Showing papers on "Chronic gastritis published in 1996"
TL;DR: H. pylori-mediated autoimmunity is involved in the pathogenesis of chronic atrophic gastritis and the grade of antigenic mimicry of the infecting H. plyori strain plays a role in the progression of chronic gastritis to atrophy.
310 citations
TL;DR: The appearance of parietal cell antibodies leads to progression of corpus atrophy and disappearance of H. pylori infection and normalization of the antral mucosa in patients followed up for 32 years.
Abstract: Background: The long-term course of Helicobacter pylori gastritis is not well known because there are few follow-up studies available, and the follow-up time has been short. Methods: The progression of H. pylori infection and chronic gastritis was retrospectively examined in 102 patients followed up for 32 years. In all patients a blind suction biopsy from the corpus mucosa was taken in 1952, and an endoscopic re-examination with biopsy specimens from the antrum and corpus was performed in 1983. Results: In the first examination 85 patients (83%) were H. pylori-positive as assessed from Giemsa-stained corpus mucosa specimens as compared with 70 H. pylori-positive patients (69%) at the end of the follow-up (1983). Two of the 17 patients who were initially H. pylori-negative became positive in 1983, implying an infection rate of 0.4% per patient-year. On the other hand, 17 of the 85 patients who were initially H. pylori-positive became negative in 1983, representing a disappearance rate of 0.6%. However, th...
265 citations
TL;DR: It is concluded that two main pathways operate in gastric carcinogenesis, both starting from H. pylori gastritis and both leading to phenotypically variable, often mixed gastric/intestinal tumor growth.
Abstract: Investigation of extensively sampled nontumor gastric mucosa from 205 early gastric cancers showed Helicobacter pylori colonization in 85% of cases, including 100% of diffuse and 78% (83% in 97 cases with Swiss rolls) of glandular or mixed cancers. Intestinal metaplasia, including its type III variant, was prominent in the mucosa associated with glandular and mixed (but not diffuse) early cancers. Both glandular (usually called intestinal) and diffuse-type cancers showed admixtures of intestinal and gastric tumor cell phenotypes. Both p53 gene mutations and p53 protein immunostaining were essentially restricted to glandular or mixed cancers and associated dysplastic lesions. Their appearance in the advanced stage of diffuse cancer was partly due to a change of the histologic pattern from glandular to diffuse during progression of some tumors. Loss of laminin, β 1 integrin, or zonula adherens junctions was a common finding in both early and advanced diffuse cancer. It is concluded that two main pathways operate in gastric carcinogenesis, both starting from H. pylori gastritis and both leading to phenotypically variable, often mixed gastric/intestinal tumor growth. However, only one of the two pathways involves intestinal metaplasia, its type III variant, p53 gene alteration, and dysplasia to end in glandular cancer. In the other pathway, diffuse cancer apparently arises directly from hyperplastic, sometimes atypical necks of mostly nonmetaplastic gastric glands, through primary involvement of genes affecting cell-cell and cell-matrix junctional proteins.
175 citations
Journal Article•
TL;DR: A review of current knowledge on the properties of H. Pylori that adapt it to its particular niche by allowing it to survive in the stomach and to colonize the gastric mucosa, as well as those that underlie its persistence and pathogenicity.
Abstract: Helicobacter pylori is a recently recognized bacterial pathogen associated with diverse pathologies of varying severity, such as chronic gastritis, peptic ulceration, mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric carcinoma. We here present a review of our current knowledge on the properties of H. Pylori that adapt it to its particular niche by allowing it to survive in the stomach and to colonize the gastric mucosa, as well as those that underlie its persistence and pathogenicity. While the bacterial determinants that preclude the persistent colonization of the gastric mucosa are better understood, those associated with pathogenicity appear to result from the possibility for some of the bacteria of the species to synthesize products that directly or indirectly damage the gastric mucosa, cause a persistent inflammatory reaction, and/or perturb the regulation of acid secretion.
144 citations
TL;DR: The pilot phase of the study in which two antioxidant preparations were evaluated on their ability to raise antioxidant levels in plasma and in gastric juice concluded that treatment 1 was the best choice and resulted in a greater increase in the plasma levels of beta-carotene and alpha-tocopherol.
