Lupus In 'Overlap' With Other Connective Tissue Diseases

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Understanding Fatigue in Lupus - and What Can Be Done

If you have lupus, you probably know how bad fatigue can be. It's one of the most common symptoms reported by people with lupus. Most lupus patients suffer with it. But exactly what causes this fatigue that goes far beyond just being tired?

A study done at Hospital for Special Surgery almost 10 years ago suggested that depression and sleep problems might contribute to fatigue in people with lupus.1 But in the women studied, those who had lupus did not have more ஐﻬdepression than those who did not. However, those who had lupus took longer to fall asleep - and slept for longer periods of time.

Over the years, other researchers have also tried to figure out how sleep and depression might play a role. Others have suggested that lack of exercise might be involved - because exercise can actually give you energy when your muscles get fit.

New Research

Recently, a Canadian group of researchers explored the question and reported at a recent meeting of the American College of Rheumatology.2 They studied 100 women with lupus. The women were given a series of different tests to look at:

the type of their fatigue,

how bad their fatigue was,

how bad their pain was,

whether they were depressed - and if so how badly,

how well - or poorly - they slept,

how much physical activity they did in their leisure time,

whether they were satisfied with the support they received from family and friends.
Finally, the women were examined by a doctor to see the level of their lupus disease activity and the impact lupus already had on their bodies.

What They Learned

As in other studies, they found that people with lupus have much more fatigue than others.

Fatigue can be influenced by everything they explored and more: depression, pain, quality of sleep, quantity sleep, exercise, ஐﻬseverity of illness, and satisfaction with your social support network - as well as flares, medications, and stress. And it varies from one patient to the next.

Because fatigue arises from so many different factors, they said treatment should try to find out what factors were involved in the patient being treated - and treat all of them to get at the fatigue. These factors can be treated - modified - changed.

Two Types of Fatigue

One thing that was different about their study was that they separated physical fatigue from mental fatigue. Many other studies have just looked at "fatigue" as one thing.

Think of physical fatigue as "I'm too tired to stand up," or "I just can't walk another block." That's easy to recognize - and you should listen to it. Rest. Sit down or just collapse in bed for awhile.

Mental fatigue can be more difficult to get a grasp on sometimes. "I can't think straight" or "I can't concentrate" or "I keep rereading this paragraph again and again" may be mental fatigue. Or it may be a sign of theஐﻬ cognitive (thinking) difficulties that are part of neuropsychiatric lupus. So any changes in your thinking or concentration should be reported to your doctor - because a change in medication may help. In the meantime, again, rest. Put the book down. Veg out in front of the TV. Cuddle up with your pet. (Studies have proven that stroking a pet can be very relaxing.) Or take a nap.

Physical Fatigue

It was not a surprise that people with more pain and poorer sleep were more likely to have physical fatigue.

Lots of research - in people without lupus - has shown exercise helps reduce depression. But this study had an interesting surprise. Only the lupus-fatigued women who did not score high on depression tests seemed to be helped by exercise. Lupus-fatigued women who were depressed did not get an improvement in physical fatigue from exercise. Does this mean you shouldn't exercise? No! You need exercise for heart fitness, muscle strength and to keep up your energy. It may even help your physical fatigue - because a finding from one research study doesn't apply to everyone.

But look to other means as well. Talk with your doctor about ways to improve your sleep and lower your pain level, especially by reducing your disease activity.

Mental Fatigue

The factors most related to mental fatigue were slightly different. They were clearly:

greater pain severity - again, talk with your doctor about how to reduce your pain level;

higher levels of depression - ask your doctor about referral to a licensed psychotherapist such as a social worker or psychologist. In some cases,r antidepressant medication may also be useful.

lower satisfaction with social support networks - talk with family and friends about what you need from them. Often they may not be aware of how you are feeling inside. Let them know what can help. ஐﻬEstablishing an understanding together of the impact of fatigue and how to problem-solve around this is important.
How Do You Cope

Fatigue is profound. It touches you to the core. It can totally disrupt your life. Fatigue itself can be stressful and fatiguing. Because you cannot "see" fatigue, and it can change so much from hour-to-hour and day-to-day, your fatigue can also be confusing to those with whom you live and work. But it's not something you can point to like a swollen joint or a rash. You can be exhausted with fatigue and your friend or family member says, "You look great."

