Necrotizing enterocolitis in the first 24 hours of life.

Necrotizing enterocolitis (NEC) is commonly thought of as occurring in the sick premature infant, usually in the first one to two weeks of life. A review of NEC at the Children's Hospital of Denver over a 5-year period, found that 13 of 79 infants (16.1%) had onset of NEC during the first day of life. These infants were larger (mean birth weight 2,624 +/- 849 g), more mature (mean gestational age 37.9 +/- 2.5 weeks), and less asphyxiated as judged by Apgar scores (mean five-minute score 8.15 +/- 1.07) than infants with onset of NEC after the first day of life (mean birth weight 1,519 +/- 586 g, mean gestational age 32.0 +/- 3.5 weeks, P less than .001, and mean five-minute Apgar score 6.81 +/- 1.84, P less than .05). Despite their large size and degree of maturity, eight of these infants (62%) showed signs of respiratory distress; four (31%) were polycythemic; four (31%) had either a partial or double-volume exchange transfusion performed; and 11 (85%) were fed prior to developing NEC. Presenting signs of disease, occurrence of sepsis (31%), requirement for surgical intervention (62%), and mortality (30%) were similar for the two groups of infants. It is suggested that term and near-term infants who have significant illness after delivery be treated more like their premature counterparts with cautious introduction of feedings after an adequate period of stabilization.

Effects of cimetidine on theophylline, acetaminophen, and zoxazolamine toxicity in the intact mouse.

3-Methylcholanthrene treatment of C57BL/6N mice induces significant amounts of cytochromes P1-450, whereas P1-450 levels in 3-methylcholanthrene-treated DBA/2N mice are no different from those in control C57BL/6N or DBA/2N mice. Comparison of 3-methylcholanthrene-treated C57BL/6N and DBA/2N mice thus provides a convenient means of determining the role of P1-450 metabolism in two strains of mice following identical drug treatment regimens. 3-Methylcholanthrene-induced P1-450 is shown to be more effective than other forms of P-450 in detoxifying theophylline and zoxazolamine and in enhancing the toxicity of acetaminophen. Cimetidine in vivo blocks these metabolic pathways, resulting in increased toxicity of theophylline and zoxazolamine and protection against acetaminophen toxicity. These data illustrate the double-edged sword nature of P1-450 metabolism and the possibility of a paradoxical effect of cimetidine during drug-drug interactions in vivo. Cimetidine is shown to inhibit in vivo and in vitro the metabolism by both 3-methylcholanthrene-induced P1-450 and control forms of P-450; these data suggest that cimetidine may be acting at the level of P-450 reduction by NADPH-P-450 oxidoreductase. This same mechanism of action has been previously suggested for ellipticine.