List of autoimmune diseases

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I was researching autoimmune disease and  found this list of many of them. It is eye opening to say the least. I was amazed how many there are. I actually have several on the list. So, in my attempt to educate others on autoimmune diseases, here is the list I found from the webpage “American Autoimmune Related Diseases Association”:

List of Autoimmune and Autoimmune-Related Diseases

 

  • Acute Disseminated Encephalomyelitis (ADEM)
  • Acute necrotizing hemorrhagic leukoencephalitis
  • Addison’s disease
  • Agammaglobulinemia
  • Allergic asthma
  • Allergic rhinitis
  • Alopecia areata
  • Amyloidosis
  • Ankylosing spondylitis
  • Anti-GBM/Anti-TBM nephritis
  • Antiphospholipid syndrome (APS)
  • Autoimmune aplastic anemia
  • Autoimmune dysautonomia
  • Autoimmune hepatitis
  • Autoimmune hyperlipidemia
  • Autoimmune immunodeficiency
  • Autoimmune inner ear disease (AIED)
  • Autoimmune myocarditis
  • Autoimmune pancreatitis
  • Autoimmune retinopathy
  • Autoimmune thrombocytopenic purpura (ATP)
  • Autoimmune thyroid disease
  • Axonal & neuronal neuropathies
  • Balo disease
  • Behcet’s disease
  • Bullous pemphigoid
  • Cardiomyopathy
  • Castleman disease
  • Celiac sprue
  • Chagas disease
  • Chronic fatigue syndrome
  • Chronic inflammatory demyelinating polyneuropathy (CIDP)
  • Chronic recurrent multifocal ostomyelitis (CRMO) 
  • Churg-Strauss syndrome
  • Cicatricial pemphigoid/benign mucosal pemphigoid
  • Crohn’s disease
  • Cogans syndrome
  • Cold agglutinin disease
  • Congenital heart block
  • Coxsackie myocarditis
  • CREST disease
  • Essential mixed cryoglobulinemia
  • Demyelinating neuropathies
  • Dermatitis herpetiformis 
  • Dermatomyositis
  • Devic’s disease (neuromyelitis optica)
  • Discoid lupus
  • Dressler’s syndrome
  • Endometriosis
  • Eosinophilic fasciitis
  • Erythema nodosum
  • Experimental allergic encephalomyelitis
  • Evans syndrome
  • Fibromyalgia**
  • Fibrosing alveolitis
  • Giant cell arteritis (temporal arteritis)
  • Glomerulonephritis
  • Goodpasture’s syndrome
  • Graves’ disease
  • Guillain-Barre syndrome
  • Hashimoto’s encephalitis
  • Hashimoto’s thyroiditis
  • Hemolytic anemia
  • Henoch-Schonlein purpura
  • Herpes gestationis
  • Hypogammaglobulinemia
  • Idiopathic thrombocytopenic purpura (ITP)
  • IgA nephropathy
  • IgG4-related sclerosing disease
  • Immunoregulatory lipoproteins
  • Inclusion body myositis
  • Insulin-dependent diabetes (type1)
  • Interstitial cystitis
  • Juvenile arthritis
  • Juvenile diabetes
  • Kawasaki syndrome
  • Lambert-Eaton syndrome
  • Leukocytoclastic vasculitis
  • Lichen planus
  • Lichen sclerosus
  • Ligneous conjunctivitis
  • Linear IgA disease (LAD)
  • Lupus (SLE)
  • Lyme disease, chronic 
  • Meniere’s disease
  • Microscopic polyangiitis
  • Mixed connective tissue disease (MCTD)
  • Mooren’s ulcer
  • Mucha-Habermann disease
  • Multiple sclerosis
  • Myasthenia gravis
  • Myositis
  • Narcolepsy
  • Neuromyelitis optica (Devic’s)
  • Neutropenia
  • Ocular cicatricial pemphigoid
  • Optic neuritis
  • Palindromic rheumatism
  • PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus)
  • Paraneoplastic cerebellar degeneration
  • Paroxysmal nocturnal hemoglobinuria (PNH)
  • Parry Romberg syndrome
  • Parsonnage-Turner syndrome
  • Pars planitis (peripheral uveitis)
  • Pemphigus
  • Peripheral neuropathy
  • Perivenous encephalomyelitis
  • Pernicious anemia
  • POEMS syndrome
  • Polyarteritis nodosa
  • Type I, II, & III autoimmune polyglandular syndromes
  • Polymyalgia rheumatica
  • Polymyositis
  • Postmyocardial infarction syndrome
  • Postpericardiotomy syndrome
  • Progesterone dermatitis
  • Primary biliary cirrhosis
  • Primary sclerosing cholangitis 
  • Psoriasis
  • Psoriatic arthritis
  • Idiopathic pulmonary fibrosis
  • Pyoderma gangrenosum
  • Pure red cell aplasia
  • Raynauds phenomenon
  • Reflex sympathetic dystrophy
  • Reiter’s syndrome
  • Relapsing polychondritis
  • Restless legs syndrome
  • Retroperitoneal Fibrosis
  • Rheumatic fever
  • Rheumatoid arthritis
  • Sarcoidosis
  • Schmidt syndrome
  • Scleritis
  • Scleroderma
  • Sjogren’s syndrome
  • Sperm & testicular autoimmunity
  • Stiff person syndrome
  • Subacute bacterial endocarditis (SBE)
  • Susac’s syndrome
  • Sympathetic ophthalmia
  • Takayasu’s arteritis
  • Temporal arteritis/Giant cell arteritis
  • Thrombocytopenic purpura (TTP)
  • Tolosa-Hunt syndrome
  • Transverse myelitis
  • Ulcerative colitis
  • Undifferentiated connective tissue disease (UCTD)
  • Uveitis
  • Vasculitis
  • Vesiculobullous dermatosis
  • Vitiligo
  • Wegener’s granulomatosis

