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At least 19 recordsLinked to original sources
PubMed1995

[Refractory peptic ulcer: the pathogenic mechanisms].

The vast majority of peptic ulcers heal after treatment with either H2 receptor antagonists or omeprazole at standard doses. However, it is also recognized that a 5-10% of peptic ulcers will not heal. The possibility of identifying the factors associated with refractory ulcers would have important repercussions. Several retrospective and prospective studies have pointed out a number of clinical, environmental or intrinsic factors. In recent years 2 factors have emerged as the main cause of peptic ulcer. Helicobacter pylori infection and NSAID use, and these two factors might be involved in the pathogenesis of refractory ulcer.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

A high frequency of detection of Helicobacter pylori in whitish exudate of gastric ulcer.

Helicobacter pylori has been implicated in the pathogenesis of chronic gastritis and peptic ulcer. However, no report to date has been made on the presence of H. pylori in the whitish exudate of peptic ulcers. We examined the biopsy specimens of 52 patients (42 men and 10 women, aged 29-78, not taking steroids or nonsteroid antiinflammatory drugs), and evaluated the frequency of detecting the organism in the whitish exudate of gastric ulcers in comparison with that in the ulcer border, gastric fundic gland, and pyloric gland using microaerobic culture and acridine-orange stain. H. pylori was detected in high rates: 38 (73%) of 52 cases by culture, and 50 cases (96%) by staining of the whitish exudate, 42 (81%) of 52 cases by culture, and 46 cases (88%) by staining of the ulcer border. The frequency for the other regions were 81% by culture and 90% by staining of the fundic gland, and 81 and 90% of the pyloric gland, respectively. Of all sites studied by the staining method, H. pylori was detected at the highest frequency in the whitish exudate. The fact that many H. pylori live in the whitish exudate of gastric ulcer, suggests a causal relationship between H. pylori and gastric ulcer.

Acridine Orange↗
PubMed1995

Peptic ulcer therapy with lansoprazole and Helicobacter pylori eradication.

This study investigated the relationship between the clearance of Helicobacter pylori and the healing rate of ulcers after treatment with lansoprazole. Lansoprazole 30 mg/day was administered to 124 gastric ulcer (GU) patients and 57 duodenal ulcer (DU) patients. The healing rates were 89.6% in GU and 96.5% in DU. The rate of shift to the S2 stage of healing was 33.1% in GU and 38.6% in DU. The H. pylori-positive rate was 69.7% in GU and 74.5% in DU. H. pylori clearance rates after lansoprazole treatment were 43.4% in GU and 51.2% in DU. In GU, the ulcer healing rate in the H. pylori-positive to -negative group was significantly higher than that in the group that remained H. pylori-positive, but there were no significant differences in the rate of shift to the S2 stage of ulcer healing. In DU, there were no significant differences in either the healing rates or the rates of shift to the S2 stage of ulcer healing. This suggests that the clearance of H. pylori results in a high healing rate in GU.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1995

No Helicobacter pylori, no Helicobacter pylori-associated peptic ulcer disease.

Virtually all duodenal ulcers (DUs) and the vast majority of gastric ulcers (GUs) are the consequence of Helicobacter pylori-associated inflammation. In DUs, the inflammation is maximal in the antrum and is associated with gastric metaplasia in the bulb. Gastrin homeostasis is disturbed by H. pylori gastritis and there is robust acid secretion. Successful eradication of the infection cures the ulcer diathesis. Amalgamated figures for ulcer relapse per year in H. pylori-positive DUs are > 60% compared with 2.6% for H. pylori-negative DU patients. The corresponding figures for GU are > 50% for H. pylori-positive and 2.0% for H. pylori-negative individuals. This striking difference in relapse rate persists, as the re-infection rate in the developed world is < 1% per year. Recurrent bleeding in bleeding-prone DUs is essentially abolished after cure of the infection. Proton pump inhibitors (PPIs) are increasingly used in eradication regimens. PPIs have intrinsic antimicrobial activity. MICs for lansoprazole (LAN) are lower than for omeprazole (OME). Two weeks of triple therapy (bismuth, tetracycline, imidazole) has, on average, a superior eradication efficacy (> or = 90%) compared with dual therapy (PPI, amoxycillin or clarithromycin) (> or = 80%). When a combination of PPI and two antibiotics has been used, results comparable to triple therapy have been reported. However, the side-effects profile and patient acceptability of PPI plus one or two antibiotic regimens are better than for traditional triple therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Bacterial Agents↗
PubMed1991

Helicobacter pylori, causation, change in natural history, and why Helicobacter-positive duodenal ulcers should not be routinely treated.

The relationship between Helicobacter pylori and duodenal ulcer is reviewed with regard to the following epidemiologic issues: causation, change in natural history, and whether there is sufficient evidence to treat H. pylori-positive peptic ulcers routinely. There is mounting evidence for a pivotal role of H. pylori as a precipitating cause of duodenal ulcers. There is insufficient data to conclude that eradication of H. pylori alone will cure peptic ulcer disease--that is, preventing instead of controlling relapse. H. pylori-positive duodenal ulcers should not be routinely treated because eradication rates need to be improved, metronidazole resistance is an increasing problem, and side-effects of currently used triple combination treatments are substantial.

Duodenal Ulcer↗
PubMedDate not supplied

Helicobacter pylori in experimental acute and chronic gastric and duodenal ulcer in Buffalo [correction of Bufallo] rats.

The experiment was performed using inbred Buffalo rats to confirm the coincidence between peptic, gastric and duodenal ulcer and Helicobacter pylori infection. The results suggest an unquestionable meaning of Helicobacter pylori appeared to be as strong ulcerogenic factor in rats as ligation of pylorus and diffusely administrated histamine.

Acute Disease↗