gastrins and Hypertension--Portal

Topics: Achlorhydria; Endoscopy, Gastrointestinal; Gastrins; Humans; Hypertension, Portal; Prevalence; Stomach Diseases

A higher incidence of gastric and duodenum ulcer was well recognized in patients with liver cirrhosis, but the mechanism has not been fully identified. In this study, serum gastrin, free portal pressure (FPP) were measured in 24 consecutively admitted cirrhotic portal hypertensive patients, and preoperative basic acid output (BAO) was measured in 13 randomized patients. Among the 24 patients, concomitant duodenal ulcers were found in 3 by both gastroduodenoscopy and barium series, and gastritis was found in all patients. It was found that most patients (71%) with liver cirrhosis have a elevated level in serum gastrin, whereas BAO is lower than normal in all patients, and the higher the FPP, the lower the BAO is. We believe that the congestive gastroduodenal mucosal lesion was underlying the ulceration most often seen in patients with portal hypertension.

Topics: Adult; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Humans; Hypertension, Portal; Liver Cirrhosis; Male; Middle Aged; Stomach Ulcer

It has been suggested that the vulnerability of gastric mucosa is increased in patients with cirrhosis as a result of a PGE2 deficiency. Therefore, we evaluated whether PGE2 mucosal generation, and gastric potential difference - a reflection of the gastric mucosal barrier - were correlated to endoscopic features and whether these alterations could be alleviated.. The potential difference was measured before (basal) and after a stimulation test by aspirin. The serum levels of gastrin and glucagon were also determined. Finally, the effects of a 1-week administration of propranolol or enprostil were tested on potential difference. The endoscopic grade of portal hypertensive gastropathy was assessed according to McCormack et al. The results are presented respectively for controls, patients with mild gastropathy, and patients with severe gastropathy. Comparisons were made using variance or covariance analysis after adjustment with age.. Basal potential difference was significantly different between the three groups: -30.6, -28.8, -24.9 mV, p <0.05, respectively. The effects of aspirin administration on potential difference parameters were significantly different between the three groups (irritability index: 35 +/- 25, 92 +/- 98, 114 +/- 74 mV2.min, p <0.05, respectively) when non-responders to aspirin were excluded. PGE2 mucosal generation was significantly increased in both the antrum (9.8, 19.5, 19.7 ng/mg proteins, p<0.05, respectively) and in the corpus (8.1, 14.0, 20.2 ng/mg proteins, p<0.05, respectively). PGE2 generation was not related to potential difference. Glucagon serum levels were related to the grade of gastropathy. A 1-week administration of 160 mg/d long-acting propranolol, 35 micro g/d enprostil or placebo did not significantly modify basal potential difference.. Portal hypertensive gastropathy is characterized by a decreased potential difference proportional to the endoscopic severity. The gastric mucosa of patients with cirrhosis seems to be more susceptible to aspirin than that of healthy subjects. It appears that the role of PGE2 is controversial in portal hypertensive gastropathy. Propranolol and enprostil do not improve this decreased potential difference.

Topics: Adrenergic beta-Antagonists; Adult; Aged; Anti-Ulcer Agents; Aspirin; Dinoprostone; Enprostil; Female; Gastric Mucosa; Gastrins; Humans; Hypertension, Portal; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Propranolol; Stomach Diseases

Gastric mucosal hyperemia associated with elevated serum gastrin level has been suggested in cirrhotic patients with portal hypertensive gastropathy (PHG). Clinical evidence has shown that these patients may benefit from propranolol administration. The aim of this study was to investigate effect of propranolol on gastric mucosal perfusion and serum gastrin level in cirrhotic patients with portal hypertensive gastropathy. Gastric mucosal perfusion was assessed by laser Doppler flowmetry. Measurements were performed under basal conditions and after observer-blind administration of propranolol (30-60 mg/day, N = 9) or placebo (N = 9) for seven days. Placebo had no effect on either gastric mucosal perfusion or serum gastrin level. In contrast, propranolol administration significantly decreased both antrum gastric mucosal perfusion (from 0.88 +/- 0.28 to 0.73 +/- 0.26 V, P < 0.05) and corpus gastric mucosal perfusion (from 0.94 +/- 0.35 to 0.78 +/- 0.25 V, P < 0.05). However, this drug had no effect on serum gastrin level. We conclude that chronic propranolol administration in cirrhotic patients with portal hypertensive gastropathy may reduce gastric mucosal perfusion without changing serum gastrin level.

