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At least 343 records · Page 19Linked to original sources
PubMed2003

Histology of gastritis and Helicobacter pylori infection in Thailand: a nationwide study of 3776 cases.

BACKGROUND: Dyspepsia is a very common problem in Thailand. Etiology of gastritis, incidence of Helicobacter pylori and mode of transmission of Helicobacter pylori infection in the country was proposed. METHODS: A nation-wide study of gastric biopsy in 3776 dyspeptic patients from six different geographic regions for incidence of gastritis, type of gastritis, incidence of H. pylori infection, gastric atrophic change and intestinal metaplasia in three age-groups of each region was done. RESULTS: 58.7% of dyspeptic patients had histological gastritis. Pangastritis was the most common type (77.3%) with mostly mild active inflammation (60.6%) and was found most commonly in the age group 31-60 years. Incidence of gastritis was slightly lower in the coastal and peninsular community compared with the mountain, jungle, semiarid plateau and fertile plain communities. Geographic factor, socioeconomic status and dietary habit were proposed to be important factors in inducing gastritis. H. pylori infection was found in 48.2% of dyspeptic patients with high incidence in the age-group 31-60 years (63.7%) and 98.2% of H. pylori infection was found to be associated with gastritis. Semi-arid plateau, mountain, jungle and fertile plain communities had high incidences of H. pylori infection varying from 54.0 to 67.1% while the coastal and peninsular communities had low incidences of 32%. Oral to oral spread is proposed to be the mode of bacterial transmission. Incidences of gastric atrophic change and intestinal metaplasia were low in this country and were found in 11.6% and 8.2% of subjects, respectively, with no significantly different distribution in geographic regions. Type I or intestinal type was found to be the most common type of intestinal metaplasia.

Adult↗
PubMed1996

Antigenic mimicry between Helicobacter pylori and gastric mucosa in the pathogenesis of body atrophic gastritis.

BACKGROUND & AIMS: The majority of patients with Helicobacter pylori infection have autoantibodies cross-reacting with gastric antigens. In this study, the relation between autoantibody status, histopathology of body mucosa, and antigenic profile of H. pylori was investigated. METHODS: One hundred patients were examined for H. pylori infection, body gastritis, and gastric autoantibodies. Balb/c mice were analyzed for serum autoantibodies after immunization with H. pylori from patients with and without atrophic gastritis. RESULTS: Immunoglobulin G autoantibodies were detected in 57 of the 87 infected patients (65.5%) but in none of the 13 patients without infection and gastritis. The autoreaction involved mainly the luminal surface of glandular cells and secretory canaliculi of parietal cells. The autoantibody status correlated with the presence and degree of inflammation and atrophy of the glands. H. pylori from patients with atrophic gastritis showed a higher capacity to induce autoantibodies than H. pylori from patients with a minimal superficial gastritis. Monoclonal antibodies showed differences in the bacterial expression of cross-reacting determinants. CONCLUSIONS: H. pylori-mediated autoimmunity is involved in the pathogenesis of chronic atrophic gastritis. The grade of antigenic mimicry of the infecting H. pylori strain plays a role in the progression of chronic gastritis to atrophy.

Adolescent↗
PubMed2002

Altered expression and allelic association of the hypervariable membrane mucin MUC1 in Helicobacter pylori gastritis.

BACKGROUND & AIMS: Infection with Helicobacter pylori causes chronic gastritis, and this confers a risk of gastric cancer. Short alleles of the membrane-bound mucin MUC1, which has a large extracellular highly glycosylated domain and is highly polymorphic due to variation in the number of tandemly repeated (TR) 20-amino acid units, have been shown to be associated with gastric cancer. Our aim was to investigate the involvement of MUC1 in chronic gastritis and, by implication, gastric cancer. METHODS: Immunohistochemical analysis was performed on endoscopic biopsy specimens from 95 patients. Gastritis was classified using the Sydney System, and H. pylori status was determined. MUC1 was detected with antibodies against different epitopes of the TR region and the cytoplasmic tail. Southern blot analysis of the MUC1 gene was performed on 57 Northern European patients to determine TR allele lengths. RESULTS: With the TR antibodies, apical staining and some perinuclear staining was seen in 34 of 41 biopsy specimens classified as histologically normal and H. pylori negative. None of the 36 biopsy specimens with gastritis and current H. pylori infection showed apical staining. In contrast, the cytoplasmic tail antibody detected apical staining in both groups. Comparison of the MUC1 allele length distributions between Northern European patients with H. pylori infection and those without H. pylori gastritis showed a statistically significant difference in distribution, with shorter alleles associated with H. pylori gastritis. CONCLUSIONS: Our results suggest that H. pylori interacts with MUC1 and that there are functional allelic differences that affect susceptibility to gastritis.

