Abstract Details

Title Anti Glutamic Acid Decarboxylase Antibody Syndromes Occur At An Earlier Age In African Americans.

Topic Autoimmune Neurology

Presentation(s) P2 - Poster Session 2 (5:30 PM-6:30 PM)

Poster/Presentation
Number 15-034

Objective The relevance of ethnicity and gender in anti Gllutamic Acid Decarboxylase antibodies (anti-GAD) associated encephalitis, stiff person syndrome and cerebellar ataxia is not well explored. In a cohort of patients at our center, we analyzed variations in age of incidence and initial anti-GAD positivity for significant differences between Caucasians (Cau) and African Americans (AA).

Background Anti-GAD associated autoimmune conditions are increasingly diagnosed in outpatient clinics. Stiff-person syndrome, cerebellar ataxia, limbic encephalitis and epilepsy, Miller Fisher syndrome are manifestations of GAD autoantibody syndrome.

Design/Methods Twenty-Eight anti-GAD positive patients were included in this retrospective study, 5 stiff person syndrome (SPS), 4 cerebellar ataxia (CA) and 19 autoimmune encephalitis (AE). Sixteen AA and 12 Cau patients were included in our study and their ages at symptom onset and at which anti-GAD antibodies were found positive were reviewed. Patients with type-1 diabetes mellitus and those with other neurological conditions (stroke, traumatic brain injury and infections) were excluded. Odds ratio was calculated to analyze the gender variation and Independent t-test was applied to analyze the variations between the ethnicities. P-value < 0.05 was considered to be significant.

Results

Titers were found positive at a younger age in AA patients compared to Cau patients, a trend close to significance (p-value= 0.06). The age of symptoms onset was also lower in AA when compared to Cau, however, this was less statistically significant due to greater variance. The average anti-GAD titer range 10 - 1442 nmol/lit in AA vs 11.7 - 999 nmol/lit in Cau group.

Conclusions Our results suggest that the AA population has a younger or more aggressive onset of these autoimmune phenomenon but the small number of patients and the variability in recall of clinical events keep the trend from reaching statistical significance. AA show more aggressive forms of other autoimmune disease, and additional patients may establish this trend.

Authors/Disclosures
Shitiz K. Sriwastava, MBBS (UT Health Houston) PRESENTER	Dr. Sriwastava has nothing to disclose.
Meghana S. Kinariwala, MD (Providence Neuroscience Instituite)	Dr. Srinivas has nothing to disclose.
Kalyan Yarraguntla, MD (University Health Center)	Dr. Yarraguntla has nothing to disclose.
Abbas Jowkar, MD (Henry Ford Health System)	No disclosure on file
Edwin B. George, MD, PhD, FAAN (Food and Drug Administration)	No disclosure on file

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