gastrins and Gastrointestinal-Hemorrhage

In the high altitude environment the oxygen and air density are decreased, the temperature and humidity are low, there es an increase in radioactivity. These environmental factors influence on the human body; it has been known for many years that people born and living at high altitude have different morphological and physiological characteristic than those at low altitude. The digestive mechanism for adaptation or acclimation to high altitude has interested physiologist and clinicians for many years. The objective of this article is to present a brief overview of the digestive physiology and pathology in the high altitude.

Topics: Altitude; Bolivia; Cholelithiasis; Colonic Neoplasms; Diverticulum, Colon; Dyspepsia; Endopeptidases; Gallbladder Neoplasms; Gastric Mucosa; Gastrins; Gastrointestinal Diseases; Gastrointestinal Hemorrhage; Gastrointestinal Transit; Humans; Intestinal Obstruction; Intestines; Peptic Ulcer; Peru

Topics: Burimamide; Chemical Phenomena; Chemistry; Cimetidine; Duodenal Ulcer; Esophagitis, Peptic; Gastric Acid; Gastrins; Gastrointestinal Hemorrhage; Histamine; Histamine H1 Antagonists; Histamine H2 Antagonists; Humans; Hypersensitivity; Intrinsic Factor; Kinetics; Malabsorption Syndromes; Metiamide; Pancreas; Pepsin A; Ranitidine; Receptors, Histamine H2; Stomach Ulcer; Stress, Psychological; Zollinger-Ellison Syndrome

Development of histamine H2-receptor antagonists has enhanced the understanding of histamine physiology and pharmacology. The effect of H2-receptor antagonists on gastrointestinal physiology has been studied extensively. These compounds inhibit gastric acid secretion in response to all known secretagogues and, in contrast to anticholinergic drugs, markedly inhibit food-stimulated acid secretion in duodenal ulcer patients. The relative roles of H2-receptor antagonists, anticholinergic drugs and antacids in the treatment of duodenal ulcer remain to be defined. Cimetidine currently is under investigation for the treatment of duodenal ulcer, gastric ulcer, reflux esophagitis, gastrointestinal bleeding and hypersecretory states. Although the long-term safety of cimetidine has not been established, in short-term clinical trials there have been no significant subjective or objective side-effects. Assuming that toxic effects do not develop, H2-receptor antagonists should improve the treatment of acid-peptic disease.

Topics: Cimetidine; Cyclic AMP; Duodenal Ulcer; Esophagitis, Peptic; Gastric Juice; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Histamine; Histamine H2 Antagonists; Humans; Intrinsic Factor; Metiamide; Pepsin A; Stomach Ulcer

Cimetidine is a specific competitive histamine H2-receptor antagonist which effectively inhibits gastric acid secretion and is advocated for the treatment of chronic peptic ulceration, haemorrhage from erosive gastritis, and the control of gastric hypersecretion and peptic ulceration in the Zollinger-Ellison syndrome. Placebo-controlled trials in outpatients have demonstrated its efficacy in promoting the healing of endoscopically diagnosed duodenal ulceration, during a period of 4 to 6 weeks, but its role in the treatment of gastric ulcer is less clear. Preliminary evidence suggests that maintenance therapy with cimetidine reduces the rate of recurrence of duodenal ulcer, but further studies are required to clarify its role in this situation and in the treatment of oesophagitis and acute gastrointestinal haemorrhage. Cimetidine controls the peptic ulceration of Zollinger-Ellison syndrome in most patients when given continuously for up to 2 years. Side-effects have generally been trivial and have very seldom necessitated withdrawal of therapy except in the rare occurrence of gynaecomastia. The haematological abnormalities particularly agranulocytosis, which lead to the withdrawal from clinical use of metiamide, have not been reported with cimetidine, except for 1 case of transient neutropenia. The safety of long-term cimetidine administration has yet to be determined.

Topics: Acute Disease; Animals; Cimetidine; Duodenal Ulcer; Gastric Juice; Gastrins; Gastrointestinal Hemorrhage; Guanidines; Humans; Intrinsic Factor; Recurrence; Stomach Ulcer; Zollinger-Ellison Syndrome

Cimetidine, a new histamine H2-receptor antagonist (H.H2.R.A.) is a potent inhibitor of basal and stimulated gastric acid secretion. Contrary to anticholinergics, it does not affect gastric emptying nor does it decrease lower oesophageal sphincter pressure; cimetidine may therefore be used as the treatment of reflux oesophagitis. After prolonged administration of currently used therapeutic doses, basal and post-prandial serum gastrin levels remain unchanged and the parietal cell mass is not increases. Cimetidine toxicity is very low. Cimetidine is effective in promoting healing and pain relief of gastric and duodenal ulcer. In the latter long-term treatment for prevention of relapse is efficient, but the appraisal of its safety remains debated. Efficiency of H.H2.R.A. in the prophylaxis of gastrointestinal haemorrhage in patients with fulminant hepatic failure has been proven. Furthermore, cimetidine has a dramatic ability to control haemorrhage from acute erosive lesions in any seriously-ill patient. It may also be of benefit in the treatment of bleeding from gastric or duodenal ulcer and, whatewer the lesion, in the prevention of bleeding recurrence. In the Zollinger-Ellison syndrome, good results have been obtained but cimetidine treatment must be decided and supervised only by well-informed specialists. Lastly, in patients with severe exocrine pancreatic insufficiency, cimetidine prevents gastric degradation of orally administered pancreatic extracts and decreases steatorrhea.

