Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài:Autoantibodies in normals – the value of predicting rheumatoid arthritis. | Arthritis Research Therapy Vol 6 No 6 Dorner and Hansen Viewpoint Autoantibodies in normals - the value of predicting rheumatoid arthritis Thomas Dorner and Arne Hansen Charite University Medicine Berlin Free University and Humboldt University Berlin Berlin Germany Corresponding author Thomas Dorner Published 15 October 2004 Arthritis Res Ther 2004 6 282-284 DOI ar1456 2004 BioMed Central Ltd Introduction The cause of rheumatoid arthritis RA remains elusive however a study demonstrating synovitis in clinically uninflamed joints 1 and several studies reporting the presence of characteristic autoantibodies IgM rheumatoid factor RF and anti-cyclic citrullinated peptide CCP antibodies prior to the appearance of disease manifestations 2 7 have provided evidence of a preclinical asymptomatic phase of the disease. Detection of autoimmune T cells has not yet reached routine diagnostics but with the development of tetramer and ELISPOT technologies it seems likely that autoantibody detection will serve as the method of choice for the identification of autoimmunity and breaches of tolerance Fig. 1 . In patients with early RA the frequency of RF is 50-66 and the prevalence of anti-CCP 41-48 compared to 7-13 and 3-9 respectively in normals 8-10 . Several recent studies have regenerated interest in the value of positive titres of autoantibodies as markers of rheumatic diseases 11-15 . Autoantibody positivity prior to symptom development disease manifestation has also been identified in other autoimmune diseases such as systemic lupus erythematosus insulin-dependent diabetes mellitus IDDM autoimmune polyendocrine syndromes and celiac disease 11-20 . Putative role of protein citrullination in rheumatoid arthritis Celiac disease is a chronic intestinal disease with an immune response to antigens in wheat gluten. Disease occurs after the target antigen gliadin has been modified by the enzyme tissue transglutaminase which allows subsequent .
