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« on: December 17, 2005, 06:16:25 pm »

Lupus and Myositis

Lupus
Many persons with lupus have muscle pain (myalgia), but few have muscle weakness due to inflammation (myositis).
The "muscle weakness" that people with lupus report is most commonly due to fatigue or high doses of cortisone.

Myositis
In polymyositis-dermatomyositis, the primary problem is muscle weakness due to muscle inflammation.
Weakness especially affects:
- the hips (inability to rise from a chair or toilet seat, or to climb stairs unassisted)
- the shoulders (inability to lift a weight onto a high shelf or comb one's hair).
- typically, there is little or no pain associated with the weakness.
People with myositis also have:
- increased blood levels of creatine kinase (CK), a substance that leaks from injured muscle
- abnormal electrical activity of muscles detected by electromyogram (EMG)
- muscle biopsy showing muscle cell degeneration and inflammation that is found in a muscle biopsy.

Treatments

Prednisone or other cortisone-like drugs are most often recommended for the treatment of myositis, and may be used in combination with other immune-suppressing drugs..
Cortisone itself, in high doses, may actually cause muscle weakness of the hips and shoulders, very similar to what occurs in myositis. But in this condition, called "steroid myopathy," the CK, EMG, and the muscle biopsy do not suggest inflammation, and recovery of strength promptly follows reduction of the cortisone dose.  www.LupusMCTD.com
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« Reply #1 on: December 17, 2005, 06:18:14 pm »

Sjogren's Syndrome and Lupus
Sjogren's syndrome
Henrik Sjögren was a Swedish ophthalmologist and the first to recognize that dry eyes and dry mouth were often found in people with connective tissue diseases.

These symptoms are caused by the accumulation of immune system cells (lymphocytes) in and around tear and saliva producing glands.
The build-up of cells disturbs the function of these glands and leads to reduced production of tears and saliva.
This condition also interferes with the protective mechanisms of the eye and mouth.
Eye inflammation and ulcers of the cornea, as well as fungal infections of the mouth (thrush), occur with increased frequency in those with Sjogren's.
Rarely, a person with this disorder develops a malignancy (cancer) affecting lymphocytes (lymphoma).
Today, Sjogren's syndrome is itself accorded the status of a distinct connective tissue disorder.

Lupus
Sjogren's syndrome also occurs in some people with lupus:
They have an increased frequency of sun-sensitive rashes and Sjogren's-related blood antibodies (anti-SSA and anti-SSB antibodies).
Women with anti-SSA antibodies are at increased risk of having babies with "neonatal lupus." Symptoms in the infant can be as minor as a temporary lupus-like skin rash, or as serious as permanent damage to the electrical system of the heart which results in a very slow heart rate (complete heart block)
Treatments

The best treatments for Sjogren's syndrome include : artificial tears (usually satisfactory) and either artificial saliva (most often unsatisfactory) or a saliva stimulant such as pilocarpine and hydroxychloroquine (Plaquenil). Eye drops containing cyclosporin have also just been introduced and have significant benefit for dry eyes in some cases . Arthritis, fatigue and skin rash in people with Sjogren's is often treated with Plaquenil.

 
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« Reply #2 on: December 26, 2005, 10:50:27 am »



Lupus is a chronic disease that causes inflammation of connective tissue. The most common form of lupus affects exposed areas of the skin, while the more serious and potentially fatal form can affect many systems of the body including the kidneys. It is an autoimmune disorder, in which the immune system for unknown reasons attacks connective tissue as though it were foreign. 
« Last Edit: July 04, 2006, 01:22:24 pm by Kathy » Logged


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« Reply #3 on: January 17, 2006, 08:59:22 pm »

Raynaud's disease 
 
Overview

Raynaud's is a condition that causes some areas of your body — such as your fingers, toes, tip of your nose and your ears — to feel numb and cool in response to cold temperatures or stress. It's a disorder of the blood vessels that supply blood to your skin. During a Raynaud's attack, these arteries narrow, limiting blood circulation to affected areas.

You can have Raynaud's without any underlying disease associated with it, in which case it's called Raynaud's disease or primary Raynaud's. Or it can be part of another disease, in which case doctors may refer to it as Raynaud's phenomenon or secondary Raynaud's.

Raynaud's affects a small percentage of Americans. Women are more likely than men are to have the disorder. It's more common in people who live in colder climates.

Treatment of Raynaud's depends on its severity and the presence or absence of associated conditions. For most people, Raynaud's is more a nuisance than a disability.


Signs and symptoms

Raynaud's is more than simply having cold hands and cold feet, and it's not the same as frostbite. Signs and symptoms of Raynaud's depend on the frequency, duration and severity of the blood vessel spasms that underlie the disorder. Signs and symptoms include:

Sequence of color changes in your skin in response to cold or stress
Numb, prickly feeling or stinging pain upon warming or relief of stress
At first during an attack of Raynaud's, affected areas of your skin usually turn white. Then, the areas often turn blue and feel cold and numb, and your sensory perception is dull. The affected skin may look slightly swollen. As circulation improves, the affected areas may turn red, throb, tingle or swell. The order of the changes of color isn't the same for all people, and not everyone experiences all three colors.

Occasionally, an attack affects just one or two fingers or toes. Attacks don't necessarily always affect the same digits. Although Raynaud's most commonly affects your fingers and toes, the condition also can affect other areas of your body such as your nose, cheeks, ears and even tongue. An attack may last less than a minute to several hours. Over time, attacks may grow more severe.

People who have Raynaud's accompanied by another disease also may have symptoms related to their underlying condition.


Raynaud's disease

Raynaud's disease is a vascular disorder that causes intermittent interruption of blood flow to the extremities. The affected body part may turn white or blue and feel cold and numb until circulation ...


Causes

Doctors don't completely understand the cause of Raynaud's attacks, but blood vessels in the hands and feet appear to overreact to cold temperatures or stress.

When your body is exposed to cold temperatures, your extremities lose heat. Your body slows down blood supply to your fingers and toes to preserve your body's core temperature. Your body specifically reduces blood flow by narrowing the small arteries under the skin of your extremities. In people with Raynaud's, this normal response is exaggerated. Stress causes a similar reaction to cold in the body, and likewise the body's response may be exaggerated.

With Raynaud's, arteries to your fingers and toes go into what's called vasospasm. This constricts the vessels, temporarily but dramatically limiting blood supply. Over time, these same small arteries may also thicken slightly, further limiting blood flow. The result is that affected skin turns a pale and dusky color due to the lack of blood flow to the area. Once the spasms subside and blood returns to the area, the tissue may turn red before returning to a normal color.

Cold temperatures are most likely to provoke an attack. Exposure to cold can be as simple as putting your hands under a faucet of running cold water, taking something out of the freezer or exposure to cold air. For some people, exposure to cold temperatures isn't necessary. Emotional stress alone can cause an episode of Raynaud's.

Some researchers are studying whether Raynaud's may be partly an inherited disorder.

Primary vs. secondary Raynaud's
Raynaud's occurs in two main types:

Primary Raynaud's. This is Raynaud's without an underlying disease or associated medical problem that could provoke vasospasm. Also called Raynaud's disease, it's the most common form of the disorder. Primary Raynaud's typically affects both hands and both feet.

Secondary Raynaud's. This is Raynaud's caused by an underlying problem. Also called Raynaud's phenomenon, secondary Raynaud's usually affects both of your hands or both feet. Although secondary Raynaud's is less common than the primary form, it's often a more complex and serious disorder.
Causes of secondary Raynaud's include:

Scleroderma. Raynaud's phenomenon occurs in about 90 percent of people who have scleroderma — a rare disease that leads to hardening and scarring of the skin. Scleroderma, a type of connective tissue disease, results in Raynaud's because the disease reduces blood flow to the extremities. It causes tiny blood vessels in the hands and feet to thicken and to constrict too easily, promoting Raynaud's.

Lupus.
About one-third of Americans with lupus — an autoimmune disease that can affect many parts of your body, including your skin, joints, organs and blood vessels — develop Raynaud's. An autoimmune disease is one in which your immune system attacks healthy tissue.

Rheumatoid arthritis. Raynaud's may be an initial sign of rheumatoid arthritis — an inflammatory condition causing pain and stiffness in the joints, often including the hands and feet.

Sjogren's syndrome. Raynaud's phenomenon can also occur in people who have Sjogren's syndrome — a rare disorder that often accompanies scleroderma, lupus or rheumatoid arthritis. The hallmark of Sjogren's syndrome, a connective tissue disease, is chronic dryness of the eyes and mouth.

Diseases of the arteries. Raynaud's phenomenon can be associated with various diseases that affect arteries, such as atherosclerosis — the gradual buildup of plaques in blood vessels that feed the heart (coronary arteries), or Buerger's disease — a disorder in which the blood vessels of the hands and feet become inflamed.

Carpal tunnel syndrome. The carpal tunnel is a narrow passageway in your wrist that protects a major nerve to your hand. Carpal tunnel syndrome is a condition in which pressure is put on this nerve, producing numbness and pain in the affected hand. The affected hand may become more susceptible to cold temperatures and episodes of Raynaud's.
Repetitive trauma. Raynaud's can also be caused by repetitive trauma that damages nerves serving blood vessels in the hands and feet. In fact, nerve damage is thought to play a role in many cases of Raynaud's. Some people who type or play the piano for long periods of time or vigorously may be susceptible to Raynaud's. Workers who operate vibrating tools can develop a type of Raynaud's phenomenon called vibration-induced white finger.

Smoking. Smoking constricts blood vessels and is a potential cause of Raynaud's.
Injuries. Prior injuries to the hands or feet, such as wrist fracture, surgery, or frostbite, can lead to Raynaud's phenomenon.

Certain medications. Some drugs — including beta blockers, which are used to treat high blood pressure; migraine medications that contain ergotamine; estrogen replacement therapy; certain chemotherapy agents; and drugs that cause blood vessels to narrow, such as some over-the-counter cold medications — have been linked to Raynaud's.

Chemical exposure. Some workers in the plastics industry who are exposed to vinyl chloride develop an illness similar to scleroderma. Raynaud's can be a part of that illness.

Other causes. Raynaud's has also been linked to an overactive thyroid gland (hyperthyroidism), to a condition in which blood pressure rises in the blood vessels of the lungs (pulmonary hypertension) and, rarely, to certain cancers.
 




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« Last Edit: May 17, 2006, 06:24:27 pm by Kathy » Logged


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« Reply #4 on: February 18, 2006, 05:20:34 pm »

Hughes Syndrome
Could you have been misdiagnosed with multiple sclerosis?
 Apparently, Hughes Syndrome can easily be mistaken for Multiple Sclerosis. It shares many of the symptoms and as many as 1 in 3 people diagnosed with MS actually have Hughes Syndrome.

Hughes Syndrome is also known as Sticky Blood Syndrome although it's proper title is Antiphospholipid Syndrome (or APS). Discovered by a Dr. Graham Hughes in 1983 while treating patients for the Lupus condition. Sticky Blood can be easily treated with Aspirin, Heparin or Warfarin but, if left untreated it can be fatal. Sticky blood can lead to the formation of blood clots which can cause Thrombosis or Strokes.

The symptoms of Hughes Syndrome can be uncannily like those of MS. They may include: difficulty with walking, foot drop, double-vision, tingling sensations, slurred speech and loss of balance. I don't know about you, but this is ringing some fairly loud alarm bells with me. Like MS, Hughes Syndrome is an autoimmune deficiency and it's cause is unknown.

Read the MS Resource Centre's article or visit the Hughes Syndrome Foundation Website
 
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« Reply #5 on: March 02, 2006, 05:13:54 pm »

Key Findings in Systemic Lupus Erythematosus, Sjögren's Syndrome, and Myositis
Robert I. Fox, MD, PhD   


Systemic Lupus Erythematosus
In the ACR State-of-the-Art Lecture on SLE, Dr. Mark Walport[1] presented the intriguing review entitled "Understanding the Pathogenesis of SLE: The Garbage Disposal Hypothesis." It has recently been demonstrated that survival and homeostasis of peripheral mature T cells depend on self-recognition.
 Thus, contrary to previous assumptions, naive T cells apparently require a constant subthreshold signal provided by their engagement with self-major histocompatibility complex (MHC)/peptide ligands to persist in a quiescent state. This self-MHC/peptide recognition in healthy patients provides a proliferation-inducing signal and leads to T-cell expansion but not autoimmunity. However, under the influence of particular background genes, a self-reactive autoimmune disease develops.

Despite key advances in an understanding of immune mechanisms in animal models, our knowledge of the relevant genetic and environmental models remains incomplete. Initial efforts to attribute autoimmunity in humans or mice to simple breakdown in "central" (thymic) tolerance (either with regard to deletions of endogenous superantigen-recognizing T cells or conventional self-peptide-recognizing transgenic mice) have been unsuccessful.

Part of the problem probably involves defects in apoptotic pathways by which activated T cells undergo cell death. However, even in lupus mice that are bred without defects in the proapoptotic FAS pathway, the reasons for underlying excessive activation remain unclear.

Against this background of autoimmunity in mice, many interesting papers were presented at the recent ACR meeting in New Orleans.

Bachmann and coworkers[2] from Oklahoma presented evidence that failure to clear the products of apoptotic cells allows "subdominant" epitopes to become antigenic. Furthermore, frame shift mutations leading to an amino acid substitution in La antigen in one patient led to a loss of a nuclear binding signal and increased antigenicity of the "self-peptide."
 Although this mutation was documented in a single patient, almost 30% of SLE sera reacted with the neoantigen created in this patient. Naik and coworkers[3] from England emphasized the role of complement C1q to "bridge" these apoptosis-derived subantigenic molecules and increase their ability to be phagocytosed for antigen re-presentation. In the presence of other background lupus genes, this mechanism can perpetuate and expand autoreactive T-cell and B-cell clones.

McClain and colleagues[4] from Oklahoma presented another interesting method for generation of autoimmune B-cell clones. It appears that anti-Ro 60-kd antigen responses in SLE patients begin by targeting an epitope that cross-reacts with the Epstein-Barr nuclear antigen 1.
Thus, apoptotic fragments can expand previous immune responses directed against exogenous (ie, Epstein-Barr virus) infections. This is particularly interesting since Epstein-Barr virus is known to have "permanent" residence in the salivary glands and oropharynx of nearly all adults, with periodic exacerbation.

Thus, a variety of candidate antigens derived from apoptotic products can either "break tolerance" or clonally expand by molecular mimicry.

Ramos and coworkers[5] from Minnesota presented the results of a genome-wide search for genetic loci that could predispose to SLE. They found some overlap with previously reported loci (7p21 and 7q11). They also found some linkage with 12q4 (previously associated with multiple sclerosis) and 12q24 (associated with inflammatory bowel disease) and a new association with 15q24. Other studies by Kawasaki and colleagues[6] in Tokyo revealed a tendency to the human BLYS (BAFF/TNFSF13B) locus, including specific nucleotide changes leading to amino acid substitution in the promoter region.

Therapy for SLE
In the area of therapy, azathioprine showed a tendency toward fewer renal relapses after successful cyclophosphamide induction in diffuse proliferative glomerulonephritis, in a study by Mok and coworkers[7] from Hong Kong. The SLE malar rashes were responsive to topical 0.1% tacrolimus, which could possibly avoid the skin thinning noted with potent topical steroids (Jones and colleagues[8] from Florida). Hydroxychloroquine was found to delay the onset of full-blown SLE in patients who present with a positive antinuclear antibody (ANA) (Jonsson and coworkers[9] from Norway) and appeared to be safe in a small number of pregnant women who gave birth while receiving this medication (Costedoat and colleagues[10] of Spain).

Although thalidomide was useful in SLE rashes, neurotoxicity was noted (Cuadrado[11] of the United Kingdom). In a phase 1/2 trial involving 18 patients, anti-CD20 chimeric antibody (rituximab, 100-375 mg/m2) was evaluated throughout 4 weekly doses, with follow-up during 1 year.
Although the medication was well tolerated and patients had decreased arthralgias, there was little decrease in anti-DNA titer or improvement in complement levels (Campbell and coworkers[12] from Rochester, New York). In a novel approach to more specific targeting of B-cell therapy, Silverman and colleagues[13] from San Diego reported that protein A will selectively bind to VH3 segments and lead to apoptotic death of this subclass of B cells.

Sjögren's Syndrome
The reports on SS this year largely represented a "consolidation" of observations that had been made in past years based on reevaluation of the data from patient cohorts using the proposed new American-European consensus criteria for SS. These new criteria require either a characteristic biopsy specimen or characteristic autoantibody (ie, SS-A, Ro) in addition to significant objective findings of oral and ocular dryness. The new criteria exclude hepatitis C and other causes of dryness.

Terenzi and coworkers[14] from New York compared patients classified under the European system (EEC) and the new consensus system and found that a main difference was that patients with dryness and fibromyalgia were no longer included in the new consensus criteria. The implementation of new methods to define disease activity and response to therapy is being developed based on scales used in SLE and previous measures called "oral health quality-of-life impact measures."

Using the revised criteria, Witte and coworkers[15] from Germany found an increased frequency of IgA anti-fodrin antibodies (as well as in SLE patients), whereas a separate study of SS patients by Sibilia and colleagues[16] failed to find a significant association with antibodies directed against the fodrin 120-kd fragment that plays a critical role in one murine model of SS (the NFS/sld mouse after thymectomy).

Patients with SS may develop antibodies to a novel centromeric antigen (cen-C), and these patients also recognize SS-A (52 kd) and SS-B (45 kd), according to Pillemer and coworkers[17] of Bethesda. This novel reactivity with a centromeric antigen is distinct from the cen A/cen B, which appears to be an antigenic target in scleroderma patients and helps explain the coexistence of some patients with antibodies to SS-A and yet having an anti-centromeric pattern on their ANA test results. Anti-citrulline antibodies may be present in some SS patients (who are ANA positive and RF negative) and were associated with synovitis previously termed rheumatoid arthritis (RA).

Jonnson and colleagues[18] from Norway reported on the expression of B-cell activating factor (BAFF) in salivary glands, as well as expression of E-cadherin and its integrin ligand aEb7 on the glandular vascular cells and cells infiltrating glandular epithelial cells, respectively. An increased level of Fas and Fas L were again noted, although the level of apoptotic cells was not increased. This activation of early steps of apoptosis appears to lead to glandular dysfunction, as measured by decreased response to muscarinic agonists, even in the absence of apoptotic changes of nuclear fragmentation and cellular blebbing.

Beutler[19] (San Diego) reviewed the important role of cell signaling through TOLL-like receptors to generate apoptotic products. These pathways involve CARD and NOD motif proteins, initially recognized as important elements in the response to lipopolysacharide and now considered as potential agents in the generation of autoantigens that maintain autoimmune T cells (as discussed above).
 Although distinct from SS, it was also noted that Blau's syndrome (granulomatous uveitis that simulates sarcoidosis) results from mutations in the nod sequences and that familial Mediterranean fever derives from interleukin 1 liberated in unopposed fashion due to mutations in the pyrin gene (Kaster and coworkers,[20] Bethesda), which normally serves as a break on this inflammatory cascade.

Kapsogeorgou and colleagues[21] from Athens reported that glandular cells could release exosomal vesicles that contain potential autoantigens and thus present additional methods to maintain autoimmune T cells similar to those described above for SLE. Lavie and coworkers[22] from France reported that rank and rank ligand, members of the tumor necrosis factor (TNF) superfamily usually associated with bone remodeling, were expressed in the SS salivary gland and could potentially lead to stimulation of T cells and B cells by salivary gland ductal epithelial cells.

Grandis and colleagues[23] from Minnesota reported analysis of complementary DNA made from SS peripheral blood using a microarray of oligonucleotides corresponding to a wide spectrum of inflammatory-related markers. They found at least 2-fold differences in more than 80 genes, including those associated with FAS, protein kinase C, BAFF, and ubiquitin. During the discussion period, the limitations of using blood (a heterogeneous population) to detect small changes in transcription and assay reliability for small changes in transcription were mentioned, but this technology may be useful in monitoring clinical response in particular patients.

Depression as measured by the Center for Epidemiologic Studies--Depression scale was more common in a cohort of SS patients than in age-matched RA patients, according to Reisine and Parke[24] in Connecticut. The dryness symptoms may be further exacerbated by certain antidepressive medications, and the symptoms of dryness (in comparison to objective findings) are further exaggerated by the depression. This creates a vicious cycle for the patient with sleep deprivation and fatigue, as well as a diagnostic and therapeutic difficulty for the rheumatologist.

