|M.Sc Student||Keren Rinat|
|Subject||Expression of Surfactant Proteins in Newborn Infants|
with Respiratory Distress Syndrome (RDS)
|Department||Department of Medicine||Supervisors||Mr. Zalman Weintraub|
|Dr. Miriam David|
|Assistant Professor Fuad Fares|
Deficiency of pulmonary surfactant is the principle cause of neonatal Respiratory Distress Syndrome (RDS). A major complication of RDS is Bronchopulmonary Dysplasia (BPD). Inability to produce surfactant protein B (SP-B) causes lethal RDS. A common SP-B mutation is the 121ins2. It was found on both alleles in approximately two thirds of SP-B-deficient patients due to early termination of translation. Recently, a 122delT mutation in SP-B gene was found associated with RDS. Polymorphism of the SP-A gene may also related to RDS. Our study examines the relationship between SP-A and SP-B levels to gestational age, RDS severity and later development of BPD. We also screened for mutations in SP-B gene in neonates in Israel.
The study population consisted of 60 preterm infants and 8 term infants. SP-A and SP-B levels were measured in bronchial lavage using ELISA. 121ins2 and 122delT mutations in SP-B gene were screened in patients who had low levels of SP-B. There was no correlation between SP-A and SP-B levels to gestational age (GA). However, in the group of infants born later than 28 weeks gestation there was some correlation between GA and SP-A levels only. In infants below 28 weeks gestation, there was inverse correlation between SP-B levels and GA. Only in infants with birth weight above 1000 g. SP-A and SP-B correlated directly with birth weight. The proteins levels increased slightly during the first 5-10 days. Higher levels of SP-A and SP-B were related to lower Mean Airway Pressure. No correlation was found between the initial proteins levels and the incidence and severity of BPD. No mutations in SP-B gene were found in the 8 term infants with severe RDS.