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Biomedical subjects

C Ferrari

Publications and source records attributed to C Ferrari.

At least 343 records · Page 19Linked to original sources
PubMed1978

Failure of lysine-acetylsalicylate and phenylbutazone to affect gastrin secretion in healthy adults.

The effect of acute parenteral and chronic oral administration of lysine-acetylsalicylate and phenylbutazone on fasting and meal-stimulated serum gastrin levels was investigated in healthy volunteers. No significant changes in gastrin secretion were induced by any treatment. The results confirm and extend previous observations suggesting that the ulcerogenic properties of salicylates and phenylbutazone are not related to increased gastrin secretion.

Administration, Oral↗
PubMed1977

Effects of short-term clofibrate administration on glucose tolerance and insulin secretion in patients with chemical diabetes or hypertriglyceridemia.

The effect of 1-wk administration of clofibrate on plasma glucose and insulin (IRI) before and during oral glucose tolerance tests (OGTT), as well as on serum lipids, uric acid, growth hormone (GH), and cortisol, were evaluated in 18 nondiabetic patients with hypertriglyceridemia and in 28 patients with chemical diabetes. Fasting plasma glucose, OGTT-glucose, and IRI areas were significantly decreased in both groups of patients, though the effects on glucose metabolism were much more marked in diabetics; 30-min IRI relative increase was unchanged; fasting plasma IRI was reduced in diabetics only. Glucose utilization during insulin tolerance tests carried out in 6 diabetics was significantly enhanced after treatment. Serum triglycerides (TG) and cholesterol (Chol) were significantly decreased in both groups of patients, as were serum free fatty acids and uric acid in diabetics; plasma GH and cortisol did not change. Significant correlations were found in diabetics between the postclofibrate decrease in OGTT-glucose area and the following: pretreatment values of serum Chol (r + 0.42, p less than 0.05) and of 30-min IRI absolute and relative increase (r + 0.44 and + 0.38, respectively, p less than 0.05); postclofibrate decreases in serum TG (r + 0.40, p less than 0.05), in fasting plasma glucose (r + 0.73, p less than 0.001), and in OGTT-IRI area (r + 0.57, p less than 0.01). These data suggest that the improvement in glucose metabolism observed during short-term clofibrate administration may be due to increased insulin sensitivity.

Adolescent↗
PubMed1976

Effect of two serotonin antagonists on prolactin and thyrotrophin secretion in man.

The effects of serotoninergic blockade on prolactin and thyrotrophin secretion in man was evaluated by determining the basal and TRH-stimulated serum prolactin and TSH concentrations in normal volunteers before and after a 3 days course of cyproheptadine or methergoline administration. Cyproheptadine, a serotonin antagonist with antihistaminic, anticholinergic and antidopaminergic properties as well, did not affect prolactin secretion, while it reduced the serum TSH response to TRH; methergoline, a specific blocker of central serotonin receptors, decreased basal and TRH-induced serum prolactin levels, without affecting TSH secretion. These results support the existence of serotoninergic stimulatory influences on human prolactin release, while suggesting that human TSH secretion is not modulated by serotoninergic inputs.

Cyproheptadine↗
PubMed1976

Failure of oral 5-hydroxytryptohan administration to affect prolactin secretion in man.

Oral 5-hydroxytryptopahn (5-HTP) administration, either 200 mg acutely or 50 mg q.i.d. fr 3 days plus 200 mg acutely, failed to modify either basal or TRH-stimulated prolactin secretion in normal subjects. This is at variance with the stimulatory action of intravenous tryptophan on human prolactin release. However, it is doubtful that 5-HTP at the dose used may increase brain serotonin concentration; moreover, the hydroxlated amino acid is also taken up by catecholaminergic neurons, from which noradrenaline and dopamine may then be released. It is concluded that the failure of 5-HTP to affect prolactin secretion in man is not a proof against the existence of serotoninergic stimulatory influences on human prolactin release.

5-Hydroxytryptophan↗
PubMed1976

Influence of L-prolyl-L-leucyl-glycine amide on growth hormone secretion in normal and acromegalic subjects.

