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)

Drug damage to the stomach provides a model for study of the development of peptic ulcer, gastritis, and duodenitis in man. Aspirin damage is the best understood. Pathophysiologically, aspirin alters the gastric mucosal barrier to hydrogen ions and lowers gastric potential difference. Ultrastructurally, aspirin damage to surface epithelial cells leads to microerosions. Macroscopically, acute hemorrhage and erosions are seen in both the stomach and duodenum by endoscopy after ingestion of a large dose of aspirin. Patients with chronic rheumatic diseases taking aspirin have a 50% incidence of gastric erosions and 20% incidence of gastric ulcer, suggesting an association between erosions and chronic ulcer formation. Acute gastric damage is lessened by neutralizing acid with bicarbonate, reducing acid secretion with cimetidine, or administering aspirin in enteric-coated form. Rheumatic patients on enteric-coated aspirin have a significantly lower incidence of gastric ulcer (5%) than those taking regular aspirin. Damage may also be prevented by increasing mucosal resistance; acute damage can be prevented by exogenous prostaglandins, regardless of their effect on acid secretion (cytoprotection). Other commonly used drugs, such as alcohol, acetaminophen, and indomethacin, reported to have paradoxical effects with respect to erosions and peptic ulcer, provide additional information on the development of gastric erosions and ulcers.
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PMID:Drugs, gastritis, and peptic ulcer. 732 Apr 67

The prevalence of Helicobacter pylori infection was studied in 152 subjects with a normal upper gastrointestinal endoscopy, 125 with duodenal ulcer, 25 with gastric ulcer, 46 with erosive gastritis and 9 with erosive duodenitis. Two biopsies from duodenum, antrum and fundus were obtained from each subject during endoscopy for histological diagnosis and Helicobacter pylori search. None of the patients with normal endoscopy and 2% of patients with duodenal ulcers had Helicobacter pylori in duodenal biopsies. These last patients had a significantly higher frequency of Helicobacter pylori in the antrum (71%) than the rest of the studied groups. Five percent of subjects with normal endoscopy and 5% of those with duodenal ulcers had Helicobacter pylori in the antrum. An active gastritis was demonstrated in almost all patients with Helicobacter infection. Intestinal metaplasia occurred almost exclusively in the absence of Helicobacter pylori infection.
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PMID:[Presence of Helicobacter pylori in the duodenum, antrum, and fundus in control subjects and patients with duodenal ulcer, gastric ulcer, gastritis, or erosive duodenitis. Histological analysis of 357 subjects]. 756 57

We here ascertain whether tryptase (a serine endoprotease released by mast cells) and cathepsin D (CD, a lysosomal hydrolase that seems able to derange the extracellular matrix) play a part in peptic ulcer disease and whether they are linked to Helicobacter pylori (Hp) infection. We studied 13 controls, 25 patients with gastric ulcer, 47 with duodenal ulcer, and 11 with duodenitis. Tryptase and CD were measured in mucosal biopsies (body and antrum of the stomach and duodenum) using IRMA methods. Hp infection was histologically evaluated (Giemsa). Tryptase and CD levels were higher (25%) in patients with active peptic ulcer, whether gastric or duodenal. In Hp-positive patients the CD mucosal content was higher while tryptase mucosal levels were lower than in Hp-negative patients. Tryptase was correlated with gastrin content. CD seems to be mainly related to the phlogistic reaction of the mucosa to Hp infection; tryptase may reflect an indirect link between Hp infection, gastrin release, and the function of mast cells.
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PMID:Influence of Helicobacter pylori on tryptase and cathepsin D in peptic ulcer. 758 35

