miércoles, 2 de febrero de 2011

Hepatitis E Virus and Neurologic Disorders | CDC EID

EID Journal Home > Volume 17, Number 2–February 2011

Volume 17, Number 2–February 2011
Synopsis
Hepatitis E Virus and Neurologic Disorders
Nassim Kamar, Richard P. Bendall, Jean Marie Peron, Pascal Cintas, Laurent Prudhomme, Jean Michel Mansuy, Lionel Rostaing, Frances Keane, Samreen Ijaz, Jacques Izopet, and Harry R. Dalton


Author affiliations: Centre Hospitalier Universitaire Rangueil, Toulouse, France (N. Kamar, P. Cintas, L. Rostaing); Université Paul Sabatier, Toulouse (N. Kamar, J.M. Peron, L. Rostaing, J. Izopet); Royal Cornwall Hospital Trust, Truro, UK (R.P. Bendall, F. Keane, H.R. Dalton); Centre Hospitalier Universitaire Purpan, Toulouse (J.M. Peron, J.M. Mansuy, J. Izopet); Centre Hospitalier de Castres, Castres, France (L. Prudhomme); Health Protection Agency, London, UK (S. Ijaz); and Peninsula College of Medicine and Dentistry, Truro (H.R. Dalton)

Suggested citation for this article

Abstract


Information about the spectrum of disease caused by hepatitis E virus (HEV) genotype 3 is emerging. During 2004–2009, at 2 hospitals in the United Kingdom and France, among 126 patients with locally acquired acute and chronic HEV genotype 3 infection, neurologic complications developed in 7 (5.5%): inflammatory polyradiculopathy (n = 3), Guillain-Barré syndrome (n = 1), bilateral brachial neuritis (n = 1), encephalitis (n = 1), and ataxia/proximal myopathy (n = 1). Three cases occurred in nonimmunocompromised patients with acute HEV infection, and 4 were in immunocompromised patients with chronic HEV infection. HEV RNA was detected in cerebrospinal fluid of all 4 patients with chronic HEV infection but not in that of 2 patients with acute HEV infection. Neurologic outcomes were complete resolution (n = 3), improvement with residual neurologic deficit (n = 3), and no improvement (n = 1). Neurologic disorders are an emerging extrahepatic manifestation of HEV infection.
Hepatitis E virus (HEV) infection is a well-known cause of acute hepatitis in developing countries (1). However, autochthonous (locally acquired) HEV infection is also emerging in industrialized countries (1), where it is caused by HEV genotype 3 and thought to be a zoonosis transmitted by pigs (2). Within the past few years, HEV has been responsible for chronic hepatitis, which can rapidly evolve to cirrhosis, in immunocompromised patients (3–8). However, little data regarding HEV-related extrahepatic manifestations have been published, although an association between neurologic manifestations (e.g., Guillain-Barré syndrome, neuralgic amyotrophy, acute transverse myelitis) and acute HEV infection has been suggested (9–13).

Previously, the association between neurologic signs and symptoms and HEV infection has been based on detection of anti-HEV immunoglobulin (Ig) M in serum. However, Rianthavorn et al. reported a case of HEV genotype 3–induced neuralgic amyotrophy in which HEV RNA was detected in the serum of patients with neurologic signs and symptoms (14), and we recently detected HEV RNA in the cerebrospinal fluid (CSF) of a kidney-transplant recipient with chronic HEV infection and neurologic signs and symptoms (15). We describe 7 cases of HEV-associated neurologic disorders in patients from the Royal Cornwall Hospital, Truro, Cornwall, UK, and Toulouse University Hospital, Toulouse, southwestern France.

In Cornwall, among 55 patients with locally acquired hepatitis E, neurologic signs and symptoms developed among 3 (5.5%). From January 2004 through April 2009, in the organ-transplant unit of Toulouse University Hospital, among 50 solid-organ–transplant patients with HEV, neurologic signs and symptoms developed among 3 (6%). In addition, from January 2005 through December 2009, in the Department of Hepatology of Toulouse University Hospital, among 21 patients with acute HEV infection, neurologic signs and symptoms developed in 1 (4.76%). We describe these 7 cases of HEV-induced neurologic disorders, which occurred in 3 nonimmunocompromised patients with acute HEV infection, in 2 kidney transplant recipients and 1 kidney–pancreas transplant recipient with chronic HEV infection, and in 1 HIV-positive patient with chronic HEV infection (Tables 1, 2).

full-text:
Hepatitis E Virus and Neurologic Disorders | CDC EID



Suggested Citation for this Article
Kamar N, Bendall RP, Peron JM, Cintas P, Prudhomme L, Mansuy JM, et al. Hepatitis E virus and neurologic disorders. Emerg Infect Dis [serial on the Internet]. 2011 Feb [date cited].
http://www.cdc.gov/EID/content/17/2/173.htm
DOI: 10.3201/eid1702.100856


Comments to the Authors
Please use the form below to submit correspondence to the authors or contact them at the following address:

Nassim Kamar, Department of Nephrology, Dialysis and Organ Transplantation, CHU Rangueil, TSA 50032, 31059 Toulouse CEDEX 9, France;
email: kamar.n@chu-toulouse.fr

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