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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The aim of our study was to evaluate the relationship between Helicobacter pylori infection and various gastroduodenal diseases. We also took into consideration alcohol intake and smoking. Two-hundred and fifty-three consecutive patients with ulcer-like symptoms underwent gastroscopic and histological examinations. H. pylori status was evaluated by means of culture, Giemsa stain and CP-test, upon obtaining bioptic samples of gastric mucosa. Two hundred eighteen patients were affected by gastritis, 171 of which were H. pylori positive (78.4%); of 164 patients with active gastritis, 158 were H. pylori positive (96.3%). In 63 patients with duodenal ulcer, H. pylori was present in 58 cases (92.1%). Of 14 patients with gastric ulcer, 11 were H. pylori positive (78.6%). Out of 133 patients with duodenitis associated with active ulcer or a history of previous ulcer, H. pylori was found in 112 patients (84.2%). Among the 27 patients with "autonomous" duodenitis, 18 were H. pylori positive (66.6%); the comparison between the two groups of patients with duodenitis concerning H. pylori infection was statistically significant (p = 0.033). Of the 119 patients tested for acquired MALT, 39 were found positive (32.7%); among these 34 patients were H. pylori positive (87.1%) and only 5 patients were H. pylori negative (12.9%). Thus our study confirms the importance of H. pylori in gastroduodenal pathology underlining its role in the development of acquired MALT (mucosa associated lymphoid tissue) for its possible evolution in low grade B cell primary gastric lymphoma. Alcohol intake and smoking do not appear to play a role in H. pylori infection.
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PMID:Clinical assessment of the relationship of Helicobacter pylori to gastroduodenal pathologies. A prospective analysis of 253 consecutive patients. 871 Mar 96

Helicobacter pylori is firmly established as a human pathogen; it fulfils all of Koch's postulates as the infectious agent causing chronic, active (type B) gastritis. Infection is strongly associated with duodenal and gastric ulcer. Recently, gastric mucosal-associated lymphoid tissue lymphoma has been successfully treated by curing H. pylori infection. Because of the evidence that the organism causes chronic gastritis and an increased risk of gastric cancer, it has been classified as a category 1 carcinogen by the World Health Organization. However, the overwhelming majority of people infected have no symptoms. Current eradication therapy is not ideal; there are treatment failures and substantial side effects. As a result, therapy should be reserved for people with clinical symptoms and complications. The infection, if present, should be treated in patients who have endoscopic evidence of mucosal ulcers in the stomach or duodenum. Current evidence does not support treating the infection to prevent gastric carcinogenesis or to alleviate symptoms of abdominal discomfort in the absence of peptic ulcers.
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PMID:Why guidelines are required for the treatment of Helicobacter pylori infection in children. 888 75

Helicobacter pylori is probably the commonest bacterial infection worldwide and is now accepted as the cause of chronic active type B gastritis. Most patients continue through life with a chronic superficial gastritis while some develop either duodenal or gastric ulcer. In a very small proportion the lymphoid reaction to H. pylori infection appears to progress to become a mucosal associated lymphoid tissue (MALT) lymphoma, while in others the evidence suggests that chronic superficial gastritis progresses to atrophy, the loss of gastric acid secretory capacity and the development of gastric cancer. The mechanisms involving H. pylori infection in peptic ulceration are increasingly well understood and H. pylori is now accepted as having a critical role in duodenal ulcer, where the prevalence of infection is 90 to 95%. 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 who ulcers have been healed but in whom the infection persists. There is also increasing evidence for the involvement of H. pylori in gastric ulcer, where infection is seen in between 60 and 80%, and there is a similar dramatic reduction in recurrence following cure of H. pylori infection. The progression of H. pylori gastritis from the acute infection to chronic superficial gastritis, predominantly antral gastritis or a pangastritis with increasing atrophy appears to be associated with the differing outcomes seen in this disease. Moreover, there is increasing data on the roles played by bacterial heterogeneity and the virulence of the organism, host factors such as the HLA genotype and immune response, environmental factors and the age of acquisition of infection play in determining these clinical outcomes of the disease.
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PMID:The role of Helicobacter pylori in pathogenesis: the spectrum of clinical outcomes. 889 29

