Fulminant hepatitis B reactivation leading to liver transplantation in a patient with chronic hepatitis C treated with simeprevir and sofosbuvir: a case report

Abstract

Introduction: Hepatitis B and C coinfection is commonly seen in clinical practice. In coinfected individuals, high levels of hepatitis C viremia are often associated with low levels of serum hepatitis B DNA. Hepatitis B reactivation in hepatitis C-infected patients treated with pegylated interferon and ribavirin has been reported, but severe or fulminant reactivation is uncommon. Hepatitis C treatment-associated hepatitis B reactivation in patients with chronic hepatitis C and isolated core antibody has not been reported previously.

Case presentation: A 59-year-old white woman with chronic hepatitis C genotype 1B and isolated hepatitis B core antibody initiated treatment with simeprevir, sofosbuvir, and ribavirin for treatment of chronic hepatitis C. She responded very well to treatment initially with near normalization of aminotransferases and hepatitis C viral load suppressed to below the level of quantification after 4 weeks of treatment. At week 11 of a planned 12-week course, she developed fulminant hepatic failure due to hepatitis B reactivation and ultimately required liver transplantation. Fortunately, her posttransplant clinical course was unremarkable.

Conclusions: This is the first report of hepatitis B reactivation in a patient with isolated hepatitis B core antibody leading to fulminant hepatic failure and liver transplantation after initiation of treatment with sofosbuvir, simeprevir, and ribavirin for hepatitis C. This case raises the concern for the risk of severe hepatitis B reactivation in hepatitis B and C-coinfected patients or chronic hepatitis C-infected patients with isolated hepatitis B core antibody treated with direct-acting antiviral drugs for hepatitis C.

Fig. 1

a Low-power magnification of a biopsy specimen from 8 months prior to presentation shows chronic hepatitis with mild steatosis, and mild portal and lobular inflammation. b High-power magnification of specimen in (a) demonstrates the component of steatohepatitis, composed of areas of steatosis, ballooned hepatocytes, and lobular inflammation. c and d Diagnostic core needle biopsy performed one week before liver transplantation shows hepatocytes with positive immunohistochemical nuclear staining for hepatitis B virus core antigen (c) and positive immunohistochemical cytoplasmic staining for hepatitis B virus surface antigen (d). Arrows in (c) and (d) indicate examples of positive immunohistochemical staining. Immunohistochemistry for hepatitis B virus surface antigen was negative on a liver biopsy specimen obtained 8 months prior to presentation (not shown). e Core needle biopsy performed 1 week before liver transplantation shows severe hepatitis with bridging and confluent necrosis, marked inflammation, and ductular reaction. f High-magnification view of liver explant specimen shows confluent necrosis and bridging necrosis with bile ductular reaction and cholestasis