Diabetes Care, Vol 16, Issue 8 1179-1183, Copyright © 1993 by American Diabetes Association

ARTICLES

HLA-DQ beta typing and non-Asp57 alleles in IDDM and nondiabetic subjects in New Zealand

LV Forbes, LJ Brown and RS Scott
Lipid and Diabetes Research Group, Christchurch Hospital, New Zealand.

OBJECTIVE--To determine the frequency of IDDM risk-associated HLA-DQ beta alleles in New Zealanders with IDDM and nondiabetic control subjects, and to examine these as susceptibility markers in relation to IDDM incidence. RESEARCH DESIGN AND METHODS--HLA-DQ beta typing was conducted in 55 juvenile-onset IDDM subjects diagnosed between 1990 and 1992, and 53 nondiabetic control subjects. Allele typing was conducted by a polymerase chain reaction-restriction fragment-length polymorphism technique. All subjects were residents of Canterbury, New Zealand. IDDM incidence data were obtained from the Canterbury, New Zealand, Diabetes Registry. RESULTS--The frequency of the susceptibility genotype DQ beta *0201/0302 was 43.6 and 5.7% in the IDDM and control groups, respectively, reflecting the increased prevalence of allele 0302 in the IDDM group. Alleles 0301, 0501, and 0602.3 were more prevalent in the control group than the IDDM group. The frequency of non-Asp57 alleles was 90.9 and 61.3% in the IDDM and control groups, respectively. Overall, the HLA-DQ beta allele distribution was similar to reports from other Caucasian populations. The 0- to 19-yr age-specific IDDM incidence rate over the period in which the diabetic subjects were diagnosed was 19.5/100,000 person-yr, the highest levels observed in Canterbury over the last decade. Our relatively high background prevalence of non-Asp57 alleles and high IDDM incidence rates were similar to results from some Scandinavian and other hotspot populations. CONCLUSIONS--HLA-DQ beta alleles are genetic susceptibility markers in New Zealand, and other Caucasian populations. Peak IDDM incidence levels observed in 1990-1992 in our population are in accordance with a high background population prevalence of non-Asp57 alleles. These results suggest that the high Canterbury incidence rates may be due to a large HLA-DQ beta non-Asp57 at-risk population.
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