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PubMed1996

Different expression of Helicobacter pylori gastritis in children: evidence for a specific pediatric disease?

BACKGROUND: Infection with Helicobacter pylori causes active chronic gastritis. Once the infection is acquired, gastritis will persist for almost the rest of one's life. To date, very few data are available on H. pylori gastritis in relation to age. Therefore, we attempted to investigate whether H. pylori gastritis in children exhibits features different from H. pylori gastritis in adults of two different age groups. MATERIALS AND METHODS: Fifty consecutive children with a median age of 11 years (range, 3-18 years) were compared with two groups of 50 adult patients, one group with a median age of 43 (range, 19-56 years) and another group with a median age of 70 years (range, 59-86 years). All patients had H. pylori gastritis unrelated to active peptic ulcer disease. Two biopsy specimens were taken from the antrum and two from the corpus, and the following gastritis parameters were evaluated: degree and activity of gastritis, H, pylori colonization, replacement of foveolar epithelium by regenerative epithelium, mucous depletion, presence of atrophic gastritis with intestinal metaplasia, and presence of lymphoid follicles. RESULTS: Degree and activity of gastritis, extent of H. pylori colonization, degree of replacement by regenerative epithelium, extent of mucous depletion, degree of atrophic gastritis with intestinal metaplasia, and the presence of lymphoid follicles in the antrum, as well as the presence of lymphoid follicles in the corpus differed significantly (chi-square test: p < .05). All these differences--except the once frequent occurrence of atrophic gastritis with intestinal metaplasia in adults--were attributable to a higher expression of these gastritis parameters in children. CONCLUSIONS: We conclude that H. pylori gastritis, particularly in the antrum, is more severely expressed in childhood. One reason for this might be a child-specific immune response to an infection with H. pylori. Alternatively, infection may represent a pediatric disease characterized by a nonatrophic, highly expressed form of gastritis, which changes its appearance once the host becomes adapted over time.

Adolescent↗

PubMed1982

Epidemiology and dynamics of gastritis in a representative sample of an Estonin urban population.

The epidemiology and dynamics of gastritis were studied in a representative sample of an urban population of Estonia. The sample consisted of 227 subjects 15-69 years old who were examined by direct-vision endoscopic biopsy, and the data were subjected to dynamic evaluation by stochastic principles. The prevalence of antral gastritis (64%) was similar to but that of body gastritis (62%) higher than that in other population samples studied by us. Correspondingly, the prevalence of atrophic antral and body gastritis was high: 38% and 37%, respectively. The prevalence of atrophic gastritis in the antrum and body increased significantly with age. On the other hand, no sex dependence of gastritis could be demonstrated. The prevalence of gastritis mainly affecting the body (32%) was significantly higher in the present than in the other Estonian sample (19%) studied by us. Complete loss of normal body glands was found in 14 subjects, and in 8 of these the antrum was normal or only slightly altered (type A gastritis). The prevalence of gastritis mainly affecting the body increased significantly with age, whereas that of gastritis mainly affecting the antrum decreased. Dynamic evaluation disclosed two basic dynamic patterns similar to those found in other population samples: the age-specific prevalences of gastritis increased with age according to the Poisson process, and gastritis started in the antrum at a younger age, but its progression was more rapid in the body mucosa. Dynamically, the chief finding of the sample was markedly more rapid progression of the body gastritis than in other samples, which explains the high prevalence of gastritis mainly affecting the body mucosa (type A gastritis) in the present series.

Adolescent↗

PubMed1990

[Chronic gastritis. Pathogenesis, clinical aspects and therapy].

