The aim of this study was to assess the effects of intravenous co-administration of ibuprofen-lysine on the pharmacokinetics of amikacin during the first days of life in preterm infants. The pharmacokinetics of amikacin were retrospectively calculated in a cohort of 73 neonates (gestational age <31 weeks) who received either ibuprofen-lysine or placebo following inclusion in the multicentre ibuprofen prophylaxis study. Assuming a one-compartment model with instantaneous input and first-order output, there was no significant difference in the median distribution volume (0.63 vs. 0.59 liters/kg), but the median serum half-life (16.4 vs. 12.4 h) of amikacin was significantly longer (p < 0.02), and the clearance (0.36 vs. 0.6 ml/kg/min; p < 0.005) of amikacin was significantly lower in infants who received ibuprofen-lysine. We conclude that the time interval between consecutive amikacin administrations should be prolonged, if ibuprofen-lysine is co-administered.

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Clara cell protein (CC16) is a 16-kD protein secreted at the surface of respiratory airways by nonciliated bronchial and bronchiolar cells, including Clara cells. Using the same immunoassay as that recently developed for CC16 in lung lavage, we have measured CC16 in amniotic fluid samples from 100 normal fetuses and 51 fetuses with various pathologies. Ouchterlony immunodiffusion analysis showed a complete identity between CC16 in amniotic fluid and the protein in lung lavages of adults. CC16 was detectable in amniotic fluid from about the 15th wk of pregnancy, then progressively increased until delivery, with a tendency to reach a plateau after the 30th wk. Between the 15th and the 39th wk of pregnancy, the concentration of CC16 in amniotic fluid increased on average 25 times. The sex of the fetus did not influence the concentration of CC16 in amniotic fluid. Compared with expected values, levels of CC16 in amniotic fluid were on average not significantly altered in cases of spina bifida (n = 9), anencephaly (n = 7), and trisomy 21 (n = 6). In contrast, CC16 was on average significantly decreased in cases of diaphragmatic hernia (n = 6), trisomy 18 (n = 14), Turner syndrome (n = 4), and diabetic pregnancy (n = 5). In cases of diaphragmatic hernia, a relation emerged between the concentration of CC16 in amniotic fluid and both the weight of the lungs and the survivorship of the fetuses. The time course of CC16 in amniotic fluid during normal pregnancy and its reduction in pathologies associated with lung hypoplasia suggest that CC16 in amniotic fluid might serve as a marker of bronchial epithelium growth. (Pediatr Res 36: 771-775, 1994)

Childhood obesity prevalence is rising in countries worldwide. A variety of etiologic factors contribute to childhood obesity but little is known about underlying biochemical mechanisms. We performed an individual participant meta-analysis including 1,020 pre-pubertal children from three European studies and investigated the associations of 285 metabolites measured by LC/MS-MS with BMI z-score, height, weight, HOMA, and lipoprotein concentrations. Seventeen metabolites were significantly associated with BMI z-score. Sphingomyelin (SM) 32:2 showed the strongest association with BMI z-score (P = 4.68 × 10−23) and was also closely related to weight, and less strongly to height and LDL, but not to HOMA. Mass spectrometric analyses identified SM 32:2 as myristic acid containing SM d18:2/14:0. Thirty-five metabolites were significantly associated to HOMA index. Alanine showed the strongest positive association with HOMA (P = 9.77 × 10−16), while acylcarnitines and non-esterified fatty acids were negatively associated with HOMA. SM d18:2/14:0 is a powerful marker for molecular changes in childhood obesity. Tracing back the origin of SM 32:2 to dietary source in combination with genetic predisposition will path the way for early intervention programs. Metabolic profiling might facilitate risk prediction and personalized interventions in overweight children.