Pasma prolactin response to the acute injection of sulpiride (1.5 mg/k BW im) was measured at 0800-0900h in 4 girls with idiopathic precocious puberty before and after 6 to 11 months of continuous therapy with 50 mg daily of cyproterone acetate (CA) orally administered. Two additional girls were examined after 26 and 28 months of therapy, respectively. Mean baseline prolactin concentrations were significantly higher in untreated girls with precocious puberty as compared to that of normal controls of the same chronological age and of a comparable degree of sexual maturation (14.5 +/- 1.9 SE vs. 7.4 +/- 1.8 SE ng/ml and vs. 9.5 +/- 1.8 ng/ml, respectively; P less than .02). Treatment with CA caused a significant further increase of plasma prolactin concentration (P less than .02 as compared to pre-treatment values); no correlation was observed between prolactin concentration and duration of treatment. No significant change in the integrated areas of prlactin response to sulpiride occurred after prolonged CA therapy. The results suggest that in idiopathic precocious puberty the action of CA upon the hypothalamic-hypophyseal complex is not solely antigonadotropic and that prolactin secretion is enhanced in patients given this drug.
Hyperprolactinemia in girls with idiopathic precocious puberty under prolonged treatment with cyproterone acetate.
ANGELI, Alberto;
1977-01-01
Abstract
Pasma prolactin response to the acute injection of sulpiride (1.5 mg/k BW im) was measured at 0800-0900h in 4 girls with idiopathic precocious puberty before and after 6 to 11 months of continuous therapy with 50 mg daily of cyproterone acetate (CA) orally administered. Two additional girls were examined after 26 and 28 months of therapy, respectively. Mean baseline prolactin concentrations were significantly higher in untreated girls with precocious puberty as compared to that of normal controls of the same chronological age and of a comparable degree of sexual maturation (14.5 +/- 1.9 SE vs. 7.4 +/- 1.8 SE ng/ml and vs. 9.5 +/- 1.8 ng/ml, respectively; P less than .02). Treatment with CA caused a significant further increase of plasma prolactin concentration (P less than .02 as compared to pre-treatment values); no correlation was observed between prolactin concentration and duration of treatment. No significant change in the integrated areas of prlactin response to sulpiride occurred after prolonged CA therapy. The results suggest that in idiopathic precocious puberty the action of CA upon the hypothalamic-hypophyseal complex is not solely antigonadotropic and that prolactin secretion is enhanced in patients given this drug.
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