Melanocyte Release-Inhibiting Peptide (MRIP-I) did not affect circulating levels of ACTH, LH, FSH, TSH,ORL, betaMSH and insulin when iv infused (5.0 mg in 5 min plus 0.4 mg/min for 70-115 min), while it significantly reduced serum GH response to hypoglycemia in normal subjects and lowered serum GH levels in acromegalics. There was no correlation between the fall in serum GH after MRIP and after dopaminergic drugs in acromegaly. These data are compatible with either a direct suppressive action exerted by MRIP-I at pituitary level or an extra-pituitary effect not involving dopaminergic pathways. It can be spec-lated that since labelled MRIP-I accumualtes in the pineal and melatonin blunts GH response to hypoglycemia, the pineal gland might be involved in the MRIP-I-induced suppression of GH secretion.

Acromegaly↗
PubMed1976

Some aspects of hypothalamic-pituitary function in patients with anorexia nervosa.

The secretion of lutenizing hormone (LH), follicle-stimulating hormone (FSH), thyrotrophin (TSH) and prolactin (PRL, was studied in 17 women suffering from anorexia nervosa. The mean basal serum LH was reduced (8.4 +/- 0.8 SE mIU/ml; P less than 0.001 vs normal controls), while LH increase after gonadotrophin-releasing hormone (LH-RH) appeared to be normal in 9 cases and impaired in 6 cases. The mean basal FSH did not significantly differ from normal subjects (3.9 +/- 0.5 mIU/ml), while LH-RH administration elicited an exaggerated increase in 7 cases and a normal increase in 8 cases: the mean FSH response was significantly higher than in controls (P less than 0.02). Plasma oestradiol-17beta was reduced (20.4 +/- 0.4 pg/ml; P less than 0.001) while the serum testosterone levels were normal (0.73 +/- 0.09 ng/ml). Clomiphene administration induced an increase in gonadotrophins in only 1 out of 7 patients. The mean serum TSH concentration was normal (2.3 +/- 0.4 muU/ml), while serum thyroxine and triiodothyronine and free thyroxine index, thought generally in the normal range, were significantly lower than values obtained in a control group (6.1 +/- 0.4 mug/100 ml, P less than 0.005; 102.3 +/- 7.7 ng/100 ml, P less than 0.005; 3.8 +/- 0.3, P less than 0.05). Though the mean serum TSH increase after thyrotrophin-releasing hormone (TRH) was normal (12.0 +/- 2.3 muU/ml), there were 4 impaired and 1 exaggerated increases, and 8 patients showed a delayed and frequently prolonged response. The increase in serum T3 after TRH appeared lower than in normal subjects (36.3 +/- 1.8 ng/100 ml, P less than 0.001). Serum PRL levels in basal conditions were higher than in the controls (19.4 +/- 4.1 ng/ml, P less than 0.001) while the increase in PRL after TRH was exaggerated in only 2 patients. The present data suggest that the primary failure in gonadotrophin secretion in anorexia nervosa occurs at hypothalamic level; moreover the data on TSH and PRL secretion also point to the existence of a hypothalamic disorder in this disease.

Adolescent↗
PubMed1975

Triiodothyronine response to thyrotrophin releasing hormone in patients with hypothalamic-pituitary disorders.

The serum triiodothyronine concentration was evaluated before and after thyrotrophin releasing hormone in fifty-six patients with hypothalamic-pituitary disorders (thirty-four had secondary hypothyroidism, twenty-two were euthyroid) and in twenty-four normal controls. Basal serum T3 was low in fifteen hypothyroid subjects and normal in the remainders. After TRH, serum T3 did not increase normally in twenty-five hypothyroid and in ten euthyroid patients; even the patients with normal or supranormal plasma TSH increase had significantly lower T3 responses than normal controls (P less than 0-0001 for hypothyroid, P less than 0-01 for euthyroid subjects). The finding of low T3 response to TRH in some euthyroid patients with hypothalamic-pituitary disorders can perhaps identify cases of preclinical secondary hypothyroidism, probably due to low biological activity of released TSH.

Clinical Trials as Topic↗