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Biomedical subjects

F Massara

Publications and source records attributed to F Massara.

At least 55 records · Page 3Linked to original sources

Arginine-induced hypophosphatemia and hyperkaliemia in man.

The effects of a 0.5 g/kg body weight arginine infusion on plasma inorganic phosphates and potassium were examined in nineteen normal subjects. Plasma phosphorus displayed a highly significant (p less than 0.001) fall with a maximum depression below baseline of 1.11 +/- 0.15 mg/100 ml or 33 +/- 3% (mean +/- SEM); there was a significant correlation (p less than 0.01) between this fall and the insulin peaks induced by arginine. Plasma potassium levels displayed a distinct and significant increase in eleven of the twelve subjects studied; the maximum increase above baseline was 1.02 +/- 0.14 mEq/1 or 27 +/- 4.5% (p less than 0.001). No change occurred in blood pH values determined in four subjects. In six normal subjects, the test was repeated with the addition of somatostatin (250 micrograms bolus, followed by 500 micrograms/hr), which abolished the insulin and growth hormone response to arginine. It also abolished the fall in plasma phosphorus but appeared (if anything) to augment the increase in potassium. These findings show that arginine is responsible for a fall in plasma phosphorus related to the insulin response, and for an increase in plasma potassium of clinical significance, the mechanism(s) of which, however, are still obscure.

Adult↗

[Use of releasing hormones in endocrinological diagnosis].

The identification and synthesis of thyrotrophin-releasing hormone (TRH) and luteinising hormone releasing hormone (LHRH) has widened our knowledge of hypothalamo-hypophyseal-thyroid and hypothalamo-hypophyseal-gonad diseases. More precisely, administration of these two releasing factors, by permitting the evaluation of pituitary TSH, LH, and FSH reserves, reveals otherwise undefinable changes in hypophyseal function. An account of the manner of execution and measurement, the administration route, and side-effects related to TRH and LHRH tests is followed by a description of the main diseases in which they offer the greatest degree of diagnostic assistance.

Acromegaly↗

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.

Acromegaly↗

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.

Adolescent↗

Carbidopa inhibits the growth hormone- and prolactin-suppressive effect of L-dopa in acromegalic patients.

The plasma GH, PRL, TSH, and dopamine (DA) responses to an infusion of L-dopa were examined in six acromegalic patients before and after pretreatment with carbidopa, a drug which inhibits the peripheral conversion of L-dopa to DA. Carbidopa neither modified baseline DA nor induced changes in baseline GH, PRL, or TSH levels. The drug instead markedly reduced the L-dopa-induced DA rise, an effect which was concomitant to a striking reduction of the suppressive effect of L-dopa on plasma GH and a partial inhibition of the suppressive effect of L-dopa on plasma PRL. TSH levels did not change either after L-dopa alone or L-dopa plus carbidopa. These data demonstrate that in "responder" acromegalics, L-dopa inhibits GH secretion through its peripheral conversion to DA and not via activation of central DA neurotransmission. For the effect of L-dopa on PRL secretion, in addition to a peripheral dopaminergic component, a central component cannot be disregarded.

Acromegaly↗

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.

Acromegaly↗

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.

Acromegaly↗

True hermaphroditism with XX/XY sex chromosome mosaicism: report of a case.

A case of true hermaphroditism with 46, XX/46, XY karyotype is reported. The propositus, reared as a male, showed ambiguous external genitalia with perineoscrotal hypospadias, and internal genitalia represented by bilateral ovotestes, normal uterus and tubes. Periodic menstrual bleedings appeared at puberty. The endocrinologic data demonstrated the secretory activity of both the ovarian and the testicular tissue. The analysis of red cell, lymphocyte and serum markers, done on the propositus and on his parents, failed to show any evidence of double fertilization. On this basis, the origin of the XX/XY condition (mosaicism versus chimerism) and its developmental consequences are discussed.

Child↗