gastrins and Liver-Cirrhosis

Topics: Animals; Dogs; Gastrins; Gastrointestinal Hormones; Humans; Intestine, Small; Kidney Failure, Chronic; Liver Cirrhosis; Malabsorption Syndromes; Peptic Ulcer; Postoperative Complications; Short Bowel Syndrome

Topics: Adrenal Cortex Hormones; Carbohydrate Metabolism; Endocrine Glands; Gastrins; Glucagon; Glucose Tolerance Test; Gonadal Steroid Hormones; Growth Hormone; Hormones; Humans; Insulin; Insulin Resistance; Liver Cirrhosis; Prolactin; Thyroid Hormones

Topics: Animals; Duodenal Ulcer; Gastrins; Gastrointestinal Diseases; Humans; Intestine, Small; Liver Cirrhosis; Liver Diseases; Peptic Ulcer

Topics: Animals; Depression, Chemical; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Liver Cirrhosis; Pancreas; Pancreatic Juice; Pepsin A; Peptic Ulcer; Stimulation, Chemical; Vagus Nerve

Topics: Aldosterone; Angiotensin II; Animals; Aprotinin; Gastric Juice; Gastrins; Hepatitis; Histamine; Humans; Hydroxyindoleacetic Acid; Kinins; Liver Cirrhosis; Liver Diseases; Peptides; Renin; Serotonin

Topics: Animals; Chronic Disease; Dogs; Duodenal Ulcer; Gastric Acidity Determination; Gastric Juice; Gastrins; Histamine; Homocysteine; Humans; Liver Cirrhosis; Liver Diseases; Stomach

Topics: Animals; Dogs; Gastric Mucosa; Gastrins; Humans; Liver Cirrhosis; Peptic Ulcer; Zollinger-Ellison Syndrome

Proton pump inhibitors (PPI) have been associated with infectious complications in cirrhosis, but their impact on distal gut microbiota composition and function is unclear. We aimed to evaluate changes in stool microbiota composition and function in patients with cirrhosis and healthy controls after omeprazole therapy. Both 15 compensated cirrhotic patients and 15 age-matched controls underwent serum gastrin measurement, stool microbiota profiling with multitagged pyrosequencing, and urinary metabolic profiling with NMR spectroscopy to assess microbial cometabolites before/after a 14-day course of 40 mg/day omeprazole under constant diet conditions. Results before (pre) and after PPI were compared in both groups, compared with baseline by systems biology techniques. Adherence was >95% without changes in diet or MELD (model for end-stage liver disease) score during the study. Serum gastrin concentrations significantly increased after PPI in cirrhosis (pre 38.3 ± 35.8 vs. 115.6 ± 79.3 pg/ml P < 0.0001) and controls (pre 29.9 ± 14.5 vs. 116.0 ± 74.0 pg/ml, P = 0.001). A significant microbiota change was seen in both controls and cirrhosis after omeprazole (QIIME P < 0.0001). Relative Streptococcaceae abundance, normally abundant in saliva, significantly increased postomeprazole in controls (1 vs. 5%) and cirrhosis (0 vs. 9%) and was correlated with serum gastrin levels (r = 0.4, P = 0.005). We found significantly reduced hippurate in cirrhosis vs. controls both pre- and postomeprazole and increased lactate in both groups post vs. preomeprazole, whereas dimethylamine (DMA) decreased in cirrhosis only. On correlation network analysis, significant changes in linkages of bacteria with metabolites (hippurate/DMA/lactate) were found postomeprazole, compared with pre-PPI in cirrhosis patients. In conclusion, omeprazole is associated with a microbiota shift and functional change in the distal gut in patients with compensated cirrhosis that could set the stage for bacterial overgrowth.

Topics: Arginine; Biomarkers; Case-Control Studies; Feces; Female; Gastrins; Hippurates; Humans; Intestines; Lactic Acid; Liver Cirrhosis; Magnetic Resonance Spectroscopy; Male; Metabolomics; Microbiota; Middle Aged; Omeprazole; Proton Pump Inhibitors; Risk Factors; Systems Biology; Time Factors; Treatment Outcome

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

Acute and chronic effect of Radix Angelicae Sinensis (RAS) on serum gastrin levels in patients with cirrhosis were investigated. The results showed that after intravenous perfusion of RAS, serum gastrin levels of inferior vana cava, hepatic and peripheral veins were significantly decreased. After long-term administration of the agent, the level fell nearly to that of control subjects. It is suggested that the effect of reducing serum gastrin level by RAS may improve portal hemodynamics and be beneficial for portal hypertensive gastroduodenal mucosal lesions in cirrhosis.

