06-P056 Acetylation and neural tube defects

Background: Gastroschisis is a congenital malformation characterized by the extrusion of the fetal bowel during intrauterine life, secondary to a defect in anterior abdominal wall. Objective: To establish an experimental model of gastroschisis in fetuses of rats exposed to acetylsalicylic acid (ASA), during pregnancy. Methods: Wistar rats were treated with an oral single ASA dose of 50, 500, 750 or 1000 mg/kg of maternal body weight on 6th, 9th or 12th days of gestation; with distilled water (group sham) and no treated (group control). It was evaluated the number of live, dead and reabsorbed fetuses, the weight and length of the fetuses and identified individuals with external malformations. Results: At dose of 500 mg was observed incidence of 18.3% of gastroschisis while at 1000 mg dose this value was 31.6%, demonstrating that increasing the dose causes an increase in the teratogenic potential of ASA. The dose of 50 mg, which reproduces the pharmacological effect in humans, was related to the occurrence of omphalocele in 7 fetuses. The 750 mg group had more fetuses reabsorbed; all groups with ASA had more omphalocele than sham and control groups. Only the group of 1000 mg on the 12th day of pregnancy had polydactyly; groups with 500 and 1000 mg had more gastroschisis. Conclusions: There was a predominance of abnormalities in the wall defect (gastroschisis and omphalocele) and present at all doses of ASA administered. The higher doses than the physiological dose showed other malformations described in a few previous studies, as polydactyly.