HLA class 1 associations in Henoch Schonlein purpura: increased and decreased frequencies
HLA class 1 associations in Henoch Schonlein purpura: increased and decreased frequencies
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DOI：
10.1007/s10067-007-0640-z
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发表时间：
2008-01-01
影响因子：
3.4
通讯作者：
Hasanoglu, Enver
中科院分区：
文献类型：
--
作者：
Peru, Harun;Soylemezoglu, Oguz;Hasanoglu, Enver
过敏性紫癜(HSP)是儿童最常见的血管炎。HSP的易感性和与HSP相关的临床异质性可能是由包括主要组织相容性复合体在内的多个遗传位点决定的。我们的目的是研究人类白细胞抗原(HLA1)类等位基因在HSP易感性中的意义，并确定HSP与肾脏、胃肠道(GI)和关节表现的可能关联。110名HSP儿童(男66名，女44名)和250名无血缘关系的健康儿童参加了这项研究。平均年龄8.65±3.59岁。根据美国风湿病学会的分类，根据临床和实验室数据对HSP进行诊断。大多数患者的诊断与皮肤和/或肾脏有关。临床和实验室检查显示：皮肤受累110例(100%)，关节表现82例(74.5%)，胃肠道症状58例(52.7%)，血尿和/或蛋白尿36例(32.7%)。通过DNA扩增鉴定出人类白细胞抗原1类等位基因，并与特定的引物序列杂交。用Fisher‘s精确检验法比较患者组和对照组的频率。用优势比(OR)作为关联性的衡量标准。HLAA2、A11和B35抗原对HSP的易感性增加(OR=1.714，95%=1.088~2.700，P=0.020；OR=2.185，95%CI=1.289~3.703，P=0.003；OR=2.292，95%CI=1.451~3.619，P=0.000)，而HLAA1、B49和B50抗原对HSP的易感性降低(OR=4.739，95%CI=1.828~12.345，P=0.0001；OR=3.268，95%CI=0.955~11.236，P=0.047)；AND OR=7.462，95%CI=0.975~55.555，P=0.024)。考虑到肾脏受累和蛋白尿的严重程度，与人类白细胞抗原1类等位基因无关。我们的结果提示，HLAA2、A11和B35等位基因频率在未选择的儿童HSP患者中的频率增加和HLAA1、B49和B50的错误携带可能被认为是HSP的易感性的危险因素。
Henoch Schonlein purpura (HSP) is the most common vasculitis of childhood. Susceptibility to HSP and associated clinical heterogeneity in HSP may be conferred by a number of genetic loci, including the major histocompatibility complex. We aimed to investigate the implications of the human leukocyte antigen (HLA) class 1 alleles in susceptibility to HSP and determine the possible associations with renal, gastrointestinal (GI), and joint manifestations of the disease. 110 children with HSP (66 boys, 44 girls) and 250 unrelated healthy controls were enrolled in the study. The mean age was 8.65 +/- 3.59 years. HSP was diagnosed on the basis of clinical and laboratory data according to the American College of Rheumatology classification. The diagnosis was supported with skin and/or kidney in most of the patients. Clinical and laboratory findings revealed: skin involvement in 110 (100%), joint manifestations in 82 (74.5%), GI symptoms in 58 (52.7%), and hematuria and/or proteinuria in 36 (32.7%) patients. HLA class 1 alleles were identified by DNA amplification, hybridized with specific primer sequences. Comparison of frequencies between patients and controls were made by using the Fisher's exact test. Odds ratio (OR) was used as the measure of association. HLA A2, A11, and B35 antigens showed an increased risk for predisposition to HSP (OR=1.714, 95%=1.088-2.700, p=0.020; OR=2.185, 95%CI=1.289-3.703, p=0.003; and OR=2.292, 95%CI=1.451-3.619, p=0.000, respectively), while HLA A1, B49, and B50 antigens revealed decreased risk for predisposition to HSP (OR=4.739, 95%CI=1.828-12.345, p=0.001; OR=3.268, 95%CI=0.955-11.236, p=0.047; and OR=7.462, 95%CI=0.975-55.555, p=0.024, respectively). Considering the renal involvement and severity of proteinuria, there was no association with HLA class 1 alleles. Our results suggest that the increased frequency of HLA A2, A11, and B35 alleles in unselected pediatric HSP patient population and miscarrying of HLA A1, B49, and B50 could be considered as a risk factor for susceptibility to HSP.