Benserazide, an extra-cerebral inhibitor of dopa-decarboxylase, elicits prolactin (Prl) release in normal subjects when administered po. The aims of this study were to characterize the effect of benserazide on Prl release and to evaluate benserazide as a diagnostic tool in hyperprolactinaemic 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 iv 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 second dose of 50 mg, administered 150 min later, is without effect on Prl release, while TRH (200 μg iv) 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, we hypothesize that, in an area involving both the hypothalamus and the pituitary gland, anti-DA drugs (benserazide), TRH, and serotonin stimulate Prl release by interacting with different kinds of receptors. When administered to hyperprolactinaemic patients, benserazide stimulated Prl release in puerperal women and in patients with functional hyperprolactinaemias, 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 second tomography or computerized axial tomography of the brain, performed respectively 3 and 6 months later, revealed a pituitary microadenoma. These results suggest that benserazide may be a valuable diagnostic tool in the differential diagnosis of hyperprolactinaemia.
|Number of pages||7|
|Publication status||Published - 1981|
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