Alleles↗
PubMed2002

Close correlation of intestinal metaplasia and corpus gastritis in patients infected with Helicobacter pylori.

BACKGROUND: The role of intestinal metaplasia as a precancerous condition for Helicobacter pylori associated gastric carcinoma has been the subject of numerous investigations. The aim of the present study was to investigate whether other diffuse gastritis markers such as H. pylori gastritis in the corpus correlate with the presence of intestinal metaplasia and gastric carcinoma. METHODS: The histological records of 2,000 patients with H. pylori gastritis were retrospectively investigated for grade/activity of gastritis, and presence of intestinal metaplasia. RESULTS: There was a strong correlation between the degree and activity of H. pylori gastritis in the corpus and the presence of intestinal metaplasia in antrum or corpus (all P < 0.001). Intestinal metaplasia and pronounced corpus gastritis were found predominately in H. pylori infected persons with gastric cancer or benign gastric ulcers. CONCLUSIONS: On the basis of its close correlation with intestinal metaplasia, pronounced corpus gastritis may be considered as a marker of gastric cancer. In comparison with intestinal metaplasia, this marker of gastric cancer risk has the advantage of being associated with less interobserver variation, and - due to its diffuse presentation - a lower risk of sampling bias.

Biopsy↗
PubMed1988

Gastritis. Bringing this enigma into sharper focus.

Type A and type B (probably Campylobacter pylori) gastritis are distinct clinical (but largely asymptomatic) and histologic entities that can be separated from other disease processes. While the association of C pylori gastritis with peptic ulcer disease is well documented, no causal relationship has been established. Acute inflammatory conditions of the stomach secondary to other disease processes, macroscopic abnormalities of the gastric mucosa, and sometimes poorly characterized epigastric pain all carry the name "gastritis." The fact that, as a disease, gastritis remains an enigma largely stems from the multiple implications of the term. An accurate classification system of the gastritides would be helpful but is not yet available. Until it is, the term "gastritis" will have more meaning if accompanied by a description of the type of gastritis or of the responsible etiologic factor, secondary disease, or toxic insult (eg, gastric mucosal injury associated with use of nonsteroidal antiinflammatory drugs). Deletion of the term "gastritis" from the clinical vocabulary and substitution of better terms (eg, "nonulcer dyspepsia," "irritable bowel syndrome") will also serve to clarify the issue.

Campylobacter Infections↗
PubMed2003

Comparative classification and grading of Helicobacter pylori gastritis in patients with gastric cancer and patients with functional dyspepsia.

BACKGROUND: It has previously been shown that corpus-dominant grade and activity of Helicobacter pylori gastritis in combination with intestinal metaplasia in the antrum or corpus are risk markers for the development of stomach cancer. If one point is scored for each of these three parameters, a gastric cancer risk index is obtained that permits prediction of the risk of gastric cancer developing on the soil of H. pylori gastritis. The aim of the present study was to evaluate the accuracy of the gastric cancer risk index based on a large number of patients compared with dyspeptic controls. METHODS: In 415 biopsied patients with gastric carcinoma, biopsy specimens taken from the antrum and corpus were investigated retrospectively. From this group of patients, 244 patients positive for H. pylori were compared with 244 sex- and age-matched H. pylori-infected patients with functional dyspepsia. RESULTS: H. pylori gastritis was detected in 395 carcinoma patients (95.2%). The 244 sex- and age-matched patients significantly more frequently had corpus-dominant H. pylori gastritis (compared with NUD controls). The incidence of intestinal metaplasia was also significantly increased. For a gastric cancer risk index score of 3 points (i.e. corpus pronounced grade and activity of gastritis, and intestinal metaplasia in antrum or corpus), a sensitivity of 93% and a specificity of 85% for the presence of gastric carcinoma can be calculated. CONCLUSION: Using the proposed risk index, the topographic grading of H. pylori gastritis in the antrum and corpus enables the diagnosis of a 'risk gastritis' to be made.

Adult↗
PubMed2005

Long-term morpho-functional development of Helicobacter pylori-induced gastritis in Mongolian gerbils.

