Abstract

Background/introductionIntraventricular hemorrhage (IVH) is a dangerous complication facing a significant proportion of preterm infants. It is multifactorial in nature, and an observed fibronectin deficiency in the germinal matrix basal lamina is among the most prominent factors that influence such rupture. Better understanding of the FN1 gene polymorphisms and their role in IVH may further clarify the presence of a genetic susceptibility of certain babies to this complication. The aim of this study was to assess if 5 single nucleotide polymorphisms of the fibronectin gene may be linked to an increased incidence of IVH.Material and methodsThe study included 108 infants born between 24 and 32 weeks of gestation. IVH was diagnosed using cranial ultrasound performed on the 1st,3rd, and 7th day after birth and classified according to Papile et al. IVH classification. The 5 FN1 gene polymorphisms assessed in the study were the following: rs3796123; rs1968510; rs10202709; rs6725958; and rs35343655.ResultsIVH developed in 51 (47.2%) out of the 108 preterm infants. This includes, 18 (35.3%) with stage I IVH, 19 (37.3%) with stage II, 11 (21.6%) with stage III, and 3 (5.9%) with stage IV IVH. Incidence of IVH was higher in infants with lower APGAR scores, low gestational age, and low birthweight. Analysis showed that IVH stage II to IV was approximately seven times more likely to occur in infants with the genotype TT FN1 rs10202709 (OR 7237 (1046–79.59; p = 0,044)). No other significant association was found with the rest of the polymorphisms.ConclusionThe results of our study indicate a sevenfold increased genetic susceptibility to IVH in preterm infants with the TT FN1 rs10202709 gene polymorphism. The fibronectin gene polymorphism may therefore be of crucial importance as a genetic risk factor for IVH in preterm infants. Further studies are warranted.

Highlights

  • Intraventricular hemorrhage (IVH) is one of the most severe complications of preterm birth

  • The following genetic factors that may predispose to IVH have been analyzed so far: polymorphisms of genes coding for proinflammatory cytokines [7, 8], coagulation pathway [9,10,11] regulation of systemic blood pressure and cerebral blood flows [12], as well as structural components of the germinal matrix [13, 14]

  • The following factors that may be associated with the development of IVH were studied: gender, gestational age (GA; weeks), and birth weight (BW, grams); mode of delivery; APGAR score; pH < 7.0 and blood base excess (BE) in cord blood; place of birth; and intrauterine infection

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Summary

Introduction

Intraventricular hemorrhage (IVH) is one of the most severe complications of preterm birth. In IVH pathogenesis are involved: irregularities in cerebral blood flow, Childs Nerv Syst (2020) 36:1729–1736 coagulation and platelet abnormalities which further accentuate the bleeding, and very critical in preterm infants in the integrity of the germinal matrix [6]. Genetic factors participating in the development of IVH are still being analyzed. The following genetic factors that may predispose to IVH have been analyzed so far: polymorphisms of genes coding for proinflammatory cytokines [7, 8], coagulation pathway [9,10,11] regulation of systemic blood pressure and cerebral blood flows [12], as well as structural components of the germinal matrix [13, 14]. There is still not enough definitive information about the connection between the increased risk of IVH and the molecular structure of the vasculature in the germinal matrix

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