Anti-Glutamic Acid Decarboxylase Antibody-Associated Ataxia as an Extrahepatic Autoimmune Manifestation of Hepatitis C Infection: A Case Report
Author(s) -
Amer Awad,
Olaf Stüve,
Marlyn J. Mayo,
Rafeed Alkawadri,
Bachir Estephan
Publication year - 2011
Publication title -
case reports in neurological medicine
Language(s) - English
Resource type - Journals
eISSN - 2090-6668
pISSN - 2090-6676
DOI - 10.1155/2011/975152
Subject(s) - medicine , cerebellar ataxia , ataxia , immunology , rituximab , antibody , autoimmune hepatitis , hepatitis c virus , glutamate decarboxylase , hepatitis , autoantibody , pathology , virus , biology , biochemistry , psychiatry , enzyme
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.
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