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txt Introduction The incidence of cholestasis related to total parenteral nutrition (TPN) among preterm infants has been estimated to be between 7% and 85%, depending on the population examined and the definition of cholestasis used [ 1].

In infants with necrotizing enterocolitis or short bowel syndrome, the prevalence of TPN-related cholestasis is 60-90% [ 2].

Although cholestasis is reversible in most patients after the successful advancement of enteral feeding, progressive liver fibrosis and cirrhosis occur in some patients even after complete enteral nutrition has been established [ 3].

Recent studies have supported the hypothesis that generation of reactive oxygen intermediates (ROIs) and elevated lipid hydroperoxides in the liver during cholestasis cause tissue injury.

Furthermore, deposition of lipofuscin, a by-product of lipid peroxidation, characterizes TPN-induced cholestasis in preterm infants [ 17].

The purpose of these studies was to determine whether TPN-induced cholestasis in preterm newborn infants is associated with increased oxidative stress secondary to increased ROIs.

The criteria for entry into the cholestasis group were direct bilirubin >2 mg/dl (34.

During this period, 36 infants qualified for the cholestasis group, and informed consent was obtained from the parents of 27.

When each eligible infant with cholestasis was enrolled, a preterm infant without cholestasis was matched for gestational age, birth weight, and severity of respiratory illness, and the parents' informed consent was requested to enroll, the infant as a control subject.

For the 27 infants enrolled in the cholestasis group, matched controls were identified for 24.

Results Twenty-seven infants were enrolled in the cholestasis group and 16 infants served as controls.

The cholestasis and control groups were not significantly different with respect to gestational age (29.

2 days of age in the cholestasis group and 38.

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