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)

Helicobacter (Campylobacter) pylori has been cultured from the antral biopsies of 85-90% of patients of gastritis, gastric ulcer and duodenal ulcer at different centres. Studies conducted all over the world have firmly implicated this organism in the aetiology of active superficial gastritis and recurrences of duodenal ulcer. Two hundred patients with upper abdominal pain, distension, vomiting and/or haemetemesis were subjected to OGD scopy. In 163 of these patients there was endoscopic evidence of gastritis; in 24 there was DU; in 3, GU and in 10 it was normal. Diagnosis of H pylori infection was made by the rapid biopsy urease test which is nearly 100% specific and 98% sensitive. 170 out of 200 patients were positive for H pylori. Among these were 138 patients of gastritis (84.6%); 22 cases of DU (91.6%); 2 cases of GU (66.6%) and 8 in whom endoscopy was normal. Histological examination of the antral biopsy specimens showed mild to severe infiltration of mucosa with lymphocytes and plasma cells. None of the 170 H pylori positive cases showed polymorphonuclear infiltration which has been stressed repeatedly by most Western authors to be characteristic of "active" superficial gastritis associated with H pylori infection. Even in those with a history of dyspepsia of barely 4 weeks duration or less there was no PMN infiltration in the mucosa. Thus the local response to infection by H pylori of the gastric mucosa is different in Indian patients.
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PMID:Unusual features of Helicobacter (Campylobacter) pylori--associated gastritis in India. A study of 200 cases. 209 22

The effect on the recurrence of gastric ulcers after suppression of Helicobacter pylori by combined treatment with cimetidine and the antimicrobial drug cefixime was investigated. Twenty one of 43 patients with endoscopically proved gastric ulcer and H pylori infection were randomly assigned to receive cimetidine 800 mg daily for 12 weeks; the remaining 22 patients received cimetidine 800 mg daily for 12 weeks plus cefixime 100 mg daily for the last two weeks. After treatment, 88% of 17 patients on cimetidine only remained H pylori positive, whereas combined administration of cimetidine and cefixime had suppressed H pylori in 78% of 18 patients (p less than 0.05). Seventeen patients in the former group whose ulcers healed but who remained H pylori positive and 18 patients in the latter group whose ulcers healed and who were no longer infected with H pylori continued to be followed after treatment. These patients underwent endoscopy to detect ulcer recurrence if symptomatic, or at 12 and 24 weeks if asymptomatic. At 12 weeks, recurrence was observed in seven of 15 (47%) patients in whom H pylori persisted, but in only one of 14 (7%) patients in whom H pylori had been suppressed (p less than 0.05). At 24 weeks, however, recurrence rates were similar between the two groups. These findings indicate that H pylori infection may be closely related to early ulcer recurrence.
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PMID:Reduction of gastric ulcer recurrence after suppression of Helicobacter pylori by cefixime. 221 Apr 64

Triple therapy has been recommended as the most effective treatment for Helicobacter pylori eradication. Despite achieving a comparatively high eradication result, however, around 10% of patients still fail to be cured. Omeprazole can enhance efficacy of single and double antibiotic protocols and is particularly effective when combined with clarithromycin and a nitroimidazole. This study examined the effect of combining triple therapy with omeprazole. A prospective, randomised, unblinded, single centre trial was carried out on consecutive patients with symptoms of dyspepsia and H pylori infection confirmed by rapid urease test, microbiological culture, and histological assessment. Patients were given a five times/day, 12 day course of colloidal bismuth subcitrate chewable tablets (108 mg), tetracycline HCl (250 mg), and metronidazole (200 mg) with either 20 mg omeprazole twice daily (triple therapy+omeprazole) or 40 mg famotidine (triple therapy+famotidine) at night. Compliance and side effects were determined using a standard questionnaire form. One hundred and twenty five of 165 triple therapy+omeprazole patients and 124 of 171 triple therapy+famotidine patients returned for rebiopsy four weeks after completion of treatment. Significantly more triple therapy+omeprazole patients achieved eradication 122 of 125 (97.6%) as assessed by negative urease test, culture, and histological assessment, when compared with 110 of 124 (89%) triple therapy+famotidine patients (p = 0.006; chi 2). There were 30 triple therapy+omeprazole (24%) and 26 triple therapy+famotidine (21%) patients with de novo metronidazole resistant H pylori included in the study. Side effects were mild and infrequent and were comparable in both groups, although pain in duodenal ulcer, gastric ulcer, and oesophagitis patients seemed to subside earlier in those taking omeprazole. Compliance (>95% of drugs taken) was achieved by 98% of patients of both groups. A 12 days regimen of triple therapy with omeprazole is more effective in achieving H pylori eradication than is triple therapy plus famotidine. Use of 20 mg omeprazole twice daily rather than 40 mg famotidine with a 12 day, low dose triple therapy enhances eradication to over 97% whether the H pylori is metronidazole sensitive or resistant.
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PMID:Omeprazole enhances efficacy of triple therapy in eradicating Helicobacter pylori. 748 31

