Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the eradication and recurrence rate of Helicobacter pylori-infected gastric ulcer patients by combination therapies. Eighty-six H. pylori-positive gastric ulcer patients were assigned randomly to one of seven groups: I, omeprazole 20 mg (n = 9); II, lansoprazole (LPZ) 30 mg (n = 16); III, LPZ 30 mg plus plaunotol 480 mg (n = 13); IV, LPZ 30 mg plus ecabet sodium 2 g (n = 11); V, LPZ 30 mg plus clarithromycin 600 mg (the first 2 weeks; n = 11); VI, LPZ 30 mg plus plaunotol 480 mg plus clarithromycin 600 mg (the first 2 weeks; n = 13); and VII, LPZ 30 mg plus ecabet sodium 2 g plus amoxicillin 1,500 mg (the first 2 weeks; n = 13). All therapy was for 8 weeks except where otherwise noted. H. pylori eradication rates as diagnosed by culture, histology, urease test, and [13C]urea breath test 4 weeks after stopping therapy were 0, 0, 8, 45, 6, 46, and 62%, respectively, in groups I-VII. No patient achieving H. pylori eradication suffered recurrence. The combination therapies with proton pump inhibitors in addition to antibiotics and antiulcer agents are safe and effective in H. pylori eradication.
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PMID:Combination therapies with a proton pump inhibitor for Helicobacter pylori-infected gastric ulcer patients. 759 30

We studied 26 gastric ulcer patients who were treated with a proton pump inhibitor to evaluate the quality of ulcer healing using endoscopic ultrasonography (EUS), and we examined the relationship between ulcer recurrence and contraction demonstrated on ulcer echoes (study I). The effect of lansoprazole versus an H2-receptor antagonist on the contraction of ulcer echoes (study II) was also investigated. In study I, gastric ulcer patients who demonstrated early healing by endoscopy often had shallow Ul-II or Ul-III ulcers and small cross-sectional areas on ulcer echoes. The early contraction on ulcer echo was associated with lower rates of ulcer relapse, and might therefore be indicative of a good quality of healing. In study II, the ulcer contraction rate after 8 weeks of treatment with lansoprazole was 71.8%, significantly higher than that achieved with H2-receptor antagonists. However, the mean cross-sectional area of gastric ulcer after 8 weeks of treatment with lansoprazole was 113.9 mm2. In conclusion, although lansoprazole was suitable for initial therapy in peptic ulcer patients, the quality of ulcer healing based on EUS findings did not appear to be adequate in patients treated for the short periods of time in this study.
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PMID:Endosonographic evaluation of the quality of ulcer healing induced by proton pump inhibitors. 759 37

The effect of lansoprazole, a new benzimidazole proton pump inhibitor, on the relationship between ulcer healing and changes in mucin content was studied in gastric ulcer patients. Twenty-one outpatients with active gastric ulcers received lansoprazole 30 mg once daily given in the morning for 8 weeks. The gastric mucin content was examined by HPLC analysis of hexosamines in gastric biopsy specimens obtained from the lesser curvature of the pylorus and the greater curvature of the upper body. The ulcer healing rate for lansoprazole was 85.7% at 8 weeks. The mucin content of both mucosal regions significantly decreased to approximately 70% (pylorus 70.9%; upper body 74.7%) of the value before drug treatment. The results of this study demonstrate that 30 mg lansoprazole once daily is remarkably effective in healing gastric ulcers because of its potent acid suppression. It appears that acid inhibition is the primary factor in initial treatment. However, maintaining an altered gastric mucosal defense mechanism may have implications for the long-term treatment of gastric ulcers.
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PMID:Effects of lansoprazole on gastric ulcer healing and mucin content. 759 39

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

We studied the effects of lansoprazole on ulcer healing and Helicobacter pylori infection in elderly patients with peptic ulcers. In a group of 24 patients with gastric ulcers, the H. pylori infection rate was 100%. In the course of gastric ulcer healing with famotidine or lansoprazole alone, the H. pylori infection showed no signs of decline. The ulcer healing rates after 8 weeks were similar between the H2-receptor antagonist famotidine (73%), and the proton pump inhibitor lansoprazole (82%). When eradication of H. pylori infection was attempted by concomitant administration of lansoprazole and amoxicillin 500 mg b.i.d. for 2 weeks, the eradication rate was 33% in the group given lansoprazole 30 mg q.d. plus ampicillin 500 mg b.i.d., whereas it was 77% in the group given lansoprazole 30 mg b.i.d. plus ampicillin 500 mg b.i.d. Lansoprazole is considered to be a useful agent for the treatment of patients with peptic ulcers and H. pylori infection and its effectiveness in H. pylori eradication is improved by b.i.d. administration along with ampicillin.
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PMID:Therapeutic effects of lansoprazole on peptic ulcers in elderly patients. 759 48

