Rheumatic diseases clinics of North America
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Corticosteroids are the drug of choice for the treatment of sarcoidosis. Because the natural course of sarcoidosis may be self-limiting and/or cause no long-term harm, treatment is not mandatory. ⋯ Efforts should be made to minimize the corticosteroid dose while keeping the risk of toxicity as low as possible. This article outlines the indications for corticosteroid therapy for sarcoidosis, discusses various dosing regimens, and suggests when alternative corticosteroid agents should be considered.
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Rheum. Dis. Clin. North Am. · Feb 2016
ReviewGlucocorticoids for Management of Polymyalgia Rheumatica and Giant Cell Arteritis.
Diagnosis of polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) is based on typical clinical, histologic, and laboratory features. Ultrasonographic imaging in PMR with assessment especially of subdeltoid bursitis can aid in diagnosis and in following response to treatment. ⋯ Methotrexate may be used in patients at high risk for glucocorticoid adverse effects and patients with frequent relapse or needing protracted therapy. Other therapeutic approaches including interleukin 6 antagonists are under evaluation.
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Rheum. Dis. Clin. North Am. · Feb 2016
ReviewCorticosteroids for Pain of Spinal Origin: Epidural and Intraarticular Administration.
Targeted interventional delivery of corticosteroids remains a mainstay of treatment for spinal pain syndromes because this approach has a wider therapeutic index than other approaches. The best evidence for analgesic efficacy is in subacute radicular syndromes associated with new-onset or recurrent lumbar radiculitis. ⋯ Considerable uncertainty persists concerning which patients with chronic pain are most likely to benefit from corticosteroid injections. Matching this treatment option with specific spinal pain syndromes remains a major challenge.
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Psoriasis is a common, chronic inflammatory skin disease most often appearing in the form of well-demarcated, scaly plaques. These lesions highlight the fundamental processes underlying its pathogenesis, namely, inflammation and epidermal hyperproliferation. ⋯ This concept is supported by results of genetic studies, pointing toward the signaling pathways of nuclear factor-κB, interferon-γ, and interleukin (IL)-23 as well as antigen presentation as central axes of the psoriatic inflammation. Efficacy of biologics targeting tumor necrosis factor-α, IL-23, or IL-17 provides further evidence in favor of this model.