Department of Pediatric General and Urogenital Surgery, Juntendo University School of Medicine, Tokyo 113-8421, Japan.
J Pediatr Surg. 2009 Dec;44(12):2364-8. doi: 10.1016/j.jpedsurg.2009.07.066.
Immaturity of neurons in normoganglionic colon in Hirschsprung disease (HD), anorectal malformation (AM), idiopathic constipation (IC), and normal controls (C) was assessed using polysialyated neural cell adhesion molecule.
Polysialyated neural cell adhesion molecule immunoreactivity in 3 sections of normoganglionic colon from HD (n = 48), AM (n = 25), IC (n = 36), and C (n = 18) were scored semiquantitatively according to age; 1 day to 11 months (G1), 1 to 4 years (G2), and 5 years and older (G3).
Neurons in all specimens appeared mature irrespective of age on hematoxylin-eosin stain. Polysialyated neural cell adhesion molecule was positive (immaturity) in all specimens during G1 (1.34 in HD, 1.60 in AM, 0.89 in IC, and 1.59 in C) and decreased significantly with age in C (0.34* for G2, 0.25* for G3; *P < .01), decreased after 4 years old in IC (0.93 for G2, 0.10(#) for G3; (#)P < .05), decreased gradually in AM (1.10 for G2, 0.75( section sign) for G3; ( section sign)P < .05), but remained strongly positive in HD (1.34 for G1, 1.26 for G2, and 1.21 for G3; P = not significant), which after 4 years was significantly higher than C (P < .05).
Postoperative colonic dysmotility may be because of persistence of immature neurons in HD and impaired maturation of neurons in AM and IC.
使用多唾液酸神经细胞黏附分子评估先天性巨结肠症(HD)、肛门直肠畸形(AM)、特发性便秘(IC)和正常对照(C)中正常神经节结肠内神经元的不成熟程度。
根据年龄对来自 HD(n = 48)、AM(n = 25)、IC(n = 36)和 C(n = 18)的正常神经节结肠的 3 个切片中的多唾液酸神经细胞黏附分子免疫反应进行半定量评分;1 天至 11 个月(G1)、1 至 4 岁(G2)和 5 岁及以上(G3)。
无论年龄大小,所有标本的神经元在苏木精-伊红染色上均显示成熟。所有标本在 G1 时多唾液酸神经细胞黏附分子均呈阳性(不成熟)(HD 为 1.34,AM 为 1.60,IC 为 0.89,C 为 1.59),并且 C 随年龄显著降低(G2 为 0.34*,G3 为 0.25*;*P <.01),IC 在 4 岁后降低(G2 为 0.93,G3 为 0.10(#);(#)P <.05),AM 逐渐降低(G2 为 1.10,G3 为 0.75( section sign);( section sign)P <.05),但在 HD 中仍保持强阳性(G1 为 1.34,G2 为 1.26,G3 为 1.21;P = 无显著性),4 岁后 HD 明显高于 C(P <.05)。
术后结肠动力障碍可能是由于 HD 中不成熟神经元的持续存在以及 AM 和 IC 中神经元成熟受损所致。