OBJECTIVE: Epidemiological studies have shown that Helicobacter pylori infection with associated chronic gastritis is the main risk factor for development of gastric cancer. The aim of this study was to investigate the long-term development of H. pylori-induced gastritis in Mongolian gerbils in terms of morphology, gastrin secretion, epithelial proliferation and gene expression of pro-inflammatory cytokines. MATERIAL AND METHODS: A total of 133 gerbils were inoculated with H. pylori and 62 served as controls. The gerbils were killed at different time-points between 6 and 94 weeks after inoculation. Serum concentrations of anti-H. pylori IgG and gastrin were determined by enzyme-linked immunoabsorbent assay (ELISA) and radioimmunoassay (RIA), respectively. Epithelial proliferation was evaluated immunohistochemically after labeling with 5-bromo-2'-deoxy-uridine. Gene expression of beta-actin, interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) were measured by real-time reverse transcriptase-polymerase chain reaction (RT-PCR). Histological parameters of gastritis were assessed semiquantitatively and expressed as a "gastritis score". RESULTS: Serum concentrations of anti-H. pylori IgG and gastrin increased over time. Epithelial proliferation in the antrum was increased 6 weeks after inoculation, followed by increased proliferation in the corpus 32 weeks after inoculation. Gene expression of IL-1beta and TNF-alpha were increased in H. pylori-infected gerbils. Beta-actin was not a reliable endogenous control for RT-PCR. With time, gastritis expanded from the antrum to the corpus and the gastritis score increased to reach a peak 32 weeks after inoculation. Pseudopyloric metaplasia (loss of specialized cells) was a characteristic feature in the corpus mucosa. Gastric ulcers, but neither dysplasia nor carcinoma, were observed during 94 weeks of infection. CONCLUSIONS: Long-term H. pylori infection in Mongolian gerbils led to progressive gastritis, glandular atrophy, hypergastrinemia, increased epithelial proliferation and elevated gene expression of pro-inflammatory cytokines.

Actins↗
PubMed2000

Chronic atrophic gastritis and Helicobacter pylori infection among Japanese Americans in Seattle.

Gastric cancer is still a major cause of mortality due to cancer worldwide. The most common type of gastric cancer is intestinal type carcinoma, which usually occurs in stomachs containing chronic atrophic gastritis. Individuals with chronic atrophic gastritis are considered to be at increased risk for developing intestinal type carcinoma of the stomach. To examine the association between chronic atrophic gastritis and other gastric cancer risk factors, a cross-sectional study was conducted using serum samples and questionnaire information collected from 776 persons of full Japanese ancestry in the greater Seattle area in 1994. The presence of chronic atrophic gastritis and Helicobacter pylori infection was determined by measurement of serum pepsinogen levels and H. pylori antibodies, respectively. Based on multiple logistic regression, the significant predictors of chronic atrophic gastritis were age over 50 years, H. pylori infection, and 20 years or more lived in Japan. Alcohol consumption, smoking, prior peptic ulcer, and history of gastric cancer in parents were not significantly associated with chronic atrophic gastritis. The results imply that H. pylori infection since earlier life and other unknown exposure factors in Japan might have played an important role in the development of chronic atrophic gastritis.

Adult↗
PubMed2001

Hyperplastic polyps of the stomach: associations with histologic patterns of gastritis and gastric atrophy.

Hyperplastic polyps are common gastric lesions characterized by hyperplastic foveolae with variable amounts of inflamed stroma. Their pathogenesis is unknown, but they have been reported to occur in association with various forms of chronic gastritis, particularly autoimmune gastritis and Helicobacter pylori gastritis. Comprehensive histologic evaluation of the background mucosal pathology in patients with hyperplastic polyps has not been previously performed. We studied 160 patients with gastric hyperplastic polyps and characterized endoscopic and histologic features of the polyps (i.e., location, multiplicity, and presence of dysplasia and adenocarcinoma) and the background gastric mucosa (i.e., intestinal metaplasia, dysplasia, carcinoma, and presence and classification of gastritis). Hyperplastic polyps were most common in the antrum (60%) and were multiple in 20% of patients. Focal intestinal metaplasia of the polyp was present in 16% and dysplasia in 4% of patients. Only one patient (0.6%) had adenocarcinoma within the polyp. Evaluation of the surrounding gastric mucosa showed at least focal intestinal metaplasia in 37% of patients, adenoma or low-grade flat epithelial dysplasia in 2%, and synchronous or metachronous adenocarcinoma in 6%. Eighty-five percent of patients had inflammatory mucosal pathology, most commonly active chronic H. pylori gastritis (25%), reactive or chemical gastropathy (21%), and metaplastic atrophic gastritis of the autoimmune (12%) or environmental (8%) type. These results indicate a strong association between various forms of gastritis and the development of hyperplastic polyps and further emphasize the importance of biopsy of the nonpolypoid gastric mucosa during endoscopic examination.

