Forbes L V, Brown L J, Scott R S
Lipid and Diabetes Research Group, Christchurch Hospital, New Zealand.
Diabetes Care. 1993 Aug;16(8):1179-83. doi: 10.2337/diacare.16.8.1179.
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.
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.
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.
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.
确定新西兰胰岛素依赖型糖尿病（IDDM）患者及非糖尿病对照人群中与IDDM风险相关的HLA-DQβ等位基因频率，并将其作为与IDDM发病率相关的易感性标志物进行研究。
对1990年至1992年间诊断的55例青少年发病的IDDM患者和53例非糖尿病对照者进行HLA-DQβ分型。采用聚合酶链反应-限制性片段长度多态性技术进行等位基因分型。所有受试者均为新西兰坎特伯雷地区居民。IDDM发病率数据来自新西兰坎特伯雷糖尿病登记处。
易感性基因型DQβ*0201/0302在IDDM组和对照组中的频率分别为43.6%和5.7%，这反映出IDDM组中等位基因0302的患病率增加。等位基因0301、0501和0602.3在对照组中比在IDDM组中更常见。非天冬氨酸57等位基因在IDDM组和对照组中的频率分别为90.9%和61.3%。总体而言，HLA-DQβ等位基因分布与其他白种人群的报道相似。在糖尿病患者被诊断的时间段内，0至19岁年龄段的IDDM发病率为19.5/100,000人年，是坎特伯雷地区过去十年中观察到的最高水平。我们相对较高的非天冬氨酸57等位基因背景患病率和较高的IDDM发病率与一些斯堪的纳维亚及其他热点人群的结果相似。
HLA-DQβ等位基因是新西兰以及其他白种人群中的遗传易感性标志物。我们人群在1990 - 1992年观察到的IDDM发病率峰值与非天冬氨酸57等位基因较高的背景人群患病率一致。这些结果表明，坎特伯雷地区较高的发病率可能归因于大量携带HLA-DQβ非天冬氨酸57的高危人群。
