We have studied the effect of the
oral administration of 200 mg
nomifensine (nom), a
drug which activates the dopaminergic system, on GH and PRL secretion in 15 normal subjects, 18 patients with idiopathic
hyperprolactinemia, and 17 patients with tumoral
hyperprolactinemia. GH levels increased significantly after nom in normal subjects (basal, 0.96 +/- 0.76 ng/ml; peak 4.6 +/- 0.61 ng/ml; P less than 0.01) and patients with
hyperprolactinemia, both idiopathic (basal, 1.0 +/- 0.38 ng/ml; peak, 4.2 +/- 1.0 ng/ml; P less than 0.05) and tumoral (basal 0.88 +/- 0.3 ng/ml, peak 6.68 +/- 1.2 ng/ml; P less than 0.01). Peak GH levels higher than 5 ng/ml were observed in 8 of 15 normal subjects, 6 of 18 patients with idiopathic
hyperprolactinemia, and 8 of 17 patients with tumoral
hyperprolactinemia. PRL levels decreased in response to nom in normal subjects, but not in patients with idiopathic or tumoral
hyperprolactinemia. A reduction in plasma PRL levels of at least 30% below the baseline was observed only in two patients with idiopathic
hyperprolactinemia and in none of the patients with tumoral
hyperprolactinemia. These results demonstrate that nom does not discriminate between idiopathic and tumoral
hyperprolactinemia. Since nom probably requires a hypothalamic pool of
dopamine to bring about its GH stimulatory effect, the suggestion that the lack of a PRL-lowering effect of the
drug is attributable to a
dopamine deficiency is not supported by our data.