This can be very frustrating. You feel that others just don't get it. Over time, see if you can learn to respond comfortably and assertively to such comments. "I wish I felt as great as I look - but I'm really fatigued right now, and it's important that I rest and take care of myself."

Those words may not be right for you - but you need to find the words that are. Because when fatigue hits, you need to let go and rest. Give in to fatigue when necessary - so you can spring back. Take that temporary break - so you can stand up and think clearly later. Whether it's an hour later or a day later doesn't matter. You will find the right moment. And only you can. Because lupus fatigue is different for everyone - what causes it, when it hits, what helps, when it goes.

Be kind to yourself, work with your doctor, and you will find the path that's best for you. Just don't give up.

Encephalopathy and severe neuropathy due to probable systemic vasculitis as an initial manifestation of mixed connective tissue disease

Matsui Hideaki, Udaka Fukashi, Oda Masaya, Kubori Tamotsu, Nishinaka Kazuto, Kameyama Masakuni
 Department of Neurology, Sumitomo Hospital, Osaka, Japan

Correspondence Address:
Matsui Hideaki
Department of Neurology, Sumitomo Hospital, 5-3-20 Nakanoshima, Kita-ku, Osaka, 530-0005


We described a 69-year-old woman with neurological manifestations due to mixed connective tissue disease (MCTD). The patient demonstrated subacute cognitive decline, seizure and gait disturbance with no connective tissue manifestation. She had been diagnosed with dementia at another hospital, later in our hospital, serological examinations disclosed high titers of anti-RNP antibody. Cognitive dysfunction in this patient was dramatically ameliorated by steroid therapy. Three months later, she developed edema of the hands, synovitis and acrosclerosis. The patient was finally diagnosed as having MCTD. We emphasized MCTD as a rare cause of "treatable dementia".

Keywords: Mixed connective tissue disease, treatable dementia, cognitive dysfunction

The occurrence of neurological or psychiatric disturbances in association with rheumatic diseases has been an area of considerable interest for many years.[1] Mixed connective tissue disease (MCTD) is characterized by clinical features of systemic lupus erythematosus (SLE), scleroderma and polymyositis occurring simultaneously or sequentially, in the presence of high titers of antibody to an Rnase-sensitive ribonuclear protein complex, U1 small nuclear RNP (ribonucleoprotein). Neurological problems in MCTD are seen in approximately 10~20% of cases;[2] however, it is difficult to diagnose patients with just neurological manifestations. We present a patient demonstrating subacute cognitive dysfunction, seizure and gait disturbance with no connective tissue manifestation. The patient was later disclosed as having MCTD. Cognitive dysfunction and seizure in this patient were ameliorated by steroid therapy. We emphasize MCTD as a rare cause of "treatable dementia".

  Case Report   

A 69-year-old woman demonstrated gait disturbance from April 2004 and the gait disturbance gradually and symmetrically progressed. The patient had no congenital disorders, no regular medicine, no history of diseases such as hypertension, diabetes mellitus or sleep disorders, no history of toxin exposure and no smoking or alcohol. In October 2004, cognitive dysfunction appeared and subacutely deteriorated. She also demonstrated aphasia and experienced transient seizure once in the previous month. The patient had been diagnosed as having dementia in another hospital, but in November 2004 was admitted to our hospital. On admission, the patient was alert and awake. She could not stay standing nor walk. There were no trophic changes in the feet. She had cognitive impairment, mainly memory disturbance. The score on a Mini-mental state examination (MMSE) was 10/30. She demonstrated incomplete transcortical motor aphasia, and sometimes palilalia, but apraxia or agnosia was not seen. Cranial nerves were intact except for right facial sensory disturbance in touch, pain and temperature. Muscle strength in upper limbs was slightly diminished, while in lower limbs all muscles revealed distal dominant weakness, as reflected by the 3 score on a manual muscle test. There was moderate atrophy in bilateral tibialis anterior muscles. Deep tendon reflexes were all symmetrical and normal in upper limbs but were absent in the lower limbs. Bilateral palmomental reflexes were positive, as was right Babinski's reflex, while left plantar reflex was equivocal. Vibration, touch, pain and temperature senses in the bilateral lower limbs were greatly and symmetrically diminished. Voluntary pain was not seen. There was no sensory level in the distribution of sensory disturbances. The neuropathy was painless. No cerebellar or autonomic manifestations were present. Neck stiffness and Kernig's sign were negative. The patient did not show any symptoms in connective tissues such as Raynaud's syndrome, synovitis, acrosclerosis, myositis, edema or sclerodactylia

