"Helicobacter pylori in areas of intestinal metaplasia in gastric antral mucosa", by Misra et al.
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Carcinoma↗
Biomedical subjects
R M Genta
Publications and source records attributed to R M Genta.
Histochemical analysis of mucous cells of congenital adenomatoid malformation of the lung: insights into the carcinogenesis of pulmonary adenocarcinoma expressing gastric mucins.
Adenocarcinomas expressing gastric mucins often are accompanied by ectopic gastric mucosa or pyloric metaplasia. We have previously described mucinous bronchioloalveolar carcinoma (mucinous BAC) producing gastric mucins. In the lung tissue, mucous cells seemingly similar to gastric mucous cells are present in congenital adenomatoid malformation (CAM). We assessed 26 cases of CAM morphologically and histochemically. Mucous cells were detected in 12 of 26 cases. These mucous cells displayed papillary growth in cystic spaces and proliferated along alveolar walls. Mucous cells in the papillary, configuration stained with galactose oxidase cold thionine Schiff reaction, and those in indented portions stained with paradoxical concanavalin A stain in all 8 cases and with pepsinogen II in 5 of 8 cases, which were available for histochemical analysis. Pepsinogen I was negative. Mucous cells in CAM were identical to those of pyloric mucosa and could be considered candidates for the origin of mucinous BAC producing gastric mucins.
Adenocarcinoma, Bronchiolo-Alveolar↗
Review article: Gastric atrophy and atrophic gastritis--nebulous concepts in search of a definition.
Epidemiological and biological evidence indicates that atrophic gastritis represents an important risk factor for gastric adenocarcinoma of the intestinal type. To estimate an individual subject's risk of gastric cancer, pathologists should be able to diagnose correctly and reliably assess gastric atrophy. However, both anecdotal evidence and recent studies suggest that pathologists have a low level of agreement on gastric atrophy. Moreover, the terms 'gastric atrophy' and 'atrophic gastritis' remain imprecisely defined, further adding confusion to the histopathological imprecision. The use of visual analogue scales proposed in the recently updated Sydney System for the classification and grading of gastritis may eventually help pathologists achieve a greater degree of interobserver agreement on the histopathological features of gastritis. However, this cannot be achieved in the absence of a stringent and widely accepted definition of atrophy. The purpose of this article is to review briefly the possible pathogenetic pathways leading to the development of atrophic changes in the gastric mucosa, explore the issue of its reversibility, and propose a working definition that could contribute to improved diagnostic reproducibility.
Adenocarcinoma↗
Acid suppression and gastric atrophy: sifting fact from fiction.
Prolonged pharmacological acid suppression is associated with various histological changes in the gastric mucosa, particularly in Helicobacter pylori infected patients. In a number of subjects these changes include a shift in the gastric inflammation from the antrum to the corpus. This finding has been interpreted as gastric atrophy, and the possibility that acid suppression accelerates the progress of lesions that may lead to gastric cancer has been considered. Two recent studies on the relation between treatment with proton pump inhibitors and atrophic gastritis have yielded apparently contradictory results. These studies are reviewed in detail here and some of the possible reasons for the discrepant conclusions are explored. In particular, the way the terms "gastric atrophy" and "atrophic gastritis" are used is examined critically.
Anti-Ulcer Agents↗
Atrophy and atrophic gastritis: one step beyond the Sydney system.
