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 role of endogenous glucagon in maintaining hepatic glucose production after an overnight fast in patients with cirrhosis of the liver was studied with arterial-hepatic-venous catheterization and using somatostatin to suppress glucagon secretion. Arterial glucagon levels were elevated in eight cirrhotics to 290 +/- 90 pg/ml (SEM) compared to 100 +/- 10 pg/ml (P less than 0.02) in five normal controls, and they were lowered during administration of somatostatin (SRIF; 250 microgram/h) by a mean of 154 pg/ml and 39 pg/ml in cirrhotics and controls, respectively. Basal net splanchnic glucose production (NSGP) was similar in patients with and without cirrhosis (approximately 100 mg/min) but declined more markedly during 30 min of SRIF in cirrhotics to a net splanchnic uptake of glucose of 30 +/- 20 ml/min, as opposed to a fall of NSGP by 44 +/- 2 mg/min in controls (P less than 0.01). To assure that NSGP declined during SRIF infusion due to the fall of glucagon levels, SRIF was combined with a glucagon infusion at 150 ng/m2 . min in four cirrhotics and in five control subjects. Arterial glucagon levels were elevated to a mean of 650 pg/ml and 559 pg/ml in cirrhotics and controls, respectively. NSGP increased after 40 min of SRIF and glucagon replacement to 179 +/- 33 mg/min in cirrhotics and significantly more, to 412 +/- 68 mg/min, in controls (P less than 0.01). Thus, hepatic glucose production during basal and elevated glucagon levels suggested hepatic resistance to glucagon in cirrhosis. Nevertheless, endogenous glucagon played an augmented stimulatory role in maintaining glucose production in the normal range since there was an exaggerated fall of hepatic glucose output during glucagon suppression.
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PMID:Evidence for an augmented glucagon dependence of hepatic glucose production in cirrhosis of the liver. 612 Sep 52

The effects of somatostatin and vasopressin on blood gases, pulmonary and systemic hemodynamics, and portal pressure assessed by the gradient between occluded and free hepatic vein pressures, were investigated in 18 patients with liver cirrhosis. In the first 10 patients, an iv bolus of 250 microgram somatostatin, followed by an infusion of 125 microgram somatostatin over 30 min, caused a sudden rise in pulmonary and systemic vascular pressures lasting 2 to 5 min and accompanied by bradycardia. There was a slight and transient increase in venous admixture (Qsp/Qt) and alveolar-arterial oxygen tension gradients (P(A-a)O2), and a transient reduction in O2 delivery (O2 del) (-11% of the baseline values) and portal pressures (-14%). In the next 8 patients, vasopressin, 0.4 U/min infused over 30 min, caused a more persistent pulmonary and systemic hypertension and bradycardia, a slight increase in P(A.a)O2 and Qsp/Qt, a reduction in O2 del (-27%) and a decrease in portal pressures (-32%). These effects were marked during the entire vasopressin infusion period. Both somatostatin and vasopressin had vasoconstrictive properties and exerted negative effects on hemodynamics and blood gases. Vasopressin appeared to be a more potent drug than somatostatin.
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PMID:Effect of vasopressin and somatostatin on hemodynamics and blood gases in patients with liver cirrhosis. 612 42

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.
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PMID:Growth hormone response to thyrotropin-releasing hormone in liver cirrhosis: unique alteration in anterior pituitary responsiveness to hypothalamic hormones. 612 95

