Can the administration of antithrombin III decrease the risk of cerebral hemorrhage in premature infants?

This study was carried out to determine whether the administration of antithrombin III decreases the risk of intraventricular hemorrhage in premature infants. In a randomized study, 60 infants born before 30 weeks of gestation were assigned to receive a loading dose of antithrombin III or placebo. There was no significant difference in the incidence of intraventricular hemorrhage between the antithrombin III and the placebo group (27.5 vs. 32%). Partial thromboplastin time, Quick's prothrombin time and platelet count were also not significantly different between the 2 groups. We conclude that the administration of antithrombin III during the first 2 days of life does not decrease incidence of intraventricular hemorrhage. Antithrombin III is a very expensive therapy and its benefits should be carefully investigated before being recommended as valuable therapy.

Increased levels of malondialdehyde and nitrite/nitrate in the blood of asphyxiated newborns: reduction by melatonin.

Free radicals have been implicated in the pathogenesis of neonatal asphyxia and its complications. This study measured a product of lipid peroxidation, malondialdehyde, and the nitrite/nitrate levels in the serum of 20 asphyxiated newborns before and after treatment with the antioxidant melatonin given within the first 6 hr of life. Ten asphyxiated newborns received a total of 80 mg of melatonin (8 doses of 10 mg each separated by 2-hr intervals) orally. One blood sample was collected before melatonin administration and two additional blood samples (at 12 and 24 hr) were collected after giving melatonin. A third group of healthy newborn children served as controls. Serum malondialdehyde and nitrite+nitrate concentrations in newborns with asphyxia before treatment were significantly higher than those in infants without asphyxia. In the asphyxiated newborns given melatonin, there were significant reductions in malondialdehyde and nitrite/nitrate levels at both 12 and 24 hr. Three of the 10 asphyxiated children not given melatonin died within 72 hr after birth; none of the 10 asphyxiated newborns given melatonin died. The results indicate that the melatonin may be beneficial in the treatment of newborn infants with asphyxia. The protective actions of melatonin in this study may relate to the antioxidant properties of the indole as well as to the ability of melatonin to increase the efficiency of mitochondrial electron transport.

Pulmonary atresia with ventricular septal defect: prevalence of deletion 22q11 in the different anatomic patterns.

BACKGROUND: Pulmonary atresia with ventricular septal defect (PA-VSD) is one of the most common cardiac defects associated with DiGeorge syndrome. The pattern of the pulmonary circulation determines the complexity of this type of heart disease. The aim of this study was to establish the prevalence of DiGeorge syndrome with deletion 22q11 in patients with simple and complex PA-VSD. METHODS: Since 1993 we have studied 128 consecutive patients affected by PA-VSD. In 90 of our patients the PA-VSD was considered "simple" (group I), because it was not associated with any other cardiac defects. In the other 38 children the PA-VSD was considered "complex" (group II) owing to the presence of heterotaxia, tricuspid atresia, a double-inlet left ventricle, transposition of the great arteries and congenitally corrected transposition of the great arteries. RESULTS: In group I, 38 patients (42%) had genetic syndromes or major extracardiac anomalies; deletion 22q11 was detected in 31% of cases. Major aortopulmonary collateral arteries were present in 50% of group I patients and in 57% of those with deletion 22q11. In group II, 10 patients (26%) had genetic syndromes or major extracardiac anomalies but none had deletion 22q11 (p < 0.005); in no case was the presence of major aortopulmonary collateral arteries observed (p < 0.005). CONCLUSIONS: PA-VSD is an anatomically and morphogenetically heterogeneous disease: in the setting of DiGeorge syndrome or velocardiofacial syndrome, PA-VSD is associated with a peculiar cardiac pattern and is due to deletion 22, whereas in case of nonsyndromic PA-VSD or when this disease is associated with different syndromes or with other types of cardiac defects, it is due to other morphogenetic mechanisms.