Abstract: A randomized chemoprevention trial on precancerous lesions of the stomach is being conducted in Tachira State, Venezuela. The aims of the study are to evaluate the efficacy of vitamin supplementation in preventing the progression rate of precancerous lesions. Here we report on the pilot phase of the study in which two antioxidant preparations were evaluated on their ability to raise antioxidant levels in plasma and in gastric juice. The study aimed also to determine the antibiotic sensitivity profiles of Helicobacter pylori isolates prevalent in the area. Forty-three subjects with precancerous lesions (chronic gastritis, chronic atrophic gastritis, intestinal metaplasia and dysplasia) of the stomach were randomized to one of two antioxidant treatments. Treatment 1 (250 mg of standard vitamin C, 200 mg of vitamin E and 6 mg of beta-carotene three times a day) or treatment 2 (150 mg of standard vitamin C, 500 mg of slow release vitamin C, 75 mg of vitamin E and 15 mg of beta-carotene once a day) for 7 days. Blood levels of total vitamin C, beta-carotene and alpha-tocopherol and gastric juice levels of ascorbic acid and total vitamin C were measured before and after treatment on day 8. Both treatments increased the plasma levels of total vitamin C, beta-carotene and alpha-tocopherol/cholesterol but not those of ascorbic acid or total vitamin C in gastric juice. Treatment 1 was the best choice and resulted in a greater increase in the plasma levels of beta-carotene and alpha-tocopherol. H. pylori was cultured from 90% of the gastric biopsies; 35 isolates were identified which were highly resistant to metronidazole, a front-line antibiotic recommended against H. pylori in other settings.
136 citations
TL;DR: Investigation of the sensitivity of detecting Helicobacter pylori in gastric biopsy and resection specimens using tinctorial and silver impregnation stains, immunohistochemistry and the polymerase chain reaction found it to be highly sensitive and easy to use.
Abstract: AIMS: To compare the sensitivity of detecting Helicobacter pylori in gastric biopsy and resection specimens using tinctorial and silver impregnation stains, immunohistochemistry and the polymerase chain reaction (PCR). METHODS: Formalin fixed, paraffin wax embedded tissue from 33 gastric biopsy specimens (26 showing chronic gastritis and seven showing low grade mucosa associated lymphoid tissue (MALT) lymphoma) together with blocks of uninvolved mucosa from gastrectomy specimens for MALT lymphoma (five cases) were studied. Consecutive sections were stained using haematoxylin and eosin, Giemsa, the Warthin-Starry silver stain, and a polyclonal antibody directed against H pylori using an immunoperoxidase technique following heat induced antigen retrieval. PCR analysis of DNA extracted from a further section was carried out using primers which amplified a 411 base pair fragment of the urease A gene. RESULTS: H pylori was detected in 14 (37%) sections stained with haematoxylin and eosin, 21 (55%) with Giemsa, 23 (61%) with Warthin-Starry, and 25 (66%) stained with the antibody. Seventeen (45%) cases were positive on PCR. Immunohistochemistry was positive in all cases in which H pylori was detected by other methods. CONCLUSION: Immunohistochemistry using an immunoperoxidase technique following heat induced antigen retrieval for detecting H pylori in gastric biopsy and resection specimens is highly sensitive and easy to use.
127 citations
TL;DR: H pylori infection although associated with an increased epithelial cell proliferation in subjects with chronic gastritis, does not influence the increased epithelium cell proliferation seen inSubjects with precancerous lesions or gastric carcinoma.
Abstract: Increased epithelial cell proliferation is associated with an increased risk of adenocarcinoma and is associated with Helicobacter pylori infection. The aim of this study was to assess both gastric epithelial cell proliferation and the influence of H pylori infection on cell kinetics in the progression from normal mucosa to gastric carcinoma. One hundred and forty four subjects were assigned to study groups based on diagnosis and H pylori status: microscopically normal mucosa and H pylori negative (n = 28); chronic active gastritis and H pylori positive (n = 83); atrophic gastritis (n = 9); intestinal metaplasia (n = 19); gastric carcinoma (n = 12). Gastric antral epithelial cell proliferation was assessed using the in vitro bromodeoxyuridine immunohistochemical technique and expressed as the labelling index per cent (LI%). Subjects with chronic atrophic gastritis, intestinal metaplasia or gastric cancer have increased gastric epithelial cell proliferation compared with normal mucosa (LI% mean (SEM): 5.14 (0.6), 4.68 (0.3), 6.50 (0.5) v 3.08 (0.2), p < 0.001). This increase in gastric epithelial cell proliferation was not influenced by H pylori status. Gastritis associated with H pylori had an increased LI% compared with normal controls or subjects with H pylori negative gastritis (4.98 (0.2) v 3.08 (0.2), 3.83 (0.2), p < 0.01). H pylori infection although associated with an increased epithelial cell proliferation in subjects with chronic gastritis, does not influence the increased epithelial cell proliferation seen in subjects with precancerous lesions or gastric carcinoma. This is further evidence that H pylori may be an initiating step in gastric carcinogenesis.
123 citations
Journal Article•
TL;DR: At the greater curvature of the body, the development of atrophy is closely associated with the increase in the severity of inflammation, which is more marked in H. pylori-positive patients.
112 citations
TL;DR: The data suggest that high ascorbic acid intake could reduce gastric cancer risk, but its protective effect might be greater if gastritis is treated (for example, by Helicobacter pylori eradication).
