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THE DECREASED BASAL AND STIMULATED PROLACTIN LEVELS IN ISOLATED GONADOTROPHIN DEFICIENCY: A CONSEQUENCE OF THE LOW OESTROGEN STATE
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Citations
19
References
1982
Year
FertilityReproductive HealthGynecologyFemale Reproductive FunctionReproductive BiologyOvarian AgingReproductive EndocrinologyFemale InfertilityReproductive MedicineWomen's PhysiologyPublic HealthEndocrine MechanismDopaminergic AntagonistBasal OestradiolEndocrinologyPharmacologyProlactin SecretionUrologyPhysiologyMenopauseMedicineEndocrine ResearchReproductive HormoneGonadotropin Biology
Prolactin secretion has been evaluated in seven male and six female patients with isolated gonadotrophin deficiency (IGD). The subjects were challenged with the dopaminergic antagonist, metoclopramide (10 mg) and TRH (200 μg) before, during and after cessation of hormonal treatment. Five females received three consecutive 21‐day courses of ethinyl oestradiol (0·1 mg daily) at monthly intervals and the remaining subject conjugated oestrogens (Premarin 0·625 mg daily) according to a similar protocol. Treatment of the males with hCG (pregnyl) 5000 iu twice weekly led to a rise in oestradiol and testosterone levels. Two males were receiving pergonal (human menopausal gonadotrophin) in addition. In the untreated state in both males and females, basal oestradiol and PRL levels were decreased as were the PRL responses to metoclopramide and TRH as compared with normal controls. During treatment in both groups, there was an increase in basal PRL levels as well as PRL response to the two stimuli, which became indistinguishable from the controls. Cessation of treatment was associated with a rapid decrease in basal PRL levels and PRL elevation following metoclopramide and TRH. In contrast to the effect of hCG, the administration of two non‐aromatizable androgens (mesterolone and fluoxymesterone) had no effect on basal and TRH‐induced PRL secretion. The administration of clomiphene citrate during hCG treatment in one male IGD patient produced a decrease in the basal and stimulated PRL response. It is concluded that the low basal PRL levels and impaired PRL responses to stimulation are not an inherent component of the syndrome of IGD, but a consequence of the abnormal steroid milieu.
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