Topics: Adult; Drugs, Chinese Herbal; Female; Gastrins; Hemodynamics; Humans; Liver Cirrhosis; Male; Middle Aged

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

To examine the effect of proximal small intestinal stimulants of gastric acid secretion in cirrhotic patients with portacaval shunt, unshunted cirrhotics, and normal subjects, a mixture of L-amino acids was administered intraduodenally, into the proximal jejunum, or intravenously to 8 cirrhotic patients with portacaval shunt and to 8 unshunted subjects (4 cirrhotic and 4 healthy volunteers). In addition, the effect of intrajejunally administered hyperosmolar mannitol (850 mosmol/kg) and intrajejunal balloon distention (40 mmHg) was determined. In the shunted and unshunted groups gastric acid secretion significantly increased equally in response to intravenous and intraduodenal amino acid infusion, whereas amino acids administered intrajejunally did not significantly alter acid secretion. Perfusion of the jejunum with hyperosmolar mannitol resulted in significant stimulation of acid secretion in the shunted subjects, whereas in the unshunted subjects it caused significant inhibition. In addition, jejunal balloon distention significantly stimulated secretion in the shunted subjects, but not in the unshunted group. Serum gastrin did not change significantly during any of the experiments and plasma amino acids were not different after jejunal compared with duodenal perfusion. These studies indicate the following: Enteral and parenteral amino acids increase gastric acid secretion similarly in subjects with and without portacaval shunt. The intestinal phase of gastric acid secretion is initiated by intraduodenal, but not intrajejunal, amino acids. As plasma amino acid concentrations were similar regardless of the route used, this suggests that the intestinal phase of acid secretion cannot be fully explained by the postabsorptive stimulation by amino acids. Intrajejunal distention with a balloon or infusion of hyperosmolar mannitol into the proximal jejunum stimulates acid secretion only in subjects with portacaval shunt.

Topics: Adult; Aged; Amino Acids; Female; Gastric Acid; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Humans; Intubation, Gastrointestinal; Jejunum; Liver Cirrhosis; Male; Mannitol; Middle Aged; Portacaval Shunt, Surgical

We herein report a case of gastric hyperplastic polyps after argon plasma coagulation (APC) for gastric antral vascular ectasia (GAVE) in the antrum of a 65-year-old man with liver cirrhosis and hypergastrinemia induced by long-term proton pump inhibitor (PPI) use. Two years after APC therapy, endoscopy demonstrated multiple gastric polyps in the antrum and angle. A gastric polyp biopsy indicated foveolar epithelium hyperplasia, which was diagnosed as gastric hyperplastic polyps. One year after switching to an H2 blocker antagonist, endoscopy revealed that the polyps and GAVE had disappeared, with normal gastrin levels suggesting that PPI-induced hypergastrinemia had caused gastric hyperplastic polyps after APC therapy, and the polyps had disappeared after discontinuing PPIs.

Topics: Aged; Argon Plasma Coagulation; Gastric Antral Vascular Ectasia; Gastrins; Humans; Liver Cirrhosis; Male; Polyps; Stomach Neoplasms

This study aims to investigate the relationship between gastrointestinal dysfunction (GD) and cirrhosis severity in cirrhotic patients, to provide evidences for the prevention and treatment of GD in cirrhotic patients.A total of 95 cirrhotic inpatients and outpatients, who were treated in the Department of Gastroenterology of Xinqu Hospital of the First Affiliated Hospital of Henan University of Science and Technology, were enrolled in the present study, and assigned as the experimental group (cirrhosis group). According to Child-Pugh classification, these patients were divided into 3 groups: group A (n = 45), group B (n = 23), and group C (n = 27). Forty healthy adults who received health check-ups during the same period served as the control group. The gastrointestinal (GI) symptoms of cirrhotic patients were scored, and the fasting serum gastrin (GAS), motilin (MTL), and vasoactive intestinal peptide (VIP) levels were measured in all subjects.The potential correlations of GI symptom scores of patients in these cirrhosis groups with GI hormone levels and cirrhosis severity were analyzed. In cirrhotic patients, the GI symptom scores significantly increased. Furthermore, the symptom scores gradually increased along with the aggravation of liver damage. Moreover, serum GAS and VIP levels were significantly higher in the cirrhosis groups than in the control group, whereas MTL levels were significantly lower. These changes were significantly correlated with cirrhosis severity. The linear correlation analysis revealed that the GI symptom score was positively correlated with GAS and VIP levels, and negatively correlated with MTL level. In addition, the linear correlation analysis revealed that GI symptom score and GAS and VIP levels were positively correlated with cirrhosis severity, whereas MTL level was negatively correlated with cirrhosis severity.Cirrhotic patients have more obvious GI symptoms and higher GI hormone levels, which are closely correlated with the progression of liver cirrhosis and the degree of liver function damage.

