Waguri N, Ichida T, Fujimaki R, Ishikawa T, Nomoto M, Asakura H, Nakamaru T, Saitoh A, Arakawa M, Saitoh K, Takahashi K
Department of Internal Medicine III, Niigata University School of Medicine, Niigata City, Japan.
J Gastroenterol Hepatol. 1998 Nov;13(11):1133-7. doi: 10.1111/j.1440-1746.1998.tb00589.x.
A 43-year-old man underwent living related-donor renal transplantation because of chronic renal failure in 1991. During the transplant period, both donor and recipient were seronegative for hepatitis B surface antigen (HBsAg). The donor was seropositive for antibody to hepatitis B surface antigen (anti-HBs) due to hepatitis B virus (HBV) vaccination. After transplantation, FK506 and methylprednisolone had been administered to the patient as immunosuppressants. In 1993, HBsAg appeared in his serum. His alanine aminotransferase level elevated gradually during 1995 and then in 1996, general fatigue, ascites and jaundice developed. At this time his serum was positive for hepatitis B e antibody, contained more than 100000 Meq/mL HBV-DNA and 100% precore mutant. Despite subsequent intensive therapy, liver dysfunction progressed and this patient died of hepatic failure 2 months following admission. At autopsy, the liver exhibited cholestasis, fibrosis extending from the portal tracts, mild inflammation and hepatocytes with a ground-glass appearance. In addition, HBsAg and hepatitis B core antigens had accumulated in the hepatocytes. Consequently, the final diagnosis was fibrosing cholestatic hepatitis (FCH) due to precore mutant HBV infection contracted after renal transplantation. It is unclear when and where the recipient liver became HBV infected. Nevertheless, after renal transplantation, while receiving immunosuppressive drugs, HBV appeared to have the potential to cause hepatic failure and FCH may have been a fatal complication for the recipient.
一名43岁男性因慢性肾衰竭于1991年接受了亲属活体供肾肾移植。在移植期间，供者和受者的乙型肝炎表面抗原（HBsAg）均为血清学阴性。供者因接种乙肝病毒（HBV）疫苗而乙型肝炎表面抗原抗体（抗-HBs）呈血清学阳性。移植后，患者接受了FK506和甲泼尼龙作为免疫抑制剂治疗。1993年，其血清中出现HBsAg。1995年其丙氨酸转氨酶水平逐渐升高，随后在1996年出现全身乏力、腹水和黄疸。此时其血清乙肝e抗体呈阳性，HBV-DNA含量超过100000 Meq/mL，且100%为前C区突变。尽管随后进行了强化治疗，但肝功能障碍仍进展，该患者入院2个月后死于肝衰竭。尸检时，肝脏表现为胆汁淤积、从门管区延伸的纤维化、轻度炎症以及呈毛玻璃样外观的肝细胞。此外，HBsAg和乙肝核心抗原在肝细胞中积聚。因此，最终诊断为肾移植后因感染前C区突变的HBV所致的纤维性胆汁淤积性肝炎（FCH）。尚不清楚受者肝脏何时何地感染HBV。然而，肾移植后，在接受免疫抑制药物治疗时，HBV似乎有导致肝衰竭的可能，FCH可能是受者的致命并发症。
