Endocrine Abstracts

Adrenal androgen synthesis involves contributions from the classic, 11-oxygenated and alternative pathways. The zona reticularis of the adrenal cortex secretes androgen precursors such as dehydroepiandrosterone (DHEA) and androstenedione (A4) which undergo conversion in peripheral tissues to active androgens such as testosterone (T) and dihydrotestosterone (DHT). The adrenals may also produce smaller concentrations of T directly. A4 can be converted by the activity of adrenal CYP11B1 into the 11-oxygenated androgen 11-hydroxyandrostenedione (11OHA4), which then undergoes peripheral conversion into potent active 11-oxygenated androgens through the activities of the enzymes HSD11B2 and AKR1C3. Classic and 11-oxygenated androgens are elevated in a number of disorders of androgen excess in women, including polycystic ovary syndrome, congenital adrenal hyperplasia and Cushing’s disease. Severe adrenal androgen excess may also be observed in adrenal tumours and in acquired or monogenic severe insulin resistance. This talk will cover the physiology and pathophysiology of adrenal androgen synthesis, as well as the diagnostic approach to patients with adrenal androgen excess.