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The newborn's persistent pulmonary hypertension is present when the respiratory vascular resistance struggles to decline at birth during the transition to postnatal life. PPHN's etiology in the majority of affected infants is unknown. In utero, nearly 80% of infants with PPHN were exposed to NSAID in utero. The reason for some neonates' sensitivity to in utero NSAID exposure remains unclear. This hypothesis will be tested in the following ways: Determine the prevalence of PTGS1 sequence variants in PPHN patients versus matched controls. The PTGS1 sequence will include all 11 exons, a minimum of 100 bp of exon flanking sequences, and 1 kbp of upstream regulatory data. Using regression analysis, the study will also quantify NSAID exposure in meconium samples and determine exposure levels to both the incidence of PPHN and the presence or absence of PTGS1 sequence variants using regression analysis.
Source link: https://clinicaltrials.gov/ct2/show/NCT00710177
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