Abstract: Epidemiological evidence suggests that high dietary ascorbic acid reduces gastric cancer risk. It may do this by either reducing N-nitroso compound formation in gastric juice, or by scavenging reactive oxygen species in gastric mucosa. The aim of this study was to discover if potential ascorbic acid protection might be increased by supplementation. Thirty two patients were supplemented with ascorbic acid, 500 mg twice daily for two weeks. Gastric juice, plasma, and upper gastrointestinal biopsy ascorbate concentrations were measured and compared with values in 48 unsupplemented patients. It was found that ascorbic acid and total vitamin C concentrations were considerably higher in biopsy specimens from oesophagus, body, antrum, duodenum, and rectum, compared with values in plasma or gastric juice. Plasma and mucosal concentrations were unaffected by the presence of chronic gastritis but gastric juice concentrations were substantially lower in patients with chronic gastritis than in patients with normal histological assessment (p < 0.01). Patients receiving ascorbic acid supplements had higher ascorbic acid concentrations in plasma (p < 0.001), gastric juice (p < 0.001), and at all biopsy sites in the upper gastrointestinal tract (p < 0.05). Gastric juice ascorbic acid and total vitamin C concentrations in gastritic patients, however, were still less after supplementation than in normal subjects (p < 0.01). These data suggest that high ascorbic acid intake could reduce gastric cancer risk, but its protective effect might be greater if gastritis is treated (for example, by Helicobacter pylori eradication).
110 citations
Journal Article•
TL;DR: Results show that H. pylori infection is associated with modifications in the proliferative compartment of the gastric mucosa, and both infection per se and chronic gastritis seem to be relevant for such changes.
109 citations
TL;DR: Chronic gastritis and H. pylori infection correlate with increased free-radical production, reduced gastric vitamin C levels, and increased glutathione turnover, and the possible implications of these changes in the pathogenesis of gastric damage and in carcinogenesis are intriguing.
Abstract: We have evaluated gastric juice pH, nitrites and vitamin C levels, mucosal glutathione, and malondialdehyde, a marker of lipid peroxidation, in patients with chronic gastritis undergoing endoscopy. Patients had chronic gastritis with (n = 28) or without (n = 60) atrophy and/or concomitant Helicobacter pylori infection. Nineteen healthy subjects, without major macroscopic or histologic changes, were included as controls. Ten subjects were studied before and after H. pylori eradication. Vitamin C levels were low in atrophic gastritis (p < 0.006) and H. pylori infection (p < 0.02). Nitrite concentrations and pH were significantly higher in atrophy (p < 0.005 and 0.0001). Glutathione turnover was higher than normal in gastritis, with higher levels of oxidized glutathione (p < 0.02). Gastric malondialdehyde levels were significantly increased by gastritis (p < 0.05) and H. pylori infection (p < 0.05). Overall, more active gastritis coincided with lower vitamin C levels and higher malondialdehyde levels. After H. pylori eradication a drop in mucosal MDA levels was observed (p = 0.04). In summary, chronic gastritis and H. pylori infection correlate with increased free-radical production, reduced gastric vitamin C levels, and increased glutathione turnover. The possible implications of these changes in the pathogenesis of gastric damage and in carcinogenesis are intriguing.
TL;DR: GHLOs were found to be common in apparently health dogs and cats and may cause histological changes comparable to chronic gastritis, but in dogs this association remain unclear.
Abstract: Summary
The occurrence and topographical mapping of the gastric Helicobacter-like organisms (GHLOs) and their association with histological changes were studied in apparently healthy dogs and cats. Multiple samples were collected for histological examination from the fundus, corpus and antrum of the stomach of 10 dogs and 10 cats. Fundus and corpus were also sampled for transmission electron microscopy (three dogs, six cats), and for culture (eight dogs, six cats). In all dogs, GHLOs were detected in the fundus and corpus, and in the antrum of nine dogs, and significantly more often in the fundus and corpus (in all sample sites examined) than the antrum (P < 0.01). In cats, GHLOs were demonstrated in 6/10 individuals, and in all regions and sample sites. In dogs GHLOs were detected in all sample sites of the fundus and corpus. Lymphocytes, plasma cells and lymphocyte aggregates were found in all dogs in all regions; there were significantly more plasma cells in the antrum than in the corpus (P < 0.05). Neutrophils were found in six dogs, and eosinophils in seven dogs. In cats, lymphocyte aggregates were found only in GHLO-positive cats, which also had more lymphocytes in the fundus and corpus than GHLO-negative ones (P < 0.05). In dogs, no statistically significant association was found between the number of GHLOs and inflammatory parameters. Four dogs showed histological changes comparable to mild chronic gastritis and another six dogs to mild active chronic gastritis. Mild chronic gastritis was found in the antrum of all cats, and it occurred significantly more often in the antrum than in other regions (P < 0.01). In cats, there was a statistically significant association between GHLOs and chronic gastritis in the fundus and corpus (P < 0.05). GHLOs resembling human ‘Helicobacter heilmannii’ were identified in all the dogs and cats studied by electron microscopy, and Helicobacter felis in one dog in addition. Culture was successful in three dogs and one cat; ‘H. heilmannii’ was identified in two of the dogs, and H. felis in the third dog and the cat. GHLOs were found to be common in apparently healthy dogs and cats. Based on the results of this study, one sample from the fundus and corpus is enough to demonstrate GHLOs. In cats, GHLOs may cause histological changes comparable to chronic gastritis, but in dogs this association remained unclear. It is also questionable if the histological criteria for human gastritis, used in the present study, are suitable for dogs and cats.
