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Causes
RA is a chronic autoimmune disorder the causes of which are not completely understood. It is a systemic (whole body) disorder principally affecting synovial tissues. There is no evidence that physical and emotional effects or stress could be a trigger for the disease. The many negative findings suggest that either the trigger varies, or that it might in fact be a chance event inherent with the immune response.[25]
Half of the risk for RA is believed to be genetic.[8] It is strongly associated with the inherited tissue type major histocompatibility complex (MHC) antigen HLA-DRB1 (most specifically the shared epitope alleles, including *0401 and *0404), and the genes PTPN22 and PADI4—hence family history is an important risk factor.[26][27] Inheriting the PTPN22 gene has been shown to double a person's susceptibility to RA. PADI4 has been identified as a major risk factor in people of Asian descent, but not in those of European descent.[28] First-degree relatives prevalence rate is 2–3% and disease genetic concordance in monozygotic twins is approximately 15–20%.[29][30]
Smoking is the most significant non-genetic risk[8] with RA being up to three times more common in smokers than non-smokers, particularly in men, heavy smokers, and those who are rheumatoid factor positive.[31] Modest alcohol consumption may be protective.[32]
Epidemiological studies have confirmed a potential association between RA and two herpesvirus infections: Epstein-Barr virus (EBV) and Human Herpes Virus 6 (HHV-6).[33] Individuals with RA are more likely to exhibit an abnormal immune response to EBV and have high levels of anti-EBV antibodies.[34]
Vitamin D deficiency is more common in people with rheumatoid arthritis than in the general population.[35][36] However, whether vitamin D deficiency is a cause or a consequence of the disease remains unclear.[37] 1α,25-dihydroxyvitamin D3 (1,25D), an active metabolite of vitamin D, affects bone metabolism indirectly through control of calcium and phosphate homeostasis. Interaction between 1,25D and the vitamin D receptor (VDR) affects the production of RANKL and delays osteoclastogenesis.[38] Some trials have found a decreased risk for RA with vitamin D supplementation while others have not.[36]
http://en.wikipedia.org/wiki/Rheumatoid_arthritis#Causes |
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