Autoimmune disease articles

[LIGA girl]

Welcome to the thread for those who want to find out more about autoimmune disease which is the underlying cause of many of the diseases we all suffer from.
I've spoken to Nick and other members about starting this thread ¦. All think it will benefit a lot of us here ¦..

My idea is that we will post articles, or links to articles, about autoimmune disease, its causes, things that aggravate or alleviate symptoms, the way it works, how it manifests itself etc. A brief summary or critique posted before the article would also be helpful in some cases.

If you gain information via a different source, eg a radio program, a TV show or newspaper article, and would like to write up a brief account of the info you found out, that would also be useful.

If you find a previous poster's article particularly useful, put up a posting saying so, but we would rather that the thread stay clear of personal recounts.

I hope this thread becomes a valuable resource for SkinCell members interested in learning about, and controlling, their skin disease.

Vicki

[LIGA girl]

This extract from Wikipedia gives a general introduction, along with a list of autoimmune diseases. They are believed to run in families, so if you have family members with some of these, it increases the chance of you having one of them too ...I have taken out the non skin related diseases from the lists.

Autoimmune diseases arise from an overactive immune response of the body against substances and tissues normally present in the body. In other words, the body attacks its own cells. Today there are more than 40 human diseases classified as either definite or probable autoimmune diseases, and they affect 5% to 7% of the population. Almost all autoimmune diseases appear without warning or apparent cause, and most patients suffer from fatigue.

The causes of autoimmune diseases are still obscure: Some are thought to be either examples of or precipitated by diseases of affluence. For example, arthritis and obesity are acknowledged to be related, and the World Health Organisation states that arthritis is most common in developed countries. Most autoimmune diseases are probably the result of multiple circumstances, for example, a genetic predisposition triggered by an infection.

Women tend to be affected more often by autoimmune disorders; nearly 79% of autoimmune disease patients in the USA are women. Also they tend to appear during or shortly after puberty. It is not known why this is the case, although hormone levels have been shown to affect the severity of some autoimmune diseases such as multiple sclerosis [1]. Other causes may include the presence of fetal cells in the maternal bloodstream. [2]

Diseases with a complete or partial autoimmune etiology:

   
    * Coeliac disease is a disease characterised by chronic inflammation of the proximal portion of the small intestine caused by exposure to certain dietary gluten proteins.
   

    * Pemphigus is an autoimmune disorder that causes blistering and raw sores on skin and mucous membranes.
   
Suspected

Diseases suspected to be linked to autoimmunity are:

    * Alopecia universalis is a suspected autoimmune disease in which the body's white blood cells attack hair and result in total baldness.
   
    * Hidradenitis suppurativa is a rare skin disease in which apocrine sweat glands become severely inflamed. Researches have found an improvement in case studies with Remicade and other biologics.
   
    * Psoriasis is a skin disorder in which rapidly-multiplying skin cells produce itchy, scaly inflamed patches on the skin.
    * Sarcoidosis is a disease wherein granulomas can form anywhere in the body but particularly in the lungs.
    * Scleroderma is a chronic disease characterized by excessive deposits of collagen. Progressive systemic scleroderma, the serious type of the disease, can be fatal. The local type of the disease is not serious.

    * Vitiligo is the spontaneous loss of pigment from areas of skin. The pigment-free areas have few or no melanocytes. Researchers have detected anti-melanocyte antibodies in some cases of vitiligo, so it seems likely that at least some instances of this condition are the result of autoimmune problems.

[LIGA girl]

From the Health Encyclopedia:


Causes and Risk Factors of Autoimmune Diseases and Disorders
Scientists believe multiple factors such as environmental toxins, heredity, viruses, and certain drugs may play a role in causing an autoimmune disease.

Stress, poor diet, lack of exercise, lack of sleep, abuse of alcohol and use of tobacco can also weaken the immune system and may play some role as well.

Diagnosis of Autoimmune Diseases and Disorders
Your doctor will take a complete medical history, perform a physical examination, and may order blood tests, radiological studies, and other studies.

Your doctor may also order tests to rule in or rule out specific autoimmune diseases. For example: for rheumatoid arthritis, the rheumatoid factor test; for myasthenia gravis, the acetylcholine receptor antibody test; and for thyroid disorders, thyroid function tests.

Treatment of Autoimmune Diseases and Disorders
Most autoimmune diseases cannot yet be treated directly, but are treated according to symptoms associated with the condition.

Doctors may prescribe corticosteroid drugs, non-steroidal anti-inflammatory drugs (NSAIDs) or more powerful immunosuppressant drugs such as cyclophosphamide, methotrexate and azathioprine that suppress the immune response and stop the progression of the disease.

Radiation of the lymph nodes and plasmapheresis (a procedure that removes the diseased cells and harmful molecules from the blood circulation) are other ways of treating an autoimmune disease.

Self Care
Boost your immunity naturally by altering your eating and exercise habits.

Nutritionists recommend a diet high in fresh vegetables and fruit, whole grains, brown rice, low-fat dairy products, fish and poultry. A daily multivitamin should be taken. Exercise daily if possible.

Questions To Ask Your Doctor About Autoimmune Diseases and Disorders
What caused this autoimmune disorder?

What type of treatment do you recommend?

What medications will you prescribe?

What are the side-effects?

Will changing current eating habits and beginning an exercise program help?

Can this condition be reversed with lifestyle changes?

[LIGA girl]

I heard a radio show about a possible link between early life experiences (at age 4 and under) and autoimmune diseases later in life. They said that kids who have exposure to more germs early in life (eg they eat dirt and get out in the open more and mix with people) are less likely to develop an autoimmune disease and that those kids who are exposed to tobacco smoke are more likely to develop an autoimmune disease.

[LIGA girl]

 Autoimmune Diseases
Very simply stated, autoimmune disorders occur when the immune system confuses normal body tissue, "self", with a foreign intruder, and attacks it. How can this happen? As a way to avoid being attacked by the immune system, some infectious organisms, such as bacteria and viruses, learn to expose only those parts of themselves that mimic "self" tissue. Bacteria and viruses are made from chains of protein as are our bodies. The foreign invader exposes a segment of it's protein chain (called an antigen) that looks something like the protein chain of self tissue; and when the immune system mounts it's attack against these foreign organisms by detecting it's antigen, it inadvertently targets the "self tissue" to be attacked and destroyed..........
..................................................................................................................................................................................

Skin is targeted in pemphigus vulgaris characterized by blistering of the skin and mouth; and psoriasis characterized by thick, scaling plaques of skin. An unidentified antigen causes sarcoidosis, a inflammation disease appearing in multiple organs, such as the lungs, livers, skin and eyes. System lupus erythematosus or Lupus affects the collagen, the connective tissue, and in turn that can affect almost every organ system in the body. Ulcerated colitis and Crohns disease affects the digestive systems.

There is no cure for stopping autoimmunity. Most treatment of autoimmune diseases is usually aimed at lessening the severity of symptoms and replacing the missing hormones when a gland is destroyed. If the immune system becomes too hyperactive, immunosuppressive drugs are administered.

Approximately half of all persons afflicted with autoimmune diseases experience periods of spontaneous remission. It is known that stress can tend to exacerbate symptoms.

[nicolespeanut]

Vicki,
Thanks for starting this thread.  I have to look back in my file to see if I can find the links between digestion and autoimmunity.  I have read a great deal of literature regarding possible causes of autoimmune diseases that explain how proteins can leak through the gut and enter the blood stream wreaking all sorts of havoc.  I will post it when I find it.  It is a theory but seems to make sense to me. 

Fondly,
Nicole

[LIGA girl]

I will be revisiting this thread in a week or so with some articles to post..... I have other issues at the moment which i need to attend to. Please anyone who is interested in posting on here continue to do so .... wil be adding to it soon

Vicki

[nicolespeanut]

Here is a helpful checklist:

http://www.thyroid-info.com/articles/autoimmune-checklist.htm

[LIGA girl]

An article on treatment of Bullous diseases, not sure of the date, but think it is around 8 years old .....


Bullous Disease Treatment

by
   

Grant J. Anhalt, MD
Head, Dermatoimmunology Department
Johns Hopkins University
Baltimore, Maryland
Vice President in charge of Scientific Affairs, The International Pemphigus Foundation
Pemphigus Vulgaris

Prior to the introduction of an effective therapy with oral corticosteroids in the 1950s, the disease had a dismal natural course with a 50% mortality rate at 2 years and 100% mortality rate by five years after the onset of the disease.

The mortality rate now is estimated at about five percent and death is almost invariably due to the complications of immunosuppressive therapy. This disease is rare enough so as to render large scale controlled treatment trials impractical.

Therefore, treatment recommendations are based on information gleaned from uncontrolled small series, case reports and the personal experience and biases of the author.

Long-term therapy for pemphigus vulgaris must be directed toward reducing autoantibody synthesis, because as long as significant levels of antiepithelial antibodies are present, the disease will persist. Therefore, topical treatments are of secondary importance, and sustained improvement occurs only with treatment of the hematipoietic system. Those that have resistant disease or are intolerant of corticosteroids should receive a second, steroid-sparing agent. In decreasing order of efficacy, these agents are cyclophosphamide, azathioprine, chlorambucil, methotrexate and gold.

Oral corticosteroids remain the first line of treatment for all cases of PV. Some individuals with PV respond rapidly and completely to treatment with moderate doses of oral corticosteroids, others are rather refractory. About one-half of patients respond to oral corticosteroids alone (prednisone 1.0 mg per kg per day, tapered slowly over 6 to 9 months).

Almost all individual treated with prednisone require every-other-day maintenance indefinitely to control their disease. It had been standard practice to use very large doses of corticosteroids in refractory cases. Typically, an individual would be treated initially with 60 or 80 mg of prednisone per day. It there was not a rapid response to therapy, the dose of corticosteroids would be doubled and often doubled again. Under this regimen, patients would be treated with several hundred milligrams of prednisone per day, often with devastating or fatal complications. With the advent of effective immunosuppressive agents, it is generally not necessary to use such massive doses of costico-steroids.

