Lupus

Monday, January 30, 2012

Connective Tissue Disease

There are many different diseases that are considered on the list of connective tissue diseases.  These are diseases such as  SLE (lupus), RA (rheumatoid arthritis), and Sjögren syndrome just to name a few.  There are a significant amount of people who have a connective tissue disease, but do not fit the criteria for diseases like lupus but suffer greatly and have an alike illness.  When people say they have a lupus like disease they are usually talking about what doctors call an Undifferentiated Connective-Tissue Disease or UCTD.  This does not mean that this person does not have a diagnosis, it just means that they have a different but alike disease.  There is also a group of diseases that make up a diagnosis such a Mixed Connective Tissue Disease or MCTD.  In this post I am going to have these diseases described in-depth and hopefully create more understanding about these illnesses.

Undifferentiated Connective Tissue Disease - In-Depth Overview 
http://www.hss.edu/conditions_undifferentiated-connective-tissue-disease-overview.asp 
Definition
The term "undifferentiated connective tissue disease" (UCTD) is used to describe people who have symptoms and certain lab test results that look like a systemic autoimmune disorder or connective tissue disease. But they don't have enough of such characteristics to meet the diagnosis for a well-defined connective tissue disease, such as rheumatoid arthritis, lupus, or scleroderma. Thus, they seem to have another, similar disorder that doctors call undifferentiated connective tissue disease."
[A systemic autoimmune disorder means that it affects your whole body (systemic) and that your immune system, which normally protects you from outside invaders such as bacteria, turns on parts of your own body and attacks them as if they were invaders. Connective tissue is the "glue" that supports and connects various parts of the body; it includes skin, cartilage, and other tissue in the joints and surrounding the heart and lungs and within the kidney and other organs.]
Although the word "undifferentiated" sounds vague, rheumatologists know this term describes a real problem. It does not mean that your doctor does not know what to call what you have.
This undifferentiated category is distinctly separate from another group of vague-sounding disorders called "overlap syndromes." People with these syndromes have enough features of more than one connective tissue disease to meet the diagnoses for several at the same time. Thus, they "overlap" two or more diseases. (For example, mixed connective tissue disease [MCTD] is just such an "overlap" syndrome.)
In contrast, patients with UCTD will not have enough of the features of any one rheumatic disease to be firmly classified as such by the currently established diagnostic criteria. However, because they may have features from several known diseases, they are said to be "undifferentiated." (See Fig. 1)
Figure 1

The term undifferentiated connective tissue disease was first used in 1980's to identify people who were recognized as being in the early stages of a connective tissue disease (CTD) but who did not yet meet the standard criteria for a well-defined CTD. At that time, it was noted that a substantial proportion of these patients remained undifferentiated - or experienced a disease remission (in which symptoms went away) - and never evolved in to a more defined rheumatic disease. Other names used early on to describe some of these patients included "latent lupus" and "incomplete lupus erythematosus," which meant that some features suggestive of lupus were present, but not enough to fulfill make the diagnosis. As many as a quarter of all patients seen by rheumatologists have UCTD.
Many researchers have been studying people with UCTD. They have been trying to identify serologic profiles (markers in the blood) that may predict who will eventually develop a well-defined connective tissue disease. They are also looking for markers to help predict whether the disease may go away, remain unchanged, or get worse. It is currently believed that less than 20% of patients with UCTD go on to develop a definite connective tissue disease. As many as one-third will experience a remission of their symptoms. The rest continue with generally mild disease in the undifferentiated form.
II. Pathogenesis
Pathogenesis refers to the origin and development of a disease. The actual cause of UCTD, like many rheumatic diseases, is not well understood. Indeed, there have been no rigorous attempts to define the basic science of UCTD. It is presumed that many of the same immunologic mechanisms that play a role in lupus and rheumatoid arthritis may be involved. Theories in those diseases include a genetic predisposition, which is subsequently triggered by some environmental factor, such as an infection, that is improperly handled by the immune system. This in turn causes the immune system to be "turned up high," or activated, when it shouldn't be and to target the tissues of one's body instead of foreign invaders (such as bacteria). Which of - or whether - these elements might be involved in UCTD remains unknown. UCTD will be difficult to study because it includes a heterogeneous population - people with so many different symptoms and blood markers. UCTD is not contagious.
III. Clinical Presentation
In the studies of patients that have been done to date, the most common symptoms of UCTD are:

  • arthralgia (joint achiness);
  • arthritis (joints that are swollen and hot, often with redness of the overlying skin;
  • rashes, usually on the face, which can worsen due to sun exposure;
  • alopecia (hair loss);
  • Raynaud's phenomenon (color changes in your hands and feet in response to cold);
  • oral ulcers (sores inside the mouth);
  • xerophthalmia (dryness of the eyes due to decreased tears);
  • xerostomia (dry mouth due to decreased saliva);
  • low-grade fever (usually under 100o f);
  • photosensitivity ( development of rashes or other symptoms after sun exposure).
Some people also develop:

  • leukopenia - decreased numbers of white cells (cells that help fight infection) in your blood;
  • anemia - decreased numbers of red blood cells (cells that carry oxygen to tissues in the body) in your blood;
  • thrombocytopenia - an abnormal decrease in the number of platelets (the parts related to blood clotting);
  • pleuritis or pericarditis - inflammation of the lining surrounding the lungs or heart, respectively, which may cause pain in the chest, especially with breathing;
  • neuropathy - abnormal nerve sensations, usually in the fingers or toes, ranging from numbness to tingling to pain.
Problems with the kidneys, liver, lungs, or brain are almost unheard of in UCTD.
The overwhelming majority of people with UCTD do not develop major organ damage or life-threatening disease. The hallmark of UCTD is its mild course and low likelihood of progression to a more serious state.
"Criteria" are the list of problems that a doctor looks for to make a diagnosis. There are no commonly accepted criteria yet for UCTD, as there are for many other rheumatic diseases. However, preliminary one has recently been proposed (See Mosca in Annotated Bibliography below) as follows:
Preliminary Classification Criteria for UCTD
  • Signs and symptoms suggestive of a CTD, but not fulfilling the criteria for any of the defined CTDs, for at least three years
  • Presence of ANA identified on two different occasions
(ANA refers to antinuclear antibodies found in the blood. These markers may indicate that your immune system is forming antibodies to parts of your body.)
At the present time, UCTD is diagnosed clinically by your doctor when the symptoms, labs and history fit the "pattern" which doctors are used to seeing with this disease. It is not based on meeting a checklist of required "criteria" alone. As doctors develop more specific criteria for UCTD, however, it will be easier to study the disease and learn about its causes and best treatments.
IV. Laboratory Findings
A. Immunologic
Some markers in your blood indicate possible abnormal function of your immune system. While most studies note that the majority of patients with UCTD are have antinuclear antibodies (ANA), a broad range of immunologic abnormalities can be seen in people with UCTD. These may include:

  • elevated erythrocyte sedimentation rate (ESR - an indicator of inflammation);
  • antiphospholipid antibodies (which can affect blood clotting and may increase your risk of miscarriage),
  • hypergammaglobulinemia (an excess of gamma globulin, often called IgG, a protein in the blood that's involved in resistance to infection);
  • hypocomplementemia, (a decreased level of complement -- proteins that help destroy bacteria and other cells -- commonly referred to as C3 and C4);
  • a false positive blood test for syphilis, known as "RPR" (meaning the lab test indicates you have syphilis but you really don't, which can be proven by a more complex test);
  • positive evidence of other markers of autoimmune disease, such as anti-dsDNA (double-stranded DNA) antibodies, anti-Ro/SSA, anti-SM (Smith), anti-RNP, rheumatoid factor (RF); and anti-Ku antibodies.
B. Hematologic
As noted above, several blood disorders - thrombocytopenia, leukopenia, and anemia - may also occur in patients with UCTD. They are rarely severe enough to require treatment alone.
C. Predictive Value of Laboratory Findings
Research has attempted to determine which, if any, of the laboratory test findings may predict the evolution of UCTD to lupus or other connective tissue diseases.
In a study of 148 patients who had detectable anti-Ro/SSA antibodies and a diagnosis of UCTD for at least one year, leukopenia was more frequent in those patients who ultimately developed a defined connective tissue disease. Anti-dsDNA antibodies were predictive of evolution to SLE. However, the majority of patients in this study who developed a connective tissue disease progressed to primary Sjogren's syndrome (50%) - which is notable for dry eyes and dry mouth.
Another study found that anti-RNP antibodies were significantly correlated with Raynaud's phenomenon and arthritis. Anti-Ro antibodies also correlated with dry eyes and dry mouth. . Most interestingly, 82% of those studied were found to have a simple autoantibody profile characterized by a single specificity. The serologic profile of these UCTD patients remained unchanged in follow-up.
Among those UCTD patients with features more suggestive of lupus (termed incomplete lupus), it has been noted in a group of 87 patients that elevated dsDNA and decreased C4 (one type of complement) were associated with subsequent development of lupus. Others have noted that the presence of homogeneous ANA (one of several "patterns" of ANA that are seen in the microscope) and presence of anti- Sm antibody predicted the development of lupus.
One physical finding which is thought to predict evolution to a defined CTD is abnormalities in the capillaries (the tiniest blood vessels) in the folds of fingernails or toenails. One study followed 43 patients with UCTD; it found that 23% of those with abnormal capillaries progressed to definite scleroderma (also called systemic sclerosis). Similar studies have suggested that the rate of progression might be even higher. If you are worried about this, your doctor - or a doctor to whom you are referred - can examine your nailfolds under a microscope. However, nailfold capillary abnormalities have been seen in many other diseases, such as dermatomyositis, lupus, and Sjogren's syndrome, and psoriasis.
It is always wise to discuss your laboratory tests with your doctor and ask for explanations of what they mean. You may want to ask for copies of your test results to keep in a folder at home so you can see how they change - or do not change - over time.
V. Differential Diagnosis
Many different diseases can cause symptoms similar to those of UCTD. Differential diagnosis is the process by which the physician figures out which one is causing your problems. This is important because diseases that may cause such symptoms are often treated in a very different manner from UCTD.
Other well-defined connective tissue diseases that need to be considered in the process of differential diagnosis include: rheumatoid arthritis, systemic lupus erythematosus (SLE), myositis, Sjogren's Syndrome, and scleroderma. Diffuse body pain without other objective features, even in the presence of a positive ANA, argues more strongly for fibromyalgia than a true connective tissue disease.
A thorough history, exam and laboratory evaluation to rule out these other rheumatic diseases is important. In this sense, the diagnosis of UCTD is one of exclusion. When the suspicion of an autoimmune disease is high in a patient because several features of one or more of these diseases is present, but signs and symptoms are insufficient to meet their criteria, UCTD is diagnosed. However, the threshold for reconsideration of a more definite CTD must be low if, and when, new symptoms present in such patients.
VI. Initial Treatment
No formal study of various treatments in patients with UCTD has been conducted. Most therapies are borrowed from physicians' experiences of their effectiveness in other rheumatic diseases. However, it is unknown to what degree a particular therapy improves the symptoms of UCTD or decreases the rate of flare or the likelihood of evolution to a more defined connective tissue disease.
Most therapies are symptomatic and include:

  1. analgesics (pain killers such as acetominophen) and non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen for musculoskeletal symptoms, such as joint and muscle aches or pains;
  2. topical corticosteroids (creams, lotions or gels that have anti-inflammatory action) and anti-malarial pills such as hydroxychloroquine (Plaquenil) for skin and mucous tissue symptoms. (Antimalarials have been found to modify immune system function.)
For symptoms that don't respond to these drugs, the physician may occasionally prescribe low dose corticosteroids in pill form (such as prednisone) for short periods of time. High doses of corticosteroids, cytotoxic agents (such as cyclophosphamide, brand named Cytoxan), and immunosuppressives (such as azathioprine, brand named Imuran) are almost never used.
However, there is one interesting study of another immunosuppressive drug, methotrexate (brand named Rheumatrex) that evaluated its use in lupus patients who did not have kidney disease and in 15 UCTD patients whose most common clinical findings were positive ANA, non-erosive polyarthritis, and Raynaud's phenomenon. Overall efficacy was noted in 53% of patients, including six out of 10 with arthritis; 60% had side effects, with 33% discontinuing the drug. It is possible that this drug may be useful for hard-to-treat joint and skin problems, although it is not commonly used at present.
VII. Long-Term Management Issues
Pregnancy: outcome, impact on flare rate and disease evolution
To date there has only been one study addressing the issue of pregnancy in patients with UCTD. Out of 25 pregnancies in 20 patients with the diagnosis for at least one year, 22 pregnancies were successfully brought to term. Complications were observed in six out of 22 of the successful pregnancies, but most were just early delivery and lower birth weight of the baby.
Some systemic autoimmune diseases tend to have alternating remissions (periods of no symptoms) and flares (periods of increased disease activity). In this pregnancy study, flares of UCTD were seen in six patients, with symptoms including arthritis, fever, and skin rash. One patient developed systemic lupus erythematosus. The flare rate was higher than the incidence of flares in a control population of non-pregnant UCTD patients. This suggests that your condition should be closely monitored during pregnancy.
Occurrence of Thyroid Disease
Thyroid disease, especially hypothyroidism (an underactive thyroid gland), is a common autoimmune condition which can be seen more frequently in patients with other autoimmune diseases, such as SLE and RA. One small study of 75 patients with UCTD showed that thyroid disease was present in 6%, suggesting that monitoring for the occurrence of thyroid disease by your doctor may be appropriate.
VIII. Prognosis
A prognosis is a forecast about the likely course of a disease. Patients with UCTD have an excellent prognosis. Almost all studies to date indicate a low likelihood of progression to any involvement of organs such as the kidney, lungs, and brain. A small minority of patients (<20%) go on to develop a well-defined connective tissue disease, but this becomes much less likely if the disease has been present unchanged for greater than five years.
In a substantial proportion of patients, the disease is mild and no treatment is needed. Rarely, in some people, the symptoms can go away completely. The majority of patients can be treated symptomatically, and very few patients ever require the use of immunosuppressive medications.
IX. When to Seek Referral to a Specialist
If your primary care physician suspects that you may have UCTD - or if you are believed to have any other systemic autoimmune or connective tissue disease - you should be seen by a rheumatologist for evaluation and to confirm the diagnosis. Consultation with a rheumatologist if UCTD is suspected is important to exclude the presence of any other definite connective tissue disease.
Once your symptoms have stabilized with effective medical management, ongoing monitoring should be done at least twice a year by the rheumatologist. Checking kidney and liver function and blood counts several times a year is sufficient unless new symptoms develop. Any new symptoms should be promptly evaluated to consider the possibility that the UCTD has evolved to a well-defined connective tissue disease that merits more aggressive treatment.
X. Annotated Bibliography
Alarcon GS. Unclassified or undifferentiated connective tissue disease. Baillieres Best Practice Clin Rheumatol. 2000 Mar;14(1):125-37.
A good review of the 10-year clinical outcomes in UCTD.