Based on clinical and histopathological features, three different types of chronic gastritis can be distinguished: gastritis A is confined to the proximal stomach and is the result of an autoimmunological process with antibodies against parietal cells and intrinsic factor. It is a rare disorder and may lead to pernicious anaemia. Distal, antral gastritis B is caused by an infection of the gastric mucosa with Helicobacter pylori (HP). Its incidence increases with age (greater than 50% above age 50). Gastritis C may be caused by drugs and alcohol but is mainly found in gastric remnants after partial resection as a consequence of biliary reflux. Gastritis A rarely causes symptoms. A relationship between gastritis B and C and non-ulcer dyspepsia (NUD) is highly controversial. Gastritis B is very closely associated with peptic ulcer disease. HP-positive antral gastritis seems to be the prerequisite for ulcer formation. All 3 types of gastritis carry an increased risk of malignancy, which seems to be positively correlated with hypoacidity, the chronicity of the inflammation and the histopathological feature of intestinal metaplasia. Noninvasive diagnostic tests (serology, breath tests, scintigraphy) are available, but the diagnosis of gastritis is still mainly based on endoscopy and biopsy. Treatment of gastritis A is not possible. Gastritis B can be healed by eradication of HP using bismuth salts and antibiotics but only combinations of 2-3 compounds seem to afford long-term positive results. Further clinical trials are needed to determine whether such treatment is justified in patients with gastritis and NUD. In patients with chronic recurrent peptic ulcers eradication of HP prevents relapses and heals ulcer disease. Gastritis C complicated by severe symptoms or ulcer can only be successfully treated by a biliary diversion, i.e. Roux-Y-gastrojejunostomy. The discovery that gastritis B is caused by HP improves our understanding of peptic ulcer disease and will change therapeutic concepts.

Algorithms↗

PubMed1998

Role of Helicobacter pylori in residual gastritis after distal partial gastrectomy.

We studied the relation between Helicobacter pylori and residual gastritis in 28 patients with gastric cancer on whom distal partial gastrectomy with Billroth I reconstruction was performed over a 13-month period. They were subjected to serologic testing along with endoscopic and histologic examinations before operation and at 3, 6, and 12 months after operation. Anti-H. pylori immunoglobulin G (IgG) and serum gastrin levels were measured by serologic tests. The presence or absence of gastritis was determined endoscopically, and gastric mucosal hexosamine levels were determined. Gastritis was measured quantitatively by histologic examination in specimens taken from the gastric mucosa using Rauws' score. After the initial histologic evaluation we divided the H. pylori-positive patients into two groups: those with a Rauws' score of 0 to 3 ("weak" gastritis group), and those with a Rauws' score of 4 to 10 ("strong" gastritis group), allowing us to compare the results of our three postoperative histologic examinations of the two groups for possible significant differences. Our endoscopic examinations showed gastric mucosal inflammatory changes in both H. pylori-positive and H. pylori-negative patients at 3, 6, and 12 months after operation, but there was no significant difference between these two groups at any point. During the histologic examinations, however, anti-H. pylori IgG assay had become negative in several patients in the "weak" gastritis group at 3 months after operation and was found to have become negative in 78% of all patients in that group 12 months after operation. In contrast, in the "strong" gastritis group H. pylori infection was still evident in the patients 12 months after operation, suggesting that "strong" histologic gastritis may have some connection to H. pylori infection, whereas "weak" histologic gastritis has no such connection. The gastric mucosal hexosamine level was higher in the "weak" gastritis group than in the "strong" gastritis group both before operation and at 6 and 12 months, indicating some relation between gastric inflammatory changes and hexosamine levels in gastric mucosa. It further suggested the possibility that H. pylori plays a role in destroying gastric mucosa by depleting mucin, thus acting as one (though not the only) cause of residual gastritis after distal partial gastrectomy. In conclusion, we found evidence that there is a relation between residual gastritis and H. pylori infection, but H. pylori is not the sole cause of residual gastritis after gastric surgery. A causal relation is difficult to detect by simple analysis of histologic findings or by endoscopic observation or clinical symptoms alone.

Female↗

PubMed2005

Gastric acidity in patients with follicular gastritis is significantly reduced, but can be normalized after eradication for Helicobacter pylori.

