Page 282 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Causes and Effects of Androgen Excess and Deficiency
Follitropin (FSH) and lutropin (LH) are released receptors. Other causes are inhibition of pulsa-
in the anterior pituitary, stimulated by pulsa- tile gonadotropin release by prolactin as well as
tile release of gonadoliberin (gonadotropin-re- damage to the hypophysis (trauma, infarct, au-
leasing hormone, GnRH) (→ A1). The pulsatile toimmune disease, tumor, hyperplasia) or to
secretion of these gonadotropins is inhibited the testes (genetic defect, severe systemic dis-
by prolactin (→ p. 260). LH controls the release ease). Lastly, androgen effects can be impaired
of testosterone from the Leydig cells in the by enzyme defects in hormone synthesis, for ex-
testes. Testosterone, by means of a negative ample, genetic reductase deficiency (→ p. 264)
feedback, inhibits the release of GnRH and LH or by a defect of the testosterone receptors.
(→ A2). The formation of inhibin, which inhib- Effects of deficient testosterone action in
its the release of FSH, and of androgen-binding the male fetus are absent sexual differentia-
protein (ABP) is promoted by FSH in the testic- tion (→ p. 278); in juveniles they are failure of
ular Sertoli cells (→ A3). the voice to break and absence of adult body
Testosterone or dihydrotestosterone (5-α- hair, delayed bone growth, but also ultimately
DHT) which is formed from testosterone in excess longitudinal growth of the limbs due to
the Sertoli cells and in some organs, promotes delayed epiphyseal fusion. Other effects (in ju-
Hormones and scrotum (→ A4). Testosterone and FSH are bido and aggressiveness, reduced muscle and
the growth of the penis, seminiferous tubules,
veniles and adults) are infertility, decreased li-
bone mass, and slightly decreased hematocrit.
both necessary for the formation and matura-
not even be any feminine pubic and axillary
stimulates the secretory activity of the prostate
9 tion of spermatozoa. In addition, testosterone If there is no androgen effect at all, there will
(reduced viscosity of the ejaculate) and the hair.
seminal vesicle (admixture of fructose and Possible causes of androgen excess are en-
prostaglandins), as well as the secretory activ- zyme defects in steroid hormone synthesis
ity of the sebaceous and sweat glands in the (→ p. 264), a testosterone-producing tumor, or
axillae and the genital region. Testosterone in- iatrogenic androgen supply (→ A2, A3).
creases skin thickness, scrotal pigmentation, Effects of testosterone excess are male sex
and erythropoiesis. It also influences height differentiation and hair growth, even in the fe-
and stature by promoting muscle and bone male, an increase in erythropoiesis, muscle
growth (protein anabolism), longitudinal and bone mass as well as of libido and aggres-
growth, and bone mineralization as well as fu- siveness. Amenorrhea (,) and impaired fertili-
sion of the epiphyseal plates. Testosterone ty (< and ,) are caused by inhibition of GnRH
stimulates laryngeal growth (deepening of the and gonadotropin release.
voice), hair growth in the pubic and axillary re- The generative function of the testes can,
gions, on the chest and in the face (beard); its however, also be impaired without apprecia-
presence is essential for hair loss in the male. ble abnormality of the sex hormones, as in
The hormone stimulates libido and aggressive undescended testis (cryptorchidism), genetic
behavior. Lastly, it stimulates the renal reten- defects, or damage to the testes (e.g., inflam-
tion of electrolytes, reduces the concentration mation, radiation, abnormal blood perfusion
of high density lipoprotein (HDL) in blood, and due to varices).
influences fat distribution.
Decreased release of androgens can be due
to a lack of GnRH. Even nonpulsatile GnRH se-
cretion stimulates androgen formation inade-
quately. Both can occur with damage to the hy-
pothalamus (tumor, radiation, abnormal per-
fusion, genetic defect) as well as psychological
or physical stress. Persistently high concentra-
272 tions of GnRH (and its analogs) decrease go-
nadotropin release by down-regulation of the
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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