Adenocarcinoma↗
PubMed1996

Symptoms of gastritis due to Helicobacter pylori in children.

Infection due to Helicobacter pylori may be associated with gastritis and peptic ulcer disease in children. The aim of this study was to compare the presentation of gastritis due to H pylori with that of gastritis not associated with H pylori infection. The medical records of 296 children who had esophagogastroduodenoscopy were reviewed; 23 (8%) had H pylori gastritis, and 51 had primary gastritis without H pylori infection. Of patients with H pylori, 43% had antral nodularity and 17% had duodenal ulcers. The incidence of epigastric pain, nocturnal pain, postprandial pain, family history of peptic ulcer disease, water brash, vomiting, weight loss, fecal occult blood, and hematemesis was similar between both groups. Periumbilical pain was less common in children with gastritis than epigastric pain, and pain in the periumbilical region was present in only 4% of children with H pylori infection, compared with 31% of patients who had gastritis without H pylori infection. The presence of H pylori should be sought in children having endoscopy for evaluation of upper gastrointestinal mucosal disease.

Abdominal Pain↗
PubMed2004

Long-standing gastric mucosal barrier dysfunction in Helicobacter pylori-induced gastritis in mongolian gerbils.

BACKGROUND AND AIMS: Helicobacter pylori infection causes chronic gastritis and leads to peptic ulcer and gastric adenocarcinoma. An impaired gastric mucosal barrier could be involved in these processes. Our aim was to investigate gastric barrier function in H. pylori-induced gastritis. METHODS: Stripped gastric mucosal tissues of H. pylori-infected Mongolian gerbils (4 weeks and 70 weeks after inoculation, respectively) and controls were mounted in Ussing chambers. (51)Cr-EDTA (paracellular probe) and horseradish peroxidase (HRP, protein antigen) were used to assess mucosal barrier function. The electrophysiological parameters of the mucosa (transepithelial potential, short circuit current, and transepithelial resistance) were monitored as measurements of barrier integrity and viability. Tissue histology was performed to assess inflammation. RESULTS: In the antrum, both short-term gastritis [4.68 (3.88-5.74) x 10(-6) vs. control 2.86 (2.34-3.77) x 10(-6) cm/s, p <.001] and gastritis of long-standing [5.72 (3.88-10.94) x 10(-6) cm/s, p <.001 vs. control] showed increased permeability to (51)Cr-EDTA. In long-standing antral gastritis there was also an increased HRP flux [9.01 (2.98-45.02) vs. control 0.52 (0.06-1.20) pmol/h/cm(2), p <.001]. In the corpus, permeability to (51)Cr-EDTA was increased only in long-standing gastritis [4.63 (3.64-7.45) x 10(-6) vs. control 2.86 (2.12-3.98) x 10(-6) cm/s, p <.01]. Gastric mucosal permeability to (51)Cr-EDTA was correlated to histological inflammation and inflammatory activity. The levels of serum anti-H. pylori immunoglobulin G were positively correlated to HRP flux and (51)Cr-EDTA permeation. CONCLUSIONS: Helicobacter pylori-induced gastritis in Mongolian gerbils was associated with a long-standing gastric mucosal barrier dysfunction. The barrier defect extended from the antrum into the corpus over time. This impaired barrier function may contribute to perpetuation of chronic inflammation and may be involved in H. pylori-associated carcinogenesis.

Animals↗
PubMed2003

Food/nutrient intake and risk of atrophic gastritis among the Helicobacter pylori-infected population of northeastern Japan.

