Carnitine in adolescents.

Carnitine, abundant in muscle and other tissues, is normally synthesized from lysine. Its major metabolic role is transport of long-chain fatty acids into muscle where beta oxidation takes place. Normative data are available for carnitine levels, but few studies define carnitine of specific age groups. This report provides data on normal male and female adolescents in relationship to age and pubertal status. The population consisted of adolescents between 10 and 18 years, seen either for routine health maintenance or minor illnesses. Concentrations of carnitine in plasma were determined by radioisotype enzyme assay. The overall mean was 45.3 +/- 8.9 mumol/L for free carnitine. There was a trend of decreasing free carnitine with increasing Tanner stage. Among the females, there was a statistically significant correlation with both age and Tanner stage. In contrast, the data for males indicated no statistically significant correlation. The data provided standards for the evaluation of carnitine status in normal adolescents. Total carnitine in plasma ranged from 43.2 to 55.9 mumol/L and was virtually all free carnitine. The significant negative correlation of concentration of free carnitine with age and pubertal stage in females was interesting, although not of clinical importance. It suggests the possibility of female hormonal influence associated with puberty.

Antenatal origin of neurologic damage in newborn infants. I. Preterm infants.

Currently, the diagnosis of white matter necrosis may be performed with echoencephalography when cysts are observed in the white matter adjacent to the lateral ventricles. One hundred twenty-seven infants with a gestational age less than 36 weeks (mean [+/- SE] gestational age = 31 +/- 3.2 weeks) were studied in the neonatal period with echoencephalography to determine the incidence of white matter necrosis and the perinatal variables associated with this complication. Twenty-three infants (18.3%) had white matter necrosis. Thirteen (10.3%) had cysts by day 3 (11 on day 1), indicating that the onset of white matter necrosis occurred antenatally. The incidence of antenatal white matter necrosis was inversely related to birth weight and was more frequent in infants weighing less than 1000 gm (19%). Stepwise logistic regression analysis of 31 antenatal variables showed that placental vascular anastomoses in multiple pregnancies, funisitis, and purulent amniotic fluid were the only complications associated with antenatal white matter necrosis. Follow-up neurologic evaluations were abnormal in four of six patients with antenatal white matter necrosis. The findings in this study focus attention on prenatal, rather than intrapartum and postnatal, factors as causative agents of neurologic morbidity and emphasize the importance of early and sequential evaluation of neonatal brain structures.