Blood analysis disclosed mild inflammatory responses, and high indexes of SS (Sj φgren syndrome) -A, RNP and TPO (thyroid peroxidase = thyroid myeloperoxidase) antibody, and hypothyroidism. Other antibodies such as DNA, SS-B, cardiolipin, Sm, or ANCA (antineutrophil cytoplasmic antibodies) were not detected. The tests for lupus anticoagulant were not performed. Antinuclear antibodies were detected at low titers. Vitamin B1, B12 and folic acid were normal. Hepatitis B surface antigen, Hepatitis C antibody, rapid plasma reagin test and treponemal tests: hemagglutination test were all negative. Cerebrospinal fluid examinations showed high total protein and increased cell counts. No bacteria or malignant cells were detected, neither was tubercle bacillus on a culture test and by DNA-PCR. Oligoclonal bands were positive while myelin basic protein was not detected. Herpes simplex virus, herpes zoster virus, mumps, measles and toxoplasma were negative during the entire clinical course. Urine examinations were normal. Ultrasonic cardiography demonstrated pulmonary hypertension (Tricuspid regurgitation peak pressure gradient = 37 mmHg). Chest computed tomography (CT) was normal. Magnetic resonance imaging (MRI) showed multiple high intensity signals in T2 and FLAIR sequences [Figure - 1]. These lesions were not enhanced. Brain and cervical magnetic resonance angiography did not show any abnormal lesions. Electroencephalography demonstrated diffuse slow activity. Motor action potentials in the bilateral tibial nerves were not evoked, while a motor conduction study demonstrated low amplitude (amplitude: 0.6 mV, conduction velocity: 30 ms) in the bilateral peroneal nerves. Motor action potentials in the bilateral ulnar nerves were intact and those in the bilateral median nerves showed slightly delayed distal latency. Action potentials in the bilateral sural nerves were not evoked, and somatosensory evoked potentials could not be detected. There was no evidence of conduction block. These nerve conduction studies demonstrated the mononeuritis multiplex pattern; severe damage in the tibial nerves in contrast to relative preservation of the peroneal nerves, which are more prone to be impaired by polyneuropathic pathology. Blink reflex test disclosed right trigeminal neuropathy [Figure - 2]. No malignant tumor was detected on chest and abdominal CT, endoscopy, sonography and tumor marker studies.

The patient was tentatively diagnosed as having neurological deteriorations due to MCTD. Corticosteroid pulse therapy was given and thereafter 60mg/day prednisolone was prescribed orally. Oral prednisolone was gradually tapered and her cognitive function improved. MMSE score was 24/30 one month after therapy. Aphasia had completely disappeared, and there were no seizures after treatment. However the trigeminal and peripheral neuropathies, and gait disturbance did not ameliorate, and brain MRI did not change significantly. Inflammatory response in blood and cerebrospinal fluid disappeared. Three months after admission, she gradually developed edema of the hands, synovitis and acrosclerosis. The patient was finally diagnosed as having MCTD. The patient did not show remarkable clinical change in further three months after the final diagnosis.


The patient fulfilled the diagnostic criteria of MCTD by Japanese study group[2] and probable diagnosis by Sharp.[3] While we could not exclude Hashimoto's encephalopathy, MCTD was strongly suggested by the concomitant pulmonary hypertension, trigeminal neuropathy and peripheral neuropathy. Especially, trigeminal neuropathy has been reported to have a close relation with MCTD compared to other collagen disease or Hashimoto's disease,[4],[5] therefore this suggested strongly that neurological manifestations in this patients were due to MCTD. Pulmonary hypertension also has been considered as a unique complication of MCTD,[6] however some authors pointed out the correlation between thyroid dysfunction and pulmonary hypertension.[7] It is unnatural to consider encephalopathy was due to Hashimoto's disease and other symptoms were due to MCTD, while all symptoms appeared in succession.

