Open AccessImpaired hepatic drug and steroid metabolism in congenital adrenal hyperplasia due to P450 oxidoreductase deficiency
Author(s) -
Dorota TomalikScharte,
Dominique Maiter,
Julia Kirchheiner,
Hannah E Ivison,
Uwe Fuhr,
Wiebke Arlt
Publication year - 2010
Publication title -
european journal of endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.897
H-Index - 148
eISSN - 1479-683X
pISSN - 0804-4643
DOI - 10.1530/eje-10-0764
Subject(s) - endocrinology , medicine , congenital adrenal hyperplasia , in vivo , drug metabolism , cyp2d6 , cytochrome p450 , cyp3a4 , pharmacology , glucocorticoid , cyp3a , biology , metabolism , genetics
Patients with congenital adrenal hyperplasia due to P450 oxidoreductase (POR) deficiency (ORD) present with disordered sex development and glucocorticoid deficiency. This is due to disruption of electron transfer from mutant POR to microsomal cytochrome P450 (CYP) enzymes that play a key role in glucocorticoid and sex steroid synthesis. POR also transfers electrons to all major drug-metabolizing CYP enzymes, including CYP3A4 that inactivates glucocorticoid and oestrogens. However, whether ORD results in impairment of in vivo drug metabolism has never been studied.
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