An international workshop to evaluate the concepts of atrophy and atrophic gastritis was held in Houston in 1998. A consensus emerged that: 1) there is a phenotype of Helicobacter pylori-associated gastritis characterized by progressive loss of glands and intestinalization; 2) this phenotype is associated with increased risk of gastric ulcer and adenocarcinoma. This pattern must be consistently recognized are reproducibly diagnosed by histopathologists. The mucosal biopsy sampling suggested in the updated Sydney System were considered adequate to evaluate a patient for atrophic gastritis. Histopathologists were advised to refrain from making a diagnosis of "atrophic gastritis" unless moderate or severe unequivocal loss of gastric glands and/or moderate or severe metaplasia is found in at least 50% of the total gastric mucosa evaluated in the biopsy specimens. When atrophic or metaplastic changes appear to be more limited, "chronic gastritis with focal atrophy or metaplasia" should be diagnosed, and more extensive sampling should be obtained before the entity "atrophic gastritis" can be diagnosed. Particular attention was devoted to the issue of "unequivocal loss of gastric glands." In general, it was felt that it is difficult to be certain about loss of glands in the presence of moderate or severe inflammation, when one cannot be sure whether the glands have actually disappeared of have been displaced by the inflammatory infiltrate. In these circumstances, the term "indefinite for atrophy" can be used and the patient should be re-evaluated several months after the eradication of Helicobacter pylori infection.
Adenocarcinoma↗
Atrophy, metaplasia and dysplasia: are they reversible?
The eradication of Helicobacter pylori results in the decrease and eventual disappearance of inflammation in the gastric mucosa. An important question with practical implications is whether treatment of H. pylori can promote the resolution of atrophy and intestinal metaplasia. If this happens, then one could infer that even in the presence of established multifocal atrophic gastritis the cure of Helicobacter pylori could reduce the risk of developing gastric cancer. Several investigators have addressed the issue, but the cumulative results remain inconclusive. The great latitude that there exists in the interpretation of the concept of atrophy and the patchy distribution of both atrophic changes and intestinal metaplasia (with resulting inevitable sampling error) are important reasons for the wide discrepancy in the conclusions reached by different authors. Controlled, long-term prospective studies conducted in different ethnic and geographic settings are needed to provide sound evidence-based answers to the question of reversibility of atrophy, intestinal metaplasia, and epithelial dysplasia.
Atrophy↗
Histologic assessment of Helicobacter pylori status after therapy: comparison of Giemsa, Diff-Quik, and Genta stains.
To compare the Giemsa, Diff-Quik, and Genta stains for detection of Helicobacter pylori in gastric biopsy specimens, we stained, coded, and randomized slides, which were then independently reviewed by two pathologists and one trainee. H. pylori was graded from 0 (absent) to 5 (maximal intensity). Negative cases were from recently cured patients to ensure that a background of chronic inflammation was present. The time required to complete the evaluation was tabulated. The pathologists interpreted 72 H. pylori-negative slides, of which 1 (1.3%), 2 (3%), and 3 (4%) were scored positive (each with the score of 1) with Diff-Quik, Genta, and Giemsa stains, respectively (P = ns). Of the 128 H. pylori-positive slides, 5 (4%) had false-negative results with Diff-Quik, 8 with Genta (6%), and 14 with Giemsa stains( 11%). No Grade 2 slides were missed by Genta or Diff-Quik stains, but 3 of 20 were missed by Giemsa stain. The combination of hematoxylin and eosin and Diff-Quik provides accuracy similar to that of the Genta stain but requires more processing time. No stain was excellent after therapy for detecting one or two bacteria per slide; this finding emphasizes the need for obtaining multiple biopsy specimen to exclude failure of H. pylori therapy.
Azure Stains↗
Mast cell involvement in gastritis with or without Helicobacter pylori infection.
BACKGROUND & AIMS: Mast cells are initiators and regulators of inflammation, but their role in the human stomach remains unclear. Therefore, the extent and distribution of mast cell involvement in gastritis with or without Helicobacter pylori infection was investigated. METHODS: Mapped biopsy specimens from 17 H. pylori-positive and 20 H. pylori-negative subjects were examined. Sections were assessed for infection and inflammation and stained with anti-human mast cell tryptase to count mucosal and epithelial mast cells. Density of mast cells in different gastric compartments, their response to infection treatment, and their relationship with other inflammatory cells were evaluated. Mast cell degranulation was evaluated by electron microscopy. RESULTS: Mast cell density was significantly greater in the mucosa with gastritis, with or without H. pylori infection, than in the mucosa of noninfected normal subjects. In the antrum, density was much greater in H. pylori-infected peptic ulcer subjects than in the other gastritis groups. It also correlated significantly with the intensity of inflammation. Mast cell degranulation was demonstrated by electron microscopy in H. pylori-infected mucosa. Mast cell density in ulcer patients decreased significantly after cure of H. pylori infection. CONCLUSIONS: Mast cells may be important effector cells in the pathogenesis of gastritis, especially in H. pylori-associated peptic ulcer.