TL;DR: A deficiency of vitamins and folate caused by chronic gastritis in H pylori infection could lead to failure of methylation by 5-methyl-tetrahydrofolic acid and thus exacerbate the accumulation of homocysteine in susceptible patients.
Abstract: Hyperhomocysteinaemia and Helicobacter pylori infection have recently been implicated in the pathogenesis of coronary artery disease. These two risk factors, though they seem unrelated, could be linked by a deficiency of vitamins and folate caused by chronic gastritis in H pylori infection. This nutritional defect could lead to failure of methylation by 5-methyl-tetrahydrofolic acid and thus exacerbate the accumulation of homocysteine in susceptible patients. Homocysteine is toxic to endothelial cells and results in coronary artery disease.
TL;DR: The ability of some strains of H pylori to produce cytotoxin and to induce the oxidative burst in neutrophils may be important in the pathogenesis of peptic ulcer disease.
Abstract: BACKGROUND: Helicobacter pylori is associated with neutrophil infiltration within the gastroduodenal mucosa. Neutrophil activation provides a major source of oxygen free radicals, which have been implicated in the pathogenesis of peptic ulceration. AIM: To investigate if cytotoxin producing strains of H pylori are associated with the generation of oxidative burst in polymorphonuclear neutrophils (PMNs). PATIENTS: 76 patients undergoing endoscopy of whom 45 had peptic ulcer and 31 chronic gastritis only were studied. METHODS: Strains of H pylori were cultured in Brucella broth. After 48 hours, bacteria were harvested by centrifugation and a bacterial suspension prepared as a stimulus for PMN oxidative burst using chemiluminescence. PMNs were prepared from health blood donors. To test the ability of strains to produce cytotoxin, culture supernatants of each were concentrated by polyethylene glycol and tested on cultured Vero cells for intracellular vacuolation. RESULTS: 30 of 45 (66.7%) peptic ulcer patients induced cell vacuolation versus nine of 31 (29%) strains from patients with chronic gastritis only (p < 0.01). Cytotoxin positive strains of H pylori regardless of the presence or absence of peptic ulcer displayed an increased induction of respiratory burst in PMNs compared with toxin negative strains from patients with chronic gastritis only (p < 0.05). Among the toxin negative strains, those from patients with peptic ulcer did not show a significant increase of the oxidative burst than those from patients without peptic ulcer (NS). CONCLUSION: Toxinogenicity of strains of H pylori seems to be correlated with neutrophil respiratory burst and peptic ulceration. The ability of some strains of H pylori to produce cytotoxin and to induce the oxidative burst in neutrophils may be important in the pathogenesis of peptic ulcer disease.
TL;DR: It is concluded that H pylori negative 'Crohn's gastritis' seems to be associated with active Crohn's disease, while H plyori negative gastritis is relatively common in patients with Crohn’s disease.
Abstract: The frequency of gastric Crohn's disease has been considered low. This study was undertaken to determine the prevalence of chronic gastritis and Helicobacter pylori infection in patients with Crohn's disease. Oesophagogastroduodenoscopy was performed on 62 consecutive patients suffering from ileocolonic Crohn's disease. Biopsy specimens from the antrum and corpus were processed for both histological and bacteriological examinations. H pylori antibodies of IgG and IgA classes were measured in serum samples by enzyme immunoassay. Six patients (9.7%) were infected with H pylori, as shown by histology, and in five of them the infection was also verified by serology. Twenty one patients (32%) had chronic H pylori negative gastritis (negative by both histology and serology) and one of them also had atrophy in the antrum and corpus. Granulomas were found in four patients. The characteristic appearance of H pylori negative gastritis was focal and mostly mild inflammation resembling the inflammatory changes seen in the gut in Crohn's disease. Patients with H pylori negative chronic gastritis had a significantly more active disease in their gut than those with normal gastric mucosa (p < 0.01). It is concluded that H pylori positive gastritis is rare, while H pylori negative gastritis is relatively common in patients with Crohn's disease. H pylori negative 'Crohn's gastritis' seems to be associated with active Crohn's disease.