Topics: Adult; Aged; Biomarkers; Disease Progression; Female; Gastrins; Gastrointestinal Diseases; Humans; Liver Cirrhosis; Male; Middle Aged; Motilin; Severity of Illness Index; Vasoactive Intestinal Peptide; Young Adult

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

Gastrin and its precursor, progastrin, are synthesized in the stomach, particularly when infected with Helicobacter pylori, and they are metabolized, at least in part, in the liver. However, little is known about their levels in various hepatic diseases.. This study was carried out on 147 patients including chronic hepatitis B (n = 35), hepatitis C (n = 52) and liver cirrhosis (n = 60) of class A (n = 38), class B (n = 15) and class C (n = 7) (Child-Pugh classification) and age- and sex-matched healthy controls (n = 65). The diagnosis of chronic hepatitis was confirmed by liver biopsy in all patients, whereas the diagnosis of liver cirrhosis was based on clinical and laboratory findings. Liver biopsy was done in 38 out of 60 patients. Blood samples were collected under basal conditions and separated plasma samples were kept frozen at -70 degrees C until radioimmunoassay of progastrin and its products, including bioactive amidated gastrins.. Median (range) plasma concentrations of total progastrin product and amidated gastrin in control subjects were 147.5 (73-345) pM and 33 (15-65), respectively. These concentrations in hepatitis B and C were not significantly different from those in controls. In cirrhosis (classes A, B and C), the concentrations of the progastrin and of gastrin were significantly (P < 0.05) higher than in controls reaching, respectively, 253.5 (135-683 pM) and 47.5 (17-385) pM. Both progastrin and gastrin levels were significantly higher in H. pylori-positive than in negative cirrhotic patients. Antibodies against H. pylori were present in about 50% of controls, 68% of hepatitis B, 57% of hepatitis C and in 83% in cirrhosis patients. The difference in H. pylori prevalence between cirrhosis and controls was statistically significant.. Plasma levels of progastrin and gastrin are significantly increased in cirrhotic patients and this could be attributed to reduced metabolism of these peptides in liver cirrhosis and to their increased release due to H. pylori infection rate in this disease.

Topics: Adolescent; Adult; Aged; Female; Gastrins; Helicobacter Infections; Hepatitis, Chronic; Hepatitis, Viral, Human; Humans; Liver Cirrhosis; Male; Middle Aged; Protein Precursors

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

A 48-year-old woman with type II diabetes developed fatigue, arthralgia and myalgia. A few weeks later she was found to have hepatomegaly. The erythrocyte sedimentation rate was raised (53/93 mm), as were liver enzyme activities (GOT 186 U/l; GPT 240 U/l; gamma-GT 199 U/l), the gamma-globulin levels (40.7%;IgG 4470 mg/dl, IgA 698 mg/dl, IgM 245 mg/dl), antinuclear antibodies and antibodies against double-strand DNA, smooth muscles and actin. Laparoscopy revealed small-nodular liver cirrhosis. The autoimmune hepatitis was treated with prednisolone (initially 60 mg daily, then reduced to 10 mg daily) and azathioprine (initially 100 mg daily, reduced to 50 mg daily). The symptoms markedly improved. But one year later, during follow-up examination, gastric polyps were found, excised and histologically found to be carcinoid. The gastrin level was raised to 765 pg/ml. Another year later the liver cirrhosis had advanced further and the type A gastritis was still present, but there was no sign of carcinoid recurrence.

Topics: Autoimmune Diseases; Azathioprine; Carcinoid Tumor; Cholangiopancreatography, Endoscopic Retrograde; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Endoscopy, Digestive System; Female; Follow-Up Studies; Gastrins; Gastritis; Hepatitis; Humans; Liver Cirrhosis; Middle Aged; Prednisolone; Stomach Neoplasms

The aim of the present study was to examine the diurnal urinary gastrin output in cirrhotics and to clarify whether in patients with hepatorenal syndrome urinary gastrin output is reduced. Thirty-two cirrhotics and 25 age- and sex-matched, controls were studied. Cirrhotics were divided into 3 groups: (I: without ascites and normal serum creatinine; II: ascites and normal creatinine; III: ascites and increased creatinine). Mean fasting serum gastrin concentration was lower in the control group than in Group I, II (p < 0.01) or III (p < 0.001). In this latter group mean serum gastrin concentration was significantly higher (p < 0.001) than in the other two groups of cirrhotics. The mean 24 h urinary gastrin output was lower (p < 0.001) in Group III patients than in the other groups of subjects studied. Also in the controls urinary gastrin output was lower (p < 0.01) than in Groups I and II. These findings suggest that: a) in cirrhotics with normal serum creatinine the average serum gastrin levels over the course of the day are indeed higher than in normals and b) In cirrhotics with hepatorenal syndrome, impaired urinary gastrin output appears to contribute significantly to their hypergastrinemia.

Topics: Adult; Aged; Case-Control Studies; Circadian Rhythm; Creatinine; Endoscopy, Digestive System; Fasting; Female; Gastrins; Humans; Liver Cirrhosis; Liver Function Tests; Male; Middle Aged; Prothrombin Time

The prevalence of peptic ulcer in cirrhotic patients is similar to that reported for the general population. Although gastric acid outputs ar normal or lower in cirrhotic subjects compared with non-cirrhotics, the frequency of non-response to histamine H2-receptor antagonists is higher. Peptic ulcer disease in the cirrhotic seems to pursue a more virulent course compared with that in the non-cirrhotic subject. Peptic ulcer prevalences in patients dying of uraemia or in uraemic patients on maintenance dialysis treatment are comparable with those in the general population. However, the frequency of peptic ulcer, especially complicated ulcer, is increased following renal transplantation. Ulcer complications in this context are associated with a high mortality rate. Pre-transplant risk factors for subsequent development of peptic ulcer remain to be identified and the value of histamine H2-receptor antagonists in prophylaxis is as yet unproven.

