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Diffuse Lung Disease |

Case of Potential Treatment Gone Rogue FREE TO VIEW

Pius Ochieng, MD; Frank Genese, MD; Doroota Korta; Donald Fishman, MD
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Mount Sinai Roosevelt Hospital, New York, NY


Chest. 2014;146(4_MeetingAbstracts):401A. doi:10.1378/chest.1993144
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Abstract

SESSION TITLE: ILD Student/Resident Case Report Posters

SESSION TYPE: Medical Student/Resident Case Report

PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM

INTRODUCTION: Anti-tumor necrosis factor (Anti-TNF) medications are accepted therapeutic armamentarium for treating refractory sarcoidosis. 1 We describe a case of anti-TNF associated pulmonary sarcoidosis and review the potential etiopathogenesis of this association.

CASE PRESENTATION: Fifty four year old Caucasian male with psoriasis was referred by his dermatologist for evaluation of positive quantiferon gold test. Notably he was on adalimumab for his psoriasis over the preceding year. He reported a prior negative PPD about a year previously. He had no dyspnea, cough, chest pain or constitutional symptoms. His examination was unremarkable. Comprehensive metabolic panel and Complete blood count were normal. Chest radiography revealed left hilar adenopathy which was new compared to a study done on unrelated visit. CT scan revealed bilateral hilar and mediastinal adenoapthy with nodules in bronchovascular distribution. Bronchoscopic transbronchial biopsy revealed peribronchovascular non-caseating granuloma consistent with sarcoidosis. The samples were negative for Acid fast bacilli and cultures negative for mycobacteria and fungi. It was also negative for malignancy. The adalimumab was stopped and the lymphadenopahty regressed.

DISCUSSION: Anti-TNF associated sarcoidosis has been documented. The chronology of adalimumab therapy, occurrence of adenopathy and resolution of the adenopathy with stopping this therapy support the diagnosis of antiTNF related sarcoidosis. This patient’s course is within the median time of 11 months described by Daı¨en in the French series. 2 The exact mechanism of antiTNF induced granuloma formation is not well defined. Since TNF activity is central in the formation of granuloma, antiTNF would intuitively counteract formation of granuloma and promote its resolution. A possible explanation is that anti-TNF may modulate the cytokines to point of restoring Th1 response which is the primary mechanism for granuloma formation.3 An alternative theory is that soluble TNF receptors may allow sufficient TNF activity with these medications to support granuloma formation. Thirdly, anti-TNF may promote reactivation or infection of yet unidentified infectious pathogen responsible for causing sarcoidosis. Treatment is stopping the inciting anti-TNF agent.

CONCLUSIONS: Clinicians should be aware of anti-TNF associate sarcoidosis.

Reference #1: Pritchard C, Nadarajah K: Tumor necrosis factor alpha inhibitor treatment for sarcoidosis refractory to conventional treatments: a report of five patients. Ann Rheum Dis 2004; 63: 318-20.

Reference #2: Daien CI et al. Sarcoid-like granulomatosis in patients treated with tumor necrosis factor blockers: 10 cases. Rheumatology. 2009;48:883-6.

Reference #3: Maurice MM et al. Treatment with monoclonal anti-tumor necrosis factor alpha antibody results in an accumulation of Th1 CD4þ T cells in the peripheral blood of patients with rheumatoid arthritis. Arthritis Rheum 1999;42:2166-73.

DISCLOSURE: The following authors have nothing to disclose: Pius Ochieng, Frank Genese, Doroota Korta, Donald Fishman

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