Forms of Ovarian Failure
Pathophysiologically, two fundamentally different variants of hypogonadism are distinguished depending on the level of the regulatory axis lesion.
Primary Ovarian Insufficiency (Primary Hypogonadism) The essence of this form is that the ovarian tissue itself loses the ability to produce adequate amounts of sex hormones. The main laboratory marker of this condition is a compensatory elevated level of follicle-stimulating hormone (FSH) in the blood. This phenomenon is explained by negative feedback: the pituitary gland "senses" the shortage of peripheral hormones and attempts to stimulate the gonads more strongly.
Acquired causes of ovarian insufficiency include:
- Autoimmune damage (immune-mediated attack directed against self-tissues).
- Infectious damage (including inflammation of the ovaries — oophoritis).
- Iatrogenic factors (exposure to radiation therapy and chemotherapeutic agents).
Secondary (Extra-ovarian, Hypogonadotropic) Hypogonadism In this form, the ovaries themselves are intact, and the problem lies in a deficiency of stimulating factors. The development of the condition is due to a lack of hypothalamic gonadotropin-releasing hormone (GnRH) or a shortage of adenohypophyseal gonadotropic hormones (such as FSH and LH). Depending on the clinical course, secondary hypogonadism can be transient or persistent, progressing to a chronic form.
Hormonal Imbalances: Hyperandrogenism and Hyperestrogenism
In addition to sex steroid deficiency, ovarian pathology is often accompanied by the excessive production of specific groups of hormones or tissue hyperreactivity to their effects.
Hyperandrogenism Syndrome This is a condition characterized by increased production and/or enhanced biological effects of androgens. The main causes include GnRH hypersecretion, ovarian tumors, hyperinsulinemia, adrenal cortical hypersecretion of androgens, and an enzymatic defect — 3β-hydroxysteroid dehydrogenase deficiency.
Typical manifestations of hyperandrogenism are divided into:
- Laboratory findings: elevated blood concentrations of testosterone and androstenedione above normal ranges, alongside altered gonadotropin ratios (the LH/FSH ratio typically exceeds 3).
- Clinical features: development of hirsutism, obesity, amenorrhea, and persistent infertility.
Hyperestrogenism Syndrome A state of excessive estrogen production or action. The primary cause lies not in direct ovarian hypersecretion, but in peripheral conversion — the transformation of excess androgens into estrogens, which actively occurs in adipose tissue and skin. Abnormally high estrogen levels are registered in the blood and urine, which, via negative feedback, leads to reduced production of gonadotropic hormones. In girls, this condition triggers isosexual precocious puberty.
Pathology of the Male Reproductive System
Disruptions in sex steroid production in males also lead to hypogonadism and reproductive disorders. Excessive production of male sex hormones is often associated with neoplastic and hyperplastic processes.
Main causes of hormonal disorders in males:
- Androgen-producing testicular tumors: Leydig cell tumors (leydigomas, actively synthesizing testosterone), as well as Sertoli cell tumors and arrhenoblastomas, which produce various androgens.
- Leydig cell hyperplasia: leads to the synthesis of massive excesses of testosterone.
- Adrenal pathology: congenital adrenal hyperplasia or tumors provoke the release of large amounts of adrenal androgens into the bloodstream.
Clinically, these pathologies, along with deficiency states, are accompanied by a decrease in libido, development of impotence, and infertility.
Male infertility is defined as the inability to conceive a child within one year of regular unprotected intercourse. It is important to note that the ability to engage in sexual intercourse may remain entirely preserved. Moreover, in so-called isolated male infertility, sexual function, voice timbre, and male body habitus may remain completely normal.