Lymphoid follicles are a common feature of Helicobacter pylori-associated gastritis. Recently, by using gastric mapping, we demonstrated lymphoid follicles in all of 62 patients with H pylori infection. This study was designed to address (1) the prevalence of lymphoid follicles in routine gastric biopsy specimens, (2) their correlation with chronic active gastritis, and (3) their predictive value with respect to H pylori infection. Slides from 174 patients whose gastric biopsy findings carried a nonneoplastic diagnosis were evaluated for the presence of (1) chronic active gastritis, (2) lymphoid follicles, and (3) H pylori. When either follicles or active gastritis was found, but H pylori could not be identified by the hematoxylin-eosin stain, additional slides were prepared with a newly developed silver-hematoxylin-eosin-alcian blue stain. Active gastritis was present in 153 patients (88%). Helicobacter pylori was identified on hematoxylin-eosin-stained slides in 123 patients and by the modified Steiner stain in 11 additional patients. Thus, 87% of the patients with chronic active gastritis had histologically detectable H pylori infection. One or more lymphoid aggregates were present in 110 patients (82% of patients with H pylori and 72% of those with chronic active gastritis). Of these, 101 (92%) had H pylori infection. In six of the nine H pylori-negative patients with lymphoid aggregates, biopsy specimens were taken from the edges of an ulcer. In summary, except when biopsy specimens are obtained from the immediate vicinity of a gastric ulcer, lymphoid aggregates in a gastric biopsy specimen are virtually always associated with chronic active gastritis and provide a useful marker for H pylori infection.
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PMID:The significance of lymphoid follicles in the interpretation of gastric biopsy specimens. 751 59

This study examines the relationship between Helicobacter pylori infection and peptic ulcer disease and gastric cancer--in particular, the presence or absence of bacteria, the grading of gastritis, and the degree of inflammation in the antral and oxyntic mucosae. The grading of gastritis and the detection of H pylori were determined by histology using the Sydney system. Of the 1006 patients examined, 34.5% had duodenal ulcer disease, 3.5% gastric ulcer disease, and 2% with coexistent ulceration. Most patients (50.2%) were classified as having non-ulcer dyspepsia. Altogether 2.4% of patients had gastric cancer and two further patients had carcinoma in the gastric stump. Of the ulcer disease patients, 87.2% had histological evidence of H pylori infection. After patients who had taken antibiotics or bismuth compounds in the preceding four weeks were excluded, 98.9% of the duodenal ulcer disease, 100% of the gastric ulcer disease, and 100% of the coexistent ulcer disease patients had evidence of H pylori infection. In patients with gastric cancer who had not taken antimicrobial agents in the four weeks before endoscopy, 83.3% had evidence of H pylori infection. Thus, there was a high rate of duodenal ulcer disease and a low rate of gastric ulcer disease in southern China, an area of low gastric cancer mortality. There was a specific topographical relationship between H pylori, the histological response, and gastroduodenal disease. Our data suggest that the status of a nation as either 'developed' or 'developing' can not be used to predict the upper gastrointestinal disease profile of its population.
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PMID:Helicobacter pylori associated with a high prevalence of duodenal ulcer disease and a low prevalence of gastric cancer in a developing nation. 788 17

Medical therapy for duodenal or gastric ulcer disease has traditionally involved gastric acid antisecretory therapy for 4 to 8 weeks to promote initial healing and indefinitely to prevent recurrences of ulcer. The discovery of Helicobacter pylori in most patients with peptic ulcer disease has led to a change in this approach. Therapy designed to eradicate H pylori may facilitate ulcer healing with acid antisecretory agents and, more important, may greatly reduce the incidence of ulcer recurrence, obviating the need for maintenance antisecretory therapy. Regimens designed to eradicate H pylori are difficult to comply with, however, and are associated with adverse effects in some patients. In this article we review the diagnosis and treatment of H pylori infection in patients with peptic ulcer disease and make recommendations regarding the use of conventional ulcer therapies and therapies designed to eradicate H pylori.
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PMID:Helicobacter pylori and peptic ulcer disease. 827 73