Sankar and colleagues[25] from Bethesda found that an elevation in serum IgM levels at presentation was associated with a serial decline in salivary gland function as measured by decreased saliva production that occurred in about half of a cohort of 46 patients followed up for 2 years, whereas surprisingly, no association was found with erythrocyte sedimentation rate or IgG levels at presentation. In long-term follow-up studies of SS patients, Quemeneur and coworkers[26] from France found progression of mild interstitial lung disease, which may have been due to aging, as measured by serial pulmonary function tests in 12 patients, for a mean of 10 years.

In a cohort of 110 patients, Ramos-Casals and colleagues[27] from Mexico found a circulating monoclonal protein in 24 patients. Although these patients had extraglandular manifestations such as purpura and pneumonitis, they did not find lymphoproliferative disease (although the length of follow-up of one patient for lymphoproliferative disease was short). In a long-term follow-up of a Greek cohort of patients by Ionnakis and coworkers,[28] purpura and low complement as well as parotid swelling at time of initial evaluation were significant predictors of development of lymphoma at 10-year follow-up.

Different aspects of therapy were presented. Dehydroepiandrosterone was not found to have significant benefit, according to Pillemer and colleagues[29] from Bethesda. Steinfeld and coworkers[30] (Amsterdam) presented favorable results from an open-label trial using infliximab (3 mg/kg) at 0.2 and 6 weeks followed by every 12 weeks in patients with at least one extraglandular manifestation (usually arthritis). These patients were not receiving concurrent methotrexate and had not previously been taking methotrexate.

With the exception of infusion reactions, Steinfeld and colleagues thought that the results were encouraging and noted that the study had now been extended to almost 100 patients with few toxic effects. However, the discussion noted that a safer medication (methotrexate) had not previously failed and that the patients showed wide variation in response (unlike the dramatic response of RA patients to infliximab). Also, the discussion pointed out the potential risks of lymphoma (increased in SS) and potential difficulty in detecting TBC (due to increased frequency of pneumonitis in this population), as well as increased risk of demyelinating disease in this population that could be exacerbated by TNF inhibitors.

Other biologic agents that may undergo trial in SS would be targeted toward B cells, including anti-CD20 (rituximab) for the hemolytic anemia or thrombocytopenia, as well as CTLA-4 Ig or anti-BAFF antibody.

Myositis
Rider and coworkers[31] from Bethesda presented the results of the International Myositis Outcomes Workshop that included 15 adult and 14 pediatric rheumatologists. Muscle strength measured by manual testing was the most important outcome with levels of improvement scored at 15% (mild) to 75% (excellent), since this function correlated with both patient and physician global assessment. Serum levels of muscle enzyme with improvement of 25% to 75% were considered important but less important than objective muscle testing. The same study group noted that extramuscular manifestations (including skin, gastrointestinal, and constitutional) correlated with muscle score and advocated the use of a visual analog scale to measure these variables.

Also of interest, dermatomyositis patients had a different HLA-DRB1 association (DR1*03) than polymyositis (DR1*07) according to Chinoy and colleagues[32] from Manchester.

Fontana and coworkers[33] from Minnesota reported that Coxsackie viral infection of mice leads to a postinfectious sequence of chronic inflammatory myopathy. This led to a lively debate about the risks and benefits of vaccination in patients with autoimmune diseases and those receiving immunosuppressive therapy.

Robin Avery[34] from Cleveland reviewed the current recommendations for vaccines (including attenuated vaccines). The general recommendations were not to use live vaccines in immunocompromised patients, but the data available for patients receiving biologic inhibitors remain incomplete. Although these patients may have suboptimal response to the vaccine, the overall benefit from vaccines against influenza appear to be justified, but varicella and mumps vaccines might be deferred (these are usually administered as combined MMR).

The current influenza vaccines are inactivated and thus differ from the swine flu vaccine of 1976 that was associated with some cases of Guillain-Barré syndrome. The issue of vaccination against smallpox and other bioterrorist agents remains unknown and specific guidelines are being developed. Other live vaccines that have been associated with neuromuscular disorders include tetanus, hepatitis B, and poliovirus; these should be used in higher-risk patients.

Avery[34] of Cleveland reviewed the data on the past proposed complications of the hepatitis B vaccine program in France (called the vaccination panic) that alleged connection of this vaccine and multiple sclerosis, noting that 2 large studies reported last year in the New England Journal of Medicine did not find any connection in large population studies. Chen and colleagues[35] from Pennsylvania reported the occurrence of arthralgias and hearing loss (ie, Cogan's syndrome) 2 weeks after anthrax vaccine. A late-breaking abstract from Brenner and coworkers[36] reviewed 183 complaints of possible anthrax vaccine-related arthritis (occurring within 30 days of vaccination). In 44 cases, they found a possible causal link to the vaccine. The arthralgias appeared self-limited and have not thus far evolved into a recurrent autoimmune disorder. Finally, subclinical myopathy after chloroquine may be more common (up to 5% of treated patients with chloroquine and less than 0.5% with hydroxychloroquine) than expected based on a serial study of 119 patients followed up by Casado and colleagues[37] from Spain.

Muscle biopsy specimens from patients with polymyositis express higher levels of interleukin 1 and TNF in clinically involved muscle than in noninvolved muscle, according to Dorf and coworkers[38] from Sweden. A particular allele in the promoter region of TNF was found by Furuya and colleagues[39] in increased frequency in Japanese myositis patients (38% compared with age-matched controls), suggesting a role for genetic predisposition to myositis.

A similar result was found among American patients, reported by Werth and coworkers[40] from Pennsylvania, who also reported polymorphisms in genes related to mannose-binding proteins that could contribute to increased cytokine levels in involved muscle in polymyositis patients. The muscle biopsy specimens are infiltrated by mature dendritic cells, TH1-type T cells that make interferon gamma and interleukin 17, according to Page and coworkers[41] in France.

In terms of therapy for chronic juvenile dermatomyositis, etanercept was well tolerated but not dramatically effective according to Miller and colleagues[42] of Chicago, whereas infliximab plus methotrexate gave more encouraging results in 3 patients described by Maillard and coworkers[43] from England. Neopterin and quinoloic acid in the urine, as measured by mass spectroscopy by Rider and colleagues[44] in Bethesda, appear to be good surrogate markers for outcome in juvenile idiopathic myositis.

The 3-year outcome results of the National Institute of Arthritis and Musculoskeletal and Skin Disease juvenile dermatomyositis registry (299 patients) were reported by Pachman and coworkers[45] from Chicago: approximately 25% of children continue to have significant weakness and, interestingly, a subset of these children developed psorias.
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« Reply #6 on: March 03, 2006, 12:49:18 pm »

From Current Opinion in Rheumatology

Musculoskeletal Manifestations and Autoimmune Diseases Related to New Biologic Agents
Posted 02/14/2006

Abstract
Purpose of Review: The anti-tumor necrosis factor agents are now widely used in the management of patients with rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis and juvenile inflammatory arthritis. One of the most common observations made during their use is the development of autoantibodies. The purpose of this paper is to review this phenomenon and its clinical implications.
Recent Findings: While the development of different autoantibodies is a common encounter, rare cases of lupus-like syndromes have been reported. On the other hand, a variety of immune-mediated clinical manifestations have been described, including vasculitis and demyelinating syndromes. Rare cases of cytopenia and non-specific lung injuries have also been reported.
Summary: While these clinical complications are rare and isolated events, clinicians must be aware of their occurrence. The experience with the anti-tumor necrosis factor agents is rather short and new, unusual immune-mediated complications may still appear. Clinicians should be prepared to recognize them.

Introduction
With the expanding use of anti-tumor necrosis factor (TNF) agents in the management of patients with different types of inflammatory arthritis, a new spectrum of biological and clinical adverse events has emerged. This review focuses on the common observation of the development of autoantibodies and its clinical implications. We also describe other immune-mediated side effects recently described during the course of anti-TNF therapy in rheumatoid arthritis (RA). The three anti-TNF agents currently available, infliximab, adalimumab and etanercept, are reviewed separately.

Infliximab
Infliximab is a chimeric monoclonal antibody directed against TNF-α. It has immunomodulatory activity leading to the development of autoantibodies and certain autoimmune syndromes. Several observations were made during the clinical trials and once the drug had been widely used in daily clinical practice.

Autoantibodies
Since the original report of the development of anti-double-stranded DNA (dsDNA) antibodies in two out of 20 patients treated with infliximab,[1] several observations of induction of autoantibodies were made, mostly without any clinical manifestations. Charles et al.[2] measured the levels of antinuclear antibodies (ANAs) and anti-dsDNA antibodies in 156 patients with RA before and after treatment with infliximab and 37 patients treated with placebo infusions.

They used three different antibody assays. Before initiation of treatment, 30 and 29%, respectively, of infliximab-treated and placebo-treated patients tested positive for ANAs. No patient tested positive for anti-dsDNA antibodies prior to therapy. In the placebo group, only one patient converted from negative to positive ANAs and none developed anti-dsDNA antibodies. The incidence of ANAs rose to 53% (82 of 156 patients) and anti-dsDNA antibodies were detected in 14% (22 of 156) by the Chritidia luciliae indirect immunofluorescence assay in the infliximab-treated group. Anti-dsDNA antibodies were of the IgM class only in all patients except in one, whose serum also contained IgG and IgA class antibodies. This particular patient was the only who developed clinical manifestations compatible with a drug-induced lupus.

Similarly, 62 patients with RA and 35 with spondylarthropathy were tested at baseline and after 30 or 34 weeks of therapy with infliximab.[3] The number of ANA-positive patients increased from 32 (52%) to 51 (82%) in the RA group and from six (17%) to 31(89%) in the spondylarthropathy group. A total of 13 patients (seven RA and six spondylarthropathy) developed new anti-dsDNA antibodies of the IgM or IgA class. No IgG antibodies were detected and none of the patients presented with lupus symptoms. A small number of patients had also anti-histone or anti-nucleosome antibodies.

In a cohort of 42 patients receiving prolonged treatment with infliximab for various rheumatic diseases, 76% developed new autoantibodies that persisted in 57%.[4] Different autoantibodies were observed, including, ANAs, anti-dsDNA antibodies, certain types of extractable nuclear antigen (anti-Sm, anti-ribonucleoprotein and anti-SSA) and rheumatoid factor. Concomitant treatment with prednisone, methotrexate or other immunosuppressive agents did not preclude the development of autoantibodies. ANAs were the earliest to appear within the fifth infusion in the majority of patients. Other autoantibodies appeared as late as the nineteenth treatment. None of the patients developed clinical manifestations of lupus.

Similar observations were made in a cohort of 125 patients with Crohn's disease treated with infliximab.[5] Seventy-one patients (57%) developed ANAs. Of the 43 patients who were tested for anti-dsDNA antibodies, 14 (33%) were positive and nine (21%) had anti-histone antibodies, of whom two presented clinical manifestations of drug-induced systemic lupus erythematosus (SLE) without major organ involvement. Anticardiolipin antibodies were also reported in association with infliximab treatment.[6]

Several hypotheses were raised to explain the production of autoantibodies. One possible mechanism is the increased presence of cytoplasmic and nuclear debris in the circulation as a result of infliximab induced cell lysis or apoptosis. It was recently demonstrated that eight out of 11 patients had higher levels of plasma nucleosomes after infliximab infusion.[7]

Systemic Lupus Erythematosus and Lupus-like Syndromes
Several case reports of lupus-like manifestations or other autoimmune symptoms have been described following infliximab treatment. They included pleural or pericardial effusions, worsening of polyarthritis and skin rashes in patients with positive ANAs and/or anti-dsDNA antibodies. Isolated cases of discoid lupus and bullous skin lesions have also been reported. No patient thus far has developed neurological or renal manifestations.

Vasculitis
In one center seven patients developed vasculitis.[8] The majority of cases involved the skin but there was one case of central nervous system vasculitis, another with mononeuritis multiplex and a third with concomitant scleritis. Of interest, five of the seven patients were receiving concomitant leflunomide. The association of vasculitis or various skin manifestations following infliximab plus leflunomide therapy has also been reported by other groups.[9,10] Some patients required corticosteroid or immunosuppressive therapy but the majority of clinical manifestations resolved after infliximab and/or leflunomide were stopped. In another report, 15 patients treated with infliximab for a variety of medical conditions developed leukocytoclastic vasculitis and some of them had confirmatory biopsy.[11**] Most of the patients recovered after drug discontinuation and one had a recurrence after rechallenge. Richette et al.[12] reported the development of a biopsy-proven necrotizing vasculitis with sensory neuropathy in one patient with RA after the sixth infliximab infusion. The patient fully recovered after corticosteroid therapy and the discontinuation of infliximab.

Other
As of August 2002, 63 cases of central demyelination, Guillain-Barré, peripheral neuropathy and polyradiculoneuropathy, and one case of transverse myelitis have been reported, which are presented in the most recent US Food and Drug Adminsitration update.[13] No cases of pancytopenia were seen during the clinical trials of infliximab; since the drug's approval, a total of 15 cases have been reported, as of September 2001.[13] Rare cases of hepatitis or non-infectious pulmonary infiltrates were also reported.
 
 ~See Part 2 For rest of Information~
 
 
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« Reply #7 on: March 03, 2006, 12:57:34 pm »

Adalimumab
Information concerning musculoskeletal manifestations of adalimumab stems from clinical trial data as of August 2002, at which time 2468 patients with RA had been treated, yielding a 4870 patient-year exposure. Through December 2003 a total of 9460 patients (9894 patient-year exposure) have been treated.

Autoantibodies
New ANAs (titre > 1:40) were observed in 12.6% of patients receiving adalimumab compared with 7.3% of placebo-treated patients.

Systemic Lupus Erythematosus and Lupus-like Syndromes
Lupus-like events have occurred in 10 patients through December 2003 giving a rate of 0.1 events/100 patient-years (Abbott Pharmaceutical, data on file). Lupus or lupus-like reactions were typically characterized by rash with positive serology. None of the 10 cases met ACR classification criteria for SLE nor met the regulatory definition of severe.

The usual course was complete recovery on discontinuing adalimumab therapy. Within the pivotal trials (793 patient-years exposure) 0.13 events/100 patient-years for SLE/lupus-like patients were observed. One patient developed features of serositis and arthritis, and positive ANAs and anti-dsDNA antibodies approx. 5 months after adalimumab therapy without renal or central nervous system involvement. The patient remitted with withdrawal of adalimumab. The post-marketing spontaneous reporting rate in the USA for SLE was 0.06/100 patient-years with an exposure of 16 860 patient-years to adalimumab treatment through December 2003.

Vasculitis
To date there are no published reports of vasculitis associated with adalimumab therapy.

Other
Within clinical trials, four cases of possible demyelination have been reported through 31 August 2002 (Abbott Pharmaceutical, data on file), including one case of optic neuritis and three cases of paresthesias - one of which had a prior diagnosis of probable multiple sclerosis and another with symptoms appearing before treatment. Three of the four cases resolved spontaneously with one patient continuing on adalimumab. Three additional cases have been reported yielding an event rate of 0.08 events/100 patient-years through 31 December 2003. Within patients treated in pivotal trials (793 patient-years exposure), 0.13 events/100 patient-years have been reported. No spontaneous post-marketing reporting reports have been made in the USA with an adalimumab exposure of 16 860 patient-years.

Rare cases of pancytopenia have been reported within the pivotal-trials treated population - 0.25 events/100 patient-years - whereas the spontaneous post-marketing reporting rate in the USA of blood dyscrasia was 0.06 events/100 patient-years. Whether these events reflect an autoimmune phenomenon is unclear.

Etanercept
Through December 2002, 3839 patients (8336 patient-years exposure) were treated in clinical trials whereas 231 000 patients (423 000 patient-years exposure; all indications) were treated.

Autoantibodies
In randomized control trials 11% of patients developed new ANAs compared to 5% with placebo. With etanercept 15% developed anti-dsDNA antibodies compared with 4% of placebo treated patients. A recent study demonstrated that prior to etanercept 18% (10/56) patients had positive anticardiolipin. After 6 months of treatment 25% of patients were positive. Increases were seen for both IgG and IgM anticardiolipin. Increasing age, a higher number of prior disease-modifying anti-rheumatic drugs and higher disease activity score (DAS) 28 were predictors of developing anticardiolipin antibodies.[14**]

Recently, several studies have compared etanercept and infliximab with respect to the induction of autoantibodies.[14**,15-17] The studies consistently demonstrated a substantial increase in autoantibody production with infliximab compared to etanercept in terms of induction of ANAs and anti-dsDNA antibodies. While one study demonstrated selectively increased IgM but not IgG anticardiolipin titers only with infliximab,[16] another study demonstrated only a slight increase in anticardiolipin antibodies with both agents.[14**] Neither infliximab nor etanercept induced other lupus-related reactivities such as anti-ENA, anti-histone, anti-smooth muscle, anti-myeloperoxidase, anti-proteinase 3 or anti-mitochondrial antibodies. Variable results were observed with anti-nucleosome antibodies with infliximab while no induction was seen with etanercept.[16,17] Anti-thyroid and anti-neutrophil cytoplasmic antibodies were rarely found in the absence of a clinical picture indicative of SLE, thryroiditis or vasculitis.[16]

Systemic Lupus Erythematosus and Lupus-like Syndromes
Shakoor et al.[18] describes four cases of SLE-like syndrome in patients treated with etanercept. Symptoms appear 6 weeks-3 months after initiation of etanercept. Clinical presentation with the four cases included fever, malaise and arthritis; discoid lupus rash; hypertension, arthritis and erythematosus facial rash; and pleuritis and malar rash. Three of the four cases were ANA and anti-dsDNA antibody-positive, whereas three cases exhibited anti-histone antibodies.

Within 2-6 weeks symptoms resolved with drug withdrawal. Brion et al.[19] reported one patient who developed a rash on etanercept, which on biopsy was diagnosed as discoid lupus. DeBandt et al.[20] also described two cases of etanercept-induced SLE in RA. In a more remote report Mohan and colleagues[21] used the US Food and Drug Administration adverse event-reporting system to identify 16 cases of new-onset SLE after etanercept use from November 1998 to February 2002, excluding Shakoor et al.'s cases. They obtained follow-up information from 13 of the 16 diagnosing physicians. Nine cases could be classified as SLE according to ACR criteria and four cases with two or three criteria as possible SLE. The median time of onset after etanercept initiation was 4 months (range 2-18 months).

Discoid rash was reported in eight cases, photosensitivity in six, and malar rash in four. No patient had renal or neurologic disorder. Five patients had elevated anti-dsDNA antibodies and four patients had anti-Sm antibodies. Of 10 patients with skin biopsies available, seven were consistent with subacute cutaneous SLE and three with discoid lupus. In 12 cases, symptoms resolved in 1-4 months after the withdrawal of etanercept and one patient improved incompletely.

Recently, two cases of biopsy-confirmed proliferative lupus nephritis and leukocytoclastic vasculitis were described in patients treated with etanercept for juvenile RA.[22,23**] Both patients had destructive joint changes, compatible with juvenile RA. Renal biopsies revealed severe hypercellularity, endocapillary proliferation wire loops and intraluminal deposits. Immunofluoresence shared positive staining for all immunoglobulin isotypes as well as C3 and Clq. Extensive electron-dense deposits were visualized by electron microscopy. The cutaneous and renal manifestations improved after etanercept withdrawal. Of note, focal proliferative lupus nephritis (Class III) was described with adalimumab.[23**]

Vasculitis
Mohan et al.[11**] summarized 28 cases of leukocytoclastic vasculitis reported with both etanercept and infliximab. The majority, 21 out of 28, resolved after stopping therapy. However, eight patients had recurrences following rechallenge.[11**] Anecdotal reports of vasculitis while receiving TNFα inhibitor have been published in patients who then received another TNF blocker without recurrence (reviewed in)[24].

The immunology of cutaneous vasculitis in a patient with Crohn's disease who developed skin lesions on etanercept, which worsened on switching to infliximab, has been described.[25] Human antichimeric antibodies were not seen but RNAs for T-helper, cytokines, chemokines and defensins as well as elevated angiogenesis factors were observed. A lymphocytic vasculitis composed of T cells was seen. Extremely high levels of chemokines and interleukin 6 were seen in a B-cell line established from the patient's peripheral blood.

