Heparin-induced inhibition of 1,25-dihydroxyvitamin D formation

Abstract

vise intrauterine transfusion because of the suspicion that normal clearance of the amniotic fluid bilirubin may be impeded by the presence of duodenal atresia, which keeps amniotic fluid bilirubin high. This theory has been previously published without case studies.’ Sources of error in amniotic fluid spectrophotometry included blood, maternal or fetal, meconium, urine, ascitic fluid, and congenital anomalies, such as anencephaly, duodenal atresia, jejunal atresia, and tracheoesophageal fistula. This report confirms that suspicion. It is believed that the bilirubin which enters the amniotic fluid returns to the fetal circulation and subsequently to the placenta by fetal swallowing and absorption from the fetal gastrointestinal tract.’ In cases of upper intestinal obstruction in the fetus, this amniotic fluid clearance of indirect bilirubin is impeded, with resulting abnormal AOD rises in amniotic fluid. To our knowledge, this is the first reported case of abnormal amniotic fluid AOD at 450 rnp with evidence of fetal duodenal atresia. The recently increasing incidence of amniocentesis for various reasons will undoubtedly create situations in which similar findings are observed, and, if so, the suspicion of fetal abnormalities should be raised in the absence of isoimmunization. Investigations done after delivery confirmed the absence of intrauterine or extrauterine hemolysis. The mild hyperbilirubinemia observed in this infant was the result of prematurity. Upper intestinal obstruction in the fetus may cause abnormal amniotic fluid spectrophotometric findings, and this should be taken into account when management of such cases is planned. Intrauterine transfusions in these cases are unnecessary and may be dangerous.