Gürünlüoğlu Semra, Ceran Canan, Gürünlüoğlu Kubilay, Koçbiyik Alper, Gül Mehmet, Yıldız Turan, Bağ Harika Gözükara, Gül Semir, Taşçi Aytaç, Bayrakçi Ercan, Akpinar Necmettin, Çin Ecem Serbest, Ateş Hasan, Demircan Mehmet
Department of Pathology Malatya Education and Research Hospital, Pathology Laboratory, Malatya, Turkey.
Department of Pediatric Surgery, Faculty of Medicine, İnönü University, Malatya, Turkey.
Pediatr Gastroenterol Hepatol Nutr. 2021 Mar;24(2):173-186. doi: 10.5223/pghn.2021.24.2.173. Epub 2021 Mar 4.
Biliary atresia (BA) is a disease that manifests as jaundice after birth and leads to progressive destruction of the ductal system in the liver. The aim of this study was to investigate histopathological changes and immunohistochemically examine the expression of glial cell line-derived neurotrophic factor (GDNF), synaptophysin, and S-100 protein in the gallbladder of BA patients.
The study included a BA group of 29 patients and a control group of 41 children with cholecystectomy. Gallbladder tissue removed during surgery was obtained and examined immunohistochemically and histopathologically. Tissue samples of both groups were immunohistochemically assessed in terms of GDNF, S-100 protein, and synaptophysin expression. Expression was classified as present or absent. Inflammatory activity assessment with hematoxylin and eosin staining and fibrosis assessment with Masson's trichrome staining were performed for tissue sample sections of both groups.
Ganglion cells were not present in gallbladder tissue samples of the BA group. Immunohistochemically, GDNF, synaptophysin, and S-100 expression was not detected in the BA group. Histopathological examination revealed more frequent fibrosis and slightly higher inflammatory activity in the BA than in the control group.
We speculate that GDNF expression will no longer continue in this region, when the damage caused by inflammation of the extrahepatic bile ducts reaches a critical threshold. The study's findings may represent a missing link in the chain of events forming the etiology of BA and may be helpful in its diagnosis.
胆道闭锁（BA）是一种出生后表现为黄疸并导致肝脏导管系统进行性破坏的疾病。本研究的目的是调查BA患者胆囊的组织病理学变化，并通过免疫组织化学方法检测胶质细胞源性神经营养因子（GDNF）、突触素和S-100蛋白的表达。
该研究包括29例BA患者组和41例接受胆囊切除术的儿童对照组。获取手术中切除的胆囊组织，进行免疫组织化学和组织病理学检查。对两组组织样本进行GDNF、S-100蛋白和突触素表达的免疫组织化学评估。表达分为存在或不存在。对两组组织样本切片进行苏木精-伊红染色的炎症活性评估和Masson三色染色的纤维化评估。
BA组胆囊组织样本中不存在神经节细胞。免疫组织化学检测显示，BA组未检测到GDNF、突触素和S-100的表达。组织病理学检查显示，BA组的纤维化更常见，炎症活性略高于对照组。
我们推测，当肝外胆管炎症造成的损害达到临界阈值时，该区域的GDNF表达将不再持续。该研究结果可能代表了构成BA病因的一系列事件中的一个缺失环节，可能有助于其诊断。
