Table of Contents Author Guidelines Submit a Manuscript
Case Reports in Neurological Medicine
Volume 2011 (2011), Article ID 975152, 4 pages
http://dx.doi.org/10.1155/2011/975152
Case Report

Anti-Glutamic Acid Decarboxylase Antibody-Associated Ataxia as an Extrahepatic Autoimmune Manifestation of Hepatitis C Infection: A Case Report

1Baton Rouge Neurology Associates, Baton Rouge General Medical Center, Baton Rouge, LA, USA
2Department of Neurology, The University of Texas Southwestern Medical Center, Dallas, TX, USA
3Neurology Section, VA North Texas Health Care Systems, Dallas, TX, USA
4Department of Internal Medicine-Digestive and Liver Diseases, The University of Texas Southwestern Medical Center, Dallas, TX, USA
5Neurological Institute, Cleveland Clinic Foundation, Cleveland, OH, USA
6Department of Neurology, University of Kansas Medical Center, Kansas, KS, USA

Received 23 May 2011; Accepted 15 June 2011

Academic Editors: Andrea Eugenio Cavanna, Massimiliano Filosto, and José Luis González-Gutiérrez

Copyright © 2011 Amer Awad et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Extrahepatic immunological manifestations of hepatitis C virus (HCV) are well described. In addition, antiglutamic acid decarboxylase (GAD) antibody-associated cerebellar ataxia is well-established entity. However, there have been no reports in the literature of anti-GAD antibody-associated ataxia as an extrahepatic manifestation of HCV infection. We report the case of a young woman with chronic hepatitis C virus and multiple extrahepatic autoimmune diseases including Sjögren syndrome and pernicious anemia who presented with subacute midline cerebellar syndrome and was found to have positive antiglutamic acid decarboxylase (GAD) antibody in the serum and cerebrospinal fluid. An extensive diagnostic workup to rule out neoplastic growths was negative, suggesting the diagnosis of nonparaneoplastic antiglutamic acid decarboxylase antibody-associated cerebellar ataxia as an additional extrahepatic manifestation of hepatitis C virus infection. The patient failed to respond to high-dose steroids and intravenous immunoglobulin. Treatment with the monoclonal antibody rituximab stabilized the disease. We postulate that anti-GAD associated ataxia could be an extrahepatic manifestation of HCV infection.