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Endocrine and Reproductive Complications
Polycystic Ovary Syndrome
➤ PCOS is characterized by hyperandrogenism, ovulatory dysfunction,
and polycystic ovaries, with obesity exacerbating insulin resistance
and hyperinsulinemia. These effects increase ovarian androgen
production and reduce sex hormone-binding globulin, elevating
free testosterone. Adiposity-driven inflammation further disrupts
hormonal balance, resulting in elevated luteinizing hormone, altered
theca cell function, and a higher risk of dyslipidemia and MetS.
Genetic and environmental factors compound these effects.
Risk Factors
• Nonmodifiable risk factors include genetic variants that impair
steroidogenesis, insulin signaling, and folliculogenesis; family history
of PCOS or T2DM; and specific ethnic backgrounds (particularly
South Asian and Indigenous populations, who experience higher
metabolic risk). Modifiable factors include an elevated BMI, increased
waist-to-hip ratio, and visceral adiposity, as well as dysregulated lipid
metabolism characterized by elevated VLDL and triglyceride levels,
and low HDL phospholipid levels. Additional modifiable contributors
include smoking, low omega-3 fatty acid intake, and alterations in
gut microbiota, such as a reduction in Bifidobacteriaceae.
➤ Clinical Manifestations
• PCOS manifests with a range of reproductive abnormalities,
including oligomenorrhea, anovulatory infertility, and polycystic
ovaries on ultrasonography, as well as dermatologic signs such as
hirsutism, acne, androgenic alopecia, and acanthosis nigricans.
Metabolic disturbances, including insulin resistance, dyslipidemia,
MASLD, and increased risk of T2DM, are common, and many
individuals experience anxiety, depression, and decreased quality
of life related to body image concerns. Patients with obesity and
PCOS tend to have more severe menstrual abnormalities and
pronounced metabolic dysfunction.
➤ Screening
• Patients with obesity should be screened for PCOS by obtaining
a thorough menstrual history to identify cycle irregularities
(<21 or >35 days in adults, or fewer than eight cycles per year);
objective assessment of hyperandrogenism using the modif ied
Ferriman-Gallwey score for hirsutism or measurement of serum
total testosterone and f ree androgen index; and evaluation of
metabolic parameters, including fasting glucose, HbA1c, and
lipid prof ile. Differential diagnoses such as thyroid dysfunction,
hyperprolactinemia, and nonclassic congenital adrenal hyperplasia
must be excluded. Pelvic ultrasonography is not recommended
for adolescents, given the high prevalence of polycystic ovarian
morphology in this group.
