Which enzyme deficiency can lead to unconjugated hyperbilirubinemia in newborns?

Unconjugated hyperbilirubinemia in newborns is primarily associated with a deficiency in UDP-glucuronyl transferase, an enzyme critical for the conjugation of bilirubin in the liver. This enzyme facilitates the conversion of fat-soluble unconjugated bilirubin into water-soluble conjugated bilirubin, which can then be excreted in bile and urine.

In newborns, especially premature infants, the liver may not yet have fully developed the necessary enzymatic pathways for effective bilirubin conjugation. A deficiency in UDP-glucuronyl transferase means that bilirubin remains unconjugated and accumulates in the blood, leading to hyperbilirubinemia. This condition is often seen in physiologic neonatal jaundice but can become more serious if levels rise too high, requiring intervention.

The other enzymes listed do not play a direct role in the conjugation of bilirubin. Heme oxygenase is involved in the breakdown of heme into bilirubin but does not affect its conjugation. Beta-glucuronidase is an enzyme that can deconjugate bilirubin, potentially exacerbating conditions like cholestasis, but does not cause hyperbilirubinemia directly. Cytochrome P450 enzymes are involved in