Excess adrenal androgens cause acne, pubic hair and armpit hair to develop before puberty, and the condition is often accompanied by a notable increase in body odor. Prepubertal hyperandrogenism is also known as premature adrenarche or exaggerated adrenarche -- too early or excessive activity of the adrenal gland resulting in increased androgen secretion.
Until recently, the standard medical advice to parents of a child suffering virilization caused by premature or exaggerated adrenarche was that the condition did not require medical treatment. But it is now clear that if left untreated, premature virilization caused by adrenal androgens has negative effects on child health.
Antiandrogens such as cyproterone acetate, spironolactone, and ketoconazole have improved behavior of boys with virilization due to adrenal androgens and may help prevent PCOS in girls.
pubarche: the development of pubic hair
In adults (or children with premature puberty) testosterone is converted to the more potent dihydrotestosterone (DHT) by Type 1 reductase in the pubic hair follicles, and by Type 2 reductase in other hair follicles. Thus a Type 2 inhibitor, such as finasteride, will reduce adult body hair but will not reduce the amount of pubic hair.
Recent data, in fact, indicate that girls with premature pubarche may not have a benign outcome. Postpubertal girls diagnosed with premature pubarche during childhood have an increased frequency of functional ovarian hyperandrogenism (45). Furthermore, hyperinsulinemia is a common feature in adolescent patients with premature pubarche and functional ovarian hyperandrogenism, and is directly related to the degree of androgen excess (46-48).
Weight gain may be a trigger for adrenarche, and obesity has also been associated with a higher incidence of premature adrenarche.... Pubarche after age 7 yr is often slowly progressive. However, that does not mean that it is normal. Evidence is emerging that premature pubarche may on occasion be a risk factor for subsequent reproductive endocrine system dysfunction....
Endocrine Reviews 21 (6): 671-696
Abnormal pubertal characteristics and polycystic ovary syndrome (PCOS) may follow a premature or exaggerated andrenarche:
The increased incidence of functional ovarian hyperandrogenism found in our cohort of postpubertal premature adrenarche patients and the hypothesis that PCOS might begin during puberty prompted us to assess the pattern of gonadotropin and ovarian steroid secretory responses to leuprolide acetate challenge throughout puberty in these patients. Recent studies performed in pubertal patients with a history of premature adrenarche suggested that increased adrenal androgen secretion was limited to childhood. In contrast, our results seem to indicate that pubertal girls with premature adrenarche have an exaggerated ovarian androgen synthesis compared with Tanner stage- and bone age-matched controls. This pattern of ovarian androgen hyperresponsiveness begins early in puberty, is most evident during mid and late puberty, and is characterized by higher basal, peak, and incremental responses of most steroid precursors to GnRH agonist challenge. This pattern of steroid secretion is suggestive of abnormal regulation of ovarian cytochrome P450C17. Even in the absence of clinical signs of androgen excess, postpubertal girls with premature adrenarche have increased ovarian androgen synthesis.
Endocrine Reviews 21 (6): 671-696
in congenital adrenal hyperplasia (CAH):
Adrenal attempts to compensate for low levels of aldosterone cause an overproduction of adrenal androgens, resulting in premature
puberty in males.
It is the combined effect of adrenal androgens, and not DHEAS alone that causes puberty to advance.
CAH affects development of the HPG axis. At any prepubertal age, prolonged exposure to adrenal androgens may cause maturation of the hypothalamic GnRH centers, and eventually central puberty is initiated. Prompt treatment of early adrenarche may prevent the premature onset of full puberty.
Adequate androgen secretion alone does not ensure normal sexual hair development in many patients with gonadal dysgenesis. Moreover, in children with a lack or delayed adrenarche long-term treatment with DHEAS at dosages such as to restore normal levels for age, failed to induce growth of sexual hair or any change in growth rate, bone maturation velocity, or to advance puberty.
GH therapy did not affect the age at pubertal onset, defined either by testicular volume >4 mL or by testosterone concentration >1.0 nmol/L (30 ng/dL). GH treatment also did not affect the pace of puberty, defined either by the rate of change in testicular volume or testosterone concentration during the 4 years after pubertal onset.
Effect of growth hormone treatment on testicular function, puberty, and adrenarche
DHEA (DeHydroEpiAndrosterone) is an adrenal androgen which metabolizes to DHEA-S (DeHydroEpiAndrosterone Sulfate)
Adrenal androgens secreted by the hypothalamus-pituitary-adrenal (HPA) axis sensitize the androgen receptors of the hypothalamus and the pituitary, eventually leading to the activation of the hypothalamus-pituitary-gonadal (HPG) axis and full puberty.
The increased secretion of androgen hormones that occurs in the earliest stages of puberty and is associated with the major changes in reproductive capacities that occur. Stimulated by ACTH from the hypothalamus.
Davies: Human Physiology
adrenarche as the threshold of puberty: the role of adrenal secretions
The tested testosterone (T) precursors androstenedione (A), dehydroepiandrosterone (DHEA) are potent activators of androgen receptors (AR).
Experimental and Clinical Endocrinology: Mechanisms of Hormone Action
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