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The origin of this virilization may be due to an impairment of P450aro (aromatase) activity, a POR-dependent microsomal P450 encoded by CYP19A1 gene, resulting in a decrease in estrogen production ( Figure 3 ). Another hypothesis is that fetal and maternal virilization in POR deficiency is due to increased gonadal DHT synthesis through an alternative ‘backdoor’ pathway ( Figure 4 ), in which 21-carbon steroid precursors are 5α-reduced and converted to DHT, bypassing the conventional precursors, androstenedione and testosterone ( Auchus, 2004 ). These broad phenotypes of POR deficiency may be due to different mutations in the POR protein, which affect the electron transfer to its partners at different degrees, and/or the same POR mutation that affects the activity of different P450 partners at different degrees since their interaction might differ ( Flück and Pandey, 2014 ), elixir steroids for sale. Thus, diagnosis of POR deficiency based on clinical features is difficult, and an analysis of plasma or urinary steroid profiles may assist in diagnosis. However, a final proof of POR deficiency relies on genetic testing.
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