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PubMedDate not supplied

Chronic gastritis and Helicobacter pylori infection in University College Hospital Ibadan, Nigeria--a study of 85 fibre optic gastric biopsies.

BACKGROUND: Fibreoptic endoscopic gastric biopsy, has revealed that chronic gastritis is not only of a complex aetiological background, but also varied topographical distribution and other clinico-pathological associations. By far, the most important aetiologic association of chronic gastritis is chronic infection by the bacillus Helicobacter pylori. This study aims to highlight some of the histopathological associations between this bacterium and chronic gastritis. METHOD: We reviewed all endoscopic gastric biopsies with a histological diagnosis of chronic gastritis, with available case records and archival tissues over an 18 year period, to determine association between the various pathological features of chronic gastritis present and the presence of H. pylori infection. RESULTS: Eighty-five cases with histological diagnosis of chronic gastritis fulfilled the inclusion criteria, and Helicobacter pylori infection was found in 22.4% of them. Most patients (83.1%) with chronic gastritis had moderate to severe grades of inflammation, and most (84.2%) of the infection involved the gastric antrum. Pangastritis was uncommon (10.5%). A greater proportion of the antral biopsies (87.5%) showed moderate to severe grades of chronic gastritis as compared with 16.7% of corporal biopsies. There was an early age of acquisition of infection, starting at the second decade of life, with a peak in the 6th decade. The frequencies of atrophic gastritis and intestinal metaplasia seen complicating chronic gastritis were 16.7% and 9.4% respectively. CONCLUSION: The study shows that Helicobacter pylori infection is associated mainly with moderate to severe chronic gastritis in Nigerians. This study confirms the antral predilection of H. pylori infection, and the finding of an antral preponderance for chronic gastritis partly explains the relatively more frequent occurrence of duodenal ulcers in Nigerians as compared to gastric ulcers. Furthermore, the finding of a low prevalence of atrophic gastritis and intestinal metaplasia, as well as the rarity of pangastritis in our patients probably explains in part, the low incidence of gastric cancer in Nigeria.

Adult↗
PubMed1984

The association of histologic gastritis with gastroesophageal reflux and delayed gastric emptying.

The aims of this study were to: 1) investigate the incidence of histologic gastritis in patients with gastroesophageal reflux (GER); 2) ascertain if gastritis in GER patients could be correlated with impaired gastric emptying; and 3) determine if the presence of histologic antral gastritis correlated with other parameters of esophageal and gastric function. Twenty-three GER patients, mean age 53.3 years (range 28-68 years) with subjective and objective evidence for GER; and 20 normal subjects (13 males and seven females), mean age 28.7 years (range 19-46 years), underwent upper gastrointestinal endoscopy. Antral biopsies obtained from the greater curvature were graded as: 0 = normal; 1 = chronic gastritis; 2 = chronic active gastritis; and 3 = chronic atrophic gastritis. All patients underwent a gastric emptying study using an isotope-labeled semisolid meal. Eighteen of the 23 GER patients (78%) had histologic gastritis compared to two (10%) of the normals. No subject had endoscopic evidence of gastritis. Gradings of histologic gastritis were significantly (p less than 0.05) correlated with delayed gastric emptying. Twelve GER patients had severe gastritis (grades 2 or 3) and their gastric emptying, 79.7% +/- 5.8 (mean +/- S.E.M.) retention of isotope at 90 minutes after the meal, was significantly slower (p less than 0.01) than the 11 GER patients with either grade 0 or 1 gastritis, 56.1% +/- 5.9 retention, or the normal subjects, 51.8% +/- 1.7. We conclude that: 1) histologic gastritis is associated with GER disease; and 2) slowing of gastric emptying can be significantly correlated with increased severity of histologic gastritis in GER patients.

Adult↗
PubMed1996

[Apoptosis in chronic gastritis: correlation of glandular apoptosis with antigastric autoantibodies].

