OBJECTIVE: To determine whether low platelet counts are related to the incidence of patent ductus arteriosus (PDA) after indomethacin treatment in preterm human infants. STUDY DESIGN: Multivariable logistic regression modeling was used for a cohort of 497 infants, who received indomethacin (within 15 hours of birth). RESULTS: Platelet counts were not related to the incidence of permanent closure after indomethacin constriction. There was a relationship between platelet counts and the initial degree of constriction; however, this relationship appeared to be primarily influenced by the high end of the platelet distribution curve. PDA incidence was similar in infants with platelet counts < 50 × 10⁹/L and those with platelet counts above this range. Only when platelet counts were consistently >230 ×10⁹/L was there a decrease in PDA incidence. CONCLUSION: In contrast to the evidence in mice, low circulating platelet counts do not affect permanent ductus closure (or ductus reopening) in human preterm infants.
OBJECTIVE: To determine whether low platelet counts are related to the incidence of patent ductus arteriosus (PDA) after indomethacin treatment in preterm humaninfants. STUDY DESIGN: Multivariable logistic regression modeling was used for a cohort of 497 infants, who received indomethacin (within 15 hours of birth). RESULTS: Platelet counts were not related to the incidence of permanent closure after indomethacin constriction. There was a relationship between platelet counts and the initial degree of constriction; however, this relationship appeared to be primarily influenced by the high end of the platelet distribution curve. PDA incidence was similar in infants with platelet counts < 50 × 10⁹/L and those with platelet counts above this range. Only when platelet counts were consistently >230 ×10⁹/L was there a decrease in PDA incidence. CONCLUSION: In contrast to the evidence in mice, low circulating platelet counts do not affect permanent ductus closure (or ductus reopening) in human preterm infants.
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