No abstract

No abstract

Intravenous metoclopramide (MET) (10 mg) induced a brisk PRL response with a mean \ m=+-\ sem peak of 85.3 \ m=+-\ 7.7 ng/ml maximal at 30 min. l-Dopa, but not atropine pre-treatment, attenuated the prolactin (PRL) response to MET. This indicates that the antidopaminergic properties of MET mediate PRL secretion. MET did not influence basal levels of TSH, LH or FSH. Neither did it affect their response to the respective releasing hormones. Our results indicate that dopaminergic blockade induced by iv MET, does not influence the secretion of the pituitary glycoprotein hormones.Dopamine, together with the other monoamines serotonin and noradrenaline modulates the secretion of the hypothalamic releasing hormones (Frohman 8c Stachura 1975). In addition, both in vivo and in vitro studies have shown that dopamine can act directly at the level of the pituitary to inhibit the

This study evaluated the effect of estrogens and androgens on TSH secretion in hypogonadal male and female patients with isolated gonadotropin deficiency (IGD). The IGD subjects were clinically euthyroid and had normal circulating levels of thyroid hormones and T4-binding globulin (TBG). The patients were challenged with TRH (200 micrograms) in the untreated state, during treatment, and 1 month after cessation of hormonal replacement therapy. For the study, five females were treated with ethinyl estradiol (0.05 mg twice daily) for 21 days; after stopping for 7 days, the treatment schedule was repeated for another two cycles. The remaining female was given a similar regimen with conjugated estrogens (0.625 mg daily). Five males were treated with hCG (5000 IU twice weekly) for 3 months; two were treated with hCG and Pergonal. The female patients had significantly decreased basal TSH levels as well as impaired TSH responses to TRH. After 3 months of ethinyl estradiol treatment, there was a rise in TBG, total serum T4 and T3 levels and a decrease in T3 resin uptake; the free T4 index was unchanged. During estrogen administration, there was no change in basal TSH, but there was an increase in the peak TSH response to TRH, which became identical to that of the controls. Cessation of estrogen was associated with a reduction in releasable TSH, and the profile reverted to the pretreatment state. In addition, serum TBG levels, with the associated changes in thyroid hormones, also returned to normal. The male patients had TSH responses to TRH identical to those of the male controls. After 3 months of hCG treatment, there was a marked rise in serum estradiol as well as testosterone. Serum T4 was reduced without a change in T3, T3 resin uptake, or TBG. Furthermore, there was no alteration in the TSH response to TRH. On the other hand, the administration of ethinyl estradiol (0.1 mg daily for 2 weeks) to two male IGD subjects produced an increase in TBG. This was associated with elevation of serum T4 and T3 levels and reduction of T3 resin uptake. During estradiol administration, there was an increase in the TSH response to TRH. These data are compatible with the hypothesis that estrogens are required to maintain a normal TSH response to TRH in the female. However, testosterone may counteract the effect of estradiol, which may explain why normal males tend to have a lower TSH response to TRH than females.

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.