Topics: Cimetidine; Gastric Juice; Gastrins; Gastrointestinal Hemorrhage; Guanidines; Humans; Peptic Ulcer; Peptic Ulcer Hemorrhage; Zollinger-Ellison Syndrome

Topics: Antacids; Asphyxia; Esophagitis; Esophagoscopy; Gastrins; Gastroesophageal Reflux; Gastrointestinal Hemorrhage; Hernia, Diaphragmatic; Humans; Methods; Parasympatholytics; Radiography; Stomach Ulcer

Topics: Digestion; Enzyme Therapy; Fats; Gastric Juice; Gastrins; Gastrointestinal Hemorrhage; Gastrointestinal Hormones; Humans; Methods; Pancreas; Pancreatectomy; Pancreatic Diseases; Pancreatic Juice; Pancreatic Neoplasms; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Animals; Aspirin; Atropine; Bile Acids and Salts; Cell Membrane Permeability; Ethanol; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Humans; Hydrogen; Hydrogen-Ion Concentration; Ion Exchange; Membrane Potentials; Pentagastrin; Pepsin A; Pyloric Antrum; Smoking; Sodium; Stomach Neoplasms

Topics: Diarrhea; Drainage; Dumping Syndrome; Duodenal Ulcer; Female; Gallbladder; Gastric Juice; Gastrins; Gastrointestinal Hemorrhage; Gastrointestinal Motility; Humans; Intestine, Small; Male; Pancreas; Peptic Ulcer Perforation; Postoperative Complications; Pyloric Antrum; Pyloric Stenosis; Pylorus; Recurrence; Stomach; Stomach Ulcer; Vagotomy

Topics: Adolescent; Adult; Aged; Anemia, Hypochromic; Anemia, Pernicious; Atrophy; Autoantibodies; Autoimmune Diseases; Chronic Disease; Female; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Humans; Male; Middle Aged; Postgastrectomy Syndromes; Stomach Neoplasms; Stomach Ulcer

Topics: Biliary Tract Diseases; Ceruletide; Cholangiography; Cholelithiasis; Duodenal Ulcer; Endoscopy; Gastrins; Gastrointestinal Diseases; Gastrointestinal Hemorrhage; Gastrointestinal Hormones; Humans; Intestinal Absorption; Lactose Intolerance; Pancreatic Diseases; Peptic Ulcer; Radionuclide Imaging; Secretin; Stomach Neoplasms

Topics: Abdomen; Duodenal Diseases; Duodenal Neoplasms; Duodenal Ulcer; Esophageal Achalasia; Esophageal Diseases; Esophageal Neoplasms; Esophagitis; Esophagoplasty; Esophagus; Female; Gastrins; Gastrointestinal Hemorrhage; Hernia, Diaphragmatic; Humans; Male; Peptic Ulcer; Peptic Ulcer Perforation; Postoperative Complications; Rupture, Spontaneous; Stomach Diseases; Stomach Neoplasms; Stomach Ulcer; Stress, Psychological; Vagotomy

Low-dose aspirin (LDA) administration prevents cerebral infarction and myocardial infarction, but many studies found an association with mucosal injury. Proton-pump inhibitors (PPIs) can prevent gastric and duodenal mucosal damage, but they may exacerbate small-intestinal mucosal injury by altering the microbiota. We aimed to assess the effect of PPIs on the intestinal flora of LDA users.. Thirty-two recruited patients, who received LDA (100 mg/day) but did not take PPIs, were divided into 15 patients additionally receiving esomeprazole (20 mg/day) and 17 patients additionally receiving vonoprazan (10 mg/day). On days 0, 30, 90, and 180, the microbiota of each patient was examined by terminal restriction fragment length polymorphism analysis, and the serum gastrin, hemoglobin, and hematocrit levels were measured.. Additional PPI administration increased the proportion of Lactobacillales in the microbiota of LDA users. This trend was more prevalent in the vonoprazan group (p < 0.0001) than in the esomeprazole group (p = 0.0024). The Lactobacillales proportion was positively correlated with the gastrin level (r = 0.5354). No significant hemoglobin or hematocrit level reduction was observed in subjects receiving LDA with additional PPI.. Additional PPI administration increased the Lactobacillales proportion in the microbiota of LDA users. The positive correlation between the gastrin level and the proportion of Lactobacillales suggested that the change in the intestinal flora was associated with the degree of suppression of gastric acid secretion. Additional oral PPI did not significantly promote anemia, but the risk of causing PPI-induced small-intestinal mucosal injury in LDA users should be considered.