In the course of time, chronic gastritis results in gastric atrophy. A typical example is type A-gastritis. Parietal cell antibodies lead to a loss of glands in the corpus mucosa. Atrophy is preceded by a preatrophic state (active type A-gastritis). Recently, gastric autoantibodies could also be detected in Helicobacter pylori induced type B-gastritis and could be specified as canalicular and luminal antibodies. The question of this study was whether apoptosis is responsible for the loss of gastric epithelium. Gastric biopsies from normal mucosa, type B-gastritis and active type A-gastritis were analysed for the presence of apoptosis using the TUNEL-method. Type B-gastritis was subdivided in cases without autoantibodies, with canalicular and luminal autoantibodies and with both types. In each case antrum- and corpus-mucosa was available and 200 cells of the foveolar as well as of the glands were counted. Normal mucosa showed only few apoptotic cells. The number of apoptosis was significantly elevated in all cases of type B-gastritis in the whole antrum and in the foveolar epithelium of the corpus. Active type A-gastritis revealed the highest number of apoptosis in the gastric glands of corpus mucosa. Subdividing type B-gastritis the most interesting result was the cases with canalicular antibodies had a similar high number of apoptosis in the corpus glands as active type A-gastritis. These cases were in this regard significantly different from cases of type B-gastritis without autoantibodies. The findings suggest that gastric atrophy might be the result of apoptosis in the gastric epithelium and that, possibly, different types of type B-gastritis lead to atrophy in different regions of the stomach.

Adolescent↗
PubMed1983

Atrophic chronic gastritis and intestinal metaplasia in gastric carcinoma. Comparison with a representative population sample.

The occurrence of chronic gastritis and intestinal metaplasia (IM) was studied in 257 patients with gastric carcinoma (GC). In all cases biopsies were available from the benign mucosal area adjacent to the tumor, and in 139 patients from the antrum and/or body mucosa outside the tumor. The results were compared with endoscopically and bioptically examined noncancer controls representing a large Finnish population sample. For every GC patient, a control subject was matched by age and sex. In addition, a mean age-adjusted score (AAS) of chronic gastritis, which expresses the progression of gastritis in GC patients as compared with that in the general population, was calculated for GC patients. The prevalences of chronic and atrophic gastritis in the antrum and body mucosa were similar in GC patients and controls when carcinoma cases were not more specifically classified according to histologic type or location of tumors. On the other hand, the location of the tumor showed a significant relation to gastritis: the progression of gastritis was more rapid (high mean AAS value) and the prevalence of atrophic gastritis was higher in the tumor-affected area (i.e., in the antrum in patients with antral [distal] tumors; in the body in patients with body [proximal] tumors), than in the general population, but were similar in the tumor-free area in both GC patients and controls. In the intestinal type of GC (IGC), the prevalence of chronic gastritis was higher and its progression was more rapid than in controls. In the diffuse type of GC (DGC), these correlations were less distinct. In GC patients, the IM adjacent to and outside the tumor area was significantly more common and extensive than in the corresponding area of controls, and a significant positive correlation was present between the location of the tumor and the distribution of IM. Like gastritis, the IM showed a closer relationship to IGC than to DGC. In all cases of GC and particularly of IGC, the antral mucosa tended to be more severely affected by gastritis and IM than the body mucosa, i.e., the prevailing type of gastritis found in this GC series was that morphologically corresponding to the so-called B-type of chronic gastritis.

Age Factors↗
PubMed1986

Fundic atrophic gastritis in an elderly population. Effect on hemoglobin and several serum nutritional indicators.