Mosca M, Neri R, Bombadieri S. Undifferentiated connective tissue diseases (UCTD): A review of the literature and a proposal for preliminary classification criteria. Clin Exp Rheumatol 1999 Sept-Oct:17(5):615-620. Review
This paper addresses need to systematically categorize those patients who should most appropriately be termed "undifferentiated." Classification criteria are proposed.

Mosca M, Neri R, Strigini F, Carmignani A, Totti D, Tavoni A, and Bombardieri S. Pregnancy outcome in patients with undifferentiated connective tissue disease: a preliminary study on 25 pregnancies. Lupus 2002;11(5):304-7.
This important study finds UCTD patients are at higher risk of pregnancy complications and argues for careful monitoring of these patients during pregnancy.

Williams HJ, Alarcon GS, Joks R, Steen VD, Bulpitt K, Clegg DO, Ziminski CM, Luggen ME, StClair EW, Willkens RF, Yarboro C, Morgan JG, Egger MJ, Ward JR. Early undifferentiated connective tissue disease (CTD). VI. An inception cohort after 10 years: disease remissions and changes in diagnoses in well established and undifferentiated CTD. J Rheumatol 1999 Apr 26(4):816-25.
This includes data on patients with UCTD followed over 10 years (the longest documented study) and makes the important observation that even with disease this far out, many patients still have not evolved into a more defined CTD.




