论文部分内容阅读
目的探讨ＨＤ并发小肠结肠炎的发病原因和发病机理。方法利用放射免疫技术及免疫组织化学方法（ＳＡＢＣ）检测ＨＤ患儿肠粘膜免疫功能。结果１３例ＨＤ患儿中，５例伴有小肠结肠炎患儿与８例无小肠结肠炎患儿相比肠腔内ＳＩｇＡ浓度明显降低，肠粘膜淋巴细胞转化能力减弱，固有层中含ＩｇＡ的浆细胞明显增多，ＣＤ４＋、ＣＤ８＋细胞分布异常。结论ＨＤ伴有小肠结肠炎患儿肠粘膜免疫功能受到抑制，多聚ＩｇＡ不能通过上皮细胞转运到肠粘膜表面形成ＳＩｇＡ，若远端肠管狭窄，粪便淤积，细菌和病毒可侵入肠粘膜大量繁殖，引起肠道炎症，进一步导致粘膜的破坏，粘膜免疫功能更加下降，形成恶性循环，这正是ＨＤ患儿并发小肠结肠炎复杂机理所在
Objective To investigate the pathogenesis and pathogenesis of HD concurrent enterocolitis. Methods Radioimmunoassay and immunohistochemistry (SABC) were used to detect intestinal mucosal immune function in children with HD. Results In 13 children with HD, 5 patients with enterocolitis had significantly lower concentrations of SIgA in the intestine and a weaker ability of intestinal mucosal lymphocyte transformation than those in 8 patients without enterocolitis. IgA-containing lamina propria in the lamina propria Plasma cells increased significantly, CD4 +, CD8 + cells were abnormally distributed. Conclusion Intestinal mucosal immune function is inhibited in children with HD accompanied by enterocolitis. Poly IgA can not transport SIgA to the intestinal mucosa through the epithelial cells. If the distal intestine is stenosed and the stool is deposited, the bacteria and virus can invade into the intestinal mucosa to proliferate, Causing intestinal inflammation, and further lead to the destruction of the mucosa, mucosal immune function is declining, forming a vicious circle, which is the complex mechanism of HD complicated with enterocolitis