Gonadal function

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Gonadal function

Sex steroid hormones

Testosterone is the principal androgen and is synthesized by the testes in the male. Oestradiol, which is secreted by the ovaries, varies widely in concentration in plasma throughout the female menstrual cycle. Steroids with oestradiol-like action are called oestrogens. Progesterone is also a product of the ovary and is secreted when a corpus luteum forms after ovulation. Normal female plasma also contains a low concentration of testosterone, about half of which comes from the ovary and half from peripheral conversion of androstenedione and dehydroepiandrosterone (DHA) sulphate, which are secreted by the adrenal cortex. Some oestradiol is present in low concentration in normal male plasma.

Testosterone and oestradiol circulate in plasma mostly bound to plasma proteins, particularly sex hormone-binding globulin (SHBG). The plasma concentration of SHBG in females is twice that in males. In both sexes the effect of an increase in SHBG is to increase oestradiol-like effects, whereas a decrease in SHBG increases androgen effects.

In females, testosterone and SHBG concentrations are sometimes reported by the laboratory as a ratio (the free androgen index), which gives a clearer indication of androgen status than does serum testosterone alone. In males, calculated free testosterone (using equations) is a more reliable indicator than measured total testosterone; free androgen index is not useful.

Male gonadal function

The testes secrete testosterone and manufacture spermatozoa. Before puberty, gonadotrophin and testosterone concentrations in plasma are very low. The development of the Leydig cells and their secretion of testosterone is influenced by LH, whereas Sertoli cell function is influenced by FSH (Fig 50.1). Testosterone is responsible for the development of the male secondary sex characteristics such as hair growth, deep voice and characteristic musculature.

Disorders of male sex hormones

Hypogonadism may result in deficient sperm production and decreased testosterone secretion. This may be due to a testicular deficiency (primary disorders or hypergonadotrophic hypogonadism) or to a defect in the hypothalamus or pituitary (secondary disorders or hypogonadotrophic hypogonadism). In hypogonadotrophic hypogonadism both gonadotrophins, or only LH, may be reduced. There may be a generalized failure of pituitary function.

Causes of primary hypogonadism include:

Causes of secondary hypogonadism include:

Dynamic tests such as stimulation with GnRH may help to establish the cause of the hypogonadism in some patients.

Female gonadal function

Oestradiol is responsible for:

Concentrations are low before puberty, but then rise rapidly and fluctuate cyclically during reproductive life. After the menopause, plasma oestradiol concentrations fall despite high circulating concentrations of the gonadotrophins.

The normal hormonal control of the menstrual cycle is shown in Figure 50.2. At the beginning of the cycle, FSH is released and initiates follicular growth. At mid-cycle a surge of LH triggers ovulation. The ruptured follicle differentiates into the corpus luteum that secretes progesterone and oestradiol whose target is the endometrium, which they prepare for implantation.

Disorders of female sex hormones

Disorders of female sex hormones include:

image Subfertility, amenorrhoea and oligomenorrhoea (see p. 102).

image Hirsutism. This is an increase in body hair with male pattern distribution. It may be idiopathic but the commonest pathological cause is obesity (insulin resistance) often in association with polycystic ovarian disease. It is essential when investigating hirsute women that serious disease is excluded. A diagnostic decision chart for the investigation of hirsutism is shown in Figure 50.3.

image Virilism. Although uncommon it is a sign of serious disease. Testosterone concentrations are markedly elevated in the virilized patient and there is evidence of excessive androgen action such as clitoral enlargement, hair growth in a male pattern, deepening of the voice and breast atrophy. Tumours of the ovary or of the adrenal are the likely cause.

The androgen screen in women

The observation of an elevated testosterone in a woman should always be investigated further. A decreased SHBG concentration is usually evidence of elevated androgen, as the synthesis of this protein in the liver is depressed by testosterone. By measuring the concentration of other androgens such as androstenedione and DHA sulphate (an ‘androgen screen’), the source of the testosterone can be pinpointed (Fig 50.4). An elevated DHA sulphate suggests that the adrenal, or an adrenal tumour, is overproducing androgens. If the ovary is the source then only androstenedione will be raised.