Drugs affecting the exchange of bilirubin
Last reviewed: 23.04.2024
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Medications can affect any stage of bilirubin metabolism. Such reactions can be predicted, they are reversible and in adults flow easily. However, in newborns with increased levels of unconjugated bilirubin, bilirubin encephalopathy (nuclear jaundice) is possible in the brain. It is enhanced by the influence of drugs such as salicylates or sulfonamides, which compete with bilirubin for binding sites on albumin. In adults with Gilbert's syndrome, chronic active hepatitis, or primary biliary cirrhosis (PBC), drugs that affect bilirubin metabolism increase bilirubinemia.
The load of bilirubin on liver cells is enhanced by hemolytic drug reactions. Hemolysis is usually combined with allergic reactions that impair the function of the liver cells. Such reactions can be observed in the treatment of sulfonamides, phenacetin and quinine. These drugs can also cause hemolysis in persons with G-6-FD deficiency.
Reactions can develop on drugs coming in with the mother's milk. Toxic effects of synthetic vitamin K preparations in newborns may partly be due to increased hemolysis.
Some drugs affect the capture of bilirubin by the hepatocyte and its intracellular transport. These include contrast agents for cholecystography and rifampicin. Newborns may have a low content of transport proteins, which causes sensitivity to drugs that compete with bilirubin for a place on the transport protein. These drugs will enhance nuclear jaundice.
Medications that affect tubular excretion of bilirubin, such as sex hormones, can cause cholestasis.
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