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Background: Tumor necrosis factor-alpha (TNF-alpha) may have an important role in the clinical exacerbation of sarcoidosis.Objective: To treat sarcoidosis with infliximab, a chimeric human-murine anti-human TNF-alpha monoclonal antibody.Design: Case report.Setting: U.S. academic medical center.Patient: A 72-year-old woman with sarcoidosis presenting with severe protein-losing enteropathy, hypoalbuminemia, and proximal myopathy who had not responded adequately to corticosteroid therapy and whose clinical course was further complicated by acute tubular necrosis and renal failure requiring long-term hemodialysis.Intervention: Intravenous infusion of infliximab, 5 mg/kg of ideal body weight; infusion was repeated at 2 and 6 weeks.Measurements: Clinical response of enteropathic and myopathic symptoms and serum albumin level.Results: Enteropathic and myopathic symptoms resolved after infliximab therapy, and the serum albumin level also improved. However, the clinical course was complicated by the development of a hypercoagulable state associated with circulating anticardiolipin antibodies, which prompted discontinuation of infliximab therapy.Conclusions: Infliximab therapy was successful in a patient with sarcoidosis. Tumor necrosis factor-alpha may be an important mediator of clinical disease in sarcoidosis and could be an attractive target for therapeutic intervention. However, infliximab may cause adverse effects associated with cytokine cascade manipulation. [ABSTRACT FROM AUTHOR]

Discusses the likelihood of persons with bacterial pneumococcal pneumonia (PP) to be homozygous for the Fc(gamma)R(Pi)a-R131 allotype than those with non-bacteremic PP through a study of a sample of hospital patients. Evidence that the severity of pneumoccocal infection may in part be genetically mediated; Evidence that such genetic factors may be generalizable to encapsulated bacteria-caused infections.