Topics: Aged; Aged, 80 and over; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Case-Control Studies; Comorbidity; Dose-Response Relationship, Drug; Esomeprazole; Female; Gastrins; Gastrointestinal Hemorrhage; Gastrointestinal Microbiome; Hematocrit; Hemoglobins; Humans; Intestinal Mucosa; Lactobacillales; Male; Middle Aged; Polymorphism, Restriction Fragment Length; Prospective Studies; Proton Pump Inhibitors; Pyrroles; Sulfonamides

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

The majority of upper gastrointestinal bleeds stop spontaneously despite the low pH and proteolytic activity of gastric juice which inhibit coagulation and platelet aggregation. In order to investigate this paradox six healthy male volunteers received intragastric infusions of 160 ml autologous venous blood or 160 ml egg white acting as control in random order on separate days. Basal acid output was calculated before infusion, net acid secretion and gastric volume emptied were calculated after intragastric infusions. Serum gastrin concentrations were also measured before and after intragastric infusions and expressed as the integrated gastrin response. Basal acid output (mmol/h) was 4.7 (1.9) (mean (SEM)) before egg white infusion and 5.9 (2.6) before venous blood infusion. After egg white infusion net acid secretion (mmol/20 min) increased to 5.6 (3.1) compared with 2.3 (1.3) after venous blood infusion (p less than 0.05). The gastric volume emptied (ml/20 min) was less after venous blood infusion at 105 (28) compared with 321 (66) after egg white infusion (p less than 0.03). Integrated gastrin response was similar after venous blood and egg white infusion. When compared with an equivalent protein meal intragastric blood stimulates less acid secretion and delays gastric emptying. This effect may facilitate haemostasis after gastric bleeding.

Topics: Adult; Blood; Egg White; Gastric Acid; Gastric Acidity Determination; Gastric Emptying; Gastrins; Gastrointestinal Hemorrhage; Humans; Male; Secretory Rate

The effects of indomethacin and carprofen on gastric secretion, serum gastrin level, electropotential difference, gastric microbleeding, DNA loss, mucosal blood flow and the production of mucosal prostaglandins (PGs) were investigated in a double-blind cross-over study in 18 healthy volunteers after one week of treatment. We did not observe any significant changes in basal and pentagastrin-stimulated gastric secretory parameters, serum gastrin level and electro-potential difference before and after treatment with these drugs. Mucosal blood flow was significantly reduced following indomethacin treatment. The most pronounced differences were found in endoscopic score studies of gastric mucosa. After indomethacin all subjects developed multiple erosions, submucosal haemorrhages, and half of them showed diffuse antral erythema. These effects were accompanied by a significant increase in both gastric microbleeding and DNA loss, and significant decrease in the production of PGE2. We concluded that carprofen, in contrast to indomethacin, did not alter gastric mucosal integrity and production of PGE2. This study indicates that the gastric mucosal damage by non-steroid anti-inflammatory compounds (NOSAC) depends upon the suppression of PGE2 biosynthesis, and that endogenous PGE2 is involved in the control of mucosal blood flow and mucosal integrity.

Topics: Adult; Anti-Inflammatory Agents; Blood Circulation; Carbazoles; Clinical Trials as Topic; Dinoprostone; Double-Blind Method; Endoscopy; Gastric Juice; Gastric Mucosa; Gastrins; Gastrointestinal Hemorrhage; Humans; Indomethacin; Male; Prostaglandins E; Stomach

The effect of carbenoxolone on the healing of gastric ulcer and erosions was compared with that of placebo. The series consisted of 20 patients with chronic gastric ulcers and 20 patients with superficial erosions of the stomach. The diagnosis as well as the follow-up of the lesions were based on gastroscopic examinations. The ulcers were measured gastroscopically. A double-blind method was used. Besides carbenoxolone 50 mg or placebo three times daily, all the patients received antacids in fixed dosage for six weeks. Subjective symptoms and cardiovascular side-effects were recorded. Maximal acid output and serum gastrin levels were measured before and after the treatment. No difference was seen between carbenoxolone and placebo groups with regard to the healing rate of the ulcers of disappearance of the erosions. The subjective symptoms subsided significantly faster in the treatment groups than in the control groups. No cardiovascular side-effects were evident during the treatment with carbenoxolone. One patient needed potassium supplements. Carbenoxolone had no effect on the pentagastrin-stimulated gastric acid secretion nor on the serum gastrin values.

