中华皮肤科杂志 ›› 2009, Vol. 42 ›› Issue (8): 548-552.

• 论著 • 上一篇    下一篇

过敏性紫癜与子宫珠蛋白基因多态性的相关性研究

朱建建1,陈静2,黄进华3   

  1. 1. 湖南省常德市第一人民医院
    2. 湖南省长沙市中南大学湘雅三医院皮肤科(04.7前在本所)
    3. 湖南省长沙市中南大学湘雅三医院皮肤科
  • 收稿日期:2008-08-07 修回日期:2008-12-09 出版日期:2009-08-15 发布日期:2009-08-10
  • 通讯作者: 朱建建

Relationship between uteroglobin gene polymorphism and Henoch-Schonlein purpura

  • Received:2008-08-07 Revised:2008-12-09 Online:2009-08-15 Published:2009-08-10

摘要:

目的 探讨子宫珠蛋白基因多态性与过敏性紫癜、紫癜性肾炎发病易感性和临床、病理表型的联系。方法 过敏性紫癜患儿118例,包括80例肾炎患者(紫癜性肾炎患者)和38例无肾炎患者,正常儿童100例。提取静脉血白细胞基因组DNA, PCR-RFLP法确定子宫珠蛋白基因G38A基因型。用χ2检验比较各组子宫珠蛋白不同基因型频率及不同基因型的紫癜性肾炎患者临床和肾脏病理特征。结果过敏性紫癜各组分别与正常对照组比较,肾炎组与无肾炎组比较,子宫珠蛋白基因3种基因型(38GG、38AG、38AA)频率差异无统计学意义(P > 0.05)。三种基因型与过敏性紫癜四种临床表型以及紫癜性肾炎患者肉眼血尿、肾病综合征等临床表型和肾脏病理损害等级无关(P > 0.05)。过敏性紫癜伴血清IgE增高组38AA型频率较血清IgE正常组明显升高(χ2 = 21.95,P < 0.01,OR = 15.51,95% CI为4.93 ~ 48.84)。紫癜性肾炎伴高血压组38GG型频率较无高血压组显著升高(χ2 = 26.17,P < 0.01,OR = 13.61,95% CI为5.01 ~ 37.01)。结论 子宫珠蛋白基因G38A多态性与过敏性紫癜、紫癜性肾炎易感性及肾脏病理损害程度无关,而子宫珠蛋白基因38AA型的过敏性紫癜患者可能容易出现血清IgE增高,38GG型的紫癜性肾炎患者可能容易出现高血压。

Abstract:

Objective To investigate the relationship of uteroglobin gene polymorphism to the susceptibility to, clinical type and pathological type of Henoch-Sch?觟nlein purpura (HSP) and Henoch-Sch?觟nlein purpura nephritis (HSPN). Methods Totally, 118 patients with clinically diagnosed HSP, including 80 cases of HSPN and 38 cases without renal involvement were recruited in this study together with 100 normal human healthy controls. Genomic DNA was isolated from peripheral blood leucocytes of all subjects. The uteroglobin G38A polymorphism was determined by PCR-restriction fragment length polymorphism (RFLP). Results The frequencies of genotypes 38GG, 38GA and 38AA in normal human controls did not differ from those in patients with HSP, patients with HSP but without nephritis, patients with HSPN, patients with HSP and joint involvement, patients with HSP and gastrointestinal involvement (all P > 0.05). Also, no significant difference was observed between patients with HSPN and patients with HSP but without nephritis (P > 0.05). Furthermore, the frequency of genotypes 38GG, 38GA and 38AA had no significant correlation to the clinical phenotype of HSP, the occurrence of gross hematuria and nephrotic syndrome or the degree of renal damage (all P > 0.05). A significant increase was observed in the frequency of genotype 38AA in patients with HSP with elevated serum IgE compared with those with normal serum IgE (58.82% vs 8.43%, χ2 = 21.946, P < 0.05, OR = 15.51, 95% CI range: 4.93% - 48.84%), whereas the frequency of genotype 38GG was significantly increased in patients with HSPN and hypertension than in those with HSPN but without hypertension(75.68% vs 18.60%, χ2 = 26.172, P < 0.05, OR = 13.61, 95% CI range: 5.01% - 37.01%). Conclusions The uteroglobin G38A polymorphism seems unrelated to the susceptibility to and degree of renal damage in patients with HSP and HSPN. The genotype 38AA may be associated with elevated level of serum IgE In patients with HSP, while genotype 38GG is associated with a high incidence of hypertension in patients with HSPN.

Key words: Uteroglobin , gene , single nucleotide polymorphism,Henoch-Schonlein purpura, Henoch-Schonlein purpura nephritis