اختبار البرولاكتين

Prolactin regulation is unique among pituitary hormones in that it is primarily under inhibitory control from the hypothalamus. Dopamine, released from the hypothalamic arcuate nucleus, tonically inhibits prolactin secretion. Any interruption of this dopaminergic inhibition — whether from a stalk-compressing tumour, dopamine-blocking medications, or autonomously secreting prolactinoma cells — results in elevated prolactin. This mechanism explains why antipsychotic drugs that block dopamine receptors are potent prolactin-elevating agents and why dopamine agonists are the first-line treatment for prolactinomas.

The clinical assessment of hyperprolactinemia requires systematic exclusion of the many physiological and pharmacological causes before attributing elevation to pathology. A careful medication history is essential. If medication is excluded and prolactin remains consistently elevated on repeat testing, macroprolactin should be excluded by PEG precipitation. Only after confirming true monomeric prolactin elevation should pituitary MRI be requested. This structured approach avoids unnecessary imaging and treatment in the substantial proportion of patients with physiological or macroprolactinaemic elevation. When pathological hyperprolactinemia is confirmed, treatment with cabergoline is highly effective, with the majority of patients achieving prolactin normalisation and tumour shrinkage within months of commencing therapy.