## Biochemical Profile in PCOD **Key Point:** PCOD is characterized by a specific hormonal signature; elevated prolactin is NOT a primary feature and should prompt investigation for other causes (prolactinoma, hypothyroidism). ### Correct Hormonal Abnormalities in PCOD | Parameter | Finding | Clinical Significance | | --- | --- | --- | | **LH:FSH ratio** | Elevated (>3:1, often >2–3:1) | Hallmark of PCOD; drives excessive androgen production | | **Free testosterone** | Elevated | Causes hirsutism, acne, male-pattern alopecia | | **Androstenedione** | Elevated | Adrenal contribution to hyperandrogenism | | **Prolactin** | Normal or mildly elevated (<25 ng/mL) | NOT a primary feature; marked elevation suggests other diagnosis | | **TSH** | Normal | Must exclude hypothyroidism (can mimic PCOD) | | **Insulin** | Elevated (fasting & post-glucose) | Present in 50–70%; drives ovarian androgen synthesis | **High-Yield:** Prolactin >25 ng/mL in a woman with suspected PCOD should raise suspicion for **prolactinoma, primary hypothyroidism, or medications** (dopamine antagonists). This is a common exam trap — students confuse mild prolactin elevation (seen in 20–30% of PCOD) with a primary feature. **Clinical Pearl:** The elevated LH drives thecal cell androgen production; hyperinsulinemia amplifies this by suppressing SHBG and increasing free androgen bioavailability. This dual mechanism explains why both hormonal and metabolic dysfunction coexist in PCOD. ### Why Prolactin Elevation Is NOT Primary in PCOD 1. Prolactin elevation in PCOD is **mild and secondary** — likely due to TRH stimulation from altered dopamine tone or mild hypothyroidism. 2. **Marked hyperprolactinemia (>25 ng/mL)** mandates MRI pituitary to exclude prolactinoma. 3. Prolactin does NOT explain the LH:FSH ratio elevation or the insulin resistance pattern seen in PCOD. [cite:Textbook of Obstetrics & Gynaecology, Jeffcoate 4e Ch 24]
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