Abdominal Wall Defects: Autopsy Findings of Distinct Groups Suggest Different Pathogenetic Mechanisms

Central and lateral abdominal wall defects are probably distinct and likely arise from different pathogenetic mechanisms. An autopsy study was done using data from a total of 45 central and lateral abdominal wall defect cases to evaluate if they are indeed separate entities and to suggest possible m...

Full description

Saved in:
Bibliographic Details
Published in:Pediatric and developmental pathology 2009-01, Vol.12 (1), p.22-27
Main Authors: Giménez-scherer, Juan Antonio, Davies, Belinda R., Reséndiz-Morán, Mario A., Durán-Padilla, Marco A.
Format: Article
Language:English
Subjects:
Abdominal Muscles - abnormalities
Abnormalities, Multiple - genetics
Abnormalities, Multiple - pathology
Amniotic Band Syndrome - pathology
Autopsy
Female
Gastroschisis - genetics
Gastroschisis - pathology
Hernia, Umbilical - genetics
Hernia, Umbilical - pathology
Humans
Infant, Newborn
Male
Triplets
Twins
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Central and lateral abdominal wall defects are probably distinct and likely arise from different pathogenetic mechanisms. An autopsy study was done using data from a total of 45 central and lateral abdominal wall defect cases to evaluate if they are indeed separate entities and to suggest possible mechanisms involved in their formation. Central defects were found to be statistically different from lateral defects; malformations that co-existed with central defects were mainly bilateral and internal and also involved “inferior” organs in relation to fetal-embryonal blood flow. Patients with lateral defects were more often female, and their coexistent defects were usually unilateral and external, with only 1 defect occurring in an “inferior” organ. These results indicate mechanisms of a vascular perfusion deficit for the majority of the central defects and of external disruption for the lateral defects.
ISSN:1093-5266
1615-5742
DOI:10.2350/06-11-0185.1