A cytotoxin produced by some Helicobacter pylori strains has recently been identified. The cytotoxin induces intracellular vacuolization of cultured cells. The aim of the present study was to examine the frequency of occurrence of cytotoxin-producing strains of H. pylori from subjects with upper gastrointestinal disease including nonulcer dyspepsia, gastric and duodenal ulcer disease, gastroesophageal reflux disease, and gastric cancer. Broth culture filtrates of clinical isolates of H. pylori recovered from 175 patients were used to inoculate Vero and HeLa cell monolayers for the detection of vacuolating cytotoxin activity. The results obtained demonstrated that the highest percentage of strains producing cytotoxin were found in subjects with peptic ulcer disease (gastric ulcer, 65%; duodenal ulcer, 66%; P < 0.01 compared with nonulcer dyspepsia, 38%). Of the 11 patients with gastroesophageal reflux disease, 4 of 5 patients in this group who had esophageal ulcers, were found to be infected with strains that produced cytotoxin. Three of the four patients with carcinoma of the stomach were also found to be infected with cytotoxic strains of H. pylori. With increasing severity of mucosal damage in subjects with a normal upper gastrointestinal tract, macroscopic gastritis, duodenitis, and peptic ulceration, there were corresponding increase in the proportion of strains producing cytotoxin; these increases were 32, 46, 50, and 66%, respectively. H. pylori strains from subjects with ulcer disease commonly produced vacuolating cytotoxin, suggesting that it may be a virulence factor in the pathogenesis of peptic ulcer disease.
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PMID:Cytotoxin production by Helicobacter pylori from patients with upper gastrointestinal tract diseases. 761 29

(A light- and electronmicroscopic study). We have examined the occurrence of Helicobacter pylori (HP) in 2937 gastric antral biopsy specimens from 979 patients with upper gastrointestinal symptoms. The incidence of HP proved to be 50.5%. The endoscopic diagnoses were: gastritis (62 cases), gastric erosion (425), gastric ulcer (51), duodenitis (22), duodenal erosion (119), duodenal ulcer (122) and the HP incidence was 29, 46, 63,, 50, 66 and 73%, respectively. Microscopic findings were: chronic gastritis (442), chronic active gastritis (356) and normal mucosa (181). The prevalence of HP in these groups was 43%, 78% and 11%, respectively. The activity of gastritis was in good correlation with HP infection. We did not see epithelial damage, and found only a few instances of mucus depletion. Electronmicroscopic examination was performed in order to investigate the morphology of bacterium and its relation to the mucosal cells. We observed mild loss of microvilli on the cell surface and did not see any cell invasion by bacteria.
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PMID:[Helicobacter pylori in benign gastroduodenal diseases]. 767 39

Biopsy samples obtained by endoscopy to diagnose infection by H. pylori usually come from the antral region. Nevertheless, there are few reports documenting the prevalence of infection at duodenal level. OBJECTIVE. To investigate the prevalence of H. pylori infection in duodenal bulb in different endoscopic diagnosis. METHODS. 331 patients with the following endoscopic diagnosis were studied: normal appearance (n = 55), gastritis (87), gastric ulcer (49), duodenal ulcer (120), and duodenitis (20). At endoscopy, different samples from duodenal bulb were obtained (apart from gastric fundus, body and antrum), which were processed for microbiology (Gram stain and culture) and histology (hematoxilin-eosin). RESULTS. Patients with duodenal ulcer or duodenitis had the highest H. pylori infection rate at duodenal bulb (47.7% and 65%, respectively). Differences were significant when compared with normal appearance (14.5%; p < 0.001) and gastritis (25%; p < 0.05). In all patients with H. pylori at duodenal bulb this organism was also detected at antral region. CONCLUSIONS. 1) The highest prevalence rates for H. pylori infection in duodenal bulb were found in patients with duodenal ulcer or duodenitis. 2) Diagnosis of H. pylori infection should not be based on the duodenal bulb samples alone, as this sample yields high false-negative results.
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PMID:[H. pylori infection at the duodenal bulb in different endoscopic diagnoses]. 778 55

We studied the prevalence of Helicobacter pylori in Sudanese subjects with gastroduodenal inflammation. H. pylori was looked for in biopsy specimens taken from the antrum by two methods: rapid urease test [Campylobacter-like organism (CLO) test] and culture using Skirrow's selective supplement. One hundred subjects were studied. H. pylori was found in 80% of patients with gastritis, 56% of patients with duodenal ulcer, 60% of patients with duodenitis and 16% of normal control subjects. It was neither detected in patients with gastric ulcer, nor in patients with oesophagitis or in those with oesophageal varices due to schistosomiasis, when using culture. However, it was found in 50% of patients with oesophagitis, when using CLO test.
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PMID:Detection of Helicobacter pylori in endoscopic biopsies in Sudan. 780 58

