Mandelic acid and phenylglyoxylic acid excretion in workers exposed to styrene under model conditions.
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Biomedical subjects
Publications and source records attributed to C Ferrari.
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One hundred ninety-one hyperprolactinemic patients (78 women and 13 men; 54 with pituitary macroadenoma, 53 with microadenoma, and 84 with idiopathic disease) were treated for 2 to 48 months with one or two of the following prolactin (PRL)-lowering drugs: bromocriptine, metergoline, and lisuride. All of the three drugs used were highly effective in lowering PRL levels and restoring gonadal function both in females and in males in the majority of patients with either idiopathic or tumorous disease. In poorly responsive patients, increasing the drug doses resulted in further PRL lowering for all the three drugs. Mild side effects were frequently encountered with initiation of drug treatment but spontaneously subsided in most cases; severe side effects, necessitating stopping of the treatment, occurred in only 12 instances, but changing of the drug allowed PRL-lowering treatment to be continued in 11 of them.
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We have previously reported that labetalol infusion increases prolactin (PRL) secretion in hypertensive patients. In an attempt to investigate the site where labetalol stimulates PRL, the drug was infused intravenously (100 mg) into healthy subjects, both under basal conditions and after pretreatment with L-dopa plus carbidopa (250 mg and 25 mg respectively every 6 h for 1 day), since this regimen has been reported to blunt the PRL responses to centrally acting stimuli. The effects of oral labetalol administration (100 and 200 mg) on PRL was also evaluated. Serum PRL concentration did not change after oral labetalol, whereas it was increased by intravenous drug administration. This effect was completely abolished by pretreatment with L-dopa plus carbidopa. These findings, though they do not demonstrate the mechanism, suggest that the hyperprolactinaemia induced by labetalol is mediated inside the blood-brain barrier.
A patient with prolactin-secreting pituitary microadenoma was treated with bromocriptine, 5 mg daily for 1 year. Despite normalization of prolactin levels throughout the treatment period, partial destruction of the sellar floor with growth of the adenoma into sphenoidal sinus were evident in a control tomography performed at the end of the treatment.
PRL secretory dynamics were evaluated by several stimulation and suppression tests in nine patients with hyperprolactinemia due to organic hypothalamic disease. Basal PRL levels ranged between 20-63 ng/ml. There was a normal PRL response to TRH in eight cases (i.e. doubling of basal levels), whereas none of the seven tested subjects responded to sulpiride. The same dissociation of responses was not observed in any of the patients who were still hyperprolactinemic after surgery. Concomitant dopamine infusion resulted in sulpiride-induced PRL release in the four subjects so studied. None of 50 other hyperprolactinemic patients (11 with macroprolactinoma, 18 with microprolactinoma, and 21 with idiopathic hyperprolactinemia) showed PRL response to TRH but not to sulpiride. The TRH-induced PRL increase was significantly higher than that induced by sulpiride in hypothalamic hyperprolactinemia and significantly lower in idiopathic disease as well as in healthy controls; no differences were found in prolactinoma patients. The administration of substances resulting in stimulation of pituitary dopamine receptors, such as dopamine and L-dopa, induced a normal PRL suppression in 7 patients with hypothalamic disease so tested, whereas central nervous system-acting dopaminergic drugs, such as carbidopa plus L-dopa and nomifensine, failed to lower PRL levels in most cases (even when normoprolactinemic after surgery). These data suggest that the mild to moderate hyperprolactinemia found in many patients with hypothalamic lesions is due to dopamine deficiency at the pituitary level, that TRH and dopamine receptors at the lactotropes are intact in this condition, and that paired TRH and sulpiride tests may be of some diagnostic utility in hyperprolactinemic patients. They further suggest that subjects with so-called idiopathic hyperprolactinemia do not suffer from the type of hypothalamic derangement exhibited by patients with organic lesions of the hypothalamus.
Hydroxyurea is a well known enzyme urease inhibitor. Bacteria strains producers of enzyme urease can be the cause of struvite calculosis. Clinical studies have shown that treatment with hydroxyurea can produce acid urine in patients suffering from struvite calculosis. In this work antiurease and antibacterial activity of hydroxyurea was valued in vitro against Proteus mirabilis strains. Our results seem not to agree with the ones obtained in vivo.
