Climacteric symptoms according to body weight in women of different socio-economic groups.

The people influence of body weight on the climacteric symptoms of 618 selected women in spontaneous post-menopause has been studied bases on data collected at a Geriatric Centre and subsequently incorporated into a postal questionnaire. These cases were divided into 3 groups according to the "obesity degree": (I) less than 5 kg (53.1% of the cases);(II) between 5 and 15 kg (31.7%); and (III) greater than 15 kg (15.2%). The data were also analysed according to the socio-economic groups to which the women belonged. Overweight women, compared with thin women, seemed to suffer less "somatic" symptoms such as hot flushes and perspiration, independently of their socio-economic level. This might well be a consequence of the higher endogenous oestrogen activity. On the contrary, "psychic" symptoms (anxiety, depression, irritability, crying spells) seemed to be more frequent and severe (a) in the "obesity degree" sub-group III, compared with sub-groups I and II, in the women belonging to the higher socio-economic group, and (b) in the sub-groups I and III, compared with sub-group II, in the women belonging to the lower socio-economic group. Such a difference between the socio-economic groups is possibility due to cultural factors. The effects of endogenous oestrogens in the overweight women seem to be easily overruled by the influence of psychological factors.

Partial remission of hyperprolactinemic amenorrhea after bromocriptine-induced pregnancy.

Clinical and/or biological improvement has been observed in 7 out of 17 patients with hyperprolactinemic amenorrhea followed for 6-15 months after the successful outcome of bromocriptine (Parlodel, Sandoz)- induced pregnancy. The ovulatory cycle was resumed in 2 out of these 7 patients (with subsequent spontaneous conception in 1); in 3 others the medroxyprogesterone acetate test became positive. In all cases, post-partum prolactin values were considerably reduced. The possible causes of this improvement are discussed, examining the present data and those in the literature. Regressive lesions, due for example to vascularization defects or hemorrhage occurring in the prolactin-secreting tissue, as a result of the hyperplastic stimulus of estrogens during pregnancy, are suggested as a possible explanation.

Effect of sulpiride on plasma prolactin levels in women with puerperal or pathological hyperprolactinaemia.

The effect of 100 mg im sulpiride on plasma Prl levels was studied in 10 normal females, 21 patients with galactorrhoea and normal plasma Prl, 10 women with puerperal hyperprolactinaemia and 27 patients with amenorrhoea-galactorrhoea and high plasma Prl levels. The response to sulpiride in patients with galactorrhoea but normal PRL was slightly higher (P < 0.05) than that observed in normal women, but only if expressed in per cent. Women with puerperal hyperprolactinaemia respond to the drug with a marked increase in Prl (mean +/- SEM: 563.0 +/- 142.8%), even though their baseline values are already very high (mean +/- SEM: 133.6 +/- 23.8 ng/ml). By contrast, there is a lower or no response to sulpiride in 13 women with pituitary tumour. The same was true in 11 patients with hyperprolactinaemia of uncertain aetiology but also 10 of these subjects presented signs suggestive of a tumour. In the last 3 patients with pathological hyperprolactinaemia in whom a consistent Prl increase after sulpiride was observed, hyperprolactinaemia was probably not of tumourous origin. On the basis of these results, the sulpiride test appears promising for discriminating between organic and 'functional' cases of enhanced Prl secretion.

Hormone patterns during bromocriptine-induced pregnancy in hyperprolactinemic patients.

Plasma prolactin (PRL) and human placental lactogen (HPL), and urinary estriol and pregnanediol were studied during pregnancies induced with bromocriptine (Parlodel, Sandoz) in 10 cases of hyperprolactinemia. Previous selective adenomectomy or intrasellar implantation of radioactive gold (198Au) failed to induce a complete remission in 3 of these subjects. PRL rapidly increases after bromocriptine withdrawal, reaching values higher than those in normal women in the same stage of pregnancy within a few weeks. At term, pathological PRL levels occurred in 3 subjects only (with distinct alterations of the sella turcica). Estriol, pregnanediol and HPL were normal in all cases. These findings suggest that PRL levels higher than those normally observed during pregnancy do not alter fetoplacental endocrine function.

Increased thyrotrophin secretion induced by sulpiride in man.

