title: Clinical significance of glutamic acid decarboxylase antibodies in patients with epilepsy.
abstract: OBJECTIVE
  Glutamic acid decarboxylase antibodies (GADAs) have been detected in patients with epilepsy, but the clinical determinants of epilepsy associated with GADA have not been defined.
  
  
  METHODS
  We analyzed GADA with a radioimmunoassay in sera of 253 well-characterized patients with epilepsy and 200 control subjects. The positive samples were confirmed by immunohistochemistry and western blotting (WB). Sera were screened for other autoantibodies.
  
  
  RESULTS
  GADA were detected in 15 patients (5.9%) and in three control subjects (1.5%) (p = 0.026). Seven patients (2.8%) had high GADA titers [>or=1,000 relative units (RUs)/ml], six of whom had temporal lobe epilepsy (TLE). All three GADA-positive control subjects had low titers. Two of the five patients with high GADA titers and available cerebrospinal fluid (CSF) samples had intrathecal synthesis (IS) of GADA; one patient had CSF oligoclonal bands. The prevalence of increased levels of GADA tended to be higher in patients with TLE than in patients with extra-TLE [odds ratio (OR) 1.32, 95% confidence interval (CI) 0.39-4.42; p = 0.657]. The patients with high GADA titers had significantly higher number of other autoantibodies compared to the patients with low GADA titers (p = 0.001) and the patients with normal GADA (p < 0.001).
  
  
  CONCLUSIONS
  High GADA titers were present in a subgroup of patients; close to 90% had TLE. The immunologic profile of these patients suggests that the most probable origin of their epilepsy is autoimmune. A positive IS of GADA may be a marker of an ongoing immune response that could identify those patients in whom a trial with immunosuppressive therapy might be warranted.
authors.affiliation: Department of Neurology and Rehabilitation, Tampere University Hospital, Tampere, Finland. suvi.liimatainen@fimnet.fi
authors.forename: Suvi
authors.initials: S
authors.lastname: Liimatainen
authors.forename: Maria
authors.initials: M
authors.lastname: Peltola
authors.forename: Lidia
authors.initials: L
authors.lastname: Sabater
authors.forename: Mahdi
authors.initials: M
authors.lastname: Fallah
authors.forename: Elham
authors.initials: E
authors.lastname: Kharazmi
authors.forename: Anna-Maija
authors.initials: AM
authors.lastname: Haapala
authors.forename: Prasun
authors.initials: P
authors.lastname: Dastidar
authors.forename: Mikael
authors.initials: M
authors.lastname: Knip
authors.forename: Albert
authors.initials: A
authors.lastname: Saiz
authors.forename: Jukka
authors.initials: J
authors.lastname: Peltola
mesh_terms: D000293:Adolescent; D000328:Adult; D017677:Age Distribution; D000368:Aged; D001323:Autoantibodies / Q000097:blood* / Q000134:cerebrospinal fluid / Q000276:immunology; D001327:Autoimmune Diseases / Q000097:blood / Q000175:diagnosis / Q000276:immunology*; D015153:Blotting, Western; D004827:Epilepsy / Q000097:blood / Q000134:cerebrospinal fluid / Q000276:immunology*; D004833:Epilepsy, Temporal Lobe / Q000097:blood / Q000276:immunology; D005260:Female; D005819:Genetic Markers; D005968:Glutamate Decarboxylase / Q000097:blood / Q000276:immunology*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D016884:Polyendocrinopathies, Autoimmune / Q000175:diagnosis / Q000276:immunology; D011863:Radioimmunoassay
chemical_list: D001323:Autoantibodies; D005819:Genetic Markers; D005968:Glutamate Decarboxylase