Of significance, three patients have recently been described who underwent therapy with etanercept and developed new-onset renal disease with antineutrophilic cytoplasmic-associated necrotizing glomerulonephritis (n = 2)[23**,26] or membranous glomerulonephritis (n = 1) with renal vasculitis.[26] An etiologic role for anti-TNF agents is supported by the temporal relation of glomerular disease to drug use in patients with long-standing RA of many years' duration and no prior renal disease and the improvement of clinical symptoms after drug withdrawal. It is notable that one patient developed a pauci-immune focal segmental necrotizing and crescentic glomerulonephritis with infliximab.[26]

Other
The number of cases of demyelination with etanercept during the clinical trials is still unclear. Mohan et al.[27] noted 17 cases of demyelination after etanercept therapy. All neurological events were temporally related to the use of Enbrel with partial of complete resolution. One patient noted return of symptoms when therapy was tried again. The most common presenting clinical symptoms among the 20 patients were paresthesias (13 of 20) followed by visual disturbances secondary to optic neuritis (8 of 20). Other signs and symptoms included confusion (25%), gait disturbance, apraxia, facial palsy and Guillain-Barré syndrome. Four patients had multiple sclerosis. Most patients respond either partially or completely with resolution of their symptoms on halting anti-TNF.

Enbrel's post-marketing experience has demonstrated that multiple sclerosis was observed (new onset of disease) in 17 patients, when the expected number was 22.1. Similarly, no excess cases of optic neuritis were seen post-marketing since 17.3 cases were expected and 13 cases were observed.

Systemic side effects of etanercept have been reported, including aplastic anemia,[28] lung injury,[29] silent thyroiditis[30] and colitis.[31]
 

Conclusion
All three anti-TNF agents, infliximab, adalimumab and etanercept, have been associated with the induction of a variety of autoantibodies. A small number of patients developed clinical manifestations; these were usually mild and subsided after discontinuation of therapy. The occurrence of other immune-mediated complications, such as skin or systemic vasculitis, nephritis or demyelinating syndromes and, more rarely, cases of cytopenia and pulmonary infiltrates, were also reported. With the relatively short experience with the anti-TNF agents and the absence of predictive factors for complications, clinicians should be on the lookout for any new unusual manifestations in patients with RA treated with these drugs
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« Reply #8 on: March 03, 2006, 01:52:21 pm »

Rheumatology Advance Access originally published online on November 8, 2005
Disease damage and low bone mineral density: an analysis of women with systemic lupus erythematosus ever and never receiving corticosteroids

Department of Radiology, Northwestern University, Feinberg School of Medicine, Chicago, IL and 4 Department of Medicine, Division of Rheumatology and Clinical Immunology, University of Pittsburgh School of Medicine and Graduate School of Public Health, Pittsburgh, PA, USA.


Objectives. To evaluate the relationship between disease damage and bone mineral density (BMD) in women with systemic lupus erythematosus (SLE).

Methods. A cross-sectional study was conducted among 307 women with SLE. Patients attended a single clinic visit that included an interview, physical examination, laboratory testing and BMD measurements (hip and/or lumbar spine). Women were stratified by the Systemic Lupus International Collaborating Clinics/American College of Rheumatology cumulative disease damage index (SDI) 1 (Damage) vs SDI=0 (No Damage), and prior use of corticosteroids (CS), yielding four groups: (1) Damage/CS+ (n=138), (2) Damage/CS– (n=23), (3) no Damage/CS– (n=100), and (4) no Damage/CS– (n=46).

Results. Mean age at SLE diagnosis was 32.7 ± 11.8 yr, 24.4% were African American, 65.0% were premenopausal, and mean SDI ± S.D. was 1.3 ± 1.8. In the unadjusted and adjusted models controlling for significant univariate risk factors for osteoporosis, the reference group (Group 1) had significantly lower mean BMD T-scores at the hip and lumbar spine than groups having no disease damage (Groups 3 and 4) independent of CS use status. Similar hip and lumbar spine mean BMD T-scores were observed in women with disease damage with and without CS exposure (Groups 1 and 2).

Conclusions. Women with SLE having disease damage and no CS use had BMD T-scores at the hip and lumbar spine similar to those of women with disease damage and prior CS use. These findings suggest an association between disease damage and lower BMD T-scores in women with SLE. [/b] [/size]
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« Reply #9 on: March 15, 2006, 01:19:29 pm »

Medical Author: William C. Shiel Jr.,

Raynaud's phenomenon (RP) is a condition resulting in discoloration of the fingers and/or the toes after exposure to changes in temperature (cold or hot) or emotional events. Skin discoloration occurs because an abnormal spasm of the blood vessels causes a diminished blood supply to the local tissues. Initially, the digit(s) involved turn white because of the diminished blood supply. The digit(s) then turn blue because of prolonged lack of oxygen. Finally, the blood vessels reopen, causing a local "flushing" phenomenon, which turns the digit(s) red. This three-phase color sequence (white to blue to red), most often upon exposure to cold temperature, is characteristic of RP.



Raynaud's phenomenon most frequently affects women, especially in the second, third or fourth decades of life. Persons can have Raynaud's phenomenon alone or as a part of other rheumatic diseases. When it occurs alone it is referred to as "Raynaud's disease" or primary Raynaud's phenomenon. When it accompanies other diseases it is called secondary Raynaud's phenomenon.

What causes Raynaud's phenomenon?

The causes of primary and secondary RP are unknown. Both abnormal nerve control of the blood vessel diameter and nerve sensitivity to cold exposure have been suspected as being contributing factors. The characteristic color changes of the digits are in part related to initial blood vessel narrowing due to spasm of the tiny muscles in the wall of the vessels, followed by sudden opening (dilation), as described above. The small arteries of the digits can have microscopic thickness of their inner lining, which also leads to abnormal narrowing of the blood vessels.

What conditions have been associated with Raynaud's phenomenon?

Raynaud's phenomenon has been seen with a number of conditions, including rheumatic diseases (scleroderma, rheumatoid arthritis, systemic lupus erythematosus), hormone imbalance (hypothyroidism and carcinoid), trauma (frostbite, vibrating tools), medications (propranolol/Inderal, estrogens without additional progesterone, nicotine, bleomycin used in cancer treatment, and ergotamine used for headaches), and even rarely with cancers.

What are the symptoms of Raynaud's phenomenon?

Symptoms of RP depend on the severity, frequency, and duration of the blood vessel spasm. Most patients with mild disease only notice skin discoloration upon cold exposure. They may also experience mild tingling and numbness of the involved digit(s) that will disappear once the color returns to normal. When the blood vessel spasms become more sustained, the sensory nerves become irritated by the lack of oxygen, and can cause pain in the involved digit(s). Rarely, poor oxygen supply to the tissue can cause the tips of the digits to ulcerate. Ulcerated digits can become infected. With continued lack of oxygen, gangrene of the digits can occur.

Less common areas of the body that can be affected by RP include the nose, ears, and tongue. While these areas rarely develop ulcers, they can be associated with a numbness sensation and pain.

Patients with secondary RP can also have symptoms related to their underlying diseases. RP is the initial symptom of 70% of patients with scleroderma, a skin and joint disease. Other rheumatic diseases frequently associated with RP include systemic lupus erythematosus, rheumatoid arthritis, and Sjogren's syndrome. For further information, please read the Scleroderma Systemic Lupus Erythematosus and Rheumatoid Arthritis articles.

How is Raynaud's phenomenon diagnosed?

In patients with the characteristic sequence of skin color changes of the digits upon cold exposure, diagnosing RP is not difficult. Sometimes, certain patterns in the tiny blood vessels (capillaries) adjacent to the fingernails of patients with RP can be seen using a magnifying viewing instrument. Abnormal nailfold capillary patterns can suggest the possibility of an associated rheumatic condition. There is, however, no single blood test to help the doctor to confirm the diagnosis. The doctor can order certain blood tests (for example, sedimentation rate, rheumatoid factor, antinuclear antibody , thyroid hormone levels, and protein levels) to exclude associated rheumatic diseases and thyroid disorder. The doctor can also perform certain maneuvers with the patient's extremities to exclude pinched blood vessels that can produce symptoms that mimic RP, such as in thoracic outlet syndrome.

Typically patients with Raynaud's phenomenon that is a manifestation of a rheumatic disease have elevated blood sedimentation rates and antinuclear antibodies. Furthermore, capillary nail fold abnormalities can frequently be found as described above.

How is Raynaud's phenomenon treated?

Management of Raynaud's phenomenon involves protecting the fingers and the toes from cold, trauma, and infection. Medications that can aggravate blood vessel spasm should be avoided by patients with RP. In patients with persistent symptoms, medications that dilate the blood vessels can be administered.

Patients with Raynaud's phenomenon who have no symptoms other than the color changes of extremities may require only measures to prevent complications. Prevention measures are important in primary and secondary RP regardless of the severity. Simple initial care involves keeping the body warm, especially the extremities. Warm clothing in colder environments is essential. Cotton gloves can be helpful while searching the freezer. Room temperatures should not be too cool. Rubber gloves protect the hands and prevent cooling while dish washing. Barefoot walking should be minimized. Compression of the blood vessels by tight-fitting wrist bands, rings or foot wear should be avoided.

Patients should guard their hands and feet from direct trauma and wounds. Any wounds or infections should be treated early to prevent more serious infections. Avoiding emotional stresses and tools that vibrate the hand may reduce the frequency of attacks. Biofeedback can also help to decrease the severity and frequency of RP in some patients.

Direct and indirect smoking should be avoided in patients with RP. The chemicals in tobacco smoke can cause blood vessel constriction and lead to hardening of the arteries, which can further impair oxygen supply to the extremities.

Care of the nails must be done carefully to avoid injuring sensitive toes and fingertips. Ulcers on the tips of the digits should be monitored closely by the doctor. These can become infected. Gently applied finger splints are used to protect ulcerated areas. Ointments that open the blood vessels (nitroglycerin ointment) are sometimes used on the sides of severely affected digits to allow increased blood supply and healing.

Medications which can aggravate symptoms of RP by leading to increased blood vessel spasm include over-the-counter cold and weight- control preparations, such as pseudoephedrine (Actifed, Chlor-trimeton, Cotylenol, Sudafed). "Beta-blockers," medicines used for high blood pressure and heart disease, can also worsen RP. These include atenolol (Tenormin), metoprolol (Lopressor), nadolol (Corgard) and propranolol (Inderal).

Patients with persistent or bothersome symptoms may be helped by taking oral medications that open (dilate) blood vessels. These include calcium antagonists, such as diltiazem (Cardizem, Dilacor), nicardipine (Cardene), nifedipine (Procardia), and other medicines used in blood pressure treatment, such as methyldopa (Aldomet) and minipress (Prazocin). Recent research has shown that the blood pressure drug losartan (Cozaar, Hyzaar) can reduce the severity of episodes of RP even more than nifedipine.

Medications that "thin" the blood, such as low doses of aspirin or dipyridamole (Persantine) are sometimes helpful.

Some patients with persistent symptoms can benefit by adding a medication called toxifylline (Trental) which makes the red blood cells more pliable, thereby improving circulation.

Severe RP can lead to gangrene and the loss of digits. In rare cases of severe disease, nerve surgery called "sympathectomy" is sometimes considered. In order to prevent blood vessel spasming, the nerves that stimulate the constriction of the vessels (sympathetic nerves) are surgically interrupted. Usually this is performed during an operation that is localized to the sides of the base of the fingers at the hand. Through small incisions the tiny nerves around the blood vessels are stripped away. This procedure is referred to as a digital sympathectomy.

Research

Researchers have reported finding a substantial genetic (inherited) contribution both to the symptoms of RP and to the associated blood vessel changes of patients with Raynaud's phenomenon.
Other researchers are studying nitric oxide and its potential relationship to Raynaud's phenomenon. A gel is being studied which might promote local production of nitric oxide in involved digits. The local nitric oxide, it seems, may open the blood vessels and improve the impaired circulation.

Raynaud's Phenomenon At A Glance
Raynaud's phenomenon is characterized by a pale-blue-red sequence of color changes of the digits, most commonly after exposure to cold.
Raynaud's phenomenon occurs because of spasm of blood vessels.
The cause of Raynaud's phenomenon is unknown, although abnormal nerve control of blood vessel diameter and nerve sensitivity to cold are suspected of being involved.
Symptoms of Raynaud's phenomenon depend on the severity, frequency, and duration of the blood vessel spasm.
There is no blood test for diagnosing Raynaud's phenomenon.
Treatment of Raynaud's phenomenon involves protection of the digits, medications, and avoiding emotional stresses, smoking, cold temperature, and tools that vibrate the hands.
For further information about Raynaud's phenomenon, please visit the following site:

The Arthritis Foundation (http://www.arthritis.org)

Or you can write to:

The Arthritis Foundation
P.O. Box 19000
Atlanta, Georgia 30326
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« Reply #10 on: April 08, 2006, 03:56:47 pm »


Treatment: Medical
Medical treatment can be defined as the use of therapies, such as prescription medications or surgeries, that are specifically ordered and supervised by a physician. There is no universal treatment for chronic fatigue and immune dysfunction syndrome (CFIDS), but medical treatments can help specific symptoms.

Pain
Most pain relief therapy begins with over-the-counter medications such as aspirin, acetaminophen (Tylenol) or ibuprofen (Advil). If these do not bring relief, moderately severe pain may be treated with a mild narcotic. Long-acting narcotics are reserved for severe, unrelenting pain. It is generally wise to avoid narcotics because of their potentially addictive qualities, but there are cases in which they become necessary. Supportive treatments, such as meditation and biofeedback, may be quite helpful. Pain management counseling is another supplemental therapy that needs to be seriously considered.

Orthostatic Intolerance
When healthy people stand, gravity causes about 750 cc (3 ¼ cups) of blood to fall to their legs and abdomen, which results in decreased blood flow to the brain. They do not experience adverse symptoms. However, persons with orthostatic intolerance (OI) do develop symptoms while standing or sitting and may become dizzy, lightheaded and/or weak.

If a person with CFIDS (PWC) has OI , their health care provider may suggest increasing water intake to at least 2 liters per day and increasing salt intake to 10-15 grams per day. This treatment is generally safe for most people, but if a person has heart or blood vessel disease, increased fluid and fluid retention could put an extra strain on the heart and blood vessels and cause serious problems. PWCs need to discuss this treatment with their primary care providers before attempting this themselves.

If symptoms do not improve with this treatment, prescription medications that treat low blood volume, increase blood pressure or prevent blood from pooling in the legs may be tried. Other potentially helpful medications are those that block the effects of epinephrine, a naturally occurring substance in the body that acts as a mediator for body chemicals that affect smooth muscles, blood vessels and other body tissues.

Central Nervous System
Studies suggest that CFIDS is associated with decreased levels of the neurotransmitters serotonin and dopamine, which may lead to disruptive sleep, a low pain threshold, irritability and depression. Low doses of selective serotonin re-uptake inhibitors (SSRIs), such as Zoloft or Paxil, or medications that affect the release of dopamine may provide relief.

Physical Malformations
Recent studies show that in some people, CFIDS-like symptoms may be caused by a narrowing of the area where the spinal cord and brain connect.  Two defects of this area include: 1) Chiari malformation and 2) cervical stenosis. Both are potentially corrected with surgery. People with CFIDS report both successes and failures after surgery. Diagnostic tests, including specialized MRIs (magnetic resonance imaging) can be ordered for PWCs to determine if surgery is an option. Surgery facts should be discussed at length with a physician and a second opinion sought.

Mental Health
A common myth about CFIDS is that it is a form of depression, but numerous research studies have successfully revealed factual information that challenges this myth. While many PWCs do have periods of depression, it is usually secondary to CFIDS, as people learn to cope with the life changes that occur with a chronic illness. Antidepressants may be prescribed, but they are not a cure-all and must be used with caution. A supportive counselor can help PWCs deal with the family issues, anxiety, depression, grief, anger and guilt that frequently accompany chronic disorders.

Sleep Disruption
Sleep disorders are reported by a great majority of PWCs. Over-the-counter sleep aids and antihistamines, such as Tylenol PM or Benadryl, can often be used to help alleviate sleep problems. Melatonin, a natural brain hormone, induces restful sleep in some people and can be purchased over the counter. The use of over-the-counter medications should always be discussed with the PWC's primary care provider to prevent unwanted side effects.

Antidepressants and hypnotics are also used for relief of sleep difficulties. Many prescription sleep medications can be habit-forming, may increase depression or interfere with thought processes; therefore, they need to be used with care. In addition, many commonly used medications, including some antidepressants, can disrupt sleep.

Cognitive Dysfunction
Many PWCs report that cognitive dysfunction is the most distressing CFIDS symptom. Impaired memory, difficulty finding words and/or using words and numbers, abstract reasoning difficulties and altered spatial perceptions are examples of cognitive-type impairment. Some PWCs experience symptom improvement when treated with the anticonvulsant, gabapentin (Neurontin). Scientists don't really know how this medication works but it appears to "even out" the nerve messages in the brain and helps the brain to respond to impulses at a steady rate.

Immune Dysfunction
Multiple studies point to irregularities with the body's immune system as a possible cause of CFIDS. To treat the irregularities, medications called immune regulators are used. Gamma globulin (see second article under additional resources) and poly(I)-poly(C12U) (Ampligen) are two medications in this category. Gamma globulin, one of the first medications used to treat CFIDS, continues to be scrutinized for its effectiveness. PWCs who have received this treatment report variable symptom relief - it appears to help some and not others. Ampligen remains in clinical trials under the supervision of the U.S. Food and Drug Administration (FDA). Availability is limited to PWCs with access to a clinical site and the financial resources to cover the cost. Symptom improvement has been inconsistent with this therapy as well, and further research is underway.

Gastrointestinal Disorders
Many PWCs experience problems with their digestive tract, particularly with irritable bowel syndrome. Nausea; diarrhea (often alternating with constipation); abdominal, pelvic or back discomfort; passage of mucus in stools; bloating and distention are common symptoms. Symptoms are worsened by stress. Drug therapy includes antispasmodics, antidiarrheal and anti-anxiety medications. Supportive therapies focus on reducing stress and adopting a high-fiber diet.

Infections
Antibiotics, antiviral, and antifungal medications are prescribed for specific infections. Infections could possibly be determined by laboratory tests, which require a body fluid sample such as blood or saliva. A word about medications: People with CFIDS often are unusually sensitive to medications and lower than usual dosages may be necessary. Primary care providers will need to prescribe low starting doses (often much lower than what is considered to be therapeutic) and increase dosages slowly.

All medications, including over-the-counter drugs, have potential side effects. The doctor and pharmacist need to be informed of every drug the PWC is taking - even a daily multivitamin or nutritional supplement. There is always the potential for an unpleasant interaction when drugs are mixed.

Medicines should always be taken as prescribed; because one works, it doesn't necessarily mean that two will work better. The medication list found on this Web site provides a list of medicines used to treat the various symptoms of CFIDS.
 [/size] [/color]
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« Reply #11 on: April 22, 2006, 10:43:45 am »



Although many cases of lupus can be brought under control using immunosuppressive medications, there remains a subset of individuals for whom current strategies are not sufficient. In this study at Northwestern University in Chicago, 48 patients with severe lupus who did not respond to standard treatments with immune-suppressing therapies had the stem cell transplantation. 

 

The name of the procedure used is autologous hematopoietic stem cell transplantation (HSCT). Stem cells are special cells in the body which can develop into different kinds of blood cells and immune system cells. These are the cells from which the body naturally replenishes circulating blood and immune cells throughout life. In HSCT, these stem cells are withdrawn from a patient’s own bone marrow (autologous = from a person’s own body). These cells are then kept alive outside the body in a disease-free environment. Meanwhile, most of the immune system cells in the patient’s body are destroyed using high doses of chemotherapy.  The stem cells then are re-implanted in the patient in an effort to regenerate a healthier immune system.

 

Although two patients died following the procedure, half of the patients were free of lupus after as long as five years.  Study participants also had significant improvement in disease activity, lung function, and in levels of anti-DNA and complement, which can be markers of lupus activity.

 

The study results suggest some reason to pursue more research in stem cell transplantation for lupus.  The LFA wants to stress for the public that this therapy is not appropriate to consider at this time for patients who do not have life-threatening or organ-threatening illness.




Nonmyeloablative Hematopoietic Stem Cell Transplantation for Systemic Lupus Erythematosus
Richard K. Burt, MD; Ann Traynor, MD; Laisvyde Statkute, MD; Walter G. Barr, MD; Robert Rosa, MD; James Schroeder, MD; Larissa Verda, MD, PhD; Nela Krosnjar, MD; Kathleen Quigley, RN; Kimberly Yaung, RN; Marcello Villa, BS; Miyuki Takahashi, MD; Borko Jovanovic, PhD; Yu Oyama, MD


JAMA. 2006;295:527-535.

Context  Manifestations of systemic lupus erythematosus (SLE) may in most patients be ameliorated with medications that suppress the immune system. Nevertheless, there remains a subset of SLE patients for whom current strategies are insufficient to control disease.

