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August 29, 2017; 89 (9) Article

Clinical phenotype and outcome of hepatitis E virus–associated neuralgic amyotrophy

Jeroen J.J. van Eijk, Harry R. Dalton, Paolo Ripellino, Richard G. Madden, Catherine Jones, Miriam Fritz, Claudio Gobbi, Giorgia Melli, Emanuela Pasi, Jenny Herrod, Rebecca F. Lissmann, Hamad H. Ashraf, Mohamed Abdelrahim, Omar A.B.A.L. Masri, Montserrat Fraga, David Benninger, Thierry Kuntzer, Vincent Aubert, Roland Sahli, Darius Moradpour, Hélène Blasco-Perrin, Shahram Attarian, Rene Gérolami, Philippe Colson, Maria T. Giordani, Johannes Hartl, Sven Pischke, Nan X. Lin, Brendan N. Mclean, Richard P. Bendall, Marcus Panning, Jean-Marie Peron, Nassim Kamar, Jacques Izopet, Bart C. Jacobs, Nens van Alfen, Baziel G.M. van Engelen
First published August 2, 2017, DOI: https://doi.org/10.1212/WNL.0000000000004297
Jeroen J.J. van Eijk
From the Jeroen Bosch Hospital (J.J.J.v.E.), 's-Hertogenbosch, the Netherlands; Royal Cornwall Hospital (H.R.D., R.G.M., C.J., J. Herrod, R.F.L., H.H.A., M.A., O.A.B.A.L.M., B.N.M., R.P.B.); European Centre for the Environment and Human Health (H.R.D., R.P.B.), University of Exeter, Truro, UK; Neurocenter of Southern Switzerland (P.R., C.G., G.M.), Lugano; Department of Neurology and Neuroscience (M.F.) and Institute for Virology (M.P.), Medical Center—University of Freiburg and Faculty of Medicine, University of Freiburg, Germany; Microbiology Department (E.P.), EOLAB (SMIC), Bellinzona, Switzerland; University Hospital Lausanne (CHUV) (M.F., D.B., T.K., V.A., R.S., D.M.), Switzerland; Université Paul Sabatier (H.B.-P., J.-M.P., N.K., J.I.), Toulouse, France; Centre Hospitalo-Universitaire Timone (S.A., R.G., P.C.); IHU—Méditerranée Infection (P.C.), Aix-Marseille Université, AP-HM, France; San Bortolo Hospital (M.T.G.), Vicenza, Italy; University Medical Center Hamburg-Eppendorf (J. Hartl, S.P.), Germany; Northumbria University (N.X.L.), Newcastle upon Tyne, UK; CHU Rangueil (N.K.); CHU Purpan (H.B.-P., J.-M.P., N.K., J.I.), Toulouse, France; Erasmus MC (B.C.J.), University Medical Centre Rotterdam; and Department of Neurology (N.v.A., B.G.M.v.E.), Donders Center for Medical Neuroscience, Radboudumc Nijmegen, the Netherlands.
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Harry R. Dalton
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Paolo Ripellino
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Richard G. Madden
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Catherine Jones
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Miriam Fritz
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Claudio Gobbi
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Giorgia Melli
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Emanuela Pasi
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Jenny Herrod
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Rebecca F. Lissmann
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Hamad H. Ashraf
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Mohamed Abdelrahim
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Omar A.B.A.L. Masri
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Montserrat Fraga
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David Benninger
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Thierry Kuntzer
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Vincent Aubert
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Roland Sahli
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Darius Moradpour
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Hélène Blasco-Perrin
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Shahram Attarian
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Rene Gérolami
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Philippe Colson
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Maria T. Giordani
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Johannes Hartl
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Sven Pischke
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Nan X. Lin
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Brendan N. Mclean
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Richard P. Bendall
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Marcus Panning
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Jean-Marie Peron
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Nassim Kamar
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Jacques Izopet
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Bart C. Jacobs
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Nens van Alfen
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Baziel G.M. van Engelen
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Citation
Clinical phenotype and outcome of hepatitis E virus–associated neuralgic amyotrophy
Jeroen J.J. van Eijk, Harry R. Dalton, Paolo Ripellino, Richard G. Madden, Catherine Jones, Miriam Fritz, Claudio Gobbi, Giorgia Melli, Emanuela Pasi, Jenny Herrod, Rebecca F. Lissmann, Hamad H. Ashraf, Mohamed Abdelrahim, Omar A.B.A.L. Masri, Montserrat Fraga, David Benninger, Thierry Kuntzer, Vincent Aubert, Roland Sahli, Darius Moradpour, Hélène Blasco-Perrin, Shahram Attarian, Rene Gérolami, Philippe Colson, Maria T. Giordani, Johannes Hartl, Sven Pischke, Nan X. Lin, Brendan N. Mclean, Richard P. Bendall, Marcus Panning, Jean-Marie Peron, Nassim Kamar, Jacques Izopet, Bart C. Jacobs, Nens van Alfen, Baziel G.M. van Engelen
Neurology Aug 2017, 89 (9) 909-917; DOI: 10.1212/WNL.0000000000004297

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Abstract

Objective: To determine the clinical phenotype and outcome in hepatitis E virus–associated neuralgic amyotrophy (HEV-NA).

Methods: Cases of NA were identified in 11 centers from 7 European countries, with retrospective analysis of demographics, clinical/laboratory findings, and treatment and outcome. Cases of HEV-NA were compared with NA cases without evidence of HEV infection.

Results: Fifty-seven cases of HEV-NA and 61 NA cases without HEV were studied. Fifty-six of 57 HEV-NA cases were anti-HEV IgM positive; 53/57 were IgG positive. In 38 cases, HEV RNA was recovered from the serum and in 1 from the CSF (all genotype 3). Fifty-one of 57 HEV-NA cases were anicteric; median alanine aminotransferase 259 IU/L (range 12–2,961 IU/L); in 6 cases, liver function tests were normal. HEV-NA cases were more likely to have bilateral involvement (80.0% vs 8.6%, p < 0.001), damage outside the brachial plexus (58.5% vs 10.5%, p < 0.01), including phrenic nerve and lumbosacral plexus injury (25.0% vs 3.5%, p = 0.01, and 26.4% vs 7.0%, p = 0.001), reduced reflexes (p = 0.03), sensory symptoms (p = 0.04) with more extensive damage to the brachial plexus. There was no difference in outcome between the 2 groups at 12 months.

Conclusions: Patients with HEV-NA are usually anicteric and have a distinct clinical phenotype, with predominately bilateral asymmetrical involvement of, and more extensive damage to, the brachial plexus. Involvement outside the brachial plexus is more common in HEV-NA. The relationship between HEV and NA is likely to be causal, but is easily overlooked. Patients presenting with NA should be tested for HEV, irrespective of liver function test results. Prospective treatment/outcome studies of HEV-NA are warranted.

GLOSSARY

ALT=
alanine aminotransferase;
gt3=
genotype 3;
HEV=
hepatitis E virus;
LFT=
liver function test;
MRC=
Medical Research Council;
NA=
neuralgic amyotrophy

Footnotes

  • ↵* These authors contributed equally to this work.

  • Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.

  • Supplemental data at Neurology.org

  • Received February 24, 2017.
  • Accepted in final form June 6, 2017.
  • © 2017 American Academy of Neurology
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