**NOTE Fibromyalgia and Chronic Fatigue are listed, not because they are autoimmune, but because many persons who suffer from them have associated autoimmune disease(s)

Hereditary??

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The jury is out when it comes to autoimmune diseases being hereditary. I say that because one study will show it can be inherited, while another will show the opposite. In the interest of being informative, I will state that in my family, we have the following autoimmune diseases:

Systemic Lupus erythrematosis

Celiac disease

Hashimotos Thyroiditis

Antiphospholipid Syndrome

Psoriasis

Of these diseases, only one is not a directly linked disease. I have a paternal aunt who has lupus. The rest of these diseases are shown in my sister, my daughter, and my sons. I would say our family makes a good case for the inherited disease. I wonder how many others out there can show the same thing?

I am hoping to enroll in yet another study (I am in one right now for benlysta) in which my sister and I are checked and followed to study the dynamics of possible inherited diseases. My sister has agreed to participate so we may get chosen to do this one.

In the meantime, I will continue to try to educate others about autoimmune diseases in an effort to bring about awareness of these diseases. Many people have heard of them, but really know nothing about them. I will try to do what I can to change that.

Celiac Disease Information

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This time I looked up celiac disease since it is another of the autoimmune diseases and can overlap with lupus. I would also like to state that my baby sister has this and it is found in 1 out of every 133 people. It does not get a lot of attention, like lupus, yet it affects so many people. In an effort to raise awareness of autoimmune diseases other than lupus, I have found this information to read. It is amazing that there are so many autoimmune diseases out there! This information was obtained from the website, www.celiac.org. If you would like more information, please see their site. Thanks and good reading!

Celiac Disease (CD) is a lifelong inherited autoimmune condition affecting children and adults. When people with CD eat foods that contain gluten, it creates an immune-mediated toxic reaction that causes damage to the small intestine and does not allow food to be properly absorbed. Even small amounts of gluten in foods can affect those with CD and cause health problems. Damage can occur to the small bowel even when there are no symptoms present.

Gluten is the common name for the proteins in specific grains that are harmful to persons with celiac disease. These proteins are found in ALL forms of wheat (including durum, semolina, spelt, kamut, einkorn and faro) and related grains rye, barley and triticale and MUST be eliminated.

The cause of Celiac Disease (CD), also known as celiac sprue or gluten sensitive enteropathy (GSE), is still a mystery. One out of 133 people in the United States is affected with celiac disease. CD occurs in 5-15% of the offspring and siblings of a person with celiac disease. In 70% of identical twin pairs, both twins have the disease. It is strongly suggested that family members be tested, even if asymptomatic. Family members who have an autoimmune disease are at a 25% increased risk of having celiac disease.

Celiac Disease is not a food allergy – it is an autoimmune disease. Food allergies, including wheat allergy, are conditions that people can sometimes grow out of. This is not the case with Celiac Disease.

Celiac Disease (CD) is unique in that a specific food component, gluten, has been identified as the trigger. When individuals with CD eat gluten, the villi (tiny hair-like projections in the small intestine that absorb nutrients from food) are damaged. This is due to an autoimmune reaction to gluten. Damaged villi do not effectively absorb basic nutrients – proteins, carbohydrates, fats, vitamins, minerals and, in some cases, water and bile salts. If CD is left untreated, damage to the small bowel can be chronic and life threatening, causing an increased risk of associated disorders – both nutritional and immune related.