Topics: Duodenitis; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Humans; Kidney Failure, Chronic; Liver Cirrhosis; Peptic Ulcer; Peptic Ulcer Hemorrhage; Uremia

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

Both H2-receptor antagonists and pirenzepine are used in the treatment of peptic ulcer disease. Since we have recently found a higher frequency of non-responders to H2-receptor antagonists among cirrhotics, we tested the effect of the combination of 50 mg pirenzepine and 300 mg ranitidine in 25 patients (12 cirrhotics and 13 controls) in whom a normal 300 mg dose of ranitidine had failed to suppress intragastric acidity. Nocturnal intragastric pH was continuously monitored for 12 hours. A rise in the intragastric pH above 4.0 for more than 6 hours following the oral dose at 18.00 h was considered as response. In all subjects, plasma concentrations of ranitidine and pirenzepine were in the therapeutic range. Coadministration of pirenzepine and ranitidine resulted in sufficient increase of the intragastric pH in only 4 of the 12 patients with cirrhosis, and in 4 of the 13 control patients. This treatment failure in most of our patients does not support the view that excessive vagal drive might play an important role in the non-response to H2-blockers. With regard to the benefit resulting from coadministration of pirenzepine and ranitidine, there seems to be no difference between cirrhotic and control patients.

Topics: Adult; Aged; Chromatography, High Pressure Liquid; Circadian Rhythm; Drug Therapy, Combination; Female; Gastric Acidity Determination; Gastrins; Humans; Hydrogen-Ion Concentration; Liver Cirrhosis; Male; Middle Aged; Peptic Ulcer; Pirenzepine; Ranitidine

To investigate whether hypergastrinemia and low serum levels of pepsinogen I are associated with gastric hypoacidity in cirrhosis with capillary ectasia of gastric mucosa and whether this alteration is secondary to the presence of atrophic gastritis, two groups of patients were studied: 1) 12 cirrhotic patients with diffuse gastric red spots at the endoscopic examination, and 2) 12 cirrhotic patients with endoscopically normal mucosa. Vascular ectasia of the gastric mucosa was histologically confirmed in all patients with gastric red spots. The study of base-line and stimulated acid gastric secretion showed that 9 of 12 (75%) cirrhotics with gastric vascular ectasia had achlorhydria and that 8 of these 9 patients had high base-line gastrin serum levels (greater than 130 pg/ml) and low base-line pepsinogen I serum levels (less than 20 ng/ml). Base-line gastrin and pepsinogen I serum levels were significantly greater and lower, respectively, in patients with gastric vascular ectasias than in cirrhotics without these lesions. None of the patients of either group had complete atrophy in the corpus of the stomach, and only 4 of the 9 cirrhotics with gastric vascular ectasia and achlorhydria had moderate atrophy. These results show that achlorhydria is frequently associated with hypergastrinemia and low pepsinogen I serum levels in patients with cirrhosis and gastric vascular ectasias and suggest that this disturbance is not secondary to a morphologic abnormality of the gastric mucosa.

Topics: Atrophy; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Liver Cirrhosis; Pepsinogens

Topics: Duodenal Ulcer; Gastrins; Humans; Liver Cirrhosis; Postoperative Period; Prognosis; Stomach Neoplasms

A clinical and anatomic analysis was made of duodenal carcinoid tumors in 5 male patients (mean age 43.2 years). The tumors were present in the areas of the major duodenal papilla (in 3 cases), those of the bulb (1) and horizontal part of the duodenum (1). They were multiple in 2 cases. Clinically, signs of gastrin activity, i. e. recurring ulcers in various segments of the gastrointestinal tract (Zollinger-Ellison syndrome), were most common. Other changes included impairments in the biliary tract and liver. The causes of death were hepatic and renal insufficiencies (2 cases), thrombohemorrhagic events (2). In the closed glands, nesidioblastosis and thyroid C cell hyperplasia were detected, one case having type I multiple endocrinal neoplasia (adrenal corticosteroma, pancreatic apudoma). In three cases, the metastases invaded into the liver and lymph nodes. Direct correlation was not established between the tumor sizes, metastases and hormonal activity signs. All the tumors had not been recognized in the patients' life. The paper discusses if it is possible to make life-time diagnosis.

