Current rheumatology reports
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Hypocomplementemic urticarial vasculitis syndrome (HUVS) is an uncommon immune complex-mediated entity characterized by urticaria with persistent acquired hypocomplementemia. First described in 1973, HUVS is associated with several systemic findings including leukocytoclastic vasculitis, severe angioedema, laryngeal edema, pulmonary involvement, arthritis, arthralgia, glomerulonephritis, and uveitis. These manifestations should be present for at least 6 months. ⋯ The disease marker is the serum presence of anti-C1q antibodies. Treatment, based on disease severity, involves corticosteroids and other immunosuppressive agents that have demonstrated some success. Patients may have significant morbidity and mortality, most commonly caused by chronic obstructive pulmonary disease and acute laryngeal edema.
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Patients with systemic lupus erythematosus (SLE) have a significantly increased risk of atherosclerotic coronary events. Traditional risk factors, such as hypertension and hypercholesterolemia, only partly account for the increased risk of coronary disease in SLE. Other important risk factors include disease and treatment-related factors. ⋯ Among these, scintigraphic myocardial perfusion defects have been shown to be predictive of subsequent coronary events, independent of traditional Framingham risk factors. Although the aggressive treatment of reversible risk factors, such as lipids and blood pressure, is advocated by many, no published studies have yet demonstrated a clear reduction in risk of coronary events with this approach. Elucidation of risk factors and preventive strategies for accelerated atherosclerosis in SLE is the subject of ongoing research.
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Calcifying tendonitis of the shoulder is a common, acute or chronic, painful disorder characterized by calcifications in the rotator cuff tendons. A natural cycle exists during which the tendon repairs itself. ⋯ Surgery is recommended when conservative treatment fails. This article discusses advances in imaging and medical, physical, and surgical management, as well as current evidence for the treatment of calcifying tendonitis of the shoulder.
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As life expectancy increases every decade, the incidence and prevalence of osteoarthritis (OA) also will increase. Despite progress in our knowledge of the pathophysiology of OA, the management of OA-mediated pain continues to challenge physicians. Concern regarding the cardiovascular effects of cyclooxygenase-2 inhibitors and the gastrointestinal and renal side effects of nonsteroidal anti-inflammatory drugs (NSAIDs) in general has limited the use of these medications in the management of chronic non-cancer pain. ⋯ When used as part of a multimodal approach to pain control, opioids are a safe and effective treatment for joint pain, including that of OA. Patients for whom NSAIDs are contraindicated, or for whom combined acetaminophen, tramadol, and NSAID therapy is ineffective, may be started on low-dose opioids and titrated as needed and tolerated. Patient education and informed consent, exercise, complementary medicine, and the use of a controlled substance agreement increases the likelihood of patient compliance with treatment guidelines, improving functional capacity and quality of life.
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Various peripheral and spinal mechanisms have been hypothesized to contribute to pain amplification and chronicity. However, the role of the brain in chronic pain states remains to be fully elucidated. Functional brain imaging techniques, such as positron emission tomography and functional magnetic resonance imaging, have frequently been used to investigate brain activity during acute/experimental pain perception, which has helped to establish the notion of the human pain network. ⋯ It has been suggested that prolonged nociceptive input to the brain might induce functional and morphologic maladaptive processes that in turn further exacerbate the experience of chronic pain. Alternatively, morphologic changes might predispose toward vulnerability to develop a chronic pain state. The purpose of this review is to examine current literature regarding altered brain morphology in patients with various chronic pain states, summarize these findings, and evaluate their implications for our understanding of the pathophysiology of chronic pain.