• E Toussirot and E Pertuiset.
• Service de rhumatologie, pôle de pathologies aiguës et chroniques, transplantation, éducation (PACTE), hôpital Minjoz, CHU, 25000 Besançon, France. etoussirot@chu-besancon.fr
• Rev Med Interne. 2010 Dec 1;31(12):828-37.

AbstractIncreased production of TNFα by alveolar macrophages and involvement of TNFα in granuloma formation suggest that this cytokine is involved in the pathophysiology of sarcoidosis. The three available TNFα blocking agents have been tested in sarcoidosis refractory to corticosteroids or immunosuppressive drugs. Data are available from isolated case reports or limited series of patients treated in open label trials with favourable issue with anti-TNFα monoclonal antibodies. Two randomized placebo controlled studies evaluated the efficacy of infliximab in pulmonary and extra-pulmonary sarcoidosis, showing that infliximab improves significantly extra-pulmonary disease. There is no significant difference between infliximab and placebo in the treatment of pulmonary manifestations. Etanercept showed no efficacy for treating ocular sarcoidosis in a controlled trial and for pulmonary disease in an open label trial. Paradoxical cases of proven sarcoidosis have been reported in patients receiving anti-TNFα agents for chronic inflammatory rheumatic diseases. A literature review identified 28 cases, including 16 with etanercept, eight with infliximab and four with adalimumab. Although these cases were mainly reported with etanercept, paradoxical sarcoidosis has been reported with the three available anti-TNFα agents, suggesting a class effect. Changes in the cytokine balance may be involved in these cases of induced sarcoidosis, which must be known by the clinician.Copyright © 2010 Société nationale française de médecine interne (SNFMI). Published by Elsevier SAS. All rights reserved.

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