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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In duodenal ulcer disease, peptic digestion and ulceration of the duodenal mucosa can be related to increased duodenal acidity, which in about half the patients is due to inherited gastric hypersecretion, with too many parietal and chief cells. The others, normosecretors, may have parietal and chief cells excessively stimulated by, and/or specially sensitive to, gastrins and the vagus, together with inadequate suppression of the release of antral gastrin and the secretion of gastric acid. The abnormality is gastric hypersecretion with inappropriate hypergastrinaemia. The reserve capacities of the duodenal defence mechanisms are probably normal, but there seems to be a functional impairment with inadequate defence by decreased bicarbonate secretion into the duodenum, but as yet no clear impairment of the release of mucosal hormones. There are marked hereditary factors in gastric ulcer too. Some ulcers are related to gastric irritants (salicylates, tobacco). Oi's anatomical dual-control mechanism explains why gastric ulcers are usually solitary and at one site. Gastritis and duodenal reflux are probably the most important factors in type 1, body ulcers. Gastric stasis may be a factor in type 2, combined ulcers. Type 3 prepyloric ulcers resemble duodenal ulcers, both in blood group and hypersecretion.
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PMID:Current views on pathogenesis of peptic ulcer. 681 36

A prospective controlled trial of proximal gastric vagotomy (PGV) in 829 patients at three surgical services is presented. Peroperative tests of vagotomy completeness were made in two of the three groups of patients. The follow-up period was four to six years. The hospital stay after PGV averaged 9.2 days. The postoperative mortality rate was 0.2%. The reduction of gastric acidity was maintained four years after PGV. Postoperatively no patient had severe diarrhoea. The incidence of dumping after PGV was 1.5% and of gastric stasis 7.3%. Though 7% of the patients reported pyrosis after PGV, only a few required treatment. Transient dysphagia was reported by 2.5% of the patients. In about 4% of the series there were relatively mild ulcer-like symptoms postoperatively, without confirmation of ulcer. Duodenal ulcer recurred in 2% of cases during the observation period and gastric ulcer appeared in 1.5%. According to the Visick classification, 74% of the series showed grade I clinical result, 18% grade II, 4% grade III and 4% grade IV. There were no intergroup differences in Visick grades.
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PMID:Proximal gastric vagotomy. A prospective study of 829 patients with four-year follow-up. 683 26

Determination was made of in situ gastric pH during early morning in fasting state (basal pH) by using wired glass electrodes, and results obtained were analyzed. Analysis of the pattern of variation in intragastric pH at night revealed no substantial difference between normal subjects and patients with peptic ulcer but a tendency to be lower in the latter group. It was also shown that sleeping waves appeared in the electroencephalogram in association with the increase in intragastric pH during sleep at night. The basal pH value was 5.4 +/- 2.1 in patients with gastric cancer, 3.0 +/- 2.2 in those with gastritis, 2.4 +/- 1.9 in those with gastric ulcer, 1.7 +/- 0.2 in normal subjects and 1.3 +/- 0.6 in patients with duodenal ulcer. In gastric ulcer patients more anal site of ulcer lesion was associated with lower mean age of the patients and higher incidence of intestinal metaplastic gastritis of the antral or non-metaplastic type. In patients who underwent partial gastrectomy for peptic ulcer, the pH value in the remnant stomach tended to become higher with the lapse of time in all cases, being constant at about 3 months postoperatively. The decrease in gastric acidity at 12 months after operation was incomplete in patients who underwent emergency gastrectomy for perforated duodenal ulcer but satisfactory in those who underwent selective vatotomy and anterectomy as elective operations.
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PMID:A study of intragastric pH in patients with peptic ulcer--with special reference to the clinical significance of basal pH value. 732 83

We reviewed 254 consecutive gastroduodenal operations done at Charity Hospital of Louisiana in New Orleans between June 1974 and June 1977. Forty-one septic complications occurred in 30 patients, for an overall infection rate of 11.8%. Statistically higher infection rates followed operations for bleeding gastric or duodenal ulcer, obstructed duodenal ulcer, gastric ulcer, and gastric malignancy when compared to those done for chronic uncomplicated ulcer or perforated duodenal ulcer. Of these 30 patients, 22 had a compromise of either gastric acidity or motility at the time of operation. These two factors appear to be most significant in controlling the organisms which reach the stomach from swallowed saliva or by reflux through the pylorus. The organisms most frequently causing infection after gastroduodenal operations are endogenous to the stomach and include aerobic enteric gram-negative bacilli and oral, penicillin-sensitive anaerobes. Exogenous bacteria such as Staphylococcus aureus are a less frequent cause of infection after these operations.
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PMID:Sepsis after gastroduodenal operations: relationship to gastric acid, motility, and endogenous microflora. 738 47