In this case, the symptoms and inflammatory response in cerebrospinal fluid and serum were ameliorated but the brain MRI after steroid therapy showed little change. This may be because the abnormal lesions in brain MRI represented irreversible damage and the symptoms in the central nervous system were ameliorated due to improvement of the encephalopathy.

Neurological problems sometimes seen in MCTD include headache, seizures, psychosis, encephalopathy, transverse myelitis, ataxia, aseptic meningitis, monocular blindness, trigeminal sensory neuropathy, polyneuropathy and entrapment neuropathy.[1],[8],[9] The neurologic features observed tend to be characteristic of the dominant clinical syndrome exhibited by each patient. For example, trigeminal and peripheral neuropathy tend to occur in MCTD patients with predominant scleroderma features, while optic neuropathy, transverse myelitis, encephalopathy and ataxia occur in patients with prominent SLE features.[1]

In this case, encephalopathy and severe neuropathy might be due to systemic vasculitis as a manifestation of MCTD. Although vasculitis is a rare feature of MCTD, there were some reports about concomitant vasculitis in patients with MCTD.[10],[11] It might account for the mononeuritis multiplex pattern peripheral neuropathy and the brain MRI findings. However, because tissue biopsy was not done in this patient, the presence of vasculitis was not confirmed in this patient.

Central nervous disorders in MCTD patients are rare, and MCTD has been never discussed in the context of "treatable dementia". Many factors have been reported to contribute to "treatable dementia", including cerebrovascular disease, tumor, normal pressure hydrocephalus, toxicity, depression, encephalopathy, multiple sclerosis, sarcoidosis, hormonal abnormalities, vitamin insufficiency, organ failure, Behηet's disease, and collagen disease.[12] In collagen disease, symptoms such as SLE, temporal arteritis, and Sj φgren syndrome have been described as a rare cause of "treatable dementia".[12] We described here "treatable dementia" due to MCTD, which while it may be rare state, it has corresponding significance because of the fact: that it is indeed treatable. Further studies will be needed to better understand the circumstances surrounding this condition.

1. Nadeau SE. Neurologic manifestations of connective tissue disease. Neurol Clin 2002;20:151-78.    [PUBMED]   
2. Miyata M, Nishimaki T. Neural disorders in mixed connective tissue disease (MCTD) and overlap syndrome. Nihon Rinsho Bessatsu Nihon Rinsho c! 2000;279-81.       
3. Sharp GC, Irvin WS, Tan EM, Gould RG, Holman RH. Mixed connective tissue disease - an apparently distinct rheumatic disease syndrome associated with a specific antibody to an extractable nuclear antigen (ENA). Am J Med 1972;52:145-59.       
4. Lecky BR, Hughes RA, Murray NM. Trigeminal sensory neuropathy. A study of 22 cases. Brain 1987;110:1463-85.    [PUBMED]   
5. Hagen NA, Stevens JC, Michet CJ Jr. Trigeminal sensory neuropathy associated with connective tissue diseases. Neurology 1990;40:891-6.    [PUBMED]   
6. Haroon N, Nisha RS, Chandran V, Bharadwaj A. Pulmonary hypertension not a major feature of early mixed connective tissue disease: A prospective clinicoserological study. J Postgrad Med 2005;51:104-8.       
7. Marvisi M, Ajolfi C, Civardi G, Delsignore R. Thyroid dysfunction and pulmonary hypertension. Recenti Prog Med 2004;95:443-6.    [PUBMED]   
8. Bennett RM, O'Connell DJ. Mixed connective tisssue disease: a clinicopathologic study of 20 cases. Semin Arthritis Rheum 1980;10:25-51.    [PUBMED]   
9. Bennett RM, Bong DM, Spargo BH. Neuropsychiatric problems in mixed connective tissue disease. Am J Med 1978;65:955-62.    [PUBMED]   
10. Kimber TE, Scott G, Thompson PD, Beare JH. Vasculitic neuropathy and myopathy occurring as a complication of mixed connective tissue disease. Aust N Z J Med 1999;29:82-3.    [PUBMED]   
11. Graf WD, Milstein JM, Sherry DD. Stroke and mixed connective tissue disease. J Child Neurol 1993;8:256-9.    [PUBMED]   
12. Abe K, Yanagihara T. Treatable dementia. Clin Neurosci 1995;13:644-5.

