Rinsho Shinkeigaku (Clinical Neurology)

Brief Clinical Note

Guillain-Barré syndrome associated with acute hepatitis A
-A case report and literature review-

Akiko Saito, M.D., Ph.D.1), Mineki Saito, M.D., Ph.D.2), Yutaka Shimoe, M.D., Ph.D.1), Takeshi Yoshimoto, M.D.1), Mari Kawakami, M.D., Ph.D.3), Hiroaki Okamoto, M.D., Ph.D.4), Keisuke Yoshikawa, M.D., Ph.D.5), Susumu Kusunoki, M.D., Ph.D.5) and Masaru Kuriyama, M.D., Ph.D.1)

1)Department of Neurology, Brain Attack Center, Ota Memorial Hospital
2)Department of Microbiology, Kawasaki Medical School
3)Department of Internal Medicine, Okayama Saiseikai General Hospital
4)Division of Virology, Department of Infection and Immunity, Jichi Medical University School of Medicine
5)Department of Neurology, KINDAI University School of Medicine

A 44-year-old female developed acute hepatitis A (HA) 5 weeks after ingesting raw oysters. She developed ascending motor weakness, bilateral peripheral facial nerve palsy, and bulbar symptoms. A diagnosis of demyelinating Guillain-Barré syndrome (GBS) was made on the basis of her clinical manifestations and the results of a nerve conduction study. The patient showed improvement following combination treatment with intravascular immunoglobulin and high dose methylprednisolone. No antibodies against specific gangliosides, sulfated glucuronyl paragloboside (SGPG), or sulfatide were detected. HA virus (HAV) RNA was isolated from her serum and its full-length genome sequence was determined. It revealed a homology of 99.9% or more with HAV genotype IA (HAV-IA) of the 2014 outbreak. No mutant virus RNA was detected.
Full Text of this Article in Japanese PDF (340K)

(CLINICA NEUROL, 58: 574|577, 2018)
key words: hepatitis A, demyelinating Guillain-Barré syndrome, facial palsy, bulbar symptoms, HAV genotype IA

(Received: 7-Mar-18)