External biliary drainage, the "routine" manner of terminating surgery on the common bile duct, should now become almost obsolete as new methods for operation and exploration during surgery are perfected. A review of cases receiving biliary surgery over a period of 20 years showed that external biliary drainage was conducted in only 4 p. cent of operations on the common bile duct (excluding biliodigestive anastomoses). External biliary drainage should be employed only after due reflection : trans-cystic drainage, the "minor" form, will be indicated less and less as investigational methods during operation develop, while Kehr's drain, the "major" form, will occupy a limited but necessary place in certain cases, primarily in angiocholitis.
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The effects of chronic prazosin treatment (3 mg/day for three weeks) on plasma renin activity (PRA) and plasma aldosterone (PA) levels were evaluated in 12 hypertensive patients, under conditions of metabolic balance. After three weeks of drug administration no significant change occurred in PRA as well as PA levels, with respect to pretreatment values, both in basal conditions and following 2 hours of ambulation. No change was observed in heart rate, while a fall in both systolic (P less than 0.02) and diastolic (P less than 0.05) blood pressure occurred in supine as well as in deambulation-stimulating condition. A mild increase in body weight (P less than 0.05) and a decrease in serum sodium (P less than 0.05) was induced by prazosin treatment. These findings are in keeping with the pharmacologic properties of prazosin, which is a selective blocker of postsynaptic alpha adrenoreceptors and therefore lowers vascular resistance without reflex sympathetic overactivity. The moderate volume expansion after prazosin does not appear to be aldosterone mediated.
A morphological and ultrastructural study was undertaken from a personal series of meningiomas. Especially the fine structure of the tumour has been described by the electron microscopic study of 16 meningotheliomatous and 4 fibroblastic meningiomas. In all cases, it was possible to distinguish certain cells with epithelial features such as desmosomes, microfilaments and interdigitating extensions. Also the cytological patterns of fibroblastic meningiomas usually were similar to the meningotheliomatous type, anyhow the intercellular space between the interdigitating extensions of adjacent cells was occupied by collagen-fibers. At present, it has been impossible to demonstrate the capability of the tumour cells to synthetize collagen. Since the tumour cells of both the meningiomas are substantially similar to the subarachnoid space meningocyte, it is concluded that the neoplasm rises from a cell with double potentiality for fibroblastic and epithelial differentiation.
The effect of acute oral administration of loperamide (4, 8 and 16 mg), a peripheral opiate agonist used in the treatment of diarrhoea, on several metabolic and endocrine variables has been evaluated in healthy volunteers in comparison with placebo. Plasma glucose was significantly raised by all three doses, whereas serum IRI and C-peptide were decreased and serum FFA was significantly increased only after loperamide 8 and 16 mg; serum PRL, GH, LH and FSH did not change. The data suggest that opiates may be involved in the regulation of glycaemia, probably by modifying islet hormone secretion by acting at a peripheral site, since loperamide does not cross the blood-brain barrier. Although the precise mechanism of these actions is unknown, it is suggested that the effects of loperamide are mediated either by stimulation of opiate receptors per se, or by suppression of acetylcholine release from cholinergic nerve endings. The lack of change in pituitary hormone secretion by loperamide is in agreement with previous observations indicating that opiate effects on PRL, GH and gonadotropins occur at the level of the central nervous system.
Acute clonidine administration is known to induce a significant rise in plasma glucose in man. In order to evaluate the possible effect of prolonged drug treatment on glucose metabolism, paired OGTTs were performed in 12 hypertensive patients (6 with normal and 6 with abnormal glucose tolerance) in basal conditions and following 1-week's administration of clonidine (0.15 mg every 8 h) Basal plasma glucose and serum insulin concentration as well as glucose tolerance and insulin response to oral glucose did not change in either group after treatment. Although the mechanism(s) mediating the transient hyperglycemic action of clonidine are not fully understood, the present findings indicate that this drug does not exert diabetogenic effects during chronic treatment, and suggest that homeostatic mechanisms may counteract the acute effect of clonidine on glucose metabolism.
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