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Fatal fulminant hepatitis caused by infection with subgenotype A1 hepatitis B virus with C1766T/T1768A core promoter mutations

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Abstract

Adults initially infected with the hepatitis B virus develop various types of hepatitis ranging from asymptomatic to fulminant, and the clinical course of infection is influenced by a variety of host and viral factors. The viral risk factors associated with fulminant hepatitis reportedly include subgenotype B1, negative HBe antigen, and mutations in the precore and core promoter regions. Here, we present a case of fatal fulminant hepatitis caused by infection with subgenotype A1 hepatitis B virus with C1766T/T1768A double mutations in the core promoter region. A 53-year-old man was hospitalized with acute hepatitis B. Immediately after admission, entecavir was administered. However, his condition deteriorated, developing into fulminant hepatitis 2 days later. Artificial extracorporeal liver support therapy with plasma exchange (PE) and hemodiafiltration (HDF) were started. At one time point, the severity of hepatic encephalopathy decreased from grade II to grade 0, and the prothrombin time also improved, increasing from 11 to 73 %. However, the total bilirubin levels remained at or above 20 mg/dL and blood creatinine levels gradually increased. HDF was restarted, and therapies such as bilirubin adsorption and PE were administered. However, neither hepatic nor renal failure was alleviated, and the patient died 78 days after admission.

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Correspondence to Takashi Hoshino.

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All experimental procedures were in accordance with the ethical standards of the responsible committee on human experimentation and the 2008 revision of the Helsinki Declaration of 1975.

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Informed consent for inclusion in this report was obtained from the patient.

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Hoshino, T., Takagi, H., Suzuki, Y. et al. Fatal fulminant hepatitis caused by infection with subgenotype A1 hepatitis B virus with C1766T/T1768A core promoter mutations. Clin J Gastroenterol 9, 160–167 (2016). https://doi.org/10.1007/s12328-016-0649-4

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  • DOI: https://doi.org/10.1007/s12328-016-0649-4

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