Antacids reduce gastric acidity by neutralization, diminish peptic activity by increasing luminal pH above that optimal for proteolysis and provide thereby the rational for their use in ulcer disease. In clinical trials antacids fastened ulcer healing in patients with duodenal ulcer but not with gastric ulcer when compared to placebo. Furthermore, the prophylactic use of antacid medication can significantly reduce the frequency of acute bleeding when gastric content is titrated to a pH greater 3.5 on an hourly basis. Cimetidine does not adequately protect seriously ill patients from acute upper gastrointestinal tract bleeding. Antacids are better for this purpose. So far the efficacy of an antacid therapy has not been proven in controlled trials in patients with chronic ulcer disease, in patients with recurring ulcers following gastric surgery and in patients bleeding from acute or chronic gastroduodenal lesions.
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PMID:[Complicated ulcer; prevention and therapy of upper gastrointestinal bleeding; indications for antacid therapy]. 741 51

Antacids have served us well for over a century. In terms of peptic ulcer disease, the attitude in the late 1950s to 1970s that antacids should be taken only on demand was unjustified and erroneous. 13 recent endoscopic controlled studies have confirmed the efficacy of antacids in the healing of duodenal ulcer, achieving about 75% healing in 4 weeks. The efficacy of antacids in promoting gastric ulcer healing has been less well studied and the results are controversial. The most appropriate and economical antacid regimens for the treatment of duodenal ulcer disease should include tablets or liquid that have acid neutralising capacity of 400 mmol/day given at least an hour after meals. As a long term therapy, antacids appear to work, but need be taken in multiple daily doses, a regimen which is unlikely to meet with long term patient compliance. Patients with gastro-oesophageal reflux disorders or pregnancy-related reflux have also benefited from the usage of antacids ad libitum. Early previous studies have clearly demonstrated the efficacy of antacids in reducing gastro-oesophageal reflux and healing of reflux oesophagitis. The acidity of the gastric contents is the major determining factor in the outcome of the aspiration pneumonitis occurring during delivery. The prophylactic use of antacids during delivery has helped to reduce the severity of this complication. Similarly, the prophylactic administration of antacid aiming to maintain gastric pH between 3.5 to 7.0 has resulted in significant reduction of bleeding due to stress associated ulcers and/or erosive haemorrhagic gastritis in critically ill patients. Antacid therapy, however, is controversial in the management of nonulcer dyspepsia or nonsteroidal anti-inflammatory drug related upper gastrointestinal mucosal damage. Undoubtedly, antacids have major roles to play in the treatment of gastric acid related disorders. They have clear advantages and disadvantages when compared with the antisecretory agents. New proton pump inhibitors in particular have certainly superseded antacids and even the H2-receptor antagonists in many respects. However, the long term safety record of antacids remains unsurpassed by any of the new antisecretory agents.
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PMID:Antacids. Indications and limitations. 751 3

We studied the action on acid secretion of lansoprazole compared with famotidine by 24-h intragastric pH monitoring, evaluated its clinical effects prospectively, and assessed the importance of acid inhibition in gastric ulcer patients. Twenty symptomatic patients with active gastric ulcers diagnosed by endoscopy were assigned to a lansoprazole (LAN) group (lansoprazole 30 mg q.d., n = 10) or a famotidine (FAM) group (famotidine 20 mg b.i.d., n = 10). There were no differences between the groups in pretreatment pH profiles or background factors such as age, sex, smoking, previous ulcer therapy, ulcer site, or Helicobacter pylori infection. The FAM group showed a continuous increase in intragastric pH during the night, with low pH values except for a transient increase associated with food intake during the day. However, the LAN group showed a more neutral pH throughout the day, with pH-3 holding time ratios of 99.0% for 24 h, 98.3% at night, and 99.8% during the day, compared with 68.0, 76.5, and 59.4%, respectively, in the FAM group. The healing rate was also higher in the LAN group. We conclude that inhibition of gastric acidity is important in ulcer therapy and that lansoprazole is superior to famotidine in promoting ulcer healing.
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PMID:Suppressive action of lansoprazole on gastric acidity and its clinical effect in patients with gastric ulcers: comparison with famotidine. 759 34