Topics: Adult; Aged; Biliary Tract; Carcinoid Tumor; Duodenal Neoplasms; Gastrins; Humans; Kidney; Liver Cirrhosis; Male; Middle Aged

Thirty-nine subjects have been studied: 14 with hepatic cirrhosis who had not been subjected to surgery, 13 cirrhotic patients in whom portacaval shunt had been performed, and 12 normal controls. In all of them, we performed serum determinations of pepsinogen I, both basal and after pentagastrin stimulation, and of basal gastrin levels, as well as analyses of basal and stimulated gastric acid secretion (basal acid output and maximal acid output). The values for pepsinogen I, basal or post-stimulation, were higher (p less than 0.001) in patients with cirrhosis who had not undergone surgical shunt than in those in the control group. However, there were no statistically significant differences when these two groups were compared with the patients who had been subjected to portacaval shunt. In this last group of patients, seven had levels similar to those of the controls, and six presented higher values. Likewise, the values for gastric acid secretion were similar in the three groups of patients, and the basal gastrin level was lower (p less than 0.001) among patients with liver cirrhosis, whether or not they had undergone surgery, than among the control population. In conclusion, the functional alterations of the gastric mucosa in patients with hepatic cirrhosis are not significantly different from those found in cirrhotic patients with portacaval shunt.

Topics: Adult; Aged; Female; Gastric Acid; Gastrins; Humans; Liver Cirrhosis; Male; Middle Aged; Pepsinogens; Portacaval Shunt, Surgical

Gastrin releasing peptide(GRP)-like immunoreactivity in human plasma was measured using radioimmunoassay of neuromedin C (NMC) in 83 healthy and 58 diseased subjects. In the healthy group, the mean value of fasting GRP-like immunoreactivity was 2.1 +/- 1.4 (mean +/- SD) pmol/L. There was a slight positive correlation between the GRP-like immunoreactivity values and aging. Postprandial serial measurements demonstrated that GRP-like immunoreactivity showed no response to a significant elevation of serum gastrin concentration. The group with chronic renal failure on hemodialysis gave the highest value, 7.1 +/- 2.1 pmol/L (p less than 0.01). There were no statistical differences between the healthy controls and groups with peptic ulcer, liver cirrhosis, diabetes mellitus or carcinomas, although some cancer patients had a marked increase in GRP-like immunoreactivity value.

Topics: Adult; Aged; Bombesin; Diabetes Mellitus; Female; Gastrin-Releasing Peptide; Gastrins; Humans; Kidney Failure, Chronic; Liver Cirrhosis; Male; Middle Aged; Neoplasms; Peptic Ulcer; Peptide Fragments; Peptides; Radioimmunoassay

Topics: Adult; Aged; Female; Gastrins; Hepatic Encephalopathy; Humans; Liver Cirrhosis; Male; Middle Aged; Neurotensin; Pancreatic Polypeptide; Somatostatin; Vasoactive Intestinal Peptide

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

We studied acid secretory responses to exogenous pentagastrin and to exogenous and endogenous gastrin in 12 stable cirrhotic subjects with portacaval shunt, 12 unshunted cirrhotics, and 12 normal subjects. Basal and stimulated serum gastrin concentrations as well as basal and maximum acid outputs were similar in the three groups. At low doses of either exogenous pentagastrin or gastrin-17 (G17), cirrhotics with portacaval shunt secreted significantly greater amounts of gastric acid than unshunted subjects. After low doses of intragastric peptone, cirrhotics with portacaval shunt secreted significantly more acid than unshunted cirrhotics and normal subjects. At each measured serum gastrin concentration after either exogenous G17 or intragastric peptone meals, cirrhotics with portacaval shunt secreted more acid than the unshunted control groups and their dose-response curve was significantly shifted to the left. Thus, in cirrhotic patients with portacaval shunt, gastric acid secretion is abnormally sensitive to both exogenously administered or endogenously released gastrin.

Topics: Aged; Diet; Dose-Response Relationship, Drug; Gastric Acid; Gastrins; Humans; Liver Cirrhosis; Middle Aged; Pentagastrin; Peptones; Portacaval Shunt, Surgical

Topics: Adult; Aged; Duodenum; Female; Gastric Mucosa; Gastrins; Hepatitis, Alcoholic; Hepatitis, Chronic; Humans; Liver Cirrhosis; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Peptic Ulcer; Stomach

In the fasting state the mean portal blood flow demonstrated by the pulsed Doppler system with the Octoson in liver cirrhosis (LC) patients (velocity (PV), 10.2 +/- 3.5 (mean +/- SD) cm/sec, 7.0 +/- 2.6 cm/sec/m2; flow (PF), 579 +/- 262 ml/min, 383 +/- 184 ml/min/m2 (n = 40)) was significantly lower than that in control subjects (PV, 21.2 +/- 5.2 cm/sec, 14.7 +/- 3.9 cm/sec/m2; PF, 966 +/- 344 ml/min, 667 +/- 220 ml/min/m2 (n = 40)). Food intake increased PV by 15% and PF by 15% in LC (n = 8) and increased PV by 56%, PF by 125% in controls (n = 8). Glucagon increased PV by 30% and PF by 52% in LC (n = 10) and increased PV by 50% and PF by 120% in controls (n = 8). Secretin increased PV by 44% and PF by 75% in LC (n = 9) and increased PV by 66% and PF by 142% in controls (n = 8). Vasopressin decreased PV by 42% and PF by 54% in LC (n = 9) and decreased PV by 48% and PF by 62% in controls (n = 8). Insulin, gastrin, and prostaglandin E1 had no effect in either group.