The ratio of pepsinogen I to pepsinogen II in the circulation decreases progressively with increasing severity of atrophic gastritis of the fundic gland mucosa. Fasting blood was obtained from 359 free-living and institutionalized elderly people (age range, 60 to 99 years). A pepsinogen I/pepsinogen II ratio less than 2.9, indicating atrophic gastritis, was found in 113 (31.5%) subjects. The prevalence of atrophic gastritis increased significantly with advancing age (P less than .05). Within the atrophic gastritis group, 84 had a pepsinogen I level greater than or equal to 20 micrograms/L, indicating mild to moderate atrophic gastritis, and 29 had a pepsinogen I level less than 20 micrograms/L, indicating severe atrophic gastritis or gastric atrophy. A significant increase in the prevalences of elevated serum gastrin levels (P less than .005), low serum vitamin B12 levels (P less than .005), circulating intrinsic factor antibody (P less than .005), and anemia (P less than .025) was observed with stepwise increases in severity of atrophic gastritis. Subjects with atrophic gastritis exhibited a lower mean serum vitamin B12 level (P less than .05) and a higher mean folate level (P less than .05), but no difference was detected in mean hemoglobin levels or serum levels of iron, ferritin, retinol or alpha-tocopherol. It is concluded that serum pepsinogen I and pepsinogen II levels can be used to determine the prevalence and severity of atrophic gastritis, that atrophic gastritis is common in an elderly population, and that atrophic gastritis is associated with vitamin B12 deficiency and anemia. Further, higher folate levels in atrophic gastritis may be related to an accumulation of 5-methyl tetrahydrofolate in serum due to vitamin B12 deficiency and/or greater folate synthesis by the intestinal flora resulting from bacterial overgrowth secondary to hypo- or achlorhydria.

Aged↗
PubMed2002

Features of gastritis predisposing to gastric adenoma and early gastric cancer.

BACKGROUND/AIMS: Helicobacter pylori gastritis is a risk factor for the development of gastric cancer. The results of several studies indicate that gastric adenomas, which are considered premalignant lesions, may also be associated with H pylori gastritis. However, it is not clear whether there are different patterns of gastritis in these patients compared with patients with gastric cancer or patients with H pylori gastritis alone. Therefore, this study was designed to investigate the patterns of gastritis in these three groups of patients. METHODS: The histological features of gastric mucosa at a distance from the tumour were analysed prospectively in 118 patients with gastric adenoma (mean age, 71.8; female to male ratio, 6 : 4). In addition, for every patient with H pylori associated gastric adenoma an age and sex matched control patient with either H pylori associated early gastric cancer of the intestinal type or H pylori gastritis only was investigated. RESULTS: Only 60 patients (50.9%) with gastric adenoma were infected with H pylori. In the remaining patients, complete atrophic gastritis predominated. In those patients with adenoma and H pylori infection, the gastritis was similar to that seen in patients with early gastric cancer (median score, 2 for activity and degree of gastritis in the antrum and corpus); intestinal metaplasia was common to both groups. These two groups differed significantly from patients with H pylori gastritis only (median grade and activity of gastritis, 1 in antrum and corpus), in whom intestinal metaplasia was rare. CONCLUSIONS: It appears that gastric adenomas and gastric intestinal cancer arise by analogous mechanisms. However, owing to severe atrophic gastritis and a lower incidence of H pylori, adenomas do not appear to be definite precursor lesions for gastric cancer.

Adenoma↗
PubMed2001

[Lymphocytic gastritis--a rare disorder of the gastric mucosa].

Lymphocytic gastritis, first described by Haot et al. in 1986, is a very rare form of gastritis (0.8-1.6% of cases) with unclear pathogenesis. On endoscopy, lymphocytic gastritis may present either a normal appearance, such as gastritis varioliformis with multiple elevated chronic erosions in the corpus and fundus, or as a giant fold gastritis in the corpus and fundus. This type of gastritis is diagnosed histologically based on an accumulation of intraepithelial lymphocytes (more than 25/100 epithelial cells) in the surface cells of the gastric mucosa. Its etiopathogenesis is currently thought to be a sprue-associated reaction or an atypical reaction to Helicobacter pylori infection. Some studies report the lymphocytic gastritis in almost 45% of cases of sprue, with the gastritis regressing in response to a gluten-free diet, while others report a correlation of lymphocytic gastritis with serologically and/or histologically confirmed H. pylori infection, with the lymphocytic gastritis being cured by H. pylori eradication treatment in a high percentage of the cases. It is possible that a similar abnormal immune reaction to an inflammatory agent underlies both pathological entities, sprue and lymphocytic gastritis--in the one case gluten and in the other H. pylori--which would mean that sprue-induced and H. pylori-induced forms of lymphocytic gastritis exist side by side.