Dermatitis Herpetiformis (DH) is the skin manifestation of celiac disease characterized by blistering, intensely itchy skin. The rash has a symmetrical distribution and is most frequently found on the face, elbows, knees and buttocks. DH patients can have intestinal damage without obvious gastrointestinal symptoms.

Dermatitis Herpetiformis (DH) is diagnosed by a biopsy of a skin lesion and staining for IgA in the tissues. More than 85% of DH patients have small bowel sensitivity to gluten. Everyone with DH needs to follow a gluten-free diet.

ASSOCIATED AUTOIMMUNE DISORDERS

Insulin-dependent Type 1 Diabetes Mellitus, Liver diseases, Thyroid Disease-Hashimoto’s Thyroiditis, Lupus (SLE), Addison’s Disease, Chronic Active Hepatitis, Rheumatoid Arthritis, Turner Syndrome, Sjögren’s Syndrome, Raynaud’s Syndrome, Alopecia Areata and Scleroderma

OTHER DISORDERS LINKED WITH CELIAC DISEASE

Down Syndrome, Fibromyalgia, Chronic Fatigue Syndrome, Williams Syndrome

Celiac Disease can appear at any time in a person’s life. In adults, the disease can be triggered for the first time after surgery, viral infection, severe emotional stress, pregnancy or childbirth. CD is a multi-system, multi-symptom disorder. Symptoms vary and are not always gastrointestinal (GI). GI symptoms can often mimic other bowel disorders.

Infants, toddlers and young children with CD may often exhibit growth failure, vomiting, bloated abdomen, behavioral changes and failure to thrive.

CLASSIC SYMPTOMS MAY INCLUDE

  • Abdominal cramping, intestinal gas
  • Distention and bloating of the stomach
  • Chronic diarrhea or constipation (or both)
  • Steatorrhea – fatty stools
  • Anemia – unexplained, due to folic acid, B12 or iron deficiency (or all)
  • Unexplained weight loss with large appetite or weight gain

OTHER SYMPTOMS

  • Dental enamel defects
  • Osteopenia, osteoporosis
  • Bone or joint pain
  • Fatigue, weakness and lack of energy
  • Infertility – male/female
  • Depression
  • Mouth ulcers
  • Delayed puberty
  • Tingling or numbness in hands or feet
  • Migraine headaches

SOME LONG-TERM CONDITIONS THAT CAN RESULT FROM UNTREATED CD

  • Iron deficiency anemia
  • Early onset osteoporosis or osteopenia
  • Vitamin K deficiency associated with risk for hemorrhaging
  • Vitamin and mineral deficiencies
  • Central and peripheral nervous system disorders – usually due to unsuspected nutrient deficiencies
  • Pancreatic insufficiency
  • Intestinal lymphomas and other GI cancers (malignancies)
  • Gall bladder malfunction
  • Neurological manifestations

Celiac Disease Diagnosis

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A person seeking diagnosis MUST be following a daily diet that contains gluten for at least 4 weeks in order for test results to be accurate. Specific antibody blood tests are the initial step in screening for CD. Patients should always consult with a physician to ensure proper diagnosis.

Recommended Blood Tests:

  • Anti-tissue transglutaminase antibody (tTG – IgA and IgG)
    commonly used whether or not symptoms are present and the most sensitive test available
  • Anti-endomysial antibody (EMA-IgA) – highly specific marker for celiac disease
  • Anti-deaminated gliadin peptide (DGP – IgA and IgG)
    used when tTG or EMA is negative and in cases where patient is IgA deficient
  • Total serum IgA – used to check levels to exclude selective IgA deficiency that results in a false negative test
  • Anti-gliadin antibody (AgA – IgG and IgA) not considered sensitive or specific enough for adults, but used for children under 2 because tTG and EMA antibodies may be absent. The anti-DGP test is sensitive in this group.

A patient with positive antibody tests and a patient with selective IgA deficiency are strongly advised to consult with their physician regarding a small bowel biopsy (which is performed endoscopically). A positive small bowel biopsy is required to confirm the diagnosis and assess the degree of damage to the villi in the intestinal lining. Antibody test results can only suggest the presence of Celiac Disease but cannot confirm it. When antibody results and biopsy are inconclusive, or when the patient is on a gluten-free diet, genetic testing of the HLA (human leukocyte antigen) DQ2/DQ8 genes may be helpful. The specific genes DQ2 and/or DQ8 are considered necessary for Celiac Disease to develop. Since one-third of the population also has these genes, the presence of DQ2 or DQ8 does not imply that the person will necessarily develop CD, rather, that they have a genetic predisposition to CD.