Topics: Adult; Aged; Female; Food; Gastrins; Glucagon; Hormones; Humans; Insulin; Liver Circulation; Liver Cirrhosis; Male; Middle Aged; Prostaglandins E; Secretin; Ultrasonics; Vasopressins

Gastric acid secretion, incidence of gastric mucosal lesion, and gut hormone responses were studied in 24 patients with liver cirrhosis. Gastric acid output in these subjects showed normal acidity and was nearly similar to that in patients with gastric ulcer. The incidence of gastric mucosal lesion was high, especially in patients whose plasma disappearance rate of indocyanine green was low. Plasma levels of both gastrin and gastric inhibitory polypeptide were higher in cirrhotic patients than in control subjects both in the fasting state and after the ingestion of a test meal. Gel chromatography of the postprandial plasma of cirrhotics showed a higher immunoreactivity at the second peak than in controls. This is because cirrhotics have a higher percentage of authentic gastric inhibitory polypeptide, although the elution patterns were similar in both groups. It is suggested that impairment of extraction of some molecular components of both gastrin and gastric inhibitory polypeptide may occur in the cirrhotic liver.

Topics: Adult; Aged; Blood Glucose; Chromatography, Gel; Female; Gastric Acid; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Humans; Insulin; Liver Cirrhosis; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Mucous Membrane; Stomach; Stomach Diseases; Stomach Ulcer

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

The serum values of PG I and gastrin have been established in a normal population and in several clinical diseases. The PG I is raised in duodenal, gastric, and pyloric ulcer even though the gastrin is normal. Both PG I and gastrin values are raised in renal insufficiency and the Zollinger-Ellison syndrome. The PG I is lowered in atrophic gastritis and alcoholic cirrhosis, and is at the limit of detection in Biermer anemia and total gastrectomy. Insulin and sham-feeding are stimulants for PG I release by patients with duodenal ulcer, but no correlation is observed between PG I output and PAO in the studied group. The results show that PG I is able to distinguish between associated hypergastrinemia and hypoacidity (Biermer anemia type) or a hyperacidity (Zollinger-Ellison syndrome type), and that PG I is a good indicator for gastric hypoacidity. Overlapping between normal and ulcer subjects is comparable to those obtained in acid output determinations.

Topics: Adolescent; Adult; Aged; Anemia, Pernicious; Duodenal Ulcer; Female; Gastrectomy; Gastrins; Gastritis, Atrophic; Humans; Kidney Failure, Chronic; Liver Cirrhosis; Male; Middle Aged; Pepsinogens; Reference Values; Stomach Ulcer; Zollinger-Ellison Syndrome

The effect of somatostatin on splanchnic hemodynamics was determined in 8 patients with cirrhosis of the liver and in 18 normal subjects using arterial-hepatic-venous catheterization. Estimated hepatic blood flow determined by indocyanine green infusion was 1.36 +/- 0.23 L/min (+/- SEM) in patients with cirrhosis and remained unaffected during 30 min of somatostatin (250 microgram/h) administration. Wedged hepatic venous pressure which was elevated to 23 +/- 1.8 mmHg was also uninfluenced. In contrast to somatostatin, an infusion of vasopressin (12 U/h for 30 min) given to the same patients, lowered estimated blood flow by 28% (p < 0.05) and wedged hepatic venous pressure by 18% (p < 0.02). Arterial gastrin and insulin levels were lowered during somatostatin infusion by 33% (p < 0.02) and by 75% (p < 0.005), respectively. In contrast to the cirrhosis, infusion of 250 microgram/h somatostatin into normal subjects was associated with a decrease of estimated hepatic blood flow from 1.20 +/- 0.16 to 0.88 +/- 0.12 L/min (p < 0.01) representing a 27% decline. Arterial gastrin and insulin concentrations were lower (p < 0.01) than in cirrhosis, but the basal levels were lowered by somatostatin to a similar degree in both groups of patients. A higher dose of somatostatin (500 microgram/h) administered to normal subjects resulted in a similar decrease of gastrin and of estimated hepatic blood flow as that seen with 250 microgram/h, whereas a lower dose (125 microgram/h) decreased gastrin but failed to influence estimated hepatic blood flow. Thus, somatostatin at a dose which has been used in the treatment of acute peptic ulcer hemorrhage (250 microgram/h) failed to influence estimated hepatic blood flow and wegded hepatic venous pressure in patients with cirrhosis but lowered splanchnic blood flow in normal subjects. Assuming that this effect contributes to somatostatin's therapeutic efficacy, these results cast doubt on its potential value in the treatment of upper gastrointestinal bleeding of cirrhotics with portal hypertension.

