Background: Tumor necrosis factor-Î± (TNF-Î±) may have an important role in the clinical exacerbation of sarcoidosis.
Objective: To treat sarcoidosis with infliximab, a chimeric humanâ€“murine antiâ€“human TNF-Î± 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-Î± 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.