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Found 3 results

  1. Hello everyone, 4 years ago, I was diagnosed with rheumatoid arthritis at age 14. My doctor put me on methotrexate, a common medication for ra, as well as folic acid. Because I was young, I was lazy when it came to taking the folic acid, and after lots of research, there seems to be a correlation between methotrexate, not taking folic acid supplements, and celiac disease. And yes, I was diagnosed with Celiac disease pretty recently as well. QUESTION: Anyways, I was wondering, did anyone else hear of this correlation between methotrexate, folic acid deficiency, and Celiac disease? How many of you have both diseases (RA and Celiac) and which diagnose did you get first? What RA medication were you prescribed? I'm really trying to see if there is correlation, and would strongly appreciate if you helped out by leaving a comment! Thanks in advance!
  2. Celiac.com 03/09/2010 - Celiac disease is a vastly growing epidemic. Those suffering from celiac have varying levels of difficulty digesting wheat, rye and barley; as celiac primarily affects the small bowel and is considered to be an autoimmune intestinal disorder. However, compounding new evidence sited in the March 2010 edition of the The Lancet Neurology, suggests that celiac disease also affects the nervous system, indicating a wider systemic disorder than previously thought. Thanks to modern science and years of testing, many neurological disorders are now being directly associated with gluten intolerance. The most common associations have been demonstrated to be, cerebellar ataxia and peripheral neuropathy. Although gluten has also been shown to impact drug resistant epilepsy, multiple sclerosis, dementia, and stiff-man syndrome among others. To accurately determine the effects gluten has on neurological health, testing by Hadjivassiliou and colleagues was done in three areas: serology, genetics, and clinical response to gluten withdrawal. As far as serological tests are concerned, IgG antibodies to gliadin (AGA) have long been considered the most accurate indicators of neurological gluten sensitivity. However, researchers are now finding that IgG AGA is no longer a relevant test for gluten sensitivity, and it is now being replaced with more dependable tests. In fact, researchers recently became aware of IgG DGP AGA as an nearly absolute marker for the connection between gluten sensitivity and celiac disease. Initial data also indicates that TG6 are markers for gluten sensitivity, while TG3 appears to be markers for dermatitis herpetiformis. Additionally, IgA antibodies to TG2, if they are detectable in the intestine, have also been shown to effectively connect neurological disease with gluten intolerance. Genetics is another important correlation between gluten intolerance and neurological disorders. Clinically speaking, the recognition of HLA DQ2 combined with a positive serology, increases the probability that gluten plays a roll in the manifestation of neurological pathogenesis. Evaluating gluten withdrawal is crucial when establishing the gluten/neurological abnormalities connection. The link has been clearly noted in patients newly diagnosed with cerebellar ataxia or peripheral neuropathy. After establishing a gluten-free diet, the patients showed considerable improvement of their neurological symptoms. However, patients that had neurological symptoms lasting longer than 12 months, did not typically show signs of neurological improvement once a gluten-free diet was initiated. The reason for this is thought to be a result of irreversible neural cell damage, such as a loss of Purkinje cells accompanied by prominent T-lymphocyte, as seen in patients with ataxia. While the findings of these studies indicated that gluten is a major factor associated with neurological disorders, further studies are needed to show conclusive evidence of the direct correlation between the two. Such findings may provide the key to determining if autoimmunity is fundamental in evoking gluten-sensitive neurological impairment. Source: The Lancet Neurology, Volume 9, Issue 3, Pages 233 - 235, March 2010
  3. Celiac.com 07/29/2010 - The underlying causes of psoriasis are not well understood. Many patients with psoriasis also have a sensitivity to gluten. In an effort to better understand any connection between psoriasis, celiac disease, and the HLA Cw6 genotype, a research team examined the expression of celiac-associated antibodies gliadin IgA, gliadin IgG, and tissue transglutaminase IgA, and possible associations the antibodies may have with the HLA Cw6 gene in people with psoriasis. The team included Sangeeta Singh, Gyanendra Kumar Sonkar, Usha, and Sanjay Singh. They are variously affiliated with the Division of Immunopathology in the Department of Pathology at the Institute of Medical Sciences, the Department of Dermatology and Venereology, and the Academic Staff College at Banaras Hindu University in Varanasi, India. Antigens are substances that are recognized by the immune system and trigger an immune reaction. Class I human histocompatibility (HLA) antigens are coded into a small cluster of structural genes at the C locus on chromosome 6. They show substantially lower immune-triggering action than the HLA-A and -B determinants, and so are not a major factor in medical donations. Researchers find them useful because of their high-risk association with certain diseases, such as spondylarthritis, psoriasis, multiple myeloma. About 50 percent of all psoriasis patients carry HLC-Cw6. For the study the team evaluated 56 patients with psoriasis, along with 60 healthy control subjects. The team used ELISA to measure antibody levels, and the microcytotoxicity method to type HLA Cw6. Blood samples of psoriasis patients showed significant HLA Cw6 expression compared with control subjects (P Psoriasis patients showed substantially higher celiac-associated antibodies for gliadin IgA/IgG and tissue transglutaminase IgA compared with control subjects (P Women showed substantially higher serum anti-tissue transglutaminase IgA (anti tTG IgA) than did men. Older patients showed higher expressions than did their younger counterparts. Antibodies showed significant positive correlation (anti-gliadin IgA with anti-gliadin IgG: r=0.67, P. From their results, the team concludes that patients with psoriasis commonly show latent celiac disease or celiac-associated antibodies, but that HLA Cw6 is not connected with expression of these antibodies in patients with psoriasis. Source: Journal of Clinical Laboratory Analysis, Volume 24 Issue 4, Pages 269 - 272
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