Adult↗
Helicobacter pylori, inflammation, mucosal damage, and apoptosis: pathogenesis and definition of gastric atrophy.
Much of what is currently accepted on the natural history of Helicobacter pylori-induced gastritis and its relationship with gastric adenocarcinoma rests on the assumption that atrophic gastritis can be correctly identified and reproducibly recognized. Recently, several studies have indicated that pathologists have a low level of agreement on this topic, and the terms "gastric atrophy" and "atrophic gastritis" remain imprecisely defined and, therefore, poorly understood. Furthermore, the genesis and progression of the atrophic changes taking place in the gastric mucosa of some, but not all, subjects infected with H. pylori are incompletely characterized. This review has three aims: (1) to briefly reexamine our current knowledge of the mechanisms involved in the injury and repair of gastric glands; (2) to present a hypothesis on the development of gastric atrophy; and (3) to propose a new, stringent definition of gastric atrophy that may be usefully applied in the clinical research arena.
Apoptosis↗
Furazolidone, amoxycillin, bismuth triple therapy for Helicobacter pylori infection.
BACKGROUND: Metronidazole-resistant Helicobacter pylori are generally the rule in developing countries such as Colombia. Developing countries need an effective, simple and inexpensive non-metronidazole therapy for H. pylori infection. AIM: To evaluate the combination of bismuth, furazolidone and amoxycillin for the treatment of H. pylori infection in Colombia. METHODS: Thirty patients with histologically documented H. pylori infection received the combination of bismuth subcitrate 240 mg b.d., furzolidone 100 mg q.d.s. and amoxycillin 500 mg q.d.s. for 14 days. Four or more weeks after ending therapy patients were re-endoscoped and gastric biopsies were obtained and examined using the Genta stain. Each slide was scored for presence, absence and density of H. pylori, active and chronic inflammation, intestinal metaplasia, erosions and atrophy. Cure was defined as the absence of H. pylori. RESULTS: All patients completed the course of therapy. Twenty-five patients were cured (86%, 95% CI: 65-94%). Mild, well-tolerated side-effects were reported by six patients (20%). CONCLUSIONS: This combination of bismuth, furazolidone and amoxycillin fulfills the criteria for successful H. pylori therapy and appears particularly well suited for developing countries since it is simple, inexpensive and effective. Furazolidone-containing therapies may become especially useful in the face of a world-wide increase in H. pylori resistance to metronidazole and macrolides.
Adult↗
Successful low-dose amoxycillin, metronidazole and omeprazole combination therapy in a population with a high frequency of metronidazole-resistant Helicobacter pylori.
AIM: Effective anti-Helicobacter pylori therapies with few side-effects are needed. We studied the effectiveness of a low-dose combination of metronidazole, amoxycillin and omeprazole for treatment of ulcer patients in Seoul, Korea. METHODS: Patients with gastric or duodenal ulcer received metronidazole (125 mg b.d.), amoxycillin (500 mg b.d.) and omeprazole (20 mg at bedtime) for 2 weeks. Endoscopic examinations were performed before treatment and at least 6 weeks after completion of antimicrobial therapy. H. pylori status was confirmed by histological examination of two gastric biopsies using the Genta stain. RESULTS: Seventy-nine patients (64 men, 15 women, mean age 46 years) with peptic ulcer were enrolled. H. pylori infection was cured in 56 (71%) 95% CI: 60-81%). The cure rate in non-smokers was significantly higher than in smokers (88% vs. 65%, P = 0.035). Twelve pre-treatment isolates were available and metronidazole resistance was noted in all; H. pylori infection was cured in 10. Thirty-six patients cured of H. pylori have been followed for 1 year (mean of 361 days) and 2 cases became reinfected (5.5%, 95% CI: 1-18%). CONCLUSIONS: The low-dose combination of metronidazole, amoxycillin and omeprazole was effective even the in face of metronidazole resistance. Recurrence of H. pylori infection is infrequent even in countries with a high prevalence of H. pylori infection.