BACKGROUND: Follicular gastritis is thought to be caused by Helicobacter pylori infection. However, the pathophysiology of it remains unclear. MATERIALS AND METHODS: We assessed gastric acidity in 15 patients with follicular gastritis, aged 20-37 years, using a 24-hour intragastric pH-metry, as well as by histologic and serologic evaluations; and compared it with that in other age-matched groups: 18 cases of H. pylori-positive antrum-predominant gastritis, 12 of pangastritis, and 24 H. pylori-negative normals. In eight cases with follicular gastritis, it was re-assessed 6 months after the eradication therapy for H. pylori. RESULTS: During nighttime, the percentage of time with intragastric pH above 3.0 in follicular gastritis was significantly higher than that in normals (p<.0001), and in antrum-predominant gastritis (p<.001), but was comparable with that in pangastritis. In the daytime period, this parameter in follicular gastritis was significantly higher than that in normal (p<.001), in antrum-predominant gastritis (p<.001), and in pangastritis (p<.05). Marked mononuclear cell and neutrophil infiltration but no apparent glandular atrophy were observed in both the antrum and corpus. Serum pepsinogen I/II ratio was significantly lower in follicular gastritis than that in normals (p<.0001) and in antrum-predominant gastritis (p<.001), whereas serum gastrin was significantly higher than that in normals (p<.0001), in antrum-predominant gastritis (p<.01) and in pangastritis (p<.05). After eradication for H. pylori, all of the parameters in follicular gastritis were altered to the same ranges as those in normals. CONCLUSIONS: In follicular gastritis, gastric acidity is significantly reduced, but can be normalized by eradication of H. pylori. It can thus be speculated that inflammatory cytokines or H. pylori-infection-induced prostaglandins might strongly inhibit gastric acid secretion in follicular gastritis.

Adult↗

PubMed1997

A comparison of Helicobacter pylori and H. heilmannii gastritis. A matched control study involving 404 patients.

BACKGROUND: Since Helicobacter heilmannii gastritis is very much rarer than H. pylori gastritis, and no systematic studies comparing these two gastritides have so far been carried out, we undertook the present study to investigate possible differences between H. heilmannii and H. pylori gastritis. METHODS: In 202 patients with H. heilmannii gastritis and 202 matched control patients with H. pylori gastritis and duodenal ulcer the following variables were graded and compared: Helicobacter colonization, chronicity of gastritis, activity of gastritis, replacement of foveolar epithelium by regenerative epithelium, mucus depletion, frequency of acquired mucosa-associated lymphoid tissue (MALT), and intestinal metaplasia. RESULTS: In contrast to the diffuse pattern of colonization in the case of H. pylori, colonization with H. heilmannii is mainly (91.2%) focal and for the most part restricted to the antrum (only 29.1% concurrent colonization of the corpus). The gradings of all gastritis variables were statistically highly significantly milder in the case of H. heilmannii gastritis. In addition, intestinal metaplasia and acquired MALT were significantly less common in patients with H. heilmannii infection. The rare cases of erosions (n = 8) and ulcerations (n = 8) in H. heilmannii gastritis were usually associated with the use of non-steroidal anti-inflammatory drugs. In a single case of H. heilmannii gastritis a concurrent gastric carcinoma and in seven cases a low-grade gastric MALT lymphoma were found. CONCLUSION: In contrast to H. pylori infection the rare colonization of the gastric mucosa with H. heilmannii, mainly circumscribed and mostly in the antrum, induces a very much milder form of gastritis in the antrum and corpus, which may also be the reason for the rarity of concurrent erosions and ulcers. Whether the observed relatively frequent association of H. heilmannii infection and gastric MALT lymphoma is coincidental, and whether H. heilmannii gastritis is more commonly associated with MALT lymphoma than is H. pylori gastritis must be investigated in further studies.

Adolescent↗

PubMed2002

Serum levels of amidated gastrin-17 and pepsinogen I in atrophic gastritis: an observational case-control study.

