INTRAUTERINE DISTRESS IMPAIRS LACTOSE ABSORPTION IN THE FULL TERM INFANT

Abstract

Meconium staining of the amniotic fluid or fetus is considered to be indicative of fetal distress. Although many infants with meconium stained amniotic fluid exhibit no signs of depression, some brief period of asphyxia may have induced passage of meconium prior to delivery. This study was designed to determine if passage of meconium in utero is associated with increased lactose malabsorption. Eighteen full term infants were studied for lactose malabsorption by breath hydrogen (H₂) testing. Breath H₂ samples were obtained through a nasopharyngeal catheter after a formula feeding. Samples were obtained preprandially and then 30, 60, 90, 150, and 180 minutes postprandially. The samples were obtained at 7 days of age to insure colonic bacterial colonization. Seven of the 18 infants were meconium stained at birth. The Apgar scores and the clinical courses of the two groups were similar. Meconium stained infants showed significantly increased breath H₂ production. Mean breath H₂ production level in the meconium stained infants was 24.14 ppm compared to 4.02 ppm in the non-meconium stained infants. Intrauterine asphyxia may impair mesenteric blood flow leading to intestinal mucosal damage and increased lactose malabsorption.

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