FSH & LH in PCOS: Hormonal Patterns, Diagnosis & Treatment Monitoring

Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) are pituitary gonadotropins central to ovarian function. In PCOS, their dysregulation drives anovulation and hyperandrogenism.

Pathophysiology in PCOS

• Elevated LH Pulse Frequency/Amplitude: Drives theca cell androgen overproduction (testosterone, androstenedione).
• Relative FSH Deficiency: Inadequate FSH → impaired granulosa cell aromatase activity → reduced estradiol, failed dominant follicle selection.
• LH:FSH Ratio: Classically > 2:1 or > 3:1 (but not universal; 30–40% of PCOS have normal ratio).

Diagnostic Utility

• Supportive, not diagnostic alone. Rotterdam criteria require 2 of 3: oligo/anovulation, hyperandrogenism (clinical/biochemical), polycystic ovaries on ultrasound.
• Exclude mimics: thyroid disease, hyperprolactinemia, non-classic CAH, androgen-secreting tumors.
• Measure in early follicular phase (days 2–5) if cycles exist; random if amenorrheic.

Treatment Monitoring

• Combined Oral Contraceptives (COCs): Suppress LH → reduce androgens. Monitor SHBG, free testosterone.
• Ovulation Induction (Letrozole/Clomiphene): Track follicular development via ultrasound + estradiol; LH surge timing for trigger/IUI.
• Metformin/GLP-1 Agonists: Improve insulin resistance → indirectly lower LH pulse frequency.

Clinical Pearl

FSH/LH levels vary cycle-to-cycle and assay-to-assay. Trends > single values. Integrate with AMH, androgen panel, and clinical phenotype for individualized management.