Patent ductus venosus does not lead to alimentary galactosaemia in preterm infants

The aim of this study was to investigate if an open ductus venosus representing 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 blood 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). Ultrasound studies of the blood flow in the ductus venosus, truncus coeliacus, superior mesenteric artery and left hepatic vein were performed before and 30 min after the meal. There was a significant rise in blood glucose after 30 and 50 min, indicating a sufficient lactose load. Galactose, however, was either 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 the ductus venosus and superior mesenteric artery after 30 min (p < or = 0.001) indicating increased entero-hepatic and portal-caval shunting.

A patent ductus venosus does not lead to a significant hypergalactosaemia in preterm infants fed human breast milk. Thus, in respect to breast-milk feeding, this is regarded safe in healthy preterm infants even with an open ductus venosus. The increased portal-caval shunting may, however, influence the hepatic metabolism of other enterally absorbed substances.