Pediatr Gastroenterol Hepatol Nutr.  2021 Mar;24(2):173-186. 10.5223/pghn.2021.24.2.173.

Glial Cell Line-Derived Neurotrophic Factor, S-100 Protein and Synaptophysin Expression in Biliary Atresia Gallbladder Tissue

Affiliations
  • 1Department of Pathology Malatya Education and Research Hospital, Pathology Laboratory, Malatya, Turkey
  • 2Department of Pediatric Surgery, Faculty of Medicine, İnönü University, Malatya, Turkey
  • 3Department of Pathology, Istanbul Bakırköy Dr Sadi Konuk Education and Research Hospital, Pathology Laboratory, Istanbul, Turkey
  • 4Department of Histology and Embryology, Faculty of Medicine, İnönü University, Malatya, Turkey
  • 5Department of Biostatistics and Medical Informatics, Faculty of Medicine, İnönü University, Malatya, Turkey

Abstract

Purpose
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.
Methods
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.
Results
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.
Conclusion
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.

Keyword

Biliary atresia; Glial cell line-derived neurotrophic factor; Synaptophysin; S-100 protein; Gallbladder
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