Celiac Disease↗
PubMed1999

Reflux gastritis in gastroesophageal reflux disease: A histopathological study.

Increased intragastric alkaline reflux has been documented in patients with reflux esophagitis; however, the effect on gastric histology has not been investigated in this population. We examined gastric biopsies from 72 non-acid-suppressed patients with gastroesophageal reflux disease (GERD) for changes of reflux gastritis or other forms of gastritis. In the Helicobacter pylori-negative GERD patients (n = 52) using the Dixon scoring system for reflux gastritis with a threshold score of >/=11, reflux gastritis was found in 15% (three of 20) of GERD patients with erosions and in no GERD patients without erosions. When the reflux gastropathy threshold score was changed to more than 8, 90% (18 of 20) of GERD patients with erosions and 19% (six of 32) of GERD patients without erosions were classified as having reflux gastritis. Regardless of the reflux gastritis threshold used, only 14% (seven of 52) of the H pylori-negative GERD patients exhibited normal gastric histology. Inactive chronic gastritis or nonspecific reactive changes were histologic findings in those gastric biopsies not classified as reflux gastritis or normal. All H pylori-positive GERD patients (n = 20) had active chronic gastritis. We conclude that most GERD patients will exhibit some form of gastric pathology: either reflux gastritis, chronic gastritis, or nonspecific reactive changes, depending on what reflux threshold score is applied and the presence of H pylori. Studies to define the intragastric alkaline content in conjunction with gastric histopathology need to be performed to further define those reflux esophagitis patients with reflux gastritis.

Adult↗
PubMed2001

Variation in serum pepsinogens with severity and topography of Helicobacter pylori-associated chronic gastritis in dyspeptic patients referred for endoscopy.

BACKGROUND: It has long been recognised that specific patterns of gastritis are linked with different gastroduodenal diseases and that serum pepsinogens vary with the histological state of the gastric mucosa. With the discovery of the role of Helicobacter pylori in chronic gastritis and the availability of noninvasive tests for H. pylori infection, individuals with H. pylori gastritis can now be identified without endoscopic biopsy. However, without a knowledge of the pattern and severity of gastritis it is impossible to predict the likelihood of significant associated gastroduodenal pathology. AIMS: The aim of this study was to evaluate the diagnostic potential of serum pepsinogens I and II in predicting the topography and severity of gastritis in H. pylori-infected dyspeptic patients attending for endoscopy. METHODS: Fasting serum was obtained from consecutive dyspeptic patients attending for endoscopy, and pairs of gastric biopsies obtained from the mid-body and antrum. Gastritis was graded according to the Sydney System, and serum pepsinogen levels determined by radio-immunoassay. RESULTS: Sixty-nine dyspeptic patients were studied (mean age: 49.6 years) of whom 34 had H. pylori-associated chronic gastritis (Hp-gastritis) - antral predominant gastritis (APG) in 41.2%, pangastritis (PAN) in 52.9%, and corpus predominant (CPG) in 5.9%. Serum pepsinogen II levels were significantly higher, and the serum pepsinogen I : II ratio significantly lower, in the H. pylori positive group than in other groups. Within the Hp-gastritis group, there was a step-wise decrease in serum pepsinogen I levels with progression from APG through PAN to CPG pattern (a cut-off value of > or = 100 ng/ml would have identified APG with a positive predictive value of 77%, though with low sensitivity). Within the Hp-gastritis group, serum pepsinogen I and II levels were correlated with antral chronic inflammation score and serum pepsinogen II levels also with antral activity score. Serum pepsinogen I and the pepsinogen I : II ratio were lowest in severe gastric corpus atrophy. CONCLUSION: In dyspeptic patients known to be infected with H. pylori, serum pepsinogen values provide an assessment of the overall topography of gastritis, the severity of antral inflammation and the presence of severe corpus atrophy.

