Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of somatostatin on splanchnic haemodynamics in patients with liver cirrhosis is not clearly defined, as some Authors reported a decrease in portal pressure and in liver blood flow during i.v. administration of this hormone, while others did not. In 19 subjects with liver cirrhosis and portal hypertension the following parameters were measured before and during i.v. infusion of somatostatin (7.5 micrograms/min): porto-hepatic gradient, effective hepatic plasma flow, specific splenic blood flow, cardiac output. Moreover the gastrin-G-17 plasma levels, those of insulin and growth hormone were measured. Effective hepatic plasma flow decreased significantly during somatostatin infusion (P less than 0.05), averaging a 15% decrease. Porto-hepatic gradient, specific splenic blood flow, cardiac output did not vary significantly. Gastrin, insulin and growth hormone plasma levels decreased significantly (P less than 0.02, 0.01, 0.05). These data indicate that somatostatin infused at the dose of 7.5 micrograms/min provokes endocrine effects, but as far as the splanchnic circulation is concerned, it induces a slight decrease in liver blood flow without affecting portal hypertension.
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PMID:[Effect of somatostatin on splanchnic hemodynamics in liver cirrhosis]. 615 Nov 51

To study the interdependence of utilization of branched chain amino acids and glucose and of hyperinsulinaemia in patients with liver cirrhosis the plasma disappearance of glucose and amino acids was estimated in seven patients with cirrhosis and portocaval shunt and in seven healthy controls following infusion of glucose and essential amino acids during suppression of endogenous hormone release by somatostatin. Exogenous insulin was infused by means of an automated glucose controlled insulin infusion system. The data demonstrate that (i) insulin requirement almost doubled in patients as compared to controls to obtain similar blood glucose responses to i.v. glucose, and (ii) the plasma disappearance rates of the infused amino acids were reduced in the patients as compared to controls despite hyperinsulinaemia sufficient to achieve normal glucose assimilation. Thus, in cirrhotic patients insulin resistance may be overcome by excess insulin as far as glucose homoestasis is concerned, whereas amino-acid metabolism still remains impaired.
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PMID:Impaired plasma amino-acid clearance in patients with cirrhosis of the liver and portocaval shunt--its relation to insulin resistance. 643 19

A patient with biopsy-proved biliary cirrhosis and previous gastrojejunostomy and portacaval anastomosis experienced episodes of severe hypoglycemia. She was found to have hyperinsulinemia and hyperglucagonemia. An oral glucose tolerance test showed postgastrectomy hypoglycemia. Results of the intravenous tolbutamide test were diagnostic for insulinoma, but results of the intravenous glucagon test and prolonged fast (96 hours) were not. Failure, on two occasions, to suppress C-peptide normally during insulin-induced hypoglycemia led to a diagnosis of pancreatogenous hyperinsulinemia. The pancreas showed a 10-fold increase in islet volume, with intensely positive staining with anti-insulin and anti-glucagon antiserums in addition to anti-somatostatin and anti-pancreatic polypeptide antiserums. Incidental findings at pancreatic exploration were a mesothelioma, which did not stain with anti-insulin antiserum, and, at autopsy one year later, a hepatoma.
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PMID:Diagnosis of pancreatic islet hyperplasia causing hypoglycemia in a patient with portacaval anastomosis. 699 72

The present double-blind study was aimed at investigating the hemodynamic and humoral effects of somatostatin or placebo in patients with cirrhosis. Patients were randomly assigned to receive either an injection of 250 micrograms of somatostatin followed by a constant infusion of somatostatin at 250 micrograms/h (n = 13), an injection of 250 micrograms of somatostatin followed by a 500 micrograms/h continuous infusion (n = 10), or an injection of placebo followed by a placebo infusion (n = 9). Placebo had no effect. Somatostatin bolus markedly decreased the hepatic venous pressure gradient: by 52% at 1 minute; P < .001; 19% at 3 minutes, P < .01; and by 13% at 5 minutes, P < .04. Azygos blood flow decreased similarly by 45% at 1 minute, P < .001; 16% at 3 minutes, P < .02; and 9.5% at 5 minutes, P = .05. Mean arterial pressure increased by 25% (P < .001). Continuous somatostatin infusions (250 or 500 micrograms/h) had no systemic effects, but significantly reduced hepatic venous pressure gradient (250 micrograms/h: -6.1%, P < .05 and 500 micrograms/h: -15%, P < .01) and hepatic blood flow (250 micrograms/h: -10%, 500 micrograms/h: -18%, P < .05). Azygos blood flow was not changed after 250 micrograms/h infusion but was reduced after 500 micrograms/h (-23%, P < .02). Somatostatin but not placebo, suppressed glucagon to normal levels. This study shows that a bolus injection of somatostatin caused an immediate and marked decrease of hepatic venous pressure gradient and azygos blood flow. Continuous infusion of somatostatin had a mild but sustained effect on splanchnic hemodynamics; this effect was more pronounced with the higher dose.
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PMID:Effects of bolus injections and continuous infusions of somatostatin and placebo in patients with cirrhosis: a double-blind hemodynamic investigation. 760