Although Helicobacter pylori (H. pylori ) infection is considered a key risk factor for atrophic gastritis, along with other environmental factors, it is still unclear which factor is involved in the development of atrophic gastritis among H. pylori-infected subjects. In the present cross-sectional study, therefore, we analyzed various dietary factors in relation to the presence of atrophic gastritis among H. pylori-infected subjects who participated in a health check-up program in a town in northeastern Japan. One thousand and seventy-one subjects (362 males and 709 females) who provided both self-administered validated food frequency questionnaires and blood samples were the basis for the study, and all of them were serologically positive for H. pylori immunoglobulin G (IgG) antibody. Among them, 663 (223 males and 440 females) were diagnosed as having atrophic gastritis on the basis of serum pepsinogen levels. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated based on tertile categories of subjects without atrophic gastritis, using logistic regression analysis. Among females, high consumptions of rice (OR = 1.6, 95% CI: 1.1-2.3), cod roe (OR = 1.5, 95% CI: 1.0-2.2) and cuttlefish (OR = 1.5, 95% CI: 1.0-2.3) were associated with a moderately increased risk of atrophic gastritis after adjustment for age (P for trend = 0.02 for these items). Among males, high consumptions of rice and miso soup showed a tendency toward an increased risk (P for trend = 0.12 and 0.13, respectively). Vegetables and fruits showed no association among either males or females. From these results, it is suggested that the dietary habits of consumers of traditional Japanese foods may play a role in the development of atrophic gastritis after H. pylori infection.

Cross-Sectional Studies↗
PubMed1998

Review article: Pathogenesis of the transformation from gastritis to malignancy.

Helicobacter pylori acquisition is the main cause of chronic gastritis in humans. In up to half of the infected subjects, chronic gastritis progresses to atrophic gastritis and intestinal metaplasia. During this course, various mechanisms are triggered that may contribute to the pathogenesis of gastric cancer. Such mechanisms include the inflammation-related cascades of cytokine and free radical reactions, up- and downregulation of growth factors and their receptors, and the atrophy-related impairment of acid output and intraluminal acidity. An array of other factors may also have become significant including overgrowth of bacteria other than H. pylori in the hypochlorhydric or achlorhydric stomach, a high dietary consumption of salt, nitrate, or nitrite, smoking, deficiency of vitamins or micronutrients, influence of sex hormones, or an inherited liability of the dividing epithelial cells to gene errors. These factors may vary in effect between populations and individuals but, if active, may affect the cell genome which may further influence the course and progression of chronic gastritis, and can finally result in overt gastric neoplasia. The molecular biology of gastric cancer has revealed a spectrum of gene errors which vary in type and extent between different histological types of cancer, and between individual cases. There now is evidence that the intestinal metaplasia or the gastric epithelium in atrophic gastritis reveal signs of abnormal expression of various regulatory genes well before the appearance of gastric neoplasia. It is possible that the mechanisms leading to mutation of the genes in epithelial cells are triggered very early in the H. pylori gastritis cascade, and that atrophic gastritis and intestinal metaplasia result from these processes.

Animals↗
PubMed2005

Occurrence and risk factors for benign epithelial gastric polyps in atrophic body gastritis on diagnosis and follow-up.

BACKGROUND: Benign epithelial gastric polyps have been reported to be more common in atrophic body gastritis. The role of Helicobacter pylori infection in the induction of gastric atrophy is well-known. The development of hyperplastic polyps may be in relation to H. pylori infection. AIM: To investigate occurrence of benign epithelial gastric polyps in atrophic body gastritis patients at diagnosis and follow-up, and the role of H. pylori and other risk factors for the development of benign epithelial gastric polyps. METHODS: A total of 259 consecutive atrophic body gastritis patients included in a follow-up programme, of whom 202 were followed up for median period of 4 years (range: 2-11). At baseline and follow-up gastroscopies, the presence of benign epithelial gastric polyps was evaluated. Biopsies for histology were obtained from all detected benign epithelial gastric polyps. RESULTS: Frequency of benign epithelial gastric polyps in atrophic body gastritis patients were 4.6% at baseline and 5.9% at follow-up. About 91.7% were hyperplastic polyps. H. pylori infection was detected in 79.2% atrophic body gastritis patients with benign epithelial gastric polyps, and in 70.8% without benign epithelial gastric polyps. Smoking was more frequent among patients with benign epithelial gastric polyps [42% vs. 20%, OR 2.8 (95% CI: 1.2-6.9)]. CONCLUSIONS: Benign epithelial gastric polyps occur in about 5% of atrophic body gastritis patients, and the vast majority are hyperplastic polyps. Smoking habit, but not H. pylori infection, increases the risk for benign epithelial gastric polyps in atrophic body gastritis patients.

Adolescent↗
PubMed1997

Effect of cisapride on functional dyspepsia in patients with and without histological gastritis: a double-blind placebo-controlled trial.

