1996 Volume 39 Issue 12 Pages 893-899
Autoantibodies to glutamic acid decarboxylase (GAD), previously reported to be the 64, 000-Mr (64K) islet cell protein, were measured by a radioimmunoassay using purified pig brain GAD in 53 patients with slowly progressive insulin-dependent diabetes mellitus (SPIDDM). When the level in a sample was higher than 5u/m/ in this method, the serum was considered to be positive. The rate of positive GAD-Ab in SPIDDM patients was 66%(35/53). Patients with SPIDDM were divided into two groups, GAD-Ab positive and negative. We compared the HLA phenotype in these two groups, HLA B44, DR13, DQ1 were significantly more common in GAD-Ab-negative-subjects than in GAD-Ab-positive-patients. The production of GAD-Ab in patients with SPIDDM may be related to their HLA phenotype.
HLA-A24 is reported to be associated with complete abolishment of β-cell function in acute onset IDDM. We estimated the β-cell function in patients with SPIDDM with the capacity of releasing insulin by loading glucagon. When the level of insulin after loading glucagon was below 0.1 ng/ml, the β-cell was thought to be complete destroyed. Therefore we compared the HLA phenotype in the two groups to determine whether theβ-cells completely destroyed or not, complete destruction of the β-cell in SPIDDM was not associated with HLA-A24 in this study.
GAD-Ab is a useful means of screening for patients with SPIDDM.
