Abstract

Sarcoidosis is an uncommon systemic granulomatous disease of unknown origin affecting lung, skin, liver, and other tissues. Noncaseating granulomas in the involved organs are the hallmark of this disease. An exaggerated immune response to an unknown antigenic stimulus could play a role in sarcoidosis development. Lung is one of the most frequently involved organs.1 Manifestations range from alveolitis to granulomatous infiltration of alveoli, bronchi, and blood vessels. The end stage of lung sarcoidosis is development of interstitial fibrosis with “honeycombing” of lung parenchyma. Interferon alfa in association with ribavirin is the treatment of choice for hepatitis C. Early treatment of acute hepatitis C with interferon alfa-2b will prevent the development of hepatic cirrhosis, but adverse effects are frequent and often can result in discontinuation of treatment.2 Most frequent adverse effects related to interferon are malaise, fever, arthralgia, and cough. Pulmonary events such as bronchial asthma, bronchiolitis obliterans, and interstitial pneumonitis have been reported. Interferon alfa is also used in the treatment of malignant melanoma, multiple myeloma, hairy-cell leukemia and HIV-associated Kaposi's sarcoma.3 Some cases of sarcoidosis after treatment with interferon alfa have been reported in the literature.4, 5, 6 Improvement of sarcoidosis has been reported with discontinuation of treatment, but in other cases an independent course of disease has been proposed, raising the belief that interferon discontinuation is unnecessary in mild-to-moderate cases of interferon-related sarcoidosis.7 We present the case of a patient with hepatitis C treated with interferon in whom pulmonary sarcoidosis developed. The sarcoidosis was initially believed to be a pulmonary neoplasm, but skin lesions developed that indicated the diagnosis of systemic sarcoidosis. The sarcoidosis finally resolved without discontinuation of interferon alfa.

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