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PubMed2001

Update on the pathologic approach to the diagnosis of gastritis, gastric atrophy, and Helicobacter pylori and its sequelae.

Biopsy sampling of the gastric mucosa at diagnostic endoscopy provides information that cannot be obtained otherwise. The most common indication for gastric biopsy is the need to know whether the patient is infected with Helicobacter pylori or not and whether the stomach is gastritic or not. Microscopic examination of gastric biopsy specimens gives, in addition to H. pylori status, information about the grade, extent, and topography of gastritis- and atrophy-related alterations in the gastric mucosa. This information provides further possibilities for the assessment of risk and likelihood of various gastric disorders. The presence of atrophy (loss of mucosal glands) results in failures in secretory functions of the corresponding mucosa and leads to errors in the homeostasis of normal gastric physiology. The grade of atrophy of the corpus mucosa linearly correlates with peak and maximal output of acid. The presence of advanced (moderate or severe) corpus atrophy indicates an extremely hypochlorhydric or achlorhydric stomach in which, for example, ordinary peptic ulcer is unlikely or impossible in spite of a possible H. pylori infection. Some well characterized and common topographic phenotypes of H. pylori gastritis and atrophic gastritis can be delineated as follows: Predominance or restriction of the H. pylori-related inflammation in antrum, in association with a nonatrophic corpus mucosa--of which phenotype is the most common--and with an increased risk of peptic ulcer disease, duodenal ulcer in particular ("duodenal ulcer phenotype" of gastritis); the presence of atrophic gastritis in corpus of the stomach ("corpus predominant gastritis"), which indicates a low risk of peptic ulcer and a reduction in the capacity of the patient to secrete acid; the occurrence of advanced atrophic gastritis and intestinal metaplasia multifocally in the stomach (advanced "multifocal atrophic gastritis"), which are features of a gastritis type and which also indicate a low acid secretion capacity and an increased risk of gastric neoplasias ("gastric cancer phenotype of gastritis"), suggesting a need for a careful exclusion of concomitant presence of small focal neoplastic or dysplastic lesions; and the presence of normal and healthy gastric mucosa, which indicates an extremely low risk of both peptic ulcer disease or gastric cancer and, therefore, is a finding of high clinical relevance. The presence of duodenal or gastric ulcer in conjunction with normal, healthy gastric mucosa suggests either aspirin or nonsteroidal antiinflammatory drugs to be the most likely cause of the ulcer.

Atrophy↗
PubMed2003

Gastritis and carditis.

Dyspepsia is a common clinical problem. Its causes include peptic ulcer disease, gastroesophageal reflux, and functional (nonulcer) dyspepsia. A detailed clinical description of pain does not reliably differentiate the cause. Approximately 80% of gastroscopies are performed for the investigation of dyspepsia. "Gastritis" is diagnosed endoscopically in 59% of all stomachs, although in only 3% are the changes severe. Pathologic examination of unselected gastric biopsy specimens reveals that abnormalities are present in 62-73%, but there is only a weak correlation between endoscopic and histologic findings. For these reasons, it is recommended that endoscopic examination should always be accompanied by biopsy. Ideally, biopsies should be taken in a systematic fashion to include sampling of antrum and corpus. Recent evidence suggests that gastric infection by Helicobacter pylori initially presents as a superficial gastritis. Later it may become atrophic with development of intestinal metaplasia. The onset of atrophic changes may be related to the duration of infection, the strain of the infecting organism, associated dietary factors, or as-yet undefined host factors related to immunity. Persistent superficial gastritis predisposes to duodenal ulcer and gastric mucosa-associated lymphoid tissue lymphoma. Atrophic gastritis predisposes to gastric ulcer and adenocarcinoma. Evidence is accumulating that in some patients, pernicious anemia may be an end result of H. pylori-induced atrophic gastritis. Reactive gastropathy is a relatively common finding in gastric biopsies; in most instances it is associated with either reflux of duodenal contents or therapy with nonsteroidal anti-inflammatory drugs. Lymphocytic gastritis, eosinophilic gastritis, and the gastritis associated with Crohn's disease are distinct morphologic entities. Lymphocytic gastritis and eosinophilic gastritis have a variety of clinical associations. Carditis is a controversial topic: currently opinions are divided as to whether it is the result of gastroesophageal reflux or a proximal extension of H. pylori infection from the remainder of the stomach.

