Case 6: Protease Inhibitor-Associated Hyperbilirubinemia

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	The patient’s presentation is most consistent with atazanavir-associated hyperbilirubinemia. The ritonavir should be discontinued and the hyperbilirubinemia should then completely resolve.

This answer is incorrect. The patient’s presentation is consistent with atazanavir-associated hyperbilirubinemia. Although this appears to be a dose-dependent effect and may occur with higher frequency with ritonavir boosting, it is not clear that removal of ritonavir reliably improves the jaundice resulting from atazanavir. Moreover, ritonavir-boosting of atazanavir is required in patients also taking tenofovir (Viread) or efavirenz (Sustiva).

	The patient’s chronic hepatitis B predisposes him to the isolated atazanavir-associated hyperbilirubinemia. Approximately 50% of patients with chronic hepatitis B virus infection will develop hyperbilirubinemia when starting atazanavir.
	Atazanavir causes hyperbilirubinemia via competitive inhibition of a key enzyme involved in bilirubin conjugation; patients with Gilbert’s syndrome are more likely to develop jaundice and severe hyperbilirubinemia when exposed to atazanavir or indinavir than those who do not have Gilbert’s syndrome.
	The differential for the jaundice includes hemolytic anemia from dapsone. The diagnosis of dapsone-associated hemolytic anemia can be made with certainty if the bilirubin is fractionated and found to be mostly unconjugated.

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