Acute pancreatitis in a female patient with HEV (GT 3) infection and a compound CLDN2 – PRSS1 genotype

Introduction:

The frequency of hepatitis E virus (HEV) cases increases. HEV infection can cause various extrahepatic manifestations including neurological and hematological disorders. Here we report a case of a patient with acute viral hepatitis E genotype 3 (GT3) presenting with acute pancreatitis (AP).

Case report:

A 70-year-old female was referred to our unit with nausea, vomiting, severe abdominal pain, and fever. Her lab tests revealed increased serum lipase activities (602 IU/l) with leukocytosis (14 G/l) and elevated CRP (70 mg/l). The CT scan showed signs of AP with pancreatic head necrosis. In the MRCP there was no cholestasis, and bile duct stones were excluded. Elastography showed increased liver stiffness (10,3 kPa). In addition to increased pancreatic enzymes, she presented with increased liver function tests (ALT 1553 IU/l, AST 507 IU/l, bilirubin 11,7 mg/dl). The patient denied alcohol abuse, and serum ethylglucuronide was normal. HAV, HBV, HCV, HDV, CMV and EBV infections as well as AIH, PBC, PSC, Wilson disease and hemochromatosis were excluded. Of note, HEV IgM antibodies and HEV-PCR were positive (150,000 IU/ml, GT3). We genotyped pancreatitis-predisposing variants (CASR, CLDN2, CTRC, PRSS1, SPINK1) and detected two variants in CLDN2 (rs12688220 homozygoous) and PRSS1 (rs10273639, heterozygous). Taken our findings together, we conclude that the HEV infection was the cause for AP. Under supportive therapy with fluids, analgetics and antibiotics, the patient recovered. She was discharged with slightly increased liver function tests but negative HEV-PCR.

Discussion:

To the best of our knowledge this is one of the first reported cases of HEV GT3-associated AP. Since 1999, approximately 50 cases of HEV-associated AP have been reported, most of them had HEV GT1 infection (Bazerbachi et al. Gastroenterol Rep 2016). We recommend inclusion of HEV testing in patients with acute pancreatitis of unknown origin. Studies analyzing the role of genetic predisposition in the risk of developing HEV-AP and other extrahepatic HEV manifestations are warranted.