Complications of infertility

Endocrine disorders and metabolic complications

In polycystic ovary syndrome (PCOS), infertility is of an anovulatory nature (primary or secondary) and is associated with the loss of the ability of luteinized cells to synthesize progesterone. However, the main danger lies in systemic complications developing against the background of dyslipidemia and carbohydrate metabolism disorders.

Severe systemic consequences include:

• Early development of vascular atherosclerotic changes.
• Onset of hypertension and coronary heart disease (CHD).
• Increased risk of developing genital hyperplastic processes.

The clinical presentation depends on the form of PCOS:

1. Typical form: disorders start with menarche, accompanied by the gradual development of hirsutism and uniform weight gain.
2. Mixed form: characterized by chronic anovulation, obligatory presence of hirsutism (on the thighs, lower legs, abdomen) with rare obesity.
3. Central form: occurs due to hypothalamic-pituitary system dysfunction (often after stress, adenovirus infection, or brain injury). It is accompanied by grade II–III obesity, trophic disorders (striae, brittle nails), and pregnancy loss.

Infectious factors and their consequences

Infectious agents also act as a cause of impaired fertility. Urogenital trichomoniasis is transmitted predominantly sexually (contagiousness is about 100%), although a household route of infection through shared underwear is not excluded in girls.

Trichomonads directly cause infertility, as they are capable of reducing sperm motility. The primary focus of infection is the vagina, but the process often spreads to the cervical canal, urethra, urinary bladder, and the excretory ducts of Bartholin's glands.

The main complication of trichomoniasis is ascending infection. The pathogen can penetrate through the uterus and fallopian tubes all the way to the abdominal cavity. The peculiarity of pathogenesis lies in the fact that trichomonads act as a kind of «transport», carrying other pathogenic microflora on their surface to the upper regions of the reproductive system. Persistent post-infection immunity does not develop, which causes a high risk of reinfection.

Hypothalamic-pituitary pathologies

Severe forms of infertility and systemic complications are observed in pituitary lesions.

Sheehan syndrome (postpartum pituitary necrosis) develops as a result of massive hemorrhage during childbirth or abortions. Blood loss leads to intravascular thrombosis and pituitary ischemia (facilitated by the physiological postpartum decrease in ACTH secretion). Thrombosis can also affect the liver, kidneys, and brain structures.

Depending on the volume of the lesion, deficiency of various hormones occurs:

• Decreased ovarian function: leads to oligomenorrhea and anovulatory infertility.
• Thyroid hormone deficiency: causes weakness, feeling cold, and headaches.
• Total hypofunction (gonadotropin, TSH, ACTH deficiency): leads to persistent amenorrhea, cachexia, hair loss (alopecia), atrophy of the mammary glands and genital organs, as well as memory impairment.

Other pituitary pathologies include gigantism (hyperplasia of eosinophilic cells with excess growth hormone), which is accompanied by hypogonadism and primary amenorrhea, as well as hyperprolactinemia. Excess prolactin often accompanies amenorrhea of hypothalamic-pituitary origin and can be provoked by certain medications (COCs, haloperidol) or damage to intrauterine receptors from frequent curettage.

Impact on pregnancy and fetal development

If pregnancy still occurs against the background of endocrine or systemic disorders, the risk of placental insufficiency (PI) and fetal growth restriction (FGR) increases manifold.

For the fetus, this is fraught with severe complications:

• High frequency of hypoxia during pregnancy and childbirth.
• Risk of meconium aspiration.
• Perinatal central nervous system injuries and impaired functional maturation.
• Adaptation disorders in the early neonatal period (hypoglycemia, hypocalcemia, hyperbilirubinemia, thermoregulation disorder).

Interesting fact: premature infants with hypotrophy are less likely to develop respiratory distress syndrome. Chronic intrauterine hypoxia stimulates a high level of endogenous steroids, which accelerates the formation of alveolar surfactant.

Long-term consequences of FGR are described by D. Barker's concept («adult diseases of fetal origin»). In such patients at an adult age (after 50 years), metabolic syndrome, diabetes mellitus, and cardiovascular diseases are reliably diagnosed much more often.

Class and exam questions

What else to study on this topic

• Pathogenesis and clinical forms of polycystic ovary syndrome (PCOS)
• Classification and stages of urogenital trichomoniasis
• Mechanisms of development of placental insufficiency and fetal growth restriction
• Physiological and pathological hyperprolactinemia
• Sheehan syndrome: etiology, diagnosis, and hormonal profile

Other topics in the "Gynecology" section

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