Adult↗
PubMed1992

Prevalence of gastritis in patients with acromegaly: untreated and during treatment with octreotide.

OBJECTIVE: It has previously been suggested that acromegalic patients treated with the somatostatin analogue octreotide invariably have chronic gastritis. We have examined the prevalence of gastritis in a large group of acromegalic patients, untreated and during treatment with octreotide. DESIGN: We studied three groups of acromegalic patients: (A) untreated; (B) octreotide-treated; (C) a subgroup of these studied both before and during octreotide therapy. PATIENTS: Forty-eight patients, grouped as above, with active acromegaly were examined for the presence of gastritis. MEASUREMENTS: Gastroscopy and histological examination of gastric biopsies for the presence of gastritis and Helicobacter organisms were undertaken. The principal outcome was quantification of the prevalence of gastritis in the various study groups. RESULTS: Group A: 10 of the 33 patients (30%) had gastritis before any therapy with octreotide. Group B: 17 of 36 patients (47%) on octreotide treatment for 6-59 months (mean 20.5) had gastritis, and this was present in five out of the sub-group of eight patients (62%) treated for over 3 years. Group C: three of 21 patients (14%) developed gastritis during treatment with octreotide for between 6 and 23 months (mean 12.4). There was a highly significant association between the presence of gastritis and the presence of Helicobacter pylori organisms. CONCLUSIONS: Octreotide therapy of acromegaly may predispose to the development of gastritis, but this remains statistically unproven. Certainly, gastritis is not an invariable consequence of octreotide therapy, even after prolonged periods of treatment. The presence of gastritis is associated with H. pylori infection.

Acromegaly↗
PubMed2001

The updated Sydney system: classification and grading of gastritis as the basis of diagnosis and treatment.

In recent years, the importance of the histological diagnosis of gastritis on the basis of routinely obtained antral and corpus biopsies has increased enormously, which is owed not least of all to the discovery of Helicobacter pylori. The introduction of the Sydney system made it possible, for the first time, to grade histological parameters, identify topographical distribution and, finally, make a statement about the etiopathogenesis of the gastritis. Of pathogenetic importance is, in the first instance, the differentiation between gastritis with and gastritis without H pylori infection. The group of H pylori-associated gastritis can be further subdivided into forms of gastritis whose morphological distribution patterns usually identify them as sequelae of H pylori infection, while the group of gastritis unassociated with H pylori, can be differentiated into autoimmune, chemically induced reactive gastritis, ex-H pylori gastritis, Helicobacter heilmannii gastritis, Crohn's gastritis and a number of special forms of gastritis.

Biopsy, Needle↗
PubMed1989

Etiology and management of chronic gastritis.

There are reasons to believe that chronic antral gastritis and chronic body gastritis are different clinical conditions. While both are associated with aging, chronic antral gastritis is much more commonly associated with gastric or duodenal ulcer. The natural history of chronic antral gastritis in asymptomatic normals and patients with peptic ulcer appears the same. Chronic body gastritis deteriorates rapidly with age in patients with gastric ulcer, but does not progress in patients with duodenal ulcer. With spontaneous healing of duodenal ulcer, chronic antral gastritis improves but persists. All these observations suggest that gastric ulcer, duodenal ulcer, and chronic antral gastritis are involved in a common mucosal inflammatory process. C. pylori occurs commonly on the antral mucosa affected by chronic gastritis, but is found to a much less extent at the site of peptic ulceration, and spontaneous ulcer healing is not affected by the presence of the organisms. It remains to be established whether C. pylori is the cause of chronic antral gastritis, is an aggravating factor of the gastritis, or is simply an inhabitant of the inflamed antral mucosa. Other known associations of chronic gastritis include pernicious anemia, bile reflux, and gastric cancer. Whether chronic antral or body gastritis is associated with clinical symptoms remains controversial. Histological improvement can be obtained with the use of prostaglandins, sucralfate, or bismuth compounds, which have one common property--they all possess mucosal-protective mechanisms.

Chronic Disease↗
PubMed1992

Natural history of gastritis and its relationship to peptic ulcer disease.

