过敏性紫癜患儿幽门螺杆菌感染及其对补体系统及炎症指标的影响

Influence of Helicobacter pylori infection on complement system and inflammatory indexes of children with Henoch-Schonlein purpura

目的 分析过敏性紫癜(HSP)患儿幽门螺杆菌(Hp)感染对补体系统及炎症指标的影响。方法 选取2017年4月-2020年4月中国医科大学附属盛京医院收治的82例HSP患儿为研究对象,根据^(14)C-尿素呼气试验结果分为Hp阳性组57例,Hp阴性组25例,分析两组患儿血清低半乳糖化IgA1(Gd-IgA1),补体片段C3a、C4a、C5a和Bb,以及单核细胞趋化蛋白-1(MCP-1)、白细胞介素18(IL-18)水平。结果 Hp阳性组出现腹痛、呕血/便血患儿的比例显著高于Hp阴性组(P<0.05),两组出现皮肤紫癜、关节肿痛、尿蛋白阳性、血尿患儿的比例均差异无统计学意义;Hp阳性组患儿血清Gd-IgA1水平显著高于Hp阴性组(P<0.05);Hp阳性组患儿的血清补体片段C3a、C5a和Bb水平显著高于Hp阴性组(P<0.05),而两组血清C4a水平比较差异无统计学意义;Hp阳性组患儿血清IL-18、MCP-1水平均高于Hp阴性组(P<0.05)。结论 Hp感染可能通过增加Gd-IgA1水平,激活补体旁路途径而促进IL-8和MCP-1的产生,进而促进过敏性紫癜的发生。

OBJECTIVE To observe the influence of Helicobacter pylori infection on complement system and inflammatory indexes of children with Henoch-Schonlein purpura(HSP). METHODS A total of 82 children with HSP who were treated in Shengjing Hospital Affiliated to China Medical University from Apr 2017 to Apr 2020 were recruited as the study subjects and were divided into the Hp-positive group with 57 cases and the Hp-negative group with 25 cases according to the result of14C-urea breath test(^(14)C-UBT). The levels of serum galactokinase deficiency IgA1(Gd-IgA1), complement fragments(C3a, C4a, C5a, Bb), monocyte chemotactic protein-1(MCP-1) and interleukin-18(IL-18) were detected for the two groups of children. RESULTS The proportions of the children who had abdominal pain, hematemesis/hematochezia were significantly higher in the Hp-positive group than in the Hp-negative group(P<0.05). There were no significant differences in the proportions of the children who had skin purpura, joint swelling and pain, positive urine protein and hematuria between the two groups. The serum Gd-IgA1 level of the Hp-positive group was significantly higher than that of the Hp-negative group(P<0.05). The levels of serum complement fragments C3a, C5a and Bb of the Hp-positive group were significantly higher than those of the Hp-negative group(P<0.05), however, there was no significant difference in the serum C4a level between the two groups. The levels of serum IL-18 and MCP-1 of the Hp-positive group were higher than those of the Hp-negative group(P<0.05). CONCLUSION The H. pylori infection may accelerate the occurrence of HSP by raising the Gd-IgA1 level and activating the complement bypass pathways to promote the production of IL-8 and MCP-1.