Adenocarcinoma↗
PubMed1975

The prevalence of chronic gastritis in patients with gastric ulcer.

Multiple gastric biopsies were performed with a duodenofiberscope in 58 Chinese subjects. All 58 cases had a gastric ulcer crater, demonstrated by endoscopy, or barium meal, or both. Histological sections of the gastric biopsies showed chronic atrophic gastritis in 12 (20.6%), chronic gastritis in 31 (53.4%), and acute-on-chronic gastritis in 11 (19%). Only two cases or 3.4% had normal gastric mucosa, while 54 cases or 93% had some form of chronic gastritis, on the gastric biopsy. The gastritis was associated with intestinal metaplasia in 16 cases (27.6%), while two cases had histological evidence of gastric atypia. No significant difference was found in the mean basal and peak acid outputs among the three groups of gastric ulcer cases with chronic atrophic gastritis, chronic gastritis, and acute-on-chronic gastritis. The high frequency of chronic gastritis (93%) occurring in patients with gastric ulcer in the present series suggests that chronic gastritis may be an important aetiological factor in the pathogenesis of gastric ulceration.

Adult↗
PubMed1971

Serum gastrin in chronic gastritis.

Fasting gastrin levels in serum were measured in 49 patients with different types of chronic gastritis and in matched controls. In 15 patients with established pernicious anaemia the mean (+/- S.E. of mean) level of gastrin was greatly raised (699 +/- 99 pg/ml). In 17 patients with chronic atrophic gastritis, seropositive for parietal cell antibody but with adequate vitamin-B(12) absorption, the level was also raised (476 +/- 74 pg/ml). By contrast, in "simple" atrophic gastritis seronegative for parietal cell antibody the gastrin levels were significantly lower for both diffuse atrophic gastritis (129 +/- 31 pg/ml) and multifocal gastritis (14 +/- 4 pg/ml). These levels were similar to those in the controls (46 +/- 7 pg/ml).The mechanism of the raised gastrin levels remains uncertain, but neither achlorhydria nor in vivo action of the parietal cell antibody wholly accounted for the hypergastrinaemia.We conclude that hypergastrinaemia is characteristic of gastritis associated with autoimmune reactions to gastric antigens and pernicious anaemia and that a raised serum gastrin is a useful marker of the type of gastritis that tends to progress to the gastric lesion of pernicious anaemia. The findings suggest that this type of gastritis is an essentially different disease from "simple" atrophic gastritis, and the differences in gastrin levels may be due to sparing of the antral mucosa in the autoimmune type but not in "simple" gastritis.

Achlorhydria↗
PubMed1999

Effect of Helicobacter pylori infection and its eradication on cell proliferation, DNA status, and oncogene expression in patients with chronic gastritis.

BACKGROUND: Helicobacter pylori, the main cause of chronic gastritis, is a class I gastric carcinogen. Chronic gastritis progresses to cancer through atrophy, metaplasia, and dysplasia. Precancerous phenotypic expression is generally associated with acquired genomic instability. AIM: To evaluate the effect of H pylori infection and its eradication on gastric histology, cell proliferation, DNA status, and oncogene expression. METHODS/SUBJECTS: Morphometric and immunohistochemical techniques were used to examine gastric mucosal biopsy specimens from eight controls, 10 patients with H pylori negative chronic gastritis, 53 with H pylori positive chronic gastritis, and 11 with gastric cancer. RESULTS: All patients with chronic gastritis were in a hyperproliferative state related to mucosal inflammation, regardless of H pylori infection. Atrophy was present in three of 10 patients with H pylori negative chronic gastritis and in 26 of 53 with H pylori positive chronic gastritis, associated in 18 with intestinal metaplasia. DNA content was abnormal in only 11 patients with atrophy and H pylori infection; eight of these also had c-Myc expression, associated in six cases with p53 expression. Fifty three patients with H pylori positive chronic gastritis were monitored for 12 months after antibiotic treatment: three dropped out; infection was eradicated in 45, in whom cell proliferation decreased in parallel with the reduction in gastritis activity; atrophy previously detected in 21/45 disappeared in five, regressed from moderate to mild in nine, and remained unchanged in seven; complete metaplasia disappeared in 4/14, and markers of genomic instability disappeared where previously present. In the five patients in whom H pylori persisted, atrophy, metaplasia, dysplasia, and markers of genomic instability remained unchanged. CONCLUSIONS: Chronic H pylori infection seems to be responsible for genomic instability in a subset of cases of H pylori positive chronic atrophic gastritis; eradication of H pylori infection can reverse inflammation and the related atrophy, metaplasia, and genomic instability.