Objective  To assess the safety of intense immunosuppression and autologous hematopoietic stem cell support in patients with severe and treatment-refractory SLE.

Design, Setting, and Participants  A single-arm trial of 50 patients with SLE refractory to standard immunosuppressive therapies and either organ- or life-threatening visceral involvement. Patients were enrolled from April 1997 through January 2005 in an autologous nonmyeloablative hematopoietic stem cell transplantation (HSCT) study at a single US medical center.

Interventions  Peripheral blood stem cells were mobilized with cyclophosphamide (2.0 g/m2) and granulocyte colony-stimulating factor (5 µg/kg per day), enriched ex vivo by CD34+ immunoselection, cryopreserved, and reinfused after treatment with cyclophosphamide (200 mg/kg) and equine antithymocyte globulin (90 mg/kg).

Main Outcome Measures  The primary end point was survival, both overall and disease-free. Secondary end points included SLE Disease Activity Index (SLEDAI), serology (antinuclear antibody [ANA] and anti–double-stranded (ds) DNA), complement C3 and C4, and changes in renal and pulmonary organ function assessed before treatment and at 6 months, 12 months, and then yearly for 5 years.

Results  Fifty patients were enrolled and underwent stem cell mobilization. Two patients died after mobilization, one from disseminated mucormycosis and another from active lupus after postponing the transplantation for 4 months. Forty-eight patients underwent nonmyeloablative HSCT. Treatment-related mortality was 2% (1/50). By intention to treat, treatment-related mortality was 4% (2/50). With a mean follow-up of 29 months (range, 6 months to 7.5 years) for patients undergoing HSCT, overall 5-year survival was 84%, and probability of disease-free survival at 5 years following HSCT was 50%. Secondary analysis demonstrated stabilization of renal function and significant improvement in SLEDAI score, ANA, anti-ds DNA, complement, and carbon monoxide diffusion lung capacity adjusted for hemoglobin.

Conclusions  In treatment-refractory SLE, autologous nonmyeloablative HSCT results in amelioration of disease activity, improvement in serologic markers, and either stabilization or reversal of organ dysfunction. These data are nonrandomized and thus preliminary, providing the foundation and justification for a definitive randomized trial.

Clinical Trial Registration  ClinicalTrials.gov Identifier: NCT00271934


Author Affiliations: Division of Immunotherapy (Drs Burt, Traynor, Statkute, Verda, Krosnjar, Takahashi, and Oyama, Mss Quigley and Yaung, and Mr Villa), Division of Rheumatology (Drs Barr and Schroeder), Division of Nephrology (Dr Rosa), and Department of Preventive Medicine (Dr Jonanovic), Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Ill. Dr Traynor is now with the Division of Hematology/Oncology, University of Massachusetts, Worcester.




RELATED ARTICLES 


This Week in JAMA
JAMA. 2006;295:469.


High-Dose Cyclophosphamide and Stem Cell Transplantation for Refractory Systemic Lupus Erythematosus
Michelle Petri and Robert Brodsky
JAMA. 2006;295:559-560.
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« Reply #12 on: April 22, 2006, 11:39:49 am »

Vardenafil Improves Blood Flow in Raynaud’s Disease
2006;166:231-233 - Archives of Internal Medicine   
 
 
Raynaud’s is a condition in which exposure to cold triggers blood vessel spasms that interrupt blood flow to the fingers, toes, ears, and/or nose. If an artery becomes blocked completely, gangrene or skin ulcers can occur. Raynaud’s is often seen in lupus patients and can be difficult to treat. This small pilot study looked at the effects on Raynaud’s of a drug for erectile dysfunction, vardenafil (Levitra®). The action of this kind of drug is to literally open up blood vessels, and it appeared in this study that vardenafil may improve both Raynaud’s symptoms and the actual blood flow in fingers and toes, both at room temperature and during cold exposure. Since this is an early study, more work will be needed to determine the safety and usefulness of this approach.
 




Phosphodiesterase Type 5 Inhibition Is a Novel Therapeutic Option in Raynaud Disease
Evren Caglayan, MD; Michael Huntgeburth, MD; Thomas Karasch, MD; Julia Weihrauch, MD; Nicolas Hunzelmann, MD; Thomas Krieg, MD; Erland Erdmann, MD; Stephan Rosenkranz, MD


Arch Intern Med. 2006;166:231-233.

Background  Raynaud disease (RD) is a common disorder affecting 3% to 5% of the healthy population, and occurs in more than 90% of patients with connective tissue diseases. The therapeutic options remain limited, particularly in patients with secondary RD due to connective tissue disease. Theoretical considerations lead to the expectation that phosphodiesterase type 5 inhibitors may improve clinical symptoms and digital blood flow in patients with RD.

Methods  We conducted an open-label pilot study in 40 patients with RD, 33 (82%) of whom had secondary and 7 (18%) of whom had primary RD. Digital blood flow was measured by laser-Doppler flowmetry at room temperature and during the cold-exposure test before medical treatment, 1 hour after the initial intake, and after 2 weeks of continuous treatment (10 mg twice a day) with the novel phosphodiesterase type 5 inhibitor vardenafil. Clinical symptoms were recorded by a patient questionnaire and summarized as the Raynaud condition score.

Results  Laser-Doppler flowmetry revealed that vardenafil improved digital blood flow in 28 (70%) patients, whereas 12 (30%) did not respond. In individuals responding, digital blood flow significantly increased by a mean ± SEM of 21.0% ± 4.9% and 30.0% ± 5.7% at 1 hour and 2 weeks of treatment at room temperature, respectively, and by 18.8% ± 4.4% and 35.1% ± 7.5% at 1 hour and 2 weeks during the cold-exposure test, respectively (P < .01 for all). Consistently, clinical symptoms improved in 27 (68%) of the 40 patients, and the Raynaud condition score declined from a mean ± SEM of 5.05 ± 0.38 to 3.54 ± 0.31 (P < .001).

Conclusion  Our data indicate that phosphodiesterase type 5 inhibition significantly improves peripheral blood flow and clinical symptoms in a large subset of patients with RD and, thus, may provide a novel therapeutic approach in such individuals.


Author Affiliations: Klinik III für Innere Medizin (Drs Caglayan, Huntgeburth, Karasch, Erdmann, and Rosenkranz) and Klinik und Poliklinik für Dermatologie (Drs Weihrauch, Hunzelmann, and Krieg), Universität zu Köln, Köln, Germany. 
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« Reply #13 on: May 02, 2006, 06:20:26 pm »

Systemic Lupus Erythematosus (Lupus) 

What is lupus?
Systemic lupus erythematosus, also known as SLE, or simply lupus, is a disease that is characterized by periodic episodes of inflammation of and damage to the joints, tendons, other connective tissues, and organs, including the heart, lungs, blood vessels, brain, kidneys, and skin. The heart, lungs, kidneys, and brain are the organs most affected. Lupus affects each individual differently and the effects of the illness range from mild to severe. Lupus can potentially be fatal.

The majority of people who have lupus are young women (late teens to 30s). This may be due to the fact that estrogen (a female hormone) seems to be associated with lupus. Lupus affects more African-Americans, Asian Americans, Latinos, and Native Americans than Caucasian Americans. Lupus in children occurs most often at the age of 10 and older; lupus is rare in children younger than 5 years of age.

The disease is known to have periods of flare-ups and periods of remission (partial or complete lack of symptoms). Children with lupus can have a large degree of kidney involvement. The severity of the kidney involvement can alter the survival rate of patients with lupus. In some cases, kidney damage is so severe it leads to kidney failure.

What causes lupus?
Lupus is an autoimmune disorder, which means the body's immune system attacks its own healthy cells and tissues.

Lupus is considered to be a multifactorial condition. Multifactorial inheritance means that "many factors" are involved in causing a health problem. The factors are usually both genetic and environmental, where a combination of genes from both parents, in addition to unknown environmental factors, produce the trait or condition. Often one gender (either males or females) is affected more frequently than the other in multifactorial traits. Multifactorial traits do recur in families because they are partly caused by genes. Females are affected with lupus three to ten times more often than males.

A group of genes on chromosome 6 codes for the HLA (human leukocyte antigens) antigens which play a major role in susceptibility and resistance to disease. Specific HLA antigens influence the development of many common disorders, many that are autoimmune related and are inherited as multifactorial traits. When a person has the specific HLA antigen type associated with the disease, they may have a genetic susceptibility to have the condition and be more apt to develop it. The HLA antigen associated with lupus is called DR2 and DR3. It is important to understand that a person without these antigens may also develop lupus, so that HLA antigen testing is not diagnostic or accurate for prediction of the condition.

**What is the immune system?
The purpose of the immune system is to keep infectious microorganisms, such as certain bacteria, viruses, and fungi, out of the body, and to destroy any infectious microorganisms that do invade the body. The immune system is made up of a complex and vital network of cells and organs that protect the body from infection.

When the immune system does not function properly, a number of diseases can occur. Allergies and hypersensitivity to certain substances are considered immune system disorders. In addition, the immune system plays a role in the rejection process of transplanted organs or tissue. Other examples of immune disorders include the following:

autoimmune diseases, such as juvenile diabetes, rheumatoid arthritis, and anemia


immunodeficiency diseases, such as acquired immunodeficiency syndrome (AIDS) and severe combined immunodeficiency (SCID)

What are the symptoms of lupus?
Lupus symptoms are usually chronic and relapsing. The following are the most common symptoms of lupus. However, each individual may experience symptoms differently. Symptoms may include:

malar rash - a rash shaped like a butterfly that is usually found on the bridge of the nose and the cheeks.


discoid rash - a raised rash found on the head, arms, chest, or back.


fever


inflammation of the joints


sunlight sensitivity


hair loss


mouth ulcers


fluid around the lungs, heart, or other organs


kidney problems


low white blood cell or low platelet count


Raynaud's phenomenon - a condition in which the blood vessels of the fingers and toes go into spasm when triggered by factors such as cold, stress, or illness.


weight loss


nerve or brain dysfunction


anemia
The symptoms of lupus may resemble other medical conditions or problems. Always consult your physician for a diagnosis.

How is lupus diagnosed?
Lupus is difficult to diagnose because of the vagueness of the symptoms each person might have. There is no single test that can diagnose lupus. A diagnosis is usually confirmed based on a complete medical history, reported symptoms, and a physical examination that may include the following:

blood test (to detect for certain antibodies that are present in most people with lupus)


blood and urine tests (to assess kidney function)


complement test (to measure the level of complement, a group of proteins in the blood that help destroy foreign substances; low levels of complement in the blood are often associated with lupus)


x-rays - a diagnostic test which uses invisible electromagnetic energy beams to produce images of internal tissues, bones, and organs onto film.
Further, the American College of Rheumatology created a set of criteria to assist physicians in making a diagnosis of lupus. The individual must have four of the 11 specific criteria to be diagnosed with lupus. It is important to remember that having some of the following symptoms does not mean that lupus is the diagnosis. The criteria include the following:

malar rash - a rash shaped like a butterfly that is usually found of the bridge of the nose and the cheeks.


discoid rash - a raised rash usually found on the head, arms, chest, or back.


sunlight sensitivity


mouth ulcers


inflammation of the joints


heart or lung involvement


kidney problems


seizures or other neurological problems


positive blood tests


changes in normal blood values
Treatment for lupus:
There is no cure for lupus. Specific treatment for lupus will be determined by your physician based on:

your age, overall health, and medical history
extent of the condition
your tolerance for specific medications, procedures, and therapies
expectation for the course of the disease
specific organs that are affected
your opinion or preference
If lupus symptoms are mild, treatment may not be necessary, other than possibly nonsteroidal anti-inflammatory medications (NSAIDs) for joint pain. Other treatment may include:

hydroxychloroquine, quinacrine, chloroquine, or a combination of these medications


corticosteroids (to control inflammation)


immunosuppressive medication (to suppress the body's autoimmune system)


liberal use of sunscreen, decreased time outdoors between 10:00 a.m. and 4:00 p.m., and wearing hats and long sleeves when outdoors, as about one-third of persons with lupus have the tendency to develop a rash in the sun


rest, including at least eight to 10 hours of sleep at night; naps and breaks during the day


stress reduction


well-balanced diet


immediate treatment of infections

Children with lupus should not receive immunizations with live viruses, including chickenpox, MMR (measles, mumps, rubella), and oral polio vaccines. Consult your child's physician regarding all vaccines.
 
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« Reply #14 on: May 08, 2006, 08:05:16 pm »

Sjögren's Syndrome
A chronic, systemic inflammatory disorder of unknown cause, characterized by dryness of the mouth, eyes, and other mucous membranes and often associated with rheumatic disorders sharing certain autoimmune features (eg, RA, scleroderma, SLE) and in which lymphocytes infiltrate mucosal and other tissues.

Sjögren's syndrome (SS) is more common than SLE but less common than RA. An association has been found between HLA-DR3 antigens and primary SS in whites. Other genetic factors may be important in other ethnic groups.

Pathophysiology, Symptoms, and Signs
SS may affect only the eyes or mouth (primary SS, sicca complex, sicca syndrome), or generalized collagen vascular disease (secondary SS) may be present. Arthritis occurs in about 33% of patients and is similar in distribution to that in RA; however, joint symptoms in primary SS tend to be milder and rarely lead to destruction. Some patients with undiagnosed SS who have rheumatic symptoms may not complain of sicca complex; SS is then diagnosed by laboratory evaluation.

Salivary and lacrimal glands become infiltrated with CD4+ T cells and with some B cells. The T cells produce inflammatory cytokines (eg, interleukin-2, -interferon). Salivary gland duct cells also produce cytokines, eventually damaging the secretory ducts. Atrophy of the secretory epithelium of the lacrimal glands causes desiccation of the cornea and conjunctiva (keratoconjunctivitis sicca--see Ch. 96). This most often produces a scratchy or irritated sensation. In advanced cases, the cornea is severely damaged, epithelial strands hang from the corneal surface (keratitis filiformis), and vision can be impaired.

One third of SS patients develop enlarged parotid glands that are usually firm, smooth, of fluctuating size, and mildly tender. Chronic salivary gland enlargement is rarely painful. Lymphocytic infiltration and intraductal cellular proliferation in the parotid gland cause luminal narrowing and eventual formation of compact cellular structures termed epimyoepithelial islands. When salivary glands atrophy, saliva diminishes, resulting in extreme dryness of the mouth and lips (xerostomia) that inhibits chewing and swallowing and promotes tooth decay and formation of calculi in the salivary ducts. Taste and smell may be diminished.

Dryness may also develop in the skin and in mucous membranes of the nose, throat, larynx, bronchi, vulva, and vagina. Dryness of the respiratory tract may lead to lung infections and sometimes to pneumonia. Alopecia may occur.

GI effects (eg, dysphagia) are associated with mucosal or submucosal atrophy and diffuse infiltration by plasma cells and lymphocytes. Chronic hepatobiliary disease and pancreatitis (exocrine pancreatic tissue is similar to that of salivary glands) may occur. Fibrinous pericarditis is an occasional complication. Sensory neuropathy is common. CNS vasculitis may also occur with SS. About 20% of SS patients have renal tubular acidosis; in many, renal concentrating ability is decreased. Interstitial nephritis is common, but glomerulonephritis is unusual. Patients with parotid enlargement, splenomegaly, and lymphadenopathy may have pseudolymphoma or malignant lymphoma. The incidence of lymphoma is increased 44-fold for SS patients, who are also at increased risk for Waldenström's macroglobulinemia.

Diagnosis
The eye is tested for dryness. The Schirmer test measures the quantity of tears secreted in 5 min in response to irritation from a filter paper strip placed under each lower eyelid. A young person normally moistens 15 mm of each paper strip. Because hypolacrimation occurs with aging, 33% of normal elderly persons may wet only 10 mm in 5 min. Most persons with SS moisten < 5 mm in 5 min, although about 15% of test results are false-positive and 15% are false-negative. Ocular staining with a drop of rose bengal solution into the eye is highly specific. In SS, the portion of the eye filling the palpebral aperture takes up the dye, and red triangles with their bases toward the limbus are seen. Slit-lamp examination is also useful.

Salivary glands can be further evaluated by salivary flow, sialography, and salivary scintiscanning. Biopsy of the readily accessible labial minor salivary glands confirms the diagnosis when multiple large foci of lymphocytes with atrophy of acinar tissue are seen.

Immunologic reactivity, detected in blood serum, is characteristic of SS; most patients have elevated levels of antibodies against -globulin (RF), nuclear protein, and many tissue constituents. Precipitating antibodies to nuclear antigens (identified by immunodiffusion analysis), termed SS-B antibodies, are frequently present but are not specific for primary SS. RF is present in > 70% of cases, ESR is elevated in 70%, 33% have anemia, and 25% have leukopenia and eosinophilia. Urinalysis may show proteinuria, reflecting interstitial nephritis.

Prognosis and Treatment
Prognosis in SS is often related to the associated connective tissue disorder, although the disease is chronic and death may also occasionally result from pulmonary infection and, rarely, from renal failure or lymphoma. There is no specific treatment for the basic process. Local manifestations can be treated symptomatically.

Ocular symptoms: See Keratoconjunctivitis Sicca in Ch. 96.

Oral complications: Dryness that promotes ductal calculi and rampant dental caries may be avoided by sipping fluids throughout the day, chewing sugarless gum, and using a saliva substitute containing carboxymethylcellulose as a mouthwash. Drugs that decrease salivary secretion (eg, antihistamines, other anticholinergics) should be avoided. Fastidious oral hygiene and regular dental visits are essential. Calculi must be promptly removed, preserving viable salivary tissue. The temporary pain of suddenly enlarged salivary glands is best treated only with analgesics. Pilocarpine can be used to stimulate salivary production if glands are not severely atrophied.

Connective tissue involvement: Because connective tissue involvement usually is mild and chronic, corticosteroids and immunosuppressive drugs are indicated only occasionally (eg, in severe vasculitis or visceral involvement). Irradiation and drugs that increase the risk of lymphoproliferative disorders and infections should be avoided.
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« Reply #15 on: May 08, 2006, 10:30:46 pm »

Saliva Management

Acetylcholine - A key chemical in nerve cells that acts as a messenger for transmitting nerve impulses across the body.

Acid Reflux/GORD - Commonly referred to as GORD, (Gastro Oesophageal Reflux Disease) a condition in which the liquid content of the stomach regurgitates (backs up, or refluxes) into the oesophagus, often creating a burning sensation for the individual

Amylase - An enzyme that helps to break starch down into sugar

Autonomic Nervous System - The autonomic nervous system automatically (without voluntary control) regulates the functioning of structures such as the heart, the smooth muscles (e.g., the muscles of the intestinal tract), and the glands.

Brainstem - The lowest part of the brain which merges with the spinal cord and sends and receives information from the spinal cord and peripheral nerves. The brainstem influences basic processes such as alertness, breathing, blood pressure, and heart rate.

Buccal Cavity - The area of the mouth outside the teeth while inside the inner cheek and lips.

Chemotherapy - A drug treatment given for cancer aimed at destroying the cancerous cells. It is usually a systemic treatment, meaning that the drugs flow through the bloodstream to nearly every part of the body.

Electrolyte - A substance that conducts the electrical current activity in the body.

Enzymes - Proteins that act to trigger or speed a specific chemical reaction

Facial Nerve (CNVII) - The seventh cranial nerve (nerve of the brain). It is responsible for supplying the muscles of facial expression, movement of the larynx in the throat and several salivary glands (submandibular, sublingual).

Glossopharyngeal Nerve CN IX - The ninth cranial nerve (nerve of the brain). It in responsible for supplying taste information from the tongue, movement of larynx and pharynx in the throat, and one of the salivary glands (the parotid gland).

Medulla - The lowest section of the brainstem.

Mucous - A viscous, slippery secretion produced by mucous secreting membranes and glands. Contains white blood cells, mucin and other substances.

Myelin - The fatty substance that covers and protects nerves.

Mylohyoid Muscle - A flat triangular muscle on each side of the mouth that connects and forms the floor of the mouth

Neurological - Referring to the nerves or the nervous system.

Parasympathetic Nerves - These nerves are the part of the Autonomic Nervous System that send impulses (messages) directed towards conserving and restoring the body's energy.

Parotid gland - The largest of the three major glands that produce saliva. It's location is in front and below the ear and behind the jaw bone.

Radiotherapy - The use of high-energy rays to destroy cancer cells, stopping them from growing and dividing. It is a local treatment that affects cancer cells only in the treated area.