Morphometric reports on animal and human spleen are very few and no studies have been carried out using stereological methods to investigate all of the tissue compartments of the human spleen. Eighteen samples of spleens, which were either surgically removed after traumatic injury or during treatment for early stage carcinoma or gastric ulcer, were investigated. The point-counting method was used to study the volume densities of the following tissue compartments: red pulp, perifollicular zone, white pulp (this tissue compartment was divided in two subcompartments: follicles and periarteriolar lymphatic sheath), marginal zone and connective tissue of trabeculas. The following stereological parameters of the follicles were investigated: the number of follicles per mm2 of spleen section, numerical density, volume density, and the mean follicular diameter. The identity of spleen tissue compartments was verified using immunohistochemical staining for B- and T-lymphocytes. The volume densities of tissue compartments, as well as stereological parameters of lymphoid follicles, were similar in both groups of splenic samples, except for the volume densities of perifollicular zone and periarteriolar lymphatic sheath, where a statistically significant difference was registered.
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PMID:Stereological study of tissue compartments of the human spleen. 893 Jun 23

Helicobacter pylori is the major causative agent of chronic gastritis. It is associated with duodenal and gastric ulcer and with the majority of primary gastric B-cell lymphomas; furthermore, there is a strong epidemiological association with gastric cancer. One intriguing aspect of this infection is the ability of H pylori to persist despite the vast array of host immune responses. This article reviews what is known about the immune responses against H pylori, emphasizing what is generally accepted and applicable while highlighting areas of controversy. The first section delineates the genesis of the inflammatory responses, which initiate with the production of tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, interleukin (IL)-1, IL-6, and IL-8 and continue with the recruitment of neutrophilic polymorphonuclear cells, lymphocytes, plasma cells, macrophages and eosinophils, and later with the development and recruitment of specifically committed cells (lymphocytes sensitized to H pylori antigens and B cells producing immunoglobulin (Ig)A, IgG, and possibly IgE antibodies against a variety of H pylori surface and flagellar proteins as well as bacterial toxins). The second part of the article focuses on the development of lymphoid follicles in the gastric mucosa, a phenomenon that for the first time links an immune response (the recruitment of mucosa-associated lymphoid tissue [MALT] to the gastric mucosa in response to H pylori infection) with the development of a neoplastic growth (the development of gastric MALT lymphomas). The local and systemic antibody responses are discussed in the light of their potential application in the development of diagnostic tests and vaccines. Particular emphasis is placed on the controversies surrounding the significance of antibodies directed against a 120 to 140 kDa protein apparently associated with more "aggressive" (sometimes also called "ulcerogenic" or "pathogenic") strains of H pylori.
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PMID:The immunobiology of Helicobacter pylori gastritis. 900 Apr 97

A 24-year-old male patient with a history of gastric ulcer was referred to our hospital in September 1995. His chief complaints were epigastralgia and weight loss of 3 kg during a short period. The upper G.I endoscopy performed on 9/22/1995 revealed multiple ulcers with a histological diagnosis of atypical lymphoid cell proliferation. Follow-up endoscopy, one month later, showed an appearance of superficial gastric lymphoma, and histology of the biopsy specimen revealed MALT lymphoma associated with H. pylori. Despite an eradication therapy for H. pylori, which consisted of lansoprazole, teprenone and amoxicillin, the progression of the ulcerative lesions was observed on the endoscopy two weeks after initiation of the treatment. However, the subsequent endoscopy, one month later, disclosed a regression both macroscopically and histologically. The lymphoma disappeared completely on the follow-up endoscopy in April 1996 with no lymphoma cells in histology. No recurrences of the lymphoma have been observed up to now.
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PMID:[Gastric lymphoma--a case report]. 947 36