Decision on breast implants welcomed
2 Richmond surgeons back FDA approval of silicone-gel product

 Nov 25, 2006

Plastic surgeons Lewis Ladocsi and Andrea Pozez say they never understood the U.S. Food and Drug Administration's rationale for restricting silicone gel-filled breast implants in the first place.

The federal agency last week agreed to allow silicone gel-filled implants back on the market, reversing a decision in the early 1990s to limit the implants because of concerns that ruptured or leaking implants caused health problems in patients, including connective-tissue disorders.

Two companies, Allergan Corp. (formerly Inamed Corp.) of Irvine, Calif., and Mentor Corp. of Santa Barbara, Calif., are being allowed to market their silicone gel-filled implants for breast reconstruction in women of all ages and for breast augmentation in women ages 22 and older.

Before Nov. 17, women received silicone gel-filled implants only as part of research studies after certain protocols. In addition, those women had to be undergoing breast reconstruction after trauma or cancer, for instance, or breast revision surgery to replace implants.

The FDA over the years has rejected applications to market the implants.

Saline-filled breast implants were still available as an option. Doctors say silicone gel-filled implants feel and behave more like natural breast tissue.

"They feel dramatically different. They are softer, warmer, more pliable," said Ladocsi of Richmond Plastic Surgeons.

"This is the most studied medical device," Ladocsi said. "They have been studied more than pacemakers. There has never been any credible evidence they were harmful."

Pozez, professor and chair of the division of plastic and reconstructive surgery at Virginia Commonwealth University, said the 1991 action to allow silicone gel-filled implants for some women and not others sent a mixed message.

"The science of implants is the same for augmentation or for reconstruction," Pozez said. "Over those 14 years, implants have been registered, and the data has been collected and analyzed. And based on continued science," the FDA approved the Mentor and Allergan products, she said.

The FDA approval comes with requirements for the companies. They have to:

conduct a large study following about 40,000 women for 10 years after receiving breast implants;
conduct a focus-group study of the patient-information labels;
continue laboratory studies to further characterize types of device failure; and
track each implant so that health professionals and patients can be notified of updated product information.
There are also requirements about what is included in information provided to patients.

Women considering implants have to be told that breast implants typically don't last forever and may have to be replaced.

"The majority of patients with breast implants of any kind can have the potential need for replacement due to implant failure or other conditions, including infection and scarring," Pozez said.

In addition, patients have to be advised about the importance of routine screening to monitor for implant rupture. Women will be told to receive a screening MRI three years after implant surgery and then every two years. Those costs can add up.

Other points that have to be highlighted include:

Many of the changes to a woman's breast after implantation are irreversible. Some women experience something called capsular contracture in which the scar tissues that form around the implant harden to the degree that it flattens the implant and increases risk of rupture.
Rupture of a silicone gel-filled breast implant is often undetectable to a woman and her doctor.
Now that the FDA is allowing silicone-filled breast implants back on the market, doctors expect many women to choose them.

Ladocsi said saline-filled implants were not a good option for some patients, particularly slim women without a lot of breast tissue. The natural folds of the implants are seen through the skin, causing a rippling or wrinkling effect.

Ladocsi said women generally do not aim for the Pamela Anderson look; most just want to better balance their figures. Some come after pregnancy and breast-feeding have changed the appearance of their breasts. Some have lost a lot of weight and want firmer breasts.

"The typical breast-enhancement patient is in her 30s, a mom, well-educated and has considered surgery for a year," Ladocsi said.

Connective tissue disease

A connective tissue disease is any disease that has the connective tissues of the body as a primary target of pathology. Connective tissue is any type of biological tissue with an extensive extracellular matrix that supports, binds together, and protects organs. These tissues form a framework, or matrix, for the body, and are composed of two major structural protein molecules, collagen and elastin. There are many different types of collagen protein in each of the body's tissues.