Lansoprazole is the first proton pump inhibitor developed in Japan. We studied the clinical efficacy of lansoprazole 30 mg q.d. on peptic ulcers and the subsequent relapse rates. The endoscopic healing rate of gastric ulcers (n = 86) after 8 weeks of treatment and duodenal ulcers (n = 52) after 6 weeks of treatment were 94.2 and 96.2%, respectively. The endoscopic S2-stage shift rates in gastric and duodenal ulcers were 45.5 and 65.4%, respectively. Factors affecting healing rates of gastric ulcers included colonization by Helicobacter pylori, the size and depth of the ulcers, pretreatment stage, and ulcer history, whereas those factors did not influence healing in duodenal ulcers. The clearance rates of H. pylori after lansoprazole treatment were 54.5% in patients with gastric ulcer and 66.7% in those with duodenal ulcer. The cumulative relapse rates after 1 year with standard maintenance therapy of H2-receptor antagonists (ranitidine, famotidine, and cimetidine) were 15.8% for gastric ulcer and 21.2% for duodenal ulcer. In conclusion, lansoprazole is highly effective in peptic ulcer disease and there are few relapses after treatment. Furthermore, it is suggested that lansoprazole is efficacious against H. pylori at usual clinical doses.
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PMID:Effect of lansoprazole on peptic ulcers. 759 50

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

Helicobacter pylori is probably the commonest bacterial infection worldwide and is now accepted as the cause of chronic active type B gastritis. It is increasingly accepted as having a critical role in duodenal ulcer, where the prevalence of infection is 90 to 100%. More important is the dramatic reduction in duodenal ulcer recurrence after successful eradication of the organism to about 4% in a year compared to recurrences of up to 80% in those whose ulcers have been healed but in whom the infection persists. There is increasing evidence that what is now clear for duodenal ulcers may also hold true for patients with a gastric ulcer who are infected with H. pylori. Moreover, evidence is accumulating that the risk of a duodenal ulcer complication, such as, bleeding, is reduced following successful eradication of H. pylori. The treatment of duodenal ulcer patients with H. pylori eradication treatment has been advocated by an international working party who met first in Sydney at the 1990 World Congress and subsequently in Athens during the First European Gastroenterology Week. The most recent recommendation suggests that the infection should be treated in any duodenal ulcer patient after the first recurrence, and that a triple therapy regimen or a proton pump inhibitor combined with either amoxicillin or clarithromycin may be prescribed. The combination of a proton pump inhibitor and an antibiotic can eradicate H. pylori in over 80% of cases and simultaneously offers the advantage of rapid symptom relief and the highest rates of duodenal ulcer healing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The current role of Helicobacter pylori eradication in clinical practice. 777 4

Gastric acid is of central importance in the pathogenesis of duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease. Pharmacological reduction of acid secretion is, therefore, the mainstay of current treatment, but the optimal degree of acid suppression remains incompletely understood. This paper considers the ideal ways of assessing and reporting the pharmacological effectiveness of acid-inhibiting drugs and relating such data to clinical efficacy. Twenty-four-hour intragastric pH measurements are widely used for this purpose, although this technique cannot measure secretion quantitatively. Data on suppression of 24-hr intragastric acidity for groups of subjects have been successfully correlated with healing rates for duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease. Three primary determinants of healing have been derived from antisecretory data. These are the degree of suppression of acidity, the duration of suppression of acidity, and the duration of treatment. The order of importance of these determinants varies depending on the disease. Data on 24-hr intragastric acidity should be accompanied whenever possible by data on 24-hr plasma gastrin levels, as the relationship between suppression of acidity and a rise in gastrin varies widely between individuals. It is not possible to predict the plasma gastrin level from the intragastric pH or any other measurement of intragastric acidity. Comparative data sets in groups of subjects may provide useful information. Proton pump inhibitors produce a greater and longer-lasting degree of suppression of acidity than conventional doses of H2-receptor antagonists. For this reason, they are more effective in healing duodenal ulcer and gastric ulcer. However, in view of the importance of duration of treatment, healing rates with the H2-receptor antagonists approach those obtained with proton pump inhibitors if treatment is continued for a longer time. In gastroesophageal reflux disease in particular, although the optimal degree of acid suppression is not yet defined, the consistently superior performance of proton pump inhibitors demonstrates that increased suppression of acidity is clinically beneficial.
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PMID:Optimizing acid suppression for treatment of acid-related diseases. 785 82

It is now generally accepted that infection with Helicobacter pylori is the most common cause of active chronic gastritis and duodenal ulceration. Although H. pylori is detected in the majority of patients with gastric ulcer, its pathogenicity and role in gastric ulceration remains unclear. One method to study this relationship is to eradicate H. pylori and observe the recurrence of gastric ulcer. In the present paper we examined the consequence of H. pylori eradication by antibiotics mono therapy with histamine H2 receptor antagonist on the recurrence of gastric ulcer. Two cases treated with proton pump inhibitor plus clarithromycin were reported. It is concluded that eradication of H. pylori infection may diminish the recurrence of gastric ulcers.
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PMID:[The role of eradication of Helicobacter pylori in healing and recurrence of gastric ulcer]. 790 21


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