BACKGROUND: Helicobacter pylori infection is often diagnosed with non-endoscopic methods, such as serology or breath or antigen stool tests. These tests provide information on the presence or absence of the H. pylori gastritis only. We investigated whether atrophic gastritis can be diagnosed and typed non-endoscopically if the serum levels of pepsinogen I (S-PGI) and gastrin-17 (S-G-17) are assayed in connection with H. pylori testing. METHODS: The present investigation is an observational case-control study comprising 100 selected dyspeptic outpatients with (cases) or without (controls) advanced (moderate or severe) atrophic gastritis. Before the blood tests, all patients underwent a diagnostic gastroscopy with multiple biopsies. The series of cases includes 56 patients. Eight had an advanced antrum limited atrophic gastritis, 13 had resected antrum (in two of whom the corpus mucosa in the stump was atrophic), and 30 had corpus-limited atrophic gastritis. Four patients had an advanced atrophic gastritis in both the antrum and corpus (multifocal atrophic gastritis), and the whole stomach was removed in one patient. Twenty of the 44 controls had a non-atrophic H. pylori gastritis. Both the antrum and corpus were normal and healthy in 24 patients. The S-PGI and S-G-17 were determined with EIA methods using monoclonal antibodies to PGI and amidated G-17. Postprandial S-G-17 (S-G-17prand) was measured 20 min after a protein-rich drink. The H. pylori antibodies were assayed with a polyclonal EIA method. RESULTS: A low S-PGI (<25 microg/l; an empirical cut-off with best discrimination) was found in 31 of 37 patients (84%) with and in 3 of 63 patients (5%) without corpus atrophy in the biopsy specimens. A low S-G-17prand (<5 pmol/l) was found in all 8 patients with H. pylori-associated antral atrophy and in 11 of 14 patients (79%) with resected antrum but in 3 of 20 control patients (15%) with H. pylori-related non-atrophic gastritis. Median and mean values of both S-G-17prand and S-PGI decreased with increasing grade of antral and corpus atrophy, respectively. Among all patients with atrophic gastritis (multifocal atrophic gastritis, or atrophic gastritis limited to antrum or corpus) or resected stomach, 50 of 56 patients (89%; Cl 95%: 81%-97%) had a low S-PGI and/or a low S-G-17prand with positive H. pylori serology. Such low values werc found in 3 of the 44 control patients (7%; CI 95%: 0%-14%). CONCLUSIONS: Low serum levels of G-17prand and PGI are conceivable biomarkers of atrophic antral and corpus gastritis, respectively. A low S-G-17prand is a sign of the multifocal or antrum-limited atrophic gastritis in patients infected with H. pylori.

Antibodies, Bacterial↗

PubMed1996

H. pylori corpus gastritis--relation to acid output.

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 ( < 30 mml/hr). Furthermore, the mean score of chronic corpus gastritis was significantly (P < 0.01) lower in those with PAO < or = 19 mmol/hr than among those with 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.

Female↗

PubMed1990

Relationship between gastrin cell number, serum, antral mucosa and luminal gastrin concentration and gastric acidity in antral atrophic gastritis.

The aim of our study was to investigate the relationship between gastrin producing cell density with antral mucosa, luminal and serum gastrin concentration in antral atrophic gastritis. Our study group consisted of 17 patients: six with mild atrophic gastritis, seven with moderate atrophic gastritis and four with severe atrophic gastritis. None of the patients had type-A atrophic gastritis but the body mucosa was affected by superficial gastritis at various extent in some. A group of 15 healthy subjects served as control. All subjects underwent gastroscopic examination with multiple bioptic sampling. Radioimmunoassay was used for gastrin determination and photomicroscopy for gastrin producing cell density assessment. Electron microscopy was used to assess the gastrin producing granule density index. Patients with moderate and severe atrophic gastritis showed a lower gastric acidity and acid output as compared to control. Serum gastrin did not show significant differences among the groups. In moderate and severe atrophic gastritis, gastrin producing cell granule density index, gastrin producing cell density and antral mucosa gastrin concentration were significantly lower when compared with control and decreased with advancing of the severity of atrophic gastritis. In atrophic gastritis, however, the latter two measurements were not correlated. In moderate and severe atrophic gastritis luminal gastrin concentration significantly increased, compared with control, after the severity of atrophic gastritis. Gastrin producing cell granule density index and luminal gastrin concentration showed a significant correlation with gastric pH. These data suggest that in antral atrophic gastritis with reduced gastric acidity, the decrement of gastrin producing cells is followed by gastrin producing cell hyperfunction with increased luminal release of gastrin.

