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Biomedical subjects

F Salerno

Publications and source records attributed to F Salerno.

At least 55 records · Page 3Linked to original sources
PubMed1990

Utility of ascitic fluid analysis in patients with malignancy-related ascites.

One-hundred and thirty-three consecutive ascitic patients hospitalized in our Liver Unit were prospectively investigated, to define the accuracy of ascitic fluid analysis in identifying malignancy. Patients with extrahepatic cancer and peritoneal carcinomatosis were characterized by positive cytology and higher ascitic levels of fibronectin, lactic dehydrogenase, carcinoembryonic antigen, and total protein than both patients with uncomplicated cirrhosis and patients with cirrhosis and liver cancer. Ascitic cytology, fibronectin, and lactic dehydrogenase (LDH) were the most sensitive and specific markers of extrahepatic malignancy. In contrast, none of these markers was useful in identifying patients with primary liver cancer complicating cirrhosis. For them, the only alteration of the ascitic fluid was an elevated alpha-fetoprotein concentration. The sensitivity, specificity, and accuracy of ascitic alpha-fetoprotein for detecting liver cancer were 87%, 95%, and 94%, respectively. Combining cytology with the determinations of fibronectin (or LDH) and alpha-fetoprotein in ascitic fluid satisfactorily differentiated 28 of 32 cases of malignancy-related ascites, with very low incidence of false-positives (4-6%). Therefore, in view of the frequent difficulties in detecting liver cancer as a complication of cirrhosis in patients with ascites, it is advisable to determine all these three markers in the same ascitic sample.

Ascitic Fluid↗
PubMed1990

Renal and humoral effects of ibopamine, a dopamine agonist, in patients with liver cirrhosis.

We investigated the renal and humoral effects of short-term administration of ibopamine, an orally active dopamine agonist, in patients with liver cirrhosis. The patients were divided into two groups on the basis of sodium excretion with a constant sodium intake of 40 mEq/d. We also compared the effects of ibopamine with those induced by intravenous infusion of dopamine hydrochloride (3 micrograms/kg per minute) in similar patients. Ibopamine caused significant increases in urine output, glomerular filtration rate, and sodium excretion throughout the 4 hours of the trial in patients with basal sodium excretion rate greater than 20 mmol/d. These renal effects were associated with a significant reduction in plasma aldosterone concentration. In contrast, only a transient increase in glomerular filtration rate and a diminution in plasma aldosterone concentration were observed after ibopamine in the patients with a basal sodium excretion rate less than 20 mmol/d. The infusion of dopamine had renal effects similar to those of ibopamine in both groups of patients. These results indicate that in cirrhotic patients with normal sodium excretion, ibopamine exerts a diuretic and natriuretic effect similar to that of dopamine infusion. However, these properties of dopaminergic agents are apparently lost in patients with avid sodium retention.

Adult↗
PubMed1990

Paracentesis: a re-evaluated procedure in the management of cirrhotic patients with ascites.

Paracentesis is the oldest method for treating patients with ascites, but the fear of serious side-effects and the coincident introduction of effective non-toxic diuretic drugs led to its abandonment during the fifties. In recent years, several studies have investigated whether abdominal evacuation of ascitic fluid is truly dangerous for cirrhotic patients. The results of some randomized controlled trials comparing paracentesis with a traditional diuretic therapy showed that the rate of complications after paracentesis, particularly when the procedure was combined with a sufficient plasma expansion, was equal to or lower than that of diuretic treatment. Moreover, the ability of paracentesis to resolve tense ascites, both in terms of number of successes and of time required to obtain ascites resolution, was similar or even higher. These data and the recent new interest of several investigators in employing ascitic fluid examination for diagnostic purposes have increased the use of this procedure in the clinical practice.

Ascites↗
PubMed1989

Brain cholecystokinin depletion in rats with acute liver failure.

A decrease of both hypothalamic and cortical CCK occurred in the brain of rats killed 8 hours after hepatic artery ligation following portocaval anastomosis. Brain CCK depletion was not reproduced by exogenously provoked hyperammonemia nor by insulin-induced hypoglycemia, thus suggesting a central mechanism for the derangement of the CCKergic system in the course of acute liver failure.

Ammonia↗
PubMed1987

Repeated paracentesis and i.v. albumin infusion to treat 'tense' ascites in cirrhotic patients. A safe alternative therapy.

To investigate the usefulness of paracentesis as an alternative treatment for ascites, 41 cirrhotic patients with 'tense' ascites were randomly assigned to treatment with either repeated paracenteses plus i.v. albumin infusion (n = 20) or diuretics (n = 21). Satisfactory mobilization of ascites was obtained with paracentesis in all but one case and with diuretics in all but two cases. Ascites disappeared within 3 or 4 days with paracentesis, but only after 15 days with diuretics. The rate of reaccumulation of ascites following paracentesis, without diuretic administration, exceeded 300 g/day in only 5 patients. The incidence of complications and the mortality rate were similar in both groups of patients during hospital stay and during follow-up. This was corroborated by the evidence that no negative changes were induced in clinical and laboratory parameters of hemodynamic, hepatic and renal function after evacuation of the ascites. These results confirm that repeated paracenteses combined with human albumin replacement are safe and effective for treating 'tense' ascites, and more rapid than traditional diuretic therapy.

Albumins↗
PubMed1987

Growth hormone hyperresponsiveness to growth hormone-releasing hormone in patients with severe liver cirrhosis.

