Background: At discharge from neonatal units, many preterm infants are vulnerable to preprandial hypoglycemia due to insufficient liver glucose production. In most preterm infants, hepatic glucose-6-phosphatase activity (the terminal step of liver glucose production) remains abnormally low postnatally.
Objective: To determine what perinatal factors are associated with changes in hepatic glucose-6-phosphatase enzyme activity.
Study design: The maximum velocity (Vmax) of the hepatic microsomal glucose-6-phosphatase enzyme, as the dependent variable, was correlated by stepwise multiple regression analysis with clinical data from a consecutive series of 45 preterm infants from a level 3 neonatal unit.
Results: Significant factors (p < or = 0.0005) were the presence of pathogenic bacteria isolated from maternal high vaginal swabs (p < or = 0.0000), hyperkalemia regimen, duration of prenatal exposure to ritodrine, and delivery mode. Further analysis revealed that the highest correlation was with positive early post-delivery infant bacterial cultures.
Conclusion: Perinatal events and clinical interventions modulate key enzyme systems necessary for human adaptation to extrauterine life.