Which syndrome involves an inability of hepatocytes to secrete conjugated bilirubin into bile?

Dubin-Johnson syndrome is characterized by an inability of hepatocytes to excrete conjugated bilirubin into the bile, leading to its accumulation in the liver and the bloodstream. This condition is caused by a defect in the multidrug resistance protein 2 (MRP2), which is responsible for the transport of conjugated bilirubin into bile canaliculi. As a result, individuals with Dubin-Johnson syndrome often present with increased levels of conjugated bilirubin in their serum, which can lead to a mild jaundice but usually does not result in severe liver dysfunction or significant complications.

In contrast, Gilbert's syndrome involves a reduced ability of the liver to conjugate bilirubin due to a deficiency of the enzyme glucuronosyltransferase, leading primarily to an increase in unconjugated bilirubin, not conjugated. Crigler-Najjar syndrome also pertains to a deficiency in the conjugation process, specifically affecting the enzyme responsible for converting unconjugated bilirubin into conjugated bilirubin, rather than the excretion of conjugated bilirubin. Wilson's disease is a disorder of copper metabolism that primarily affects the liver but is unrelated to bilirubin transport. Thus, the key feature of Dubin-Johnson syndrome makes