Cyclophosphamide (Cytoxan), is an extremely effective agent in the treatment of PV, but it is also very toxic. It is very effective in reducing autoantibody synthesis, and has a preferential cytotoxic affect on proliferative plasma cells. It is generally reserved for patients who have the most therapy-resistant forms of PV in a dose of 1 or 2 mg per kg per day of by intermittent intravenous pulse. Major side effects include a predictable leukopenia, toxic effects of urinary metabolites causing hemorrhagic cystitis, and an increased lifetime risk of malignancy. The precise risk of lymphoma, leukemia, or bladder carcinoma secondary to treatment with cyclophophamide has not been established for patients with PV, but in patients treated with similar dosed for Wegener's granulomatosis, the lifetime risk may approach 5% to 10%. In addition, treatment may produce sterility in patients with childbearing potential. Chlorambucil (Leukeran) is a useful alternative to cyclophosphamide if a patient has developed hemorrhagic cystitis due to cyclophoshamide therapy but still requires an alkylating agent to reduce anitbody synthesis. Major potential problems of chlorambucil include its carcinogenic potential, and prolonged and unpredictable neutropenia.

Azathioprine (Imuran) is more widely used for the control of corticosteroid-resistant pemphigus. It is preferentially used under several circumstances: 10 In young individuals, it is more desirable to use a less toxic agent to reduce the lifetime risk of malignancy and potential for sterility. 20 If a patient cannot be monitored closely by complete blood counts and urinalysis or is not compliant. 3) If the patient is intolerant of cyclophosphamide due to profound leukopenia, thrombocytopenia or hemorrahagic cystitis. Azathioprine, however must be used in adequate doses for proper effect. Initial doses of 2 to 3 mg per kg per day are usually required to produce reduction of anitbody synthesis. Again, it should be used in conjunction with a low dose of oral corticosteroids.

Methotrexate was used for the treatment of pemphigus before other agents were available. It is a less effective but generally well-tolerated therapy for patients who cannot use alkylating agents or azathioprine.

Intramuscular gold has also been reported widely to be effective in management of both PV and pemphigus foliaceus. Response to this therapy has not been generally recognized, and the drug is not uniformly beneficial in everyone's experience. The incidence of allergic phenomena, such as nephritis and cutaneous or pulmonary hypersensitivity reactions, is very high and approaches 25%. Therefore gold is being used with much less enthusiasm now than it has been in the past.

The side effects appear to be the same whether one administers gold by mouth or intramuscularly.

Plasmapheresis has been used with mixed results in the therapy of pemphigus. If plasmapheresis alone is used, it can produce a short-term decrease in circulating autoantibody levels with subsequent clinical improvement. However, it must be recognized that the levels with subsequent clinical improvement. However, it must be recognized that the autoantibodies are under feedback inhibition control. If one simply removes the end-product, the B cells that produce the antibody are actually stimulated to produce more and a rebound flare with worsening of the disease will occur several weeks after plasmapheresis has been discontinued. Therefore, it is best to reserve plasmapheresis as an adjunct to therapy and to use it in conjunction with an alkylating agent. After the plasmapheresis has been discontinued, the loss of circulating anitbody from the serum causes a preferential stimulation of the B cells producing the autoantibody. As they proliferate, they are preferentially destroyed by the cyclophosphamide. The patients who are treated with this combination of plasmapheresis and an alkylating agent sometimes go into prolonged disease-free remissions after 1 or 2 years of therapy.

Cyclosporin (Sandimmune) has been used with benefit in some cases of PV, but it is not generally accepted to be particularly effective. The high incidence of pephrotoxicity also limit its usefulness.

Finally, treatment should always be adjusted according to the disease activity that is clinically apparent, without being unduly influenced by autoantibody titers as estimated by indirect immunofluorescence. The anitbody titers generally are high when the disease is active and are low or undetectable when the disease is in remission. If a patient is in apparent clinical remission but has persistent low titers, that should not prevent planned reduction of drug dosages. The indirect immunofluorescent titer is most useful during maintenance if a patient develops a flare of disease activity. In this circumstance, a low or negative anitbody titer would be reassuring that the flare may be self-limited and may not require increased drug dosages. On the contrary, a high titer raises more concern and prompts earlier intervention.

Pemphigus Foliaceus

Most cases of pemphigus foliaceus can be controlled by oral corticosteroids alone. A starting dose of 0.5 to 1.0 mg per kg per day, with a slow taper over a period of six months and the use of an alternative-day steroid regimen, is usually effective. Topical or intralesional steroids are somewhat effective in limited cases of pemphigus foliaceus. The list of drugs that are useful as a second or steroid sparing agents is identical to that in PV, with ;the possible addition of anitmalarials such as hydroxychloroquine (Plaquenil), 200 mg twice daily. The necessity of using an immunosuppressive agent, such as cyclophosphamide, azathioprine, or other agents such as gold or methotrexate in management of this disease is less frequent than in PV. Efficacy and toxicities of these therapies have already been outlined.

[LIGA girl]

This article comes with an assurance that it is written by a medical or research professional ....  I think it goves a good overview of autoimmunity and some different aproaches that are non medical. It also expplains clearly why there is a link between cancer and taking immuno suppressants.


Pemphigus: An Ayurvedic Approach

by Jay Glaser, MD, a board-certified internist, researcher and medical director at the Lancaster Ayurveda Medical Centers based in Sterling, MA. He can be reached at 978-422-5044. Answers to many questions about Ayurveda can be found on the Lancaster web site, www.AyurvedaMed.com, where you can subscribe to their free online newsletter, The Spirit of Health.

Sufferers of pemphigus are in a good position to aid well meaning administrators in politics, social policy, security, intelligence and defense who are currently grappling with how to re-engineer a free society immune to disruption from within or without, because this disorder recapitulates issues in domestic security. Understanding the immunology of autoimmune disorders sheds light on critical issues of individual and societal health, so we will examine immunology from both a western and eastern perspective.

A Sanskrit expression from Charaka Samhita, the oldest textbook of medicine, states, yatha pinde tatha brahmande, i.e. œas is the individual physiology, so is the universe.� This means that the body is an expression of an underlying field of intelligence, the same intelligence that also governs the functioning of larger structures such as galaxies, ecosystems and societies. In the wake of recent horrific events, we have all wondered if there is any intelligence at all at work in a human society. Quantum mechanics and chaos theory both insist, œYes! But like biology, it is an intelligence that operates with probabilities and uncertainty.� This also means that social systems have their own physiology.

The ancient Ayurvedic texts call this intelligence Veda, and describe it as a blueprint for the physiology, indeed for the cosmos. Veda functions as a constitution of the universe, describing the laws of nature at work as unmanifest, unexpressed intelligence that expresses itself into a human, a virus or a star. The verses of Veda and the Vedic literature also have a discrete structure, an architecture defined by the relationships between the syllables, words, chapters and rhythms.

If Veda indeed provides the blueprint for nature including for humankind, one would expect that human physiology and anatomy reflects the architecture and functioning of Veda. Tony Nader, MD, PhD, a Harvard-trained neuroscientist investigated whether the structure of Veda could be found in the human neuroanatomy. Dr. Nader analyzed all 40 areas of Veda and the Vedic literature and discovered that each Vedic text has an almost identical corresponding structure in the human anatomy. For example, Rg Veda, the primordial Vedic text which gives rise to all others, is composed of 192 groups of verses. Similarly, the human autonomic nervous system governing our vital functions consists of 192 nerves.

This recent insight from neuroscience provides one of the strongest confirmations of the existence of an underlying blueprint for creation and that every human individual is cosmic. This correspondence also validates the biblical understanding that man is made in the image of the divine.

Agnivesha, a medical student who lived thousands of years ago, poses in the ancient Ayurvedic medical text a question about immunity that is still pertinent today. œWhy is it that some people eat all the right things and they still get disease and infections, while some people never eat well and they seem to never fall sick?� His professor, Atreya, gives an answer that prophesies our modern understanding. œPredisposition to disease also depends on how and when the food is eaten, the environment of the individual, as well as on genetics.�

Immune disorders, like problems with security systems or militias, can be categorized as either 1) weak immunity or 2) strong immunity, but lacking organization and leadership. AIDS is an example of the former because the immune cells are both scarce and weak. Pemphigus and other autoimmune disorders and allergies are examples of the latter. In allergic conditions, a strong immune system aims its formidable weapons at a non-threatening foreign irritant, the proverbial cannon against the mosquito.

Autoimmune disorders are the most interesting to a student of social policy and domestic security because they represent an imbalance between adequate internal vigilance and tolerance of individuality. Autoimmune diseases are caused by activation of immune cells for no apparent reason such as an infection. The immune response is directed against one's own tissues, perhaps tissues that, to a T cell, look a lot like an invader. This includes not only pemphigus, but common disorders such as hypothyroidism, rheumatoid arthritis, psoriasis, juvenile diabetes and probably multiple sclerosis, as well as more uncommon problems such as lupus, spondylitis and inflammatory bowel disease.

Immune cells are not designed simply to discriminate self from foreign, but to attack in an environment of inflammation triggered by chemical signals. Autoimmune disease usually implies both a genetic predisposition and the presence of triggers such as viruses or bacteria, drugs, a woman's natural estrogen or even stress. It seems that Atreya was right: genes and one's environment are just as important as a good diet.

Pemphigus and other immune disorders of the skin may be more common than immune disorders involving other organs simply because the skin, our largest organ, is responsible with the toughest immune task in the body: keeping the interior sterile in the face of an unsterile hostile environment. The intelligence to accomplish this difficult task, according to Ayurveda, comes from the source of intelligence in Veda, whose first biological expression is our DNA.

The standard medical approach is to subdue the immune system using harmful steroids and other risky immune suppressants otherwise used for preventing transplant rejection. Continuing our analogy, this is comparable to so weakening the FBI and other domestic security agencies, simply because they lacked perfect discrimination between the innocent citizenry and subversives, that it endangers the whole society.

It has long been known that stress aggravates allergic disorders like asthma, eczema and hives. What experienced ER doc hasn't seen kids with severe wheezing at home, who are fine as soon as they enter the hospital, knowing that they wouldn't suffocate? Now several studies have shown that stress can also be a trigger for autoimmune disorders, including Grave's disease, lupus, colitis, and rheumatoid arthritis. Our forebears fleeing a saber-tooth tiger had a good chance of being wounded, and needed an immune system that would be mobilized and stimulated from the chase alone. Today the tiger and its like are extinct, but we go about our business with our nervous systems in high gear as if these dangers were present, creating neuropeptides and stress hormones in the brain that circulate through our bodies to turn our immune systems on inappropriately. Serenity, on the other hand, allows proliferating cells to be quiescent.

