RESUMO
OBJECTIVE: Immature antioxidant and oxygen-sensing mechanisms are involved in the pathogenesis of the patent ductus arteriosus (PDA). We conducted a prospective, observational, pilot study to test the hypothesis that antioxidant activity is low at birth in preterm infants at risk for symptomatic PDA. STUDY DESIGN: Blood and urine samples were collected within 24 to 48 hours of life in 53 preterm infants (≤32 weeks' gestation) who developed early PDA symptoms and in 30 term (≥37 weeks' gestation) control infants. Thirty preterm infants developed hemodynamically significant PDA (hsPDA) and required pharmacologic treatment and/or PDA ligation. For these infants, blood and urine samples were also collected at 24 hours posttreatment. Samples were analyzed for biomarkers of antioxidant activity, oxidative stress, and lipid peroxidation. RESULTS: At 24 to 48 hours after birth, plasma superoxide dismutase (SOD), urinary catalase, and plasma and urinary 8-isoPGF2α were significantly lower in preterm infants who developed hsPDA. Plasma 8-isoPGF2α levels rebounded post-PDA treatment, while urinary prostaglandin E2, plasma and urinary thromboxane B2, and plasma SOD declined. CONCLUSION: The antioxidant status is low in preterm infants at risk for developing hsPDA. SOD may be a key antioxidant regulating functional ductus arteriosus closure. Therefore, low levels may result in persistence of a hsPDA.
Assuntos
Antioxidantes/uso terapêutico , Biomarcadores/sangue , Biomarcadores/urina , Inibidores de Ciclo-Oxigenase/uso terapêutico , Permeabilidade do Canal Arterial/terapia , Estresse Oxidativo/efeitos dos fármacos , Permeabilidade do Canal Arterial/sangue , Permeabilidade do Canal Arterial/urina , Feminino , Humanos , Ibuprofeno/uso terapêutico , Indometacina/uso terapêutico , Lactente , Recém-Nascido , Recém-Nascido Prematuro/sangue , Recém-Nascido Prematuro/urina , Ligadura , Masculino , Projetos Piloto , Estudos ProspectivosRESUMO
Fetal and neonatal thyrotoxicosis from maternal Graves disease is a very rare entity. Fetal symptoms result from the transplacental passage of thyroid-stimulating immunoglobulins, which persist in the neonate resulting in neonatal symptoms. We present a case of fetal and neonatal thyrotoxicosis from maternal Graves disease. Fetal symptoms were controlled with maternal administration of antithyroid drugs leading to fetal thyroid inhibition. We present this case with a brief review of the literature.