Chronic gastritis is a common inflammatory disease. In a number of patients, the inflamed gastric mucosa shows a gradual tendency to become atrophic (atrophic gastritis). Gastritis tends to be lifelong, and spontaneous healing is rare. With very few exceptions (e.g. in patients with autoimmune chronic corpus gastritis), gastritis is associated with the presence of the bacterium Helicobacter pylori. Inflammation and atrophy of the gastric mucosa result in impairment of gastric secretory functions (e.g. secretion of gastric acid, pepsin and gastrin). Such impairment is dependent on the topographic type of gastritis; i.e. whether the inflammation and atrophy occur in the antrum (chronic antral gastritis), corpus (chronic corpus gastritis) or in both the antrum and corpus simultaneously (chronic pangastritis). Gastritis of different topographic types associates with different gastric diseases. In patients with H. pylori-related antral or pangastritis, peptic ulcer disease, and in particular duodenal ulcer, is common (with an incidence exceeding 20% after 10 years' follow-up), as compared with peptic ulcer disease, which is very rare in patients with a normal stomach. Gastric ulcer may sometimes occur in patients with a rather atrophic stomach, but both gastric and duodenal ulcers are extremely rare in patients in whom the gastritis accompanies severe atrophic changes in the corpus mucosa. Routine biopsies from the antrum and corpus, and interpretation of the results in the light of the data on gastritis and its atrophic sequelae, allow the gastroenterologist to predict the risk and likelihood of peptic ulcer disease in patients with gastritis.

Adult↗
PubMed2002

Radiographically diagnosed antral gastritis: findings in patients with and without Helicobacter pylori infection.

The purpose of this study was to characterize the radiographic findings of antral gastritis and to determine whether there are differences in the appearance of antral gastritis in patients with and without Helicobacter pylori infection. A search of radiology, endoscopy and pathology files revealed 90 patients with antral gastritis on double contrast upper gastrointestinal tract studies who had endoscopy with testing for H. pylori. The barium studies were evaluated to further characterize the findings of antral gastritis without knowledge of the H. pylori status of the patients or of the endoscopy or pathology findings. The radiographic findings of antral gastritis included thickened folds in 67 patients (74%), polypoid antral gastritis (a subset of patients with thickened folds) in 6 (9%), antral erosions in 21 (23%), enlarged areae gastricae in 14 (16%), crenulation of the lesser curvature in 4 (4%), mucosal nodularity in 2 (2%), a hypertrophied antral-pyloric fold in 2 (2%) and antral striae in 1 (1%). 43 patients (48%) with antral gastritis were H. pylori positive and 47 patients (52%) were H. pylori negative. Thickened folds were detected in 39 H. pylori-positive patients (91%) with antral gastritis vs 28 H. pylori-negative patients (60%) (p<0.001); polypoid gastritis in 6 H. pylori-positive patients (14%) vs 0 H. pylori-negative patients (p<0.05); enlarged areae gastricae in 14 H. pylori-positive patients (33%) vs 0 H. pylori-negative patients (p<0.0001); and antral erosions in 2 H. pylori-positive patients (5%) vs 19 H. pylori-negative patients (40%) (p<0.0001). Our experience suggests that antral gastritis caused by H. pylori infection is associated with characteristic features on double contrast studies (including thickened folds, polypoid gastritis and enlarged areae gastricae) and that this condition is rarely associated with antral erosions. Thus, radiologists can often suggest whether the patient's gastritis is caused by H. pylori on the basis of radiographic findings.

Adult↗
PubMed2003

Epithelial cell proliferation and glandular atrophy in lymphocytic gastritis: effect of H pylori treatment.

