Patent ductus venosus does not lead to alimentary galactosaemia in preterminfants

The aim of this study was to investigate if an open ductus venosus represen ting a portal-caval shunt can lead to transient "alimentary galactosaemia" in preterm infants fed human breast milk. Twenty-six preterm infants (28-34 wk of gestational age) with open ductus venosus were included. Capillary b lood samples for measurement of galactose and glucose were collected before , 30 and 50 min after a meal with breast milk (range 12-23 mL/kg). Ultrasou nd studies of the blood flow in the ductus venosus, truncus coeliacus, supe rior mesenteric artery and left hepatic vein were performed before and 30 m in after the meal. There was a significant rise in blood glucose after 30 a nd 50 min, indicating a sufficient lactose load. Galactose, however, was ei ther not detectable or was just above the detectable limit (0.1-0.4 mmol/L) , with no changes after the meal. An increased flow velocity was found in t he ductus venosus and superior mesenteric artery after 30 min (p less than or equal to 0.001) indicating increased entero-hepatic and portal-caval shu nting. Conclusion: A patent ductus venosus does not lead to a significant hypergal actosaemia in preterm infants fed human breast milk. Thus, in respect to br east-milk feeding, this is regarded safe in healthy preterm infants even wi th an open ductus venosus. The increased portal-caval shunting may, however , influence the hepatic metabolism of other enterally absorbed substances.