Adult↗
PubMed1999

Corpus gastritis is protective against reflux oesophagitis.

BACKGROUND: Gastric acid is important in the pathogenesis of reflux oesophagitis. Acid production by the gastric corpus is reduced in corpus gastritis. AIMS: To determine whether corpus gastritis protects against reflux oesophagitis. METHODS: Patients presenting for elective oesophagogastroduodenoscopy were studied. Two biopsy specimens were taken from the antrum, corpus, and cardia and stained with haematoxylin/eosin and Diff-Quick II stains. The presence and severity of gastritis were graded according to a modified updated Sydney classification. RESULTS: Of 302 patients, 154 had endoscopic signs of reflux oesophagitis. There was no difference between patients with and controls without oesophagitis in the overall infection rates with Helicobacter pylori. Acute or chronic corpus gastritis occurred less often in patients with than those without reflux oesophagitis. Compared with controls, corpus gastritis was less severe in patients with reflux oesophagitis. The presence of acute or chronic gastritis in the corpus was significantly correlated with either type of gastritis in other areas of the stomach. In a multivariate logistic regression, age, sex, smoking status, and the presence of chronic corpus gastritis all exerted a significant influence on the presence of reflux oesophagitis. Chronic corpus gastritis was associated with a 54% reduced risk for reflux oesophagitis. CONCLUSIONS: While infection with H pylori alone may not affect the occurrence of reflux oesophagitis, the development of chronic corpus gastritis seems to be protective.

Acute Disease↗
PubMed2000

Atrophic gastritis and Helicobacter pylori infection in outpatients referred for gastroscopy.

BACKGROUND: Atrophic gastritis has been shown to be one of the long term sequelae of Helicobacter pylori infection. AIMS: To determine the prevalence of atrophic gastritis in outpatients, to study the accuracy of serological methods for revealing atrophy, and to define the association of H pylori infection with atrophic gastritis in these patients. PATIENTS/METHODS: A total of 207 consecutive outpatients referred for gastroscopy were included. Biopsy specimens from the antrum and corpus were assessed histologically according to the Sydney system. Serum samples were studied for H pylori IgG and IgA antibodies by enzyme immunoassay, CagA antibodies by immunoblot, pepsinogen I by an immunoenzymometric assay, gastrin by radioimmunoassay, and parietal cell antibodies by indirect immunofluorescence. RESULTS: Histological examination revealed atrophic gastritis in 52 (25%) of 207 patients. H pylori and CagA antibodies were strongly associated with atrophic antral gastritis but poorly associated with atrophic corpus gastritis. Low serum pepsinogen I was the most sensitive and specific indicator of moderate and severe atrophic corpus gastritis. All six patients with moderate atrophic corpus gastritis had H pylori infection but eight of 10 patients with severe atrophic corpus had increased parietal cell antibodies and nine had no signs of H pylori infection. CONCLUSIONS: Atrophic antral gastritis was strongly associated with CagA positive H pylori infection. Severe atrophic corpus gastritis was not determined by H pylori tests but low serum pepsinogen I, high gastrin, and parietal cell antibodies may be valuable in detecting these changes.

Adult↗
PubMed2001

Post-immunisation gastritis and Helicobacter infection in the mouse: a long term study.