AIM: Lymphocytic gastritis is commonly associated with Helicobacter pylori infection. The presence of glandular atrophy and foveolar hyperplasia in lymphocytic gastritis suggests abnormalities in cell proliferation and differentiation, forming a potential link with the suspected association with gastric cancer. Our aim was to compare epithelial cell proliferation and morphology in H pylori associated lymphocytic gastritis and H pylori gastritis without features of lymphocytic gastritis, and to evaluate the effect of H pylori treatment. METHODS: We studied 14 lymphocytic gastritis patients with H pylori infection. For controls, we selected 14 matched dyspeptic patients participating in another treatment trial whose H pylori infection had successfully been eradicated. Both groups were treated with a triple therapy and followed up with biopsies for 6-18 months (patients) or 3 months (controls). Blinded evaluation for histopathological features was carried out. To determine the cell proliferation index, the sections were labeled with Ki-67 antibody. RESULTS: Before treatment, lymphocytic gastritis was characterized by foveolar hyperplasia (P=0.001) and glandular atrophy in the body (P=0.008), and increased proliferation in both the body (P=0.001) and antrum (P=0.002). Proliferation correlated with foveolar hyperplasia and inflammation activity. After eradication therapy, the number of intraepithelial lymphocytes decreased in the body (P=0.004) and antrum (P=0.065), remaining higher than in controls (P<0.001). Simultaneously, the proliferation index decreased in the body from 0.38 to 0.15 (P=0.043), and in the antrum from 0.34 to 0.20 (P=0.069), the antral index still being higher in lymphocytic gastritis than in controls (P=0.010). Foveolar hyperplasia and glandular atrophy in the body improved (P=0.021), reaching the non-LG level. CONCLUSION: In lymphocytic gastritis, excessive epithelial cell proliferation is predominantly present in the body, where it associates with foveolar hyperplasia and glandular atrophy. These characteristic changes of lymphocytic gastritis are largely related to H pylori infection, as shown by their improvement after eradication. However, some residual deviation was still seen in lymphocytic gastritis, indicating either an abnormally slow improvement or the presence of some persistent abnormality.

Atrophy↗
PubMed1992

Difference in expression of Helicobacter pylori gastritis in antrum and body.

Seven hundred seventy biopsy specimens obtained from 10 different sites in stomachs of 77 patients were examined for the presence of active chronic gastritis (ACG) and Helicobacter pylori to investigate the characteristics of gastritis in the antrum and body. Forty-eight patients with ACG at one or more sites were all H. pylori positive. H. pylori was not found in 20 patients who had chronic gastritis with no activity or in 9 patients who had histologically normal mucosa. In patients with ACG in at least one biopsy site, a strong positive topographic association between H. pylori colonization and ACG was seen in the Warthin-Starry stain. The frequency of H. pylori colonization was similar in the antrum and body. However, the incidence of ACG declined significantly proximal to the borderline between the antrum and body (P less than 0.001). The average grade of gastritis at the individual biopsy sites was distributed evenly throughout the antrum but decreased markedly in the body (P less than 0.0001). In the same manner, the average grade of H. pylori colonization decreased in the body (P less than 0.0027). The grade of H. pylori colonization in the individual biopsy specimens was closely related to the grade of gastritis (r = 0.51); also, the grade of neutrophil infiltration was related to the grade of gastritis (r = 0.79). A good correlation existed between the grade of H. pylori colonization and the grade of neutrophil infiltration (r = 0.70). The results of this study show a different expression of H. pylori gastritis in the antrum and body, which is the main subtype of chronic type B gastritis. The close topographic and graded association between the presence of H. pylori and the activity and grade of gastritis lend further support to the major pathogenic role of H. pylori in active chronic gastritis. The different expression of gastritis in antrum and body is suggested to be increased reactivity of the antral mucosa to the infection, possibly on the basis of an enhanced immunologic response to H. pylori in this region.

Adult↗
PubMed2002

Atrophic corpus gastritis and Helicobacter pylori infection in primary biliary cirrhosis.