So intimately are the nervous and immune systems connected that a new science called psychoneuroimmunology has arisen that may make this connection not only legitimate but also practical. Brains and immune cells both have memories and intellects, and even share some common cells. Most importantly, a nervous system free of anxiety and depression creates a neurochemistry that signals the immune system to deactivate. Countries at peace, like Switzerland and Costa Rica, marshal small, inconspicuous armies.

The western approach to pemphigus and other autoimmune disorders is to take corticosteroids and other powerful immunosuppressants. The Ayurvedic approach to autoimmunity is to put the immune system to rest rather than to suppress it. Transcendental Meditation has been shown to improve the inflammatory response of gingivitis and to lower cortisol and increase DHEA, exactly the opposite of the stress response. Several Ayurvedic herbs, including guggulu, have powerful anti-inflammatory effects and have been shown effective in rheumatoid arthritis, the autoimmune disorder that wreaks the most widespread suffering.

When I was in medical school, we thought that the body naturally eliminates clones of cells that attack one's self, leaving intact only the T and B cells which react against foreign antigens such as bacteria. Now we understand that a low level of autoreactivity is natural and even critical to normal immune function. Apparently, tissues that provoke an immune response help naïve immune cells to differentiate and survive. In addition, since our bodies create cancer cells every day, a hint of autoreactivity may be one of the ways the immune system is recruited to eliminate these abnormal cells, which don't look quite like œself.�

It seems that the healthiest condition for the body is akin to a benign yet testy society that is perpetually challenging the domestic security agencies to keep them on their toes. In these challenging times, may we have the humility to take a few lessons from Nature in establishing our new world order. Perhaps we can take a few lessons from the ancient sages of Ayurveda in overcoming pemphigus.

[LIGA girl]

This article is specific to pemphigus, but may have applications to other autoimmune skin diseases. It gives a broad overview of possible triggers for the autoimmune response for pemphigus:

PEMPHIGUS
An Acronym for a Disease with Multiple Causes

by Sarah Brenner, MD, Jacob Mashiah, MD, Einat Tamir, MD, Ilan Goldberg, MD and Yonit Wohl, MD, Department of Dermatology, Tel Aviv Sourasky Medical Center, and Sackler Faculty of Medicine, Tel Aviv University, Israel

Pemphigus is generally considered to stem from a genetic predisposition to the disease triggered and/or aggravated by one or more external factors. An acronym has been suggested from the name of the disease, PEMPHIGUS, to encompass those factors:
PE       PEsticides
M       Malignancy
P       Pharmaceuticals
H       Hormones
I       Infectious agents
G       Gastronomy
U       UV radiation
S       Stress

Pesticides

Gardening materials and pesticides are a major group of agents implicated in the development of the disease. The medical literature documents numerous cases provoked by pesticides all over the world. Organochlorine pesticides, and organophosphates, a new generation of pesticides, have been tied to the disease.

How pesticides work on the skin is unclear. It is speculated that the immune system is activated via contact or systemic exposure, resulting in the generation of autoantibodies targeting desmosomal antigens. Interestingly, in most of the reported cases the patients had a first-time, long-duration exposure to the offending substance, and developed the disease only after a massive additional exposure, resembling the induction and elicitation phases of allergic contact dermatitis.

Malignancy

Pemphigus has been associated with malignant processes, mainly hematolymphoproliferative diseases such as Hodgkin's lymphoma, chronic lymphocytic leukemia, Castelman's disease, and others. These constitute a specific clinicopathological variant called paraneoplastic pemphigus. A few reports on cases of pemphigus associated with malignant diseases that did not meet the above criteria raised the possibility of simple co-existence. In both events, the physician should perform a malignancy-directed work-up on a pemphigus patient.

Pharmaceuticals

Drugs reported to induce pemphigus are divided into three main groups according to their chemical structure: drugs containing a sulfhydryl radical such as penicillamine; phenols such as rifampin, levodopa and aspirin; and nonthiol nonphenol drugs, such as calcium channel blockers, angiotensin converting enzyme inhibitors, NSAIDS, dipyrone, and glibenclamide.

Again, speculated mechanisms are chemical insult and immune system activation by a complicated mechanism involving diverse molecules (autoantibodies, cytokines). Calcium channel blockers are emphasized in view of the fact that the calcium ion is critical to maintaining an intact epithelium.

Hormones

Pregnancy is closely related to autoimmune diseases and thus to immunoblistering diseases, an association seen in the aggravation of pemphigus vulgaris during pregnancy, and pregnancy- or postnatally-induced herpes gestationis and neonatal pemphigus. These diseases are attributed to the passage of pathogenic autoantibodies via the placenta that target different placental antigens or skin antigens in the newborn. The role of sex hormones, mainly estrogen, in the pathogenesis of pemphigus has not yet been established.

Infection

Different infectious agents and immunizations can induce or exacerbate pemhigus, mainly by activating the cellular immune system. The most frequently incriminated infectious agents are the viruses of the herpetoviridae family, namely herpes simplex, EBV, CMV, and even HH8.

Despite the confusing clinical similarities of viral diseases and pemphigus, and because of the different outcomes of the two conditions, it is important to diagnose viral infection in a pemphigus patient and initiate early antiviral therapy, often as an adjunct to immunosuppressive therapy. Viral isolation remains the most reliable laboratory means for viral diagnosis, followed by molecular biology techniques, which are more sensitive but less reliable and indicated only in cases in which the results of the former are not conclusive.

In addition, bacteria such as coagulase positive staph aureus are capable of inducing pemphigus. Gram negative bacteria and even Actinomyces have been cultured in patients before the pemphigus becomes manifest, and were therefore described as its possible triggers.

Gastronomy

Although rarely mentioned in the literature, recent studies indicate that certain foods can induce or trigger pemphigus. Some nutritional components are chemically similar to known causative drugs, and may act in the same way. The following chemicals and related foodstuffs have been associated with pemphigus:

PHENOLS
Fruits: mango, bananas, potatoes, tomatoes
Nuts: pistachio, cashew
Pinenes: baked goods, smoked and grilled food, candy, chewing gum, ice cream, black pepper
Cow's milk
Food additives: aspartame, sodium benzoate, tartrazine, vanillin, eugenol, caffeic acid, cinnamic acid, vitamis C and E

TANNINS
Nuts: Kola, betal, walnuts
Fruits: cassava, cranberry, raspberry, blackberry, cherry, banana, apple, pear, grape skins, peach avocado
Drinks: tea, mate, fruit juice, beer, wine, liquors, water, coffee, guarana
Food additives: vanillin
Spices: ajowan, coriander, cumin, black pepper, red chilies, rosemary, garlic, ginger

THIOLS
Vegetables: garlic, onion, shallot, chive, leek
Assuming that foods containing thiol, phenol, and polyphenolic compounds may contribute to pemphigus, avoidance of certain foods may lead to remission.

Ultraviolet radiation

Pemphigus is considered a photosensitive disease, especially the superficial variant pemphigus erythematosus. Ultraviolet radiation, either occupation- or leisure-related, can induce or exacerbate the clinical manifestation. Whether the phototoxic reaction is a simple one or entails specific immune system stimulation remains to be determined.

Physical factors such as x- ray radiotherapy, burns, major surgery and cosmetic procedures have also been reported capable of inducing pemphigus.

Stress

The well-known connection between the immune and nervous systems raises the possibility that a psychoneural disorder can influence the onset and course of autoimmune disease. Several studies and case reports point to the possible contribution of emotional stress as a precipitating factor in pemphigus. Hence, avoiding emotional stress may be therapeutic in pemphigus patients, hastening the healing process and reducing or stopping the use of immunosuppressive drugs.

In summary, while the myriad causes of pemphigus complicate the differential diagnosis and course of the disease, it also points to the numerous factors that can help in its diagnosis and treatment. These factors have been documented in the studies cited here. The acronym is suggested to give clinicians a tool to pinpoint possible causes and prevent flare-ups in every newly diagnosed pemphigus patient.

[LIGA girl]

This article is again focussing on Pemphigus, but may have wider applications. It looks at predictors for remission ..... written in 2000

Remissions in Pemphigus

by
   

Jean-Claude Bystryn, M.D.
Professor of Dermatology
Director of Immunofluorescence Laboratory
The Ronald O. Perelman
Department of Dermatology
New York University Medical Center

Pemphigus vulgaris (PV) can enter into remissions in which all manifestations of the disease disappear and all therapy can be discontinued. How often, and when this occurs is unclear. Review of all major studies of PV conducted during the past four decades describes remissions as occurring in less than one-third of patients.1 However, a problem with these studies is that the incidence of remissions is usually provided at only a single time point. Thus, it is unclear how long it takes for remissions to appear, how long they last and what happens when therapy is discontinued. Further complicating interpretations of the results is that the meaning of remission is often unclear. The criteria used by different investigators to define this event differ and/or are not provided. The practical outcome of this incomplete information is uncertainty about the management of pemphigus. It is unclear whether treatment simply suppresses the manifestations of the disease and must be continued permanently, or whether complete and durable remissions can be induced that permit therapy to be safely discontinued.

To answer these questions we examined the induction of remissions in 40 patients with pemphigus vulgaris who were followed for a prolonged period (on the average of 7.7 years) by the same investigator. The results of the study have recently been published in the Journal of the American Academy of Dermatology.2

A strict set of entry criteria was used to include patients in the study, to minimize the effects of patient selection bias on the results. These included: a) diagnosis of PV confirmed by clinical, histologic and immunofluorescence criteria; b) first seen shortly (<3 months) after the diagnosis of pemphigus, to exclude bias from early death; c) seen continuously by the same investigator during the course of their illness; and d) a minimum of two years of follow-up information from onset of disease. All patients were treated conventionally with steroids, with or without adjuvants, using guidelines that have previously been published.3 All patients were followed and evaluated using defined criteria for disease activity and remissions, to ensure a consistent evaluation of clinical outcome. Scores were recorded for the most severe phase of the disease during the first year of treatment, yearly on the anniversary of diagnosis, and at last follow-up. Complete remission was defined as a period greater than one month during which the patient was on no systemic therapy and lesion-free. Partial remission was defined as a period greater than one month during which the patient was lesion-free and on no more than 15 mg./day of prednisone or its equivalent; or on only 100 mg./day or less of cyclophosphamide or azathioprine; or only on gold or dapsone. Duration of remission was classified as short if at least one month but less than 6 months, and as long if 6 months or longer. Time to partial or complete remission was calculated from date of diagnosis to onset of partial or complete remission. The results show that pemphigus improved with time in almost all patients. Improvement was particularly rapid during the first two years of therapy, with the severity score declining 64% from an average of 5.3 during the most severe phase of the illness to 1.9 two years after diagnosis (see Figure 1). Severity continued to decline, albeit more slowly, during the ensuing years. Five years after diagnosis the average severity score was only 1.4, indicating the disease was inactive or treated with <15 mg./day of Prednisone in most patients.