Experimental data suggest that somatostatin is metabolized by both liver and kidneys. Results in humans are conflicting. By studying a group of cirrhotic patients with surgically induced end-to-side portacaval shunts, basally and during a somatostatin infusion, we have been able to analyze separately the hepatic and splanchnic metabolism of this peptide. After catheterization, samples were obtained from the pulmonary artery, portal and hepatic veins. Basal pulmonary artery immunoreactive somatostatin (IRS) was significantly higher (p less than 0.001) in the cirrhotic patients (96 +/- 11 pg per ml) than in a sex- and age-matched control group (31.4 +/- 5.8 pg per ml). During the infusion of exogenous somatostatin, IRS values were higher in arterial (12,269 +/- 1,198 pg per ml) than in hepatic venous blood (7,648 +/- 1,234 pg per ml), indicating hepatic extraction of the peptide; but there was also a substantial splanchnic extraction demonstrated by higher arterial (12,269 +/- 1,532 pg per ml) than portal values (6,754 +/- 1,040 pg per ml) of IRS. During the somatostatin infusion, at very high circulation IRS levels, the liver was able to extract 38% of the peptide. This suggests that the high basal IRS levels found in liver cirrhosis are not likely to be due to hepatic failure. Possible mechanisms may involve increased somatostatin secretion, predominance of high molecular weight moieties of IRS which may not be as effectively removed by the liver, and/or portal-systemic shunting.
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PMID:Splanchnic and hepatic metabolism of somatostatin: a study in cirrhotic patients with a portacaval shunt. 613 59

The effects of 1 and 4 micrograms/kg/h somatostatin on pentagastrin-stimulated gastric mucosal blood flow and acid secretion were investigated in 12 normal subjects and in 12 patients with cirrhosis of the liver. Each dose of somatostatin was given intravenously to six normal subjects and to six patients. Gastric mucosal blood flow was measured by the neutral red clearance of the stomach. Pentagastrin at a dose of 0.67 micrograms/kg/h stimulated acid secretion less in patients with cirrhosis of the liver than in normal subjects. In normal subjects 1 micrograms/kg/h somatostatin induced a parallel decline of gastric mucosal blood flow and gastric secretion; with 4 micrograms/kg/h somatostatin mucosal blood flow was inhibited more than gastric secretion. In patients with cirrhosis of the liver gastric mucosal blood flow remained unaffected by both doses of somatostatin, while acid secretion was slightly decreased. It is concluded that somatostatin can affect gastric mucosal blood flow independently of acid secretion. Somatostatin may be ineffective in the treatment of gastric haemorrhage in patients with cirrhosis of the liver.
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PMID:Somatostatin reduces gastric mucosal blood flow in normal subjects but not in patients with cirrhosis of the liver. 613 13

As medical treatment of haemorrhage from esophageal varices vasopressin is discussed. The analogue triglycyl-vasopressin has less side-effects and a longer plasma half-life. According to the first randomized study with only a small number of patients bleeding from varices triglycyl-vasopressin was superior to vasopressin. The efficacy of somatostatin to reduce splanchnic blood flow in patients with liver cirrhosis is controversial. In a placebo-controlled trial propranolol prevented rebleeding from varices in patients with cirrhosis. However, beta-blockers should not be given to patients with advanced cirrhosis. Several controlled studies prove cimetidine not to be effective in ulcer bleeding. Somatostatin and secretin could be candidates for pharmacotherapy of haemorrhage from ulcers and erosions. In an own randomized and multicenter trial on 100 patients with stopped ulcer bleeding it was proven that the combination of the synergistically acting receptor antagonists cimetidine and pirenzepine prevent rebleeding significantly better than a prophylactic treatment of either cimetidine or pirenzepine alone. An improvement of mortality rates of upper gastrointestinal bleeding seems also to be possible by using such a combined prophylaxis. As prophylaxis of stress-ulcer bleeding cimetidine - recently ranitidine, too - and antacids are applied. Instead of a widely used enhancement of the doses of H2-blockers a combined application of H2-receptor antagonists and pirenzepine is also recommended in this indication which offers theoretical and practical advantages.
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PMID:[Drug therapy and prevention of acute upper gastrointestinal hemorrhage]. 613 16

Haemorrhages in the course of cirrhosis and portal hypertension are surgical emergencies. Nevertheless medical treatment may be necessary both to revive the patient and temporarily to check the haemorrhaging itself. Some views are presented on the use of drugs, both those already in clinical use and others at the experimental stage, which appear to be effective in the treatment of haemorrhaging in portal hypertension (Vasopressin, glypressin, prostaglandin, somatostatin, propranolol, cimetidine and ranitidine).
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PMID:[Recent developments in the medical treatment of emergency cirrhotic hemorrhage. Vasopressin and glipressin, prostaglandins, somatostatin, propranolol, cimetidine and ranitidine]. 613 72

