Tumor necrosis factor sarcoidosis

Yee AM, Pochapin MB. Treatment of complicated sarcoidosis with infliximab anti-tumor necrosis factor-alpha therapy. Ann Intern Med 2001 135(1) 27-31. 

Massara A, Cavazzini L, La Corte R, Trotta F. Sarcoidosis appearing during anti-tumor necrosis factor alpha therapy a new class effect paradoxical phenomenon. Two case reports and literature review. Semin Arthritis Rheum 2010 39 (4) 313-9. 

Clementine RR, Lyman J, Zakem J, Mallepalli J, Lindsey S, Quinet R. Tumor necrosis factor-alpha antagonist-induced sarcoidosis. J Clin Rheumatol 2010 16 (6) 274-9. 

Cuchacovich R, Hagan J, Khan T, Richer A, Espinoza LR. Tumor necrosis factor-alpha (TNF-a) -blockade-induced hepatic sarcoidosis in psoriatic arthritis (PsA) case report and review of the literature. Clin Rheumatol 2011 30(1) 133-7. 

Grutters JC, Sato H, Pantelidis P, et al. Increased frequency of the uncommon tumor necrosis factor -857T allele in British and Dutch patients with sarcoidosis. Am J Respir Crit Care Med 2002 165(8) 1119-1124. 

Sweiss NJ, Welsch MJ, Curran JJ, et al. Tumor necrosis factor inhibition as a novel treatment for refractory sarcoidosis. Arthritis Rheum 2005 53 788-791. 

Baughman RP. Tumor necrosis factor inhibition in treating sarcoidosis the American experience. Rev Port Pneumol 2007 13(suppl 2) S47-S50. 

Ulbricht KU, StoU M, Bierwirth J, et al. Successful tumor necrosis factor alpha blockade treatment in therapy-resistant sarcoidosis. Arthritis Rheum 2003 48 3542-3543. 

Baugbman RP, Strobofer SA, Buebsbaum J, et al. Release of tumor necrosis factor by alveolar macrophages of patients with sarcoidosis. J Lab Clin Med 1990 115 36-42. 

Fehrenbach H, Zissel G, Goldmann T, et al. Alveolar macrophages are the main source for tumor necrosis factor-alpha in patients with sarcoidosis. Eur Respir J 2003 21(3) 421 28. 

Seitzer U, Swider C, Stuber F, et al. Tumor necrosis factor alpha promoter gene polymorphism in sarcoidosis. Cytokine 1997 9(10) 787-790. 

Mrazek F, HoUa LI, Hutyrova B, et al. Association of tumor necrosis factor-alpha, lymphotoxin-alpha and HLA-DRBl gene polymorphisms with Lofgren s syndrome in Czech patients with sarcoidosis. Tissue Antigens 2005 65(2) 163-171. Somoskovi A, Zissel G, Seitzer U, et al. Polymorphisms at position -308 in the promoter region of the TNF-a and in the first intron of the TNF-P genes and spontaneous and lipopolysaccharide-induced TNF-a release in sarcoidosis. Cytokine 1999 11(11) 882 87. 

Dai H, Guzman J, Costabel U. Increased expression of apoptosis signaling receptors by alveolar macrophages in sarcoidosis. Eur Respir J 1999 13(6) 1451 1454. Kieszko R, Krawczyk P, Chocholska S, et al. Tumor necrosis factor receptors (TNFRs) on T lymphocytes and soluble TNFRs in different cUnical courses of sarcoidosis. Respir Med 2006 101(3) 645-654. 

Dai H, Guzman J, Chen B, et al. Production of soluble tumor necrosis factor receptors and tumor necrosis factor-alpha by alveolar macrophages in sarcoidosis and extrinsic allergic alveolitis. Chest 2005 127(1) 251-256. 

Hino T, Nakamura H, Shibata Y, et al. Elevated levels of type II soluble tumor necrosis factor receptors in the bronchoalveolar lavage fluids of patients with sarcoidosis. Lung 1997 175(3) 187-193. 

COPE with Cytokines. 2006. Available at http //www.copewithcytokines.de/. Kunitake R, Kuwano K, Miyazaki H, et al. Apoptosis in the course of granulomatous inflammation in pulmonary sarcoidosis. Eur Respir J 1999 13(6) 1329-1337. Agostini C, Zambello R, Sancetta R, et al. Expression of tumor necrosis factor-receptor superfamily members by lung T lymphocytes in interstitial lung diseases. Am J Respir Crit Care Med 1996 153 1359-1367. 

Tumor necrosis factor-a (TNF-a) inhibitors (particularly infliximab) have been used, with anecdotal success, to treat refractory sarcoidosis (particularly lupus pernio) (166,189-192). Data in pulmonary sarcoidosis are limited (193—195). In a recent multicenter trial, 138 patients with chronic pulmonary sarcoidosis were randomized to placebo or infliximab (3 mg/kg) or infliximab (5 mg/kg) (194). At 24 weeks, the primary endpoint AFVC% predicted was shghtly higher among infliximab-treated patients (2.5% above baseline) compared to placebo-treated patients (no change). This difference, although statistically significant, is of doubtful chnical significance. 

Tumor necrosis factor alpha (TNF-a) is a cytokine that is secreted by macrophages associated with sarcoid granulomas (46). Antagonists of TNF-a including thalidomide (47), and infliximab (48) have been shown to be useful for the treatment of cutaneous sarcoidosis. Infliximab appears to be particularly useful for the treatment of lupus pernio (48). The use of infliximab is limited by its high cost and the need for intravenous administration. Fatal cases of tuberculosis have been associated with infliximab administration (49). Therefore, a tuberculin skin test is required prior to its use, and patients on the drug must be monitored closely for the development of tuberculosis. 

Steffen M, Petersen J, Oldigs M, et al. Increased secretion of tumor necrosis factor-alpha, interleukin-1-beta, and interleukin-6 by alveolar macrophages from patients with sarcoidosis. J Allergy Clin Immunol 1993 91 939-949. 

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