Background

Connective-tissue diseases (CTDs) manifest with a wide range of clinical findings and laboratory abnormalities. The diversity of signs and symptoms frequently complicates the diagnosis of a rheumatic disease.
Diagnostic and classification criteria have been established for many CTDs, including rheumatoid arthritis (RA),[1] systemic lupus erythematosus (SLE),[2, 3] systemic sclerosis (SSc),[4] polymyositis (PM), dermatomyositis (DM),[5] mixed connective-tissue disease (MCTD),[6] and Sjögren syndrome (SS).[7, 8]
Some of these disease criteria overlap, further complicating the diagnostic workup in patients with a potential CTD. Unclassifiable symptoms, physical examination findings, or serological results suggestive of a CTD frequently lead to diagnoses such as incomplete lupus, latent lupus, overlap syndrome, and undifferentiated connective-tissue disease (UCTD). Conceptually, these terms may seem synonymous; however, specific definitions are necessary for appropriate diagnostic, therapeutic, and prognostic determinations.
In 1980, LeRoy et al proposed the concept of undifferentiated connective-tissue syndromes (UCTS) to characterize mixed or overlapping syndromes.[9] Since that time, innumerable case reports, case series, and clinical studies have used variable criteria to define UCTD. Such variation in the definition of UCTD results in ambiguity of study results and difficulty with interpreting the findings and conclusions. In 1999, Mosca et al proposed preliminary classification criteria for UCTD that have become increasingly accepted and used.[10] The authors suggested defining cases of UCTD as those in which signs and symptoms are consistent with a CTD but that do not fulfill the classification or diagnostic criteria for any one of the defined CTDs (ie, RA, SLE, SSc, PM/DM, MCTD, SS). In order to fulfill the criteria for UCTD, antinuclear antibodies must be present, along with a disease duration of at least 3 years. Cases with a shorter duration should be described as early UCTD.
Other definitions for UCTD have been proposed.[9, 11, 12, 13, 14, 15, 16, 17] However, many of these definitions are limited by the fact that they may lead to the inclusion of a defined CTD manifesting early or in an incomplete form. In 2008, Mosca et al admitted that, while their proposed classification criteria exclude most patients with an evolving definite CTD, limitations are evident. Their criteria do not allow the diagnosis of UCTD to be made at onset. In addition, the criteria do not exclude a slowly evolving or an incomplete definite CTD.[18] To avoid the misdiagnosis of transitory or early defined CTD, exclusion criteria were appended to the proposed classification criteria above.[19] These preliminary classification criteria for UCTD are listed in Table 1, although no mutual agreement has been reached regarding the criteria for diagnosis of UCTD.[20]
Table 1. Preliminary Classification Criteria for Undifferentiated Connective-Tissue Disease (Open Table in a new window)
Inclusion CriteriaClinical



Exclusion Criteriaa

Laboratory Exclusion Criteriaa
1. Signs and symptoms suggestive of a CTD but not fulfilling the diagnostic or classification criteria for any of the defined CTDs b for at least 3 years c



2. Presence of antinuclear antibodies determined on two different occasions

Malar rash



Subacute cutaneous lupus



Discoid lupus



Cutaneous sclerosis



Heliotrope rash



Gottron papules



Erosive arthritis

Anti-dsDNA



Anti-Smith



Anti-U1-RNP



Anti-Scl70



Anticentromere



Anti-La/SSB



Anti-Jo1



Anti-Mi2

a Applicable to patients at disease onset
b Using established classification criteria for SLE, MCTD, SSc, PM/DM, RA and SS
c If the disease duration is less than 3 years, patients may be defined as having an early UCTD.
Adapted from Mosca et al[10] and Doria et al[19]

Mixed Connective Tissue Disease

Mixed connective tissue disease is a rheumatic disease that has features shared by lupus,  scleroderma, polymyosistis or dermatomyositis and rheumatoid arthritis.

Symptoms of Mixed Connective Tissue Disease

When symptoms first appear, they may suggest that the person affected has any one of several rheumatic diseases. However, when a person has mixed connective tissue disorder, the symptoms aren't as severe or as widespread as they would be if the person has lupus, scleroderma, rheumatoid arthritis or other rheumatic disorder.

This condition has many symptoms, including:

  • Pain in two or more joints. Almost all persons with mixed connective tissue disease have this symptom. Three out of four persons with the condition have arthritis and may have the swollen, deformed joints of rheumatoid arthritis.
  • Raynaud's phenomenon. This symptom may appear years before any other.
  • Skin changes. These can be like those of lupus or red patches over the knuckles, violet discolorations of the eyelids, loss of hair over the body and abnormal opening up (dilation) of the capillaries of the hands and face that may form a tumor
  • Swollen hands. This is the most common symptom. With time, the fingers look more and more like sausages.
  • Muscle weakness. There may sometimes also be tenderness.
  • Difficulty swallowing and keeping food in the stomach.
  • Loss of sensation in the nerves of the face and head.
  • Lung disorders. Nearly 80% of the people with mixed connective tissue disease have some involvement of the lungs. Symptoms can include inflammation of the lining that covers the lungs and the inside of the chest, difficulty breathing or pulmonary hypertension.
  • Kidney disease. Only about one out of every 10 patients has this symptom, which is often mild. In some cases, however, it can become life threatening.

Causes and Risk Factors for Mixed Connective Tissue Disease

It isn't yet known what causes this disease. In some cases, it gets worse and develops into scleroderma or lupus. Several factors, however, suggest that mixed connective tissue disease is a distinct disorder in its own right. These include symptoms shared by several rheumatic conditions, the presence of certain antibodies, abnormalities in the system that regulates the body's immune response and frequent pulmonary hypertension.