Chronic atrophic corpus gastritis, termed as autoimmune corpus gastritis or type A gastritis, and primary biliary cirrhosis (PBC) are characterized by a common immunological process against the exocrine glandular structures of both the stomach and bile duct. However, there has been controversy over whether atrophic corpus gastritis is associated with PBC. Recently, it has been suggested that Helicobacter pylori plays an important role in the early stage of atrophic corpus gastritis due to the induction of autoantibodies that are reactive with a protein in the gastric parietal cells. One hypothesis is that molecular mimicry, possibly resulting from H. pylori infection, might be responsible for initiating an autoimmune response in a predisposed host due to cross-reactivity among gastric mucosal, bile ductular, and bacterial antigens. The aim of this study is to assess whether atrophic changes of the gastric corpus could affect patients with PBC, and to determine the correlation with H. pylori infection. Sixteen patients with PBC were enrolled in this study. All patients were examined by serological studies of anti-pyruvate dehydrogenase (PDH) antibody, anti-H. pylori antibody, gastrin and vitamin B12. Gastroscopy was performed on all patients in order to verify the histological findings and to microscopically identify H. pylori. Atrophic corpus gastritis was found in 2 of 16 patients with PBC (12.5%), one of whom was confirmed to have pernicious anemia, a developed stage of atrophic corpus gastritis. H. pylori infection in the gastric corpus and the anti-H. pylori antibody were found in 7 (43.8%) and 11 (68.8%) of 16 patients, respectively. Anti-H. pylori antibody was confirmed to be positive in both of the patients with atrophic corpus gastritis, although H. pylori was absent in the gastric biopsy specimen. There was a positive correlation between anti-PDH antibodies and anti-H. pylori antibodies in sera from patients with PBC. Atrophic corpus gastritis is not frequently involved in PBC. However, H. pylori is a possible pathogenic factor in atrophic corpus gastritis in PBC patients because of the presence of anti-H. pylori antibody. A positive correlation between the titer of anti-PDH antibodies and the titer of anti-H. pylori antibodies was confirmed. Consequently, H. pylori infection could induce autoimmune responses in the development of both PBC and atrophic corpus gastritis. H. pylori infection associated with PBC requires further study.

Adult↗
PubMed2000

Collagenous gastritis: a case report, morphologic evaluation, and review.

Collagenous gastritis is rare; there are only four previous case reports. Histologic features seem to overlap with the other "collagenous enterocolitides"; however, pathologic criteria are not yet established for the diagnosis of collagenous gastritis. We describe an additional case of ostensible collagenous gastritis in a patient who initially presented with celiac sprue and subsequently developed colonic manifestations of mucosal ulcerative colitis. Endoscopic biopsies of the stomach revealed deposition of patchy, very thick bandlike subepithelial collagen in gastric antral mucosa, focal superficial epithelial degeneration, numerous intraepithelial lymphocytes, and a dense lamina propria lymphoplasmacytic infiltrate. Image analysis evaluation of gastric antral biopsies demonstrated a mean thickness of subepithelial collagen of 27.07 micron. Morphologic comparison was made with age-matched control groups of 10 patients who had normal gastric mucosal biopsies and 10 patients who had "chronic" gastritis, which revealed mean subepithelial collagen measures of 1.37 micron and 1.19 micron, respectively. We compared these morphologic findings with those of all previous case reports of collagenous gastritis and propose a pathologic definition based on the limited combined data. It seems that subepithelial collagen is dramatically thickened in reported cases of collagenous gastritis, with a cumulative mean measure of 36.9 micron. It is also apparent from this and previous reports that the thickened subepithelial collagen is accompanied by a chronic or chronic active gastritis and sometimes intraepithelial lymphocytes and surface epithelial damage. Recently described associations of lymphocytic gastritis, sprue, and lymphocytic colitis as well as collagenous and lymphocytic colitis suggest a common pathogenesis that empirically may include collagenous gastritis in the same disease spectrum. We propose that collagenous gastritis can be confidently identified by using analogous defined features of collagenous colitis: subepithelial collagen more than 10 micron in a patchy distribution, lamina propria lymphoplasmacytic infiltrates, intraepithelial lymphocytes, and surface epithelial damage. Collagenous gastritis also seems to have the same spectrum of associated clinical findings as collagenous colitis, including frequent coexistence of celiac sprue, watery diarrhea syndrome, and female predominance.

Adolescent↗