Spontaneous reactivation of hepatitis B virus with S gene mutations in an elderly patient with diabetic nephropathy
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CASE REPORT
Spontaneous reactivation of hepatitis B virus with S gene mutations in an elderly patient with diabetic nephropathy Noriyuki Obara1 · Jun Inoue2 · Hiroyuki Endo1 · Eiji Kakazu2 · Masashi Ninomiya2 · Tomoaki Iwata2 · Akitoshi Sano2 · Mio Tsuruoka2 · Atsushi Masamune2 Received: 16 March 2020 / Accepted: 2 June 2020 © Japanese Society of Gastroenterology 2020
Abstract Generally, reactivation of hepatitis B virus (HBV) infection is induced by the administration of immunosuppressants or anticancer agents, but reactivation without such drugs has rarely been reported. Here we report an elder case with spontaneous reactivation of HBV replication accompanied by hepatitis B surface antigen (HBsAg) mutations. A 69-year-old man with a history of diabetes mellitus and chronic kidney disease (CKD) was found to be positive for HBsAg (0.072 IU/ ml) in June 2018. In May 2019, marked hepatic dysfunction and increased HBsAg (2533.2 IU/ml) were observed when he visited the hospital due to diarrhea and worsening of CKD. At that time, hepatitis B surface antibody (HBsAb) was positive (268.9 mIU/ml) and HBV DNA was 6.0 log IU/ml. After treatment with entecavir, HBV DNA and HBsAg rapidly decreased. Full-genome HBV sequence analysis revealed that the patient was infected with HBV of subgenotype B1 and it had an “a” determinant mutation M133L in the S gene coding HBsAg. Notably, both HBsAg and HBsAb were positive at the time of HBV reactivation, suggesting that the HBV with these mutations escaped from neutralization by HBsAb. This case suggests that immune escape mutations could play an important role in spontaneous HBV reactivation. Keywords HBV · M133L · CKD · Immune escape
Introduction Hepatitis B virus (HBV) infection is one of the most common infectious diseases in the world. It is estimated that almost one third of people in the world experience HBV infection and more than 248 million people are persistently infected with HBV [1]. Persistently HBV-infected patients who are positive for hepatitis B surface antigen (HBsAg) can progress to cirrhosis and liver cancer. When patients with persistent HBV infection are treated with immunosuppressants or anti-cancer chemotherapy, reactivation of HBV can lead to severe hepatitis including fulminant hepatitis [2, 3]. Even if people who had been * Jun Inoue jinoue‑[email protected] 1
Department of Gastroenterology, Japan Community Health Care Organization (JCHO) Sendai Hospital, 3‑16‑1 Tsutsumi‑machi, Aoba‑ku, Sendai 981‑8501, Japan
Division of Gastroenterology, Tohoku University Graduate School of Medicine, 1‑1 Seiryo‑machi, Aoba‑ku, Sendai 980‑8574, Japan
2
exposed to HBV become HBsAg-negative, reactivation of HBV can be caused by immunosuppressants or chemotherapy, and sometimes de novo hepatitis has a fatal course [4]. However, not all people experience HBV reactivation when treated with immunosuppressants and there are still many unclear points about the mechanism. As one of the mechanisms of HBV reactivation, HBV mutations in the S gene coding HBsAg are considered t
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