Adult↗
Is the sanctuary where Helicobacter pylori avoids antibacterial treatment intracellular?
The sanctuary site where Helicobacter pylori evades antimicrobial therapy is unknown, but considerable data exist about an intracellular location for H pylori. Ten H pylori-infected volunteers received standard triple antimicrobial therapy for 2 weeks. Gastric mucosal biopsy specimens were obtained with jumbo forceps on therapy days 0, 3, 14, and 42. Hematoxylin-eosin staining was used for classification of gastritis and the Genta stain for the visualization of H pylori. Immunohistochemical staining was used to detect HLA-DR antigens, human heat shock protein (HSP60), and the bacterial HSP60 antigen. Bacterial HSP60 was expressed on the mucosal surface and within epithelial cells. No such expression of human HSP60 was found, which supports a bacterial origin for the intracellular HSP60. Coexpression of bacterial HSP60 and HLA-DR was always observed, indicating an ongoing local immune response. Infection was cleared on day 14, but when examined 4 weeks after completion of therapy, Genta staining indicated that only five volunteers remained free of H pylori. However, results of immunohistochemical staining were negative at this time for only two volunteers. Disappearance of intracellular expression of bacterial HSP60 remained after therapy and correlated with the intensity of chronic inflammatory cell infiltration. These data are consistent with the intracellular localization of H pylori having a role in inflammation and as a protective strategy against extracellular antibacterial activity.
Adult↗
Failure to isolate Helicobacter pylori from stray cats indicates that H. pylori in cats may be an anthroponosis--an animal infection with a human pathogen.
The recent isolation of Helicobacter pylori from cats obtained from a commercial supplier has potentially important public health implications. The present study investigated whether H. pylori infection was common in stray cats. Twenty-five cats were examined for the presence of H. pylori by histological examination, culture and two polymerase chain reaction (PCR) assays. Histologically, the gastric biopsy specimens from all cats showed large spiral organisms typical of H. felis and not H. pylori. Samples from 23 cats yielded bacterial growth and two had no growth. Colonies grossly similar to H. pylori were tested for catalase, oxidase, urease and Gram's stain reactions. None was H. pylori. All samples tested as positive by the Helicobacter 16S rRNA genus-specific PCR assay and only six cats and a mouse stomach infected with H. heilmannii gave positive results with the adhesin subunit A (hpaA)-specific PCR assay, which is consistent with either H. pylori or H. heilmannii. The helicobacters identified in these samples by PCR were not cultivable and hence were probably H. heilmannii. H. pylori infection is uncommon in stray cats and owning pet cats should not be a threat to public health in relation to H. pylori infection.
Adhesins, Bacterial↗
Histological classification of gastritis and Helicobacter pylori infection: an agreement at last? The International Workshop on the Histopathology of Gastritis.
An international workshop has assessed and revised the Sydney System for the reporting of gastritis. Much of the original approach was retained including division into acute, chronic and special forms, and grading of chronic inflammation, polymorph activity, atrophy, intestinal metaplasia and H. pylori density into mild, moderate and marked categories. Visual analog scales have been introduced as a simple guide to grading. The four biopsy sites have been changed to optimize detection of H. pylori, and supplemented by a fifth biopsy from the incisura angularis, the site which is most likely to yield premalignant changes. Chronic gastritis is classified into non-atrophic and atrophic forms with the latter divided into autoimmune (diffuse corpus atrophy) and multifocal. Histological reporting of gastritis should take into account the topographical pattern (antral or corpus predominant), and the final diagnostic term should ideally combine morphology and etiology to maximize the clinical value of gastric biopsy diagnosis.
