Hepatitis B virus associated with severe acute respiratory syndrome coronavirus 2 infection: a case report.

Background: After secondary respiratory failure, liver failure is often reported in the literature on coronavirus disease 2019 infection. Angiotensin-converting enzyme 2 receptors in hepatocytes make the liver directly susceptible to the severe acute respiratory syndrome coronavirus 2 virus. An exacerbated immune response, drug-induced hepatotoxicity, and hypoxia secondary to respiratory failure are further possible causes of hepatocytolysis in coronavirus disease 2019 patients. Pre-existing infection with the hepatitis B virus can aggravate coronavirus disease 2019 or be aggravated/reactivated by it. This case report describes unusually severe liver damage in a coronavirus disease 2019 patient with well controlled hepatitis B, where the evidence points to coronavirus disease 2019-related factors as the main causes of hepatic cytolysis.

Case presentation: A 70 year-old patient of Romanian ethnicity with a 5-year history of chronic hepatitis B presented to the emergency department complaining of fever, chills, and marked physical asthenia with an onset of 2 weeks. Blood tests revealed an inflammatory syndrome and incipient liver cytolysis. Low-intensity opacities were visible on chest X-ray, and the severe acute respiratory syndrome coronavirus 2 polymerase chain reaction test was positive, so the patient was transferred to the infectious diseases hospital. His condition then aggravated atypically, with increasingly severe hepatic cytolysis that was not noted in other coronavirus disease 2019 patients with hepatitis B.

Conclusion: The patient's history of well-controlled hepatitis B suggests that, in this case, liver dysfunction was secondary to coronavirus disease 2019 manifestations such as the cytokine storm, respiratory failure, and drug-induced hepatotoxicity. The patient eventually recovered, and there was no demonstrable reactivation of hepatitis B after discharge. Coronavirus disease 2019 can thus affect liver function severely and primarily, yet without necessarily interacting with adequately managed hepatitis B.