Genetic testing does not diagnose Celiac Disease – its largest benefit is that the absence of DQ2 and DQ8 essentially excludes CD.

The onset of Celiac Disease can occur at any time in a person’s life. Once a person is diagnosed, family members should be urged to get tested as well.

Treatment of Celiac Disease

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Celiac Disease/Dermatitis Herpetiformis (CD/DH) are chronic disorders. The only treatment is the lifelong adherence to the gluten-free diet. When gluten is removed from the diet, the small intestine will start to heal and overall health improves. Medication is not normally required. Consult your physician regarding specific nutritional supplementation to correct any deficiencies. The diagnosed celiac should have medical follow-up to monitor the clinical response to the gluten-free diet.

Adapting to the gluten-free diet requires some lifestyle changes. It is essential to read labels which are often imprecise, and to learn how to identify ingredients that may contain hidden gluten. Even small amounts of ingested gluten can affect those with CD and cause health problems.

Dietary compliance increases the quality of life and decreases the likelihood of osteoporosis, intestinal lymphoma and other associated illnesses.

Because osteoporosis is common and may be profound in patients with newly diagnosed CD, bone density should be measured at or shortly after diagnosis.

Potential harmful ingredients include:

  • unidentified starch
  • binders
  • fillers
  • excipients
  • extenders
  • malt

Gluten may also be used as a binder in some pharmaceutical products.  Request clarification from food and drug manufacturers when necessary.

  

 

 

Recent Lupus News 10.06.2010

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Hey everyone! I am taking the easy way out tonight and posting an article I found on medicalnewstoday.com. Hope you enjoy the article and tomorrow I hope to post a new post. Thanks and enjoy!

Lupus Research Investigator Says Breakthrough Holds Potential For New Treatment To Quiet Lupus

   

 

   

 

   

Researchers at the Dana-Farber Cancer Institute in Boston have identified a new type of cell in mice that dampens the immune system and protects the animal’s own cells from immune system attack.

This “suppressor” cell reduces the production of harmful antibodies that can drive lupus and other autoimmune diseases in which the immune system mistakenly turns on otherwise healthy organs and tissues.

The discovery, published in a recent issue of Nature (H Kim, et al.; Vol 467 in Letters), resulted from Lupus Research Institute funding to Harvey Cantor, MD, and colleagues on a separate immune system topic.

Now the discovery will be used to explore therapies that might control the hyperactive immune system in lupus. “These CD8+ T suppressor cells represent a potential new lever for lowering the strength of the immune response in autoimmune diseases such as lupus,” Dr. Cantor said.

Staying Open to Discovery

Until now, scientists searching for cells involved in quieting the immune system response had focused their hunt on “regulatory CD4+ T cells” – also known as CD4+ Treg. Some of these cells have been shown to prevent harmful inflammatory diseases and infections.

In the Nature study, Harvey Cantor, MD, and his team reported that not just CD4+T cells but CD8+ T cells as well include a subset that helps dampen the immune response. Instead of reducing inflammation like their CD4 cousins, the CD8+ T regulatory cells ensure that the immune system doesn’t produce antibodies that attack normal cells.

Lead author Hye-Jung Kim and colleagues made the discovery as they were winding up unrelated LRI-funded work into the role in autoimmunity of a protein found inside immune cells called osteopontin.

“Our LRI funds allowed us to carry out the early experiments that led to the definition of the CD8 suppressor cells.” – Dr. Cantor.

“We were testing osteopontin’s activity against a population of cells known as follicular T helper cells,” explained Dr. Cantor. “We noted that the cells were responsive to osteopontin but also that they expressed what we knew to be the target of suppressor CD8+ T cells.”

As next steps, Dr. Cantor and his team will investigate whether defective CD8+ T suppressor cells actually could be a cause of lupus and might serve as a powerful drug target for quieting the immune system response in autoimmunity.

About Lupus

Systemic lupus erythematosis is a chronic complex and potentially fatal autoimmune disease that affects more than 1.5-million Americans, mostly young women in their child-bearing years. Lupus causes the immune system to become hyperactive, forming antibodies that attack and damage the body’s own tissues and vital organs including the heart, brain, kidneys and lungs. Lupus is a leading cause of cardiovascular disease, kidney disease and stroke among young women. As yet, there is no known cause or cure but the progress of recent discoveries is highly promising.

Source:
Liane Stegmaier
Lupus Research Institute