Serous - A thin, watery fluid

Sjogren's Syndrome - An autoimmune disease in which exocrine (mucous-producing) glands become infected and inflamed, leading to gradual loss of lubrication throughout the body. Symptoms include dry eyes, dry mouth and diseases of the connective tissues such as rheumatoid arthritis (a disease involving chronic inflammation of the joints).

Sublingual Gland - The smallest of the three major glands that produce saliva. It is located underneath the tongue in the floor of the mouth close to the midline.

Submandibular Gland - The second largest of the three major glands that produce saliva. It is located deep to the mandible (jaw bone).

Superior Salivatory Nucleus - Located in the medulla in the brainstem, it is the starting point of specific nerves. It contains nerve cell bodies that receive information from areas of the body and send impulses to the Submandibular and Sublingual glands.

Sympathetic Nerves - The nerves in the Autonomic Nervous System that prepare the body for an emergency. They send impulses (messages) to the heart and lungs, muscles of blood vessel walls, hair follicles, glands and digestive and reproductive organs.
 
 


 
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« Reply #16 on: May 08, 2006, 11:06:08 pm »

What is Saliva and where is it made?

Saliva is made by salivary glands that are found in the underlying tissues of our mouths. The basic unit of salivary glands are clusters of cells called acini. These cells secrete a fluid that contains water, electrolytes, mucus and enzymes all of which flow out into a series of collecting ducts.
The main salivary glands are the:
1.Parotid glands
2.Submandibular glands
3.Sublingual glands

Each gland is found in symmetrical pairs in the head. Each gland has a tube shaped duct that carries the saliva produced into the mouth. There are also smaller saliva-producing glands that are dotted throughout the mouth and contribute to the overall amount of saliva produced.


How the glands make Saliva
The type of nerve system that controls saliva production is the autonomic nervous system, which controls both the volume and type of saliva secreted15. The secretion of saliva by each gland is controlled by two different types of nerves; sympathetic and parasympathetic nerves.

The parasympathetic nerve supply is most active during the day, whilst eating and creates more watery, or serous saliva; predominantly produced by the parotid gland, and partly by the submandibular gland.

The parasympathetic system turns up the flow of saliva by releasing a chemical, acetylcholine, which stimulates the glands to make more saliva. If these glands get diseased, damaged, or affected by drugs, they may not make enough saliva, leading to dry mouth .

The sympathetic nerve supply produces predominantly thicker mucous saliva mainly by the sublingual and partly the submandibular glands. This may occur when in certain situations, fear, stress or anger are aroused. This is also the case during hard physical exercise.

The Parotid gland
The Parotid glands are the largest of the glands and lie between the back of the jaw and each ear1 and secretes about 25% of the total saliva amount at rest2. Each gland is surrounded by a hard capsule called the parotid capsule. The parotid mainly produces watery, or serous saliva. It's duct opens in the mouth just opposite the crown of the 2nd upper molar tooth. The gland's productions are predominantly controlled by a nerve called the Glossopharyngeal Nerve (CN IX) which originates in the superior salivatory nucleus of the medulla in the brainstem. For a more detailed description of neuroanatomy and function related to saliva

The Submandibular Gland
The submandibular glands are of intermediate size and lie just inside the lower-back parts of the mandible (jaw) in the floor of the mouth. A part of the gland curls inwards around the mylohyoid muscle. The submandibular produces most of the saliva at rest (about 60%)4 and its ducts are 5cm long, emptying underneath the tongue at the floor of the mouth. The type of saliva produced is both serous and mucous saliva: the amount of each is altered depending on which nerves (parasympathetic or sympathetic) are in control.

The submandibular gland is innervated predominantly by the facial nerve (CNVII). The nerve fibres begin in the superior salivatory nucleus in the pons of the brainstem. More information

The Sublingual Glands
The sublinguals are the smallest glands and are located just under the floor of the mouth, above the mylohyoid muscle. You can feel it as a ridge under your tongue. These secrete around 5% of total saliva at rest and produces mainly mucous saliva secreting glands, although some serous saliva is also produced. It's major and minor ducts also empty at the at the floor of the mouth in a row along with the submandibular duct2. The nerve controlling sublingual production follows the same pathway as the nerve controlling the submandibular gland


Where does Saliva go?
Saliva is primarily involved at the beginning of the swallowing process.

When food is placed before the nose or eyes, the sight and smell of food stimulates the autonomic nervous system which in turn sends messages to the glands instructing them to produce saliva. The saliva created is secreted into the mouth. It is mixed up with the food and swallowed.

Why have Saliva?
Saliva has many uses within the human body. It primarily:

Begins digestion
The enzyme Amylase in saliva begins the process of the breaking down of carbohydrates of food in the mouth.
Lubricates the tongue and lips for smooth and clear articulation of speech
Protects the lining of the mouth from damage caused by abrasive foods and objects
Assists with acidity levels in the digestive tract. Bicarbonate ions regulates the pH levels in the mouth and eosphagus
Acts as a solvent so that substances in the mouth can be tasted.
Maintains a clean and hygienic mouth Carries anti-bacterial agents (immunoglobulins). They destroy micro-organisms and remove toxic substances
Influences on saliva production
The general pattern of saliva production is that it is greater during the day than at night and when upright rather than lying down. However, from person to person, the production of saliva can vary . Many external and internal elements can influence saliva production:

Mood (eg. Anxiety, depression)
Gender. Evidence has shown that males produce greater amounts and rates of flow of saliva than females.
Age. Although there is conflicting evidence in regards to this, several studies have found that the prevalence of oral dryness increases with aging and that the resting flow rate of saliva decreases with age.
The amount of water you drink. Reducing bodywater content may lead to less saliva flow at rest.
Chewing. It is generally agreed that chewing creates more whole saliva flow, particularly of the parotid secretions and thus serous saliva. Nerve endings or receptors (periodontal mechanoreceptors) ascertain the force and frequency of chewing and feedback the information so that the amount of saliva secreted from the parotid is adapted accordingly
Taste. Research has found that saliva contains specific proteins that are growth factors that make taste buds develop and mature. Without these growth factors, taste buds degenerate. Decreased salivary flow results in a clinically significant oral imbalance that may manifest as altered taste sensation.
Smoking. Saliva production may be increased.
Sight of Food. It is commonly thought that saliva is produced upon the sight of food.
Facts and Figures
Most mature salivary glands produce about 600mls per day. Resting or unstimulated whole saliva is produced at a rate of 0.3-0.5ml/minute while stimulated saliva is 1.0-3 ml/minute.
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« Reply #17 on: May 10, 2006, 11:34:39 am »

**I went searching for information Re: I keep expeirancing with my mouth burning, especially my tongue. ~Kathy

By: Cheryl Guttman 
Dermatology Times 
 

New Orleans — Xerostomia can complicate the diagnosis and management of various oral diseases and is an important condition to recognize and treat, said Susan L. Zunt, D.D.S., M.S., at the 63rd Annual Meeting of the American Academy of Dermatology, here.


Dr. Zunt
 
"Many physicians do not realize the impact of dry mouth on oral diseases and may also not be aware that it can often be successfully treated using medications to restore salivary flow," according to Dr. Zunt, professor of oral pathology and chair, oral pathology, medicine and radiology, Indiana University School of Dentistry, Indianapolis.

She adds that while artificial saliva substitutes may be a more familiar management technique, pharmacologic restoration of salivary flow with prescription medications provides a better, more comfortable option for patients. She explains that in patients who present with burning mouth syndrome, xerostomia needs to be included in the differential diagnosis.

"About 20 percent of patients with burning mouth syndrome have dry mouth that has not been previously diagnosed, and those individuals often get better if treated with a salivary flow stimulant," Dr. Zunt observes.


Patient experienced burning tongue for 15 months. The condition was unresponsive to gabapentin and clonazepam, but resolved with medication to restore salivary function. Photo: Susan L. Zunt, D.D.S, M.S.
 
Also, patients with oral conditions such as recurrent aphthous ulcers, painful geographic tongue, candidiasis, erosive lichen planus, cicatricial pemphigoid and CREST may not respond as expected to usual interventions if they have untreated salivary gland hypofunction. Comorbid xerostomia may also increase the risk of developing oral yeast infections in patients who are receiving steroid treatment for their oral disease.

Making the diagnosis The presence of xerostomia may be suggested by history and examination of the oral cavity. However, accurate diagnosis of salivary gland hypofunction requires sialometry — a simple, in-office test that measures saliva flow rate over a five-minute period.

"Sialometry should be performed if there is no pool of saliva in the floor of the mouth. However, it is important to be aware that patients with an oral infection or erosive lesions might have stimulated flow and they should be tested or retested after the mouth is healed," Dr. Zunt says.

Unstimulated sialometry is performed when the patient has been fasting for at least an hour. Patients identified as having abnormally low salivary flow are then tested with stimulated sialometry to determine if there is functional salivary gland tissue present, indicating the patient may be a candidate for treatment with salivary gland stimulating medications.

In the unstimulated test, Dr. Zunt uses a result of 0.1 ml/min to diagnose salivary gland hypofunction. However, a value of 0.2 ml/min is also recommended in the literature.

"Both of these measures are indicative of a very low amount of saliva flow, but I prefer using the more stringent 0.1 ml/min rate so that I can be more certain the patient has salivary gland hypofunction. However, there are times when I will go on to salivary stimulation testing in patients with a higher flow rate if they also have marked signs and symptoms of xerostomia, such as oral discomfort, high dental caries rate or frequent oral yeast infections," she says.

The stimulated salivary flow rate test is performed by applying citric acid to the tongue, chewing unflavored paraffin, or after a test dose of secretagogue. Patients in whom saliva production increases are considered candidates for salivary stimulant treatment. However, even patients who have advanced destruction of salivary gland tissue, such as secondary to previous head and neck radiation therapy or in association with various autoimmune diseases, and who do not show any response in the stimulated testing may still be given a trial with a salivary stimulant.

"Since the sialometry is performed over such a short period of time, I am willing to start some patients on a three-month trial and see if they benefit based on assessment of clinical endpoints, such as improvement in problems with oral infections, dental decay, comfort, and ease of swallowing and speech," she says.

In all patients, re-evaluation for response to a salivary stimulant is not performed for three months because it can take that long for maximum subjective benefit to be achieved.

Medications used for stimulating salivary flow are muscarinic cholinergic agonists and include pilocarpine (Salagen, MGI Pharma) and cevimeline (Evoxac, Daiichi). The usual doses are pilocarpine 5 mg to 7.5 mg three to four times daily and cevimeline 30 mg three times daily.

Both agents have minimal side effects and are fairly well-tolerated. Sweating is the most commonly occurring adverse event, although it can usually be minimized by having the patient take the medication with food and a full glass of water and usually does not necessitate treatment discontinuation.

Some patients should not be treated with cholinergic agonist drugs, particularly those experiencing recent (six months) myocardial infarction or stroke, acute iritis, narrow angle closure glaucoma, uncontrolled asthma or known hypersensitivity to the medication.

Lifelong treatment As there is no cure for salivary gland hypofunction, patients who start and respond to salivary stimulation treatment should expect to continue on chronic maintenance therapy. For optimal saliva production, it is also important that patients be well-hydrated, and so they should be instructed to drink eight glasses of water a day.

Patients with salivary gland hypofunction who are just starting steroid treatment for another oral disease might also be started on an antimicrobial mouthwash to protect against the development of candidiasis.

Dr. Zunt has been a lecturer for continuing education courses sponsored by Daiichi Pharmaceuticals (Evoxac, cevimeline) and MGI Pharma (Salagen, pilocarpine).
 
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« Reply #18 on: June 03, 2006, 04:43:59 pm »

Preventing a Lupus Flare

Your doctor has put together a treatment plan that is designed specifically for you and your lupus. This probably includes physical and emotional rest, aggressive treatment of infections, good nutrition, and avoidance of direct sunlight and other sources of ultraviolet light. Your doctor may have also prescribed medications to control disease symptoms and other health problems that you might have. One of the most important ways you can help yourself is to understand your treatment plan and the things you need to do to keep your disease under control.

Sometimes, despite the treatment plan and your efforts, you may experience a lupus flare. A flare is a worsening of symptoms that signals increased disease activity. A variety of factors can cause a flare, and you should contact your doctor immediately if you suspect a flare is developing. The doctor will evaluate your condition and take steps to control the seriousness of the flare. He or she will also reevaluate your overall treatment plan and make any needed changes.

Warning Signs of a Flare  bflyfever

Increased fatigue
A new or higher fever
Increased pain
Development or worsening of a rash
Upset stomach
Headache or dizziness
Development of symptoms you haven’t had before
What Triggers a Flare?

A flare can be triggered by one factor or a combination of factors.
The most common are

overwork or not enough rest;
stress or an emotional crisis;
exposure to sunlight or other sources of ultraviolet light;
infection;
injuries or surgery;
pregnancy or the time right after the baby’s birth (the postpartum period);
sudden stopping of medications for lupus;
sensitivities or allergies to items that you put on your skin, such as hair dye, hair permanent solution, makeup, and skin creams;
certain prescription drugs;
over-the-counter medications, such as cough syrup or laxatives; and
immunization
Caring For Yourself

Learn to recognize the warning signals of a flare and tell your doctor about them.


Maintain your physical health. Be sure to visit your doctor regularly, even if you are feeling well. Schedule regular dental, eye, and gynecological exams.


Get enough sleep and rest. Be flexible with your schedule of daily activities.


Try to limit your stress. Because this may be hard to do at times, consider developing a plan for dealing with potentially stressful situations. Develop a support system that includes family, friends, medical or nursing professionals, community organizations, and support groups. Remember, it helps to talk to someone when you’re feeling stressed.


Participate in a well-planned exercise program to help you maintain physical fitness and reduce stress.


Eat a healthy diet.


Limit your exposure to the sun and other sources of ultraviolet light, such as fluorescent or halogen lights.


Tell your doctor right away about any injury, illness, or infection or if you do not feel well in any way.


Delay elective surgery (including dental surgery and teeth pulling) until your lupus is under control or in remission.


Lupus may cause problems for a pregnant woman and her baby. As a result, women with lupus should carefully plan any pregnancy. Do not stop using your method of birth control until you have discussed the possibility of pregnancy with your doctor and he or she has determined that you are healthy enough to become pregnant.


Talk with your doctor before you stop taking any prescribed medications.


Check with your doctor or nurse before taking any over-the-counter medications.


Be careful when trying any over-the-counter preparations used on your skin or scalp. First, determine whether you have a sensitivity or an allergy to it. Put a small amount of the preparation on the inside of your forearm or on the back of your ear. If any redness, rash, raised areas, itching, or pain develops, do not use the preparation.


Be aware that certain prescription drugs may trigger a flare. Tell any doctor, nurse, or health care professional you visit that you have lupus. Also tell your lupus doctor or nurse if any new medications have been prescribed for you.


Be sure to check with your lupus doctor before receiving any immunization. Routine immunizations, including those for the flu and pneumonia, are an important part of maintaining your health, and you should get them if your doctor approves.
 
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« Reply #19 on: June 09, 2006, 09:58:51 am »

Definition
A great deal of debate has surrounded the issue of how best to define CFS. In an effort to resolve these issues, an international panel of CFS research experts convened in 1994 to draft a definition of CFS that would be useful both to researchers studying the illness and to clinicians diagnosing it. In essence, in order to receive a diagnosis of chronic fatigue syndrome, a patient must satisfy two criteria:

Have severe chronic fatigue of six months or longer duration with other known medical conditions excluded by clinical diagnosis; and
Concurrently have four or more of the following symptoms: substantial impairment in short-term memory or concentration; sore throat; tender lymph nodes; muscle pain; multi-joint pain without swelling or redness; headaches of a new type, pattern or severity; unrefreshing sleep; and post-exertional malaise lasting more than 24 hours.

The symptoms must have persisted or recurred during six or more consecutive months of illness and must not have predated the fatigue.

The 1988 chronic fatigue syndrome (CFS) working case definition (Holmes, et al) did not effectively distinguish CFS from other types of unexplained fatigue. For this reason, it was decided during a 1993 meeting of CFS investigators to develop a logical revision of that definition. The ensuing effort led to the 1994 definition. Following years of use of the 1994 definition a working group prepared the following document:

Identification of ambiguities in the 1994 chronic fatigue syndrome research case definition and recommendations for resolution.
This publication addresses problems in applying the 1994 CFS Research Case Definition and recommends an approach to guide systematic reproducible application of the case definition in research studies. The article should also be helpful to health care professionals who care for persons with CFS.



Other Commonly Observed Symptoms in CFS

In addition to the eight primary defining symptoms of CFS, a number of other symptoms have been reported by some CFS patients. The frequencies of occurrence of these symptoms vary from 20% to 50% among CFS patients. They include abdominal pain, alcohol intolerance, bloating, chest pain, chronic cough, diarrhea, dizziness, dry eyes or mouth, earaches, irregular heartbeat, jaw pain, morning stiffness, nausea, night sweats, psychological problems (depression, irritability, anxiety, panic attacks), shortness of breath, skin sensations, tingling sensations, and weight loss. These symptoms do not contribute to the diagnosis of CFS



Basic Facts




Chronic fatigue syndrome, or CFS, is a debilitating and complex disorder characterized by profound fatigue that is not improved by bed rest and that may be worsened by physical or mental activity. Persons with CFS most often function at a substantially lower level of activity than they were capable of before the onset of illness. In addition to these key defining characteristics, patients report various nonspecific symptoms, including weakness, muscle pain, impaired memory and/or mental concentration, insomnia, and post-exertional fatigue lasting more than 24 hours. In some cases, CFS can persist for years. The cause or causes of CFS have not been identified and no specific diagnostic tests are available. Moreover, since many illnesses have incapacitating fatigue as a symptom, care must be taken to exclude other known and often treatable conditions before a diagnosis of CFS is made.



Definition of CFS

A great deal of debate has surrounded the issue of how best to define CFS. In an effort to resolve these issues, an international panel of CFS research experts convened in 1994 to draft a definition of CFS that would be useful both to researchers studying the illness and to clinicians diagnosing it. In essence, in order to receive a diagnosis of chronic fatigue syndrome, a patient must satisfy two criteria:

Have severe chronic fatigue of six months or longer duration with other known medical conditions excluded by clinical diagnosis; and
Concurrently have four or more of the following symptoms: substantial impairment in short-term memory or concentration; sore throat; tender lymph nodes; muscle pain; multi-joint pain without swelling or redness; headaches of a new type, pattern or severity; unrefreshing sleep; and post-exertional malaise lasting more than 24 hours.
The symptoms must have persisted or recurred during six or more consecutive months of illness and must not have predated the fatigue.

Similar Medical Conditions

A number of illnesses have been described that have a similar spectrum of symptoms to CFS. These include fibromyalgia syndrome, myalgic encephalomyelitis, neurasthenia, multiple chemical sensitivities, and chronic mononucleosis. Although these illnesses may present with a primary symptom other than fatigue, chronic fatigue is commonly associated with all of them.



Other Conditions That May Cause Similar Symptoms

In addition, there are a large number of clinically defined, frequently treatable illnesses that can result in fatigue. Diagnosis of any of these conditions would exclude a definition of CFS unless the condition has been treated sufficiently and no longer explains the fatigue and other symptoms. These include hypothyroidism, sleep apnea and narcolepsy, major depressive disorders, chronic mononucleosis, bipolar affective disorders, schizophrenia, eating disorders, cancer, autoimmune disease, hormonal disorders*, subacute infections, obesity, alcohol or substance abuse, and reactions to prescribed medications.



Other Commonly Observed Symptoms in CFS
In addition to the eight primary defining symptoms of CFS, a number of other symptoms have been reported by some CFS patients. The frequencies of occurrence of these symptoms vary from 20% to 50% among CFS patients. They include abdominal pain, alcohol intolerance, bloating, chest pain, chronic cough, diarrhea, dizziness, dry eyes or mouth, earaches, irregular heartbeat, jaw pain, morning stiffness, nausea, night sweats, psychological problems (depression, irritability, anxiety, panic attacks), shortness of breath, skin sensations, tingling sensations, and weight loss.




Risk Factors for CFS

People of every age, gender, ethnicity and socioeconomic group can have CFS.
CFS affects women at four times the rate of men.
Research indicates that CFS is most common in people in their 40s and 50s.
Although CFS is much less common in children than in adults, children can develop the illness, particularly during the teen years.