Topics: Carbenoxolone; Clinical Trials as Topic; Double-Blind Method; Drug Evaluation; Follow-Up Studies; Gastric Juice; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Humans; Stomach Ulcer; Triterpenes

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Topics: Duodenal Ulcer; Epidermal Growth Factor; Gastrins; Gastrointestinal Hemorrhage; Humans; Stomach Ulcer

 To explore the predictive value of serum gastrin (GAS), epidermal growth factor (EGF) levels in gastric ulcer complicated with acute upper gastrointestinal bleeding.. A descriptive study.. Department of Emergency, Beijing Jiangong Hospital, China, from January 2019 to June 2020.. One hundred and twenty-five patients with gastric ulcer and acute upper gastrointestinal bleeding were selected as Group A. One hundred and twenty-five patients with gastric ulcer and no upper gastrointestinal bleeding were selected as Group B. Logistic regression analysis was used to analyse the risk factors of gastric ulcer complicated with acute upper gastrointestinal bleeding. The value of serum GAS, EGF in early diagnosis of gastric ulcer with upper gastrointestinal bleeding was evaluated by receiver operating characteristic (ROC) curve.. Univariate analysis showed statistically significant differences between Group A and Group B in taking non-steroidal anti-inflammatory drugs (NSAIDs), helicobacter pylori (Hp) infection, serum GAS and EGF (all p <0.001). Logistic regression analysis showed that raised serum GAS and serum EGF were independent risk factors for gastric ulcer and upper gastrointestinal bleeding (both p <0.001). The ROC area of serum EGF to predict gastric ulcer and acute upper gastrointestinal bleeding was 0.810 (95% CI: 0.753-0.867, p <0.001), greater than ROC area of serum GAS. At serum EGF of ≤109.95 pg/mL, had the 84.8%, sensitivity to predict gastric ulcer and acute upper gastrointestinal bleeding with specificity of 68.8%.. The predictive value of serum GAS and EGF is high for gastric ulcer complicated with acute upper gastrointestinal bleeding; the predictive value of serum EGF is greater than that of serum GAS. Key Words: Gastric ulcer, Acute upper gastrointestinal bleeding, Serum, Gastrin (GAS), Epidermal growth factor (EGF), Logistic regression, Receiver operating characteristic (ROC) curve.

Topics: Anti-Inflammatory Agents, Non-Steroidal; China; Epidermal Growth Factor; Gastrins; Gastrointestinal Hemorrhage; Helicobacter Infections; Helicobacter pylori; Humans; Risk Factors; Stomach Ulcer

To evaluate the local risk factors of traumatic brain injury (TBI) patients developing gastrointestinal (GI) bleeding during the early hospitalization in neurosurgery intensive care unit (NICU).. From September 2005 to February 2006, 41 patients admitted to NICU and 13 healthy volunteers were involved in our study. Blood samples at 24 hours, 2-3 days and 5-7 days were obtained from each patient via arterial line at 8 a.m. to measure the concentrations of serum adrenocorticotropic hormone (ACTH), total cortisol and gastrin. The collected serum was immersed in an ice bath and tested by the Immulite 1000 systems. Data were analyzed by SPSS 11.5.. Within 24 hours following TBI, the concentrations of total cortisol, ACTH and gastrin increased proportionally to the severity of injury, especially significant in the experimental group (P less than 0.05). The concentrations of ACTH and gastrin were higher in the GI bleeding positive group than in the GI bleeding negative group, (F equal to 1.413, P less than 0.253) for ACTH and (F equal to 9.371, P equal to 0.006) for gastrin. GI bleeding had a positive correlation with gastrin concentration (r equal to 0. 312, P less than 0.05) and a negative correlation with serum hemoglobin (Hb) (r equal to -0.420, P less than 0.01). The clinical incidence of GI bleeding was 24.39% (10/41) in the experimental group. Within 24 hours, GI bleeding had a strong correlation with gastrin concentration (OR equal to 26.643, P less than 0.05) and hematocrit (Hct) (OR equal to 5.385, P less than 0.05). High ACTH concentration ( larger than 100 pg/ml) increased the frequency of GI bleeding. For patients with severe TBI and treated with routine antacids, the incidence of GI bleeding was 40.91% (9/22) and the mortality rate was 20% (2/10).. Low Glasgow coma scale scores, low Hb, high concentrations of gastrin and ACTH (larger than 100 pg/ml) are risk factors and can be predictive values for post-traumatic GI bleeding. Severe TBI patients have high risks of GI bleeding with high mortality.