Journal Article•
TL;DR: Hp infection, frequently found in patients with non-ulcer dyspepsia, is associated with gastric mucosal inflammation; of the indices studied, serum IgG and PGC most accurately indicated Hp infection; their product may be proposed as an aid in diagnosing Hp infections in dyspeptic patients.
TL;DR: The results indicate that apoptosis plays a crucial part in the morphogenesis of gastritic mucosa including intestinal metaplasia, and that the process is correlated both with tumourigenesis and with proliferative activity.
Abstract: We examined the existence and distribution of apoptotic cells in human gastric mucosa, chronic gastritis, adenomatous dysplasias and carcinomas in 15 surgically removed stomachs in which dysplasia and carcinoma were found simultaneously. Serial sections were cut for immunohistochemistry for p53 oncoprotein and Ki-67 antigen, and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labelling (TUNEL). TUNEL signal-positive apoptotic cells were rare in normal mucosa, while a few apoptotic cells were noted in gastritic mucosa and intestinal metaplasia, intermingled with Ki-67 antigen-positive cells forming a generative cell zone. This suggests the cell-cycle-dependent apoptosis of gastric mucosa. The frequency of apoptotic cells per crypt was higher in incomplete than in complete metaplasia, implying greater underlying DNA damage in the former. TUNEL indices (TI; percentage of TUNEL-positive cells in tumour cells) were slightly higher in adenomatous dysplasias (4.9±2.1) than in carcinoma (3.9±1.1), but there was no no statistical difference. Ki-67 indices (KI; percentage of Ki-67 antigen-positive cells in tumour cells) were significantly (P<0.05) higher in carcinomas than in dysplasias. Thus, gastric adenomatous dysplasias were characterized by relatively higher TI and lower KI, which might reflect a more static growth potential. The expression of p53 oncoprotein in cancer cells is thought to be an apoptosis-suppressing event, although its precise role remains to be elucidated. Overall, these results indicate that apoptosis plays a crucial part in the morphogenesis of gastritic mucosa including intestinal metaplasia, and that the process is correlated both with tumourigenesis and with proliferative activity.
TL;DR: In genuine hypersecretors, H. pylori colonization and subsequent gastritis with atrophic and metaplastic sequelae may be limited to the antrum, while in hyposecretors gastritis predominates in the corpus, and in the latter, atrophic gastritis in the Corpus then leads to further impairment of acid output.
Abstract: Helicobacter pylori is the main cause of chronic gastritis in humans. Autoimmune mechanisms and Helicobacter heilmannii infection are other causes, both of which are of minor significance in a worldwide perspective. Atrophic gastritis is a quite common late consequence of H. pylori gastritis and will develop on a multifactorial basis, but not in all infected persons. The evolution of atrophic gastritis is a slow and gradually worsening process leading to subtypes, in which the antrum and corpus are affected to dissimilar extent and degree. The distal part of the stomach is the site where the atrophic sequelae (atrophic gastritis and intestinal metaplasia) of H. pylori infection occur most often. A minority of cases develop corpus-limited, or corpus- predominant atrophic gastritis. Along with the worsening of atrophic gastritis, inflammation and density of colonization of the mucosa by H. pylori tend to decrease in grade. In general, the degree of gastric mucosal inflammation, acute and chronic, is positively related to the degree of colonization of the mucosa by H. pylori. Acid secretion and local acidity are factors which modulate the ecology and density of colonization of H. pylori in the stomach, and may thus also modulate the evolution of chronic gastritis into topographically dissimilar subtypes. Acid secretion varies among individuals, this variation being perhaps caused by hereditary differences in parietal cell mass, or by differences in the sensitivity of parietal cells to hormonal or neural stimuli. It is hypothesized that in genuine hypersecretors, H. pylori colonization and subsequent gastritis with atrophic and metaplastic sequelae may be limited to the antrum, while in hyposecretors gastritis predominates in the corpus. In the latter, atrophic gastritis in the corpus then leads to further impairment of acid output. In these cases, H. pylori infection and gastritis may, finally, heal in the antrum, resulting in hypochlorhydria and atrophic gastritis that is limited to, or predominant in the corpus.
TL;DR: The results suggest that a combination of serum pepsinogen levels and Helicobacter pylori serology could be useful as a biomarker strategy for detection of individuals at increased risk of gastric carcinoma and for non-invasive investigation of the natural history of Helicobacterial gastritis.
