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THE RESPONSE OF PROLACTIN TO CHLORPROMAZINE STIMULATION IN MEN WITH HYPOGONADOTROPHIC HYPOGONADISM AND EARLY PUBERTAL BOYS: RELATIONSHIP TO SEX STEROID EXPOSURE*

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SUMMARYThe effect of chlorpromazine (CPZ) on prolactin (PRL) secretion was studied in fourteen sexually immature males; nine with idiopathic hypogonadotrophic hypogonadism and five who proved to be normal early pubertal boys. Initially, clinical features and basal levels of testosterone, LH and FSH in serum collected in the morning and the gonadotrophin responses to LHRH stimulation were similar in all subjects. Following CPZ the early pubertal boys increased PRL levels by at least 15 ng/ml, responses similar to those of normal men, whereas no subject with complete hypogonadotropism increased PRL by more than 5 ng/ml. Two subjects with incomplete hypogonadotropism (‘fertile eunuchs’) exhibited responses similar to normals.Treatment with human chorionic gonadotrophin (hCG) or testosterone enhanced the PRL response to CPZ in three of six hypogonadotrophic subjects. Ten additional hypogonadotrophic men studied while receiving long term treatment with hCG or testosterone also manifested normal responses to CPZ. These data indicate that lack of sex steroid exposure, rather than a more generalized hypothalamic disorder, explains the attenuated PRL response to CPZ found in untreated men with idiopathic hypogonadotrophic hypogonadism. Moreover, CPZ‐stimulated PRL secretion may prove to be of practical value in distinguishing hypogonadotrophics from boys with delayed puberty.
Title: THE RESPONSE OF PROLACTIN TO CHLORPROMAZINE STIMULATION IN MEN WITH HYPOGONADOTROPHIC HYPOGONADISM AND EARLY PUBERTAL BOYS: RELATIONSHIP TO SEX STEROID EXPOSURE*
Description:
SUMMARYThe effect of chlorpromazine (CPZ) on prolactin (PRL) secretion was studied in fourteen sexually immature males; nine with idiopathic hypogonadotrophic hypogonadism and five who proved to be normal early pubertal boys.
Initially, clinical features and basal levels of testosterone, LH and FSH in serum collected in the morning and the gonadotrophin responses to LHRH stimulation were similar in all subjects.
Following CPZ the early pubertal boys increased PRL levels by at least 15 ng/ml, responses similar to those of normal men, whereas no subject with complete hypogonadotropism increased PRL by more than 5 ng/ml.
Two subjects with incomplete hypogonadotropism (‘fertile eunuchs’) exhibited responses similar to normals.
Treatment with human chorionic gonadotrophin (hCG) or testosterone enhanced the PRL response to CPZ in three of six hypogonadotrophic subjects.
Ten additional hypogonadotrophic men studied while receiving long term treatment with hCG or testosterone also manifested normal responses to CPZ.
These data indicate that lack of sex steroid exposure, rather than a more generalized hypothalamic disorder, explains the attenuated PRL response to CPZ found in untreated men with idiopathic hypogonadotrophic hypogonadism.
Moreover, CPZ‐stimulated PRL secretion may prove to be of practical value in distinguishing hypogonadotrophics from boys with delayed puberty.

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