Current rheumatology reports
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Obesity and osteoarthritis are two commonly encountered clinical problems that can lead to significant physical and emotional disability. This report examines the association between obesity and osteoarthritis, and discusses potential mechanisms by which obesity influences osteoarthritis. Special attention is devoted to reviewing the molecular and genetic mechanisms that underlie the development of clinical obesity. Improved understanding of obesity will hopefully lead to improved treatment and subsequent amelioration of this important risk factor for osteoarthritis.
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This article reviews current understanding of the relationship between antiphospholipid antibodies and the endothelium. In vitro antiphospholipid antibodies produce endothelial cell activation. Clinical data in this area are scanty and worthy of future research, which could lead to new therapies in the management of antiphospholipid syndrome.
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The antiphospholipid antibody syndrome is an autoimmune condition in which venous or arterial thrombosis and recurrent pregnancy losses occur in patients having serologic evidence of antibodies against anionic phospholipid-protein complexes. The pathophysiologic mechanisms of this syndrome have not yet been established. ⋯ We propose that thrombosis and pregnancy loss in the antiphospholipid syndrome may be caused by disruption of this Annexin-V shield by antiphospholipid (and cofactor) antibodies, thereby increasing the net quantity of thrombogenic phospholipids exposed to the circulating blood. The data accumulated from tissue immunohistochemistry, trophoblast and endothelial cell culture studies, coagulation studies using noncellular phospholipids, and competition studies on artificial phospholipid bilayer are consistent with the hypothesis that interference with the binding of Annexin-V to anionic phospholipid surfaces is an important mechanism of thrombosis and pregnancy loss in the antiphospholipid syndrome.
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This paper examines the use of neuroimaging to measure change in regional cerebral blood flow (rCBF) produced by pain in patients with fibromyalgia and in healthy individuals. Fibromyalgia patients differ from healthy persons in rCBF distribution in several brain structures involved in pain processing and pain modulation both at rest and during experimental pain induction. These abnormalities may contribute to abnormal pain sensitivity as well as the maladaptive pain behaviors that characterize many patients with fibromyalgia. We anticipate that future neuroimaging studies will enhance our understanding of abnormal pain sensitivity and of pain management interventions aimed at altering central nervous system function in patients with fibromyalgia.