BACKGROUND AND AIMS: Helicobacter pylori is a major cause of peptic ulcers and gastric cancer. Vaccine development is progressing but there is concern that immunisation may exacerbate Helicobacter induced gastritis: prophylactic immunisation followed by challenge with H felis or H pylori can induce a more severe gastritis in mice than seen with infection alone. The aim of this study was to investigate the relationship between immunity to Helicobacter infection and post-immunisation gastritis. METHODS: (1) C57BL/6 mice were prophylactically immunised before challenge with either H felis or H pylori. Histopathology and colonisation were assessed one month post-challenge. (2) C57BL/6 mice were prophylactically immunised against H felis infection and gastritis assessed up to 18 months post-challenge. RESULTS: Prophylactic immunisation induced a reduction in bacterial colonisation following H felis challenge which was associated with increased severity of active gastritis with neutrophil infiltration and atrophy. However, immunised mice challenged with H pylori SS1 had little evidence of pathology. Long term follow up showed that post-immunisation gastritis was evident at three months. However, from six months onwards, although immunised/challenged mice still developed gastritis, there was no significant difference between inflammation in these mice and infected controls. Post-immunisation gastritis was not associated with the serum antibody response. Immunisation prevented the formation of secondary lymphoid aggregates in the gastric tissue. CONCLUSION: The H felis mouse model of post-immunisation gastritis is the most extreme example of this type of pathology. We have shown in this model that post-immunisation gastritis is a transient event which does not produce long term exacerbation of pathology.

Analysis of Variance↗
PubMed1998

Lymphocytic gastritis and coeliac disease: evidence of a positive association.

AIMS: To investigate the prevalence of lymphocytic gastritis in patients with coeliac disease. METHODS: Gastric biopsies from 70 patients with coeliac disease were examined by light microscopy for the presence of lymphocytic gastritis, defined as 25 or more intraepithelial lymphocytes/100 gastric columnar epithelial cells. RESULTS: Lymphocytic gastritis was found in seven cases. Positive cases had a mean of 32.1 intraepithelial lymphocytes/100 columnar cells, compared with a mean of 13.9 in negative cases, and 5.15 in noncoeliac controls. No differences were found for age, sex, gastric corpus or antrum, or degree of inflammation in the gastric lamina propria. All intraepithelial lymphocytes were of T cell lineage. Cases not showing lymphocytic gastritis did however show significantly increased gastric intraepithelial lymphocytes compared with non-coeliac controls. Eighteen of 70 cases were positive for Helicobacter pylori, and four of seven cases of lymphocytic gastritis were H pylori positive; no significant difference was observed between H pylori positive and negative patients. Three cases had concomitant ulcerative enteritis, of which none showed lymphocytic gastritis, while five cases had concomitant enteropathy associated T cell lymphoma, of which one showed lymphocytic gastritis. CONCLUSIONS: Lymphocytic gastritis occurred in 10% of patients with coeliac disease. Cases without lymphocytic gastritis nevertheless showed increased gastric intraepithelial lymphocytes. Coeliac disease may on occasion be a diffuse lymphocytic enteropathy occurring in response to gluten. Lymphocytic gastritis outside coeliac disease may involve an immune response to luminal antigens, such as H pylori, not unlike the response to gluten in patients with coeliac disease.

Adult↗
PubMed1985

Chronic gastritis: dynamic and clinical aspects.

A simple method for grading gastritis is to assess the severity of round cell infiltration and the loss of normal glands, and this may be applied to both antral and body changes. However, there is, as yet, no satisfactory classification of gastritis. In population samples, gastritis shows a linear increase in age-specific prevalence so that the annual increase in the body atrophic gastritis pool up to geriatric age is constant (1.5%). In the elderly, there appears to be a retardation of the process, particularly in the antral mucosa, where some healing trend is demonstrable. This dynamic behaviour is qualitatively similar in all population samples collected in Finland and Estonia. On the other hand, the dynamic behaviour of gastritis in different subpopulations differs markedly from that in the population at large. In pernicious anemia patients and their first-degree relatives, the progression of body atrophic gastritis in its final stages is about 20 times more rapid than in a general population, while, simultaneously, antral gastritis displays a distinct healing tendency. A behaviour opposite to that in pernicious anemia is seen in patients with active or healed duodenal ulcer disease and in duodenitis: antral gastritis behaves, on the whole, similarly to that in the general population, but in the body mucosa there occurs virtually no progression with age, and the mucosa generally remains normal or at the stage of superficial gastritis. However, after antrectomy body gastritis progresses rapidly in the remnant at first, but it slows down later and then closely resembles that in the general population.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1995

Helicobacter pylori infection, serum gastrin, and gastric acid secretion in teen-age subjects with duodenal ulcer, gastritis, or normal mucosa.

