Benserazide, a stimulator of prolactin release: a new test in the diagnosis of pituitary prolactin-secreting tumours

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Abstract
Benserazide, an extra-cerebral inhibitor of dopa-decarboxylase, elicits prolactin (Prl) release in normal subjects when administered orally. The aims of this study were to characterize the effect of benserazide on Prl release and to evaluate benserazide as a diagnostic tool in hyperprolactinemic patients. In normal subjects, the effect of 50 mg benserazide is reduced to a greater extent by 500 mg than by 200 mg L-dopa, and is nullified by dopamine (DA, 50 mg i.v. in 180 min), which also decreases fasting plasma Prl levels. Doses of 25, 50 and 150 mg benserazide elicit Prl responses which are slightly and progressively but not significantly higher; a 2nd dose of 50 mg, administered 150 min later, is without effect on Prl release, while TRH (200 .mu.g i.v.) elicits a further Prl peak. Since it is known that consecutive doses of TRH yield progressively lower PRl responses while 5-hydroxytryptophan (the precursor of serotonin) further increases PRl release in response to benserazide, in an area involving both the hypothalamus and the pituitary gland, anti-DA drugs (benserazide), TRH and serotonin may stimulate Prl release by interacting with different kinds of receptors. When administered to hyperprolactinemic patients, benserazide stimulated Prl release in puerperal women and in patients with functional hyperprolactinemias, but was totally ineffective in patients with pituitary adenomas, whatever the fasting plasma Prl levels. In 2 patients with a normal sellar tomography in whom benserazide induced no Prl release, a 2nd tomography or computerized axial tomography of the brain, performed respectively 3 and 6 mo. later, revealed a pituitary microadenoma. Benserazide may be a valuable diagnostic tool in the differential diagnosis of hyperprolactinemia.