Gastritis↗
Primary gastric MALT lymphoma: trivial condition or serious disease?
BACKGROUND: Primary gastric B-cell lymphomas originating from the mucosa-associated lymphoid tissue (MALT) have been demonstrated to be closely associated with Helicobacter pylori infection. Approximately 70% of these tumors regress within 1 year of eradication of H. pylori. Currently, there is little consensus on the best strategies for diagnosing, treating, and following up these lymphomas. Our objective was to review the current strategies for the diagnosis and management of MALT lymphomas and to describe the management guidelines used in our own institution. METHODS: Our approach consisted of a review of the literature and personal experience. RESULTS: Rigorous histopathological criteria (Isaacson's criteria) must be applied to the diagnosis of gastric biopsies with atypical lymphoid aggregates. Molecular and immunohistochemical studies might play have a role in determining the clonality of the lesions, but correlation with the histopathological aspects is crucial. CONCLUSIONS: Little solid information exists on the natural history and evolution of MALT lymphomas. While studies are being carried out, we suggest that even a suspected MALT lymphoma in a gastric biopsy specimen should be treated as a potentially serious condition. The diagnosis should be confirmed by an experienced histopathological laboratory, and H. pylori infection must be sought and treated. Because the response of lymphomas to antibacterial therapy cannot be predicted, close follow-up of affected patients is essential.
Helicobacter Infections↗
Invasive Helicobacter-like organisms in feline gastric mucosa.
BACKGROUND: Helicobacter-like organisms (HLOs) usually are present in the stomachs of cats. Although the histopathology of natural (H. felis or H. heilmannii) infections has been reported, their invasion into the lymphoid aggregates has not been described previously. MATERIALS AND METHODS: Gastric tissues were obtained from 17 adult cats living in a natural urban environment. Biopsy sites were selected by the presence of urease on the mucosal surface stained by Genta stain and periodic acid-Schiff stain. RESULTS: Spiral organisms morphologically similar to H. felis or to H. heilmannii were detected in all the cats, distributed predominantly over the oxyntic mucosa. Seven cats had prominent lymphoid follicles with germinal centers within the oxyntic mucosa, and in six of these seven cats, extracellular organisms were present within the lymphoid follicles. Scattered organisms also were found over sites of gastric metaplasia in the duodenum of six cats. CONCLUSIONS: This study extends previous observations by showing that HLO infection in cats is associated with large lymphoid follicles in the stomach. In addition, HLOs were demonstrated submucosally within gastric lymphoid follicles and on patches of gastric metaplasia in the duodenum.
Animals↗
Cure of Helicobacter pylori infection improves gastric acid secretion in patients with corpus gastritis.
BACKGROUND: For more than 30 years it has been known that gastric acid secretion is inversely related to the extent and severity of corpal gastritis. We therefore evaluated the effect of cure of Helicobacter pylori infection on basal and pentagastrin-stimulated acid secretion. METHODS: Basal acid output (BAO) and maximal acid output (MAO) were assessed in 11 H. pylori-infected dyspeptic patients (8 women and 3 men; mean age, 28 years) before and after successful anti-H. pylori therapy. RESULTS: The gastritis index was significantly lower after therapy and was associated with an increase in both BAO and MAO after cure of the H. pylori infection (BAO from 0.3 mmol/h and MAO from 4.8 mmol/h to 19 mmol/ h). Basal and stimulated acid concentrations also increased (29.1 +/- 36.6 to 54 +/- 31 mmol/l and 72.5 +/- 46 to 120.1 +/- 30 mmol/l, respectively, for basal and stimulated acid concentrations; P < 0.05 for peak and MAO, P = 0.07 for BAO). CONCLUSION: Gastric acid secretion increased into the normal range after successful treatment of H. pylori infection, suggesting that gastric function can recover to normal or almost normal after cure of H. pylori infection.
Adult↗
The immunobiology of Helicobacter pylori gastritis.
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.
Gastritis↗