The Medical clinics of North America
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Med. Clin. North Am. · Jan 1997
ReviewPathogenesis and treatment of the antiphospholipid antibody syndrome.
Antiphospholipid antibody syndrome (APS) is one of the most important causes of thrombophilia, presenting most often as venous or arterial thrombosis, recurrent pregnancy loss, or thrombocytopenia. Both the lupus anticoagulant and anticardiolipin antibody are associated with APS. The mechanism of the prothrombotic state is not understood, but may involve beta-2 glycoprotein 1 (a naturally occurring anticoagulant), platelet aggregation, the protein C pathway, or endothelial cell function. The current treatment recommendation, after a venous or arterial thrombosis, is high-intensity, long-term warfarin therapy.
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Cognitive-behavioral approaches appear to offer a viable alternative for the management of arthritis pain. Controlled studies have documented the efficacy of CBT protocols for managing pain in individuals having OA and RA. ⋯ A number of clinical and research issues need attention if CBT is to be incorporated into rheumatology practice settings. These issues include identifying the most important components of CBT, developing strategies for matching CBT interventions to patients' readiness for behavior change, testing the efficacy of different therapy formats (e.g., individual versus group), broadening the scope of CBT to address issues other than pain, and insurance reimbursement.
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Chronicity and destructive potential are characteristic features of the inflammatory response in the synovial membrane typical for RA. The dominant paradigm has proposed that an exogenous antigen, likely an infectious organism, targets the synovia and elicits a chronic immune response. Support for this disease model has come from describing the cellular components of the inflammatory lesions, which are composed of macrophages, T cells, and B cells. ⋯ A sequence polymorphism in the HLA-DR B1 gene appears to be a strong genetic risk factor in several ethnic groups. Correlation of clinical presentation of RA and the inheritance of the RA risk gene suggests that the gene product is not necessary in disease initiation but functions by modulating disease pattern and severity. The next decade in RA research will be dedicated toward unraveling how genetic determinants can introduce pathology (e.g., how HLA genes can function as progre