Showing papers on "Chronic gastritis published in 1990"

Bacterial adhesion and disease activity in Helicobacter associated chronic gastritis.

Abstract: Ultrastructural examination of biopsies showing Helicobacter pylori associated chronic gastritis reveals close attachment between gastric surface epithelial cells and the organism. The finding of 'adhesion pedestals', which represents a cellular response to the presence of the organism, is analogous to the response of intestinal cells to enteropathogenic E coli. Thus the development of bacterial attachment sites in H pylori associated gastritis might be an indication of pathogenicity. We have therefore explored the relationship between the proportion of organisms forming attachment sites and histological indices of disease 'activity'. Antral biopsies from 40 patients with H pylori positive gastritis were examined histologically and ultrastructurally, and the percentage of attached organisms compared with subjective assessments of epithelial degeneration, mucin depletion, polymorphonuclear and chronic inflammatory cell infiltration. We found a significant increase in the proportion of attached bacteria in cases showing histological epithelial degeneration, and a significant decrease in cases showing intraepithelial polymorph infiltration. The direct relationship between bacterial attachment and cellular degeneration lends further support to a pathogenic effect. Reduced attachment in the face of polymorph infiltration might indirectly reflect aspects of the immune response--namely, blocking of adhesion by IgA, with complement activation and generation of leucotactic factors.

Cumulative 10-year risk of symptomatic duodenal and gastric ulcer in patients with or without chronic gastritis. A clinical follow-up study of 454 outpatients.

Abstract: The cumulative rate of symptomatic peptic ulcer (PU) was examined in a 10-year clinical follow-up study of 454 consecutive outpatients who had undergone diagnostic gastroscopy, from whom routine biopsy specimens were taken from the antral and corpus mucosa, and who were found to be ulcer-free before and at the time of this initial gastroscopy. During the follow-up period 34 (11%) of 321 patients who showed gastritis in the biopsy specimens at the initial gastroscopy had contracted symptomatic PU (18, 5, 7, and 4 cases of duodenal, pyloric, antral, and angular or corpus ulcer, respectively), which was verified by endoscopy. Only 1 (0.8%) of 133 patients with normal antral and corpus mucosa had contracted PU. It was calculated that the 10-year cumulative probability of PU was 10.6% (95% confidence interval (CI95), 7.2-14.0%) in the patients with gastritis, whereas this probability was only 0.8% (0-2.2%) in the patients who had normal antral and corpus mucosa in the initial specimens. The cumulative probability of PU was found to be highest, 27.3% (1.0-53.6%), in middle-aged men (41-60 years of age) who had chronic antral gastritis or chronic pangastritis (gastritis in both antrum and corpus). It is concluded that chronic gastritis precedes the appearance of PU and that the cumulative 10-year risk of PU is very low when both antral and corpus mucosa are normal but may be high if chronic gastritis is present.

Helicobacter pylori infection and chronic gastritis: clinical, serological, and histologic correlations in children treated with amoxicillin and colloidal bismuth subcitrate

Abstract: Twenty-three children with Helicobacter (Campylobacter) pylori-associated chronic gastritis are reported. Family history of peptic disease, previous digestive procedures, and nonspecific epigastric pain were the most frequently encountered clinical features. Antral nodularity at endoscopy and histologic evidence of follicular gastritis were characteristic morphological aspects. Rapid urease tests suggested the diagnosis in 90% of patients. Significant increases of serum IgG and IgA against Helicobacter pylori allowed the identification of infected children with 95% cumulative sensitivity. Treatment with amoxicillin and bismuth subcitrate eradicated the infection and improved gastritis in 13 of 19 children. These findings provide further evidence for the etiologic role of Helicobacter pylori in chronic antral gastritis in children.

Relation of Helicobacter pylori to the human gastric mucosa in chronic gastritis of the antrum.

Abstract: The spatial relations between bacteria and the affected tissues can indicate pathogenic mechanisms. This study was undertaken to define the spatial relation of Helicobacter pylori to the human gastric mucosa. Antibodies against gastric mucus and ruthenium red were used to stabilise the glycoprotein structure of the mucus and glycocalyces in antral biopsy specimens from eight patients infected with H pylori. The location of organisms and ultrastructural features were assessed using systematic scanning and transmission electron microscopy: 92 (2)% (mean (SE] of H pylori were in the pit mucus, and 7 (3)% were in the surface mucus; 60 (12)% of H pylori were close to epithelial cells, with only 5 (2)% located near the epithelial intercellular junctions. Fine filamentous strands extended between organisms and nearby epithelial cells, with few organisms in membrane to membrane contact. H pylori were not observed between, beneath, or within cells of the gastric mucosa. The preferred location of H pylori in the gastric antrum is within the pit mucus close to the epithelial cell surface, with no evidence that they have a direct toxic effect on the mucosa.

Relation between T cell number and epithelial HLA class II expression quantified by image analysis in normal and inflamed human gastric mucosa.

