Abstract
Dubin–Johnson syndrome is a worldwide prevalent familial conjugated hyperbilirubinaemia. The identification of multidrug resistance-associated protein 2 provided an understanding of the complex metabolic impairment involved in this syndrome. We report the first family with modified clinical expression of Dubin–Johnson heterozygous state due to genotypic interaction with co-inherited β and δβ thalassaemia, an interaction that has never been described.
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