M. Fukui et al., DIAGNOSTIC-SIGNIFICANCE OF ANTIBODIES TO GLUTAMIC-ACID DECARBOXYLASE IN JAPANESE DIABETIC-PATIENTS WITH SECONDARY ORAL HYPOGLYCEMIC AGENTS FAILURE, Clinical immunology and immunopathology, 85(2), 1997, pp. 182-186
Some non-insulin-dependent diabetes mellitus (NIDDM) patients are posi
tive for antibodies to glutamic acid decarboxylase (anti-GAD), and the
y tend to develop insulin deficiency. The aim of this study was to eva
luate the prevalence of anti-GAD in NIDDM with secondary failure of su
lfonylurea agents (NIDDM-SF) and to investigate the diagnostic signifi
cance of seropositivity for anti-GAD in NIDDM-SF patients by evaluatin
g human leukocyte antigen (HLA)-DRB1 alleles concurrently, The prevale
nce of anti-GAD in NIDDM-SF, NIDDM, and new-onset (within 1 year after
onset) insulin-dependent diabetes mellitus (IDDM) was 9.3% (39/420),
3.1% (12/392), and 65.0% (13/20), respectively, Pancreatic beta cell f
unction deteriorated in NIDDM-SF patients positive for anti-GAD. HLA-D
RB1 allele typing revealed that NIDDM-SF patients positive for anti-GA
D were significantly associated with DRB1()0901 (RR = 2.81, P < 0.01)
, which is one of the susceptible alleles to IDDM. Shorter interval be
fore development of secondary failure and insulin deficiency were sign
ificantly associated with the presence of DRB1()0901 (P < 0.05) in NI
DDM-SF patients positive for anti-GAD, In conclusion, nearly 10% of NI
DDM-SF patients are positive for anti-GAD, suggesting that an autoimmu
ne mechanism might play an important role in the pathogenesis of NIDDM
-SF patients, In addition, a combination of serological marker (anti-G
AD) and genetic marker (HLA-DRB1) is useful for predicting clinical co
urse of NIDDM patients with secondary failure of sulfonylurea agents.
(C) 1997 Academic Press.