gastrins and Esophageal-and-Gastric-Varices

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

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

To characterize bleeding from gastric red spots in patients with cirrhosis, three groups of patients were studied: (a) 11 cirrhotic patients bleeding from gastric red spots, (b) 18 nonbleeding cirrhotic patients without gastric red spots, and (c) 13 noncirrhotic patients with endoscopic normal mucosa (controls). Histologic examination of antral biopsy specimens revealed a diffuse capillary ectasia without inflammation in 8 of the 11 cirrhotic patients with gastric lesions. Morphometric analysis disclosed a significantly greater mean mucosal capillary cross-sectional area in cirrhotic patients with gastric lesions (mean +/- SE, 1371 +/- 320 microns2) than in those without gastric lesions (541 +/- 61 microns2) (p less than 0.005) or controls (353 +/- 20 microns2) (p less than 0.001). Hypergastrinemia was detected in 8 of the 11 cirrhotic patients with lesions, in 2 of the 18 cirrhotic patients without gastric lesions, and in none of the controls (p less than 0.001). Gastrin serum levels correlated significantly (r = 0.80) with mean mucosal capillary cross-sectional area in patients with cirrhosis. Pepsinogen I serum levels below 20 ng/ml were observed in 7 of the 11 cirrhotic patients with lesions, in 1 of the 18 cirrhotic patients without lesions, and in none of the controls. These data indicate that bleeding from gastric red spots in patients with cirrhosis is a distinct entity characterized by vascular ectasia of the gastric mucosa. This condition seems to be associated with hypergastrinemia and low serum levels of pepsinogen I.

Topics: Capillaries; Esophageal and Gastric Varices; Female; Gastric Mucosa; Gastrins; Gastrointestinal Hemorrhage; Humans; Liver Cirrhosis; Male; Middle Aged; Pepsinogens

The present study was designed to investigate basic and clinical problems of intraluminal lower esophageal sphincter (LES) manometry. As for the basic study, manometry apparatuses, measuring conditions and methods were revalued. For clinical study, effects of gastric contents and gastrin were studied with special reference to the asymmetry of the LES. The results obtained may be summarized as follows: Occlusion test performed in a LES model and dogs showed that the rate of pressure increase was greater in proportion to the greater perfusion rate as well as to smaller calibre of the manometry tube. The lower esophageal sphincter pressure (LESP) became greatest when the perfusion rate was increased up to a certain level and also when the withdrawal speed of a manometry tube was slowed down to a certain speed. Analysis of LES from the point of respiratory reversal disclosed that the pressure was greatest at the direction of 8 o'clock followed by those at 0 and 4 o'clock. The length of LES was longest at 4 o'clock followed by those at 0 and 8 o'clock. These differences in length of LES was mostly in accordance with the length of LES caudal to the point of respiratory reversal. LESP measured in different postures was greatest in the prone position suggesting the effect of intraabdominal pressure. Intragastric instillation of saline resulted in increase of intragastric pressure and LESP. Asymmetry of the LES in patients with sliding hiatal hernia, esophageal varices and achalasia showed profiles specific to the individual lesion.

Topics: Adult; Aged; Animals; Dogs; Esophageal Achalasia; Esophageal and Gastric Varices; Esophagogastric Junction; Fasting; Gastrins; Hernia, Hiatal; Humans; Intubation, Gastrointestinal; Male; Manometry; Middle Aged; Perfusion; Posture; Respiration

Topics: Adult; Aged; Esophageal and Gastric Varices; Esophagogastric Junction; Estrone; Female; Gastrins; Humans; Liver Cirrhosis; Male; Manometry; Middle Aged; Progesterone

Lower esophageal sphincter pressure (LESP) was measured in 10 biopsy-proved cirrhotics with esophageal varices and tense ascites before and after diuresis to evaluate of ascites might play in the development of variceal bleeding. In the 10 cirrhotic men studied, basal LESP was 30.9 +/- 1.7 mm Hg before and 22.7 +/- 1.3 mm Hg (P less than 0.01) after a diuresis which resulted in a mean 12-kg weight loss. LESP responses to abdominal compression were also evaluated. The change in LESP in response to a standard degree of abdominal compression was greater in the presence of ascites (8.5 +/- 0.4) than in its absence (6.3 +/- 0.4) (P less than 0.01). Basal gastric pH and fasting plasma gastrin concentrations did not differ during the two testing periods. Based on these data and the rarity with which cirrhotic patients with ascites complain of heartburn, it is concluded that reflux esophagitis caused by failure of the lower esophageal sphincter to remain competent is unlikely to be a significant etiological factor in the development of variceal bleeding.

Topics: Adult; Esophageal and Gastric Varices; Esophagogastric Junction; Fasting; Gastric Juice; Gastrins; Gastroesophageal Reflux; Gastrointestinal Hemorrhage; Humans; Hydrogen-Ion Concentration; Liver Cirrhosis; Male; Middle Aged; Pressure

The purpose of this study is to determine whether lower esophageal sphincter (LES) incompetency is a common occurrence in patients with liver cirrhosis and contributes to the development of variceal bleeding. Resting LES pressure (17.8 +/- 1.1 mm Hg) in 35 patients with cirrhosis was similar to that of our control population (17.3 +/- 2.0 mm Hg). No differences were found among patients with ascites, variceal hemorrhage, or with different degrees of hepatic decompensation. In both patients and control subjects the LES responded with a significant pressure increase to gastric alkalinization. Symptoms and radiological evidence of gastroesophageal reflux were extremely uncommon in patients with liver cirrhosis. Based on these data it is unlikely that acid-pepsin regurgitation is a significant factor in the development of variceal hemorrhage.

Topics: Adult; Aged; Ascites; Esophageal and Gastric Varices; Esophagitis, Peptic; Esophagogastric Junction; Gastric Acidity Determination; Gastrins; Gastroesophageal Reflux; Gastrointestinal Hemorrhage; Humans; Liver Cirrhosis; Liver Function Tests; Manometry; Middle Aged; Muscle Contraction

Vasopressin and its analogs are used inthe treatment of bleeding esophageal varices. Since gastrointestinal reflux may have a deleterious effect on variceal hemorrhage, the effect of 2,3-phenylalanine-8-lysine-vasopressin upon the lower esophageal sphincter (LES) was studies by rapid pull-through manometry in 24 persons. PLV infusion up to a dosis of 2.7 mU/kg/h raised LES pressure from 15.1 +/- 1.3 (SEM) to 17.9 +/- 2.0 mm Hg. Higher doses lowered LES pressure progressively to 12.1 +/- 0.7 mmHg at 54 mU/kg/h. The serum gastrin level did neither correlate with basal LES pressure not with LES pressure changes during PLV infusion. Therefore, PLV does not appear to act indirectly through serum gastrin. Because of the danger of systemic side effects and of the undesirable in LES pressure with the usual high doses of vasoactive substances, a continuous infusion of lower doses of vasopressin analogs appears to be advantageous.

Topics: Adult; Esophageal and Gastric Varices; Esophagogastric Junction; Female; Gastrins; Gastrointestinal Hemorrhage; Humans; Lypressin; Male; Methods; Vasopressins

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