Remissions were found to be much more common than previously reported. This is probably because the incidence of remissions increases with time, and we studied patients for prolonged periods. Remissions that were complete and long-lasting (no evidence of disease and no systemic therapy for at least 6 months) occurred in 25%, 50% and 75% of patients 2, 5 and 10 years after diagnosis. These remissions were durable, lasting on the average over 4 years. Actual duration is probably longer, since most patients in remission were still in remission at last follow-up. The bulk of the remaining patients were in partial remissions or had mild disease controlled on 15 mg./day or less of Prednisone or with only an adjuvant (see Fig 1).3
Study results.

The course of pemphigus in different patients as evidenced by induction of remissions and flare in disease activity was variable, but followed one of 4 patterns. In pattern 1, the disease responded rapidly to treatment and went into a remission that was complete and long lasting. This occurred in 17% of the patients. There was no flare in disease activity when treatment was stopped. The average time to complete remission was 15 months and the remissions were maintained to last follow-up for an average of over 4 years. In pattern 2, seen in 37% of patients, response to therapy was slower and intermittent but complete and long-lasting remissions were also eventually induced in all patients. Pemphigus in these patients fluctuated between periods of partial or complete remissions of various length, which were punctuated by flares in disease activity as the intensity of therapy was decreased. Relapses were usually less severe than initial disease activity. With continued therapy, all patients eventually had long-lasting, complete remissions that persisted for longer than 6 months following termination of all systemic therapy. The average time to the first complete long-lasting remission was 35 months. In the third pattern, seen in 35% of patients, disease activity also fluctuated but no long-lasting complete remissions were induced during the course of this study. This may be because these patients were on the average followed for a shorter period of time.

However, disease activity in most of these patients eventually became mild and could be controlled by low doses of Prednisone (15mg/day or less), or with only an adjuvant. There was no mortality in patients whose disease followed these three patterns. In pattern 4, seen in 10% of patients, the disease was resistant to therapy and never went into a remission of any type. Mortality in this small group was high, occurring in two of four patients.

Two factors were identified as predictive of the course of pemphigus. One was initial severity and extent of disease. Patients with mild or moderate disease at diagnosis were twice as likely to enter a long-lasting complete remission as those with severe disease. The other was early response to treatment. Patients who responded rapidly to treatment were over twice as likely to enter a long and complete remission as those with a slower response.

These results indicate that the outlook of pemphigus is more favorable than currently believed. The disease can be converted into an inactive state in the majority of patients. Most patients will eventually enter a complete and durable remission that permits systemic therapy to be safely discontinued without an exacerbation in disease severity. The remaining patients will usually have only mild disease controllable with low doses of Prednisone or an adjuvant. The practical implication of these observations is that the ultimate goal of treatment in pemphigus vulgaris is to discontinue all treatment.
References

1. Bystryn J-C, Steinman NM. The adjuvant therapy of pemphigus - an update. Arch Dermatol 1996; 1 32:203-212.

2. Herbst A, Bystryn JC. Patterns of remission in pemphigus vulgarism. J Am Acad Dermatol 2000; 42:422-7.

3. Bystryn J-C. Therapy of pemphigus. Semin Dermatol 1988;7:186-194.

August 2000

[bunnie]

[

[LIGA girl]

Link to an articel on the judas enzyme ... provided by Andi on another thread...

http://www.innovations-report.de/html/berichte/biowissenschaften_chemie/bericht-74690.html

[LIGA girl]

A little more on the Judas enzyme ....

http://www.ntnu.no/gemini/2002-06e/43.htm

[LIGA girl]

This link has some good definitions of autoimmune diseases and if you look around the site there is some info on autoimmune skin diseases as well.....


http://autoimmunity.pathology.jhmi.edu/whatis_disease.cfm#circumstantial

[LIGA girl]

There is more discussion taking place on autoimmune diseases of the skin at

http://www.skincell.org/yabbse/index.php/topic,21129.740.html

the Linear IGA thread ..... please feel free to have a look or to join in.

Vicki 

[CalamityJane]

A little more on the Judas enzyme ....

http://www.ntnu.no/gemini/2002-06e/43.htm

Hi Vicki:  I emailed the doctor today at the institution.  It's a great theory, and I'm glad the mice/rats all recovered from their psoriasis.  However, what I have (and you have, methinks, isn't psoriasis).  All this though adds enormously to our knowledge and research!

[LIGA girl]

Yes, I agree that I certainly dont have psoriasis, thankfully, and that this new brekthrough wont help me directly, but I think that if any of us have an autoimmune disease and a treatment is being developed to treat any other autoimmune disease, there is a chance that further developments in that area may help us, especially when they are looking at the whole autoimmune process. The bit that interested me in that link is the following ....


"If the blockers are patented, rights in them can either be sold to a pharmaceutical company able to develop a drug, or a spin-off firm from the research environment may develop the concept further," says Professor Berit Johansen.
She explains that knowledge about the enzyme phospholipase A2 and the method of blocking unwanted activity in the cells most probably can be applied to the treatment of other diseases.
"This new knowledge is of more general interest, not least in relation to chronic diseases such as allergies, asthma, rheumatism, chronic enteric diseases, and cardiovascular diseases. A symptom common to all these diseases is a physical inflammatory reaction."

Vicki

[LIGA girl]

Jane

PS from my last posting ... if you hear back from them can you let us know what they say, please? It will be interesting to find where they are up to with their research ....

[CalamityJane]

Jane

PS from my last posting ... if you hear back from them can you let us know what they say, please? It will be interesting to find where they are up to with their research ....

Of course!  Of that, there is no doubt, but I'll be *very surprised* if I get an answer. And I agree with your post before this one.  Anything that can come from research and newly discovered treatments is valued.

I wonder......in 50 - 70 years........what'll they be treating our skin problems with?  Sorry that I won't be here.....but our children might!  That's a warm thought in my frozen environment!

Jane
PS do you have the spell check button on your 'post reply' window?  I think I've lost my mind.........*sigh*

[bunnie]

This is the link for the Immunology Scientist Polly Matzinger. However, if you type in the name loads of links will come up. I first heard of this scientist in 1993 in a BBC Documentary. I sent for a transcript of the programme, and I still have it. reading about this Judas enzyme and Polly Matzingers school of thought, closely resemble one another, except that I think the process of this "mechanism" or activation is given another name.
http://www.genetics.wayne.edu/asg/polly.html

[bunnie]

More Interesting links.
http://www.niaid.nih.gov/publications/pdf/ADCCFinal.pdf

[LIGA girl]

Hi Bunnie

this document, above, is very interesting and contains lots of great stuff for informing in all sorts of areas. I hope the report gets acted upon so that autoimmune disease sufferers get some relief and people at risk of getting an autoimmune disease can take preventative steps. How and where did you find it?

[bunnie]

HI LG i was doing a search, because I had read somewhere that diseases such as ours have devastating affects on a persons life and that they were trying to have this listed onto the stat books for disabilities. Most interesting to me was page 18 (introduction, last paragraph) because everything on there has happened to me, giving up my business and livlihood, just everything, and I'm now trying to find out if I as a sufferer can help to have this passed in the government.
Link to the meaning of the word Heterogeneous
http://www.yawiki.org/h/1148368091637.html

[LIGA girl]

Hi Bunnie

I agree re the devastating effects on life ...I now have a disability pension that both derms did not want to support me in getting, tho I am fortunate that eventually one of them and my GP did, but it was a difficult process and I had to go thru the first level of the appeal  process to get it. I will have to reapply  in future too if I do not get better as it is not a permanent thing. There is a list of conditions here that automatically qualify one for the disability pension but autoimmune diseases are not mentioned. Blindness, BTW is one that automatically qualifies here.

Some lobbying to govt may make things easier for those who follow on from us .....

V

[bunnie]

Hi LG, its the same thing...of or pertaining to heterogenisis.

[bunnie]

Hi LG Sorry you are correct it is my spelling . I have corrected it. Here a link with photos of LIGA, for anyone reading.
http://dermnetnz.org/immune/linear-iga.html

[bunnie]

A good link for Lupus....
http://www.lupusuk.com/sitemap.asp

[LIGA girl]

A nice overview article from the  Pemphigus Foundation website: no author is cited for this one ...

What Are Autoimmune Diseases?

The word "auto" is the Greek word for self. The immune system is a complicated network of cells and cell components (called molecules) that normally work to defend the body and eliminate infections caused by bacteria, viruses, and other invading microbes. If a person has an autoimmune disease, the immune system mistakenly attacks self, targeting the cells, tissues, and organs of a person's own body. A collection of immune system cells and molecules at a target site is broadly referred to as inflammation.

There are many different autoimmune diseases, and they can each affect the body in different ways. Pemphigus vulgaris, the most common of the pemphigus diseases, effect the skin and mucous membranes. In multiple sclerosis the autoimmune reaction is directed against the brain. In Lupus, one person may have affected skin and joins whereas another may have affected skin, kidney, and lungs.

Ultimately, damage to certain tissues by the immune system may be permanent.

How Does the Immune System Work?
The immune system defends the body from attack by invaders recognized as foreign. It is an extraordinarily complex system that relies on an elaborate and dynamic communications network that exists among the many different kinds of immune system cells that patrol the body. At the heart of the system is the ability to recognize and respond to substances called antigens whether they are infectious agents or part of the body (self antigens) Most immune system cells are white blood cells of which there are many types. An antibody binds to an antigen and marks the antigen for destruction by other immune system cells.

How Are Autoimmune Diseases Diagnosed?
The diagnosis of an autoimmune disease is based on an individual's symptoms, findings from a physical examination, and results from laboratory tests. Autoimmune disease can be difficult to diagnose, particularly early in the course of the disease. Symptoms of many autoimmune diseases – such as fatigue – are nonspecific.

In some cases, A specific diagnosis can be made. A diagnosis shortly after onset of a patient's symptoms will allow for early aggressive medical therapy; and for some diseases, patients will respond completely to treatments if the reason for their symptoms is discovered early in the course of the disease.

