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Treatment of Complicated Sarcoidosis with Infliximab Anti–Tumor Necrosis Factor-α Therapy

Arthur M.F. Yee, MD, PhD; and Mark B. Pochapin, MD
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From Hospital for Special Surgery and New York Presbyterian Hospital, Weill Medical College of Cornell University, New York, New York.

Acknowledgments: The authors thank Drs. Flavia A. Golden, Stephen A. Paget, and Lionel B. Ivashkiv for critical reading of the manuscript.

Requests for Single Reprints: Arthur M.F. Yee, MD, PhD, Hospital for Special Surgery, 535 East 70th Street, New York, NY 10021.

Current Author Addresses: Dr. Yee: Division of Rheumatic Diseases, Hospital for Special Surgery, Weill Medical College of Cornell University, 535 East 70th Street, New York, NY 10021.

Dr. Pochapin: Division of Digestive Diseases, New York Presbyterian Hospital, Weill Medical College of Cornell University, 525 East 68th Street, New York, NY 10021.

Author Contributions: Conception and design: A.M.F. Yee.

Analysis and interpretation of the data: A.M.F. Yee, M.B. Pochapin.

Drafting of the article: A.M.F. Yee.

Critical revision of the article for important intellectual content: A.M.F. Yee, M.B. Pochapin.

Final approval of the article: A.M.F. Yee, M.B. Pochapin.

Provision of study materials or patients: A.M.F. Yee, M.B. Pochapin.

Administrative, technical, or logistic support: A.M.F. Yee.

Collection and assembly of data: A.M.F. Yee, M.B. Pochapin.

Ann Intern Med. 2001;135(1):27-31. doi:10.7326/0003-4819-135-1-200107030-00010
Text Size: A A A

Background: Tumor necrosis factor-α (TNF-α) may have an important role in the clinical exacerbation of sarcoidosis.

Objective: To treat sarcoidosis with infliximab, a chimeric human–murine anti–human TNF-α 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-α 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.


Grahic Jump Location
Changes in serum albumin level.

Asterisks denote intravenous methylprednisolone pulses (1.0 g/d for 3 days). White arrows denote intravenous administration of infliximab (5 mg/kg of ideal body weight). The black arrow denotes initiation of oral thalidomide, 100 mg/d.

Grahic Jump Location




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Summary for Patients

A New Anti-Inflammatory Therapy (Infliximab) for Complicated Sarcoidosis

The summary below is from the full report titled “Treatment of Complicated Sarcoidosis with Infliximab Anti–Tumor Necrosis Factor-α Therapy.” It is in the 3 July 2001 issue of Annals of Internal Medicine (volume 135, pages 27-31). The authors are AMF Yee and MB Pochapin.


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