Hepatic sarcoidosis complicating treatment-naive viral hepatitis

Abstract

Hepatic sarcoidosis is usually asymptomatic but rarely leads to adverse liver-related outcome. Co-existence of viral hepatitis and hepatic sarcoidosis is a rare, but recognised phenomenon. Obtaining a balance between immune suppression and anti-viral therapy may be problematic. Immunosuppression in the presence of viral hepatitis can lead to rapid deterioration of liver disease. Similarly, anti-viral therapy may exacerbate granulomatous hepatitis. Here we present two cases of viral hepatitis co-existing with sarcoidosis that illustrate successful management strategies. In one, hepatitis B replication was suppressed with oral anti-viral therapy before commencing prednisolone. In the second, remission of hepatic sarcoidosis was achieved with prednisolone, before treating hepatitis C and obtaining a sustained virological response with pegylated interferon and ribavirin therapy.

Keywords: Anti-viral therapy; Chronic hepatitis B infection; Chronic hepatitis C infection; Hepatic sarcoidosis; Immune suppression.

Figure 1

The histological features of hepatic sarcoidosis complicating chronic hepatitis B virus infection. A: Portal tract showing minimal portal inflammation attributable to hepatitis B virus [haematoxylin eosin (HE) staining ×20]; B: Portal fibrosis (reticulin ×40); C: Ground glass hepatocytes (HE ×40); D: Hepatitis B surface antigen immunostain showing accumulation in cytoplasm (×20); E: Granulomatous portal tract inflammation with duct irregularity (HE ×20); F: High power portal granulomatous inflammation (HE ×40).

Figure 2

The changes in alanine transaminase, alkaline phosphatase and angiotensin converting enzyme levels in patient 1. The dotted arrow and the solid arrow mark the commencement of antiviral treatment and steroid treatment respectively. ALT: Alanine transaminase; ALP: Alkaline phosphatase; ACE: Angiotensin converting enzyme.

Figure 3

Histological features of hepatic sarcoidosis complicating chronic hepatitis C virus infection. A: Portal inflammation including lymphoid follicle and interface activity [haematoxylin eosin (HE) staining ×20]; B: Parenchymal inflammation and necroinflammation with acidophil bodies (HE ×20); C: Architectural stain showing parenchymal granulomatous inflammation and fibrosis (Chromotrope-Aniline Blue ×10); D: Parenchymal granulomatous hepatitis (HE ×20).

Figure 4

The changes in alanine transaminase, alkaline phosphatase and angiotensin converting enzyme levels in patient 2. The arrow marks the commencement of steroid treatment. ALT: Alanine transaminase; ALP: Alkaline phosphatase; ACE: Angiotensin converting enzyme.