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The clinical significance of pathological studies of congenital intestinal atresia.

AbstractOBJECTIVE:
The purpose of this study was to explore the mechanisms of postoperative intestinal motility disorders in intestinal atresia patients by investigating the expression profiles of proteins, including calretinin (CR), glial-derived neurotrophic factor (GDNF), bone morphogenetic protein 2 (BMP-2), c-kit, α-smooth muscle actin (α-SMA), and S-100 protein; to decipher the correlation between the area of the pathological segment and the alteration of the above 6 proteins; and thereby to provide a clinical specific reference values to determine the removal length for intestinal tract resection.
METHODS:
Immunohistochemistry technique was applied to detect the CR, c-kit, GDNF, BMP-2, α-SMA, and S-100 protein in specimens of atretic, proximal, and distal intestine from 25 cases of intestinal atresia and samples of intestinal walls from 10 non-atresia control specimens. The alteration of the enteric nervous system, nerve growth and its regulatory factors, the interstitial cells of Cajal (ICCs), and the enteric muscle system were examined, with particular attention being paid to pathological changes and the lesion area.
RESULTS:
The expression of all of the abovementioned 6 proteins in the proximal side of the atresia was significantly lower than in control group. The expression of the abovementioned proteins tended to be higher farther away from the atresia site. The expressions of both GDNF and BMP-2 had returned to normal level at 10 cm proximal to the atresia site, whereas the expressions of CR, c-kit, α-SMA, and S-100 protein only returned to normal at 15 cm proximal to the atresia site. On the distal side, the expression of all 6 markers at 3 cm distal to the atresia site was normal.
CONCLUSION:
Pathological deterioration of the myenteric ganglia, nerve growth factor, and ICCs are the causes of intestinal motility disorders after the surgical repair of intestinal atresia. Our data support resecting an intestinal segment extending from 15 cm proximal to 3 cm distal to the atretic segment. In proximal jejunal atresia, when it is not possible to resect 15 cm, we suggest resecting as much of the hypertrophic proximal intestine as possible. Based on our data, we believe this surgical practice could improve postoperative dysmotility in these patients.
AuthorsXiuliang Wang, Chendong Yuan, Li Xiang, Xiaoqing Li, Zhanbo Zhao, Xianqing Jin
JournalJournal of pediatric surgery (J Pediatr Surg) Vol. 48 Issue 10 Pg. 2084-91 (Oct 2013) ISSN: 1531-5037 [Electronic] United States
PMID24094962 (Publication Type: Evaluation Study, Journal Article)
CopyrightCopyright © 2013 Elsevier Inc. All rights reserved.
Chemical References
  • ACTA2 protein, human
  • Actins
  • BMP2 protein, human
  • Biomarkers
  • Bone Morphogenetic Protein 2
  • CALB2 protein, human
  • Calbindin 2
  • GDNF protein, human
  • Glial Cell Line-Derived Neurotrophic Factor
  • S100 Proteins
  • Proto-Oncogene Proteins c-kit
Topics
  • Actins (metabolism)
  • Biomarkers (metabolism)
  • Bone Morphogenetic Protein 2 (metabolism)
  • Calbindin 2 (metabolism)
  • Case-Control Studies
  • Female
  • Glial Cell Line-Derived Neurotrophic Factor (metabolism)
  • Humans
  • Ileus (etiology, metabolism, prevention & control)
  • Immunohistochemistry
  • Infant, Newborn
  • Intestinal Atresia (complications, metabolism, pathology, surgery)
  • Male
  • Postoperative Complications (etiology, metabolism, prevention & control)
  • Proto-Oncogene Proteins c-kit (metabolism)
  • S100 Proteins (metabolism)

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