Androgens

Androgens are steroid hormones produced in the gonads (ovaries in women, the testes in males) and in the adrenal glands.

Effects of Androgen Excess: Hirsutism and Virilization

Androgens promote hair growth at puberty, although to different extents in each sex. Females, with low levels of androgens, develop visible pubic and axillary hair. Males, with greater concentrations of androgen, get additional hair g growth on the face and chest, as well as masculinization (i.e., increased mus

» cle mass, broadening of shoulders, and deepening of the voice).

Excess androgen in women will also result in these changes as well. In this J2 context, these effects are termed hirsutism and virilism.

S Hirsutism—the development of increased terminal hairs on the chest, ab domen, and face in a woman.

Virilization—the development of masculine characteristics in a woman, such as deepening of the voice, clitoromegaly, loss of female body contour, decreased breast tissue, and male pattern balding.

Hair Types

Vellus hairs are fine hairs found on most parts of the body. They are barely visible. Terminal hairs are the coarse, darker hairs found, for example, in the axilla and pubic region. Androgens facilitate the conversion of vellus to terminal hairs.

Production of Androgens

In women, androgens are produced in two locations: The adrenals and the ovaries (in males, they are produced in the adrenals and testes).

Adrenal Production of Androgens

The zona fasciculata and the zona reticularis of the adrenal cortex produce androgens, as well as Cortisol. ACTH regulates production.

A third layer of the adrenal cortex, the zona glomerulosa, produces aldosterone and is regulated by the renin-angiotensin system.

All three hormones—cortisol, androgens, and aldosterone—are derived from cholesterol. Androgen products from the andrenal are found mostly in the form of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone-sulfate (DHEAS). Elevation in these products represents increased adrenal androgen production.

Ovarian Production of Androgens

In the ovaries, first, LH stimulates the theca cells to produce androgens (an-drostenedione and testosterone). Then, FSH stimulates granulosa cells to convert these androgens to estrone and estradiol. When LH levels become disproportionately greater than FSH levels, androgens become elevated.

Pathologies

Excess androgen can be either ovarian etiology or adrenal, neoplastic, or benign.

Adrenal Etiologies

Cushing's Syndrome and Cushing's Disease

Cushing's syndrome is a general term meaning hypercortisolism along with the clinical picture that goes with it—moon face, buffalo hump, weakness, etc. Exogenous or endogenous cortisol can be the cause.

Cushing's disease is a subset of Cushing's syndrome, in which the increased cortisol level is due to ACTH hypersecretion by the pituitary, usually secondary to a benign pituitary adenoma. It accounts for 70% of Cushing's syndromes. Virilism and hirsutism are associated with this condition because the ACTH stimulates androgen production as well.

Paraneoplastic syndromes in which tumors (usually small cell lung cancer) produce ectopic ACTH are another cause of increased cortisol. These account for 15% of Cushing's syndromes.

Adrenal tumors (adenoma or carcinoma) account for the remaining 15% of Cushing's syndromes. In general, adenomas produce only cortisol, so no hir-sutism or virilization is present. Carcinomas, by contrast, often produce andro-gens as well as cortisol, so they may present with signs of hirsutism and viril-ization.

Congenital Adrenal Hyperplasias

Congenital adrenal hyperplasia is a general term for disease entities involving defects in steroid, androgen, and mineral corticoid synthesis. Two such common entities that result in virilism and hirsutism due to increased androgens are 21-hydroxylase deficiency and 1iP-hydroxylase deficiency.

Cortisol production in the adrenals: Where? zonas fasciculata and reticularis Regulated by? ACTH Derived from? Cholesterol

DHEA and DHEAS are androgen products from the adrenals. Increased levels of these indicate that the source is adrenal.

High LH:FSH ratio in the context of androgen excess indicates that ovary is the source.

21-Hydroxylase deficiency typical scenario:

A baby with ambiguous genitalia, dangerously hypotensive, and with elevated 17-hydroxyprogesterone.

11 P-Hydroxylase deficiency:

Low cortisol, high mineral corticoids (hypertensive) and high androgens. 11-Deoxycortisol is elevated vs.

21-Hydroxylase deficiency: Low cortisol and mineral corticoids (hypotensive),

17-Hydroxyprogesterone is elevated.

PCOS typical scenario: A

24-year-old obese woman with facial hair comes in with complaints of amenorrhea. LH:FSH ratio is elevated. Treat with oral contraceptives.

Typical scenario: A baby with ambiguous genitalia is born to a mother who complains of increased facial hair growth over last few months. Think: Luteoma of pregnancy.

21-Hydroxylase deficiency—this is the most common congenital adrenal hyperplasia. The condition has various levels of severity. Affected individuals lack an enzyme crucial to cortisol and mineral corticoid production. Therefore, hormone synthesis is shunted to excessive production of androgens. Elevated serum 17-hydroxyprogesterone levels are found as well. In the severe form, affected females have ambiguous genitalia at birth, along with severe salt wasting and cortisol insufficiency. A milder form presents simply with virilization and hirsutism of females after puberty.

11 P-Hydroxylase deficiency—this condition is associated with decreased cortisol, but increased mineral corticoids and androgens. The resultant picture is a severe hypertension with virilization/hirsutism (which results in pseudohermaphroditism of female babies). 11-Deoxycortisol levels are high.

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