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 pylori infection is usually acquired during childhood, and evidence-based guidelines regarding diagnosis and treatment of infected children have been recently published. Diseases associated with H. pylori infection are gastritis, duodenal ulcers, mucosal-associated lymphoid-type (MALT) lymphoma, and gastric adenocarcinoma. The association of specific symptoms with H. pylori infection in children and adults (ie, recurrent abdominal pain and nonulcer dyspepsia) remains controversial. Additionally, the role of H. pylori in gastroesophageal reflux disease or in extra-gastrointestinal diseases (ie, coronary artery disease) lacks sufficient evidence to demonstrate causality. The diagnosis of H. pylori-associated diseases in children can reliably be made through gastroduodenal endoscopy with biopsies. Clinical trials are underway for the validation of noninvasive diagnostic tests for the H. pylori-infected child, and current guidelines recommend eradication therapy for infected children with duodenal and gastric ulcer, gastric lymphoma, and atrophic gastritis with intestinal metaplasia. The natural history of childhood H. pylori infection is poorly described. Moreover, rational approaches to the prevention and control of childhood H. pylori infection are critically needed, requiring characterization of the determinants for acquisition and persistence and the disease outcomes following eradication.
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PMID:New approaches to Helicobacter pylori infection in children. 1135 61

The discovery of Helicobacter pylori (H. pylori) has revolutionised the pathophysiological and clinical approach to gastric and duodenal ulcer. Since the first paper identifying H. pylori was published only 19-20 years ago, it has been found out that this bacterium causes probably the commonest human infection. Like other revolutions in history, the original directions of the H. pylori story have changed in response to conflicting ideologies, observation, and practices. It is known that once H. pylori is acquired, colonisation continues for life unless the organism is eliminated by antimicrobial treatment or by the usually late-in-life development of the atrophic gastritis. If any recent achievement in the world of medicine is to be called revolutionary, then it is the discovery of the role of this spiral bacterium in the etiopathogenesis of gastritis, gastric ulcer, duodenal ulcer, gastric adenocarcinomas and gastric mucosa-associated lymphoid type (MALT) B-cell lymphomas. Essentially everyone who carries the organism in the gastric mucous layer has evidence of tissue reaction (termed chronic active gastritis), but most colonised persons remain asymptomatic for life. In the absence of treatment, the presence of H. pylori can be determined with a high degree of confidence by endoscopy (with culture, histologic examination, or urease testing of gastric biopsy specimens), by serologic testing, or by urea breath tests. After successful treatment, specific antibody levels decrease so slowly that serologic testing cannot be used to document success for at least 6 months. In most patients, elimination of H. pylori changes the natural history of peptic ulcer disease and of gastric MALT lymphomas. It is now recommended that these patients have to be treated to eliminate H. pylori because the benefits seem to substantially outweigh the risks and costs. Currently, enthusiasts, drug companies, and the lay press are putting pressure on physicians to eliminate H. pylori from all patients, symptomatic or not, in whom it is detected. There is little evidence that this is appropriate, and management will continue to change as new knowledge emerges and socioeconomic environments change in ways that are relevant to H. pylori and clinical medicine.
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PMID:[Is the only good Helicobacter a dead Helicobacter?]. 1205 16

