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Objective: To measure the oxidant/antioxidant status of newborn babies with oesophageal atresia and their mothers, compared with healthy control subjects., Methods: This case-control study included 40 participants: 10 newborns with oesophageal atresia and their mothers, and 10 healthy newborns and their mothers. Whole blood malondialdehyde (MDA) levels and the activities of antioxidant enzymes (catalase, carbonic anhydrase [CA], glucose-6-phosphate dehydrogenase [G-6-PD], and superoxide dismutase [SOD]) were measured., Results: MDA levels and CA activity were significantly higher, and catalase, SOD and G-6-PD activities were significantly lower, in newborns with oesophageal atresia and their mothers than in healthy newborns and their mothers. Although CA activity was similar between the newborns and mothers in the patient group, it was significantly lower in newborns than in mothers in the healthy group., Conclusions: Increased lipid peroxidation might play an important role in the pathogenesis of oesophageal atresia. Impairment of the free radical/antioxidant balance may lead to increased free radical and decreased antioxidant levels in oesophageal atresia.

A unique case of newborn biliary atresia associated with esophageal atresia and tracheoesophageal fistula, ano-rectal atresia, Reovirus type 3 infection and an early switch of fetal into adult hemoglobin is reported. At birth, the infant, who had only one umbilical artery, was operated on by primary anastomosis of the esophagous, and descending colostomy. At six weeks of age the baby underwent a "Kasai hepatic portoenterostomy-Type I" for a EHBA Type III, Subtype C2, Subgroup O ("aplasia" of all extrahepatic biliary ducts, including the gallbladder). The absence of an artery branch for the left lobe of the liver was observed. Histologically, the liver showed a hyperplasia of the intrahepatic bile ducts due to persistence of an excess of embryologic bile ducts in "ductal plate malformation" (DPM). Specific Reovirus type 3 antibodies were found in both the mother's and baby's sera. In the postoperative period the infant developed rapid and severe liver failure and underwent a successful liver transplantation. Although in most cases EHBA appears to be a perinatal event due to a necro-inflammatory process of unknown etiology, cases associated with complex extrahepatic anomalies, may be due to different pathogenetic mechanisms supported by different causative agents operating very early in the fetal period. Viral infection seems to be the most reliable etiology.

This study was undertaken to evaluate the relationship between maternal serum alpha-fetoprotein (MSAFP) levels and oesophageal atresia (OA). OA occurred in 16 fetuses of mothers who had an MSAFP test in the study interval. The multiple of the median (MOM) value for MSAFP averaged 1.54 +/- 0.65 (range 0.5-2.9 MOM), which was significantly higher than the value seen in controls. The median MOM was 1.35. Using a cut-off of 2.5 MOM, the sensitivity of MSAFP for detecting OA was 19 per cent. Although OA should be considered in the differential diagnosis of an elevated MSAFP level, MSAFP cannot be considered an appropriate screening test for OA given the low sensitivity.

To investigate extraesophageal anomalies in infants with esophageal atresia, preoperative plasma gastrin was measured in 12 infants. The median plasma gastrin was 32 ng/L (interquartile range, 24 to 44). There was significant correlation with birth weight (rs = .73, P less than .05) and gestational age (rs = .74, P less than .05). Within this group 9 infants of greater than 36 weeks' gestation were matched to a group of 20 control infants without esophageal atresia. Infants with esophageal atresia had a significantly lower median plasma gastrin (38 ng/L v 55 ng/L, P less than .05). This may indicate preexisting vagal abnormalities in esophageal atresia unrelated to surgical intervention.

The human fetus swallows a considerable amount of amniotic fluid which appears to be in balance with the urine output. Since amniotic fluid intake is considered to be compromised in fetuses with atresia of the upper gastrointestinal tract, glomerular function development in such infants may be delayed. Plasma creatinine level determined in 6 neonates with atresia of the upper gastrointestinal tract was similar to the level measured in neonates with lower obstruction, and both groups were within the range of values obtained during other studies in normal newborns. Glomerular functional development is probably not affected in neonates with atresia of the upper gastrointestinal tract.

A subnormal maternal serum alpha-fetoprotein level associated with elevated alpha-fetoprotein level in amniotic fluid was found in a case of trisomy 21 combined with esophageal atresia in a fetus at 36 + 5 weeks of gestation. The significance of this observation is discussed in view of the possible biologic mechanisms resulting in maternal serum alpha-fetoprotein reduction in cases of fetal autosomal trisomies. The most likely hypotheses seem to be a reduced fetal alpha-fetoprotein production and/or an alteration of the placental regulation of the alpha-fetoprotein transfer from fetal to maternal blood via the placenta.

A blood group change from A2 to Ax is described in a boy who had Fallot's tetralogy, oesophageal atresia, and a tracheo-oesophageal fistula. The change of blood group created a transfusion problem. The unusual serology is discussed.

The preliminary results of the use of high frequency positive pressure ventilation (HFPPV) in six newborn infants presenting a type III oesophageal atresia during the thoracic stage of surgical repair are reported. HFPPV allowed correct gas exchange during the surgical procedure. In the six cases, a significant decrease in PaCO2 (p less than 0.05) was observed, whereas the effects on PaO2 were variable. The technical problems, mechanism of gas transport during HFPPV and clinical interest of HFPPV in thoracic surgery are discussed.