OBJECTIVES: In the current prospective study our aim was to analyse the distribution of the factor V Leiden (G1691A) mutation in preterm and full-term neonates with grade I intraventricular haemorrhage and in control neonates. STUDY METHOD: A group of 125 individually selected neonates with grade I intraventricular haemorrhage and 128 controls were investigated. RESULTS: The allele frequency was 7.2% in the total population of affected infants while it was 3.9% in the controls (p < 0.05); the latter corresponds to an average European allele frequency in healthy populations. When the infants were grouped as premature (<2,500 g and < or =36 weeks of gestational age) and appropriate for gestational age full-term infants the statistical analysis revealed an increased prevalence of the mutation in the premature group (10% allele frequency vs. 4.8% in the controls, p < 0.05), and a normal prevalence in the mature group (4.6 vs. 3.1%, respectively); therefore, the overall increase was due to the increase of incidence rate in preterm neonates. CONCLUSIONS: These data confirm our previous results and suggest that as the preterm and term infants differ from each other in haemorrhage susceptibility in many clinical particulars, carrying of the mutation has probably also a different impact in premature and in full-term infants with respect to the intraventricular haemorrhage.
OBJECTIVES: In the current prospective study our aim was to analyse the distribution of the factor V Leiden (G1691A) mutation in preterm and full-term neonates with grade I intraventricular haemorrhage and in control neonates. STUDY METHOD: A group of 125 individually selected neonates with grade I intraventricular haemorrhage and 128 controls were investigated. RESULTS: The allele frequency was 7.2% in the total population of affected infants while it was 3.9% in the controls (p < 0.05); the latter corresponds to an average European allele frequency in healthy populations. When the infants were grouped as premature (<2,500 g and < or =36 weeks of gestational age) and appropriate for gestational age full-term infants the statistical analysis revealed an increased prevalence of the mutation in the premature group (10% allele frequency vs. 4.8% in the controls, p < 0.05), and a normal prevalence in the mature group (4.6 vs. 3.1%, respectively); therefore, the overall increase was due to the increase of incidence rate in preterm neonates. CONCLUSIONS: These data confirm our previous results and suggest that as the preterm and term infants differ from each other in haemorrhage susceptibility in many clinical particulars, carrying of the mutation has probably also a different impact in premature and in full-term infants with respect to the intraventricular haemorrhage.