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Biomedical subjects

A Spada

Publications and source records attributed to A Spada.

At least 145 records · Page 8Linked to original sources
PubMed1982

In vitro effect of dopamine on growth hormone (GH) release from human GH-secreting pituitary adenomas.

The effect of dopamine (DA) on GH release was studied in monolayer cultures obtained from 21 GH-secreting pituitary adenomas. DA at a concentration of 10(-6) M inhibited GH release in 13 adenomas (group 1: inhibition from 27--74%), had no effect in 3 (group II), and elicited a marked stimulation in 5 (group III: stimulation from 62--170%). The adenomas of acromegalic patients which were preoperatively responsive to DNA infusion (4 micrograms/kg . min) al fell into group I, whereas adenomas from patients not responsive to DA in vivo fell into groups II and III. The dose dependency of the effect of DA on GH secretion was studied in groups I and III. In group I adenomas the maximal inhibition was from 32--76% between 10(-7) and 2 x 10(-5) M DA. At high concentrations DA elicited a stimulatory effect. In group III adenomas the maximal stimulation was from 95--310% between 10(-7) and 10(-5) M DA. The dopaminergic ergot derivative CH 29--717 was as potent as DA in inhibiting GH release but, in contrast to DA, was nearly ineffective in stimulating the secretion of the hormone. We hypothesize that the different in vitro responsiveness of GH-secreting pituitary adenomas to DA could be due to the presence of multiple forms of DA receptors.

Adenoma↗
PubMed1980

[A rare case of acute mandragora poisoning. Diagnostic and therapeutic criteria].

After mentioning the botanic characteristics of mandragora, its territorial distribution, morphological characteristics and the toxicological properties of its alkaloids, a clinical case of accidental mandragora poisoning is reported. The case was successfully treated with atropinic block antagonists, namely cholinesterase inhibitors. Apart from its serious symptomatology, mandragora poisoning also involves considerable metabolic commitment of liver and kidney, which present evident signs of disturbance. Information about these and other insidious plants should be spread to prevent such cases of poisoning, whose gravity is enhanced by the fact that they are exceptional and not often encountered in clinical practice.

Acute Disease↗
PubMed1979

Thyrotropin secretion in patients with central hypothyroidism: evidence for reduced biological activity of immunoreactive thyrotropin.

TSH concentration was measured in plasma before and after TRH administration (200 micrograms, iv) in 89 patients with documented hypothyroidism consequent to various hypothalamic-pituitary disorders. Basal plasma TSH was less than 1.0 microI/ml in 34.8%, between 1.0-3.6 microU/ml in 40.5% and slightly elevated (3.7-9.7 microU/ml) in 24.7% of the cases. The plasma TSH response to TRH was absent in 13.5%, impaired in 16.8%, normal in 47.2%, and exaggerated in 22.5% of the cases, with delayed and/or prolonged pattern of response in 65% of the cases. The dilution curves of several plasmas drawn before and after TRH were parallel to those obtained with TSH standard preparation. After gel filtration, the elution pattern of TRH-stimulated plasmas from 4 patients did not show any major difference from that of pooled plasmas from normal subjects given TRH or from that of patients with primary hypothyroidism. Plasma TSH values determined by cytochemical bioassay on both basal and TRH-stimulated samples of 5 patients were markedly lower than those obtained by RIA. The serum T3 response to TRH was absent or low in 40 out of 53 patients in whom it was evaluated. The administration of T3 (100 micrograms/day for 3 days) or dexamethasone (3 mg/day for 5 days) respectively suppressed or reduced both basal and TRH-induced plasma TSH levels. Two patients became hypothyroid shortly after pituitary surgery in spite of basal and TRH-induced plasma TSH levels similar to or higher than those before surgery. Though thyroid atrophy due to chronic understimulation could explain the low T3 response to TRH in secondary hypothyroidism, it is difficult to reconcile thyroid understimulation with normal or increased plasma TSH unless the immunoreactive material has low biological activity. Present data suggest that several patients with hypothyroidism consequent to hypothalamic-pituitary diseases secrete a material which is immunologically similar to pituitary standard TSH and responds to stimulatory and suppressive agents in a manner similar to normal TSH but has low or absent biological activity. Thus, hypothyroidism due to insufficient TSH stimulation can be termed central hypothyroidism and can be due 1) to pituitary insufficiency (secondary hypothyroidism), 2) to a hypothalamic defect (tertiary hypothyroidism), or 3) to the secretion of biologically inactive TSH.

Biological Assay↗
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↗