## Endocrine Profile in PCOD **Key Point:** The hallmark endocrine abnormality in PCOD is an elevated LH:FSH ratio, typically 2.5:1 or higher (normal is 1:1 to 1.5:1), with absolute LH elevation and relatively normal or low-normal FSH. ### Mechanism 1. **Abnormal GnRH pulsatility** — increased frequency of GnRH pulses preferentially stimulates LH secretion over FSH 2. **Increased LH bioactivity** — drives excessive androgen production by theca cells 3. **Relative FSH suppression** — due to elevated inhibin B from granulosa cells and elevated estradiol ### Other Endocrine Findings in PCOD | Feature | Finding | Frequency | | --- | --- | --- | | **Hyperandrogenism** | Elevated free/total testosterone, androstenedione | 70–80% | | **Insulin resistance** | Fasting hyperinsulinemia, impaired glucose tolerance | 50–70% | | **LH:FSH ratio** | Elevated (>2.5:1) | 60–80% | | **Prolactin** | Mildly elevated (rarely >25 ng/mL) | 20–30% | | **TSH** | Normal (thyroid disease in ~20% of PCOD patients) | — | **High-Yield:** The elevated LH:FSH ratio is so characteristic that a normal ratio should prompt investigation for other causes of anovulation (e.g., hypothyroidism, hyperprolactinemia, Cushing syndrome). **Clinical Pearl:** Measurement of LH and FSH on day 3 of the menstrual cycle (or any day if amenorrheic) is part of the diagnostic workup for PCOD, though Rotterdam criteria do not mandate it.
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