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Patients with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency have impaired cortisol synthesis.  Subsequent lack of feedback causes the hypothalamus to increase adrenocorticotropic hormone (ACTH) secretion by the anterior pituitary.  This results in stimulation of the adrenal cortex and adrenal androgen overproduction (eg, dehydroepiandrosterone, androstenedione).

Treatment of 21-hydroxylase deficiency involves low (ie, physiologic) doses of exogenous corticosteroids that suppress ACTH secretion via negative feedback mechanisms.  Without excess ACTH stimulation, androgen production by the adrenal cortex decreases.

(Choice B)  Deficiency of 21-hydroxylase impairs cortisol synthesis; further suppression of cortisol production could precipitate an adrenal crisis (eg, hypoglycemia, hypotension).

(Choice C)  Luteinizing hormone (LH) stimulates the testes to produce testosterone.  Decreasing LH levels would decrease testosterone production by the testes but would not affect excess adrenal androgen production in CAH.

(Choice D)  Hyperprolactinemia disrupts GnRH secretion, which leads to decreased testosterone production and hypogonadism.  Prolactin suppression would further elevate testosterone levels and would not be beneficial in this patient.

(Choice E)  This patient's symptoms are the result of excessive production of adrenal androgens (eg, dehydroepiandrosterone and androstenedione), which can subsequently undergo peripheral conversion to testosterone.  Blockade of testosterone alone would not be sufficient to prevent progression of this patient's symptoms, as the androgenic effects of these testosterone precursors would remain unopposed.

Educational objective:
Treatment of congenital adrenal hyperplasia due to 21-hydroxylase deficiency involves low doses of exogenous corticosteroids to suppress excess ACTH secretion, which reduces production of androgens by the adrenal cortex.