BACKGROUND: Helicobacter pylori (HP) infection is very prevalent worldwide, and has been associated with the presence of duodenal ulcer, gastric ulcer and chronic active gastritis. It is also speculated that HP may have a role in gastric cancer development. Triple drug schemes have been shown to be the most effective approach to erradicate HP infection. Nevetheless, high rates of resistance against some antibiotics as well as high costs affect the effectiveness of these therapies. The goal of the present study is to assess the effectiveness of the combination of tetracycline, furazolidone and bismuth in erradicating HP, as well as the changes in the histology.METHODS: Patients with diagnosis of HP infection, found in their antral gastric biopsies (hematoxylin and eosin staining (H-E)), were included. They received the following scheme for 10 days: tetracycline 500 mg qid., furazolidone 100 mg qid., and colloidal bismuth subcitrate 120 mg qid. Patients were instructed to come back for follow-up 6 to 8 weeks after starting the therapy. At that time a control upper endoscopy was performed and 3 antral biopsies were taken. Biopsies were stained with H-E and read by experienced pathologists. In both, the biopsy before treatment and the control biopsy, the following parameters were looked for: presence and density of HP; presence, depth and grade of chronic gastritis (lymphoplasmocytic infiltrate); presence and grade of inflammatory activity (polymorphonuclear inflitrate); presence of glandular atrophy; presence, grade (partial or total) and extent (focal or multifocal) of mucinous damage (epithelial damage); presence of intestinal metaplasia; and presence of lymphoid follicles.RESULTS: Fifty-nine patients (30 men and 29 women) completed per protocol. Mean age was 43 +/- 18 (range: 14-73). HP erradication was achieved in 54 patients (91.5%). Control biopsies showed improvement in the following parameters: presence and density of HP (p<0.001); presence, depth and grade of chronic gastritis (p<0.001); presence and grade of inflammatory activity (p<0.001); presence, grade and extent of mucinous damage (p<0.001); and presence of lymphoid follicles (p<0.001). Neither the presence of glandular atrophy nor the presence of intestinal metaplasia showed any significant change. Patients who did not erradicate HP showed no significant difference in any of the parameters.CONCLUSIONS: The triple drug scheme including tetracycline, furazolidone and bismuth is effective in HP erradication. Erradication of HP is followed by an improvement in the following histologic parameters: presence, depth and grade of chronic gastritis (LMN infiltrate); presence and grade of inflammatory activity (PMN infiltrate); presence, grade and extent of mucinous damage; and presence of lymphoid follicles. This scheme is a cost-effective alternative for the therapy of HP infection in low income populations with a high prevalence of infection with this bacteria.
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PMID:[HELICOBACTER PYLORI INFECTION ERRADICATION IN DISPEPTIC PATIENTS WITH AND WITHOUT PEPTIC ULCER] 1220 4

Gastric Helicobacter pylori (Hp) infection in Mongolian gerbils is an established experimental model of gastric carcinogenesis resulting from the long-term Hp infection but functional aspects accompanying this Hp-induced progression from gastritis to the cancer, especially changes in gastric acid secretion, gastric blood flow (GBF) and gastrin-somatostatin link have been little studied. It is unclear whether Hp eradication therapy alters the functional and the histopathological changes in this animal model of Hp-infection. We examined the effects of intragastric (i.g.) inoculation of Mongolian gerbils with Hp strain (cagA+ vacA+, 5 x 10(6) CFU/ml) that had been isolated from a patient with gastric ulcer as compared to those induced by vehicle (saline) in gerbils with or without gastric fistula (GF) at 1.2, 4, 6, 9, 12 and 30 wks upon gastric inoculation with this bacteria. An attempt was made to evaluate the influence of anti-Hp triple therapy with omeprazole, amoxicillin and tinidazol on gastric Hp-infection and Hp-induced functional impairment of the gastric mucosa. Gastric mucosal biopsy specimens were taken for the assessment of the morphological changes and the presence of Hp infection using rapid urease test (CLO-test) and the density of Hp-colonization were assessed by counting of the number of bacterial colonies per plate. Gastric blood flow (GBF) was measured by H2-gas clearance technique and the venous blood and the gastric content were collected for the measurement of plasma gastrin levels and the gastric luminal somatostatin level by radioimmunoassay (RIA). The Hp in gastric mucosa was detected in all animals by culture and rapid urease test at various periods upon Hp inoculation. Basal gastric acid in non-infected conscious gerbils with GF reached the level of about 28 +/- 4 micromol/h and this was reduced by over 50% immediately upon the Hp-inoculation and persisted for time intervals tested up to 30 wk. Early lesions were seen 4 wks after the Hp-inoculation and consisted of chronic gastritis with thickened gastric mucosal foldings and elongated interfoveolar ridges. Edema and congestion as well as significant mucosal inflammatory infiltration with lymphoid infiltrate in lamina propria of the mucosa occurred in all infected gerbils. Adenomatous hyperplasia with cellular atypia was observed at 12 wk upon Hp-inoculation together with increased mitotic activity and numerous apoptotic bodies formation, while lamina propria was reduced leaving dilated atypical gastric gland situated "back-to-back". This glandular atypia failed to show lamina propria or submucosa infiltration corresponding to gastric intraepithelial neoplasia. The GBF in Hp-infected gerbils was significantly lower, and a 6-7 fold increase in plasma gastrin levels combined with a significant fall in gastric luminal somatostatin contents observed at all tested periods as compared to vehicle-controls and these effects were counteracted by anti-Hp triple therapy. We conclude that: 1). Hp-infection in Mongolian gerbils in early stages before adenocarcinoma formation results in the development of typical functional and pathological changes such as suppression of gastric secretion and impairment of both, gastric mucosal microcirculation and gastrin-somatostatin link, and 2). this deleterious influence of Hp on gastric morphology and gastric functions is greatly attenuated in gerbils treated with Hp-eradication therapy.
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PMID:Triple eradication therapy counteracts functional impairment associated with Helicobacter pylori infection in Mongolian gerbils. 1267 17

