Maternal obesity mediated predisposition to respiratory complications at birth and in later life: understanding the implications of the obesogenic intrauterine environment.

More women than not are entering pregnancy either overweight or obese. This presents a significant health care burden with respect to maternal morbidities and offspring complications at birth and in later life. In recent years it has also become clear that maternal obesity is an even greater global health problem than anticipated, because the effects are not limited to the mother but are also programmed in the fetus, known as the 'intergenerational cycle of obestiy'. Despite a large body of epidemiological evidence reporting outcomes of obese pregnancies, including offspring respiratory complications, much less is known about the molecular effects of maternal obesity on fetal lung development. This review focuses on the influence of altered substrate supply associated with the obesogenic intrauterine environment on fetal lung development. Understanding the molecular mechanisms contributing to altered fetal lung development will lead to improved respiratory outcomes for offspring at birth and in later life.

Surfactant deficiency in full-term newborns with transient tachypnea delivered by elective C-section.

INTRODUCTION: Previous studies have suggested that full-term newborns delivered by elective cesarean section who develop transient tachypnea have low gastric microbubble counts. In the present study, microbubble concentrations in oral fluid samples were used to evaluate pulmonary maturity. OBJECTIVE: To evaluate lung maturity in full-term newborns delivered by elective caesarean section using the stable microbubble test in oral aspirates collected at birth. METHOD: The study involved newborns with gestational age >37 weeks delivered by elective cesarean section. Oral fluid samples were obtained in the delivery room immediately after birth, and gastric fluid was collected within the first hour of life. Samples were frozen and analyzed by two blinded researchers. RESULTS: The sample comprised 544 newborns. Twenty-two were diagnosed with transient tachypnea of the newborn by the assisting physician, and required admission to the Neonatal Intensive or Intermediate Care Unit. The median (interquartile range) of the number of microbubbles in the oral samples of these patients was 67.5 (45-150) microbubbles/mm(2) . The remaining 498 newborns without respiratory difficulties had a count of 350 (150-750) microbubbles/mm(2) -P < 0.001. Gastric fluid tests revealed a count of 150 (82.5-700) microbubbles/mm(2) for neonates with respiratory difficulties, and of 600 (216-1125) microbubbles/mm(2) -P < 0.05 for those without respiratory symptoms. CONCLUSION: The present results suggest that transient tachypnea of the newborn is associated with surfactant dysfunction. Pediatr Pulmonol. 2016;51:596-600. © 2015 Wiley Periodicals, Inc.

Polymorphism of the angiotensin-converting enzyme gene and angiotensin-converting enzyme activity in transient tachypnea of neonate and respiratory distress syndrome.

BACKGROUND: Transient tachypnea of neonate (TTN) and respiratory distress syndrome (RDS) of the newborn are the most common cause of early respiratory distress in the immediate neonatal period. There is increasing evidence to support the role for the activation of the renin angiotensin system during acute lung injury. OBJECTIVES: The purpose of this study was to determine if there is a relationship between angiotensin-converting enzyme (ACE) I/D polymorphism, ACE activity and TTN and respiratory distress syndromes. METHODS: Nineteen neonates with TTN, 20 neonates with RDS and 21 control infants are studied for ACE polymorphism and serum ACE activity. RESULTS: Twenty six (43.3%) patients have DD polymorphism, 19 (31.7%) patients have ID polymorphism and 15 (25%) patients have II polymorphism. Serum ACE activity is 43.5 ± 1.8 (40-46) U/L in DD, 31.5 ± 2.3 (28-36) U/L in ID and 22.1 ± 2.1(19-46) U/L in II patient. CONCLUSIONS: The study could not find any difference in DD alleles and ACE activity between control group and TTN group. ACE polymorphism was not different between RDS group and control group in this study.