What is a potential cause of neonatal physiological jaundice of the hepatic type?

Neonatal physiological jaundice is a common condition in newborns characterized by elevated levels of bilirubin in the blood. The hepatic type of this jaundice specifically relates to the newborn's immature liver function and its inability to effectively conjugate bilirubin.

A deficiency in the bilirubin conjugation enzyme system, particularly the enzyme UDP-glucuronosyltransferase, is a well-recognized cause of this condition. In neonates, this enzyme is often underdeveloped, leading to an accumulation of unconjugated bilirubin. As a result, the liver fails to convert this fat-soluble bilirubin into a water-soluble form that can be excreted in bile. This deficiency usually resolves as the liver matures, typically within the first week of life.

The other options do not pertain to the hepatic type of jaundice as directly. For instance, hemolytic episodes (due to ABO or Rh incompatibilities) result in increased production of bilirubin due to the breakdown of red blood cells. While these conditions certainly contribute to neonatal jaundice, they primarily cause hemolytic jaundice rather than physiological jaundice linked to hepatic maturation. Similarly, structural abnormalities of the common bile duct can lead to obstructive jaundice rather