Follicular gastritis is an important histological entity, because it may progress to overt gastric MALT lymphoma. However, there is no universal agreement on whether there is any correlation of follicular gastritis with histological features of the antral mucosa or on the prevalence of follicular gastritis. To shed further light on these issues, we studied antral biopsies obtained from 735 adult patients, who had participated in six consecutive clinical trials. They included 348 patients with duodenal ulcer, 82 with gastric ulcer, and 305 with nonulcer dyspepsia. The Sydney classification system of gastritis was used, using a score of 0-3 to grade degree and activity of inflammation, gland atrophy, intestinal metaplasia, and H. pylori colonization density. Follicular gastritis was defined as prominent lymphoid follicles with no lymphoepithelial lesion. None of the H. pylori-negative patients (N = 159) had follicular gastritis. Among H. pylori-positive patients, 80/340 (23.5%) with duodenal ulcer, 5/77 (6.5%) with gastric ulcer, and 20/159 (12.6%) with nonulcer dyspepsia had follicular gastritis (P < 0.001). Multivariate discriminant analysis selected the following four significant predictor variables for follicular gastritis (Wilks lambda = 0.91, chi2 = 70.6, df = 4, P < 0.001): gastritis sum score, atrophic gastritis, age of the patient, and disease. The prevalence of follicular gastritis was linearly correlated (gamma = 24.55 - 0.98chi, r = -0.62, F1,11 = 6.12, P = 0.03) with the age groups of the 576 H. pylori-positive patients studied. In conclusion, follicular gastritis is highly correlated with H. pylori-caused severe, active gastritis. It is mostly prevalent in the young H. pylori-infected patients with duodenal ulcer.
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PMID:Predictive factors and prevalence of follicular gastritis in adults with peptic ulcer and nonulcer dyspepsia. 1038 88

In the pediatric population, the associations of Helicobacter pylori with gastritis, gastric ulcer, duodenitis and duodenal ulcer, and with duodenal gastric surface metaplasia and disorders of the D cell- G cell axis resulting in hypergastrinemia, are well established and in many ways resemble their counterparts in adults. Eradication of H pylori invariably results in the reversal of these diseases with time. There are also suggestions that gastric surface metaplasia is more extensive in children with H pylori, and may be the site of duodenal H pylori infection and associated duodenal erosions or ulcers. There is no consensus as to whether H pylori in children is more or less severe than in adults. In one pediatric cohort, H pylori was associated with increased intensity of inflammation, while other studies suggest that acute inflammation may be less intense in children overall but that chronic inflammation may be increased in intensity, including lymphoid hyperplasia, which in turn may correlate with endoscopic nodularity. Lymphoid hyperplasia and nodular gastritis appear to be more frequent in children than in adults and usually regress following H pylori eradication. However, in children, other diseases or morphological abnormalities, including some loss of glands (atrophy), occasionally intestinal metaplasia, lymphoproliferative diseases including low grade mucosal-associated lymphoid tissue lymphoma, lymphocytic gastritis and hypertrophic gastritis/Menetrier's disease, are much less frequently associated with H pylori than in adults. Other associations are rarely seen in children, primarily because the time required for these to develop takes the individual to adulthood; for example, while intestinal metaplasia occurs in the pediatric population, the complications of adenoma/dysplasia and carcinoma are rare. In adults, inflammatory and hyperplastic polyps, atrophic gastritis and pernicious anemia, and in some patients granulomas (granulomatous gastritis), may also be associated with H pylori infection. Greater awareness of the spectrum of diseases associated with H pylori may well lead to their increased recognition in the pediatric population. Some diseases, particularly Crohn's disease, but also human immunodeficiency virus infection, have a negative association with H pylori that appears not to be simply a result of the excess antibiotic therapy that these patients receive. These variations in association and reactions to H pylori, some of which are age-related, may allow the different host responses to H pylori that occur in humans to be examined.
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PMID:Pathobiology of Helicobacter pylori infection in children. 1051 59

The histopathology of the antral mucosa of patients with acid peptic disease was studied in relation to Helicobacter pylori infection. Three hundred and fifty-five patients underwent gastroscopy and biopsy on 443 occasions. During each gastroscopy, two antral samples were taken for Rapid Urease Test (RUT) for H. pylori and two antral samples for histopathology. Haematoxylin and Eosin and modified Giemsa stained sections were studied. Histopathological changes in the antrum and the density of H. pylori were graded according to the Sydney System criteria. There was a significant association between the RUT and histology results for detection of H. pylori. The overall prevalence of H. pylori was 61.4% with a maximum incidence in the third and fourth decades of life, and an equal sex distribution. H. pylori colonisation was seen in 90.7% of patients with duodenal ulcer, 66.7% with gastric ulcer and 44.3% with non-ulcer dyspepsia. H. pylori colonisation was associated with more severe antral chronic active gastritis, lymphoid follicles, intestinal metaplasia and dysplasia. Elimination of H. pylori by treatment with anti-H. pylori regimens resulted in regression of the changes.
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PMID:Antral histopathological changes in acid peptic disease associated with Helicobacter pylori. 1112 73


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