Although autoimmune diseases are chronic, the course they take is unpredictable. A doctor cannot foresee what will happen to the patient based on how the disease starts. Patients should be monitored closely by their doctors so environmental factors or triggers that may worsen the disease can be discussed and avoided and new medical therapy can be started as soon as possible. Frequent visits to the doctor are important in order to the physician to manage complex treatment regimens and watch for medication side effects.

What causes autoimmunity?
The immune system normally can distinguish "self" from "non-self." Some lymphocytes are capable of reacting against self, resulting in an autoimmune reaction. Ordinarily these lymphocytes are suppressed. Autoimmunity occurs naturally in everyone to some degree; and in most people, it does not result in diseases. Autoimmune diseases occur when there is some interruption of the usual control process, allowing lymphocytes to avoid suppression, or when there is an alteration in some body tissue so that it is no longer recognized as "self" and is thus attacked. The exact mechanisms causing these changes are not completely understood.

Are they inherited?
The genes people inherit contribute to their susceptibility for developing an autoimmune disease. Certain Diseases can occur among several members of the same family. The ability to develop an autoimmune disease is determined by a dominant genetic trait that is very common (20 percent of the population). This suggests that a specific gene or set of genes predisposes a family member. The genetic predisposition alone does not cause the development of autoimmune diseases. It seems that other factors need to be present as well in order to initiate the disease process. In addition, individual family members with autoimmune diseases may inherit and share a set of abnormal genes, although they may develop different autoimmune diseases. For example, one first cousin may have lupus, another pemphigus, another Sjorgen's syndrome. It is important for families with members who have an autoimmune disease to mention this fact when another member of the family is experiencing medical problems that appear to be difficult to diagnose.

What are the types of autoimmunity?
Particular autoimmune disorders are frequently classified into organ-specific disorders and non-organ-specific types. Autoimmune processes can have various results, for example, slow destruction of a specific type of cells or tissue, stimulation of an organ into excessive growth, or interference in its function. Organs and tissues frequently affected include the endocrine gland, such as thyroid, pancreas, and adrenal glands; components of the blood, such as red blood cells; and the connective tissues, skin, muscles, and joints. Some autoimmune diseases fall between the two types. Patients may experience several organ-specific diseases at the same time. There is, however little overlap between the two ends of the spectrum.

In organ-specific disorders, the autoimmune process is directed mostly against one organ. Examples, with the organ affected, include Hashimoto's thyroiditis (thyroid gland), pernicious anemia (stomach), Addison's disease (adrenal glands), and insulin-dependent diabetes mellitus (pancreas) and pemphigus (skin).

In non-organ-specific disorders, autoimmune activity is widely spread throughout the body. Examples include rheumatoid arthritis, systemic lupus erythematosus (SLE or lupus), and dermatomyositis.

Are they Contagious?
No autoimmune disease has ever been shown to be contagious or "catching." Autoimmune diseases do not spread to other people like infections. They are not related to AIDS.

[LIGA girl]

This article is unfortunately 8 years old but may be a good one for family members .....
   
Autoimmunity and Your Family:
Researchers Looking at Genetics

by Sal Capo

One out of every five Americans has some kind of autoimmune-disease. Put another way, that's over 50 million people. Seventy-five percent of those 50 million are women (pemphigus is one of a few autoimmune diseases which treat the sexes equally). Autoimmune problems cause over 80 different diseases, including lupus, scleroderma,, rheumatoid arthritis, multiple sclerosis, autoimmune hepatitis, and of course, pemphigus. So far none of these illnesses can be cured. Noel Rose, M.D., Ph.D., Professor of Molecular Microbiology and Immunology and Pathology at Johns Hopkins University was quoted as saying: "This nation involves some $86 billion of its health care money in the treatment of autoimmune disease. We're talking about a major health problem in the United States. Autoimmune disease in the aggregate is right up there with cancer and heart disease as major disease problems in this country, both from the point of view of the number of people involved and the amount of our health care effort that goes into autoimmune disease."

"Despite their devastating human and economic toll, autoimmune diseases are among the least investigated, most difficult to diagnose, and physically and emotionally painful diseases that face Americans today," said Susan Wood, Ph.D., and newly appointed Acting Deputy Assistant U. S. Secretary for Women's Health, Department of Health and Human Services for the National Institutes of Health.

Stephen Katz, M.D., Ph.D., Director of the National Institute of Arthritis and Musculoskeletal and Skin Diseases, stated: "Two of the hottest areas in medicine today are genetics and immunology. Advances in these areas will have a direct impact on our understanding of autoimmunity. With regard to genetics, the fact that autoimmune diseases can run in families indicates that the development of these diseases has a genetic basis." Several genetic studies released recently have identified genes that may play a role in autoimmune diseases.

Towards that end, one study by the Yale University School of Medicine and St. Mary's Hospital in Connecticut isolated an antibody which is a "common thread" in families. This antibody, known as the antiphospholipid antibody (APL), is an "auto-antibody" protein produced by the body to attack itself. When APL levels are too high disease occurs. If at least one family member suffers from an autoimmune disorder associated with high levels of APL, others did also.

Twenty-three family members, 87 blood relatives, 18 spouses and 37 controls were included in the Yale and St. Mary's study. Auto-antibodies were found in almost 60% of the blood relatives. Only one spouse showed the same. One third had APL antibodies, while another 37% had other autoantibodies. The control subjects showed no positive results. Eight relatives were found to have lupus or lupus-like syndrome, two had suffered premature stroke, and three had recurrent fetal loss.

Thomas Greco, M.D., assistant clinical professor of medicine at the Yale University School of Medicine said "While the study is relatively small, it is supported by other previous studies that suggest APL antibodies may actually be genetically transmitted from family member to family member, from generation to generation. More important, the APL antibody may be associated with one disease process in one family member and yet another disease process in another family member."

Independent research by Duke University scientists into the genetic patterns of 12 unrelated families with APL found the possibility that a single inherited genetic defect may be at fault. These findings support Dr. Greco's research, and in fact, Dr. Greco has begun a study with Duke University researchers to define the genetic defect which causes these diseases. This would put Dr. Greco on the evening news and be a major step in medicine for humankind.

Recent data presented by French researchers shows families with APL antibodies had diseases related to these proteins, as well as many other immune system troubles such as rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis, among others.

Dr. Greco pointed out that while these proteins are seen in only about one or two percent of the population of patients nationwide, in affected families the rate may be as high as 50%.

"If an APL inheritance pattern can be firmly established in future studies, the good news is that we may be able to prevent premature stroke, heart attack, recurrent miscarriage and the other APL-associated diseases by performing simple and inexpensive tests and taking more thorough family histories," Dr. Greco predicted.

"It may be premature to say, but APL may end up being one of the common threads that ties together all of the seemingly unrelated 80 known autoimmune diseases," said Virginia Ladd, president of the American Autoimmune Related Diseases Association (AARDA). "If it turns out that APL is a common factor in autoimmune diseases, then the next step for researchers is to begin looking for an autoimmune gene."

Unlock one autoimmune disease and perhaps they all open. These are very exciting times in research labs. Many are involved and progress is made daily. Stay tuned.

June 1998

 

[LIGA girl]

homepage link for Australasian Blistering Diseases Foundation:

The pic of Linear iga in the About Blistering Diseases Page is of my back!!! Taken a few months ago ... not very nice either ....


http://www.blisters.org.au/BDHome.html

LG

[CalamityJane]

Hi Vicki:  Thank you for that link.  Your back looks painful and sore.  I didn't realize the blisters are so large.  But that poor person's foot, dreadful.

Guess you take the dubious accolade of being very rare. Do you have a photo album here on SC?

Jane

[LIGA girl]

Hi Jane

I suppose I should put some pics into an album here  - have just been too slack and/or shy - dont really want lots looking at me! I also have a great one on my fone of my L foot when it was really bad but cant download it - I may be able to borrow a lead that will let me do that and then  I will put up a few. I was actually surprised to see that pic of me when I looked at it today on the web - had forgotten I'd sent it to my derm!

Guess you take the dubious accolade of being very rare.

They all like looking at my lesions as some of them are the classic linear iga circle of blisters called a crown of jewels ... as one doc said to me "the last thing you need is to be interesting to doctors!"

I agree re that foot foto - a shocker!

[CalamityJane]

Hi V:

Some of these pics in the gallery, and on the web and shocking, for sure. The pic of that foot just made me cringe and shrivel up.

I made an album here, and I have a folder on my PC--everyhting has to be resized for the album here.  At the time I have the pics taken I wonder why the heck I'm doing it, but then many months later, I look at them and can see (and again feel) the difference.  I remember all the circumstances leading-up to their taking.  The sort of day, the time, who I was with, doing what, how it felt, etc.  Such has been the impact on the PPP upon me.

I feel you are very blessed with Bunnie, and her sage advice.  She's been there, and I really pray that it's never revisited for her.

Jane
PS  How the heck do you cope with your disease and the heat you are in.  If you read the PPP thread, you'll know my doc blames my PPP for my cellulitis (staph & strep).  That's one of the reasons I emailed you regarding the swimming. I realize that the foot is more prone to that sort of stuff in a pool/water, but any open skin at all seems to me to be an invitation (where I live, anyway).



Jane

[bunnie]

Hi Girls, Your back V looks like mine is now but at the shoulder level though, I don't think its quite as bad but near enough. I have an album Jane in the gallery, showing the disease and epidermal necritis which exascerbated the disease, due to a toxic reaction from a drug. Theres also a pic of my OOKP surgery on my left "eye".

How the heck do you cope with your disease and the heat you are in.

I always think of you V in the heat! As you know I have often said I don't know how you stand it! It really makes me worse in the summer , I dread it truly.
Couldn't you copy that picture of you and add it to the album I have created for the disease?
Just another point here...
Did you know that any photograph taken of you at the hospital, even with your permission belongs to you, and cannot be used publicly without your permission?
When the photos of my eye were made public, even though I could not be recognised my permission was still sought before He published the "paper". I was told this by two consultants, who look after me, and you can have copies although you may have to pay for them. They must seek your permission every time they use those photos.

[bunnie]

PS LG, Can you not scan the photo, save it to my pictures, and then using this re-size web-site, re-size it if necessary, save the now smaller version to my pictures, and then click on it on the additional options at the bottom here?
Nick taught me how to do this!
http://www.resize2mail.com/

[LIGA girl]

Hi ladies

 I have just been trying to post and unable to due to the large size of the photos i have ... i have the original of that one plus some others that are more recent. it is good to compare and I wil have a go at resizing them. It is getting late now tho and if i cant do it tonight, I will do it tomorrow.