Diagnosing Mixed Connective Tissue Disease

A rheumatologist may suspect mixed connective tissue disease if a patient appears to have lupus, scleroderma, vasculitis, polymyositis, Sjögren's syndrome, lymphoma or viral pericarditis but also has symptoms of the other conditions as well.
Your doctor may order:
  • Blood tests to measure antibodies or the presence of the rheumatoid factor, among other things
  • Electromyogram. This is a type of image that is made by recording the electrical activity of the muscles. It helps measure how well the nerves and muscles are communicating with each other.
  • Muscle biopsies. This involves taking a sample of muscle tissue to exam under a microscope. If a person has mixed connective tissue disease, there will be signs of damage to the muscle fibers.

Treating Mixed Connective Tissue Disease

This condition is treated much like lupus. Corticosteroids, especially when given early in the course of the disease, can be helpful in managing the symptoms.

Mild forms of the condition can be controlled with nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, antimalarial drugs or very low doses of corticosteroids. In some patients, the symptoms disappear for many years (go into remission) and don't require ongoing corticosteroids.

Mixed connective tissue disease can cause life-threatening complications such as pulmonary hypertension, kidney failure, heart attack, infections, stroke or the development of holes in the colon (the lower part of the large intestine). In these cases, patients need stronger treatment. This usually includes larger doses of corticosteroids.



Thursday, January 26, 2012

Lupus and hair loss

Hair loss or alopecia is a common symptom of lupus, it happens in about 45% of people, although some places have the statistic at around 70%.  This is a very emotionally taxing problem that a lupus patient can have, it can have devastating affects on ones self esteem.  Hair is so important especially to woman, it is part of our sexuality, beauty, and confidence.  I had thin hair on and off for years at first I had no idea why it would get so thin but after my SLE diagnosis, I knew the culprit.  Alopecia also runs in my family in absence of lupus, it can happen alone and is considered an autoimmune disease itself.  This symptom can come and go, so  depending on the cause, it is not usually permanent.  

Hair loss (alopecia)
http://www.lupus.org/webmodules/webarticlesnet/templates/new_empty.aspx?articleid=453&zoneid=76 
Hair loss occurs in about 45 percent of people with lupus at some time during the course of their disease. Most frequently the hair loss occurs at the onset of the illness, and may be one of the first symptoms of the disease recognized by the person. Most often, the hair loss is from all over the head, but sometimes the hair falls out in patches. When the disease is brought under control, the hair should grow back. Sometimes there is a rash in the scalp—usually subacute or chronic discoid—that interferes with the hair follicle. In this situation, the individual is left with a permanent area of alopecia. Drugs used to treat lupus, such as prednisone and immunosuppressive therapies, also may be the cause of reversible hair loss.

Coping with Lupus-Related Hair Loss

http://www.lupus.org/webmodules/webarticlesnet/templates/new_donate.aspx?articleid=496&zoneid=6 

A lupus diagnosis often brings many physical changes-from skin rashes to weight gain. And often, the most upsetting of these changes can be losing your hair.
"For so many people, it is a major quality-of-life issue," says Victoria Werth, M.D., a professor of dermatology and medicine at the University of Pennsylvania School of Medicine in Philadelphia.
Although hair loss can be overwhelming, it needn't be totally devastating. These days it's easier than ever to face the problem head-on. Hair loss is a common side effect of both lupus and the medications used for treatment, so work with your doctor to discover the cause. "There are many reasons for hair loss," says Werth. "Some is caused by scarring associated with discoid scalp lesions, and some is diffusive and does not result from scarring, as with systemic lupus."
If hair loss is caused by medication, you may have to wait until your lupus is under control. Luckily, says Werth, this type is "mostly reversible." Hair loss associated with discoid lesions and scarring is generally permanent, so early treatment is key.
But don't experiment with over-the-counter medications, like Rogaine, without your doctor's approval. "Rogaine is for treating male- and female-pattern alopecia, which is a completely different type of hair loss than we usually see in lupus," says Werth.
Brittle hair also is common, and many treatments-including steroids and immunosuppressives-cause hair to thin.
Once your diagnosis is clear, maximize your assets. If your hair loss is mild, try a new haircut. Long hair is weaker than short, so consider a shorter 'do' with layers to hide thinning or bald patches. Wash fragile hair with baby shampoo, and use a leave-in conditioner with sun block. Avoid adding more stress to your hair from using curlers and alcohol-based styling products, which can irritate sensitive skin.
Finally, don't shy away from wearing a hairpiece, hair extensions, or a wig. Hairpieces and extensions can be added into thin areas to create a fuller look. Just make sure that these aren't too tight, because tension on weakened hair also can lead to hair loss. Wigs come in a wide range of styles, colors, and lengths. And don't forget your scalp! Keep it dry to prevent chafing, and remove the wig occasionally to allow your skin to breathe.
Whether you decide to go with a wig or a new hairstyle, remember that there's no wrong way to deal with hair loss. "Everyone has a different comfort level," says Werth. "It should be an individual decision." 