Elastin has the capability of stretching and returning to its original length - like a spring or rubber band. Elastin is the major component of ligaments (tissues that attach bone to bone) and skin. In patients with connective tissue disease, it is common for collagen and elastin to become injured by inflammation.ஐﻬ Many connective tissue diseases feature abnormal immune system activity with inflammation in tissues as a result of an immune system that is directed against one's own body tissues (autoimmunity).

Diseases in which inflammation or weakness of collagen tends to occur are also referred to as collagen diseases. Collagen vascular disease is a somewhat antiquated term used to describe diseases of the connective tissues that typically include diseases which can be (but are not necessarily) associated with blood vessel abnormalities.

Connective tissue diseases can have strong or weak inheritance risks, and can also be caused by environmental factors.

Heritable Connective Tissue Disorders
Marfan syndrome - a genetic disease causing abnormal fibrillin.
Ehlers-Danlos syndrome - causes progressive deterioration of collagens, with different EDS types affecting different sites in the body, such as joints, heart valves, organ walls, arterial walls
Osteogenesis imperfecta (brittle bone disease) - caused by insufficient production of good quality collagen to produce healthy, strong bones.

 Weakly or Non-Heritable Connective Tissue Disorders
These are the autoimmune CTDs, where the cause is unknown but may have both genetic and environmental links. Weaker genetic factors may create a predisposition towards developing these autoimmune diseases.

They are characterized as a group by the presence of spontaneous overactivity of the immune system which results in the production of extra antibodies into the circulation. The classic collagen vascular have a "classic" presentation with typical findings that doctors can recognize during an examination. ஐﻬ Each also has "classic" blood test abnormalities and abnormal antibody patterns. However, each of these diseases can evolve slowly or rapidly from very subtle abnormalities before demonstrating the classic features which help in the diagnosis. The classic collagen vascular diseases include:

Scurvy - caused by a dietary deficiency in vitamin C, leading to abnormal collagen.

Systemic Lupus Erythematosus (SLE) - An inflammation of the connective tissues, SLE can afflict every organ system. It is up to nine times more common in women than men and strikes black women three times as often as white women. The condition is aggravated by sunlight.

Rheumatoid Arthritis - Rheumatoid arthritis is a systemic disorder in which immune cells attack and inflame the membrane around joints. It also can affect the heart, lungs, and eyes. Of the estimated 2.1 million Americans with rheumatoid arthritis, approximately 1.5 million (71 percent) are women.
Scleroderma - Scleroderma is an activation of immune cells which produces scar tissue in the skin, internal organs, and small blood vessels. It affects women three times more often than men overall, but increases to a rate 15 times greater for women during childbearing years, and appears to be more common among black women.
Sjogren's Syndrome - Sjögren's syndrome (also called Sjögren's disease) is a chronic, slowly progressing inability to secrete saliva and tears. It can occur alone or with rheumatoid arthritis, scleroderma, or systemic lupus erythematosus. Nine out of 10 cases occur in women, most often at or around mid-life.
Myositis - Myositis involves inflammation that results in damage to muscle fibers and skin. Myositis is a term that describes several illnesses including polymyositis, dermatomyositis and inclusion body myositis. Polymyositis involves inflammation of the muscles and can affect many parts of the body. Dermatomyositis involves inflammation of skin. Inclusion myositis is similar to polymositis, but its onset is generally slower and more relentlessly progressive. All of these fall into the category of inflammatory muscle diseases — "myo" means "muscles" in Greek; "itis" means "inflamed." "Derma," which means "skin," implies the skin-related signs and symptoms that accompany the muscle inflammation of dermatomyositis
Mixed Connective Tissue Disease - Mixed connective-tissue disease (MCTD) is a disorder in which features of various connective-tissue diseases (CTDs) such as systemic lupus erythematosus (SLE); systemic sclerosis (SSc); dermatomyositis (DM); polymyositis (PM); and, occasionally, Sjögren syndrome can coexist and overlap. The course of the disease is chronic and usually milder than other CTDs. In most cases, MCTD is considered an intermediate stage of a disease that eventually becomes either SLE or Scleroderma.


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