Topics: Double-Blind Method; Female; Gastric Mucosa; Gastrins; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Laser-Doppler Flowmetry; Liver Cirrhosis; Male; Middle Aged; Pepsinogens; Propranolol; Regional Blood Flow; Stomach Diseases

This randomized controlled trial was conducted to compare the efficacy of intravenous infusion of octreotide (a synthetic long-acting somatostatin analogue) with vasopressin in 48 cirrhotic patients with endoscopically proven bleeding esophageal varices. Twenty-four patients received a continuous infusion of octreotide 25 micrograms/h for 24 h after an initial bolus of 100 micrograms and another 24 patients received a continuous infusion of vasopressin 0.4 U/min for 24 h. Bleeding was initially controlled after 6 h of drug infusion in 88% (21/24) and 54% (13/24) of the patients treated with octreotide and vasopressin respectively (p = 0.03). Complete control of bleeding after 24 h of drug infusion was achieved in 15 (63%) patients receiving octreotide and in 11 (46%) patients receiving vasopressin (p > 0.05). Side effects during drug infusion such as headache, chest pain and abdominal pain were significantly lower in the octreotide group (3/24) than in the vasopressin group (11/24). Serum gastrin and insulin levels fell significantly following octreotide infusion, but plasma glucose levels remained unchanged. Mortality related to bleeding esophageal varices was no different between the two groups. This report showed that octreotide infusion was more effective and had fewer side effects than vasopressin in initial controlling of acute esophageal variceal bleeding until an elective endoscopic sclerotherapy could be performed.

Topics: Aged; Blood Glucose; Esophageal and Gastric Varices; Female; Gastrins; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Injections, Intravenous; Insulin; Liver Cirrhosis; Male; Middle Aged; Octreotide; Vasopressins

This investigation was designed to assess the effects of oral administration of melatonin (10 mg) and tryptophan (Trp) (500 mg) on fasting and postprandial plasma levels of melatonin, gastrin, ghrelin, leptin and insulin in 10 healthy controls and in age-matched patients with liver cirrhosis (LC) and portal hypertension. Fasting plasma melatonin levels in LC patients were about five times higher (102 +/- 15 pg/mL) than in healthy controls (22 +/- 3 pg/mL). These levels significantly increased postprandially in LC patients, but significantly less so in controls. Treatment with melatonin or L-Trp resulted in a further significant rise in plasma melatonin, both under fasting and postprandial conditions, particularly in LC patients. Moreover, plasma gastrin, ghrelin, leptin and insulin levels under fasting and postprandial conditions were significantly higher in LC subjects than in healthy controls and they further rose significantly after oral application of melatonin or Trp. This study shows that: (a) patients with LC and portal hypertension exhibit significantly higher fasting and postprandial plasma melatonin levels than healthy subjects; (b) plasma ghrelin, both in LC and healthy controls reach the highest values under fasting conditions, but decline postprandially, especially after oral application of melatonin or Trp; and (c) plasma melatonin, gastrin, ghrelin and insulin levels are altered significantly in LC patients with portal hypertension compared with that in healthy controls possibly due to their portal systemic shunting and decreased liver degradation.

Topics: Administration, Oral; Basal Metabolism; Case-Control Studies; Data Interpretation, Statistical; Gastrins; Ghrelin; Humans; Hypertension, Portal; Insulin; Leptin; Liver Cirrhosis; Male; Melatonin; Peptide Hormones; Postprandial Period; Tryptophan

The prevalence of duodenal ulcer (DU) in adult patients with portal hypertension is higher than in patients without portal hypertension. This study investigates the prevalence and characteristics of DU in children with portal hypertension.. From January 1997 to December 2001, 80 children with portal hypertension who had undergone upper intestinal endoscopic examinations were enrolled. Possible factors contributing to the development of DU including severity of liver disease, portal hypertension, H. pylori, and serum gastrin level were studied. The control group consisted of 80 age-and sex-matched children with gastrointestinal symptoms but no liver disease and who underwent endoscopic examination during the same period.. The prevalence of DU was significantly higher in children with portal hypertension than in children with digestive symptoms only (22.5%v 8.8%; P =0.017). DU was more common and appeared earlier in children with a history of variceal bleeding. The presence of DU was independent of the severity of liver disease, H. pylori infection and serum gastrin level.. DU occurs commonly in children with portal hypertension, especially in those who have had variceal bleeding. It is mandatory to screen a patient with gastrointestinal bleeding for DU even in the presence of esophageal varices. Elevated portal pressure might be a factor contributing to the development of DU.