Adult↗

PubMed1999

Predictive factors and prevalence of follicular gastritis in adults with peptic ulcer and nonulcer dyspepsia.

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.

Adolescent↗

PubMed1999

Expression of bcl-2 in autoimmune and Helicobacter pylori-associated atrophic gastritis.

Chronic atrophic gastritis can be induced either by H. pylori or by an autoimmune process. The protein product of bcl-2, which is a protooncogene, blocks apoptosis. Aberrant bcl-2 expression has been found in 68% of atrophic gastritis patients. The aim of this study was to compare bcl-2 expression in 20 autoimmune atrophic gastritis patients to that in 20 H. pylori-associated atrophic gastritis patients. Twenty patients with H. pylori antral gastritis but without atrophy served as controls. The bcl-2 expression was assessed by immunohistochemical staining of gastric biopsies, using mouse anti-human bcl-2 monoclonal antibodies. Autoimmune atrophic gastritis patients were younger, mainly females, with a significantly higher serum gastrin level than the H. pylori-associated atrophic gastritis group (P < 0.001). The bcl-2 was expressed in 10/20 (50%) of autoimmune atrophic gastritis patients, in 9/20 (45%) of H. pylori-associated atrophic gastritis patients (P = 0.73), and in 2/20 (10%) of controls. There was no correlation between bcl-2 expression and the presence of intestinal metaplasia (P = 0.35). Our findings confirm that H. pylori-associated atrophic gastritis and autoimmune atrophic gastritis are two different conditions, but with equal expression of bcl-2. Excessive expression of bcl-2 is found only in atrophic gastritis, but not in H. pylori antral gastritis without atrophy.

Adult↗

PubMed1996

The relationships between chronic gastritis and gastric acid secretion.

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.

Adolescent↗

PubMed2000

Relationship between serologically diagnosed chronic atrophic gastritis, Helicobacter pylori, and environmental factors in Japanese men.

BACKGROUND: Whereas chronic atrophic gastritis is known to be an intermediate stage in gastric carcinogenesis, information is sparse about factors associated with this precancerous lesion except for Helicobacter pylori. METHODS: In a cross-sectional study of 566 men aged 50-55 years in the Japan Self-Defense Forces, we examined the relation of H. pylori infection, smoking, alcohol use, and dietary factors to the prevalence of chronic atrophic gastritis as determined by serum pepsinogen I and pepsinogen II (I/II ratio < 3.0. and pepsinogen I < 70 ng/ml). Chronic atrophic gastritis was classified as severe when the pepsinogen I/II ratio was < 2.0, and as moderate otherwise. RESULTS: The overall prevalence of chronic atrophic gastritis was 35.7% (202 of 566). The seropositivity of H. pylori was associated with a 10-fold increase in the risk of chronic atrophic gastritis, and the association was much stronger for moderate atrophic gastritis. Neither cigarette smoking nor alcohol consumption was related to the overall risk of chronic atrophic gastritis. Consumption of vegetables and fruits was each unrelated to chronic atrophic gastritis whether examined as a whole or separately for moderate and severe atrophic gastritis. Green tea was related to decreased risk of severe atrophic gastritis, although not statistically significant, whereas garlic consumption showed no protective association. CONCLUSIONS: The findings corroborate that H. pylori infection has an important role in the development of chronic atrophic gastritis in middle-aged Japanese men. Green tea consumption may be protective against the advance of atrophic gastritis. Vegetables, fruits, or garlic had no protective effect against the development of atrophic gastritis in the study.

Alcohol Drinking↗

PubMed2001

Atrophic body gastritis patients with enterochromaffin-like cell dysplasia are at increased risk for the development of type I gastric carcinoid.