The heat doesnt worry my skin too much ... it is mainly the excessive sweating I have now that makes it unpleasant. I do stick to my clothes a bit nore in the heat tho, but as you will see from my mroe recent photos when I post them, my back is healing pretty well and only a few of them 'stick' nowadays, as it were.

Apparently I gave permission to use that photo, George tells me, but my memory is so bad these days i dont remember - maybe i have blisters on the brain too ....

[LIGA girl]

I couldnt do it tonight so just emailed you both a photo and will have another go tomorrow - just warning you in case it comes thru and clogs up your inbox, you may have to go in and delete it from your server.

[bunnie]

 

but my memory is so bad these days i dont remember - maybe i have blisters on the brain too ....

Don't worry Lg, it happens to us all! I'm sure I'm in the first stages of Alzeimers
I went to the shop for some glue, remembered to get it , but can't remember what I want to stick with it!! It will come back to me!
PS I think we are using the wrong thread for this small talk!

[CalamityJane]

Hi Bunnie:

What a very useful link for resizing!  I use Microsoft Office Picture Manager to do mine, which is pretty simple and you can adjust the brightness and saturation also.  Comes with XP I think.  I resize to post here and on other forums, but always keep the larger ones in My Pictures.

For just resizing, that site looks brilliant!

Jane
PS Hope you remember what you want to stick with the glue

[LIGA girl]

I think we are using the wrong thread for this small talk!

You are right - back to the other thread .....

....maybe others will have their photos used for publications and might be aware  of that need for their permission ....

[LIGA girl]

Can this thread be made sticky? It has a lot of reads ... and anyone is welcome to post on it too ...

[totalfolly]

Can this thread be made sticky? It has a lot of reads ... and anyone is welcome to post on it too ...

All stickied. 

totalfolly

[LIGA girl]

All stickied. 

Many thanks TF! 

[bunnie]

What causes autoimmunity?
The immune system normally can distinguish "self" from "non-self." Some lymphocytes are capable of reacting against self, resulting in an autoimmune reaction. Ordinarily these lymphocytes are suppressed. Autoimmunity occurs naturally in everyone to some degree; and in most people, it does not result in diseases. Autoimmune diseases occur when there is some interruption of the usual control process, allowing lymphocytes to avoid suppression, or when there is an alteration in some body tissue so that it is no longer recognized as "self" and is thus attacked. The exact mechanisms causing these changes are not completely understood.

Just to say that this extract I have taken from the above post from the pemphigus foundation, is what I have learned and understood to be the case concerning autoimmunity, and indeed the whole post says it all, it's unpredictability, the fact that auto is self, and it explains that the self mechanisms that are causing or have caused these changes at the molecular level, are not as yet understood.

[andyb]

This is a most interesting thread - although I must admit I did pass rather quickly over some of the photos.

I don't think I would have come across this if TF hadn't stickied....(thanks) and I was able to follow one of your listed links and confirm some more symptoms with my own current problem - fibromyalgia - which was misdiagnosed as lupus at first - thank you for that  

btw I looked up Linear IGA on Wikipedia but they don't have an article - perhaps you ladies should write one after doing all this research....

andyb  

[LIGA girl]

hi Andyb

thanks for the feedback. It struck me that it is a common element that exists for many skin conditions. Didnt know you have fibromyalgia, too. I know another with it. I was also wrongly told i had lupus at one stage last year ...not nice.

Writing up on Linear iga for Wikipedia sounds rather daunting  , but thanks for your vote of confidence in us ....

LG

[bunnie]

Hi Andyb, we have been discussing autoimmunity on our LIGA thread for a long time, all the info is there about our disease,and of course it applies to all autoimmune bullous diseases.  LG thought it a good idea to have this seperate thread for any articles found on the subject of autoimmunity because all of these diseases are under that umbrella. There's loads of info out there Andy on our condition, mostly about us, or the drugs used, many of which I was personally the guinea pig for!
This thread is good, because the articles in it pertain to what an auto immune disease is, something I have been trying to get people namely friends and family to understand for many years. It occurs and is of self.. I'm glad you have found bits of it interesting.

Bunnie

[LIGA girl]

Andyb, if yu found some good stuff regarding your own condition, why not post links to it here ...?

[LIGA girl]

Link to article on a study using IVIG treatment for an autoimmune disease .... combining it with prednisone was not an effective treatment:

http://neurology.org/cgi/content/abstract/56/3/323

And another one which was also not effective:

http://www.neurology.org/cgi/content/abstract/51/6/S37

I included these links just in case people are having this treatment suggested to them, they can make an informed choice about whether to accept it.

[LIGA girl]

Just notiing that in the few weeks since this thread was made sticky it has received several hundred (about 300 or 400) reads!

[bunnie]

I see theres a lot!

[LIGA girl]

Yes, it's good ... I must have a look for more stuff for it ....

[LIGA girl]

I happened to hear a small thing on the radio about an emotional disorder being associated with plaque psoriasis. The emotional disorder is an anxiety disorder to do with fear of losing a loved one.

[bunnie]

http://www.cop-boop.org.uk/steroid_use_&_effects.htm
The above link is to information regarding the side effects of prednisone and prednisolone -steroids.

[LIGA girl]

That link is a really good one, thanks Bunnie. It gives a better overview than many others I have read.

[bunnie]

Excellent Link explaining how the Immune System workshttp://www.merck.com/mmhe/sec16/ch183/ch183a.html#sec16-ch183-ch183a-10

[LIGA girl]

Abstract of an article which I think is interesting, supposing the genetic skin fragility referred to is our diseases ....

J Dermatol Sci. 2006 Sep 22; : 16996720      
Molecular and diagnostic aspects of genetic skin fragility.
[My paper] Cristina Has , Leena Bruckner-Tuderman
Genetic syndromes with skin fragility represent a heterogeneous group of very rare disorders caused by mutations in genes encoding proteins or protein subunits important for the mechanical resistance of keratinocytes and for cell-cell or cell-extracellular matrix adhesion. The common symptoms are skin blistering or peeling, with various degrees of severity and distribution, ranging from localized to generalized forms. Associated features include involvement of skin annexes, mucous membranes, teeth, muscles or the digestive tract. Morphological investigation of skin samples provides evidence for the tissue level of blister formation, while immunostainings may reveal defective proteins, providing clues concerning the genetic origin of the disease. Extensive mutation analysis and subsequent identification of new gene defects provide accurate diagnostics, and lead to better understanding of the functions of the respective proteins, with the potential for new therapeutic strategies.

[bunnie]

The link below concerns Bullous disease in the mouth.
Note that ALL Autoimmune bullous conditions can affect all mucous membranes and epithelial tissue throughout the body. Bullous conditions which affect these tissues, are almost indistinguishable from one another, and all are medically treated the same. Scarring, which occurs from these lesions left by blisters in these tissues; unlike the skin, continues to grow, the scarring becoming thicker. In Ocular tissues this results in blindness, or other serious complications in other parts of the body where this tissue is affected.
http://www.priory.com/den/pemphigoid.pdf

[bunnie]

 link to recent research article in autoimmune disease.
http://www.nlm.nih.gov/medlineplus/news/fullstory_44202.html

[LIGA girl]

See footnote 1 on this article for some research regarding DHEA and SLE (lupus)

http://en.wikipedia.org/wiki/Dehydroepiandrosterone

[bunnie]

Questions and answers about Autoimmunity
http://www.niams.nih.gov/hi/topics/autoimmune/autoimmunity.htm
The componants of the immune system, and their role in the body's defence.
http://en.wikipedia.org/wiki/Antigen
NB. An autoimmune response which occurs in anyone with an (auto=greek for self)-immune disease, is different from an immune response. 

[bunnie]

http://autoimmunedisease.suite101.com/blogs.cfm
I found this exert from the above link particulary interesting. It mentions that Vit D is deficient in cases of autoimmune disease.
May 22, 2007

The Importance of Vitamin D

Posted by  Elaine Moore

Vitamin D is important for a healty immune system as well as proper bone metabolism and muscle strength; blood tests are used to determine the need for supplements.


Several studies have shown a link between higher levels of Vitamin D and a lower incidence of multiple sclerosis. Similarly, studies have shown low blood levels of vitamin D are associated with numerous autoimmune diseases. Vitamin D offers benefits for autoimmune diseases because of its ability to influence T cell development and inactivate Natural Killer cells. Besides its beneficial effects on immunity, which include cancer prevention, vitamin D helps the body absorb calcium, ensuring proper bone metabolism, and it has also been shown to improve muscle strength, particularly leg muscle strength. The question of how much vitamin D is enough is of prime importance for patients with autoimmune diseases.

Sources of Vitamin D

Vitamin D is absorbed through the skin from sunlight or from supplements and foods fortified with vitamin D. The body then converts it into 25-OH vitamin D and then into the active hormone 1,25-dihydroxy vitamin D (1,25OH-D).


The recommended daily dose of vitamin D is 200-600 IU.
The optimal blood range for 1, 25 hydroxy vitamin D is 75-125 nmol/L.
Studies show that most people in the United States do not get adequate vitamin D, especially in the winter months. Studies show that the action of vitamin D in the body also depends on adequate sources of calcium from a normal to high calcium diet.

Because of the widespread use of sunscreen and a trend towards limited exposure to sunlight, the incidence of vitamin D deficiency has reached epidemic levels. Blood tests are available for measuring vitamin D levels with tests for 1, 25 hydroxy vitamin D. This test is necessary for determining if a vitamin D deficiency exists. Serum levels in the optimal range have been associated with improved bone health and muscle strength, as well as protection against numerous cancers,


The recommended dose of vitamin D3 supplementation is 800-1,000 IU daily.
However, some people need at least 5,000 IU vitamin D3 daily to bring levels into the optimal range.
According to the Life Extension Foundation, toxicity is unlikely at daily intake levels less than 10,000 IU (250 mcg).


Vitamin D Toxicity

Blood tests are important to guard against toxicity. Excess vitamin D can cause dangerous blood calcium levels, poor muscle and nerve function. Long-term elevations of vitamin D can increase the risk of kidney stone. Patients taking extremely high doses of vitamin D should be monitored for signs and symptoms of toxicity, including nausea, vomiting, poor appetite, constipation, weakness, heart arrhythmias, and elevated levels of cholesterol, calcium or liver enzymes. People with kidney disease and patients using digoxin or other heart medications should check with their doctor before using vitamin D.

