A 24-year-old woman presents with fatigue, weight gain, cold intolerance, and a serum TSH of 0.3 mIU/L (low-normal) with low free T4. Prolactin is mildly elevated at 45 ng/mL. MRI of the pituitary is normal. The clinician suspects primary hypothyroidism with hypothalamic compensation. Which mechanism best explains the hyperprolactinemia in this setting?

• A ADH co-secreted with CRH stimulates prolactin release
• B Low T3 directly stimulates pituitary prolactin gene transcription
• C Dopamine synthesis in the arcuate nucleus is increased
• D TRH stimulates lactotrophs to secrete prolactin ✓

Explanation

In primary hypothyroidism, elevated TRH (due to loss of thyroid hormone negative feedback) stimulates not only TSH but also prolactin secretion from lactotrophs, because TRH receptors are present on both cell types. This causes mild hyperprolactinemia and explains galactorrhoea sometimes seen in hypothyroidism. Dopamine synthesis would be reduced, not increased, by the same feedback loss. ADH has no prolactin-stimulating role. Low thyroid hormone does not directly upregulate prolactin transcription.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

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Written and medically reviewed by the StethoPrep medical team.