BACKGROUND/AIMS: In the presence of atrophic body gastritis, gastric carcinoid develops from gastric-body mucosa enterochromaffin-like cells. Few data exist on the prevalence of enterochromaffin-like dysplastic lesions in atrophic body gastritis patients and their presumed risk of evolution to carcinoid has never been assessed prospectively in humans. The aim of the present study was to investigate the prevalence and incidence of dysplastic and neoplastic enterochromaffin-like cell lesions in a consecutive series of patients with atrophic body gastritis. METHODS: A total of 130 atrophic body gastritis patients at diagnosis and 96 atrophic body gastritis patients at follow-up (median 30 months) underwent gastroscopy with multiple biopsies and fasting gastrinaemia evaluation. In patients with enterochromaffin-like cell dysplasia, a more detailed bioptic sampling at follow-up was performed. RESULTS: Of the 130 atrophic body gastritis patients, only one (0.7%) had a gastric carcinoid polyp, whereas enterochromaffin-like cell dysplasia was found in five patients (3.8%). At follow-up only one out of the 96 atrophic body gastritis patients (1%) was diagnosed as having a carcinoid polyp at 41 months. Enterochromaffin-like cell dysplasia was present in four additional patients (4.2%). Two atrophic body gastritis pernicious anaemia patients with enterochromaffin-like cell dysplasia developed a gastric carcinoid in the follow-up. Among nine atrophic body gastritis patients with enterochromaffin-like cell dysplasia, the incidence of carcinoid tumour was 22% compared to 1.1% of atrophic body gastritis patients without dysplasia (odds ratio: 26.00; 95% confidence interval: 2.089-323.52). During the follow-up, fasting gastrin levels increased significantly only in atrophic body gastritis patients with enterochromaffin-like cell dysplasia (mean 677.4 +/- 66.1 vs 1112.2 +/- 185.6; P = 0.0287). CONCLUSION: This study provides the first clinical evidence that, in hypergastrinaemic atrophic body gastritis patients, enterochromaffin-like cell dysplasia carries a markedly increased risk for development of type I gastric carcinoid. This suggests that a more detailed endoscopic/bioptic procedure in this subgroup of atrophic body gastritis patients is able to detect gastric carcinoid at an early stage.

Adult↗

PubMedDate not supplied

The Sydney System: epidemiology and natural history of chronic gastritis.

Chronic gastritis is a common disease which forms an important background to the pathogenesis of several gastric diseases. In most instances, gastritis seems to be a bacterial (microbial) disease. It begins as long-lasting, chronic inflammatory reaction directed against Helicobacter pylori (HP), or occasionally against other spiral bacteria, which colonize in the space between the surface epithelium and the mucous layer. Gastritis may, irrespectively of the HP-related or HP-independent origin, progress to an atrophy (chronic gastritis with atrophy) in the underlying mucosa. Prevalence of gastritis increases with increase in age, but great variations exist in the age-specific prevalence and in mean age of onset of the gastritis in different populations. A high rate and an early onset of the HP-related gastritis associates with low socio-economic status. Chronic gastritis, and the gastritis with atrophy in particular, may interfere with the function of the affected gastric mucosa, and may subsequently increase or decrease the risk of some gastric diseases, such as cancer and peptic ulcer. Both antral and corpus gastritis with coexistent severe atrophic changes have been shown to be associated with an increased risk of gastric cancer. In addition, gastritis seems to also play an important role in the pathogenesis of peptic ulcer. Virtually all patients with DU and GU have coexisting and preceding gastritis. The cumulative risk of ulcer has been estimated to be high in subjects with gastritis, but, in contrast, to be low in subjects who have normal gastric mucosa.

Adolescent↗

PubMed1990

The occurrence and extent of Helicobacter pylori colonization and antral and body gastritis profiles in an Estonian population sample.