In a prospective study 27 patients (13 women, 14 men; mean age 62 [45-83] years) with Helicobacter (H.) pylori associated disease received over 7 days pantoprazole (40 mg twice daily), clarithromycin (500 mg twice daily) and metronidazole (500 mg twice daily). Six patients had gastric ulcer, 4 duodenal ulcer, 4 erosive gastritis, 6 erosive duodenitis and 7 had H. pylori-positive functional dyspepsia. Pre-treatment oesophago-gastro-duodenoscopy was combined in 4 patients with antral and in 4 others with body-of-stomach biopsies to demonstrate H, pylori (urease test, specific culture and histology). The H. pylori status was checked with the 13C-urea breath test 4 weeks after the end of treatment. In addition, 9 patients with peptic ulcer were examined endoscopically at least 2 weeks after onset of the treatment to check for any healing of the ulcers, 25 of the patients completed the study according to the protocol. The H. pylori eradication rate was 100% (25 of 25 patients), while the "intention to treat" analysis gave a rate of 92.6% (25 of the 27 patients). The peptic ulcers were found to be healed in all 9 patients who had been endoscoped. One woman developed a reversible stomatitis, but the drug treatment did not have to be stopped. -These findings indicate that short-term triple treatment in the described manner is efficacious in curing H. pylori infection and any peptic ulcer. It is thus a highly promising treatment of H. pylori-associated diseases.
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PMID:[Short-term triple therapy with pantoprazole, clarithromycin and metronidazole for the healing of Helicobacter pylori infection]. 788 16

Quality of Life was investigated in patients with suspected duodenal ulcer. In self-administrated questionnaires general well-being was evaluated with the Psychological General Well-Being Index (PGWB). Patients were required to fill out the questionnaires before endoscopy. This was done by 1526 patients who, after endoscopy, were divided into five groups; esophagitis (192), gastric ulcer (109), duodenal ulcer (426), duodenitis/gastritis (296) and negative endoscopy (401). Another 70 patients were found to have other diagnoses. Endoscopy was not performed in 32 patients who filled out questionnaires. All five patient groups reported low general well-being with the PGWB index. No statistical significant differences could be seen between the different groups. This study shows that patients complaining of gastrointestinal symptoms have a low degree of general well-being. Among patients with symptoms suspected for duodenal ulcer other diagnoses were common.
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PMID:Assessment of Quality of Life among patients with suspected duodenal ulcer. 817 Dec 97

The pathogenesis of peptic ulcer is a complex phenomenon and several factors are thought to be involved in this process. Among others, Helicobacter pylori infection, hypergastrinaemia and some proteases seem to play an essential role in inducing peptic ulceration. We investigated whether tryptase (a serine endoprotease released by mast cells) and cathepsin D (a lysosomal hydrolase which seems able to derange the extracellular matrix) play a part in peptic ulcer disease and whether they are linked to Helicobacter pylori infection and mucosal content of gastrin. We studied 13 controls, 25 patients with gastric ulcer, 47 with duodenal ulcer and 11 with duodenitis. Tryptase and cathepsin D were measured in mucosal biopsy specimens (body and antrum of the stomach and duodenum) using IRMA methods. Gastrin was assayed in the antral mucosa by means of a RIA method. Helicobacter pylori infection was histologically evaluated (Giemsa). Tryptase and cathepsin D levels were higher (25%) in patients with active peptic ulcer, whether gastric or duodenal. The mucosal content of cathepsin D, but not that of tryptase, was associated with Helicobacter pylori infection. Tryptase, on the other hand, was related to gastrin content. No correlation was found between the two enzymes. It is concluded that tryptase and cathepsin D probably reflect different pathophysiological modifications in ulcer disease. Cathepsin D seems to be mainly related to the phlogistic reaction of the mucosa to Helicobacter pylori infection; tryptase may reflect and indirect link between the action of gastrin and the function of mast cells.
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PMID:Are tryptase and cathepsin D related to Helicobacter pylori infection and mucosal gastrin in peptic ulcer? 820 35


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