Helicobacter pylori (H pylori) eradication heals chronic active type B gastritis and dramatically changes the natural history of duodenal ulcer disease. There are few data concerning the role of anti-H pylori treatment in gastric ulcer disease. A total of 83 patients presenting with H pylori positive active gastric ulcer disease were treated with omeprazole and antibiotics (amoxicillin, ciprofloxacin, roxithromycin) in seven different clinical protocols, each of which included the attempt to eradicate H pylori infection and to evaluate the post-therapeutic course of ulcer disease. The overall proportion of H pylori eradication was 67.9% (53 of 78 patients available for follow up). Best results were obtained with two week treatment regimens comprising omeprazole 20 mg twice daily and amoxicillin 500 mg four times a day or 1000 mg twice daily (eradication > 80%). Eradication of H pylori speeds up ulcer healing, with a six week healing rate of 84.9% compared with 60% in patients with persistent H pylori infection (p = 0.0148). In a subgroup of 11 patients with refractory ulcers, H pylori eradication (n = 10) was associated with ulcer healing on continued acid suppression in nine cases. One male patient with chronic antral ulcer did not respond to treatment within the next six months (H pylori and ulcer persistence), and in one female patient a resistant body ulcer was identified as gastric lymphoma. Fifty patients with healed ulcers were followed up for one year. Patients with (n = 32) and without (n = 18) bacterial eradication had similar demographic and clinical characteristics. H pylori eradication was associated with a statistically significant reduction of ulcer recurrences (3.1 v 55.6%, p<0.001). This study concludes that H pylori eradication considerably changes the natural history of H pylori associated gastric ulcer disease. In addition, H pylori eradication speeds up ulcers healing and is associated with healing of previously refractory ulcers. Thus, treatment aimed at bacterial eradication should be considered in all patients with gastric ulcers severe enough to contemplate further treatment options.
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PMID:Evidence for the essential role of Helicobacter pylori in gastric ulcer disease. 830 43

The hypothesis that non-secretors of ABO blood group antigens, a group shown to be more susceptible to certain bacterial infections, may be at greater risk of gastroduodenal disease because of increased susceptibility to Helicobacter pylori infection was investigated. Of 101 patients with symptoms of dyspepsia who were undergoing endoscopy, 32% were non-secretors (determined from Lewis blood group phenotype), 36% had endoscopically visible gastroduodenal disease (antral gastritis, gastric ulcer, erosive duodenitis, duodenal ulcer or some combination), and 58% had H pylori detected in antral biopsy specimens. Non-secretors and patients with H pylori infection were significantly more likely to have gastroduodenal disease (p = 0.02 and p = 0.002 respectively). There was, however, no significant association between secretor status and H pylori infection, logistic regression analysis confirming that these were independently associated with gastroduodenal disease. Overall, the relative risk of gastroduodenal disease for non-secretors compared with secretors was 1.9 (95% confidence intervals 1.2, 3.2). Non-secretion of ABO blood group antigens is not related to H pylori infection but is independently and significantly associated with endoscopic gastroduodenal disease. The mechanism of this remains to be explained.
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PMID:Secretor status and Helicobacter pylori infection are independent risk factors for gastroduodenal disease. 847 82

To determine the prevalence and distribution of gastric lymphoid follicles in patients with Helicobacter pylori infection, to evaluate their relationship with gastroduodenal pathology, and to assess their evolution after eradication of H pylori, mapped gastric biopsy specimens were obtained from 20 H pylori-negative normal volunteers, 25 asymptomatic volunteers with H pylori infection and no ulcer disease, 21 duodenal ulcer patients, and 16 patients with gastric ulcer. Nine infected subjects were treated by triple therapy, and biopsy specimens were obtained at 1, 4, and 12 months posttreatment. Lymphoid follicles were counted and other histologic features were scored semiquantitatively. None of the noninfected subjects had lymphoid follicles. All subjects with H pylori had follicles, which were more numerous in the antrum than in the corpus (P < .001) and on the lesser rather than on the greater curvature (P = .003). Ulcer patients had greater numbers of follicles than asymptomatic infected volunteers (P < .05). There was no relationship between number or distribution of follicles and patients' age, sex, or other mucosal inflammatory responses (except for numbers of lymphocytes: r = .785, P < .001), intensity of H pylori infection, or intestinal metaplasia. Eradication of H pylori resulted in a slow decrease (but not in the disappearance) of lymphoid follicles in all patients. Our results indicate that the careful examination of multiple specimens will reveal lymphoid follicles in the gastric mucosa of all patients with H pylori infection. The normal stomach does not contain mucosa-associated lymphoid tissue, and this study supports the concept that H pylori may be a precursor in the development of primary gastric lymphomas.
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PMID:Gastric lymphoid follicles in Helicobacter pylori infection: frequency, distribution, and response to triple therapy. 801 55

To study the association of Helicobacter pylori with peptic ulcer and the associated histopathological changes, to characterize the isolated strains in terms of their protein profile, 83 peptic ulcer cases were studied. A high association of H pylori with peptic ulcer (duodenal ulcer 77%, gastric ulcer 75%) and gastritis (74%) was observed. Age and smoking did not have any relationship with H pylori infection. The infection was predominantly associated with the 'quiescent' form of chronic gastritis. Comparative sodium dodecyl sulfate polyacrylamide gel electrophoresis of whole cell extracts of the local isolates and a reference strain from Australia showed a general homogeneity between the strains with obvious interstrain differences. However, the difference between the local isolates and the reference strain was more marked. Significant association of H. pylori with peptic ulcer along with strain variations were observed.
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PMID:Isolation and characterization of Helicobacter pylori strains from peptic ulcer patients in Dhaka, Bangladesh. 886 53


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