Growth spurt

The adolescent growth spurt is an acceleration of growth in most skeletal dimensions. The peak height velocity (PHV) is 9–10 cm per year and lasts for about 2 years. There is no difference in the PHV of girls and boys, and both sexes grow between 25 and 28 cm during puberty. However, girls start their growth spurt 2 years earlier than boys, at which time they are 10 cm shorter than when boys start theirs. This accounts for the difference in adult height between the sexes.

This large increase in height is mediated by an increase in growth hormone (GH) production by the pituitary gland. The greatest increase in the frequency and amplitude of GH takes place at night in a similar fashion to luteinizing hormone (LH) pulses (Figure 1.1).

Figure 1.1 Luteinizing hormone (LH) levels during puberty. Changes in the pulse frequency and amplitude of luteinizing hormone during puberty. REM, rapid eye movement.

Hormonal changes

The hormonal changes of puberty produce two main effects: maturation of the ovary so that reproduction can occur, and development of secondary sexual characteristics (breasts, axillary and pubic hair).

During childhood, serum levels of the gonadotrophins – LH and follicle-stimulating hormone (FSH) – are low. During early to mid-puberty, however, there is a striking increase in the magnitude and frequency of LH pulses at night during sleep (see Figure 1.1). In late puberty, there is an increase in magnitude during the day, but not as marked as at night. Only when puberty is complete do the LH pulses lose their diurnal variation and settle into an adult pattern, with pulses approximately every 90 minutes during the follicular phase, and between 120 and 180 minutes in the luteal phase.

These events are probably initiated by the maturation of the hypothalamus and the onset of secretion of gonadotrophin-releasing hormone (GnRH). However, it is impossible to prove the exact sequence of events initiating puberty because the experiments required would be unethical in humans.

The increase in both LH and FSH activity has a trophic effect on the ovary, stimulating the production of estradiol. The primordial follicles (the oocyte and surrounding support cells), present from birth, begin to mature into antral follicles lined by granulosa cells. This process of maturation takes about 10 weeks. LH acts mainly on the theca cells which surround the follicles, causing them to produce testosterone, which is then converted by an aromatase into estradiol in the granulosa cells under the influence of FSH.

The increase in estradiol secretion stimulates breast development. The five stages of breast development take about 4 years to complete (Figure 1.2). Menarche (the first menstruation) usually occurs once breast development is quite well advanced – between stages III and IV¹. Rapid breast development or increase in breast size, common during pregnancy and less common on the oral contraceptive pill, may cause stretch marks to develop, especially in the lateral margins of the breast, which may be of concern, particularly to younger women.

Figure 1.2 Breast development. The Tanner stages I–V of breast development.

Several other changes also occur, which are important in understanding the physiologic changes in the skin. The first is adrenarche. This is an increase in the production of adrenal androgens, dehydroepiandrosterone (DHEA) and its sulfate (DHEAS), which starts at about 8 years of age and continues until 13–15 years of age in both sexes. This increase is thought to stimulate the development of axillary and pubic hair, as hair growth and changes in sebum secretion are modulated predominantly by androgens in both sexes. Pubic and axillary hair growth usually starts before the breasts change following the increase in adrenal androgen levels, but reaches the mature stage at around the same time. The testosterone level increases in girls, as in boys, under the influence of LH, but most of it is converted into estradiol.

During puberty, the concentration of the main binding protein of the sex hormones (sex hormone-binding globulin, SHBG) declines in both sexes, despite the increase in estradiol concentrations in girls². SHBG has a greater affinity for testosterone than for estradiol, with the result that, in most girls, more than 90% of circulating testosterone is bound to SHBG, thus limiting the effect that testosterone may have peripherally. The decrease in SHBG seems to be mediated by an increase in insulin concentration, which has been demonstrated in both sexes³.

Polycystic ovary syndrome

There is a group of girls who produce an excess of testosterone accompanied by morphologic changes in their ovaries, a phenomenon known as polycystic ovaries (PCO)⁴. Typically these girls never establish regular menstruation and have increased hair growth, usually of a male pattern, with an abdominal escutcheon, moustache, or other facial hair growth (Figure 1.3). They may also develop acne. Many girls with acne and/or hirsutism have polycystic ovary syndrome. These girls also have higher insulin concentrations and lower SHBG concentrations than their weight-matched contemporaries⁵.

Figure 1.3 Polycystic ovary syndrome. Facial hirsutism associated with polycystic ovary syndrome.

A lower SHBG concentration, together with an increased circulating testosterone level, will lead to an increased free testosterone level. It is the fraction of free testosterone that is thought to be active peripherally on the skin, sebaceous glands, and hair follicles.

Acne

Testosterone has major effects on the hair follicle and sebum secretion. Acne vulgaris⁶ (Figure 1.4) and hirsutism are never seen in prepubertal children with normal adrenal function, providing further evidence that puberty-related changes trigger these events. Although there is no evidence of increased androgen production in men with acne, most women with acne do have increased ovarian androgen production and a reduced SHBG concentration. Undoubtedly, genetic factors also play an important part in determining which girls will suffer and which will not. The pilosebaceous gland becomes more differentiated, increases in size, and changes its sebum composition. These changes are most marked on the scalp and around the nose, chin, and cheeks, as well as on the upper chest and back (see Chapter 2

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A Systematic Approach to the Dermatoses of Pregnancy of Therapeutics for Vulvovaginal Disease Pemphigoid (Herpes) Gestationis Physiologic Skin Changes of Pregnancy Vaginitis Disorders of Pigmentation

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