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Urinary trypsin inhibitor present in fetal urine prevents intraamniotic meconium-induced intestinal damage in gastroschisis.

BACKGROUND/PURPOSE: Contact with amniotic fluid causes intestinal damage in gastroschisis, and intraamniotic meconium has been shown to be responsible. Meconium has been shown to contain a significant amount of IL-8, which may be the responsible cytokine for harmful effects of meconium. Neonatal urine contains high amount of urinary trypsin inhibitor (UTI) compared with adult human urine. Urinary trypsin inhibitor has been shown to exert inhibitory effects on IL-8. Therefore, far from being destructive, presence of fetal urine in the amniotic fluid might be beneficial because human urine contains UTI. An experimental study has been performed to investigate whether presence of intraamniotic human urine (consequently UTI) besides meconium is beneficial on intestines of chick embryo with gastroschisis.

METHODS: Five-day-old fertilized chick eggs were used. Gastroschisis was created through amniotic cavity without opening the allantoic cavity. Sterile urine and meconium were obtained from newborn humans. Study was conducted in 2 stages. In the first stage, gastroschisis was created, and meconium suspensions at minimal harmful meconium concentration were prepared using natural and denatured human neonatal urine and instilled into the amniotic cavity. In the second stage of study, various concentrations of UTI plus meconium suspension at minimal harmful meconium concentration was instilled into the amniotic cavity.

RESULTS: Serosal thickening, inflammation, and focal fibrin deposits were observed in intestines of the groups with meconium and meconium in denatured urine. Histopathologic features of intestines of the group with meconium in natural urine did not differ from the intestines of the control group. Histopathologic examination of intestines of groups with meconium and meconium plus 50 U/mL UTI showed serosal thickening, inflammation, focal fibrin, and collagen deposits. Histopathologic features of intestines of the groups with 1:400 intraamniotic meconium plus 100 and 200 U/mL UTI did not differ from the intestines of control group.

CONCLUSION: Urinary trypsin inhibitor 100 U/mL prevented the intestinal damage via inhibiting IL-8, which is contained by 1:400 concentration of meconium. Therefore, besides the existence of threshold level of meconium, the existence of UTI, which is capable of inhibiting IL-8 contained by threshold level of meconium, may be a factor in the occurrence of intestinal damage in gastroschisis.

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