BACKGROUND: Many studies have confirmed the close association of Helicobacter pylori with duodenal ulcer (DU) in adults. However, in the subtype of DU known as 'childhood' or 'early onset DU' genetic factors seem to play a prominent role in the pathogenesis. The aim of this study was to investigate the prevalence of H. pylori in teen-age subjects with DU, gastritis, and normal mucosa and to examine the relationship of H. pylori to serum gastrin levels and gastric acid secretion. METHODS: Sixty-one teen-age subjects (24 with DU, 14 with gastritis, and 23 normal subjects) were investigated for the presence of H. pylori, antral histology, gastrin levels, basal acid output (BAO), and maximal acid output (MAO). RESULTS: All 24 patients with DU and 8 of 14 with gastritis were infected with H. pylori; none of the normal subjects were infected. Mean gastritis scores and fasting serum gastrin levels were significantly higher in patients with DU or H. pylori-positive gastritis than in subjects with H. pylori-negative gastritis or normal mucosa (p < 0.05). The difference in serum gastrin levels was also significant when patients with DU were compared with those with H. pylori-positive gastritis (p < 0.05). BAO and MAO were significantly higher in patients with DU than in subjects with H. pylori-positive gastritis or normal mucosa (p < 0.05), but there was no difference between subjects with H. pylori-positive gastritis and those with normal mucosa. CONCLUSION: H. pylori infection is associated closely with teen-age DU and gastritis and with hypergastrinemia but does not affect BAO and MAO in most infected teen-age subjects.

Adolescent↗
PubMed2004

Adaptive cytoprotection through modulation of nitric oxide in ethanol-evoked gastritis.

AIM: To assess the mechanisms of protective action by different mild irritants through maintenance of gastric mucosal integrity and modulation of mucosal nitric oxide (NO) in experimental gastritis rats. METHODS: Either 200 mL/L ethanol, 50 g/L NaCl or 0.3 mol/L HCl was pretreated to normal or 800 mL/L ethanol-induced acute gastritis Sprague-Dawley rats before a subsequent challenge with 500 mL/L ethanol. Both macroscopic lesion areas and histological damage scores were determined in the gastric mucosa of each group of animals. Besides, gastric mucosal activities of NO synthase isoforms and of superoxide dismutase, along with mucosal level of leukotriene (LT)C4 were measured. RESULTS: Macroscopic mucosal damages were protected by 200 mL/L ethanol and 50 g/L NaCl in gastritis rats. However, although 200 mL/L ethanol could protect the surface layers of mucosal cells in normal animals (protection attenuated by NG-nitro-L-arginine methyl ester), no cytoprotection against deeper histological damages was found in gastritis rats. Besides, inducible NO synthase activity was increased in the mucosa of gastritis animals and unaltered by mild irritants. Nevertheless, the elevation in mucosal LTC4 level following 500 mL/L ethanol administration and under gastritis condition was significantly reduced by pretreatment of all three mild irritants in both normal and gastritis animals. CONCLUSION: These findings suggest that the aggravated 500 mL/L ethanol-evoked mucosal damages under gastritis condition could be due to increased inducible NO and LTC4 production in the gastric mucosa. Only 200 mL/L ethanol is truly "cytoprotective" at the surface glandular level of non-gastritis mucosa. Furthermore, the macroscopic protection of the three mild irritants involves reduction of LTC4 level in both normal and gastritis mucosa, implicating preservation of the vasculature.

Animals↗
PubMed2006

Expression of cytokeratins in Helicobacter pylori-associated chronic gastritis of adult patients infected with cagA+ strains: an immunohistochemical study.