In the present double-blind placebo-controlled study the effect of cisapride on functional dyspepsia was evaluated in patients with and without histological gastritis. Patients with functional dyspepsia and whose symptoms persisted after a 2 week run-in period with antacid treatment were randomized to receive cisapride (10 mg) or matching placebo three times daily for 4 weeks. Symptoms of epigastric pain, bloating, nausea, belching, early satiety and heartburn were graded on a four-point scale based on patients' feedback and diary card recording. A global response was also formulated by the investigators. One hundred and four patients entered the study and 76 completed the trial, comprising 36 patients with histological gastritis and 40 patients without gastritis. Symptom scores in both gastritis and non-gastritis groups were significantly improved by both cisapride and placebo; however, the improvement was not statistically different between the two treatment groups. Cisapride produced a good or better global response in 58% of subjects with histological gastritis and in 53% of subjects without gastritis compared with 47% and 52%, respectively, of patients on placebo; this difference was not statistically significant. Gastric histology did not influence the effect of cisapride on the symptoms of functional dyspepsia.

Adult↗
PubMed1995

HLA-DR expression on CD8 lymphocytes from gastric mucosa in urease-positive and urease-negative gastritis.

We isolated lymphocytes from chronically inflamed gastric mucosa. We analysed the expression of IL-2 receptors (CD25), transferin receptors (CD71) and HLA-DR molecules on T lymphocytes by flow cytometric analysis in 16 patients with urease-positive and in 7 patients with urease-negative chronic gastritis. In G0, G1 and G2 histological type (Sydney classification) of gastritis the number of lymphocytes obtained from the gastric mucosa biopsies was too low for the flow cytometric analysis. However, in G3 histological type of chronic gastritis we obtained enough cells for the flow cytometric analysis in 75%. We demonstrated a significant increase in HLA-DR expression on CD8 cells from patients with urease-positive gastritis compared to urease-negative gastritis. We also observed a statistically non-significant increase in HLA-DR expression on CD3 cells, and in CD71 expression on both CD3 and CD8 cells in urease-positive gastritis. However, no difference in CD25 expression was found between the two types of gastritis.

CD3 Complex↗
PubMed1988

Campylobacter pylori is associated with chronic gastritis but not with active peptic ulcer disease.

Campylobacter pylori is supposed to be involved in the pathogenesis of gastroduodenal peptic ulcer diseases and chronic gastritis. In order to study whether the Campylobacter pylori in the stomach of peptic ulcer patients is related to ulcer itself or to a co-existing chronic gastritis, we examined the frequency of the bacteria in Giemsa stained histological sections of biopsy specimens from a series of patients with active peptic ulcer and from series of non-ulcer control subjects. We found no difference in the frequency of Campylobacter- positive cases between ulcer patients and non-ulcer controls when the comparison was done within the same category of chronic gastritis; e.g., within the category of chronic superficial gastritis 74% and 78% of cases showed the bacteria in antral biopsies from ulcer patients and from non-ulcer controls, respectively. In both ulcer patients and control subjects, in similar way in both antral and body mucosa, the Campylobacter pylori was strongly associated with chronic superficial gastritis but was more weakly associated with chronic atrophic gastritis, and the bacteria were only occasionally seen in normal mucosa. We conclude that Campylobacter pylori is associated with chronic gastritis in peptic ulcer patients but is not related to active ulcer.

Adult↗
PubMed1992

Chronic gastritis and the distribution of parietal cells in duodenal ulcer patients and normals.

Pentagastrin-stimulated acid secretion and parietal cell density were studied in 51 patients with duodenal ulcer (DU) and 26 patients without ulcer disease (non-DU). Chronic gastritis was assessed for a comparative study between parietal cell density and grade as well as the extent of gastritis. Parietal cell density was estimated with a high degree of accuracy, since the difference in cell counts of two adjacent biopsies and the inter- and intra-observer variation never exceeded 10%. The density calculated from three regional biopsies was representative for the density of the entire corpus mucosa. Parietal cell density was similar in normal mucosa, superficial chronic gastritis and mild atrophic gastritis, while fewer parietal cells were found in severe chronic atrophic gastritis. Nonuniform distribution of chronic gastritis was more frequent in DU than in non-DU, and may explain the lack of correlation between acid secretion and parietal cell number. If severe chronic atrophic gastritis is found to be localized, parietal cell density investigations will require multiple biopsies.

Chronic Disease↗