Sood A, Midha V, Sood N. TUBB3 been reported in Korea [2-8]. Most individuals of acute hepatitis E illness are self-limiting and require no treatment. Moreover, a small number of individuals with acute HEV genotype 1 or 3 illness have been treated with antiviral therapy [9-11]. However, reports within the clinical significance of use of steroid in individuals with cholestatic hepatitis E are very limited. Guillain-Barr syndrome (GBS) is triggered by a preceding illness including acute hepatitis A, B, and C. Occasionally, it has been triggered by HEV illness [12-14]. We reported a case of prolonged cholestasis caused by an autochthonous HEV illness that was resolved with steroid treatment. After 2.5 months, the patients developed weakness of the lower limbs, and were diagnosed with GBS associated with acute hepatitis E. CASE Statement On 20 March 2014, a 58-years-old Korean male was referred to our hospital with severe hepatitis of unfamiliar cause. On 10 March 2014, the patient had presented with anorexia, pruritus, and jaundice. He was a heavy alcohol drinker, having a usage rate of 120 g/day time of alcohol for 30 years. He had not travelled outside South Korea. There was no history of blood transfusions, risky sexual behavior or drug habit. Three months before hospitalization, he ingested uncooked deer meat with the intention of improving his stamina. He had ingested about 200 g of uncooked meat from a crazy deer captured on Jiri-mountain in the Gyeongnam province, South Korea. On physical exam, he had jaundice, right top quadrant tenderness and an enlarged liver, but showed no feature of hepatic encephalopathy. Initial laboratory data showed white blood cell count of 6.36103/mm3 (polymorphonuclear neutrophils, 60.1%; lymphocytes, 24.1%; and eosinophils, 2.2%), serum total bilirubin level of 23.59 mg/dL, serum aspartate aminotransferase (AST) level of 292 IU/L, and serum alanine aminotransferase (ALT) level of 525 IU/L. Tenofovir hydrate Prothrombin time, electrolytes and renal function checks were normal. Serologic study was bad for immunoglobulin (Ig) M anti-hepatitis A disease (HAV) antibody and positive for IgG anti-HAV antibody. Hepatitis B disease surface antigen and antibody to hepatitis C were absent, and HCV RNA was bad. Abdominal computed tomography showed findings compatible with chronic liver disease with splenomegaly. Within the ninth day time of admission, laboratory data showed a maximum total bilirubin level of 35.0 mg/dL and liver biopsy and blood test for IgM and IgG anti-HEV (Dia. Pro, Milan, Italy for IgG anti-HEV ELISA and DSI, Milan, Italy for IgM anti-HEV ELISA) were performed. On liver biopsy (Fig. 1), the lymphocyte-dominant inflammatory cells were accumulated in the periportal area. There was no fatty switch. Swelling and focal apoptosis of hepatocytes were present. Periportal fibrosis with bridge necrosis was observed. Sixteen days after admission, we started 30 mg/day time of prednisolone despite the normal prothrombin time because of a steady increase in total bilirubin levels and pruritus. Within the fourteen day time of admission, commercially available immunoassay for IgM anti-HEV and IgG anti-HEV were both positive. The optical denseness value of IgM anti-HEV was 0.849 (cut-off value 0.294) and IgG anti-HEV was 3.356 (cut-off value: 0.367). Open in a separate window Number 1. Liver biopsy of acute hepatitis E. (A) Inflammatory cells had accumulated in the periportal area. There was no fatty switch. Swelling and focal apoptosis of hepatocytes were present. Periportal fibrosis with bridging was observed (H&E, 100). (B) Lymphocytes were the dominating inflammatory cells in Tenofovir hydrate the portal area (H&E, 400). At the time of the analysis of acute HEV, we Tenofovir hydrate decided to taper steroid therapy, but the total bilirubin level was elevated (17.8 mg/dL to 21.3 mg/dL) after steroid tapering (30 mg/day to 5 mg/day over 10 days) (Fig. 2). Thereafter, prednisolone was given at a dose of 20 mg/day time, and the dose of steroid was tapered and discontinued after 5 weeks. Two months after admission, laboratory data showed a total bilirubin level of 2.30 mg/dl, AST level of 24 IU/L, and ALT level.