scholarly journals Associations between insulin-dependent diabetes mellitus and HLA-DQA1 alleles

1995 ◽  
Vol 41 (4) ◽  
pp. 3-5
Author(s):  
I. I. Mersiyanova ◽  
Yu. A. Knyazev ◽  
M. V. Burdenko ◽  
T. V. Sebko ◽  
О. V. Yevgrafov

The incidence of HLA-DQA1 alleles was assessed in patients with insulin-dependent diabetes mellitus (IDDM), their relatives, and healthy controls using HLA-DQA1 genotyping by digestion of PCR amplified DNA with allele-specific restriction enzymes. A significant increase in the incidence of HLA-DQA1*0301 allele was observed in diabetics although the ratio of DQA1*0301 homozygotes to heterozygotes was similar in the patients and controls. The presence of one DQA 1*0301 allele in the genome appeared to be sufficient for susceptibility to IDDM. Comparison of the incidence of other DQA1 "Arg52" alleles in diabetics and healthy controls revealed no differences between the groups. The incidence of DQA1 "non-Arg52" alleles (specifically DQA1*0201) was reduced in diabetics as compared to normal controls. The presence of these alleles may be considered as the "protective" factor.

1999 ◽  
Vol 84 (10) ◽  
pp. 3721-3725 ◽  
Author(s):  
Koji Nakanishi ◽  
Tetsuro Kobayashi ◽  
Toshio Murase ◽  
Taeko Naruse ◽  
Yoshisuke Nose ◽  
...  

Abstract The aim of this study is to identify insulin-dependent diabetes mellitus (IDDM)-susceptible HLA antigens in IDDM patients who do not have established risk allele, HLA-DQA1*0301, and analyze relationship of these HLA antigens and the degree of β-cell destruction. In 139 Japanese IDDM patients and 158 normal controls, HLA-A, -C, -B, -DR and -DQ antigens were typed. Serum C-peptide immunoreactivity response (ΔCPR) to a 100-g oral glucose load ≤ 0.033 nmol/l was regarded as complete β-cell destruction. All 14 patients without HLA-DQA1*0301 had HLA-A24, whereas only 35 of 58 (60.3%) normal controls without HLA-DQA1*0301 and only 72 of 125 (57.6%) IDDM patients with HLA-DQA1*0301 had this antigen (Pc = 0.0256 and Pc = 0.0080, respectively). ΔCPR in IDDM patients with both HLA-DQA1*0301 and HLA-A24 (0.097 ± 0.163 nmol/L, mean ± sd, n = 65) were lower than in IDDM patients with HLA-DQA1*0301 only (0.219 ± 0.237 nmol/L, n = 45, P < 0.0001) and in IDDM patients with HLA-A24 only (0.187 ± 0.198 nmol/L, n = 14, P = 0.0395). These results indicate that both HLA-DQA1*0301 and HLA-A24 contribute susceptibility to IDDM independently and accelerate β-cell destruction in an additive manner.


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