The significance of changes in plasma somatostatin level at patients with vascularly decompensated liver cirrhosis was investigated. The plasma level of somatostatin, glucagon, gastrin and blood glucose concentration were determined under basal condition and after testmeal in patients with vasculary decompensated cirrhosis, in cirrhotic-patients without ascites formation and in control subjects. The basaline levels and the postprandial increases of plasma somatostatin concentrations were significantly lower in cirrhotic patients with ascites, compared to the other two groups. The glucagon concentrations--both the basaline and the postprandial--were significantly higher in the cirrhotic patients-groups, compared to the controls. The gastrin and blood glucose levels were not different in the three groups. The decrease in plasma somatostatin concentration present in cirrhosis associated with ascites represents a secondary phenomena, and suggest that endogen somatostatin plays a role in maintaining body fluid homeostasis.
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PMID:[Somatostatin plasma level in patients with liver cirrhosis]. 776 Oct 79

The task of pharmacotherapy in acute haemorrhage from oesophageal varices in patients with cirrhosis of the liver and portal hypertension is to arrest bleeding by reducing the blood pressure and blood flow in the oesophageal varices. The mechanism of action of the majority of drugs used is vasoconstriction of the arterioles in the splanchnic region. Somatostatin seems to be more effective and in particular safer than vasopressin, terlipressin or their combination with the vasodilatator nitroglycerin. Initial pharmacotherapy for rapid control of haemorrhage is simple and effective treatment, however, it cannot be considered an alternative of sclerotherapy, which remains the method of choice in acute haemorrhage from oesophageal varices and is effective in 90-95%. Pharmacotherapy is useful also in the prevention of relapsing haemorrhage from oesophageal varices. A combination of sclerotherapy with somatostatin or nitrates to reduce early relapses of haemorrhage is particularly effective. The effectiveness of beta-blockers to reduce the risk of relapsing haemorrhage is less clear. Prophylactic treatment for the prevention of the first haemorrhage from oesophageal varices (pharmacological, but also endoscopic or surgical) is justified only in strictly selected patients with a high risk of haemorrhage.
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PMID:[Pharmacotherapy of portal hypertension]. 776 77

Glucose reduces the hepatic conversion of aminonitrogen to urea, quantified by the functional hepatic nitrogen clearance (i.e., the slope of the linear relation between urea synthesis rate and blood alpha-aminonitrogen concentration). This is due to a direct effect of glucose and to inhibition of glucagon. In this study, the effect of glucose on functional hepatic nitrogen clearance was examined during spontaneous hormone responses and during hormonal control by somatostatin. In 7 control subjects (study 1) and 9 patients with cirrhosis (study 2), functional hepatic nitrogen clearance was assessed twice in each subject: during infusion of alanine and during alanine administration superimposed on a continuous glucose infusion (blood glucose, on average = 8.4 mmol/L). In study 3, 6 patients with cirrhosis had functional hepatic nitrogen clearance determined on three occasions: during infusions of alanine and of alanine superimposed on infusion of somatostatin with either euglycemia or hyperglycemia (blood glucose = 8.4 mmol/L). In the control subjects (study 1), functional hepatic nitrogen clearance was 32.5 +/- 1.9 L/hr, and glucose reduced it to 18.4 +/- 0.9 L/hr (p < 0.01). In the cirrhotic patients, functional hepatic nitrogen clearance was only 9.8 +/- 1.3 L/hr (p < 0.01 vs. controls), and glucose did not change it. In the control subjects, glucose reduced the glucagon response to alanine from 204 +/- 36 ng/L to 106 +/- 8 ng/L (p < 0.05). In the cirrhotic patients the mean fasting glucagon level was increased twofold (180 +/- 21 ng/L). The response to alanine increased to 968 +/- 265 ng/L; it was not reduced by glucose. In study 3, somatostatin and hyperglycemia reduced functional hepatic nitrogen clearance from 13.2 +/- 1.5 L/hr to 6.4 +/- 0.7 L/hr (p < 0.01). Somatostatin and euglycemia reduced functional hepatic nitrogen clearance to 9.2 +/- 1.2 L/hr (p < 0.01 vs. alanine and hyperglycemia). The results show that the reduction by glucose of hepatic aminonitrogen conversion is lost in cirrhotic patients. The markedly increased glucagon response to alanine was not suppressed by glucose. Inhibition of the glucagon response by somatostatin reestablished the glucose effect, which was in part due to inhibition of glucagon in itself. Thus hepatic aminonitrogen conversion in cirrhosis depends on increased glucagon levels. The hormone-independent effect of glucose is preserved if the hyperglucagonemia is abolished, but the spontaneous high glucagon level overrules the glucose effect. The results indicate reduced hepatic contribution to the nitrogen-sparing effect of glucose in cirrhotic patients.
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PMID:Effects of glucose on hepatic conversion of aminonitrogen to urea in patients with cirrhosis: relationship to glucagon. 790 54