Vitamin D and the Immune System

The highest concentration of vitamin D is found in the immature immune cells of the thymus and the mature CD-8 T Lymphocytes. Studies show that vitamin D3 supplements can either prevent or markedly suppress experimental autoimmune encephalomyelitis, rheumatoid arthritis, systemic lupus erythematosus, type I diabetes, and inflammatory bowel disease.

With adequate calcium, vitamin D stimulates transforming growth factor-beta1 and interleukin-4 production, which in turn may suppress inflammatory T-cell activity.

Resources:

Hector F. Deluca and Margherita T. Cantorna, Vitamin D: Its role and uses in immunology, FASEB J. 15, 2579-2585, 2001.

Tiesha D. Johnson, Guarding Against the Dangers of Vitamin D Deficiency, Life Extension Journal, May 2007: 43-50.

Janet Raloff, Vitamin Boost, From muscle strength to immunity, scientists find new vitamin D benefits, Science News Online, Oct 9, 2004, accessed May 8, 2007

[bunnie]

Diagnosis of Autoimmune disease. Note important factors in Bold.

http://www.niams.nih.gov/hi/topics/autoimmune/autoimmunity.htm

Medical tests—No one test will show that you have an autoimmune disease. But doctors may find clues in a blood sample. For example, people with lupus or rheumatoid arthritis often have certain autoantibodies in their blood. Autoantibodies are blood proteins formed against the body’s own parts.

Not all people with these diseases have these autoantibodies. And some people without autoimmune disease do have them. So blood tests alone may not always help. But if a person has disease symptoms and autoantibodies, the doctor can be more sure of a diagnosis.

The key is patience. Your doctor may be able to diagnose your condition quickly based on your history, exam, and test results. But the process often takes time. It may take several visits to find out exactly what’s wrong and the best way to treat it.

[bunnie]

Regarding Infection in persons immunocompromised.

Immunocompromised patients have alterations in phagocytic, cellular or humoral immunity = (antibody production, and all the accessory processes that accompany it)  that increase both the risk of infection and the ability to combat infection.

Immunocompromised patients are vulnerable to a broad-range of infectious agents and, due to the state of immunosuppression, presentation will be atypical =(not conforming to type) and the course fulminant.=(Occurring suddenly, rapidly, and with great severity or intensity, usually of pain.)

Commensals such as Candida and other fungi, and viruses such as cytomegalovirus, can lead to serious infection. 
Broad-spectrum antibiotic use increases the risk of secondary fungal infections.

Skin and mucous membrane infections can be very widespread and highly visible.  In contrast, it is often difficult to identify the site of infection.  Signs of inflammation other than fever are often mild or absent and, in patients undergoing cytotoxic chemotherapy, the side-effects of the treatment may mimic infection eg. pain or mucositis.

http://www.bsac.org.uk/pyxis/Immunocompromised%20patient/Principles/Principles%20of%20management%20of%20infection%20in%20the%20immunocompromised%20patientF.htm

[bunnie]

Very simple and Fun explanation of how the cells of the immune system work.
http://nobelprize.org/educational_games/medicine/immunity/immune-overview.html

http://nobelprize.org/educational_games/medicine/immunity/immune-detail.html

This is a game...
http://nobelprize.org/educational_games/medicine/immunity/index.html
and another DNA game
http://nobelprize.org/educational_games/medicine/dna_double_helix/dnahelix.html

[bunnie]

not sure if I have already posted this here or not, so just in case I haven't...
http://ww2.arthritis.org/research/researchupdate/04march_april/exploring.asp

[CalamityJane]

Hi all:

My current and second bout of sinusitis, this time w/bronchial involvement is making me wonder now that my PPP is in remission if my immune system has gone from overdrive back to a more normal state.

Any thoughts anybody. I find this quite difficult to understand w/my somewhat challenged mentality, so hope this is not a foolish question.

Jane

[bunnie]

hi jane, If you have had no signs whatsoever of your ppp then, I think you may have had or are going through a period of remission. It is this that confuses people with autoimmune diseases, because they are idiopathic, which means they are spontaneous. Remissions unlike waxing and waning, are total, the disease disappears quite naturally, and can last from a few months to many years, sometimes as with some children, it disappears altogether at puberty. My own disease went into remission for 18 years! and was far more severe than the first time. Some, depending on the disease, gradually "burn out" , for want of a better expression.
PPP I understand is quite rare and the rarer the disease the less likely that bacteria could be an enviromental factor involved in this, as we are exposed constantly to bacteria. As we have discussed before, it is a combination of mutated genes, (of which I understand there are in some cases as many as 30) other multigenous factors, along with either an exogenous factor and/or alone. endogenous factors which cause these conditions. Basically what I am saying is that the sinusitis bears no relation to your ppp, that is an immune response to an exogenous or non-self factor, whereas PPP is an abnormal immune response to endogenous or self factors.
One can have an allergy to something, or even just a reaction to something and will have an immune response to that, and still have an autoimmune response going on at the same time. This is because the genes involved in dealing with the allergy or reaction, are normal for you , whereas others in the presence of self factors, (or even stimulated by an allergy in some cases) are mutated, one at least in you, carrying the direct hereditary predisposition to Psoriasis, so once stimulated, if that gene is involved, you will get psoriasis or one of it's phenotypes. (subclasses) With autoimmune diseases the regulatory T cells are the ones involved in intense research, because these, having been "given the wrong command "
are unable to act, their job being to regulate the immune response and switch it off. I will be explaining all of this on my blog. If you have had no signs of your PPP at all for over a year I would take that as remission personally. Hope this makes sense Jane!
fondly Bunnie

[CalamityJane]

Hi bunnie:

Basically what I am saying is that the sinusitis bears no relation to your ppp, that is an immune response to an exogenous or non-self factor

Darn it bunnie I was hoping to be able to explain all this illness I've had this year. I started the Doxy again today. I couldn't manage to throw it off on my own. Started in throat, down bronchial tubes, nasty cough. Spent much of last night coughing & felt rough enough this morning to know I needed help.

Was hoping I could say my immune system had calmed down, therefore, I was more susceptible to virus' etc.

The PPP is in remission, (thank you Cellulitis & Doxy) I'm sure. All the time I had it I didn't once have a sniffle, cold, or anything.

Thanks bunnie........

[sallyann]

I just wanted to jump in here because everyone in my family has been sick with the crud.  The majority of people at work also have had a bad flu.  Several grandchildern also have had the flu recently. I have PPP and can't understand why I have not gotten it yet.  I hope I don't, but wondered if my body is too busy working on the PPP that it blocked the virus that is going around. 

I don't understand the autoimmune system yet but thanks to the forum I am learning.

Sally

[LIGA girl]

My current and second bout of sinusitis, this time w/bronchial involvement is making me wonder now that my PPP is in remission if my immune system has gone from overdrive back to a more normal state.

Jane, the last three winters before I got my skin illness I seemed to have no resistance to winter flus and had them constantly during those 3 winters. When I got a major autoimmune disease I wondered if there was a connection. And since having the skin disease I have been almost free of the flu ... had one bout last year made worse by being on immunesuppressants but that is all.

LG

[bunnie]

The autoimmune response is a response to self molecules. An immune response is a response to non self exogenous factors, that is why one can have two different things going on, say having a cold or flu-like symptoms. It isn't a case of having two different immune systems , but a case of the genetics involved, ie the specific genes which are involved. A virus can stimulate the predisposition in some cases, but that virus would be identified, and would still manifest symptoms just as an allergy does. I have had awful colds and other infections and still had the autoimmune disease manifesting, and had the same when I was in remission.
Basically, from what I understand anyway, (and I will be posting a link to my blog soon concerning this, that's if it is allowed of course to do that; I just need to finish presenting it, ) A protein of self, transcribes the stored information in the genes and presents that information as a protein. As the gene is mutated, so is the information transcribed from it, therefore every subsequent immune cell produced is also mutated and "acts" differently than it should, within that specific response, and the other cells (regT cells) which regulate the immune response , also fail to regulate properly and are unable (apart from other things) to switch the response "off" as normal. In order for these mutated genes to be stimulated in the first place, it takes a combination of multigenous and endogenous factors ( such as hormones, or molecular mimicry, there are others  ) and possibly exogenous factors in some cases, such as viruses or drugs etc. Another point is that say a person had a nail in their foot,  the complement system would be there in a trance stimulating inflammation to prevent infection entering the body. The complement system (the first part of the immune defence to act) is very rapid to answer and very deadly, it also assists antibodies in fighting invaders. The genes and immune cells involved in this response may be fine, and they don't prevent or stop another abnormal response involving other genes and the subsequent production of cells from that abnormal response from occuring. In other words cells could be fighting two seperate invasions of non-self factors at the same time, say a nail in the foot and a head cold occuring at the same time, or an abnormal response and a normal one going on at the same time. They are unrelated.
Its like sending a battalion of an army to fight in IraQ and another to Afghanistan. My geography is hopeless by the way, so don't pull me up on that!
Forgot to add LG, probably the reason that you have not had this flu symptom since getting Liga, is that you were on high dose steroids, (still are?) also immunosuppressants although they suppress the immune system making it more vunerable to infection, they are never the less suppressing all the cells involved in the immune response particulary inflammation, a key factor in head colds.
Bunnie

[CalamityJane]

Hi all:

Just as I thought I was getting a grasp of this, I'm soooo lost (again)....My head is thicker than 'normal' today Bunnie But I do understand the difference between autoimmune and immune! Got that! Yippee.....

Jane, the last three winters before I got my skin illness I seemed to have no resistance to winter flus and had them constantly during those 3 winters. When I got a major autoimmune disease I wondered if there was a connection. And since having the skin disease I have been almost free of the flu ... had one bout last year made worse by being on immunesuppressants but that is all.

LG

Hi LG: The 3 years before my PPP I had no colds or flu and nothing while the PPP was active. Even though I had Doxy last year it was not for sinus/bronchial things. Don't know why that would be as son is often (it seems) full of it (colds I mean)! I've not caught them.

Jane

[bunnie]

Don't know why that would be as son is often (it seems) full of it (colds I mean)!

Hi jane, maybe because your son is more susceptible than you regarding these bugs. My brother and I were serious as kids, one getting better the other starting, terrible symptoms , streaming inflamed eyes, raw nose, streaming nose, real "coryza", (which means boiling over from the head!" describes it exactly!) Mum and my two other siblings never got a thing! My siblings still don't, whereas my brother and I are serious, my poor brother getting terrible asthma. My son too has this problem, coryza and asthma, bless him, I am sorry to say, it is so miserable.
fondly Bunnie

[CalamityJane]

Hi Bunnie........

which means boiling over from the head!" describes it exactly!)