Abstract: This study aimed to estimate the prevalence and type of chronic gastritis in an asymptomatic working population and to determine whether a combination of serum pepsinogen levels and Helicobacter pylori serology could be used to identify a subgroup with atrophic gastritis at elevated risk of gastric carcinoma. A 10% subsample of 544 male volunteer factory workers aged 18-63 years and participating in a larger study underwent endoscopy and biopsy. Of these men, 29 were seropositive for Helicobacter pylori; all but three (89.7%) had chronic gastritis. Serum pepsinogen A levels increased with progression from a corpus predominant pattern of gastritis through pangastritis to an antral predominant pattern. Nine subjects had corpus atrophy, which was in most cases accompanied by fasting hypochlorhydria and hypergastrinaemia. A combination of pepsinogen A below 80 ng ml-1 and Helicobaceter pylori seropositivity detected corpus atrophy with sensitivity 88.9% and specificity 92.3%. A second screening stage, using a pepsinogen A/C ratio of below 2.5 as a cut-off, resulted in a reduction in numbers requiring further investigation but with some loss of sensitivity (77.8%). Application of this two-stage screening programme to the original sample of 544 workers would have resulted in 11 (2.2%) men being selected for follow-up, excluding 25 (5.1%) false negatives. Our results suggest that a combination of serum pepsinogen levels and Helicobacter pylori serology could be useful as a biomarker strategy for detection of individuals at increased risk of gastric carcinoma and for non-invasive investigation of the natural history of Helicobacter pylori gastritis.
TL;DR: This work has shown an accurate method for detecting Helicobacter pylori in histological sections and its application in food spoilage and wound healing is feasible and effective.
Abstract: BackgroundAttempts have been made to develop an accurate method for detecting Helicobacter pylori in histological sections.
Materials and Methods.Biopsy specimens were obtained from the stomachs of 167 patients with gastric ulcer (33), duodenal ulcer (52), gastroduodenal ulcer (15), chronic gastritis (45), and normal mucosa (22) before antimicrobial treatment and from 108 of these patients after treatment. Biopsy specimens were (1) cultured, (2) fixed in 10% buffered formalin, or (3) fixed in Carnoy's solution. The latter method was employed to preserve the surface mucous gel layer (SMGL) covering gastric surface mucous cells. Histological sections were stained with hematoxylin and eosin (H&E), with immunostaining using a commercially available polyclonal anti-H. pylori antibody.
Results.Cultures were positive for H. pylori in 61% of the cases before treatment and in 16% after treatment; by HE by immunostaining using formalin-fixed materials: 78% and 21%; and by immunostaining using Carnoy-fixed materials: 85% and 41% of biopsy speciemens, respectively. The difference in detection rates between materials fixed in formalin and those in Carnoy's solution was due to the detection of H. pylori in the SMGL by the latter, especially after antimicrobial treatment.
Conclusions.Immunostaining for H. pylori using materials fixed in Carnoy's solution revealed H. pylori in the SMGL as well as on the surface mucous cells and in the gastric pits and permitted the optimal detection of H. pylori in tissue sections.
TL;DR: Investigating the acquisition rate of Helicobacter pylori infection among Finnish adults who were shown to have histologically normal, noninfected gastric mucosa in 1974–76 concluded that the current prevalence of chronic gastritis in Finland is not explained.
Abstract: Background and methods: To investigate the acquisition rate of Helicobacter pylori infection among Finnish adults, we obtained, in 1991, serum samples from 181 subjects who were shown to have histo...
TL;DR: It is concluded that the detection of a clonal population in a suspicious lymphoid infiltrate does not confirm the diagnosis of lymphoma, nor does the absence of such a population imply benignity.
Abstract: The significance of the demonstration of a clonal B-cell population in gastric lymphoid infiltrates was investigated by analysis of immunoglobulin heavy chain (IgH) gene rearrangements using sensitive polymerase chain reactions, employing fluorescently labelled primers to target the FR3 and FR1 regions. Tissue blocks were studied showing different histological features (high-grade lymphoma, low-grade lymphoma, and chronic gastritis) from 12 gastrectomies for primary gastric lymphoma, together with blocks showing chronic gastritis from 13 cases of gastric adenocarcinoma and biopsies from 33 patients with active Helicobacter-associated chronic gastritis. Clonal IgH gene rearrangements were detected in lymphoma samples from eight of the gastrectomies for lymphoma (67 per cent). In four of these eight specimens, clonal rearrangements were also detectable in the samples showing only chronic gastritis. Three of 28 (11 per cent) informative biopsies showing active Helicobacter-associated chronic gastritis had detectable clonal populations. Clonal rearrangements were also demonstrated in two of eight (25 per cent) informative blocks showing chronic gastritis from eight gastrectomies for adenocarcinoma. It is concluded that the detection of a clonal population in a suspicious lymphoid infiltrate does not confirm the diagnosis of lymphoma, nor does the absence of such a population imply benignity.
TL;DR: It is suggested that H pylori may induced duodenogastric reflux which may be important in the pathogenesis of H pylonori gastritis or carcinogenesis, or both.