Action steps 

http://www.lupusny.org/about-lupus/newsletters/winter-2010/what-do-about-lupus-hair-loss

Losing hair can be scary, but it’s usually treatable and often can be covered up. It may take a while for hair to grow back—sometimes 6 months or more—but eventually it usually does unless it’s caused by skin (“cutaneous”) lupus that leads to a “discoid rash.” (Patches of thick and scaly red “discoid” rash can scar hair follicles and cause lasting hair loss, so be sure to talk to your doctor about your options if these develop. “Alopecia” is the medical term for hair loss.)
For most hair loss, you aren’t powerless! Here are some strategies to try:

  • Refresh your hair style. Ask a hairdresser for ideas to cover up bald spots. To make hair look thicker, try a cut that layers. When blow drying, try lifting hair up and away from the head. Or ask about dying hair to cover up bare scalp that otherwise might show through.
  • Consider hair extensions.  If you still have some healthy hair and are just missing some patches on the sides (not the top)—and aren’t actively losing hair—consider hair extensions. Pre-made and custom-made extensions are available, and different ways to attach them (sewing, knotting, or adding in through tiny links are often best to avoid contact with chemicals, adhesives (glues) and heat.
  • Try a wig. These days wigs are so well-made that most people can’t tell you have one on. To start take a friend to just look around. You may well feel a lot better when you see what options there are!
  • Experiment with hair wraps, scarves, bandanas, accessories—tips are on the Internet! Enter “hair loss” along with the term “wrap,” or “scarf” in Youtube.com and you’ll get more free video demonstrations and ideas than you can handle!  
  • Last resort: cosmetic surgery. For extreme and permanent hair loss, stretching the remaining hair to cover what’s been lost may be an option, or even transplanting hair from another part of the scalp.
If you have lupus and are losing hair, do NOT experiment with over-the-counter hair loss treatments. Talk to your doctor about treatment options.  

What’s NOT to blame for lupus hair loss? 

While it’s only common sense to avoid harsh chemicals or even very tight braids that pull on your scalp, you can’t really blame serious hair loss on a lack of vitamins, washing your hair a lot, or using hair colorings or other common hair products. Some hair loss follows the pattern that your mother or father experienced as well, and is totally normal.

Alopecia

http://www.hopkinslupus.org/lupus-info/lupus-affects-body/skin-lupus/ 

About 70% of people with lupus will experience hair loss (alopecia) at some point during the course of the disease. Hair loss in lupus is usually characterized by dry, brittle hair that breaks, and hair loss is more common around the top of the forehead. Physical and mental stress can also cause hair loss, as can certain medications, including corticosteroids such as prednisone. In many cases the hair will grow back, but hair loss due to scarring from discoid skin lesions may be permanent. There is no cure-all for hair loss, but treatments such as topical steroids and Rogaine may be prescribed. Sometimes dealing with the cosmetic side effects of lupus can be difficult, but some people find using hairpieces and wigs to be an effective means of disguising hair loss.

Natural Help for Hair Loss

Always ask your doctor before trying any new treatments even if it is natural.

By Kathleen Halloran  http://www.motherearthliving.com/natural-beauty/natural-help-for-thinning-hair.aspx
May/June 2000
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Sometimes what we see in the mirror every morning can affect our self-esteem more directly than any other event of the day. For men and women who are losing their hair, the mirror provides an unpleasant documentation of the problem. The extent to which hair loss and balding affects people’s lives is reflected in the millions of dollars spent each year on expensive products—both prescription and alternative—that purport to cure the problem. The few prescription drugs available for balding work in some cases, but not for all. Some can be accompanied by serious side effects.
If you’re experiencing hair loss, don’t rule out natural alternatives. Although no remedy will work for everyone, natural approaches have helped many.
“Herbal medicine has a variety of ways to contribute to the extreme slowing down of this process and the minor expression of genetics—as opposed to being completely bald like our ancestors,” says Thomas Lee, a naturopathic physician in Phoenix who has worked with dozens of balding men. Most of these men came to him for other health problems and began noticing within a few months that the herbal support and lifestyle changes were also resulting in thicker hair and less gray, he says.

