The collagen turnover profile is altered in patients with inguinal and incisional hernia

Nadia A Henriksen, Joachim H Mortensen, Lars T Sorensen, Anne C Bay-Jensen, Magnus S Ågren, Lars N Jorgensen, Morten A Karsdal

33 Citationer (Scopus)

Abstract

Background Disturbed metabolism in the extracellular matrix (ECM) contributes to formation of abdominal wall hernias. The aim of this study was to gain deeper insight into the ECM turnover in hernia patients by analyzing serum biomarkers specifically reflecting collagen synthesis and breakdown in the interstitial matrix (types I, III, and V collagens) and in the basement membrane (type IV collagen). Material and Methods Patients with 3 different types of hernias were included: Primary unilateral inguinal hernia (n = 17), multiple hernias defined as ≥3 hernias (n = 21), and incisional hernia (n = 25). Patients without hernias scheduled to undergo elective operation for gallstones (n = 18) served as controls. Whole venous blood was collected preoperatively. Biomarkers for synthesis of interstitial matrix (PINP, Pro-C3, P5CP) and basement membrane (P4NP) as well as corresponding degradation (C1M, C3M, C5M, and C4M) were measured in serum by validated, solid-phase competitive assays. Results In inguinal hernia patients, the turnover of the interstitial matrix collagens type III (P <.042) and V (P <.001) was decreased compared with controls, whereas the turnover of the basement membrane collagen type IV was increased (P <.001). In incisional hernia patients, the turnover of type V collagen was decreased (P =.048) and the turnover of type IV collagen was increased compared with the hernia-free controls (P <.001). Conclusion Hernia patients demonstrated systemically altered collagen metabolism. The serologic turnover profile of type IV collagens may predict the presence of inguinal and incisional hernia. Regulation of type IV collagen turnover may be crucial for hernia development.

OriginalsprogEngelsk
TidsskriftSurgery
Vol/bind157
Udgave nummer2
Sider (fra-til)312-21
Antal sider10
ISSN0039-6060
DOI
StatusUdgivet - 1 feb. 2015

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