P63 Neurological sequelae of acute and chronic HEV genotype 3 infection. (16th November 2010)

• Record Type: Journal Article
• Authors: Dalton, H; Kamar, N; Dalton, H R; Bendall, R; Keane, F; Peron, J M; Cintas, P; Pruhomme, L; Mansuy, J M; Rostaing, L; Ijaz, S; Izopet, J
• Is Part Of: Gut. Volume 59(2010)Supplement 2
• Page Start: A36
• Page End: A36
• Publication Date: 2010-11-16
• Subjects: Gastroenterology -- Periodicals; 616.33
• DOI: 10.1136/gut.2010.223362.89
• Languages: English
• ISSNs: 0017-5749

Abstract

Abstract : Introduction: HEV is an emerging infection in the developed world. It differs from HEV endemic in developing countries as it is caused by HEV genotype 3, is thought to be a porcine zoonosis, has a predilection for middle aged/elderly males, and can cause chronic infection in the immunosuppressed. Neurological symptoms associated with HEV infection have been described in both developed and developing countries. However, to date, no systematic study of the neurological sequelae of HEV has been undertaken. Aim: To describe the clinical and laboratory features of the neurological complications of HEV genotype 3 infection. Method: Retrospective review of 126 patients with locally acquired acute and chronic HEV genotype 3 infection from two University Hospitals: Truro (UK) and Toulouse (France). Results: Neurological complications were seen in 7/126 (5.5%) of patients with HEV. The neurological complications included inflammatory polyradiculopathy (n=3), Guillain-Barré Syndrome (n=1), bilateral brachial neuritis (n=1), encephalitis (n=1), ataxia/proximal myopathy (n=1). Three cases occurred during acute HEV infection in non-immunocompromised patients and four occurred in immunocompromised patients with chronic HEV infection (three transplant patients, and one HIV-positive patient). HEV RNA was detected in the cerebrospinal fluid (CSF) of all four patients with chronic HEV infection and neurological symptoms. In one of these cases unique HEV quasispecies were documented in the CSF. In patients with acute HEV who had neurological symptoms, HEV RNA was absent in the CSF (n=2). Follow-up was up to 4 years and neurological outcomes were: complete resolution (n=3), improvement with residual neurological deficit (n=3), no improvement (n=1). Conclusion: Neurological symptoms are an emerging extra-hepatic manifestation of HEV infection. The pathophysiology is not understood, but HEV may be neurotropic, as unique HEV quasispecies were isolated from the CSF of one of our cases.