To evaluate endogenous and exogenous factors affecting the quality of ulcer healing produced by proton pump inhibitors, gastric acid pH, serum gastrin, and serum pepsinogen (PG) I and II were measured in peptic ulcer patients before and after treatment with lansoprazole 30 mg once daily. Lansoprazole achieved more rapid scarring in duodenal ulcer (n = 34), with a healing rate of 97.1% after 6 weeks, than in gastric ulcer (n = 56), with a healing rate of 92.8% after 8 weeks. Scarring was the most rapid in gastroduodenal ulcer (n = 8), with a healing rate of 100% after 8 weeks, but the rate of complete scarring was the lowest (37.5%). Lower gastric acidity and lower PG I:II ratio were associated with poor quality ulcer scarring in patients with gastric ulcers, but the opposite was true for those with duodenal and gastroduodenal ulcers. For gastric ulcers, not only ulcer size but also mucosal atrophy was an important factor in ulcer healing. Smoking and alcohol consumption had little effect on the quality of ulcer healing during treatment. These results suggest that there are a number of differences between gastric ulcers and duodenal ulcers in terms of the quality of ulcer healing after lansoprazole treatment.
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PMID:Factors affecting quality of ulcer healing after lansoprazole treatment. 759 44

Omeprazole plus amoxicillin cures Helicobacter pylori infection. The hypothesis was tested that low acidity is a predictor of outcome. Fifty patients with relapsing or complicated, or both H pylori positive duodenal (n = 25) or gastric ulcer (n = 25) were randomly treated with either omeprazole 20 mg twice daily plus amoxicillin 1 g twice daily or with omeprazole 40 mg twice daily plus amoxicillin 1 g twice daily over two weeks. After one week of combined treatment, a 24 hour gastric pH measurement was performed in all patients. H pylori cure rate was 67%. Patients who later turned out to be cured had higher pH values during night time and after meals (p < 0.05). In an explorative analysis drug compliance, smoking, location of the ulcer (duodenum versus stomach), age, and grade of body gastritis were additional predictors of the outcome. Smoking (p = 0.006), compliance (p = 0.037), duodenal ulcer disease (p = 0.065), and young age (p = 0.021) were related to high acidity. In conclusion, the success of eradication treatment with omeprazole and amoxicillin in ulcer patients infected with H pylori depends on intragastric pH. Drug compliance, smoking habits, location of ulcer, age, and activity of body gastritis are other predictors and in part related to intragastric acidity.
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PMID:Intragastric acidity as a predictor of the success of Helicobacter pylori eradication: a study in peptic ulcer patients with omeprazole and amoxicillin. 767 77

Until recently, suppression of gastric acid secretion in patients with peptic ulcer was empirical and of unproven value. Anticholinergic drugs had only modest inhibitory effects on acid secretion, many side effects, and uncertain efficacy. Controlled trials using antacids demonstrated the value of reducing gastric acidity for healing duodenal ulcer. The discovery of histamine-2 (H2) receptor antagonists in the 1970s and the introduction of H+,K(+)-ATPase inhibitors in the 1980s made reduction of acid secretion the first-choice modality for healing and preventing recurrences of duodenal and gastric ulcers. The demonstration in the late 1980s and early 1990s that Helicobacter pylori (Hp) was a major risk factor for duodenal and gastric ulcer recurrences suggested that peptic ulcer could be cured by eradicating this organism from the stomach. However, antibiotic eradication of Hp can be difficult, often requiring simultaneous administration of a drug that suppresses acid secretion. Therefore, H2 and proton pump inhibitors continue to play a role in the management of duodenal and gastric ulcers associated with Hp and also play a primary role in the therapy of other acid-related disorders, such as gastroesophageal reflux diseases, stress ulcers, ulcers associated with nonsteroidal anti-inflammatory drugs, and gastrinoma (Zollinger-Ellison syndrome) and other acid hypersecretory states.
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PMID:Suppression of acid secretion in peptic ulcer disease. 767 7


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