Hypogonadism is, in short, a defect of the reproductive system, associated with hormonal failure of the testicles and ovaries and their symptoms. This disease is caused, inter alia, by dysfunction of the testes, Leydig cells or impaired functioning of the ovaries in adolescence or adulthood. Hypogonadism can be primary or secondary.
BRIEF CHARACTERISTICS OF THE EFFECT OF TESTER HORMONES
The biologically active sex hormones produced by the male gonad are steroidal compounds: testosterone and its derivatives: dihydrotestosterone (DHT) and estradiol. Dihydrotestosterone is formed from testosterone with the participation of the enzyme 5-?alpha -reductase and has 3 times greater affinity for the androgen receptor (the most biologically active androgen) than that of testosterone. Estradiol is formed from testosterone with the participation of the aromatase enzyme and acts through the estrogen receptor.
The Leydig cells of the testicular interstitial gland are the main site for the biosynthesis of male sex hormones. The luteinizing hormone (lutropin, LH) activates the enzymes involved in the steroidogenesis process, thanks to which testosterone is produced from cholesterol in the highest amounts. The target sites for follicle stimulating hormone (follitropin, FSH) are Sertoli cells and spermatogoniums in sperm-forming tubules. Follitropin stimulates the maturation and growth of sperm-forming tubules, influences the activity of Sertoli cells, and through them regulates the spermatogenesis process. Feedback is an important mechanism in the regulation of the activity of the hypothalamic-pituitary-nucleus axis. By way of negative feedback, respectively high levels of testosterone and estradiol in the blood reduce the secretion of gonadoliberin (GnRH) and LH, and the protein hormones of the testes inhibit (inhibin) or stimulate (activin) the secretion of FSH. Inhibin is synthesized in Sertoli cells and consists of two?alpha i?beta. Inhibin A contains the subunits of ??alpha i?betaA. Inhibin B contains the subunits of?alpha i?betaB and is the main form of this hormone that is found in the circulation of men.
The biological effects of male sex hormones vary depending on the period of life in which they act:
1. In the early stage of fetal life (6- 20 weeks) testosterone causes differentiation of male internal genitalia (epididymis, vas deferens, seminal vesicles, prostate), and its derivative – DHT – external (penis and scrotum).
2. In the perinatal period (8th month of fetal life -4th month after birth) testosterone and its derivatives participate in the descent of the testicles to the scrotum, as well as in the differentiation of sexually dimorphic brain structures and determine the male psychological gender.
3. During puberty in boys testosterone and its derivative – estradiol – induce growth acceleration (growth jump) and its termination by closing the epiphyses of long bones, initiate full spermatogenesis, and also influence the development of secondary male sexual characteristics (including male body shape and male hair shaping, penile growth) and the development of sex drive.
4. In the period of maturity androgens participate in the maintenance of spermatogenesis and secondary male sexual characteristics, and maintain metabolic effects such as anabolic effect on liver function, hematopoietic, muscular, bone and immune systems.
Hypogonadism – types and symptoms
Classically, the term “hypogonadism” is defined as a disorder of the endocrine and gameteogenic function of the gonads. In men, hypogonadism is manifested by hypoandrogenism and a lack of testicular sperm-forming activity. These disorders can be caused by abnormal gonadal function (primary, hypergonadotrophic, nuclear) or the hypothalamus and / or pituitary (secondary, hypogonadotrophic, pituitary).
Both primary and secondary hypogonadism may occur in the form of partial hypogonadism. The disorder may involve primarily the testicular interstitial gland (with Leydig cell agenesis or metabolic block in Leydig cell steroidogenesis) or only sperm-forming tubules. Secondary hypogonadism may also occur in the form of an isolated deficiency of only one gonadotropin (FSH or LH).
Recently, a new concept has been introduced – the so-called late hypogonadism (late onset hypogonadism – LOH), which is associated with decreased testicular function in aging men. The concentration of testosterone decreases slightly here, and the concentration of gonadotropins slightly increases (the values may be close to the lower limit recognized as the normal). The concentration of sex steroid binding globulin (SHBG) is significantly increased, which results in a decrease in the concentration of free, biologically active testosterone.
However, there are still doubts as to whether the physical and mental changes, similar to some clinical symptoms of hypogonadism, are associated with poorer testicular function or rather with deteriorating health in aging men, e.g. with the appearance of such diseases as:
- atherosclerosis,
- diabetes,
- cardiovascular disease,
- lifestyle, e.g. with little physical activity.
Increased secretion of prolactin (Prl) from the pituitary gland is sometimes thought to be the cause of hypogonadism. Hyperprolactinaemia may disrupt the pulsatile secretion of gonadotrophins and therefore disrupt the function of the gonads. However, unlike in women, hyperprolactinaemia is rare in men and is of little importance in the pathogenesis of hypogonadism.
Source: A. Cajdler-Łuba, S. Mikosiński, A. Sobieszczańska-Jabłońska, I. Nadel, I. Salata, A. Lewiński: “FUNCTIONAL DIAGNOSTICS OF HORMONAL DISORDERS WITH ELEMENTS OF DIFFERENTIAL DIAGNOSTICS; Czelej Publishing House