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Aged; Brain Injuries; Female; Gastrins; Gastrointestinal Hemorrhage; Glasgow Coma Scale; Humans; Logistic Models; Male; Middle Aged; Risk Factors

Melatonin and its precursor, l-tryptophan, have been shown to exert gastroprotective effects in animals, but their influence on the gastric damage by aspirin (ASA) in humans has been sparingly investigated. In this study, we designed to determine the effects of melatonin and l-tryptophan on ASA-induced gastric mucosal damage, gastric microbleeding, mucosal generation of prostaglandin E(2), and plasma melatonin, and gastrin levels. Three groups of healthy male volunteers (n = 30) with intact gastric mucosa received daily for 11 days either ASA alone or that combined with melatonin or tryptophan. Gastric blood loss and mucosal damage were evaluated at 3rd, 7th, and 11th days of ASA administration by endoscopy using Lanza score. ASA alone caused a marked rise of gastric damage and gastric blood loss, mainly at day 3rd and 7th, but they were significantly reduced at 11th day. Pretreatment with melatonin or tryptophan remarkably reduced ASA induced gastric lesions and microbleeding. Gastric mucosal generation of PGE(2) was suppressed by about 90% in all subjects treated with ASA alone without or with addition of melatonin or tryptophan. Plasma melatonin was markedly increased after treatment with melatonin or tryptophan plus ASA, but it was also raised significantly after application of ASA alone. Plasma gastrin levels were raised in subjects given melatonin or tryptophan plus ASA, but not in those with ASA alone. We conclude that melatonin and its precursor tryptophan given orally significantly reduce gastric lesions induced by ASA possibly due to (a) direct gastroprotective action of exogenous melatonin or that generated from tryptophan and (b) gastrin released from the gastric mucosa by melatonin or tryptophan.

Topics: Adult; Aspirin; Dinoprostone; Gastric Mucosa; Gastrins; Gastrointestinal Hemorrhage; Humans; Male; Melatonin; Middle Aged; Severity of Illness Index; Statistics, Nonparametric; Stomach Ulcer; Tryptophan

Upper gastrointestinal (GI) bleeding is a feared consequence of open heart surgery in children. Increased gastric acid secretion is a known key factor in the pathogenesis of gastritis and upper intestinal ulcerations. The aim of this study is to evaluate the serum kinetics of acid-stimulating factors and associated perioperative parameters after heart surgery in children.. Fifteen pediatric patients after open heart surgery and 15 children with cardiac catheterization were included in this study. Serum levels of gastrin, histidine, alanine, and tryptophan were analyzed before and up to 26 h after surgery.. In the postoperative period there was a significant elevation of gastrin with a peak at 4 h after surgery. Serum histidine was increased significantly immediately after surgery only in patients undergoing heart surgery with cardioplegia. No association of gastrin and histidine elevation with ischemia, perfusion time or lactate was observed.. Factors that are responsible for postoperative gastrin elevation still have to be determined. Circumstances of extracorporeal circulation (ECC) in low-risk patients most likely do not lead to relevant elevation of amino acids with acid-stimulatory effect in our study population.

Topics: Cardiac Surgical Procedures; Child; Child, Preschool; Gastric Acid; Gastric Acidity Determination; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Humans; Infant; Postoperative Complications

Peptic ulcers due to nonsteroidal anti-inflammatory drug (NSAID) use may have contributed to the static prevalence of ulcer disease in Asia.. We aimed to determine the current etiology of peptic ulcer disease in Singapore.. Consecutive patients undergoing esophagogastroduodenoscopy who had not been exposed to antibiotics, or antiulcer therapy within the past 6 months, and in whom peptic ulcers were found, were prospectively studied. Before endoscopy, patients were interviewed regarding the use of NSAID or aspirin. During endoscopy, antral biopsies were obtained for urease test and histology. Serum thromboxane B2 levels were compared with those of healthy volunteers.. Peptic ulcers were detected in 600 patients during a 2-year period. The ulcers were negative for Helicobacter pylori in 212 patients (35.3%) and these H. pylori negative ulcers were related to NSAID use in 68.9% of cases. On the basis of serum thromboxane B2 levels, 30.8% of the patients with non-H. pylori non-NSAID were considered to have consumed NSAID.. H. pylori negative peptic ulcer makes up a significant proportion of peptic ulcer in Singapore. Most of these ulcers were related to NSAID use. Serum thromboxane profile suggested surreptitious NSAID use in many of the non-H. pylori and apparently non-NSAID patients.

Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Female; Gastrins; Gastrointestinal Hemorrhage; Humans; Male; Middle Aged; Peptic Ulcer; Prospective Studies; Singapore; Thromboxane B2

Topics: Anti-Ulcer Agents; Cysts; Female; Gastric Mucosa; Gastrins; Gastrointestinal Hemorrhage; Gastrostomy; Humans; Infant; Jejunostomy; Peptic Ulcer; Pyloric Antrum; Ranitidine; Stomach Diseases; Vagotomy

Topics: Carcinoma, Islet Cell; Fatal Outcome; Female; Gastrins; Gastrointestinal Hemorrhage; Humans; Liver Neoplasms; Middle Aged; Pancreatic Neoplasms

Two strains of rat, Sprague-Dawley and inbred Piebald Virol Glaxo pigmented (PVG) strain, were dosed orally with hypertonic sodium chloride at a dose of 0.25, 0.5, 1.0 or 1.33 g/kg. Gastric epithelial cell proliferation was compared 16 hours after a single dose. The rats were given intraperitoneal bromodeoxyuridine (20 mg/kg) 1 hour before sacrifice, and cells undergoing DNA synthesis (S-phase) were assessed using a monoclonal antibody to bromodeoxyuridine. The number of labelled cells per gastric gland was counted using video image analysis, assessing ten low-power fields (160-180 gastric glands) per rat. Tissue injury was graded for submucosal oedema, inflammation and necrosis; it was minimal after dosing with 0.25 and 0.5 g/kg of sodium chloride. The PVG rats were more susceptible to tissue injury after dosing with 1.0 or 1.33 g/kg of sodium chloride: submucosal oedema, 80% in the PVG and 10% in the Sprague-Dawley; inflammation, 70% compared with 10%; necrosis, 70% compared with 20%. The number of labelled cells per fundic gland increased with increasing dose concentration of sodium chloride and the response was similar for both strains of rat. Plasma gastrin concentration at the time of sacrifice was significantly higher in the PVG rat for the 0.5, 1.0 and 1.33 g/kg doses. These strain differences may be useful in the further evaluation of the mechanisms of sodium chloride-induced tissue damage and repair.

Topics: Animals; Cell Count; DNA; Epithelium; Gastric Mucosa; Gastrins; Gastrointestinal Hemorrhage; Mitosis; Rats; Rats, Inbred Strains; Saline Solution, Hypertonic

Topics: Acute Kidney Injury; Gastrins; Gastrointestinal Hemorrhage; Hemofiltration; Humans; Male; Middle Aged; Postoperative Complications; Shock, Septic; Stress, Physiological

Topics: Gastric Acid; Gastrins; Gastrointestinal Diseases; Gastrointestinal Hemorrhage; Humans; Telangiectasis; Uremia

During the past 9 years, we have treated 23 patients with gastrointestinal hemorrhage following corrective surgery for biliary atresia. Ulcers or erosions of the stomach, duodenum or intestinal wall were observed endoscopically in 20 cases. In other 3 cases, bleeding point was not determined endoscopically, but massive bleeding was recognized frequently. Ten patients bled within 6 months of surgery, and the incidence of bleeding was also seen even after the age of 10 years. A history of cholangitis, the presence of jaundice and the use of cholagogues were related to the postoperative gastrointestinal bleeding. Serum concentrations of gastrin and gastric inhibitory polypeptide showed high values after surgery in almost half the biliary atresia patients examined, however, no clear relationship between the concentration of these factors and gastrointestinal hemorrhage was established.

Topics: Biliary Atresia; Child; Child, Preschool; Female; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hemorrhage; Humans; Infant; Jaundice; Male; Peptic Ulcer Hemorrhage; Postoperative Complications

Serum concentration of gastrin was measured before and after renal transplantation in 97 consecutive patients in order to assess possible correlations to gastrointestinal bleeding, allograft function, or graft rejection. In patients with transient signs of allograft rejection (N = 29) or upper gastrointestinal bleeding (N = 12) there was a nonsignificant trend towards higher postoperative gastrin levels, and in patients in whom the graft was removed (N = 29), this tendency was more pronounced (p = 0.06). The study demonstrated that monitoring of serum concentrations of gastrin following renal transplantation is of little clinical value. However, increased gastrin levels in serum may indicate that graftectomy may be the ultimate result.

Topics: Cadaver; Cimetidine; Female; Gastrins; Gastrointestinal Hemorrhage; Graft Rejection; Humans; Immunosuppressive Agents; Intraoperative Period; Kidney Transplantation; Male; Peptic Ulcer Perforation; Predictive Value of Tests

Over a five-year period, we measured concentrations of gut hormones in plasma samples from 353 patients in whom diagnoses of pancreatic endocrine tumors were subsequently confirmed. A median of 19 months (range, 7 to 120) after the initial diagnosis, 24 of these patients (6.8 percent) had elevated concentrations of other hormones in association with new clinical symptoms. In 13 of these patients (8 with glucagonomas, 3 with tumors secreting vasoactive intestinal polypeptide, and 2 with insulinomas), hypergastrinemia developed along with the clinical features of a gastrinoma; 5 patients died of gastrointestinal perforation or bleeding, apparently caused by this second tumor. We conclude that patients with pancreatic endocrine tumors, regardless of their initial clinical picture, require continued surveillance for new elevations of hormones.