Defining CFS Symptoms

CFS is marked by extreme fatigue that has lasted at least six months; is not the result of ongoing effort; is not substantially relieved by rest; and causes a substantial reduction in daily activities.
In addition to fatigue, CFS includes eight characteristic symptoms:
postexertional malaise (relapse of symptoms after physical or mental exertion);
unrefreshing sleep;
substantial impairment in memory/concentration;
muscle pain;
pain in multiple joints;
headaches of a new type, pattern or severity;
sore throat; and
tender neck or armpit lymph nodes.
Symptoms and their consequences can be severe. CFS can be as disabling as multiple sclerosis, lupus, rheumatoid arthritis, congestive heart failure and similar chronic conditions. Symptom severity varies from patient to patient and may vary over time for an individual patient.


Diagnosis of CFS

There are no physical signs that identify CFS
There are no diagnostic laboratory tests for CFS.
People who suffer the symptoms of CFS must be carefully evaluated by a physician because many treatable medical and psychiatric conditions are hard to distinguish from CFS. Common conditions that should be ruled out through a careful medical history and appropriate testing include mononucleosis, Lyme disease, thyroid conditions, diabetes, multiple sclerosis, various cancers, depression and bipolar disorder.
Research conducted by the Centers for Disease Control and Prevention (CDC) indicates that less than 20% of CFS patients in this country have been diagnosed.


Treatment of CFS

Since there is no known cure for CFS, treatment is aimed at symptom relief and improved function. A combination of drug and nondrug therapies is usually recommended.
No single therapy exists that helps all CFS patients.
Lifestyle changes, including prevention of overexertion, reduced stress, dietary restrictions, gentle stretching and nutritional supplementation, are frequently recommended in addition to drug therapies used to treat sleep, pain and other specific symptoms.
Carefully supervised physical therapy may also be part of treatment for CFS. However, symptoms can be exacerbated by overly ambitious physical activity. A very moderate approach to exercise and activity management is recommended to avoid overactivity and to prevent deconditioning.
Although health care professionals may hesitate to give patients a diagnosis of CFS for various reasons, it’s important to receive an appropriate and accurate diagnosis to guide treatment and further evaluation.
Delays in diagnosis and treatment are thought to be associated with poorer long-term outcomes. For example, CDC’s research has shown that those who have CFS for two years or less were more likely to improve. It’s not known if early intervention is responsible for this more favorable outcome; however, the longer a person is ill before diagnosis, the more complicated the course of the illness appears to be.


Recovery from CFS

CFS affects each individual differently. Some people with CFS remain homebound and others improve to the point that they can resume work and other activities, even though they continue to experience symptoms.
Recovery rates for CFS are unclear. Improvement rates varied from 8% to 63% in a 2005 review of published studies, with a median of 40% of patients improving during follow-up. However, full recovery from CFS may be rare, with an average of only 5% to 10% sustaining total remission.


Possible Causes of CFS

Despite an intensive, nearly 20-year search, the cause of CFS remains unknown. Many different infectious agents and physiologic and psychological causes have been considered, and the search continues.
Much of the ongoing research into a cause has centered on the roles of the immune, endocrine and nervous systems may play in CFS. More recently, interactions among these factors are under evaluation.
Genetic and environmental factors may play a role in developing and/or prolonging the illness, although more research is needed to confirm this. CDC is applying cutting-edge genomic and proteomic tools to understand the origins and pathogenesis of CFS.
CFS is not caused by depression, although the two illnesses often coexist, and many patients with CFS have no psychiatric disorder.

Symptoms  What's the clinical course of CFS?


Chronic fatigue syndrome can be misdiagnosed or overlooked because its symptoms are common to other many disorders. Fatigue, for instance, is found in hundreds of illnesses. The nature of the symptoms, however, can help distinguish CFS from other illnesses.


Primary Symptoms

As the name chronic fatigue syndrome suggests, this illness is accompanied by fatigue. However, it's not the kind of fatigue we experience after a particularly busy day or week, after a sleepless night or after a single stressful event. It's a severe, incapacitating fatigue that isn't improved by bed rest and that may be worsened by physical or mental activity. It's an all-encompassing fatigue that results in a dramatic decline in both activity level and stamina.

People with CFS function at a significantly lower level of activity than they were capable of prior to becoming ill. The illness results in a substantial reduction in occupational (work-related), personal, social or educational activities.

The fatigue of CFS is accompanied by characteristic symptoms lasting at least six months. These symptoms include:

difficulties with memory and concentration
problems with sleep
persistent muscle pain
joint pain (without redness or swelling)
headaches
tender lymph nodes
increased malaise (fatigue and sickness) following exertion
sore throat


Other Symptoms

The symptoms listed above are the symptoms used to diagnose this illness. However, many CFS patients may experience other symptoms, including:

irritable bowel
depression or psychological problems (irritability, mood swings, anxiety, panic attacks)
chills and night sweats
visual disturbances (blurring, sensitivity to light, eye pain)
allergies or sensitivities to foods, odors, chemicals, medications or noise
brain fog (feeling like you're in a mental fog)
difficulty maintaining upright position, dizziness, balance problems or fainting


It's important to tell your health care professional if you're experiencing any of these symptoms. They may be related to CFS, or they may indicate that you have another treatable disorder. Only a health care professional can diagnose CFS.


What's the clinical course of CFS?

The severity of CFS varies from patient to patient, with some people able to maintain fairly active lives. For most symptomatic patients, however, CFS significantly limits work, school and family activities.

While symptoms vary from person to person in number, type and severity, all CFS patients are functionally impaired to some degree. CDC studies show that CFS can be as disabling as multiple sclerosis, lupus, rheumatoid arthritis, heart disease, end-stage renal disease, chronic obstructive pulmonary disease (COPD) and similar chronic conditions.

CFS often follows a cyclical course, alternating between periods of illness and relative well-being. Some patients experience partial or complete remission of symptoms during the course of the illness, but symptoms often reoccur. This pattern of remission and relapse makes CFS especially hard for patients to manage. Patients who are in remission may be tempted to overdo activities when they're feeling better, which can actually cause a relapse.

The percentage of CFS patients who recover is unknown, but there is some evidence to indicate that the sooner a person is treated, the better the chance of improvement. This means early diagnosis and treatment are important.


Treatment Options

Coping with CFS
Common Difficulties
Professional Counseling
Cognitive Behavioral Therapy (CBT)
Alternative Therapies
Support Groups
Recent Articles
Managing Activity and Exercise
Avoiding Extremes
Developing an Exercise Program
Severely Ill Patients
Introduction

Managing chronic fatigue syndrome can be as complex as the illness itself. There is no cure yet, no prescription drugs have been developed specifically for CFS, and symptoms vary considerably over time. These factors complicate the treatment picture and require you and your health care team to constantly monitor and frequently revise treatment strategies.

It may take some time to find a combination of traditional and alternative therapies that works for you, but it’s important not to delay symptom management. For instance, untreated sleep problems can actually make other symptoms—like pain and memory problems—worse.

One key to managing CFS is working with your doctor and other health care practitioners to create an individualized treatment program for you. This program should be based on a combination of therapies that address coping techniques, symptoms and activity management.

A multidisciplinary team of health care professionals working together to develop this individualized care plan is ideal. This team might include physicians and other primary care professionals, mental health professionals, rehabilitation specialists and physical or exercise therapists. Other professionals, like a sleep therapist or dietician, can be added as needed, and you may only need one or two consultations with such specialists.

If you live in an area where you don’t have access to specialists, or if your insurance professional doesn’t cover such consultations, you can still work with your primary care professionals to develop an effective treatment plan.


Coping with CFS
Living with chronic fatigue syndrome can be difficult. Like other debilitating chronic illnesses, CFS can have a profound impact on daily life, requiring patients to make significant lifestyle changes and adapt to a series of new limitations.

Common Difficulties

Common difficulties for CFS patients include problems coping with:
the severe, changing and unpredictable symptoms of varying severity
a decrease in stamina that interferes with activities of daily living
memory and concentration problems that seriously impact work or school performance
an uncertain prognosis that makes it hard to plan for the future
loss of independence, livelihood and economic security
alterations in relationships with family and friends
worries raising children
concerns about the potential impact of decreased sexual activity on intimate relationships
skepticism and misconceptions about the illness
Feelings of anger, guilt, anxiety, isolation and abandonment are common in CFS patients. While it's normal to have such feelings, unresolved emotions and stress can make symptoms worse, interfere with pharmacological therapies and make recovery harder. It's important for patients to acknowledge the life-altering changes imposed by their illness and to develop effective coping strategies to deal with these changes.


Professional Counseling
Consulting a trained professional will help most patients build effective coping skills. A supportive counselor can help you cope with the prospects of long-term illness, as well as the anxiety, depression, grief, anger and guilt that often accompany chronic illness. A competent therapist, using problem-solving techniques and standard psychotherapy and counseling methods, can help you work through these issues. In some cases, a therapist may recommend a combination of medication and psychotherapy.
Because chronic illnesses like CFS impact the entire family, not just the patient, you may want to consider family education and counseling. Consulting a behavioral health professional may be helpful to address changes in family dynamics related to living with CFS.


Cognitive Behavioral Therapy (CBT)
Cognitive behavioral therapy, or CBT, is often prescribed to help chronically ill patients cope with illness and develop behaviors and strategies that help alleviate symptoms. It has been successful in helping patients with cardiovascular disease, diabetes and cancer, and recent studies indicate that CBT can be useful in treating some CFS patients.
CBT is frequently prescribed as part of therapeutic process; it help patients learn to manage activity levels, stress and symptoms. Optimally, CBT can help you better adapt to the impact of CFS and improve your level of function and quality of life.


Alternative Therapies
Deep breathing and muscle relaxation techniques, massage and healing touch, and movement therapies like stretching, yoga and tai chi can be beneficial for some CFS patients in reducing anxiety and promoting a sense of well-being.

Be sure to discuss all potential alternative therapies with your health care professional since many so-called cures and treatments for CFS that are promoted on the Internet are unproven and could be dangerous.


Support Groups

Many people with CFS find it therapeutic to meet with other people who have this illness. Support groups can provide patients with useful, current information, and they can provide a sense of community with people who understand what you're going through.

For information on how to select a support group, what kinds of groups to avoid and how to find a group in your area, click here.

Managing Activity and Exercise
Avoiding Extremes


For patients with CFS, learning to manage activity levels is key to managing the illness itself. This requires a new way of defining exercise. While vigorous aerobic exercise is beneficial for many chronic illnesses, CFS patients can't tolerate traditional exercise routines. Exercise programs aimed at optimizing aerobic capacity are not recommended.
The majority of people with CFS are affected by postexertional malaise, which is defined as an exacerbation of symptoms following physical or mental exertion, with symptoms typically worsening 12-48 hours after activity and lasting for days or even weeks. It's important, however, not to avoid activity and exercise altogether. Such avoidance leads to serious deconditioning and can actually worsen other symptoms. It's also important not to engage in an endless "push-crash" cycle in which patients do too much, crash, rest, start to feel a little better, do too much again, and so on.

Instead, CFS patients must learn to pace activities and work with their health care professionals to create an individualized exercise program that focuses on interval activity or graded exercise. The goal is to balance rest and activity to avoid both deconditioning from lack of activity and flare-ups of illness due to overexertion. Effective activity management may help improve mood, sleep, pain and other symptoms so patients can function better and engage in activities of daily living.


Developing an Exercise Program


It is imperative that any activity plan be started slowly and increased gradually. When beginning an activity program, some CFS patients may only be able to exercise for as little as a few minutes Patients who are severely deconditioned or who are caught in the "push-crash" cycle should limit themselves to the basic activities of daily living - getting up, personal hygiene, dressing, essential tasks - until they have stabilized.

Several daily sessions of brief, low-impact activity can then be added. Simple stretching and strengthening exercise using only body weight for resistance is a good starting place for most people with CFS. All exercise needs to be followed by a rest period at a 1:3 ratio, exercising for one minute, then resting for three minutes. These sessions can be slowly increased by one to five minutes a week as tolerance develops.

Daily exercise can be divided into two or more sessions to avoid symptom flare-ups. Activity should be intermittent, brief, spread throughout the day and followed by rest. If patients experience a worsening of symptoms, they should return to the most recent manageable level of activity.

Strength and conditioning exercises are an important component of the overall activity program. Standard rehabilitative methods, such as resistance training and flexibility exercises, may help improve stamina and function, increase strength and flexibility, reduce pain and increase range of motion.

Activity should begin slowly with simple stretching and strengthening exercises. Examples of functional exercises include repeated hand stretches, sitting and standing, wall push-ups or picking up and grasping objects. Patients can begin with a set of two to four repetitions, building to a maximum of eight repetitions. Once this stage is mastered, resistance band exercises can be added to build strength and flexibility. Patients should be careful to adhere to the principle of brief intervals of exercise, followed by adequate rest, to avoid postexertional malaise.


Severely Ill Patients

A subset of people with CFS are so severely ill that they're largely housebound or bedbound. They require special attention, including a modified approach to exercise. Hand stretches and picking up and grasping objects may be all that can be managed at first. Gradually increasing activity to the point patients can handle essential activities of daily living-getting up, personal hygiene and dressing-is the next step.
A realistic goal with severely ill patients is focusing on improving flexibility and minimizing the impact of deconditioning so they can increase function enough to manage basic activities.




« Last Edit: June 09, 2006, 10:09:18 am by Kathy » Logged


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« Reply #20 on: June 10, 2006, 09:05:43 am »

~NOTE I get asked alot about the differences of Fibro and CFS versus Lupus and other Mixed Connective Tissues Disorders. To  help dispell the myth Re: Fibro  & CFS being the same as Lupus & MCTD, Fibro & CFS are not autoimmune disorders. Please read the following article:

What are autoimmune diseases?
Our bodies have an immune system that protects us from disease and infection. But if you have an autoimmune disease, your immune system attacks itself by mistake, and you can get sick. Autoimmune diseases can affect connective tissue in your body (the tissue which binds together body tissues and organs). Autoimmune disease can affect many parts of your body, like your nerves, muscles, endocrine system (system that directs your body’s hormones and other chemicals), and digestive system.

Who is at risk for getting autoimmune diseases?

Most autoimmune diseases occur in women, and most often during their childbearing years. Some of these diseases also affect African American, American Indian, and Latina women more than white women. These diseases tend to run in families, so your genes, along with the way your immune system responds to certain triggers or things in the environment, affect your chances of getting one of these diseases. If you think you may have an autoimmune disease, ask your family members if they have had symptoms like yours. The good news is that if you have an autoimmune disease, there ARE things you can do to feel better!

What are the most common symptoms of autoimmune diseases?
There are more than 80 types of autoimmune diseases. Learning the symptoms of some of the more common autoimmune diseases can help you recognize the signs if you get one. But some autoimmune diseases share similar symptoms. This makes it hard for doctors to find out if you really have one of these diseases, and which one it might be. This can make your trip to doctors long and stressful. But if you are having symptoms that bother you, you need to persist to make sure you get relief.

Below are descriptions of some common autoimmune diseases.Disease Symptoms Tests to help find out if you have it

Hashimoto’s thyroiditis (underactive thyroid)  tiredness
depression
sensitivity to cold
weight gain
muscle weakness and cramps
dry hair
tough skin
constipation
sometimes there are no symptoms
 blood test for thyroid stimulating hormone (TSH)
 
Graves’ disease (overactive thyroid) insomnia (not able to sleep)
 irritability
weight loss without dieting
heat sensitivity
sweating
fine brittle hair
weakness in your muscles
light menstrual periods
bulging eyes
shaky hands
sometimes there are no symptoms
 blood test for thyroid stimulating hormone (TSH)
 
Lupus  swelling and damage to the joints, skin, kidneys, heart, lungs, blood vessels, and brain
“butterfly” rash across the nose and cheeks
rashes on other parts of the body
painful and swollen joints
sensitivity to the sun
 exam of your bodylab tests (antinuclear antibody [ANA] test, blood tests, and urine tests)
 
Multiple sclerosis (MS)  weakness and trouble with coordination, balance, speaking, and walking
paralysis
tremors
numbness and tingling feeling in arms, legs, hands, and feet
 exam of your body
exam of your brain, spinal cord, and nerves (neurological exam)
x-ray tests (magnetic resonance imaging [MRI] and magnetic resonance spectroscopy [MRS])
other tests on the brain and spinal cord fluid to look for things linked to these diseases
 
Rheumatoid arthritis inflammation begins in the tissue lining your joints and then spreads to the whole joint (hand joints are the most common site, but it can affect most joints in the body)
muscle pain
deformed joints
weakness
fatigue
loss of appetite
weight loss
becoming confined to bed in severe cases
 blood tests may show that you have anemia (when your body does not have enough red blood cells) and an antibody called rheumatoid factor (RF). (Some people with RF never get this disease, and others with the disease never have RF.)
 

 Are chronic fatigue syndrome and fibromyalgia autoimmune diseases?
Chronic fatigue syndrome (CFS) and fibromyalgia (FM) are not autoimmune diseases, but they often have symptoms—like being tired all the time and pain—that may seem like other autoimmune diseases.


CFS can cause you to be very tired, have trouble concentrating, feel weak, and have muscle pain. Symptoms of CFS come and go. The cause of CFS is not known.
FM is a disorder with symptoms of widespread muscle pain, fatigue (feeling tired and having low energy), and multiple tender points. Tender points are located in the neck, spine, shoulders, hips, and knees and are painful when pressure is applied to them. FM mainly occurs in women of childbearing age, but children, the elderly, and men are sometimes diagnosed with FM. The cause is not known.

What are flare ups?
Symptoms of autoimmune diseases can come and go, ranging in how bad they are, or all go away for a while (called remission). Flare-ups, or the sudden and severe onset of symptoms, can also happen. It’s best to work closely and often with your doctor and other members of your health care team to manage your illness. If you have a flare-up, it is best to first call your doctor. Don’t try a “cure” you heard about from a friend or relative.

Are there medicines to treat autoimmune diseases?
You can take medicines to help your symptoms, which your doctor(s) will talk with you about. The type of medicine you take depends on which disease you have and what your symptoms are. Some people can take over-the-counter drugs, like aspirin and ibuprofen for pain. Others with more severe symptoms may have to take certain kinds of prescription drugs that can help with pain, swelling, depression, anxiety, sleep problems, fatigue, or rashes. You also might be able to take medicine to help slow the progress of your disease. New treatments for autoimmune diseases are being studied all the time.

How can I manage my life now that I have an autoimmune disease?
Although there is no cure for autoimmune diseases, you can treat your symptoms and learn to manage your disease, so you can enjoy life! Women with autoimmune diseases lead full, active lives. Your life goals should not have to change. It is important, though, to see a doctor who specializes in these types of diseases.

What are some things I can do to feel better?
If you are living with an autoimmune disease, there are things you can do each day to feel better:

Eat a healthy diet. Keep your immune system as healthy as can be! The list of nutrients that you need for a healthy immune system is long. But don’t try to overload on vitamins because that could be worse for your health. Try to get all you need from food, rather than from vitamin pills. Eat balanced meals with foods from all of the food groups. Include yummy fruits and vegetables and whole grains. Also eat calcium-rich foods, such as fat-free or low-fat milk and yogurt. Avoid fatty foods.

Get regular exercise (but be careful not to overdo it). Thirty minutes most days of the week is best, but talk with your doctor about what types of exercise you can do. A gradual and gentle exercise program often works well for people with long-lasting muscle and joint pain. Some types of yoga or tai chi exercises may be helpful.

Get enough rest. Rest allows your body tissues and joints the time they need to repair. Sleeping is a great way you can help both your body and mind. If you don’t get enough sleep, your stress level and your symptoms could get worse. You also can’t fight off sickness as well when you sleep poorly. With enough sleep, you can tackle your problems better and lower your risk for illness. Try to get at least seven hours of sleep every night.
Reduce stress and try “self” pain management. You also might be able to lessen your pain or muscle spasms and deal with other aspects of living with your disease if you try meditation or self-hypnosis. You can learn to do these through self-help books, tapes, or with the help of an instructor. You also can use imagery (use the power of your thoughts to “destroy” your pain) or distract your focus on your pain by doing a hobby or something else you enjoy.
You have some power to lessen your pain!
Try using imagery for 15 minutes, two or three times each day.
 
Put on your favorite calming music.
Lie back on your favorite chair or sofa. Or if you are at work, sit back and relax in your chair.
Close your eyes.
Imagine your pain or discomfort.
Imagine something that confronts this pain and watch it “destroy” the pain.
 
 

 

What kinds of doctors will I need to treat my autoimmune disease?

Juggling your health care needs among different doctors and other types of health care providers can be hard. But visiting other types of health care workers, along with your main doctor, may be helpful in managing some symptoms of your autoimmune disease. If you are visiting many types of health care workers, make sure you have a supportive main doctor to help you. Often, your family doctor may help you coordinate care. Here are some other kinds of health care workers that may be useful.