AIM: To investigate the expression of different cytokeratins (CKs) in gastric epithelium of adult patients with chronic gastritis infected with Helicobacter pylori (H pylori) cagA+ strains. METHODS: The expression of CK 7, 8, 18, 19 and 20 was studied immunohistochemically in antral gastric biopsies of 84 patients. All the CKs were immunostained in cagA+H pylori gastritis (57 cases), non-H pylori gastritis (17 cases) and normal gastric mucosa (10 cases). RESULTS: In cagA+ H pylori gastritis, CK8 was expressed comparably to the normal antral mucosa from surface epithelium to deep glands. Distribution of CK18 and CK 19 was unchanged, i.e. transmucosal, but intensity of the expression was different in foveolar region in comparison to normal gastric mucosa. Cytokeratin 18 immunoreactivity was significantly higher in the foveolar epithelium of H pylori-positive gastritis compared to both H pylori-negative gastritis and controls. On the contrary, decrease in CK19 immunoreactivity occurred in foveolar epithelium of H pylori-positive gastritis. In both normal and inflamed antral mucosa without H pylori infection, CK20 was expressed strongly/moderately and homogeneously in surface epithelium and upper foveolar region, but in H pylori -induced gastritis significant decrease of expression in foveolar region was noted. Generally, in both normal antral mucosa and H pylori-negative gastritis, expression of CK7 was not observed, while in about half cagA+ H pylori-infected patients, moderate focal CK7 immunoreactivity of the neck and coiled gland areas was registered, especially in areas with more severe inflammatory infiltrate. CONCLUSION: Alterations in expression of CK 7, 18, 19 and 20 together with normal expression of CK8 occur in antral mucosa of H pylori-associated chronic gastritis in adult patients infected with cagA+ strains. Alterations in different cytokeratins expression might contribute to weakening of epithelial tight junctions observed in H pylori-infected gastric mucosa.

Adult↗
PubMed2005

Gastritis in Saudi Arab children.

OBJECTIVE: Information on childhood gastritis in developing countries is rare; hence, the objective of this study is to report the pattern of this condition in Saudi Arab children. METHODS: Data analysis were carried out in all children <18 years of age who were referred for endoscopy at King Khalid University Hospital, Riyadh, Kingdom of Saudi Arabia from 1993 to 2002. Only children with histology-proven gastritis were included. RESULTS: One hundred and seventy-five patients out of 851, referred for the investigation of gastrointestinal symptoms, had histology-proven gastritis; whereas only 110/851 (13%) had endoscopic features of gastritis. Most of the children (96%) were Saudi nationals, the age ranged between 4 days to 18 years, and the male to female ratio was 0.4:1. The most common presentation of gastritis was abdominal pain in 42%, followed by combination of abdominal pain and vomiting in 20% and vomiting alone in 18% of the children. Rare but important presentations included refractory anemia, melena and halitosis. The prevalence of gastritis increased with age from 9% in children <5 years of age to 42% in adolescents 16-18 years of age. Likewise, the prevalence of Helicobacter pylori (H. pylori) gastritis increased from 47% in children <5, to 62% in the 6-15 year age group, and 69% in the 16-18 years old adolescents. Endoscopy was normal in 74/175 (42%) of histologic gastritis and the prevalence of H. pylori gastritis was the highest in cases of endoscopic nodularity (92%) CONCLUSION: Compared to findings from various parts of the world, this report document a similar clinical pattern, but high prevalence of H. pylori gastritis in Saudi Arab children.

Adolescent↗
PubMed2006

[Corpus gastritis -- Helicobacter pylori -- gastrin].

OBJECTIVE: Corpus gastritis is a common diagnosis. Studies have shown that about 25% of patients that undergo gastroscopy receive this diagnosis. This study was undertaken to investigate etiological associations in patients with corpus gastritis in our northern Icelandic population. MATERIAL AND METHODS: Patients who had had a histological diagnosis of chronic corpus gastritis between the years of 1994 to 1998 were retrieved from the computer files of the department of pathology. In all 172 patients fulfilled the Sydney pathological criteria. Pathology review was performed by the same pathologist. Blood samples were also taken for variable serology and a urea breath test for Helicobacter pylori (H. pylori) was performed. RESULTS: Mean age 71 year old (24-99 year). Males were 57%. H. pylori infection was diagnosed in 39%. There appears to be a relationship between active gastritis and H. pylori positivity, especially if there was only chronic gastritis without atrophy or metaplasia. Atrophy was significantly greater if anti-parietal antibody was present. No connections were found between anti-parietal antibody and anti-microsomal antibody. There was significantly higher mean gastrin levels in patients with atrophy or metaplasia compared with only chronic gastritis (p<0.05), present also in patients with chronic gastritis vs active gastritis (p<0.01). There was no difference in mean gastrin levels between H. pylori positive and H. pylori negative patients. Significantly higher mean gastrin levels were seen in patients with anti-parietal antibody (p<0.001). No difference was found in mean gastrin levels between patients with or with out antimicrosomal antibody. CONCLUSIONS: There is a high probability that corpus gastritis and related complications are related to H. pylori infection in a large proportion of our population. Serum gastrin may well be a predictor of the histological grading of the chronic gastritis. We did not see a relationship with antimicrosomal activity.