Fasting level of somatostatin-like immunoreactivity (SLI) in plasma was measured by a highly sensitive radioimmunoassay in 36 patients with alcoholic liver disease verified by histopathology (10 patients with steatosis and 26 with cirrhosis of the liver). The median value of SLI was markedly elevated in patients with steatosis of the liver as compared to normal subjects, P less than 0.01, while the median value of SLI in the cirrhotic group was even higher, P less than 0.05, as compared to the steatotic group. Correlations of SLI to se-bilirubin and p-coagulation factors 2, 7 and 10 were significant, P less than 0.001 and P less than 0.01, respectively, whereas no correlation to plasma insulin could be elicited. These results suggest that in alcoholic liver disease fasting plasma somatostatin is correlated to the degree of hepatic failure and indicate that the liver is an important site for clearance of portal vein somatostatin.
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PMID:Fasting plasma somatostatin in alcoholic liver disease. 614 Jul 48

The influence of intravenous somatostatin infusion (7.6 micrograms/min) on systemic and splanchnic haemodynamics was examined in 10 patients with liver cirrhosis and portal hypertension. The hepatic vein catheter technique was employed and indocyanine green dye was injected to evaluate hepatic blood flow. Mean wedged hepatic venous pressure fell from 24.9 +/- 2.8 in the basal state to 21.4 +/- 3.2 mmHg (P less than 0.2) at 60 min of infusion and the mean arterial pressure decreased from 87 +/- 5 to 80 +/- 6 mmHg (P less than 0.05). The rate of indocyanine green dye disappearance decreased from 8.7 +/- 1.9 to 6.6 +/- 1.7%/min (P less than 0.001) during the infusion, indicating decreased hepatic blood flow. Arterial-hepatic venous oxygen differences rose from 69 +/- 11 to 78 +/- 11 ml/l. Blood glucose levels fell from 4.84 +/- 0.31 to 3.79 +/- 0.33 mmol/l at 60 min of infusion (P less than 0.005). It is concluded that a continuous infusion of somatostatin in patients with liver cirrhosis and portal hypertension causes a decreased hepatic blood flow with augmented hepatic oxygen extraction and a modest reduction in mean wedged hepatic venous pressure. In view of the magnitude of the observed haemodynamic changes the findings do not suggest an important role for somatostatin in the treatment of patients with bleeding oesophageal varices.
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PMID:Influence of somatostatin on splanchnic haemodynamics in patients with liver cirrhosis. 614 61

The purpose of our study was to evaluate the effect of somatostatin (500 microgram/h intravenously) upon insulin, c-peptide, glucagon and plasma amino acids concentrations in patients with and without cirrhosis of the liver. The typical plasma amino acid pattern in cirrhosis is characterised by increased concentrations of the aromatic amino acids and decreased concentrations of the branched chain amino acids and of alanine and glycine. After administration of somatostatin insulin, c-peptide and glucagon concentrations decreased and those of the branched chain amino acids in both groups increased; in addition in patients with cirrhosis the plasma concentrations of threonine, serine, glycine, alanine, lysine, and arginine increased also. Infusion of somatostatin plus insulin in patients with cirrhosis succeeded in preventing the increase in the branched chain amino acid concentrations, while the infusion of somatostatin plus glucagon decreased threonine, serine, glycine, alinine, phenylalanine, tyrosine, lysine and arginine concentrations. It is therefore suggested that the effect of somatostatin on the plasma amino acids may be because of the reduction of insulin and glucagon concentrations; however, other effects of somatostatin cannot be excluded at present.
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PMID:Correction of altered plasma amino acid pattern in cirrhosis of the liver by somatostatin. 614 82


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