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• W2416456476 abstract "Rheumatoid arthritis is a relatively common (0.5±1%) chronic inflammatory systemic disease that primarily affects peripheral joints. Its clinical course is characterized by insidious progression and destruction of the affected joints, resulting in significant morbidity and mortality. Despite considerable efforts to ascertain its cause, the etiology of RA remains an enigma. Extensive investigation of metabolic, endocrine, nutritional, as well as psychosocial, geographic, ethnic and occupational factors suggests that some or all may influence the course of the disease but there is very little evidence that they are involved in its cause. In recent years, research in this area has concentrated on the interplay between genetic susceptibility and environmental exposure [1]. Family and twin studies indicate that RA probably involves many genes as attested to by only 15±30% concordance for RA in monozygotic twins and its incomplete penetrance. RAassociated HLA molecules that stem from the HLA-DR4 locus have been considered to be genetic markers for disease evolution. In patients with RA, certain HLA-DR4 subtypes, i.e., Dw4, Dw10, Dw13, Dw14 and Dw15, predominate. In HLA-DR4negative RA patients other HLA-DR molecules ± DR1, DR6 and DR10 ± share structural homology with the above-mentioned subtypes [2]. The shared epitope (HLA-DRB1) theory generated considerable promise that individuals at risk would be identified relatively easily. However, population-based studies have not shown an association between HLA-DR and RA [3]. The HLA genes probably modify disease expression, as HLADRB1-negative patients tend to have a milder, less aggressive form of the disease [4]. While the HLA system has been the focus of most of the genetic studies, the polygenic nature of RA mandates that candidate genes other than HLA-DR alleles be considered and that these, independently or in combination with HLA-DR alleles, may significantly influence disease initiation and expression [5,6]. While some progress has been made in the genetic characterization of patients at risk for developing progressive destructive RA, the search for putative environmental mechanisms that initiate tissue injury in RA has been unsuccessful. An attractive avenue of study has been the pursuit of an infectious etiology for RA [7]. Bacterial and viral infectious agents have been shown to produce polyarthritis, often resembling RA, in animals and humans. Extensive investigation into the possible role of viruses (HTLV-1, parvovirus B19, herpesviruses, papillomavirus, adenovirus) has largely revealed data that support an attenuated immune response, systemically and in the synovium, to these viruses rather than a causative role in RA. For example, parvovirus has been isolated from the joints of a small percentage of patients with inflammatory arthritis. However, the disease is often mild and rarely destructive [8]. By and large, microorganisms have not been cultured from the synovium, and a direct relationship between a putative infectious agent and chronic arthritis has eluded investigators. The identification in the synovium of breakdown products derived from the cell walls of dead bacteria as well as bacterial antigens that can induce synovitis are indirect lines of evidence that lend credence to the postulate that RA may have an infectious etiology. Alteration of the intestinal flora in patients with RA, examples of therapeutic response to antimicrobial agents, the detection of cellular and humoral immune responses to some bacteria, and the localization of bacterial DNA or RNA in the joints of RA patients have received and continue to receive unabated attention." @default.
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• W2416456476 title "Rheumatoid arthritis: the future is not yet now." @default.
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