Peru Harun, Soylemezoglu Oguz, Gonen Sevim, Cetinyurek Aysun, Bakkaloğlu Sevcan Azime, Buyan Necla, Hasanoglu Enver
Department of Pediatric Nephrology, Gazi University Hospital, Besevler, Ankara, Turkey, 06540.
Clin Rheumatol. 2008 Jan;27(1):5-10. doi: 10.1007/s10067-007-0640-z. Epub 2007 May 9.
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%CI = 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.
过敏性紫癜（HSP）是儿童期最常见的血管炎。HSP的易感性以及HSP相关的临床异质性可能由多个基因位点决定，包括主要组织相容性复合体。我们旨在研究人类白细胞抗原（HLA）I类等位基因在HSP易感性中的作用，并确定其与该疾病的肾脏、胃肠道（GI）及关节表现之间可能存在的关联。本研究纳入了110例HSP患儿（66例男孩，44例女孩）和250名无亲缘关系的健康对照。平均年龄为8.65±3.59岁。根据美国风湿病学会的分类标准，依据临床和实验室数据诊断HSP。大多数患者通过皮肤和/或肾脏活检来辅助诊断。临床和实验室检查结果显示：110例（100%）有皮肤受累，82例（74.5%）有关节表现，58例（52.7%）有胃肠道症状，36例（32.7%）有血尿和/或蛋白尿。通过DNA扩增、与特定引物序列杂交来鉴定HLA I类等位基因。采用Fisher精确检验比较患者和对照之间的频率。比值比（OR）用作关联度量。HLA A2、A11和B35抗原显示HSP易感性增加（OR分别为1.714，95%CI = 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HLA A1、B49和B50抗原显示HSP易感性降低（OR分别为4.739，95%CI = 1.828 - 12.345，p = 0.001；OR = 3.268，95%CI = 0.955 - 11.236，p = 0.047；OR = 7.462，95%CI = 0.975 - 55.555，p = 0.024）。考虑到肾脏受累情况及蛋白尿的严重程度，与HLA I类等位基因无关联。我们的结果表明，在未选择的儿科HSP患者群体中，HLA A2、A11和B35等位基因频率增加以及HLA A1、B49和B50等位基因缺失可被视为HSP易感性的危险因素。