A series of 143 subjects representing an Estonian urban population was examined for the occurrence and extent (absent, mild, moderate, severe) of Helicobacter pylori colonization in antral and body biopsy specimens (Giemsa staining). These data were correlated with the presence and grade of chronic gastritis (normal, mild, moderate, or severe superficial chronic gastritis; mild, moderate, or severe atrophic gastritis) in the antrum and the body. Gastritis of any grade was found in the antrum and/or the body in 140 (98%) subjects. The overall extent of H. pylori colonization in the whole series did not differ between the antrum and the body. Of 93 subjects with superficial gastritis, H. pylori was found in the antrum and/or the body in 87 (94%) cases. Of 47 subjects with atrophic gastritis in the antrum and/or the body. H. pylori was not found in 12 (25%). In subjects with gastritis the absence of H. pylori either in the antrum or in the body was relatively common (in 30 of 143 subjects). The grade of superficial gastritis showed a highly significantly positive correlation with the extent of H. pylori colonization in the antrum but not in the body. Correspondingly, the grade of atrophic gastritis in the antrum correlated negatively to the grade of colonization. The total absence of H. pylori was particularly associated with the absence of gastritis in the antrum. Conversely, severe body H. pylori colonization was found in subjects who had atrophic antral gastritis, and severe antral colonization in subjects who had at least moderate superficial antral gastritis and who showed a coexistent normal or slight superficial gastritis in the body.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1996

Severity of Helicobacter pylori gastritis predicts duodenal ulcer recurrence.

BACKGROUND: Helicobacter pylori gastritis is suggested to be the underlying condition leading to duodenal ulcer disease. The aim of the study was to investigate the relationship between chronic active H. pylori gastritis and the risk of duodenal ulcer (DU) recurrence. METHODS: One hundred and eighty-eight patients were followed up with regard to the evolution of their H. pylori gastritis after they had received antibacterial or acid-suppressing treatment for their DU. Four weeks, 1 year, and 2 years after treatment and in the case of DU recurrence several morphologic indicators of gastritis were studied histologically in the antrum and corpus. RESULTS: In patients who were cured of H. pylori infection a significant and long-lasting regression of all gastritis variables were observed. patients with persistent H. pylori infection after antibacterial treatment showed only a temporary regression of all gastritis variables. In the overall group of patients who received acid-suppressive therapy there was no change in gastritis. However, in the subgroup of patients who received omeprazole monotherapy, no change in the antrum but a statistically significant increase of gastritis in the corpus was observed. The grade of antral gastritis at the end of treatment was significantly and positively correlated with the risk of DU recurrence and was independent of the kind of pretreatment (18.5% recurrences in grade-2 versus 86% in grade-4 gastritis). CONCLUSIONS: The data show that the grade of gastritis is an important risk factor for duodenal ulcer recurrence. Cure of H. pylori infection is associated with healing of chronic H. pylori-associated gastritis. These data lend considerable support to the hypothesis that H. pylori gastritis is the most important factor among those leading to duodenal ulcer disease.

Chronic Disease↗

PubMedDate not supplied

[Prevalence of the various types of gastritis in patients with upper dyspeptic symptoms].

Multiple site biopsy specimens from 153 patients were examined retrospectively for the presence of gastritis and Helicobacter-like organisms (HLO). Chronic gastritis was classified as superficial gastritis, diffuse antral gastritis, postgastrectomy (reflux) gastritis, diffuse corporal atrophic gastritis, and multifocal atrophic gastritis. In some cases technical problems did not make possible to define the type of chronic gastritis and we introduce the terms unclassified gastritis and minimal inflammatory changes to name those cases. In our opinion they represent superficial biopsies from cases of diffuse antral gastritis. Diffuse antral gastritis was found in 60% of patients followed by multifocal atrophic gastritis found in 20% of patients. HLO was searched in histological sections stained by a modified Giemsa stain. The typical curved bacilli were seen in the gastric mucus or closely attached to the top of superficial or foveolar epithelial cells in 83% of patients. Although we have noted high correlation between activity of chronic gastritis and infection by HLO such correlation was not possible between the degree of activity and the degree of infection.

Adolescent↗