作者: William E.R Ollier , Beverley Harrison , Deborah Symmons
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摘要: Inflammatory polyarthritis can be a self-limiting disease, develop into rheumatoid arthritis (RA) or differentiate another form of chronic arthritis. It remains clinical and scientific challenge to understand the relationship between these phenotypes, determine their aetiologies predict course outcome for individual patients. Even patients labelled as having RA show wide spectrum phenotypes. Disease definition is major problem in studying aetiology currently used classification criteria were derived using with established disease. thought result from combination genetic susceptibility exposure an appropriate environmental trigger. The component probably oligogenic. association HLA has been known over 25 years. now associated conserved sequence amino acids number HLA-DRB1 alleles, called shared epitope. However, epitope appears chronicity severity more than susceptibility. Other potential genes include IL-1, aromatase, corticotropin-releasing hormone region on X chromosome. Hormonal reproductive factors also influence severity. common women men, especially before menopause. Men may protected by hormonal require stronger Although infectious triggers have long suspected, no definitive evidence obtained. Previous blood transfusion, smoking obesity are possible risk factors. Chronicity remission important aspects natural history early RA. we identify at adverse prognosis some accuracy, remain unable remission. Functional disability radiological damage most studied outcomes Radiological often occurs RA, but erosion first time several years after symptom onset. Many studies demonstrated features severe This related gene dosage.