Background: Pathogenesis of intraventricular hemorrhage (IVH) in premature infants is multifactorial. Little is\nknown about the impact of genetic variants in the vitamin K-dependent coagulation system on the development\nof IVH.\nMethods: Polymorphisms in the genes encoding vitamin K epoxide reductase complex 1 (VKORC1 -1639G>A) and\ncoagulation factor 7 (F7 -323Ins10) were examined prospectively in 90 preterm infants <32 weeks gestational age\nwith respect to coagulation profile and IVH risk.\nResults: F7-323Ins10 was associated with lower factor VII levels, but not with individual IVH risk. In VKORC1-wildtype\ninfants, logistic regression analysis revealed a higher IVH risk compared to carriers of the -1639A allele. Levels of\nthe vitamin K-dependent coagulation parameters assessed in the first hour after birth did not differ between\nVKORC1-wildtype infants and those carrying -1639A alleles.\nConclusions: Our data support the assumption that genetic variants in the vitamin K-dependent coagulation system\ninfluence the coagulation profile and the IVH risk in preterm infants. Further studies focussing on short-term changes\nin vitamin K-kinetics and the coagulation profile during the first days of life are required to further understand a\npossible link between development of IVH and genetic variants affecting the vitamin K-metabolism.
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