A 71-year-old man was admitted to our hospital because of systemic edema and exertional dyspnea. Chest radiographs revealed infiltrative shadows in both lung fields, pleural effusion, and pericardial effusion. Seven years before, he had undergone gastric surgery for a gastric ulcer with lymphoid hyperplasia. In the pathologic diagnosis based on the percutaneous lung biopsy, hyalinizing granuloma was suspected. For a more thorough diagnosis, the patient was subjected to an open lung biopsy, and the final diagnosis was low-grade B-cell lymphoma of the MALT (mucosa-associated lymphoid tissue) type. Gallium scintigraphy showed accentuated accumulation in the left neck and hypothyroidism was present. Histologic re-examination of the resected stomach revealed infiltration of centrocyte-like cells and lymphoepithelial lesions, compatible with the pathologic features of MALT lymphoma. We considered that the gastric neoplasm and the pulmonary, pleural, and thyroid tumors of MALT lymphoma had occurred seven years apart in this case. Thyroid hormone replacement and CHOP therapy improved the symptoms and decreased the lung tumor size by 73%. MALT lymphomas tend to remain localized for a long period. The multiorgan involvement seen in this case is rather rare.
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PMID:[A case of pulmonary low-grade B cell lymphoma (MALT type) presenting seven years after gastric lymphoma resection]. 1272 33

Helicobacter pylori (H. pylori) is a causative agent for peptic ulcers as well as some types of gastric lymphoma; however, the relationship between a peptic ulcer history in combination with H. pylori infection and the risk of gastric lymphoma has not been fully evaluated. To examine this point, we conducted a case-control study with 645 patients histologically diagnosed as having malignant lymphomas and 3225 non-cancer controls. Plasma H. pylori IgG status was assessed for subgroups for which blood samples were available (116 cases and 114 controls). An association with a history of gastric, but not duodenal ulcers was found for gastric lymphoma [odds ratio (OR) = 5.41, 95% confidence interval (CI): 3.12-9.39]. In the examination according to histological subtype, the OR was high for both gastric mucous-associated lymphoid tissue (MALT) lymphoma (OR = 5.54, 95% CI: 2.56-12.01) and diffuse large B-cell lymphoma (DLBCL) (OR = 7.23, 95% CI: 2.62-19.90). In the analysis of H. pylori antibody, the risk of total gastric lymphoma was associated with H. pylori infection (OR = 5.34, 95% CI: 1.42-20.05). A high prevalence of H. pylori infection was also found for both gastric MALT lymphoma (8 out of 10: 80.0%) and DLBCL (8 out of 9: 88.9%). Further, in subgroup analysis of subjects with H. pylori infection, gastric ulcer history, but not duodenal ulcer history was associated with the risk of gastric lymphoma (OR = 4.15, 95% CI: 1.02-16.89). In conclusion, we found a positive association with a past history of gastric ulcer and H. pylori infection for gastric lymphoma, while duodenal ulcer history was no association. These results suggested the risk of gastric lymphoma increased by interaction between H. pylori infection and gastric ulcer history. Further studies are warranted.
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PMID:A past history of gastric ulcers and Helicobacter pylori infection increase the risk of gastric malignant lymphoma. 1640 Jan 89

Helicobacter pylori (H. pylori) is a gram-negative bacteria infecting more than 50% of human population. H. pylori selectively colonizes gastric mucosa and represents the major cause of gastroduodenal pathologies, such as gastric ulcer, autoimmune gastritis, gastric cancer and B cell lymphoma of mucosa associated lymphoid tissue (MALT). In this review interplay between H. pylori and both innate and adaptive immune responses is discussed. The second part of this article presents current knowledge about the relationship between H. pylori infection and neoplasia.
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PMID:Interplay between Helicobacter pylori and the immune system. Clinical implications. 1703 3