Patients with severe liver disease often have high baseline plasma GH levels and/or paradoxical GH release in response to several secretagogues, e.g. TRH. In this paper, we have investigated in a group of cirrhotic patients the GH response to GH-releasing hormone (GHRH) and evaluated the effectiveness of GHRH to cause GH release in TRH responder and non-responder patients. Ten patients and seven age- and sex-matched control subjects were given bolus injections of GHRH (0.1 and 1.0 microgram/kg i.v. on separate occasions). GHRH 0.1 microgram/kg failed to cause a GH response in both control and cirrhotic subjects, but 1.0 microgram/kg caused a significantly higher GH response in patients than in controls. Evaluation of the GH response curve after GHRH revealed a similar pattern of secretion in the TRH-responders (four subjects) and non-responders (six subjects). These results suggest that the enhanced GH responsiveness to GHRH in cirrhotic patients may contribute to their high baseline GH levels and/or secretory rate, and the mechanism(s) of the paradoxical GH rise after TRH seems to be separate from that for GH hyperresponsiveness to GHRH.

Aged↗
PubMed1986

Humoral and renal effects of ibopamine in normal subjects.

The acute effects of 50 mg of ibopamine (SB-7505), the 3,4-diisobutyryl ester of N-methyldopamine, were investigated after oral administration to 10 adult subjects without evidence of renal, hepatic or cardiovascular disease. Blood pressure and heart rate did not change while diuresis and urinary electrolyte excretion increased significantly during the 240 min of the study. Glomerular filtration rate (GFR) was also increased at 80 min after ibopamine, whereas plasma aldosterone and prolactin were slightly decreased. In contrast to dopamine, ibopamine did not stimulate plasma renin activity. These results are attributable to the ability of ibopamine to be rapidly deesterified to N-methyldopamine (epinine) which has been previously shown to exert peripheral effects similar to those of dopamine. Therefore, the increased GFR can be ascribed to an enhanced renal blood flow. On the contrary, taking into account the significant increase of the fractional excretion of sodium (FeNa) the rise in sodium excretion seems to be the consequence of a direct tubular effect of epinine, even though the slight decrease in peripheral aldosterone concentration would have been a contributing factor. Urinary flow rate might be enhanced by the high sodium delivery to the distal nephron, rather than by a postulated dopaminergic inhibition of arginine-vasopressin release.

Adult↗
PubMed1984

Effect of clonidine on the secretion of anterior pituitary hormones in heroin addicts and normal volunteers.

Neuroendocrine effects of intravenous injections of clonidine, 0.15 mg, were investigated in 13 heroin addicts and 14 normal control subjects. The study was designed to determine whether continuous opiate administration leads to the development of hypersensitive alpha 2-adrenergic receptors. The peak increments in levels of plasma growth hormone (GH) and beta-endorphin induced by clonidine did not differ between heroin addicts and normal control subjects. At no time interval could the clonidine-induced rise in GH levels in addicts be differentiated from that induced by placebo. Clonidine failed to alter plasma prolactin, gonadotropin, or thyrotropin levels in either heroin addicts or controls. Since clonidine's neuroendocrine effects are reportedly due to the activation of postsynaptic alpha 2-adrenoceptors, it appears that (1) continuous opiate use does not lead to the development of hypersensitive alpha 2-adrenergic receptors involved in neuroendocrine mechanisms and (2) brain norepinephrine does not play a role in the regulation of tonic prolactin, gonadotropin, and thyrotropin secretion in man.

Adolescent↗
PubMed1983

Brain cholecystokinin-8 immunoreactivity in rats with experimental liver cirrhosis.

Cholecystokinin-8 like immunoreactivity (CCK-8 IR) was measured in different brain regions of rats with experimental liver cirrhosis. A statistically significant reduction of CCK-8 content was observed in the hypothalamus of cirrhotic rats. No significant modification of brain CCK fractionation pattern was observed in treated animals as compared to controls. The decrease of CCK-8 IR parallels the recently reported hypothalamic depletion of beta endorphin in cirrhotic rats confirming that central neuropeptides are affected by chronic liver failure.

Animals↗
PubMed1983

Effect of pyridoxine alpha-ketoglutarate (PAK) on ammonia and pyruvic and lactic acid blood levels in patients with cirrhosis.

Administration of PAK to patients with hepatic cirrhosis significantly reduced hyperammonaemia and plasma levels of pyruvic and lactic acid. No significant changes in glycaemia were found. PAK treatment increased plasma levels of glutamic acid and decreased plasma levels of glutamine. This double-blind placebo controlled trial showed that PAK administration has a positive effect on some metabolic disturbances in cirrhotic patients.

Aged↗
PubMed1982

Growth hormone response to thyrotropin-releasing hormone in liver cirrhosis: unique alteration in anterior pituitary responsiveness to hypothalamic hormones.

Patients with chronic liver diseases were evaluated for: 1) the ability of somatostatin to affect the thyrotropin-releasing hormone (TRH) induced growth hormone (GH) rise; 2) the competence of luteinizing-hormone releasing hormone (LH-RH) to release GH; 3) the non-specific releasing effect of TRH and LH-RH on other anterior pituitary (AP) hormones. In 6 patients, infusion of somatostatin (100 micrograms iv bolus + 375 micrograms i.v. infusion) completely abolished the TRH (400 micrograms i.v.)-induced GH rise; in none of 12 patients, of whom 7 were GH-responders to TRH, did LH-RH (100 micrograms i.v.) cause release of GH; 4) finally, LH-RH (12 patients) did not increase plasma prolactin (PRL) and TRH (7 patients) did not evoke a non-specific release of gonadotropins. It is concluded that: 1) abnormal GH-responsiveness to TRH is the unique alteration in AP responsiveness to hypothalamic hormones present in liver cirrhosis; 2) the mechanism(s) subserving the altered GH response to TRH is different from that underlying the TRH-induced GH rise present in another pathologic state i.e. acromegaly, a condition in which the effect of TRH escapes somatostatin suppression and LH-RH evokes GH and PRL release.

Adult↗