Acute hepatitis E virus infection after liver transplant is a challenging clinical phenomenon. Due to its unspecific clinical and histological presentation, the diagnosis of acute or chronic hepatitis E virus infection can be difficult in unclear cases of elevated liver enzymes. Here, we report the case of a 56-year-old male patient who presented to our center for 17-year follow-up after liver transplant with α1-antitrypsin deficiency. The patient was asymptomatic but had remarkably increased transaminases and cholestasis parameters. Blood levels for immunosuppressives were in the normal range, and cholestasis and deteriorated liver perfusion were excluded by ultrasonographic examination. A liver biopsy was performed that was histologically interpreted as acute cellular rejection grade I. Accordingly, the patient was treated with 5-day high-dose intravenous steroids and increased doses of the maintenance immunosuppressive agents, resulting in the slow normalization of the liver enzymes. Extended laboratory examinations revealed presence of acute hepatitis E virus infection, and a retrospectively immunohistologic staining of the liver biopsy was positive for hepatitis E virus antigen. Acute hepatitis E virus infection can be a reason for acute allograft dysfunction after liver transplant. This differential diagnosis should be kept in mind, especially when graft dysfunction occurs long after transplant.

Non‑alcoholic fatty liver disease (NAFLD) is a widespread health concern, and there is currently insufficient understanding regarding its pathogenesis and treatment. The present study aimed to explore the effects of Artemisia capillaris formula (ACF) on high‑fat diet‑induced hepatic steatosis and fatty acid‑induced intracellular lipid accumulation, by micro (mi)RNA regulation. A total of 72 Sprague‑Dawley rats were divided into six groups (n=12/group). One group was designated as the control group and fed a normal diet, and the remaining five groups were allowed ad libitum access to a high‑fat diet for eight weeks, in order to establish an NAFLD rat model. The rats were subsequently administered polyene phosphatidylcholine (PP; 0.076 g/kg body weight/day), low dose of ACF (0.462 g/kg body weight/day), middle dose of ACF (0.924 g/kg body weight/day) or high dose of ACF (1.848 g/kg body weight/day) intragastrically for four weeks. HepG2 human hepatocellular carcinoma cells were treated with oleic acid and palm acid, followed by treatment with various concentrations of ACF. Serum alanine transaminase (ALT), aspartate aminotransferase (AST), triglycerides (TG), total cholesterol (TC), high‑density lipoprotein cholesterol (HDL‑C), low‑density lipoprotein cholesterol (LDL‑C), and steatotic HepG2 human liver carcinoma cell TC and TG levels were measured. ACF and PP treatments attenuated high‑fat diet‑induced hepatic steatosis and fatty acid‑induced intracellular lipid accumulation. A modified high‑fat diet significantly increased ALT, AST, TG, TC, LDL‑C levels and decreased HDL‑C levels. Treatment with ACF and PP abrogated the increase in liver enzymes and TG, TC and LDL‑C levels, but did not influence HDL‑C levels in a high‑fat diet induced rat model of steotosis. Steatotic HepG2 cells exhibited significantly increased levels of both TG and TC. Treatment with ACF significantly decreased TC and TG levels in vivo, and ACF and PP treatment decreased the expression levels of fatty acid synthase (FASN) and increased miR‑122 in vivo and in vitro. In conclusion, these results suggested that ACF may inhibit hepatic steatosis via miR‑122‑induced downregulation of FASN in vivo and in vitro.