Abstract
Background
The etiology of incisional hernias in the population of morbidly obese patients remains
unclear. Most likely, factors other than purely mechanical are at play; it has been
ascertained that nonobese patients suffering from inguinal and incisional hernias
display alterations in the architecture of the connective tissue. The goal of this
study has been to evaluate and compare the relative expression of collagen type I
and III genes in the rectus abdominis muscle sheath (RMS) of obese and nonobese individuals
to investigate their possible influence on the quality of the connective tissue.
Materials and methods
RMS specimens were harvested in the early stages of either bariatric or non-bariatric
laparotomies; total RNA was isolated and enzymatically purified from the tissue samples.
The resulting material was subjected to a quantitative and qualitative analysis; reverse
transcription reactions were then performed and the resulting complementary DNA was
used in real-time reverse transcription polymerase chain reactions. The biopsy specimens
were also examined by scanning electron microscopy.
Results
The real-time reverse transcription polymerase chain reactions, performed on complementary
DNA, provided specific amplicons for individual genes. The efficacy of the reactions
was rather low. An almost twofold decrease of the relative expression level for type
I and III collagen was observed between the two patient groups; the results did not
reach statistical significance. Scanning electron microscope photographs have documented
a marked difference in the ultrastructure of the RMS in both groups.
Conclusions
The authors have shown that changes in messenger RNA levels for collagen type I and
III genes may be related to the pathogenesis of incisional hernia through alterations
in the ultrastructure of the RMS fascia. Our report should be considered preliminary;
the results should be verified on a larger group of patients.
Keywords
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Article info
Publication history
Published online: January 20, 2015
Accepted:
January 7,
2015
Received in revised form:
December 22,
2014
Received:
July 1,
2014
Identification
Copyright
© 2015 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