Nephrologist. A doctor who will look at how well your kidneys are working. Kidneys are organs that clean the blood and produce urine.

Rheumatologist. A doctor who specializes in arthritis and other diseases.

Endocrinologist
. A doctor who specializes in diseases that affect your glands (organs in your body that make hormones). Glands help control the body’s reproduction, energy levels, weight, food and waste production, and growth and development.

Physical therapist. A health care worker who can help you with stiffness, weakness, restricted body movement, and with finding out the proper level of exercise for your body.

Occupational therapist. A health care worker who can help you find devices or make changes in your home or workplace to make life easier for you. They also can teach you ways to do all you have to despite your pain and other health problems.

Speech therapist. A health care worker who can be helpful for people with MS who have speech problems.

Vocational therapist. A health care worker who offers job training for people who cannot do their current jobs because of their illness or other health problems. You can find this type of person through both public and private agencies.
 
Counselor for emotional support. A health care worker who is specially trained to help you to find ways to cope with your illness. You can work through your feelings of anger, fear, denial, and frustration.

Support groups.
Some women find that talking with others who have the same health problem is helpful in finding new ways to cope with it.

Chiropractor.
A type of doctor who might be helpful in relieving some of your symptoms, such as muscle spasms and backaches. But you should only see this type of doctor along with your regular autoimmune disease doctor, not in place of him or her.

For More Information . . .
For more information about autoimmune diseases, contact the National Women’s Health Information Center at 1-800-994-9662 or the following organizations:

National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), NIH, HHS
Phone: (877) 226-4267
Internet Address: http://www.nih.gov/niams

National Institute of Neurological Disorders and Stroke (NINDS), NIH, HHS
Phone: (800) 352-9424
Internet Site: http://www.ninds.nih.gov

American Autoimmune Related Diseases Association (AARDA), Inc.
Phone: (800) 598-4668
Internet Address: http://www.aarda.org

Lupus Foundation of America (LFA), Inc.
Phone: (800) 558-0121
Internet Site: http://www.lupus.org

Thyroid Foundation of America (TFA), Inc.
Phone: (800) 832-8321
Internet Address: http://www.tsh.org
« Last Edit: June 10, 2006, 09:42:50 am by Kathy » Logged


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« Reply #21 on: June 17, 2006, 11:05:46 am »

WHAT IS MYOSITIS?

Myositis literally means 'inflammation of the muscles'.  This term covers a number of related illnesses including Dermatomyositis, Polymyositis, Juvenile Dermatomyositis/Polymyositis and Inclusion Body Myositis. These diseases fall under the classification of 'autoimmune' diseases, in that they are the result of abnormal immune responses (which the body would normally use to fight off diseases) attacking normal tissues - in this instance, the muscles.  Thankfully these diseases are very rare and to date no-one really knows what causes them.

As these diseases affect the muscles and connective tissues of the body, the main symptom is muscular weakness, which may be progressive and can be severely disabling, affecting in the majority of cases the whole body.  People of any age and sex can develop 'Myositis', and depression and a general feeling of misery can frequently ensue. These diseases are not catching and there is no way to predict who may become affected.

They can usually be suppressed by drugs which often have side effects which can promote worrying problems of their own. Often patients need physiotherapy to prevent muscle shrinkage and to keep them mobile. As yet there is no true cure for the disease, but some patients can go into partial or complete remission. Some fortunately do get better, but for the majority it is a case of coping with the disease and trying to live as near a normal life as possible. The less fortunate may need a wheelchair, particularly whilst the disease is at its height.

Polymyositis and Dermatomyositis are related illnesses affecting muscle and connective tissues of the body. Joints may also occasionally be involved. A rarer form of Polymyositis is known as Localised Nodular Myositis. The most serious and very rare form of disease is Inclusion Body Myositis.  In Polymyositis, the main problems are weakness and inflammation of the muscles. (‘Poly’ means many, ‘myo’ means muscle, ‘itis, means inflammation.)

In Dermatomyositis, the problems are similar to Polymyositis but also include skin rashes. (‘Derma’ means skin.)

Localised Nodular Myositis is a condition appearing in single muscle or muscle groups where painful tender lumps can be felt.

Inclusion Body Myositis is usually progressive and very difficult to treat.

In most of these conditions, the voluntary muscles undergo degenerative changes due to inflammation. The main symptom of these diseases is muscular weakness, which may be progressive and can be severely disabling. Initially it is not usually painful in children and noticeable weakness may develop gradually over several months.

Because Polymyositis and Dermatomyositis affect individuals differently, they are probably caused by several factors. These diseases are often referred to as being autoimmune diseases. This means that it they are a result of a defect in the immune system, which is the body’s natural defence against disease.

 For example, in healthy people, the immune system attacks the bacteria and viruses that cause disease. In people with an autoimmune disease, there is a defect in the immune system that causes it to turn against the body’s own tissues. Other doctors feel that autoimmunediseases such as Polymyositis and Dermatomyositis may be caused by a virus or the combination of a viral infection and defective immune system.

These diseases can vary greatly from patient to patient, and few cases are identical and follow the same pattern. Some people may have had the disease for months or even years before it is noticed. However, the majority find within weeks they have developed muscular weakness. This is sometimes accompanied by pain and tenderness especially in adults.

The large muscles about the hips and shoulders are usually the first to be affected. The weakness results in difficulty in walking, lifting arms and getting up from the sitting and lying down positions. There may even be some trouble in swallowing and the voice may become nasal in quality. Other muscles sometimes affected are those in the neck making if difficult to raise the head when lying down. Depression and a general feeling of misery particularly in children, is very noticeable and can be an indication of the disease before any sign of muscle weakness.

The diseases can affect people of any age and sex. It affects about twice as many women as men in adult life. In children the ratio is equal. Although the condition affects adults and children, the childhood form possibly has different underlying causes and behaves very differently from the adult form. Children can be expected to make a complete recovery. However, it is a rare disease in any of its forms.

So! There is no evidence to suggest it can be transmitted to other people as an infection. The disease is also not inherited, and as yet there is no way one can predict who in the general population will be affected.

The muscular weakness in Dermatomyositis is accompanied by a patchy, dusky red rash, medically termed, an ‘erythematous’ rash. It usually appears over the cheeks, about the eyes, where it can be violet in colour particularly over the eyelids, on the neck, shoulder, and upper chest. It can be quite prominent over the knuckles and elbows and sometimes on the knees and ankles.

Tiny blood vessels may be seen in the skin in the reddened areas, and the skin may become shiny and tight. In severe cases the entire skin may take on a reddish hue. There may also be a degeneration of blood vessels (vasculitis) underlying the muscle damage and the development of calcinosis especially in children.
This is where there are deposits of calcium salt in the skin and in the muscle. In the skin these can feel hard and sometimes can erupt and drain a white, chalky fluid. This may lead to a secondary infection which will need to be treated with antibiotics. Calcinosis may require surgical removal of troublesome deposits. This feature is more common in children.

Polymyositis while defined as an inflammation of the muscle can also be a feature of a more general autoimmune illness such as Systemic Lupus Erythematosus, Scleroderma or even Rheumatoid Arthritis. Other possible symptoms of both diseases include fever and with loss.

A few people have an extreme sensitivity and reaction to cold that is most often felt in the fingers and toes. The problem is called Raynaud’s phenomenon and is caused by a narrowing of the blood vessels in the fingers and toes. This reduces blood flow and turns the fingers and toes white, then gradually to blue. They may also feel numb and may develop shiny red areas around and under the nails. In this situation it is very important to keep hands and feet warm.

There is no association with malignancy in children and only a weak association with an underlying tumour in adults with Dermatomyositis.

Experienced doctors at a centre familiar to the disease will recognise the disease after a simple examination. It will then need to be confirmed by the measurement of certain blood enzymes and other tests. Blood tests alone will not confirm the disease particularly in the childhood form. Examination of the electrical activity of the muscle, known as electromyography, and in addition a muscle biopsy maybe done which will help make the diagnosis. This involves a small piece of muscle tissue being taken and then examined under a microscope.

Once the disease has been diagnosed most patient respond well to steroids. The childhood form is very sensitive to steroids and practically all of them will respond, whereas the adults are much more variable. A second line of treatment is immunosuppressive medication.

Like steroids these drugs suppress the body’s immune system and limit the inflammation. These drugs are monitored under a strict regime, with regular blood tests to monitor their effect and progress. In children the steroid treatment has to be carefully tailored as to the child’s needs, as too little treatment might not adequately suppress the condition. If the patient did not respond to these treatments then intermittent (pulsed) treatment can be given intravenously or plasma exchanges would be considered.

Steroids are prescribed because they are thought to be able to ‘modify’ the immune response against tissue. Immunosuppressants are prescribed because they slow down the immune system, reducing its ability to attack disease agents or healthy tissue. The two may be used together with good effect, but the reasons for this are not fully understood.

Steroid drugs and immunosuppressants are very powerful agents and can have a number of side effects even when correctly administered. These can be shown by weight gain, rounding of the face ('moon face'), increased hairiness, hair thinning, hair loss and easy bruising. More serious side effects may include thinning bones (osteoporosis), depression, high blood pressure, cataracts, bringing on or worsening of diabetes, and in very rare cases, bleeding from the stomach.

These symptoms are rarely encountered if the disease has been managed correctly, and there has been no overlap or influence from another illness. The sufferer, because the immune system has been suppressed, will be open to increased risk of infection from common ailments they would usually fight off. Also the way these ailments express themselves may not follow the normal pattern when these drugs are taken. In children growth may be restricted.

 During the medication by steroids, the body slows production of its own steroids. For this reason, any time the dose is to be lowered, the doctor will gradually reduce the level of steroids a patient is taking, tapering off over a period of weeks or months. During this time the body will gradually increase its own steroid production.

Opinions vary among doctors as to how long to continue treatment but the majority prefers to give drugs for a least two to three years. During this period regular muscle function tests are given as a guide to the disease activity and to make sure the necessary dose of drugs are prescribed to control the disease.

 The period of time may need to be longer, although in children this period can be less if the disease has ‘burnt out’, or is under control until it goes away. While the disease remains active the drugs only suppress its activity. As yet there is no totally satisfactory treatment of Polymyositis and Dermatomyositis which is going to effectively cure all of the patients all of the time.

It  is possible that the untreated condition may stop deteriorating and may even improve. However, usually this is not the case and muscles may have been permanently damaged and weakened by inflammation as a result of the lack of medication. The muscles may even shrink and cause deformity. The untreated illness may even be severe enough to put the sufferer’s life at risk. Before the days of steroids and particularly in children the disease carried an appreciable mortality, mainly as a result of involvement also of the breathing and swallowing muscles.

Approximately a third got better and about a third might have had some general improvement, but be left with quite marked disability. The prognosis using modern treatment is better now. Therefore, treatment at a centre familiar with these conditions is essential.

During the active phase of the illness rest is probably advisable, but once the inflammation has died down active exercise becomes important, for without exercises the muscles become weak and wasted. Your doctor, in conjunction with you physiotherapist will decide at what point to change from resting to active exercise.
The physiotherapist is also very important, as there is a need to stretch muscles to prevent or limit contractures. Contractures are a condition where the muscle fibres have become fibrous and loose their elasticity. This in turn causes a tightness of the muscle to a degree where joint ranges can become restricted.

Rest is also another aspect that is very important. During times of increased muscle weakness you need to take frequent rest periods during the day, and to limit activity to a tolerable level. As the condition improves and inflammation has died down, fewer rest periods are needed. Complete inactivity is harmful and can actually increase muscle weakness. The physiotherapist is invaluable in advising on an exercise programme to balance rest and activity.

The density of the rash in Dermatomyositis can vary from the very faint to the severe involvement of the skin. This can be seen in some case as a very faint hue over the eyelids. In other cases it can appear as a type of nettle rash, blisters, or bumpiness. Sometimes there can be redness and scaling of the scalp. These conditions are not always permanent and can be treated with topically applied steroids.

 The more severe the rash the stronger the required strength of the steroid cream. Regular baths using oily creams or emollients are advisable, for these will cleanse the skin without removing the natural oil layer. Detergents must be avoided, even ‘simple soap’.

It is also advisable to remember that sufferers of Dermatomyositis should keep out of harsh, bright sunlight for long periods. Firstly it can effect the medication and secondly the skin, because of the nature of the disease, the skin becomes very sensitive to the effects of direct sunshine. When going on holiday it is advisable to use a total sun-blocking agent.

As it is not fully understood how the disease developed initially, it can be triggered off again. In women there is always a slight chance that there could be a flare up because of hormonal changes particularly in pregnancy and a medical opinion should he sought before this is envisaged. This can also apply when deciding to take oral contraception.

Some sufferers have found by following a diet and eating certain foods it has been beneficial to their general condition. As yet there is not medical proof to support any claims that diet plays a big role in controlling the disease. However, a balanced, healthy diet containing fresh food etc., low in saturated fat and supplemented in certain kinds of fish oil can to a degree be beneficial.

Children may expect their symptoms to go away. In adults a small percentage do get well within two years. For most it is a case of living with the disease and understanding as much about your illness as possible, so that even during the periods of increased pain and weakness a nearly normal life can be led. It cannot be denied that it is a chronic illness but the disease is rarely fatal, and as long as the prescribed medication is taken the future is always hopeful.

Some patients may well need a wheel chair from time to time. Other equipment such as callipers or splints may be needed while the illness is at its height. An unfortunate few may even need more permanent help if there is serious damage of the muscles.
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« Last Edit: October 17, 2006, 07:26:49 am by ♥ The Pumpkin Smilie Faced Girl ♥ » Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
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« Reply #22 on: July 05, 2006, 11:02:40 pm »

Patient Information - Serious conditions associated with lupus     
 
   
Although lupus can be well controlled in many people, serious medical conditions caused by or associated with the disease can still occur. It is important that you know about these conditions and how they may make you feel so that you can call your doctor right away. The sooner a problem is detected and evaluated, the sooner it can be treated to prevent or reduce damage to your body’s organs.

Kidney disease:
 Many people with lupus develop some form of mild kidney disease. Others, however, develop kidney disease serious enough to lead to kidney failure.

Warning signs include:

swelling around your ankles, hands, and eyes;

increased fatigue or tiredness, especially if you have not altered your rest and activity patterns; and

increased need to urinate at night.


Pericarditis:
 Pericarditis is an inflammation of the thin sac that surrounds the heart.

Warning signs include:

chest pain,
shortness of breath, and
new or higher-than-usual fever.

Myocarditis:
Myocarditis is an inflammation of the heart muscle. Warning signs include:

chest pain,
shortness of breath, and
new or higher-than-usual fever.

Atherosclerosis:
 This is a condition in which fatty deposits build up on the inside of arteries. These deposits can reduce or block blood flow. A blockage or reduced blood flow through an artery that supplies the heart can cause a heart attack to occur.

Warning signs include:

burning, choking, squeezing, or pressing chest pain felt in the center of the chest that may radiate to the left shoulder and arm (anginal pain); it can last up to 5 minutes and will become much less intense or go away completely if you rest;
crushing, prolonged chest pain that is not
relieved by rest;
shortness of breath;
unrelieved indigestion; and
a weak or faint feeling.



Pleuritis:
 Pleuritis is an inflammation of the lining of the lung. Warning signs include:
shortness of breath, and
chest pain, especially when taking a deep breath.

Central nervous system (CNS) disease:
 CNS disease covers a variety of problems that may or may not be related to lupus. Problems can include seizures, memory loss, headache, confusion, hearing and visual changes, muscle weakness, depression, and emotional disturbances. Because many of these problems can be related to use of medications or indicate other conditions, it is often difficult to make a definite diagnosis of CNS disease.

Warning signs include:

severe or chronic headaches;
seizures;
periods of forgetfulness, restlessness, or confusion;
new or increased hearing and vision problems;
bizarre or erratic changes in behavior;
mood swings; and
signs of a stroke, including weakness or numbness in the arms, legs, face, or down one side of the body; a change in speech; confusion; or severe headaches
.

Depression:
With depression, people may feel helpless, hopeless, or overwhelmed. They may find it difficult to get through the day. Depression can occur as a result of lupus or be caused by the drugs used to treat it, especially cortico-steroids.
Warning signs include:


depressed mood;

significant weight loss or gain;

trouble sleeping or sleeping too much;

extreme tiredness and lack of energy;

decreased concentration or an inability to make a decision;
feelings of being overwhelmed and unable to carry out simple tasks, such as personal hygiene, housework, or childcare;
feelings of hopelessness about various aspects of life;
unusual anger or irritability; and
recurrent thoughts of death and suicide
.

Osteonecrosis:
This is a condition that usually affects the hip joint, but may occur in other joints such as the knees, ankles, or shoulders. Blood supply to the hip is reduced and, over time, leads to severe degenerative arthritis. Osteonecrosis is considered to be a side effect of corticosteroid therapy and not a manifestation of SLE itself.
 Warning signs include:

sharp pain in the groin or buttocks that may radiate down the back of the leg,
decreased exercise tolerance,
stiffness of the hips, and
increased pain and difficulty in walking after exercise
.

Pancreatitis:
In pancreatitis, the pancreas (an organ involved in digestion and in producing hormones that regulate blood sugar levels) becomes inflamed. It is a very serious problem that must be treated immediately.
Warning signs include:

sharp, intense pain at the level of the belly button that radiates around to the back;
nausea and vomiting; and
new or higher-than-usual fever.


Acute abdomen:
This is a condition that describes the sudden onset of abdominal pain. A variety of serious problems can cause this condition. You should see your doctor immediately if you develop acute abdomen.
Warning signs include:

abdominal pain that may be severe and radiate throughout the abdominal area;
nausea, vomiting, or loss of appetite;
change in usual bowel movements; and
vomiting blood or blood in the stool.


Vision problems:
Changes in vision can be a result of lupus or because of the corticosteroids and antimalarials used to treat lupus. Problems can include inflammation of the eye, glaucoma, cataracts, general changes in vision, and blocked tear ducts. On very rare occasions, blindness can result.
 Warning signs include:


development of a rash over the eyelids;
mucus discharge from the eye;
blurred vision;
sensitivity to light;
headaches;
a sore, red eye;
lack of tears, and eyes that hurt and are dry; and
episodes of flashing lights and partial blindness.
 
« Last Edit: July 05, 2006, 11:04:04 pm by Kathy » Logged


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« Reply #23 on: July 13, 2006, 02:52:53 pm »

Side Effect of Long-term Cyclosporine Therapy for Dry Eye in RA and Lupus Patients

Question
What is the most common side effect of long-term cyclosporine therapy for dry eye in RA and lupus patients?

 Response from  Robert I. Fox, MD, PhD
Member, Rheumatology and Medicine Department, Scripps Memorial Hospital, La Jolla, California




There have been no reports on Medline or Medwatch (FDA.gov) of late adverse events in patients using topical cyclosporin (Restasis, Allergan). Early discontinuations were due to intolerance (burning) and late discontinuations were due to lack of efficacy.

Comment

Cyclosporin is a potent immunomodulator that acts locally when administered at the ocular surface. On the basis of 2 randomized double-blind studies,[1] 0.05% cyclosporin ophthalmic emulsion has been approved by the US Food and Drug Administration for treatment of keratoconjunctivitis sicca (KCS; dry-eye disease). After topical application, cyclosporin accumulates at the ocular surface and cornea, reaching concentrations (≥ 0.236 mcg/g) that are sufficient for immunomodulation.[2] Very little drug penetrates through the ocular surface to intraocular tissues. In experimental studies, cyclosporin is not metabolized in rabbit or dog eyes and may also not be metabolized in human eyes. Cultured human corneal endothelial and stromal cells exposed to cyclosporin in vitro exhibited no adverse effects and only minor effects on DNA synthesis. No ocular or systemic toxicity was seen with long-term ocular administration of cyclosporin at concentrations up to 0.4%, given as many as 6 times daily for 6 months in rabbits and 1 year in dogs.[2] Systemic blood cyclosporin concentration after ocular administration was extremely low or undetectable in rabbits, dogs, and humans, obviating concerns about systemic toxicity. In 12-week and 1-year clinical safety studies in dry-eye patients,[1] the most common adverse event associated with the ophthalmic use of cyclosporin emulsion was ocular burning. No serious drug-related adverse events occurred.


