Decreased serum cortisol levels stimulate ACTH release via negative feedback. The adrenal glands undergo hypertrophy, apparently because of ACTH-stimulated production of insulinlike growth factor–2 (IGF-2). Increased ACTH secretion also produces overproduction of both the adrenal steroids preceding the missing enzyme and those not requiring the missing enzyme (ie, build-up of compounds both before the block and ”sideways” from the block). Treatment with exogenous glucocorticoid results in decreased ACTH secretion and subsequent suppression of the overproduced steroids. An 8-kilobase (kb) gene, HSD3B2 , located on the p11-13 region of chromosome 1 encodes 3-beta–hydroxysteroid dehydrogenase. [3] Two isoenzymes of 3-beta–hydroxysteroid dehydrogenase have been described, differing by only 23 amino acids. Conditional Bet – a no gg multi bet on irrelevant outcomes. Various mutations in the HSD3B2 gene have been shown to be responsible for the varying phenotypic presentations.
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