Acute fulminant hepatitis B during hepatitis C virus therapy with direct-acting antivirals in a patient co-infected with HIV.

Co-infection with hepatitis C (HCV) and B (HBV) viruses is common in clinical practice. We report a case of fulminant hepatic failure as a consequence of reactivation of HBV in a patient with human immunodeficiency virus (HIV) after HCV treatment. This was a 53-year-old man diagnosed in 1998 with HIV infection following detection of pulmonary tuberculosis, with a good current response to antiretroviral therapy. In addition, he had chronic HCV genotype 1a infection and a history of previous HBV infection with positive IgG (anti-HBc IgG) core antibody, negative surface antigen (HBsAg) and antibodies (anti-HBs) and undetectable levels of HBV DNA, prior to initiation of treatment with direct-acting antivirals (DAA). For his HIV infection, the patient had previously followed several treatment regimens with multiple failures and development of resistance. In 2011, he was prescribed treatment with tenofovir (TDF), abacavir and ritonavir-boosted atazanavir. The TDF was subsequently withdrawn after a slight worsening of his renal function, and the treatment was simplified to darunavir/cobicistat monotherapy. Since then, his viral load has been undetectable and his CD4 T-cell lymphocytes 500–800/mm3 (CD4 T lymphocytes 800/mm3 at most recent testing, prior to starting HCV treatment). In October 2013, the patient started treatment for HCV according to the regimen pegylated interferon alpha-2a 180 g, one weekly injection, and ribavirin 1000 mg daily (3-0-2), resulting in a 3log decrease in HCV viral load by week 4 of treatment. The idea of adding first-generation direct-acting antivirals (telaprevir) was proposed, but the patient refused to continue treatment because of poor tolerance to interferon. In December 2015, his HCV viral load was 2,181,330.11 IU/ml with a liver stiffness measurement of 12 kPa. Since we already had DAA, he was started on treatment with sofosbuvir and ledipasvir for 12 weeks.1 In week 2, his viral load had dropped to 284.51 IU/ml, by week 4 it was down to 30.45 IU/ml and by week 8 it was less than 15 IU/ml, with a sustained viral response at week 4 post-treatment. A month later, the patient consulted with abdominal pain, nausea and jaundice, with total bilirubin 10.98 mg/dl, direct bilirubin 8.75 mg/dl, GOT 1025.40 IU/l, GPT 642 IU/l and INR 1.30. An HBV