Understanding hair loss

Hairs are made of the protein keratin, the same substance in nails and skin, and their growth is most often triggered by hormones. When a man reaches puberty and testosterone levels start to rise, he begins to develop underarm, pubic, and facial hair. For many men, the hormones at this stage are also believed to initiate what in later years will become male pattern baldness.
Each hair, which rises out of a bulblike follicle, goes through a cycle of growth for up to about five years. It then stops growing and shifts into a period of rest, after which it falls out and a new hair begins to grow. This cycle happens throughout our lives, and even people with healthy hair lose up to 100 hairs a day.
Hair loss can be caused by a number of factors, including circulation, stress, hormonal changes, and nutrition. But the most potent influence—and the toughest to combat—is genetics. In people experiencing genetic hair loss, there are believed to be more hormone receptors in the balding areas of the scalp. One male hormone that is converted from testosterone, called dihydrotestosterone (DHT), damages the hair follicles so that the hairs gradually become finer and the growth cycles shorter. The conversion of healthy male hormones to unwanted DHT is driven by an enzyme produced mainly in the prostate and adrenal glands. DHT also plays a role in prostate enlargement, so the two conditions are linked.
According to the American Hair Loss Council, more than half of all American men experience significant hair loss by the age of forty-five. Although pattern baldness also occurs in women, they have much lower levels of DHT, and the problem is ­almost always much less pronounced, resulting in thinning hair rather than bald heads; in women, the hair loss is often linked to the adrenal glands, Lee says.
Other causes of hair loss include auto-immune diseases, stress, poor nutrition, and side effects of radiation or medication for conditions ranging from arthritis and gout to heart problems and depression. Dealing first with those problems may well eliminate further hair loss.

What to do

Once the hair follicles die and a man has been bald for some time, it becomes impossible to revive the follicles and reverse the process. The lesson here is a common refrain today: Prevention is the best cure. Don’t wait until it’s too late or your only options are a toupee, a transplant, or some hair product that comes in a spray can.
The first drug approved by the Food and Drug Administration (FDA) for treatment of hair loss was Rogaine (minoxidil), originally developed to fight hypertension. Applied as a cream, Rogaine doesn’t work for everyone and doesn’t block the formation of DHT, so its effects on hair growth last only as long as a man uses the treatment, and it doesn’t prevent the deterioration of the follicle. More recently, a DHT blocker, Propecia (finasteride), won approval, but for a small number of men it has unfortunate side effects, including decreased sexual desire and impotence. Propecia doesn’t prevent baldness in women, and because it has been associated with birth defects, the FDA recommends that pregnant women avoid contact with the drug.
The natural treatment approaches, which have not been studied and tested for hair loss the way the pharmaceuticals have, generally focus on substances that help block the formation of DHT and restore vitality to the remaining hair follicles.

Alternative approaches

Among the herbs that naturopathic physicians often use to slow down hormonal effects are saw palmetto, pygeum, horsetail, corn silk, and licorice. (See “Healthy hair, the natural way” on page 56 for more detail.) Rosemary, horsetail, and nettle are among another category of herbs that encourage hair growth by promoting blood circulation to the scalp and unclogging pores so that nutrients get to the follicle more easily. General herbs for circulation such as ginkgo are also sometimes used, and women experiencing ­pattern baldness will most often respond to herbs that target adrenal insufficiency such as Siberian ginseng, astragalus, or licorice.
Vitamins, minerals, and amino acids are a critical part of having healthy hair and keeping it. Not only is it important to maintain sufficient quantities of these ­nutrients, but also that you take in a ­proper balance of them, because excessive amounts of one can create deficiences in another. The answer is good nutrition and a good multivitamin and mineral supplement, or work with an expert on a personal approach that is best for you.
Remember that hair growth is slow and the process takes time. Lee, the Phoenix naturopath, says at least 80 to 85 percent of his patients begin to see a noticeable improvement in their hair within four to six weeks, or sometimes as long as six months.
“Whether the improvement is as dramatic and complete as they would have liked is hard to say,” he says. With an issue such as balding, where vanity plays a powerful role, it’s difficult to keep expectations in bounds. So as you approach your own hair thinning, try to be patient and reasonable. The results may be a pleasant surprise.