Adult↗
PubMed1979

Endoscopic, histological and ultrastructural correlations in chronic gastritis.

Thirty-three patients presenting with dyspepsia were examined with the Olympus Fiber-gastroscope. An endoscopic diagnosis was made in each case and multiple gastric biopsies were obtained for histological and ultrastructural assessment. The endoscopic, histological and ultrastructural findings were compared with each other. Of 33 patients endoscoped, 29 were found to have endoscopic evidence of various types of gastritis and all of these latter had histological evidence of some form of gastritis. Histological confirmation of specific types of endoscopically diagnosed gastritis, however, was only found in 3/9 cases of chronic atrophic gastritis (CAG), 10/14 cases of chronic (superficial) gastritis (CG) and in none of six cases of acute gastritis (AG), indicating that endoscopic diagnosis of specific types of gastritis is relatively inaccurate. Endoscopic diagnosis should thus be restricted to presence or absence of gastritis, leaving the specific typing to histological assessment of the gastric biopsies. Multiple gastric biopsies should be obtained even though the gastric mucosa appears normal endoscopically, since histological evidence of gastritis was found in three out of four cases with endoscopically normal gastric mucosa. Comparison of histological diagnosis with electron microscopy showed that generally there is good correlation between the severity of the histological changes and the ultrastructural grade of damage as defined in this study. It would appear that E.M. examination of the gastric biopsies will not significantly increase the diagnostic accuracy of light microscopy, although it has elucidated the various cellular changes which characterize chronic gastritis. The rough surface contours, the large gastric pit and the increasing number of surface microvilli, seen by scanning E.M., aid the grading of the disease process. Some of these changes are reflected in observations made by transmission E.M. where in addition the basal intercellular edema of the mucosal layer and the appearance of electron-dense mucosal lining cells are observed. The latter, which are the counterpart of "intestinal metaplasia", possess mucus granules which resemble those of gastric mucosal lining cells or intestinal goblet cells, or both.

Adult↗
PubMed1995

[Residual gastritis after gastrectomy and Helicobacter pylori--its clinical significance].

Residual gastritis after gastrectomy brings the various symptoms such as abdominal pain, nausea, emesis and loss of appetite, and often hazards quality of life of the patient. Bile reflux to the stomach is believed as one of the important pathogenesis of residual gastritis, however the prevention for bile reflux cannot always heal the gastritis. Helicobacter pylori (H. pylori) is considered as one of the most important pathogenesis of gastroduodenal ulcer and gastritis, and H. pylori may possibly cause residual gastritis after gastrectomy. However, the association between infection with H. pylori and the residual gastritis has not revealed yet. In the present study, the association with H. pylori and the residual gastritis after gastrectomy was investigated in 56 patients who had undergone gastrectomy before. Twenty-four patients (42.9%) had H. pylori infection at their stomachs and the incidence of the infection in the patients with gastrectomy was significantly higher with subtotal gastrectomy. As for the histological gastritis score of Rauws (Rauws' score), Rauws' score of H. pylori positive group was significantly higher than H. pylori negative group. Furthermore, the eradication of H. pylori for the patients with serious symptoms of gastritis improved the symptoms and decreased significantly Rauws' score. These results suggest that H. pylori was associated with the pathogenesis of residual gastritis after gastrectomy.

Adult↗
PubMed1982

[Morphology of chronic gastritis].

The objective of the paper is the specification of morphological criteria for the diagnostics of chronic gastritis. Biopsies, taken from the antral and corporal mucosa of 317 patients, were studied. Light chronic superficial gastritis was established in 184 cases. Manifested chronic superficial gastritis--in 178 cases, 119 of them in the antrum. Chronic gastritis with initial atrophy of the glands was established in II cases, and complete--in one. Chronic gastritis with intestinal metaplasia was observed in the antral mucosa mainly, and with various degrees of glandular atrophy both in case of the chronic superficial gastritis and chronic gastritis. The chronic gastritis with some changes in the glands, but without atrophy--47 cases, is of particular interest. The intestinal metaplasia as well as the pylorization of the corporal glands in chronic gastritis with changes in the glands without atrophy are a manifestation of dysregeneratory disorders and disturbance in the coordination between the phases of proliferation and differentiation.

Biopsy↗