M. Fukui et al., ANTIBODIES TO GLUTAMIC-ACID DECARBOXYLASE IN JAPANESE DIABETIC-PATIENTS WITH SECONDARY FAILURE OF ORAL HYPOGLYCEMIC THERAPY, Diabetic medicine, 14(2), 1997, pp. 148-152
Some patients with non-insulin-dependent (Type 2) diabetes mellitus (N
IDDM) are positive for antibodies to glutamic acid decarboxylase (anti
-GAD), which have been shown to be a useful marker for the diagnosis a
nd prediction of insulin-dependent (Type 1) diabetes mellitus (IDDM).
Anti-GAD positive NIDDM patients tend to develop insulin deficiency. W
e investigated the prevalence of anti-GAD in 200 NIDDM with secondary
failure of oral hypoglycaemic therapy (SF) and 200 NIDDM well controll
ed by diet and/or sulphonylurea agents (NSF). Twenty-two of 200 (11%,
p < 0.05) SF patients and 6 of 200 (3%) NSF patients were anti-GAD pos
itive. The positive rate for anti-GAD was as high as 23.8% in the non-
obese and insulin deficient SF patients. The SF patients with anti-GAD
tended to be non-obese and to have an impaired release of endogenous
insulin. The interval before development of secondary failure was not
associated with the presence of anti-GAD in this study. In conclusion
we found that anti-GAD was positive in as many as 11% of the SF patien
ts, suggesting that autoimmune mechanisms may play an important role i
n the pathogenesis of secondary failure of sulphonylurea therapy.