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目的 探讨肥大细胞在先天性巨结肠(Hirschsprung’s disease,HD)各表型中的分布差异,进而研究肥大细胞在HD发病机制中的作用.方法 选取2010年3月至2012年9月在上海交通大学附属儿童医院行HD根治术患儿的狭窄段和扩张段肠壁石蜡标本23例.根据病史资料,将其分为常见型12例,长段型6例,全结肠型5例.同时,选取先天性肛门直肠畸形行造瘘术患儿的肠壁石蜡标本13例作为对照组.肥大细胞采用甲苯胺蓝染色和免疫荧光染色.然后,通过显微镜观察并统计HD各表型组及对照组的黏膜层、黏膜下层和肌层中肥大细胞的数量.结果 常见型组、长段型组及全结肠型组的狭窄段黏膜层肥大细胞数量(分别为34.5±7.2、42.6±11.1、54.0±4.6)和黏膜下层的肥大细胞数量(分别为21.8±6.1、27.0±6.5、37.2±12.9)均多于自身扩张段及对照组黏膜层肥大细胞数量(分别为24.3±8.3、24.9±8.9、25.4±9.5、25.7±11.1)和黏膜下层的肥大细胞数量(分别为13.8±5.3、14.9±6.9、13.6±6.6、13.7±6.2),差异均有统计学意义(P＜0.05).对常见型组、长段型组和全结肠型组的狭窄段黏膜层及黏膜下层肥大细胞数量进行两两比较,发现各组黏膜层及黏膜下层的肥大细胞数量存在差异(P＜0.05).许多肥大细胞存在明显的脱颗粒现象.结论 肥大细胞在HD各表型中的分布是有差异的,这也说明肥大细胞可能在HD的发病机制中扮演重要的角色.“,”Objective To explore the role of mast cells (MCs) in the pathogenesis of Hirschsprung’s disease (HD) through examining the distribution of MC in different phenotypes of HD.Methods Twenty three hospitalized HD patients between March 2010 and September 2012 were recruited and another 13 undergoing colostomy for congenital anorectal malformations selected as control group.Based on medical history,they were divided into common type (n =12),long segment type (n=6) and total colon type groups (n =5).The MCs in colonic wall were stained by toluidine blue and immunofluorescence.And their numbers of MCs were counted microscopically in mucosal,submucosal and muscular layers.Results The numbers of MCs in mucosa (34.5 ± 7.2,42.6 ± 11.1,54.0± 4.6) and submucosa (21.8 ± 6.1,27.0 ± 6.5,37.2 ± 12.9) of aganglionic segments from common type,long-segment type and total colon type groups were all higher than those in mucosa (24.3 ± 8.3,24.9 ± 8.9,25.4 ±9.5,25.7 ± 11.1)and submucosa(13.8 ± 5.3,14.9 ± 6.9,13.6 ± 6.6,13.7 ± 6.2)from ganglionic segments and control group(P＜0.05).Through pairwise comparisons among aganglionic segments from common type,lon,segment type and total colon type groups,the numbers of MCs were different in both mucosa and submucosa of all groups(P＜0.05).Marked degranulation occurred.Conclusions The distributions of MCs vary in different phenotypes of HD.Thus MCs may play an important role in the pathogenesis of HD.