Topics: Adolescent; Case-Control Studies; Child; Child, Preschool; Duodenal Ulcer; Endoscopy, Gastrointestinal; Esophageal and Gastric Varices; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Hypertension, Portal; Infant; Male; Prevalence

The gastric mucosa of patients with portal hypertension frequently manifests changes in its appearance that are readily identifiable by endoscopy. Many of these can be sources of bleeding, and some imply the presence of systemic disease. Although portal hypertension is critical in development of portal hypertensive gastropathy (PHG), the role that other factors might play in its pathogenesis is uncertain.. Four groups of subjects were studied prospectively: 37 with portal hypertension due to cirrhosis, 26 noncirrhotic subjects with portal hypertension due to extrahepatic portal vein obstruction (PVO), nine cirrhotic patients with extrahepatic PVO, and 57 control subjects. The diagnosis in each case was based on a combination of clinical data, needle liver biopsy, ultrasonography, splenoportography, and upper GI endoscopy.. Snake skin, scarlatina rash, diffuse hyperemia, and diffuse bleeding were frequent endoscopic gastric findings in cirrhotic patients. These findings were seen less frequently in noncirrhotic patients with portal hypertension due to PVO than in cirrhotic patients (p< 0.0001). The highest incidence was seen in cirrhotic patients with PVO (P< 0.001). Positive correlations existed among the endoscopic findings, the clinical estimate of the cirrhosis severity (Child-Pugh grade), and the size and appearance of esophageal varices (Beppu score). No endoscopic findings of the gastric mucosa enabled one to distinguish between groups. Hypergastrinemia was present in cirrhotics with and without PVO but not in noncirrhotic patients with portal hypertension resulting from isolated PVO.. These findings suggest that the endoscopic findings of PHG are affected by the severity of the underlying liver disease and the presence or absence of coexisting PVO. There is no association between PHG and the presence of gastric varices. Thus, the development of the gastric lesions characteristic of PHG requires not only portal hypertension but also some other consequence of parenchymal liver disease.

Topics: Adult; Biopsy; Endoscopy, Digestive System; Esophageal and Gastric Varices; Fasting; Female; Gastrins; Humans; Hypertension, Portal; Liver; Liver Cirrhosis; Male; Portography; Ultrasonography

The stomachs of cirrhotic patients are frequently subject to a number of alterations, detectable by endoscopy, the presence of which indicates a disturbance in the mucosa. Several investigators believe that portal hypertension plays an etiopathogenetic role. Three groups of subjects were studied prospectively: 83 cirrhotic patients with portal hypertension, 53 cirrhotic patients without portal hypertension, and 135 control subjects. Snake skin, scarlatina rash, and petechia were the most frequent endoscopic findings in the cirrhotic patients with portal hypertension (P less than 0.001); these findings were also most frequently present in association with each other in this group. There was no correlation between the endoscopic findings, the clinical gravity of liver cirrhosis (Child-Pugh grade), and the gravity of esophageal varices (Beppu score). There were no characteristic inflammatory findings in the gastric mucosa. Hypergastrinemia was often observed in cirrhotic patients with and without angiodysplasias.

Topics: Aged; Biopsy; Chronic Disease; Cluster Analysis; Female; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Gastroscopy; Humans; Hypertension, Portal; Liver Cirrhosis; Male; Middle Aged; Prospective Studies

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.

Topics: Adult; Female; Gastrins; Growth Hormone; Humans; Hypertension, Portal; Injections, Intravenous; Insulin; Liver Circulation; Liver Cirrhosis; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Somatostatin; Spleen

Topics: Adult; Ammonia; Female; Gastric Acidity Determination; Gastric Juice; Gastrins; Humans; Hypertension, Portal; Liver; Male; Middle Aged

Topics: Animals; Ascites; Bile; Biliary Tract Diseases; Digestive System Physiological Phenomena; Esophageal and Gastric Varices; Gastric Juice; Gastrins; Gastrointestinal Diseases; Hepatic Encephalopathy; Humans; Hypercholesterolemia; Hypertension, Portal; Liver; Liver Cirrhosis; Liver Regeneration; Liver Transplantation; Pancreas; Preservation, Biological; Radioimmunoassay; Rats