The Helicobacter pylori duodenal ulcer promoting (dupA) gene has been previously described as a risk marker for duodenal ulcer (DU) development and a protective factor against gastric cancer (GC). Recent studies which have assessed the application of dupA in the prediction of clinical outcomes have been controversial. In the current study, the association of dupA with the clinical outcomes and histopathological changes following H. pylori infection was evaluated in Iranian patients. A total of 157 H. pylori-infected patients with DU (n=30), gastric ulcer (n=23), gastritis (n=68) or GC (n=36) were assessed. The presence of jhp0917 and jhp0918 genes was determined by gene specific PCR. Gastric histopathological changes were recorded according to the updated Sydney system. Seventy-eight (49.7 %) and 71 (45.2 %) of the 157 tested strains, respectively, were positive and negative for both genes. The remaining 8 (5.09 %) of the 157 strains were jhp0917-positive/jhp0918-negative. Univariate analysis showed inverse associations between dupA and histological features including dysplasia as the penultimate stage of GC and lymphoid follicles as a consequence of relatively long-standing H. pylori-associated gastritis. The degrees of nucleotide sequence identity of Iranian strains to Colombian, Brazilian and Indian strains ranged from 86.1 to 100 % for the aligned regions of jhp0917, from 88 to 98.8 % for jhp0918 and from 93.4 to 99.5 % for the partial sequences of the dupA gene. Despite the fact that possession of the dupA gene showed no association with any disease category in our population as reported in several other countries, association of dupA-negative strains of H. pylori with pre-malignant lesions calls for additional studies to evaluate the role of this gene as a protective marker against GC.
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PMID:dupA as a risk determinant in Helicobacter pylori infection. 1843 87

Myrrh (Commiphora molmol) has been widely used as an anti-inflammatory and wound healing commercial product. As white blood cell (WBC)/leukocyte counts have been used as an indicator by clinicians to monitor progress of healing in patients, the purpose of this study was to examine effects of myrrh supplementation on blood WBC numbers before an injury and during healing. Male rats (7-8-wk-of-age) were randomly assigned to four groups. Group 1 (SIM) served as "skin injury treated + myrrh treatment (500 mg/kg/day)," Group 2 (SI) as "skin injury alone", Group 3 (GUM) as "gastric ulcer treated + myrrh treatment", and Group 4 (GU) as gastric ulcer only. Myrrh treatments (via drinking water) began 4 wk before induction of injury and continued for a 2 wk period post-injury. Baseline values for each WBC type were recorded before start of the myrrh treatments. Counts were performed again on Day 1 of the 5th wk (1-2 hr before injury) and post-injury on Days 4 and 7 of the 5th wk, and a final time on Day 4 of the 6th wk. Results showed that levels of all WBC types were significantly (P < 0.05) elevated before either injury in myrrh-treated rats (Groups 1 and 3) as compared with levels in rats in Groups 2 and 4. At all timepoints, there were neither significant differences between the values seen with rats in Groups 1 and 3, nor between those in Groups 2 and 4. Treatment with myrrh also induced an initial increase in WBC levels that persisted through the post-injury healing period. Levels of most cell types only increased in the Group 2 and 4 rats once the injury was induced, but then declined over the healing period. Since myrrh enhanced WBC levels before injury, we conclude that myrrh likely contains substances that could induce an apparent antigen-driven response. As the myrrh also helped maintain elevated WBC levels throughout the healing period, this implied it was also able to induce maturation/differentiation/activation of both myeloid and lymphoid cell types during the effector phase of the immune responses involved in wound healing.
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PMID:Effect of myrrh (Commiphora molmol) on leukocyte levels before and during healing from gastric ulcer or skin injury. 1999 43

Helicobacter pylori infection is associated with gastritis, gastric ulcer, gastric adenocarcinoma, and mucosal associated lymphoid tissue lymphoma. Documenting the presence of H pylori in a gastric biopsy is essential for appropriate patient care. Several special stains and immunohistochemistry (IHC) stain for H pylori are available, and many laboratories are routinely using one of them. We introduced routine IHC for H pylori about a year ago, and this study aims to investigate the value of this protocol. A total of 224 patients qualified for the study criteria during this period. The diagnoses were chronic active gastritis (68), chronic gastritis (76), no pathologic abnormality (50), reactive gastropathy (24), and polyps (6). Fifty-four cases were positive for H pylori on IHC, including 50 chronic active gastritis and 4 chronic gastritis. The IHC positive rate was 73.5% (50/68) in chronic active gastritis, 5.3% (4/76) in chronic gastritis, and 0% (0/80) in other diagnoses. The sensitivity/specificity of finding H pylori by blindly reviewing hematoxylin and eosin slides was 100%/100%, 100%/100%, 95%/100%, and 100%/100% from the 4 authors. Our results showed that many gastric biopsies (35.7%, 80/224) had no pathologic abnormality or reactive gastropathy and did not need a routine IHC for H pylori. Hematoxylin and eosin slide review had a very good sensitivity and specificity with all levels of observers. In summary, IHC for H pylori should not be routinely used, especially during these economically challenging times. Immunohistochemistry should be reserved for unexplained gastritis and previously treated patients with likely low organism density.
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PMID:The role of routine immunohistochemistry for Helicobacter pylori in gastric biopsy. 2063 30


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