Topics: Dose-Response Relationship, Drug; Gastrins; Humans; Insulin; Liver Circulation; Liver Cirrhosis; Middle Aged; Regional Blood Flow; Somatostatin; Splanchnic Circulation; Vasopressins; Venous Pressure

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

The concentration of gastrin was determined in arterial and venous serum from the head, lung, liver, kidney, and legs in six fasting patients with mild hepatic parenchymatous disease. Extraction of gastrin could not be demonstrated in any of the vascular beds examined. The results indicate that gastrin degradation is not confined to certain specific organs but takes place in many organs or perhaps in the total volume of distribution for gastrin.

Topics: Adult; Biological Transport; Fatty Liver; Femoral Artery; Femoral Vein; Gastrins; Hepatic Veins; Humans; Jugular Veins; Liver; Liver Cirrhosis; Middle Aged; Pulmonary Artery; Renal Veins

The effect of glucagon on fasting gastrin levels was studied in normal subjects and in patients with advanced liver cirrhosis. Intravenous glucagon was given e.v. at a dose of 200 ng/kg/h and produced a significant decrease of serum gastrin levels at 50 min in controls while in cirrhotic patients there was no significant decrease. (p less than 0,01) Gastrin inhibition in normal subjects during glucagon infusion was significantly correlated to a simultaneous increase found in plasma cAMP and glucose levels. These findings suggest that hypergastrinemia in cirrhosis could be consequence of the failure of glucagon metabolic interactions.

Topics: Cyclic AMP; Gastrins; Glucagon; Humans; Liver Cirrhosis

Topics: Female; Gastric Juice; Gastrins; Humans; Liver Cirrhosis; Male; Middle Aged; Pepsin A; Secretin; Stomach Ulcer

Topics: Duodenal Ulcer; Female; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Liver Cirrhosis; Male

Fasting gastrinemia in cirrhotics (48.35 +/- 2.77 pg/ml) was higher than in normal controls (32.93 +/- 0.75 pg/ml; P less than 0.001). After insulin-induced hypoglycemia, the mean increase of gastrin above basal level was 42.29 +/- 1.92 pg/ml in controls and 10.85 +/- 5.05 pg/ml in cirrhosis (P less than 0.001). BAO was 2.53 +/- 0.36 mEq/h in controls and 0.42 +/- 0.004 mEq/h in cirrhotics (P less than 0.001). After i.v. insulin, TAO was 8.42 +/- 0.72 mEq/h in controls and 3.06 +/- 0.26 mEq/h in cirrhotics (P less than 0.001). The authors suggest that the lack of an adequate gastrin and acid response to the hypoglycemic stimulus in cirrhotics might be accounted for by a decreased insulin sensitivity.

Topics: Adult; Aged; Gastric Juice; Gastrins; Humans; Hypoglycemia; Insulin; Liver Cirrhosis; Male; Middle Aged

Immunoreactive serum gastrin from portal and peripheral veins was determined in five controls and in five cirrhotic patients with indwelling portal catheters in basal conditions, during and after 30 min arginine infusion, in order to assess whether the human liver is involved in gastrin metabolism. A significant difference was found between portal and peripheral gastrin concentrations in controls at 0, 60 and 90 min; no significant differences were found in cirrhotics. Our findings support the hypothesis of an at least partial breakdown of endogenous gastrin in the human liver.

Topics: Adult; Arginine; Arm; Gastrins; Humans; Liver; Liver Cirrhosis; Male; Middle Aged; Portal Vein

Topics: Adult; Aged; Duodenal Ulcer; Female; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Liver Cirrhosis; Male; Middle Aged; Stomach Ulcer

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

Topics: Aged; Blood Glucose; Dietary Proteins; Gastrins; Growth Hormone; Humans; Insulin; Insulin Secretion; Liver Cirrhosis; Male; Middle Aged

Topics: Duodenal Ulcer; Gastrins; Humans; Liver Cirrhosis; Peptic Ulcer

After days of standardized conditions of life and standardized diets, serum gastrin levels were measured in 6 patients with liver cirrhosis on 3 consecutive days and in 14 normal controls on 1 day. Blood samples were drawn every 4 h. In patients as well as in controls, a significant serum gastrin circadian rhythm was noted. The daily mean serum gastrin levels of patients were not significantly different from those of controls. These results suggest a secondary role of the liver in gastrin metabolism.

Topics: Aged; Circadian Rhythm; Female; Gastrins; Humans; Liver Cirrhosis; Male; Middle Aged; Radioimmunoassay

Topics: Gastrins; Humans; Liver Cirrhosis; Portacaval Shunt, Surgical; Renal Veins; Splenic Vein

