Inhibition of cyclic gonadotropin secretion by endogenous human prolactin

Abstract

The resumption of cyclic uterine bleeding reportedly accompanies the use of human prolactin (HPRL)-suppressing agents in postpill galactorrhea-amenorrhea. In this laboratory, HPRL suppression with L-dopa was variable and short lived. Basal plasma HPRL levels were elevated before and after as much as five months of therapy. Galactorrhea persisted and mean gonadotropin concentrations were subnormal. An immediate and sustained attenuation of HPRL secretion ( less than 200 per cent) followed the use of 2-Br-alpha-ergocryptine (CB-154). Cyclic gonadotropin secretion resumed and was accompanied by ovulation and, in one instance, pregnancy. The cessation of galactorrhea was positively correlated with the rise in the daily concentration of 17 beta-estradiol. Cyclic postovulatory menstruation continued after the cessation of CB-154 treatment. HPRL levels remained normal. The daily patterns of human follicle-stimulating hormone (HFSH) and human tuteinizing hormone (HLH) secretion created by the suppression of HPRL displayed an inherent rhythmicity identical to that observed at the time of menarche. The inhibitory effects of HPRL appeared directed at cyclic rather than tonic gonadotropin secretion. At the same time, diminished ovarian estrogen production seemed to increase mammary gland sensitivity to HPRL, leading to lactation. One may postulate, therefore, that the ingestion of sex steroids is associated with an over-all suppression of endogenous cyclic and, to a lesser extent, tonic gonadotropin secretion secondary to which ovarian function is attenuated. Without physiologic concentration of circulating estrogen, HPRL induces mammary alveolar function with the production of a milklike secretion.

PIP: Agents used to induce cyclic menstruation following nonpuerperal galactorrhea and amenorrhea, such as l-dopa, appear to decrease the plasma concentration of human prolactin (HPRL). This study presents preliminary data on the clinical activity of such drugs with regard to HPRL and gonadotropin secretion in postpill galactorrhea-amenorrhea. 5 women suffering from this postpill syndrome after using Depo-Provera for various periods of time were given l-dopa (2 gm daily); HPRL suppression by l-dopa was variable and short-lived. However, an immediate and sustained attenuation of HPRL secretion of greater than 200 percent was found after administration of 2-Br-alpha-ergocryptine (CB-154); women so treated resumed cyclic bleeding and ovulation; 1 pregnancy occurred. Cessation of galactorrhea was positively correlated with the rise in daily concentration of 17-beta-estradiol. Cyclic postovulatory menstruation continued after cessation of CB-154. HPRL levels remained normal. Daily patterns of human follicle stimulating hormone and luteinizing hormone created by suppression of HPRL showed an inherent rhythmicity identical to that observed at menarch. HPRL inhibitory effects were directed at cyclic rather than tonic gonadotropin secretion. Diminished ovarian estrogen production also seemed to increase mammary gland sensitivity to HPRL, resulting in lactation. It is postulated that the use of sex steroids is associated with an overall suppression of endogenous cyclic gonadotropin secretion secondary to which ovarian function is attenuated.