Topics: Adenoma, Islet Cell; Adult; Aged; Gastrins; Gastrointestinal Hemorrhage; Glucagon; Glucagonoma; Hormones; Humans; Insulinoma; Middle Aged; Pancreatic Neoplasms; Time Factors; Vasoactive Intestinal Peptide; Vipoma; Zollinger-Ellison Syndrome

In 15 undialyzed (UD) patients and 26 hemodialyzed (HD) patients, (1) basal and test meal-stimulated gastrin concentrations, (2) basal and pentagastrin-stimulated gastric acid outputs, and (3) endoscopic examinations were studied. Also studied were the morphological and functional differences of the gastrointestinal tract between UD and HD patients. HD patients had lower gastric acid outputs and higher circulating gastrin levels in the fasting state. After a test meal, the peak increment of serum gastrin in UD and HD patients occurred 30 and 60 min later, respectively, and the response was prolonged in each group. Endoscopic findings showed that the incidence of abnormalities in each group was very similar, that is, the most predominant lesions in each group were hemorrhagic and atrophic gastritis. The data suggested that the response to gastrin of parietal cell and the defensive mechanism of gastrointestinal mucosa in HD patients may be impaired.

Topics: Adult; Eating; Female; Gastric Juice; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Gastroscopy; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis

Topics: Adult; Aged; Calcitonin; Female; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis

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

Topics: Adolescent; Adult; Aged; Female; Gastric Acidity Determination; Gastrins; Gastrointestinal Hemorrhage; Humans; Male; Middle Aged; Peptic Ulcer; Stress, Physiological

During a 3-year period proximal gastric vagotomy without drainage and selective gastric vagotomy with drainage were performed in 61 patients with duodenal ulcer. Of these, 57 patients were followed for 3-6 years. 77% were symptom-free (Visick I); 8,3% were improved but still have periods of dyspepsia (Visick II) and 14% were failures because of recurrent ulcer (Visick III). There were seven duodenal recurrences in the bulb, and one prepyloric recurrence. There were no operative deaths or major complications. The side effects, like diarrhoea and dumping, after proximal gastric vagotomy and selective vagotomy were mild and rare. The majority of our patients gained their ideal body weight within the first six months from surgery. Blood chemistry did not show any deficiency in haemoglobin secondary to vagotomy, but plasma basal level of gastrin was constantly higher after surgery. It is concluded that 3-6 years after proximal gastric vagotomy and selective gastric vagotomy for duodenal ulcer there was a 14% recurrence rate, but the absence of mortality, severe complications or significant side effects seems to be at least as important as the high recurrence rate.

Topics: Adolescent; Adult; Aged; Body Weight; Diarrhea; Drainage; Duodenal Ulcer; Follow-Up Studies; Gastrins; Gastrointestinal Hemorrhage; Humans; Male; Middle Aged; Postoperative Complications; Recurrence; Retrospective Studies; Vagotomy; Vagotomy, Proximal Gastric

Endoscopy of the upper gastrointestinal tract was performed on 84 patients with end-stage chronic renal failure undergoing hemodialysis. Gastric acid secretion and fasting plasma gastrin levels were also examined in these patients. Hemorrhagic gastritis was most frequently observed (23 cases) followed by erosive gastritis (18 cases). No patients had gastric ulcers. Duodenal ulcers were observed in only two patients. Gastrointestinal bleeding was observed in 15 cases (17.9%). Thirteen of these 15 cases had hemorrhagic gastritis, one of which had a duodenal ulcer as a complication. Fasting plasma gastrin levels (359.6 +/- 336.5 pg/ml) were significantly higher than those of normal subjects (35.2 +/- 37.1 pg/ml), but no acceleration in gastric acid secretion was observed either in the basal condition (BAO 0.8 +/- 0.7 mEq/h) or following tetragastrin stimulation (MAO 9.0 +/- 6.9 mEq/h). Our results were inconsistent with the previous reports that high frequencies of peptic ulcers and increased gastric acid secretion were observed in patients with chronic renal failure. Our data suggest that the defensive factors rather than the aggressive factors of the gastroduodenal mucosa may be involved in chronic renal failure.

Topics: Adolescent; Adult; Aged; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Gastroscopy; Humans; Kidney Failure, Chronic; Male; Middle Aged

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

After administration of antacids, gastric stress lesions due to hemorrhagic shock appear in the pig stomach quicker and more markedly than in animals which have been similarly treated with an indifferent substance or not at all. However, once treated, the administration of antacids seems to favor the healing of mucosal lesions after the end of the stress. At the same time it was observed that after administration of antacids in hemorrhagic shock, the serum gastrin level rises and does not remain constant, as in the control group. An attempt is made to explain the favorable effect of antacids on the genesis of hemorrhagic stress lesions in the pig's stomach through this observation.