Abstract: Helicobacter pylori and duodenogastric reflux are both recognised as playing aetiological roles in chronic gastritis. This study investigated whether H pylori colonisation of the antral mucosa and duodenogastric reflux are independent phenomena or have a causal relationship. Thirty eight patients (15 men, 23 women) aged (mean (SD)) 48 (17) years participated. Each patient underwent gastroscopy. Antral biopsy specimens were taken to investigate H pylori colonisation. In addition BrIDA-99mTc/111In-DTPA scintigraphy was used to quantify duodenogastric reflux. H pylori positive patients who were found to have duodenogastric reflux were treated with amoxycillin (1 g/d) and metronidazole (1.5 g/d) for seven days and four tablets of bismuth subcitrate daily for four weeks. Follow up antral biopsies and scintigraphy were repeated at six months. Duodenogastric reflux could not be found in 18 patients, including eight (44%) who were H pylori positive. Ten of the 11 patients who had duodenogastric reflux (reflux % 11.6 (9.2)), however, were H pylori positive (chi 2 = 6.26, p = 0.01). These 10 patients were given eradication treatment. At six months, in six patients who became H pylori negative, duodenogastric reflux was significantly reduced from a pretreatment value of 14.3% to 3.3% (two tail, paired t = 2.57, p = 0.016). These data suggest that H pylori may induced duodenogastric reflux which may be important in the pathogenesis of H pylori gastritis or carcinogenesis, or both.
Journal Article•
TL;DR: The findings support the precancerous nature of the various gastric lesions and the etiological role of H. pylori infection in CG.
Abstract: Gastric biopsies from 1477 participants in a chemoprevention trial for precancerous lesions of the stomach in Venezuela were evaluated for the prevalence of precancerous lesions and Helicobacter pylori infection. These study subjects were selected from participants in an early detection program for gastric cancer using double-contrast X-ray. Overall, 94% had some type of chronic gastritis (CG) and were positive for H. pylori using Giemsa stain, 49% had atrophic gastritis, 34% had intestinal metaplasia (IM), and 6.5% had dysplasia. There were only three subjects (0.2%) with normal gastric mucosa, and 4% had only superficial gastritis. The prevalence of all of these precancerous lesions increased with age, but there was no clear difference by gender. The prevalence of the various lesions was higher in the antral mucosa than in the fundic mucosa. H. pylori infection was strikingly frequent in our study population, with prevalence rates ranging from 73% in subjects with superficial gastritis to 95% in those with atrophic gastritis and IM and 98% in those with CG. The prevalence of H. pylori was equally high in males and females, and it was significantly positively associated with the degree of infiltration of poly- and mononuclear cells and with that of active regeneration; it was inversely correlated with the degree of atrophy, IM, and dysplasia. Our findings support the precancerous nature of the various gastric lesions and the etiological role of H. pylori infection in CG.
TL;DR: H. pylori played a crucial role in the local boosting of B-cell lymphoproliferation, but the underlying B- cell disorder was that associated with the autoimmune disease and was nonmalignant.
TL;DR: The results indicate that the high epithelial turnover, expressed by PCNA LI, may be an indicator of increased risk of neoplastic changes in long-standing untreated HP+ chronic gastritis.
Abstract: Helicobacter pylori (HP) infection is the main etiopathogenetic agent responsible for inflammatory and ulcerative changes in gastroduodenal mucosa and the basis for both intestinal and diffuse types of gastric carcinoma. In this latter case, intestinal metaplasia is the intermediary between gastritis and cancer. In this study we describe the proliferative activity of gastric epithelium in the progressive stages of HP infection. The expression of proliferating cell nuclear antigen (PCNA), which has proven to be a reliable method for this evaluation, was used as a marker. The study was performed on endoscopic biopsies of the gastric antrum of 40 patients, who were divided into five groups, eight in each group: normal histology and endoscopy, HP−; histological HP+ gastritis with normal endoscopy; histological HP+ gastritis with endoscopic evidence of chronic erosions; complete and incomplete intestinal metaplasia in a HP+ stomach. PCNA was detected by immunohistochemistry and expressed as labeling index, ie, percentage of positive nuclei either in the whole or upper third of foveolae. Our data show a progressive increase of epithelial proliferation in the successive stages of HP infection ranging from gastritis alone to the development of incomplete intestinal metaplasia, a well-known precancerous condition. The proliferative pattern tended to expand towards the upper foveolar third, which in normal conditions does not represent a site of epithelial renewal. These alterations may be related to the development of neoplastic transformations of gastric epithelium. It is well known that genetic mutations are facilitated in proliferating cells. Therefore, our results indicate that the high epithelial turnover, expressed by PCNA LI, may be an indicator of increased risk of neoplastic changes in long-standing untreated HP+ chronic gastritis.
Journal Article•
TL;DR: It is concluded that the intensity of chronic inflammation (gastritis) in the corpus mucosa is inversely related to PAO, which supports the hypothesis that acid output may affect the course of H. pylori gastritis and can modulate the topographic distribution of gastritis in the stomach.
