PHOSPHATIDYLGLYCEROL STUDY AS FETAL LUNG MATURATION PARAMETER AFTER DEXAMETHASONE ADMINISTRATION FOR WOMEN AT RISK OF PRETERM BIRTH

Phosphatidylglycerol is an important indicator of fetal lung maturation, which plays a role in stabilizing surfactant lipoprotein complex. Corticosteroid antenatal can stimulate the synthesis of pulmonary surfactant in infants with preterm birth. The objective of this study is to examine the phosphatidylglycerol levels as fetal lung maturation parameter after dexamethasone administration in women with preterm birth compared to L/S ratio parameter. This study was prospective longitudinal (cohort). The samples were pregnant women with preterm birth risk at 28-34 weeks gestation getting the therapy of antenatal dexamethasone 6 mg IM every 12 hours given 4 times in 48 hours. The samples were 17 patients. Determination of L/S ratio and PG levels was performed by ELISA. The study was conducted from May - November 2015 and reviewed to obtain ethics eligibility permit by the research ethic committees of Dr. Soetomo General Hospital. The results show that the mean value of L/S ratio is 2.28 with a range of 1.35 to 9.06 and the mean of PG level is 1.17 with a range from 0 to 3.79. L/S ratio and PG show no significant relationship between the two of them. Increased levels of PG on the gestational age of 28-32 weeks have not demonstrated clinically significant changes yet. The highest PG level occurs in the gestational age of 32-34 weeks.

Lymphatic function is required prenatally for lung inflation at birth

Mammals must inflate their lungs and breathe within minutes of birth to survive. A key regulator of neonatal lung inflation is pulmonary surfactant, a lipoprotein complex which increases lung compliance by reducing alveolar surface tension (Morgan, 1971). Whether other developmental processes also alter lung mechanics in preparation for birth is unknown. We identify prenatal lymphatic function as an unexpected requirement for neonatal lung inflation and respiration. Mice lacking lymphatic vessels, due either to loss of the lymphangiogenic factor CCBE1 or VEGFR3 function, appear cyanotic and die shortly after birth due to failure of lung inflation. Failure of lung inflation is not due to reduced surfactant levels or altered development of the lung but is associated with an elevated wet/dry ratio consistent with edema. Embryonic studies reveal active lymphatic function in the late gestation lung, and significantly reduced total lung compliance in late gestation embryos that lack lymphatics. These findings reveal that lymphatic vascular function plays a previously unrecognized mechanical role in the developing lung that prepares it for inflation at birth. They explain respiratory failure in infants with congenital pulmonary lymphangiectasia, and suggest that inadequate late gestation lymphatic function may also contribute to respiratory failure in premature infants.