That's exactly how I feel, but hadn't heard that word before.

I get it now -- came to me as I sneezed along walking Rolo -- my cold/sinus thing is an immune response to whatever...........the PPP is autoimmune, not related.

Right.............

Jane

[LIGA girl]

An overview of the latest treatment I have had (rituximab) and its application to skin diseases: (See especially the last page with the grey box for a good summary.)

http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1365-2230.2006.02151.x?cookieSet=1

[bunnie]

http://www.cureautoimmunity.org/Common%20Cause.htm

http://www.cureautoimmunity.org/common%20cause%20white%20paper%2012-05.htm

[bunnie]

A link to my blog on disorders of the immune system, which includes all disorders inluding autoimmunity.
http://wassail-allthatilove.blogspot.com/2008/03/disorders-of-immune-system-immune.html
bunnie

[sallyann]

Please see my post in the PPP thread.  I contacted roundworm we think from my cat.  I found a very interesting article which I am linking.  Roundworm can cause an autoimmune response.

I posted some of the information in the PPP thread.  for Now I am only including the link. http://members.aol.com/SynergyHN/roundworm


Bunnie should be very interested in this.

Sally

[gerrybhoy]

Hi all
 
i have being given the drug low dose naltrexone for mt ppp but since looking into it have found out that it dose cover alot more autoimmune disease's as well

some people having difficult in find site so ill leave a link to see what you all think or if you've hear of it before

www.lowdosenaltrexone.org

thanks gerald

[CalamityJane]

The link below is excellent article, only published last month, and makes reference to the difference between allergic dermatitis and atopic dermatitis.

Well worth reading for all of us with autoimmune diseases.

http://emedicine.medscape.com/article/1049216-overview?src=emed_whatnew_nl_0#causes

Jane

 

[CalamityJane]

Hi all, received this today from an ezine that I subscribe to, www.drmirkin.com

Here it is:

"Women are three times more likely than men to develop lupus, multiple sclerosis, or rheumatoid arthritis, currently thought to be autoimmune diseases that are caused by a person's immunity attacking her own body, instead of doing its job of killing germs. This increased risk may be caused in some way by the process of pregnancy, or it may be due to the fact that women are twice as likely as men to become infected with a sexually transmitted disease and 10 times more likely to become infected with HIV. See report #G144 on mycoplasma, chlamydia and ureaplasma.

Several papers have shown that multiple sclerosis may be caused by infection with human herpes-6 (39,40), lupus by parvovirus B-19 (27,38) and rheumatoid arthritis by mycoplasma (2-26).

People with autoimmune diseases usually have proteins called antibodies that attach to and damage a person's own body proteins and cells, rather than attaching to and killing known germs that enter the body. For example, antinuclear antibodies, double-stranded DNA antibodies and anticardiolipin antibodies are often fond in people who have lupus and the rheumatoid factor is found in rheumatoid arthritis. These autoantibodies can be caused by infections with Hepatitis B and C viruses, the human immunodeficiency virus, and parvovirus B19 (1,38). Several papers have suggested that rheumatoid arthritis may be caused by mycoplasma bacteria (2-26), lupus by parvovirus B19 (27), Crohn's disease by bacteroides and klebsiella bacteria (28-37), and multiple sclerosis by HHS-6 and JC viruses (39,40) and many doctors are treating rheumatoid arthritis and Crohn's disease with antibiotics. Future studies will show if these autoimmune diseases are really caused by infections."

[Seattlejeff]

Hi all, received this today from an ezine that I subscribe to, www.drmirkin.com

Here it is:

"Women are three times more likely than men to develop lupus, multiple sclerosis, or rheumatoid arthritis, currently thought to be autoimmune diseases that are caused by a person's immunity attacking her own body, instead of doing its job of killing germs. This increased risk may be caused in some way by the process of pregnancy, or it may be due to the fact that women are twice as likely as men to become infected with a sexually transmitted disease and 10 times more likely to become infected with HIV. See report #G144 on mycoplasma, chlamydia and ureaplasma.

Several papers have shown that multiple sclerosis may be caused by infection with human herpes-6 (39,40), lupus by parvovirus B-19 (27,38) and rheumatoid arthritis by mycoplasma (2-26).

People with autoimmune diseases usually have proteins called antibodies that attach to and damage a person's own body proteins and cells, rather than attaching to and killing known germs that enter the body. For example, antinuclear antibodies, double-stranded DNA antibodies and anticardiolipin antibodies are often fond in people who have lupus and the rheumatoid factor is found in rheumatoid arthritis. These autoantibodies can be caused by infections with Hepatitis B and C viruses, the human immunodeficiency virus, and parvovirus B19 (1,38). Several papers have suggested that rheumatoid arthritis may be caused by mycoplasma bacteria (2-26), lupus by parvovirus B19 (27), Crohn's disease by bacteroides and klebsiella bacteria (28-37), and multiple sclerosis by HHS-6 and JC viruses (39,40) and many doctors are treating rheumatoid arthritis and Crohn's disease with antibiotics. Future studies will show if these autoimmune diseases are really caused by infections."

Dear Calimity Jane:

I am very impressed with your knowledge of autoimmune diseases and have some questions for you if you don't mind.  I am a 56 yr old man, immune depressed, who developed a strange rash in January 09.  My dermatologist suspected lupus and my Elisa came back as such.  However when I was referred to a rheumatologist his findings which were complicated and intricate tests done at the local University, concluded a false positive.  Relieved, I still have been dealing with this rash to this day.  My endocrinologist sees no connection as my thyroid functions are normal.  And my nephrologist said, even though my kidneys are functioning at a moderate level, he sees no correlation to a rash.

My derm took three biopsies, one showing folliculitus which was taken from this initial rash which is on my upper chest neck and beard area.  Also effecting my shoulders now.  And another taken shortly after on my back which showed Grover's.  In her mind they are completely seperate of each other.  The latest biopsy on my initial rash on my upper chest showed follicular distress, especially with an unusually high amount of white blood cells at its base.  It is my idea, as my derms, this could be an auto immune type situation, I think they call it auto immune reconstitution.

I saw an allergist/immunologist, although nice, my case seemed to complicated, and he was not helpful.  It does seem from the presentation on my neck, upper neck, beard, and upper back, symptoms that my CD 4s are over reacting and my body is sending too many white blood cells to  site causing all this inflammation.

I know this is rather vague, but since this is a public site, I don't want to get into a whole lot of specifics, but thought you may have some ideas of if indeed this is autoimmune related, if there is a particular type of physician I should see who I haven't, and if there is a medication I should be on.

I'm kind of at my wit's end.....  I should underscore this I have made very healthy diet changes, and exercise regularly.  But have been under some stress lately.

Thanks for any opinions you might have,

SeattleJeff

[CalamityJane]

Hi Seattlejeff, we are geographically neighbours, and thank you for your post.

I'm not a doctor or a nurse or an expert in auto immune diseases (but thank you!). I'm just somebody who has one. I'm glad to see you are investigating and learning on your own. It's good to research, be informed and take an active role in your condition and treatment.

From what you say, it seems that you have seen all the right doctors and specialists who can help you. As some tests came back a false positive, perhaps you could consider repeating them?  Your derm in discussion w/your other specialists would have prescribed something for the inflammation you have. Or the other way around, the other specialists in consultation with your derm.

Auto immune diseases are difficult and treatment can be problematic because so many things are involved. They come and go at will adding to the problem. I understand you being at your wit's end. I've been at my wit's end, along with many others. It's a long and twisting road it seems. What helped me will not necessarily help you. It's individual and is "in" you so to speak, like freckles, wavy hair, etc.

"Auto immune reconstitution" is a new one to me. Tell me more!

In my humble opinion, you are doing all the right things and seeing all the right people, who will follow the trail and eventually all the pieces will fit together to solve your puzzle. I know it's frustrating but it seems to be the nature of the beast. Have you tried a course of antibiotics?

You might glean some more info by going to the site that produces the ezine I receive. It's well worth signing up, again my opinion. It's www.drmirkin.com

I wish I could be of more help.........

Jane

[Seattlejeff]

Hi Seattlejeff, we are geographically neighbours, and thank you for your post.

I'm not a doctor or a nurse or an expert in auto immune diseases (but thank you!). I'm just somebody who has one. I'm glad to see you are investigating and learning on your own. It's good to research, be informed and take an active role in your condition and treatment.

From what you say, it seems that you have seen all the right doctors and specialists who can help you. As some tests came back a false positive, perhaps you could consider repeating them?  Your derm in discussion w/your other specialists would have prescribed something for the inflammation you have. Or the other way around, the other specialists in consultation with your derm.

Auto immune diseases are difficult and treatment can be problematic because so many things are involved. They come and go at will adding to the problem. I understand you being at your wit's end. I've been at my wit's end, along with many others. It's a long and twisting road it seems. What helped me will not necessarily help you. It's individual and is "in" you so to speak, like freckles, wavy hair, etc.

"Auto immune reconstitution" is a new one to me. Tell me more!

In my humble opinion, you are doing all the right things and seeing all the right people, who will follow the trail and eventually all the pieces will fit together to solve your puzzle. I know it's frustrating but it seems to be the nature of the beast. Have you tried a course of antibiotics?

You might glean some more info by going to the site that produces the ezine I receive. It's well worth signing up, again my opinion. It's www.drmirkin.com

I wish I could be of more help.........

Jane

Thanks so much Jane for getting back to me so quickly.  It's nice that we are geographical neighbors.  A small world it is.

You point out some very good ideas.  I am seeing my dermatologist and GP this week.  I think a round of antibiotics might help, although about three months I was on a three week course of Avelox and didn't see much improvement.  Prendisone (sp) helps while I'm on it, but I relapse even worse soon after.  I think a round of tetracycline or something like that might be of help.

Also, I feel I do need to repeat my ANA lupus tests.  Thyroid tests all check out fine.  And kidneys too.

I'll check the link you gave me as well.  Thanks for that.  I hope you are doing well.

Will be in touch, and thanks so much for responding.  By the way, I have Grover's as well, so I am in the Grover's group on Skin Cell, and a wonderful group they are as is yours.  I feel so blessed to have found this site.

Best wishes to you Jane,

Jeff