100 mg i.m. sulpiride (a dopamine-receptor-blocking drug) led to a significant rise in plasma TSH in normal womem, in female patients with galactorrhoea, and, to a much more marked degree, in male and female patients with primary hypothyroidism. In the hypothyroid patients, there was a significant positive correlation between basal TSH and its maximum increment after sulpiride. The drug proved to be an even more potent stimulator of PRL, at least in subjects with normal blood PRL. Normal males, on the other hand, displayed no significant changes in TSH after sulpiride. Continuous administration (150 mg/day per os for 15 days) also resulted in enhancement of TSH in normal women. These results suggest that TSH release is controlled by a dopaminergic mechanism in man. The more accentuated TSH response in hypothyroid patients may perhaps be attributable to the absence of negative-feedback on the part of thyroid hormones.

Inhibition of thyrotropin and prolactin secretion by dopamine in man.

The effect of dopamine on thyrotropin (TSH) and prolactin (PRL) levels was studied in 5 normal subjects, 7 women with galactorrhea, 9 acromegalics and 4 patients with primary hypothyroidism. Dopamine infused at the rate of 280 micrograms/min produced significant decrease in plasma TSH and PRL levels in all four groups, though a lower fall in TSH was noted in acromegalics. A similar reduction in PRL was also noted after 28 micrograms/min dopamine. Phentolamine infusion (0.5 mg/min) had no effect on PRL response to dopamine. These results indicate that a dopaminergic stimulation led to an inhibition of TSH and PRL secretion. Since the high polarity of dopamine impedes its passage through the blood-brain barrier, its site of action should be outside this barrier, probably in the pituitary.

Long-term treatment with 2-Br-alpha-ergocryptine in acromegaly.

Thirty acromegalic subjects underwent chronic CB154 therapy (10-20 mg daily) for periods ranging from 3 months up to 2 years. In 18 out of 21 patients, who exhibited consistent HGH reduction following acute administration of the drug, there was also during chronic treatment, a suppression of the plasma HGH levels exceeding 50% of base line values, e.g. from mean daily values between 14-197 ng/ml (mean +/- SEM = 57.8 +/- 12.4 ng/ml pre-treatment) to 2-19 ng/ml (mean 8.3 +/- 1.2 ng/ml post-treatment). In 12 of the subjects who responsed to chronic CB154 treatment, the mean daily values of HGH were below 10 ng/ml. The suppression of plasma HGH was maintained unaltered throughout the whole course of therapy. In the 9 subjects, in whom no consistent HGH decrease was evidenced with acute CB154 administration, there was accordingly a minor or no suppression of HGH values during the chronic treatment. In 13 subjects, irrespective of the degree of their GH responses, the plasma prolactin levels were constantly inhibited by CB154; instead the drug failed to modify significantly the TRH or insulin-induced GH release. These changes in the hormonal parameters were paralleled by marked clinical amelioration and improvement of some of the metabolic alterations frequently encountered in acromegaly, e.g. reduced carbohydrate tolerance, increased insulin resistance, diminished fall of plasma phosphorus after insulin, decreased urinary excretion of phosphate, hyper-hydroxyprolinuria and hyper-calciuria. Collectively, these data demonstrate that CB154 thrapy is effective in reducing HGH hyper-secretion in many acromegalic patients during long-term treatment.

Effect of dopamine on plasma growth hormone and prolactin levels in normal and acromegalic subjects.

In contrast with other dopaminergic drugs (L-dopa, apomorphine or bromocriptine) a 280 mug/min dose of dopamine infused for 120 min failed to induce an increase in plasma GH in 9 normal subjects. During dopamine infusion, no significant change in the GH response to arginine was also noted, whereas prolactin displayed a significant fall. In 15 acromegalic patients, on the other hand, the drug caused a marked fall in both GH (mean+/-SE; 71.1%+/-5.6) and prolactin (mean+/-SE; 67.6%+/-4.0) followed by a distinct rebound after the end of the test. There was a very close relation (P less than 0.001) between the maximum per cent decrease in GH during dopamine and after 2.5 mg bromocriptine by mouth. Dopamine also inhibited the GH response to TRH (4 patients). Since dopamine does not readily cross the blood-brain barrier, these results suggest that the stimulating effect of dopaminergic drugs on GH secretion in the normal subject is exerted via the CNS, whereas in acromegaly there is a direct action on structures lying outside the blood-brain barrier, probably in the hypophysis. Dopaminergic inhibition of prolactin is primarily the result of action on the hypophysis, as well as on the hypothalamus, in both normal and acromegalic subjects.