Abstract: H. pylori acquisition is the main cause of chronic gastritis in humans. After acquisition, non-atrophic gastritis appears which develops with time into atrophic gastritis in approximately one third of infected subjects. Gastritis may affect the gastric antrum, both antrum and corpus or, occasionally, corpus alone. Acid secretion and local acidity are factors which are considered to influence the ecology and flourishing of H. pylori infection in the stomach, and can, therefore, also modulate the evolution of gastritis into topographically dissimilar subtypes. In the present study, we analysed whether there occurs an association between the intensity of chronic gastritis (inflammation) of the corpus mucosa and the pentagastrin stimulated peak acid output (PAO) in 94 subjects who had an H. pylori positive, non-atrophic gastritis. It appeared that the mean PAO was significantly higher in subjects who had mild or no chronic corpus gastritis than in those who had severe corpus gastritis. The prevalence of subjects with mild or no gastritis was highest among those with a high PAO ( > or = 30 mmol/hr) and lowest among those with a low PAO ( or = 40 mmol/hr. We conclude that the intensity of chronic inflammation (gastritis) in the corpus mucosa is inversely related to PAO. This supports the hypothesis that acid output may affect the course of H. pylori gastritis and can modulate the topographic distribution of gastritis in the stomach.
TL;DR: In patients with Helicobacter pylori positive chronic gastritis, eradication of HP was accompanied by a marked reduction of the inflammatory infiltrate, and elevated levels of IL-1 beta, IL-8, TGF-beta 1, putrescine and spermidine/spermine ratio significantly dropped, while EGF mucosal content significantly increased.
Abstract: In 10 patients with Helicobacter pylori (HP) positive chronic gastritis, gastric mucosal content of lnterleukin (IL)-1β IL-8, Transforming Growth Factor (TGF)-β1, Epidermal Growth Factor (EGF) and Polyamines (putrescine, spermine and spermidine) was evaluated before and after eradicating treatment. Histologically, in all patients eradication of HP was accompanied by a marked reduction of the inflammmatory infiltrate. At the same time, at the end of the therapeutical regimen, elevated levels of IL-1β, IL-8, TGF-β1, putrescine and spermidine/spermine ratio significantly dropped, while EGF mucosal content, significantly increased.Results are discussed in terms of the reciprocal role of inflammatory cytokines, growth factors and polyamines in the evolution of the HP-associated chronic gastritis.
TL;DR: The high prevalence of Hp infection confirms the primary role of the microorganism in the pathogenesis of chronic gastritis with antral atrophy, although the bacterium is no longer present in the advanced stages of such disease.
Abstract: It has been suggested that there may be a correlation between Helicobacter pylori (Hp) infection and precancerous lesions of the stomach. However, histological evaluation of bacterial colonization in chronic atrophic gastritis shows a relatively low prevalence of the microorganism, which does not support the hypothesis. The aim of our study was to investigate the Hp serology in 95 patients with chronic gastritis with antral atrophy, with (27 cases) and without (68 cases) intestinal metaplasia, and without Helicobacter-like organisms in antral and corpus biopsy specimens. For all subjects, serum anti-Hp immunoglobulin IgG was identified by a fluorescent immunoenzymatic method (Helori-test; Eurospital), and mucosal atrophy and activity were graded histologically (Sydney System score). The serum Hp-antibody status documented the presence of current bacterial infections in 64 of 95 (67.4%) patients and previous infections in another 17 subjects. In only 14.7% of cases was there no evidence of current or previous infection. These subjects had less severe mucosal atrophy and lower inflammatory scores. In addition, there were no cases of intestinal metaplasia in such subjects. The high prevalence of Hp infection confirms the primary role of the microorganism in the pathogenesis of chronic gastritis with antral atrophy, although the bacterium is no longer present in the advanced stages of such disease. The histological evaluation of Hp colonization following the criteria of the Sydney System appears from our study to underestimate the true prevalence of the infection in the stomach when there is mucosal atrophy.
Journal Article•
TL;DR: There is a considerable interindividual variability in UBT-results for the same degree of gastritis indicating that besides the number of bacteria other factors must be of significance for the severity of inflammation.
Abstract: The urea breath test (UBT) reflects the intragastric urease activity and thus the extent of H. pylori (H.p.) burden of the mucosa. We compared UBT results with gastroscopic and histologic findings in 174 patients. H.p.density, grade and activity of the chronic gastritis type B were semiquantitatively assessed. 46% of patients were H.p.-positive. A type B gastritis was significantly (p < 0.01) associated with H.p. colonization. UBT-results significantly correlated with the grade (r = 0.53) and the activity (r = 0.45) of gastritis. They correlated better with grade and activity of the inflammation than did the H.p.-density in histology (r = 0.38 and r = 0.37). There is a considerable interindividual variability in UBT-results for the same degree of gastritis indicating that besides the number of bacteria other factors must be of significance for the severity of inflammation. Endoscopic findings apart from ulcers do not predict the presence of H.p.