Extra‐hepatic manifestations of autochthonous hepatitis E infection

Abstract

Summary Background Autochthonous (locally acquired) hepatitis E is increasingly recognised in developed countries, and is thought to be a porcine zoonosis. A range of extra‐hepatic manifestations of hepatitis E infection have been described, but have never been systematically studied. Aim To report the extra‐hepatic manifestations of hepatitis E virus. Methods Retrospective review of data of 106 cases of autochthonous hepatitis E (acute n = 105, chronic n = 1). Results Eight (7.5%) cases presented with neurological syndromes, which included brachial neuritis, Guillain‐Barré syndrome, peripheral neuropathy, neuromyopathy and vestibular neuritis. Patients with neurological syndromes were younger (median age 40 years, range 34–92 years, P = 0.048) and had a more modest transaminitis (median ALT 471 IU/L, P = 0.015) compared to cases without neurological symptoms [median age 64 years (range 18–88 years), median ALT 1135 IU/L]. One patient presented with a cardiac arrhythmia,twelve patients (11.3%) presented with thrombocytopenia, fourteen (13.2%) with lymphocytosis and eight (7.5%) with a lymphopenia, none of which had any clinical consequence. Serum electrophoresis was performed in 65 patients at presentation, of whom 17 (26%) had a monoclonal gammopathy of uncertain significance. Two cases developed haematological malignancies, acute myeloid leukaemia and duodenal plasmacytoma, 18 and 36 months after presenting with acute hepatitis E infection. Conclusions A range of extra‐hepatic manifestations can occur with hepatitis E. Neurological and haematological features of hepatitis E infection are relatively frequent in this UK cohort, and result in significant morbidity which warrants further study.

Characteristics of 20 Patients with Autochthonous Acute Hepatitis E in Hokkaido, Japan: First Report of Bilateral Facial Palsy Following the Infection with Genotype 4 Hepatitis E Virus

“…These complications include neurological disorders (Kamar et al 2011;Cheung et al 2012;Santos et al 2013;van den Berg et al 2014;Woolson et al 2014), myasthenia gravis (Belbezier et al 2014), thrombocytopenia (Fourquet et al 2010), aplastic anemia (Shah et al 2012) glomerulonephritis (Kamar et al 2012) and acute pancreatitis (Deniel et al 2011). Among them, neurological complications are more frequently reported, including Guillain-Barré syndrome, brachial neuritis, transverse myelitis, cranial nerve palsy and peripheral neuropathy (Kamar et al 2011;Cheung et al 2012;van den Berg et al 2014;Woolson et al 2014). However, such neurological complications as extrahepatic manifestations of clinical or subclinical HEV infection have not yet been reported in the literature in Japan, although cases of autochthonous acute or fulminant hepatitis E are increasingly being seen in this country.…”

Distinct Entry Mechanisms for Nonenveloped and Quasi-Enveloped Hepatitis E Viruses

“…There is, however, an increasing concern with the persistence of HEV, particularly gt 3 viruses, in individuals with weakened immune systems, resulting in accelerated progression to cirrhosis (7,8). In addition, extrahepatic manifestations have been reported, raising the possibility that infection involves multiple cell types (9). Because HEV gt 3 infection appears to be more common than expected and sometimes can persist, the possibility of transmission through the blood supply has been recognized recently (10).…”

A Rare Association between Left Lobe Secondary Biliary Cirrhosis and Budd-Chiari Syndrome Secondary to Hepatocellular Carcinoma in the Non-Cirrhotic Right Liver Lobe

“…Although it is a common cause of self-limited acute viral infection, HEV infection is often unrecognized or misdiagnosed with drug-induced liver injury [16]. Hepatitis E virus infection may cause decompensation in patients with underlying chronic liver disease, in whom the prognosis is poor [6,16], and is responsible for up to 10-15% of cases of acute liver failure. A recent study shows that from five HEV infected patients with underlying chronic liver injury, three died of acute-onchronic liver failure [6].…”

“…Hepatitis E virus infection may cause decompensation in patients with underlying chronic liver disease, in whom the prognosis is poor [6,16], and is responsible for up to 10-15% of cases of acute liver failure. A recent study shows that from five HEV infected patients with underlying chronic liver injury, three died of acute-onchronic liver failure [6]. Treatment with ribavirin may be effective for these patients [17].…”

“…[5]. However, there is new evidence to support the opinion that HEV represents a greater problem than previously thought, especially for patients with underlying chronic liver disease [6]. Of the four human HEV-genotypes, in developed regions genotypes 3 and 4 are considered pathogenic, with zoonotic transmission, predominantly after ingestion of infected pork meat [5,7].…”