Novel inflammatory markers of labor following premature preterm rupture of membranes

N Marczuk,A Torbè,A Rajewska,B Dołęgowska,S Kwiatkowski,R Rzepka,K Nurek

doi:10.12891/ceog4607.2019

Abstract

The aim of the study was comparison of levels of resistin (RE), soluble receptor for advanced glycation end products (sRAGE), soluble receptor activator for nuclear factor-κB ligand (sRANKL), osteoprotegerin (OPG), glucose (GL), total protein (TP), and albumin (AL) between women with preterm and term rupture of fetal membranes and evaluation of prognostic values of all above in diagnostic of premature labor. Ninety-eight women in singleton pregnancy presenting with premature rupture of fetal membranes were included and divided into two groups: A - 49 women after 37 weeks and B - 49 women before 36 weeks of gestation. Plasma levels of sRAGE, OPG, TP, and AL were significantly lower in group B, and RE and GL plasma levels were higher in this group. The high prognostic values for sRAGE and sRANKL in the prognosis of spontaneous delivery after preterm rupture of membranes (pPROM) were found. The authors concluded that sRAGE and sRANKL serum levels could be a useful prognostic factors after pPROM. Resistin can play role in pathogenesis of rupture of membranes in premature pregnancy.

Highlights

According to the World Health Association’s data, the prevalence of preterm delivery all over the world is as high as thirteen million per year [1]
45–50% of preterm births are idiopathic, 30% are related to preterm rupture of membranes, and another 15–20% are attributed to medically indicated or elective preterm deliveries [2-3]
Plasma levels of soluble receptor for advanced glycation end products (sRAGE), OPG, total protein (TP), and AL were significantly lower in group B than in group A

Summary

Introduction

According to the World Health Association’s data, the prevalence of preterm delivery all over the world is as high as thirteen million per year [1]. 45–50% of preterm births are idiopathic, 30% are related to preterm rupture of membranes (pPROM), and another 15–20% are attributed to medically indicated or elective preterm deliveries [2-3]. Premature birth causes 28% of perinatal deaths of the neonates [4]. Despite many years of research, the actual cause of pPROM remains unclear. Working as the activators of Toll-like receptors (TLRs), mainly TLR2 and TLR4, these agents increase cytokine production. This leads to the onset of arachidonic acid cascade, oxidative stress accumulation, and the rise in production of prostaglandins, and different types of proteases, especially matrix metalloproteinase (MMP) [5-7]. The last group is believed to be the most important destructive factor in fetal membranes [8]

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