Cirrhosis is characterized by paradoxical growth hormone secretion in response to glucose and insulin infusion. To ascertain whether this abnormality contributes to insulin resistance, euglycemic hyperinsulinemic glucose clamps were performed on six patients with cirrhosis and six normal control subjects. Each patient with cirrhosis underwent two clamps in random order, a clamp with somatostatin (250 micrograms/hr) together with insulin and glucagon replacement, and a control clamp without somatostatin. The normal subjects underwent the control clamp only. During the control clamp, growth hormone levels were considerably higher in the patients with cirrhosis (6.1 +/- 0.4 vs. 0.5 +/- 0.4 mU/L, p < 0.02), and glucose uptake was considerably lower (3.29 +/- 0.56 vs. 9.52 +/- 1.14 mg/kg/min, p < 0.001). Indirect calorimetry indicated that the defect was accounted for by lower nonoxidative glucose disposal (1.23 +/- 0.45 vs. 6.00 +/- 0.73, p < 0.001). Peripheral glucose uptake, exemplified by forearm glucose uptake (0.27 +/- 0.04 vs. 1.22 +/- 0.42 mg/100 ml/min, p < 0.02), and calculated insulin sensitivity (24 +/- 8 vs. 114 +/- 20 microliters/kg/min per mU/L) were particularly diminished. In the patients with cirrhosis somatostatin suppressed growth hormone levels (6.1 +/- 1.2 to 1.2 +/- 0.4 mU/L, p < 0.05). However, no significant changes occurred in whole-body glucose uptake (3.29 +/- 0.56 vs 3.01 +/- 0.54 mg/kg/min), forearm glucose uptake (0.27 +/- 0.04 vs 0.30 +/- 0.01 mg/100 ml/min) or insulin sensitivity (24 +/- 8 vs, 35 +/- 10 microliters/kg/min/mU/L, p = 0.42).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth hormone, insulin-like growth factor-1 and insulin resistance in cirrhosis. 790 78

Transmural variceal pressure was measured by fine-needle puncture following a 250-micrograms bolus injection of somatostatin given intravenously, together with a slow infusion of 250 micrograms/h, and compared with results following a 500-micrograms bolus and with placebo in 19 patients with cirrhosis who had recently bled. Pressure was recorded continuously for a 4-min period. Placebo did not alter variceal pressure (n = 6), whereas a 250- or 500-micrograms bolus produced a rapid decrease in pressure from 33 +/- 7 cmH2O to 20 +/- 6 (n = 7) and from 35 +/- 5 cmH2O to 24 +/- 6 (n = 6), respectively. The difference between the two groups was not significant. This decrease occurred within 30 to 90 s, but was followed by a progressive increase in variceal pressure over the next 2 min in all except two patients. After 3-4 min, variceal pressure still remained below pretreatment levels. Further studies are needed to evaluate the optimal infusion rate. These results seem to indicate that future clinical studies using somatostatin in the treatment of variceal haemorrhage should include repeated bolus injections to arrest variceal bleeding.
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PMID:The effect of different doses of a bolus injection of somatostatin combined with a slow infusion on transmural oesophageal variceal pressure in patients with cirrhosis. 791 Nov 36

Somatostatin and endoscopic sclerotherapy are widely used in the treatment of acute variceal bleeding. Although objective evidence does exist about the advantages of either treatment, data comparing both procedures are scarce. In order to compare the effectiveness and safety of somatostatin and sclerotherapy in the treatment of acute variceal bleeding, 70 consecutive cirrhotic patients suffering from esophageal variceal hemorrhage and meeting the inclusion criteria were randomly assigned to treatment with somatostatin (35 patients) or sclerotherapy (35 patients). No differences in age, sex, alcohol intake, etiology of cirrhosis and severity of liver failure were found between groups. Failure of treatment (defined as persistence of bleeding despite therapy or subsequent rebleeding within the 48-hr trial period) occurred in seven patients (20%) in the somatostatin group and in six (17.1%) in the sclerotherapy group (NS). Early rebleeding occurred in seven of 28 patients (25%) in the somatostatin group and in five of 29 (17.2%) in the sclerotherapy group (NS). Mortality within the first 6 wk was no different between both groups: 10 (28.5%) and eight (22.8%) in the somatostatin and sclerotherapy groups, respectively. Sclerotherapy, but not somatostatin, was associated with major complications in five cases (14.2%) (p = 0.026), two of which resulted in patient's death. These results suggest that somatostatin is safer, and as effective as sclerotherapy, in controlling acute variceal bleeding until an elective treatment can be established.
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PMID:A prospective randomized trial comparing somatostatin and sclerotherapy in the treatment of acute variceal bleeding. 791 7


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