Posted 06/05/2006


--------------------------------------------------------------------------------

References
Sall K, Stevenson OD, Mundorf TK, Reis BL. Two multicenter, randomized studies of the efficacy and safety of cyclosporine ophthalmic emulsion in moderate to severe dry eye disease. CsA Phase 3 Study Group. Ophthalmology. 2000;107:631-639.
Tang-Liu DD, Acheampong A. Ocular pharmacokinetics and safety of ciclosporin, a novel topical treatment for dry eye. Clin Pharmacokinet. 2005;44:247-261.
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« Reply #24 on: July 15, 2006, 08:25:20 am »

The Facts about Systemic Lupus Erythematosus

Lupus is one of many disorders of the immune system known as autoimmune diseases. In autoimmune diseases, the immune system turns against parts of the body it is designed to protect. This leads to inflammation and damage to various body tissues. Lupus can affect many parts of the body, including the joints, skin, kidneys, heart, lungs, blood vessels, and brain. Although people with the disease may have many different symptoms, some of the most common ones include extreme fatigue, painful or swollen joints (arthritis), unexplained fever, skin rashes, and kidney problems.

Lupus is characterized by periods of illness, called flares, and periods of wellness, or remission. At present, there is no cure for lupus. However, lupus can be effectively treated with drugs, and most people with the disease can lead active, healthy lives.

Many more women than men have lupus. Lupus is three times more common in African American women than in Caucasian women and is also more common in women of Hispanic, Asian, and Native American descent. In addition, lupus can run in families. There are three main types of lupus:

Systemic lupus erythematosus (SLE) is the form of the disease that most people are referring to when they say "lupus." The word "systemic" means the disease can affect many parts of the body. The symptoms of SLE may be mild or serious. Although SLE usually first affects people between the ages of 15 and 45 years, it can occur in childhood or later in life as well. This article focuses on SLE.

Discoid lupus erythematosus is a chronic skin disorder in which a red, raised rash appears on the face, scalp, or elsewhere. The raised areas may become thick and scaly and may cause scarring. The rash may last for days or years and may recur. A small percentage of people with discoid lupus have or develop SLE later.

Drug-induced lupus is a form of lupus caused by medications. Many different drugs can cause drug-induced lupus. Symptoms are similar to those of SLE (arthritis, rash, fever, and chest pain) and they typically go away completely when the drug is stopped. The kidneys and brain are rarely involved.

Causes
Lupus is a complex disease, and its cause is unknown. It is likely that a combination of genetic, environmental, and possibly hormonal factors work together to cause it. The fact that lupus can run in families indicates that its development has a genetic basis, but no specific "lupus gene" has been identified. Scientists believe that genes alone do not determine who gets lupus and that other factors also play a role. Some of the factors include sunlight, stress, certain drugs, and infectious agents such as viruses.

In lupus, the body's immune system does not work as it should. A healthy immune system produces proteins called antibodies and specific cells called lymphocytes that help fight and destroy viruses, bacteria, and other foreign substances that invade the body. In lupus, the immune system produces antibodies against the body's healthy cells and tissues. These antibodies, called autoantibodies, contribute to the inflammation of various parts of the body and can cause damage to organs and tissues.

Symptoms
Each person with lupus has slightly different symptoms that can range from mild to severe and may come and go over time. However, some of the most common symptoms of lupus include painful or swollen joints (arthritis), unexplained fever, and extreme fatigue. A characteristic red skin rash - called a butterfly or malar rash - may appear across the nose and cheeks. Rashes may also occur on the face and ears, upper arms, shoulders, chest, and hands. Because many people with lupus are sensitive to sunlight (called photosensitivity), skin rashes often first develop or worsen after sun exposure.

Common Symptoms of Lupus

Painful or swollen joints and muscle pain
Unexplained fever
Red rashes, most commonly on the face
Chest pain upon deep breathing
Unusual loss of hair
Pale or purple fingers or toes from cold or stress (Raynaud's phenomenon)
Sensitivity to the sun
Swelling (edema) in legs or around eyes
Mouth ulcers
Swollen glands
Extreme fatigue
Other symptoms of lupus include anemia (a decrease in red blood cells), headaches, dizziness, depression, confusion, or seizures. New symptoms may continue to appear years after the initial diagnosis, and different symptoms can occur at different times. In some people with lupus, only one system of the body, such as the skin or joints, is affected. Other people experience symptoms in many parts of their body. Just how seriously a body system is affected varies from person to person. The following systems in the body also can be affected by lupus.

Kidneys: Inflammation of the kidneys (nephritis) can impair their ability to get rid of waste products and other toxins from the body effectively. There is usually no pain associated with kidney involvement, although some patients may notice swelling in their ankles. Most often, the only indication of kidney disease is an abnormal urine or blood test. Because the kidneys are so important to overall health, lupus affecting the kidneys generally requires intensive drug treatment to prevent permanent damage.

Lungs:
Some people with lupus develop pleuritis, an inflammation of the lining of the chest cavity that causes chest pain, particularly with breathing. Patients with lupus also may get pneumonia.

Central nervous system:

In some patients, lupus affects the brain or central nervous system. This can cause headaches, dizziness, memory disturbances, vision problems, seizures, stroke, or changes in behavior.

Blood vessels:
Blood vessels may become inflamed (vasculitis), affecting the way blood circulates through the body. The inflammation may be mild and may not require treatment or may be severe and require immediate attention.

Blood:
People with lupus may develop anemia, leukopenia (a decreased number of white blood cells), or thrombocytopenia (a decrease in the number of platelets in the blood, which assist in clotting). Some people with lupus may have an increased risk for blood clots.

Heart:
In some people with lupus, inflammation can occur in the heart itself (myocarditis and endocarditis) or the membrane that surrounds it (pericarditis), causing chest pains or other symptoms. Lupus can also increase the risk of atherosclerosis (hardening of the arteries).

Diagnosis
Diagnosing lupus can be difficult. It may take months or even years for doctors to piece together the symptoms to diagnose this complex disease accurately. Giving the doctor a complete, accurate medical history (for example, what health problems you have had and for how long) is critical to the process of diagnosis.

No single test can determine whether a person has lupus, but several laboratory tests can help the doctor to make a diagnosis. The most useful tests identify certain autoantibodies often present in the blood of people with lupus. The doctor may order a biopsy of the skin or kidneys if those body systems are affected. Other laboratory tests are used to monitor the progress of the disease once it has been diagnosed. A complete blood count, urinalysis, blood chemistries, and the erythrocyte sedimentation rate (ESR) test can provide valuable information. Another common test measures the blood level of a group of substances called complement.

Treatment
Diagnosis and treatment of lupus are often a team effort between the patient and several types of health care professionals that might include a family doctors or internists, rheumatologists, immunologists, nurses, psychologists, social workers, nephrologists, hematologists, dermatologists, and neurologists.

NSAIDs:
 For people with joint or chest pain or fever, drugs that decrease inflammation, called nonsteroidal anti-inflammatory drugs (NSAIDs), are often used. While some NSAIDs, such as ibuprofen and naproxen, are available over the counter, a doctor's prescription is necessary for others. Common side effects of NSAIDs can include stomach upset, heartburn, diarrhea, and fluid retention.

Antimalarials:
These drugs were originally used to treat malaria, but doctors have found that they also are useful for lupus. A common antimalarial used to treat lupus is hydroxychloroquine. It may be used alone or in combination with other drugs and generally is used to treat fatigue, joint pain, skin rashes, and inflammation of the lungs. Clinical studies have found that continuous treatment with antimalarials may prevent flares from recurring. Side effects of anti-malarials can include stomach upset and, extremely rarely, damage to the retina of the eye.

Corticosteroids:

The mainstay of lupus treatment involves the use of corticosteroid hormones, such as prednisone, hydrocortisone, methylprednisolone, and dexamethasone. Corticosteroids work by rapidly suppressing inflammation. Corticosteroids can be given by mouth, in creams applied to the skin, or by injection. Because they are potent drugs, the doctor will seek the lowest dose with the greatest benefit.
Short-term side effects of corticosteroids include swelling, increased appetite, and weight gain. These side effects generally stop when the drug is stopped. It is dangerous to stop taking corticosteroids suddenly, so it is very important that the doctor and patient work together in changing the corticosteroid dose.
Long-term side effects of corticosteroids can include stretch marks on the skin, weakened or damaged bones, high blood pressure, damage to the arteries, high blood sugar, infections, and cataracts. Typically, the higher the dose and the longer they are taken, the greater the risk and severity of side effects. People with lupus who are using corticosteroids should talk to their doctors about taking supplemental calcium and vitamin D or other drugs to reduce the risk of osteoporosis (weakened, fragile bones).

Immunosuppressives:
For some patients whose kidneys or central nervous systems are affected by lupus, a type of drug called an immunosuppressive may be used. Immunosuppressives such as cyclophosphamide and mycophenolate mofetil restrain the overactive immune system by blocking the production of immune cells. These drugs may be given by mouth or by infusion. Side effects may include nausea, vomiting, hair loss, bladder problems, decreased fertility, and increased risk of cancer and infection. The risk for side effects increases with the length of treatment. As with other treatments for lupus, there is a risk of relapse after the immunosuppressives have been stopped.


Methotrexate: in some patients, methotrexate, a disease-modifying antirheumatic drug, may be used to help control the disease.

Alternative and Complementary Therapies: Some alternative approaches people have tried include special diets, nutritional supplements, fish oils, ointments and creams, chiropractic treatment, and homeopathy. Although these methods may not be harmful in and of themselves, and may be associated with symptomatic or psychosocial benefit, no research to date shows that they affect the disease process or prevent organ damage. Some alternative or complementary approaches may help the patient cope or reduce some of the stress associated with living with a chronic illness. If the doctor feels the approach has value and will not be harmful, it can be incorporated into the patient's treatment plan. However, it is important not to neglect regular health care or treatment of serious symptoms.


Lupus and Quality of Life
Despite the symptoms of lupus and the potential side effects of treatment, people with lupus can maintain a high quality of life overall. Learning to recognize the warning signs of a flare can help the patient take steps to ward it off or reduce its intensity. Many people with lupus experience increased fatigue, pain, a rash, fever, abdominal discomfort, headache, or dizziness just before a flare. Developing strategies to prevent flares can also be helpful, such as learning to recognize your warning signals and maintaining good communication with your doctor.

It is also important for people with lupus to receive regular health care, instead of seeking help only when symptoms worsen. Results from a medical exam and laboratory work on a regular basis allows the doctor to note any changes and to identify and treat flares early. The doctor can provide guidance about such issues as the use of sunscreens, stress reduction, and the importance of structured exercise and rest, as well as birth control and family planning. Because people with lupus can be more susceptible to infections, the doctor may recommend yearly influenza vaccinations or pneumococcal vaccinations for some patients.

Women with lupus should receive regular preventive health care, such as gynecological and breast examinations. Men with lupus should have the prostate-specific antigen (PSA) test. Both men and women need to have their blood pressure and cholesterol checked on a regular basis. If a person is taking corticosteroids or antimalarial medications, an eye exam should be done at least yearly to screen for and treat eye problems.

Staying healthy requires extra effort and care for people with lupus, so it becomes especially important to develop strategies for maintaining wellness. Wellness involves close attention to the body, mind, and spirit. One of the primary goals of wellness for people with lupus is coping with the stress of having a chronic disorder. Some approaches that may help include exercise, relaxation techniques such as meditation, and setting priorities for spending time and energy.

Developing and maintaining a good support system is also important. A support system may include family, friends, medical professionals, community organizations, and support groups. Participating in a support group can provide emotional help, boost self-esteem and morale, and help develop or improve coping skills.

Learning more about lupus may also help. Studies have shown that patients who are well-informed and participate actively in their own care experience less pain, make fewer visits to the doctor, build self-confidence, and remain more active.

Pregnancy For Women With Lupus
Although a lupus pregnancy is considered high risk, most women with lupus carry their babies safely to the end of their pregnancy. Women with lupus have a higher rate of miscarriage and premature births compared with the general population. Pregnancy counseling and planning before pregnancy are important. Ideally, a woman should have no signs or symptoms of lupus and be taking no medications for at least 6 months before she becomes pregnant.

Some women may experience a mild to moderate flare during or after their pregnancy; others do not. Pregnant women with lupus, especially those taking corticosteroids, also are more likely to develop high blood pressure, diabetes, hyperglycemia (high blood sugar), and kidney complications, so regular care and good nutrition during pregnancy are essential. It is also advisable to have access to a neonatal intensive care unit at the time of delivery in case the baby requires special medical attention.
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« Reply #25 on: August 03, 2006, 02:52:27 pm »

Epstein-Barr virus and lupus

What problem was studied?
Epstein-Barr virus is one of the most common viruses that infect humans, generally resulting in a very mild and brief illness in children. When EBV affects adolescents or young adults, it can result in infectious mononucleosis, a condition that results in fever, sore throat, swollen lymph glands and severe fatigue. Although symptoms usually stop within a few months, EBV remains dormant or latent in the body for the rest of the infected person's life and can become reactivated. EBV infection is more common in people with systemic lupus erythematosus (SLE or lupus) but it is not clear whether this is a cause or effect of a faulty immune system in these individuals. In addition, people with lupus often take drugs that suppress the immune system, making them more susceptible to infections and cancer. To help prevent these complications, research is needed to better understand how the immune system in people with lupus defends against foreign invaders.

Arthritis Foundation-funded researchers involved in the study: Insoo Kang, MD, supported by an Arthritis Investigator Award; Timothy Quan, MD, supported by an AF/American College of Rheumatology Physician Scientist Development Award; and Joseph E. Craft, MD, supported by a Biomedical Science Grant and a Southern New England Chapter grant, Yale University, New Haven, CT

What was done in the study?
The research team collected blood samples from people with lupus and from healthy individuals to look at signs of EBV infection (called "viral loads"). They also examined how the immune system in both groups handled EBV infection by studying subsets of immune cells, called "T cells," which normally play a key role in defending the body against viral infections.

What were the study results?
The researchers found that the patients with lupus had a 40-fold increase in signs of EBV infection compared to the healthy subjects. The people with lupus had a higher frequency of one type of T cell (CD4) but a lower frequency of another type of T cell (CD8). The team concluded that people with lupus have a defect in their ability to control latent EBV infection that probably results from altered T cell responses to the virus.

What's the relevance to people with lupus?
This study is important because it begins to provide insights about how people with an abnormal immune system, such as in lupus, respond to infection. Adds Dr. Kang, "This is clinically important research since patients with autoimmune diseases like lupus are frequently treated with strong immunosuppressive drugs that may suppress immune responses against infection. In this study, we have shown that patients with SLE have defective control of latent EBV infection. However, the clinical significance of such a defect is still elusive and should be determined with future studies."
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« Reply #26 on: September 12, 2006, 01:18:22 pm »

New Insights Into How Estrogen May Trigger Activation of the Immune System

 
Lupus is nine times more frequent among women of childbearing ages than men. This overwhelming difference, coupled with the way that flares seem to occur with certain phases of the menstrual cycle, has spurred research into the role of sex hormones in the development of lupus and disease activity.  In particular, the interactions of immune cells (B and T cells) and estrogen has been the subject of growing attention.  Estrogen is known to regulate genes involved in inflammation, and the way the immune system cleans up the residue of inflammation in the bloodstream (programmed cell death, or “apoptosis”). Estrogen also regulates genes involved in the ways that immune cells communicate with each other using chemical signals.

 

In this study, researchers compared the effects of one type of estrogen (estradiol 17-β) on the T cells of women with lupus and healthy women. Their research focused specifically on the activity of two estrogen receptors (ER), known as ER-α and ER-β. Receptors are the docking molecules, where estrogen binds and sends its regulating signals to the genes of a cell. The receptors are present in both lupus T cells and normal T cells.

 

The researchers found that in the lupus T cells — but not in the T cells of healthy people — the ER-α and ER-β receptors responded to estrogen by turning on the immune response, sending signals to two agents called CD154 and calcineurin. There was also a greater variation in the amount of ER-α among the lupus T cells. This suggests that the lupus patients have a quicker turnover of the docking receptors in their cells. This might make the cells more sensitive to estrogen and contribute to problems with immune function in women with lupus.

 

It is not known how estrogen increases CD154 and calineurin expression. However, the researchers point out that better understanding of these mechanics (how estrogen acts inside the cells of healthy people and lupus patients) could lead to new approaches to treat gender-biased autoimmune diseases such as lupus.

 

Read the Abstract:

http://www.jrheum.com/abstracts/abstracts06/1093.html

 
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« Reply #27 on: September 12, 2006, 01:21:00 pm »

Protein May Regulate How Cells in the Body Grow or Self-Destruct

Individuals affected by Sjögren’s syndrome and lupus have immune system proteins (autoantibodies) that target a protein called Ro52. They also make unusually high amounts of Ro52. However what the purpose of this protein is in the body, or why the immune system is zeroing in on it in these patients, is not yet understood. The researchers wanted to study what effect on the immune system having extra Ro52 might have.

 

Using B cells from a mouse model of lupus, the researchers manipulated these cells to make excessive amounts of Ro52 to see how this would affect the cell. They found that if you give these cells with extra Ro52 protein triggering signals, which usually cause cell activation and death (the CD40 signaling pathway), this caused decreased cell growth and increased cell death over what would otherwise be expected. Next, when they then reduced the amount of Ro52 made by these cells, it restored the ability of the cells to live longer.

 

The findings suggest the possibility that increased manufacture of Ro52 by patients with Sjögren’s and lupus could be part of the reason why they have unbalanced immune cell activation and problems with regulated immune cell disposal (programmed cell death or apoptosis).  The killing-off and disposal of expired immune cells needs to proceed in an orderly manner in order to prevent further inflammation in the bloodstream. This might contribute to the dysregulation of the immune system in people with Sjögren’s syndrome and lupus.


 

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« Reply #28 on: September 12, 2006, 01:30:09 pm »

TNF-Alpha Protein May Contribute to Lupus Skin Rashes

 Tumor necrosis factor alpha (TNF-a) is an immune-regulating protein (cytokine) that is manufactured and released by cells to act in the bloodstream. Increased amounts of this protein can be found in many inflammatory diseases, and also can be produced by the body in response to toxic substances in bacteria. Tumor necrosis factor is important because it stimulates another regulating protein called interleukin (IL)-1, which regulates other immune responses, such as activating white blood cells, called lymphocytes, and helping to trigger fever. TNF-a increases tissue damage by IL-1, stimulates immune cells to make destructive proteins (collagenases) which degrade tissues, and plays a role in how the immune system recognizes specific triggering agents.

 

In this study researchers examined tissue biopsy samples taken from patients with lupus skin rashes (called subacute cutaneous lupus) that had not responded to the usual treatments, such as antimalarial drugs, immunosuppressive drugs, and thalidomide.  The researchers compared what was found in these skin samples with biopsies from patients with other inflammatory and cancerous skin diseases. The skin rash samples from patients with lupus showed a strong presence of TNF-α particularly in the skin’s outer layer (the epidermis). However, TNF-α was not seen in healthy skin samples from the same group of lupus patients, or in skin biopsies from the non-lupus group. 

 

These findings suggest that TNF-α is produced by the surface region (epidermal layer) of skin in this kind of lupus rash, and might have a role in causing of this kind of rash. This finding might help to develop superficial skin treatments for this rash that might work better and/or be less toxic than medicine which is taken by mouth or put directly into the bloodstream.

 

Read the Abstract:

http://ard.bmjjournals.com/cgi/content/abstract/65/4/545

 

 
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« Reply #29 on: October 01, 2006, 09:07:59 am »

How lupus is diagnosed
Diagnosis of SLE may be suspected on the basis of symptoms, but is confirmed by a series of blood tests. Of particular interest is the antinuclear antibody (ANA), which is present in virtually all the patients with lupus. Other tests such as the anti-double strand DNA (dsDNA) and anti-smith antibodies (Sm) are more specific and are used to confirm the diagnosis of lupus. The levels of certain complement proteins (a part of the immune system) are also used to help diagnose and monitor the disease.

If anti-phospholipid antibodies are present, this not only helps to establish a diagnosis of lupus, but also indicate there is an increased risk of specific complications. These include an increased risk of miscarriage and an increased risk for developing blood clots that may lead to stroke or lung injury.

Typical clinical features include:

Fever, fatigue, and weight loss

Arthritis involving multiple joints for several weeks

Butterfly-shaped rash over the cheeks or other rashes

Skin rash appearing in areas exposed to the sun

Sores in the mouth or nose for more than a month

Loss of hair, sometimes in spots or around the hairline

Seizures, strokes and mental disorders

Blood clots in different locations

Miscarriages in some patients

Blood or protein in the urine or tests that suggest poor kidney function

Low blood counts (anemia, low white blood cells or low platelets)

Other symptoms include chest pain when the patient breathes deeply, heartburn, abdominal pain and poor circulation to the fingers and toes.

All of these symptoms can develop gradually, making lupus hard to diagnose.

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