What is Hypogonadism?
Hypogonadism is a collective concept that includes all conditions accompanied by hypofunction of the testicles.
Causes of Hypogonadism
Hypogonadism includes conditions caused by the pathology of the testicles proper or the function of the hypothalamic-pituitary system that regulates them, or insufficient production of androgens in embryogenesis, which leads to impaired sex differentiation, as well as conditions that arise correlatively as a result of the primary pathology of other endocrine glands and organs involved in androgen exchange.
Violations of gender differentiation, leading to hermaphroditism, and proper hypogonadism are closely related problems. In fact, hermaphroditism is hypogonadism, if we consider it as androgen deficiency relative to a genetically programmed male body.
The androgen deficiency underlying hypogonadism is the result of both a quantitative decrease in androgen secretion and a violation of its biosynthesis. If the pathology begins with damage to the tissues of the testis, it is attributed to primary hypogoyadism, if with a violation of the structure and function of the pituitary gland or hypothalamic centers regulating its activity, it is secondary.
Primary and secondary hypogonadism can be congenital and acquired.
The current level of science does not yet allow us to explain all the mechanisms of the primary lesion of individual elements of testicular tissue, in particular the pathogenesis of the inconsistency in the functional state of the germinal epithelium and interstitial endocrinocytes.
One of the causes of primary testicular insufficiency is chromosomal abnormalities, as a result of which the testicular tissue is absent or remains underdeveloped, incapable of secreting sex hormones in general, or as a result of disruption of the testosterone biosynthesis in it remains incapable of secreting sex hormones in an amount sufficient for the development of androgen-dependent organs and tissues and secondary sexual characteristics.
The pathology of their prolapse leads to a hypogonadal state of the testicles. For the occurrence of chromosomal and other congenital pathologies, the infectious, toxic, medicinal, chemical, radiation and other harmful effects on the mother’s body play a detrimental role.
The cause of the primary acquired hypogonadism is often acute and chronic infectious diseases transferred in the pre-pubertal period. In particular, mumps complicated by orchitis in the future in 60% of cases causes a violation of the spermogram. Traumatic testicular damage, early castration, varicocele, postoperative atrophy and hypoplasia of the testicles (after herniotomy, orchipexy, and operations on the scrotum organs) lead to the development of symptoms of eunuchoidism and infertility.
Secondary hypogonadism (hypogonadotropic) is the result of primary insufficiency of the gonadotropic function of the adenohypophysis, which can be combined with a deficiency in the production of other triple hormones. Gonadotropic insufficiency, leading to hypoandrogenism, is associated either with inflammatory, tumor, vascular disorders in the pituitary or hypothalamus, or with impaired embryonic development of the pituitary gland. Clinical symptoms depend on the severity of hypopituitarism and androgen deficiency, as well as the age of the pathology (including the embryonic period).
Pathogenesis during Hypogonadism
The pathogenesis of primary hypogonadism is closely associated with a decrease in the level of androgens in the blood, a compensatory reaction of the adrenal androsteroid, and activation of the secretion of gonadotropic hormones. Symptoms can occur with prostatopathies and other visceropathies (cirrhosis, hepatitis, etc.). The testicles are damaged a second time. However, the pathogenetic mechanisms in this case develop as the primary (hypergonadotropic) disco-correlation hypogonadism.
Symptoms of Hypogonadism
If androgen deficiency of any genesis arose in the early stages of the formation of the male body (up to 20 weeks), then severe sex differentiation develops, clinically expressed by intersexuality (hermaphroditism) and always proceeding with the clinical picture of hypogonadism. After 20 weeks of embryogenesis, anorchism, unilateral (monorchism) or bilateral testicular aplasia, unilateral or bilateral testicular hypoplasia occur. This leads to the underdevelopment of the external and internal genital organs, delayed or lack of development of secondary sexual characteristics and sexuality.
If androgen deficiency occurs after birth, but before puberty, puberty does not occur and signs of eunuchoidism develop. Early castration (more often due to testicular injury) also leads to the formation of eunuchoidism.
The occurrence of androgen deficiency in the post-pubertal period, in addition to a slight regression of sexual hair growth, leads to the extinction of libido, a decrease in potency, and symptoms of premature involution.
Diagnosis of Hypogonadism
Male hypogonadism is diagnosed on the basis of complaints, anamnestic data, an assessment of the general somatic status using anthropometric techniques (taking into account age), examination and palpation of the external and internal genitalia, an assessment of the clinical signs of hypoandrogenia, and the rate of puberty. To diagnose hypogonadism, X-ray data are important: bone age, bone mineralization status, size of the Turkish saddle, the presence of petrificates over the Turkish saddle, indicating the presence of a tumor.
Bone age accurately enough allows you to determine the onset of puberty. It is associated with the appearance of a sesamoid bone in the I metacarpophalangeal joint (within 13.5-14 years). The appearance of synostoses, that is, the disappearance on the x-ray of the transverse dense bone strips at the site of the distal epiphyses of the ulna and radius, indicate complete puberty. This feature allows you to distinguish between prepubertal age and puberty. Bone age standards for the timing of ossification of the wrist joint and hand.
When assessing bone age, it is necessary to take into account the options for the earliest and late ossification. For patients in the southern regions of the country, it is necessary to focus on earlier, northern ones on later dates. You should also pay attention to other possible signs of violation of osteogenesis (asymmetry of ossification, distortion of sources of osteogenesis), which may be due to other factors.
The most important in the diagnosis of hypogonadism is the determination of the level of sex and gonadotropic hormones (T, E2, LH, FSH, PRL) and functional tests with chorionic gonadotropin and with chorionic gonadotropin against a background of dexamethasone.
The treatment of hypogonadism depends on the clinical form of the pathology, the nature and degree of manifestations of disorders of the hypothalamic-pituitary-gonadal system, concomitant anomalies, the timing of occurrence, and the age of its detection. In this regard, a common terminology and gradation of various forms is important.
Hypogonadism treatment is carried out strictly individually. The goal of treatment is to prevent future retardation of infertility, infertility and testicular malignancy. Adult treatment is the correction of androgen deficiency and sexual dysfunction, which due to infertility due to congenital and pre-pubertal hypogonadism is unpromising, especially in cases of aspermia. The following principle must be observed: in case of primary congenital and acquired hypogonadism, in case of preserved reserves of endocrinocytes, stimulating therapy of testicles in children with non-hormonal agents (symptomatic therapy) is shown in adults – with hormonal (low doses of androgens, gonadotropins); in the absence of reserve testicular activity (negative choriogonin test), androgen therapy is indicated according to the substitution principle. In secondary hypogonadism in children and adults, stimulating hormone therapy with gonadotropins should be used. Treatment of correlative forms of hypogonadism begins with therapy of the underlying disease.