The basal acid output (BAO), post-pentagastrin acid output (MAO), fasting and post-prandial gastrin levels in 40 patients with proven cirrhosis of the liver were compared with those in 20 normal controls. The mean BAO and MAO were significantly lower than normal, the mean fasting gastrin level was significantly higher than normal, and the postprandial gastrin response was significantly increased and prolonged. These differences were still significant even when the patients were divided into cryptogenic and alcoholic subgroups. A significant inverse relationship between MAO and the integrated gastrin response to meal was observed both in the normal controls and in the cirrhotic patients. The MAO and integrated gastrin response of the cirrhotic patients did not correlate with the degree of liver function impairment. In five cirrhotic patients fasting and postprandial gastrin levels were unchanged after splenorenal shunt operation. A more consistent abnormality of the gastric mucosa as assessed by endoscopy and biopsies appeared to be mucosal congestion with occasional atrophic gastritis. the severity of mucosal abnormality, however, was unrelated to the degree of hypoacidity. these results indicate, firstly, that the hypergastrinaemia in cirrhotic patients is a reflection of gastric hypoacidity and bears no direct relationship to hepatic dysfunction. Secondly, the gastric hypoacidity does not accrue solely from mucosal abnormality. It is suggested that this hypoacidity may result from the presence of excessive amounts of circulating acid-inhibiting intestinal peptides, which the diseased liver fails to metabolise.

Topics: Adult; Aged; Female; Food; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Liver Cirrhosis; Liver Function Tests; Male; Middle Aged; Pentagastrin; Secretory Rate; Stimulation, Chemical; Time Factors

Topics: Adult; Chronic Disease; Duodenal Ulcer; Gastric Juice; Gastric Mucosa; Gastrins; Hepatitis; Humans; Liver; Liver Cirrhosis; Middle Aged; Peptic Ulcer; Stomach Ulcer

Fifty patients with cirrhosis of the liver had gastrin concentrations in serum above normal when measured in the fasting state. Hypergastrinaemia predominated in non-alcoholic cirrhosis. In both groups of patients, serum gastrin levels were higher in patients with inactive cirrhosis than when cirrhosis was slightly active.

Topics: Aged; Alcoholism; Female; Gastrins; Humans; Liver Cirrhosis; Male; Middle Aged

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

In 28 patients with cirrhosis of the liver, histologically confirmed by liver biopsy, serum gastrin concentrations were determined radioimmunologically afer an overnight fast. Mean value and standard deviation in the patients with cirrhosis (30.1 +/- 19.3 pg/ml) was not found to be significantly different from the mean value established in 275 normal subjects (39.7 +/- 21.3 pg/ml).

Topics: Gastrins; Humans; Liver Cirrhosis

Topics: Adult; Aged; Gastric Acidity Determination; Gastric Juice; Gastrins; Glycine; Histamine; Humans; Iodine Radioisotopes; Liver Cirrhosis; Liver Function Tests; Middle Aged; Radioimmunoassay; Secretory Rate; Stimulation, Chemical; Time Factors

Topics: Biopsy; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastrointestinal Hemorrhage; Gastroscopy; Humans; Liver Cirrhosis; Water-Electrolyte Balance

Topics: Acromegaly; Dietary Proteins; Gastrectomy; Gastrins; Gastrointestinal Diseases; Humans; Kidney Diseases; Liver Cirrhosis; Peptic Ulcer; Radioimmunoassay; Stomach Neoplasms

Topics: Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Liver Cirrhosis; Pentagastrin; Peptic Ulcer; Secretory Rate; Stimulation, Chemical

Topics: Animals; Gastrins; Liver; Liver Cirrhosis; Peptic Ulcer; Rats

Topics: Blood Glucose; Gastric Juice; Gastrins; Gastrointestinal Hormones; Humans; Insulin; Insulin Secretion; Liver Cirrhosis; Portacaval Shunt, Surgical

Topics: Adult; Anemia; Fasting; Female; Gastrins; Humans; Immune Sera; Iodine Isotopes; Liver Cirrhosis; Male; Middle Aged; Radioimmunoassay

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

Topics: Cholelithiasis; Duodenal Ulcer; Fatty Liver; Gastric Acidity Determination; Gastrins; Gastrointestinal Diseases; Hepatitis; Humans; Lipid Metabolism; Liver Cirrhosis; Liver Diseases; Pancreas; Postgastrectomy Syndromes; Secretin; Sulfobromophthalein

Topics: Animals; Dogs; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Intestine, Small; Liver Cirrhosis; Peptic Ulcer; Portacaval Shunt, Surgical; Postoperative Complications

Topics: Aged; Blood Glucose; Bronchial Neoplasms; Carcinoma; Coronary Disease; Gastrins; Humans; Insulin; Liver Cirrhosis; Middle Aged; Osteochondritis; Peptides

Topics: Adolescent; Adult; Child; Female; Gastrins; Hemangioma; Humans; Hypersplenism; Liver Cirrhosis; Liver Diseases, Parasitic; Male; Middle Aged; Portacaval Shunt, Surgical; Portal Vein; Postoperative Complications; Schistosomiasis; Zollinger-Ellison Syndrome

Topics: Animals; Dogs; Gastrins; Liver Cirrhosis; Liver Cirrhosis, Experimental; Liver Diseases; Peptic Ulcer; Physiology; Ulcer

Topics: Animals; Dogs; Gastrins; Liver Cirrhosis; Liver Cirrhosis, Experimental; Peptic Ulcer; Research