Sarcoidosis and chronic hepatitis C: a case report

Abstract

Several case reports deal with the relationship between hepatitis C virus (HCV) infection and pulmonary or hepatic sarcoidosis. Most publications describe interferon α-induced sarcoidosis. However, HCV infection per se is also suggested to cause sarcoidosis. The present case report describes a case of biopsy-verified lung and liver sarcoidosis and HCV infection, and the outcome of antiviral therapy. In March 2009, a 25-year-old man presented with moderately elevated liver enzymes without any clinical symptoms. The patient was positive for HCV antibodies and HCV RNA of genotype 1b. Four months later the patient became dyspnoic and pulmonary sarcoidosis was diagnosed by lung biopsy and radiography. A short course of corticosteroid treatment relieved symptoms. Three months later, liver biopsy showed noncaseating granulomas consisting of epithelioid histiocytes and giant cells with a small amount of peripheral lymphocyte infiltration, without any signs of fibrosis. Chronic HCV infection with coexistence of pulmonary and hepatic sarcoidosis was diagnosed. Antiviral therapy with peginterferon α and ribavirin at standard doses was started, which lasted 48 wk, and sustained viral response was achieved. A second liver biopsy showed disappearance of granulomas and chest radiography revealed normalization of mediastinal and perihilar glands. The hypothesis that HCV infection per se may have triggered systemic sarcoidosis was proposed. Successful treatment of HCV infection led to continuous remission of pulmonary and hepatic sarcoidosis. Further studies are required to understand the relationship between systemic sarcoidosis and HCV infection.

Keywords: Hepatitis C virus infection; Peginterferon α; Pulmonary and hepatic sarcoidosis; Ribavirin; Sustained viral response.

Figure 1

Thoracic computer tomographic scans of mediastinal, hilar lymph nodes and pulmonary nodules. Enlarged lymph nodes (A, white arrows) and small pulmonary nodules in the right upper lobe before prednisolone treatment (B, black arrow; July 2009) are revealed.

Figure 2

Biopsy taken from a pulmonary lymph node. Two tight naked round well-formed granulomas are surrounded by a small amount of lymphocytic infiltration. The granulomas consist of epithelioid cells; there are no necrosis, giant cells, Shaumann or asteroid bodies. Stained with hematoxylin and eosin, magnification × 200 (A) and × 400 (B).

Figure 3

Liver biopsy revealing a noncaseating granuloma consisting of epithelioid histiocytes and giant cells with a small amount of peripheral lymphocyte infiltration. Stained with hematoxylin and eosin, magnification ×200 (A) and × 400 (B).

Figure 4

Thoracic computer tomographic scans of mediastinal, hilar lymph nodes and pulmonary nodules. A significant decrease in size of mediastinal and hilar lymph nodes (A, white arrows) is shown before initiation of antiviral treatment but pulmonary nodules remain at the same levels (B, black arrow; October 2009). At the end of treatment no progression of lymph nodes is revealed (C, white arrows) and pulmonary nodules are absorbed (D, black arrow; December 2010).

Figure 5

Liver biopsy revealing the absence of granuloma formation with vesicles of steatosis. Stained with van Geason, magnification × 200.