Topics: Animals; Antacids; Disease Models, Animal; Female; Gastric Mucosa; Gastrins; Gastrointestinal Hemorrhage; Male; Shock, Hemorrhagic; Stomach Diseases; Stomach Ulcer; Stress, Physiological; Swine; Time Factors

An awareness of the modes of presentation in childhood duodenal ulcer disease is necessary for prompt diagnosis and treatment. Therapy should be based on the rationale of decreasing acid secretion and providing adequate buffering of gastric acid throughout the day. Because of the high incidence of recurrence in children, aggressive diagnosis and treatment of duodenal ulcer are indicated in any child suspected of having the disease.

Topics: Adolescent; Antacids; Child; Child, Preschool; Duodenal Ulcer; Duodenum; Feeding Behavior; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastrointestinal Hemorrhage; Gastroscopy; Histamine H2 Antagonists; Humans; Infant; Infant, Newborn; Parasympatholytics; Radiography; Wound Healing

Twenty-one chronic hemodialysis patients were investigated. While only two had radiologic evidence of peptic ulceration, three had markedly elevated basal acid outputs, thirteen had significantly elevated maximal acid outputs and seven had fasting duodenogastric reflux. Elevated fasting serum gastrin levels and prolonged gastrin circulation following stimulated endogenous release were also demonstrated. The abnormalities in gastric function may be explained by fasting and stimulated hypergastrinemia.

Topics: Adult; Female; Gastric Juice; Gastrins; Gastrointestinal Hemorrhage; Humans; Hypercalcemia; Kidney Transplantation; Male; Middle Aged; Peptic Ulcer; Renal Dialysis; Uremia

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

Alterations in gastric physiology caused by selective embolization and vasopressin infusion of the left gastric artery were evaluated in 29 dogs. Gastric acidity was not significantly altered following Gelfoam embolization but decreased sharply with vasopressin infusion. These results suggest that the segmental occlusion caused by Gelfoam embolization permits significant collateral blood flow to the gastric mucosa, while the arteriolar and capillary constriction caused by vasopressin effectively decreases mucosal blood flow. These findings are consistent with the clincal observation that embolization is more effective in controlling bleeding ulcers, while vasopressin infusion is more effective for controlling hemorrhagic gastritis.

Topics: Angiography; Animals; Dogs; Embolization, Therapeutic; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Histamine; Models, Biological; Peptic Ulcer Hemorrhage; Stomach; Vasopressins

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: Adult; Age Factors; Aged; Blood Group Antigens; British Columbia; Female; Gastrectomy; Gastric Acidity Determination; Gastrins; Gastroenterostomy; Gastrointestinal Hemorrhage; Humans; Male; Middle Aged; Peptic Ulcer; Postoperative Complications; Recurrence; Sex Factors; Substance-Related Disorders; Time Factors; Vagotomy

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

Topics: Animals; Electric Stimulation; Gastric Mucosa; Gastrins; Gastrointestinal Hemorrhage; Hypothalamus; Injections, Intravenous; Rats; Stimulation, Chemical; Stomach Ulcer

Topics: Acetates; Animals; Chlorides; Dogs; Female; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastrointestinal Hemorrhage; Hydrogen-Ion Concentration; Injections, Intramuscular; Male; Prednisolone; Sodium; Vagotomy

Topics: Adult; Aged; Carcinoid Tumor; Cholestasis; Duodenal Neoplasms; Duodenal Obstruction; Duodenal Ulcer; Female; Gastrins; Gastrointestinal Hemorrhage; Histamine Release; History, 19th Century; History, 20th Century; Humans; Insulin; Insulin Secretion; Male; Middle Aged; Neoplasm Metastasis; Peptic Ulcer Perforation; Peptides; Prognosis; Serotonin

Topics: Adenoma, Islet Cell; Bile Acids and Salts; Dietary Fats; Enzyme Repression; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastrointestinal Hemorrhage; Humans; Hydrogen-Ion Concentration; Jejunum; Lipase; Lipid Mobilization; Male; Middle Aged; Pancreas

Topics: Adrenocorticotropic Hormone; Adult; Cushing Syndrome; Gastrins; Gastrointestinal Hemorrhage; Humans; Hyperparathyroidism; Male; Multiple Endocrine Neoplasia; Parathyroid Hormone

Topics: Adenocarcinoma; Adenoma; Aortography; Diagnosis, Differential; Diarrhea; Gastrectomy; Gastric Juice; Gastrins; Gastrointestinal Hemorrhage; Gastrointestinal Motility; Humans; Hyperplasia; Intestine, Small; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Absorption; Animals; Aspirin; Bethanechol Compounds; Denervation; Dogs; Gastric Mucosa; Gastrins; Gastrointestinal Hemorrhage; Hemorrhage; Histamine; Intestinal Absorption; Ion Exchange; Pharmacology; Research; Salicylates; Salicylic Acid; Sympathomimetics; Toxicology