Abstract: Epithelial expression of HLA class II determinants and the number of lamina propria and intraepithelial T cells were quantified in gastric body mucosa by means of paired immunofluorescence staining which was subjected to computerised image analysis. In normal mucosa, epithelial HLA-DR expression was virtually absent. A significantly increased expression was seen in simple chronic gastritis, most extensively in the isthmus zone, where a positive reaction was seen in 34% of the epithelial area when the gastritis was of low degree and in 85% when it was of moderate severity. The most extensive HLA-DR expression was found in moderate 'stump gastritis' 28 to 32 years after Billroth II resections. In these patients the epithelial area in the foveolar and isthmus zones showed 83% and 92% positive responses, respectively. The HLA subregion products were expressed in a differential manner (DR greater than DP greater than DQ). The number of both intraepithelial and lamina propria T cells increased significantly with increasing severity of gastritis, and the fraction of putative memory T cells was also raised. Correlation analyses showed a positive relation between the epithelial expression of HLA-DR and the intraepithelial as well as the lamina propria density of T cell. These results suggest a biological link between T cells, aberrant HLA-DR expression, and gastritis, although the pathogenic importance of this relation is unknown. Enhanced epithelial presentation of autoantigens or luminal antigens, or both leading to increased activation of T cells is one possible explanation.

Evidence for gastric mucosal cell invasion by C. pylori: an ultrastructural study.

Abstract: It is now generally accepted that Campylobacter pylori is closely associated with peptic ulcer disease and chronic type B gastritis. Whether C. pylori is the direct etiologic cause of either or both of these illnesses remains unclear. Possible pathophysiologic effects of C. pylori are still a matter of debate and conjecture. Utilizing a small group of patients with gastric ulcers and chronic gastritis, we examined the ultrastructural relationship between C. pylori and gastric cells. Forty-eight percent of our gastric ulcer patients and 57% of our chronic gastritis patients had C. pylori in their lower corpus mucosa. Examination with the transmission electron microscope indicated a very close proximation by C. pylori to the surface epithelial cells strongly suggesting adherence. We also describe for the first time the invasion of gastric cells by C. pylori. Although an uncommon occurrence, we had repeated observations of C. pylori invading surface epithelial cells, parietal cells, and chief cells. Most of the intracellular C. pylori were intact but other forms appearing to be degenerating organisms were also seen. We suggest that cell invasion may be one mechanism by which C. pylori causes pathologic changes in the gastric mucosa. These observations may also explain why C. pylori chronically infects gastric cells and frequently recurs after treatment.

Gastroduodenal mucosa in uraemia: endoscopic and histological correlation and prevalence of helicobacter-like organisms.

Abstract: This study aimed to determine the prevalence of endoscopic and histological gastroduodenitis as well as helicobacter-like organisms in patients with end stage renal failure undergoing maintenance dialysis treatment. A total of 322 out of 422 patients in our dialysis programme underwent endoscopy and gastroduodenal biopsy specimens were taken from 260. Endoscopic gastroduodenitis occurred in 158 (49%). Histological gastritis occurred in the gastric body or antrum in 134 patients (52%) and duodenitis in 52 (21%). There was no correlation between endoscopic and histological gastritis in contrast to a significant correlation for duodenitis. Helicobacter-like organisms occurred in the body or antrum in 81 (31%). Their presence was associated with gastritis--in particular acute and acute on chronic gastritis rather than chronic gastritis. Patients with gastritis were significantly older than those without (p less than 0.001) and had lower basal and peak acid outputs.

The gastric juice urea and ammonia levels in patients with Campylobacter pylori.

Abstract: The authors studied gastric juice ammonia and urea nitrogen levels to determine how they are altered by gastric Campylobacter pylori (CP) infection. Patients with chronic gastritis (20), peptic ulcer (24), hepatic cirrhosis (10), chronic renal failure (13), or gastric remnant (20) were included. Endoscopic biopsy specimens stained with the Warthin-Starry stain were evaluated for the presence of CP. Blood and gastric juice analysis was performed for 11 of the patients with chronic renal failure and 37 patients from the remaining groups. CP was identified in gastric biopsies from 50 of 87 (57.5%) patients, including 87.5% with peptic ulcer and 40-50% of those with chronic gastritis, cirrhosis, chronic renal failure, or gastric remnant. CP infection had no effect on blood urea nitrogen or blood ammonia levels in any group of patients. The urea nitrogen level of gastric juice was higher in patients with chronic renal failure than in other groups but was not related to CP infection. CP infection was associated with a significant increase in gastric juice ammonia levels, both in patients with chronic renal failure (23.3 mmol/L vs. 2.90 mmol/L; [P less than 0.05]) and in other groups (5.48 mmol/L vs. 1.26 mmol/L [P less than 0.0001]). The authors conclude that elevation of gastric juice ammonia level is an indicator of gastric CP infection.

The Occurrence and Extent of Helicobacter pylori Colonization and Antral and Body Gastritis Profiles in an Estonian Population Sample

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

Experimental pathogenesis: drugs and chemical lesions in the gastric mucosa.

Abstract: The goals of this article are to review the similarities and differences in the pathogenesis of acute gastric mucosal injury induced by alcohol, exemplified mostly by ethanol, and aspirin, as a representative of nonsteroidal anti-inflammatory drugs, and to deduce implications from pathogenetic studies for a better understanding of the concept of gastric cytoprotection. The main similarity between the hemorrhagic erosions caused by ethanol and aspirin is their localization in the acid-producing glandular stomach, the rate-limiting step in their pathogenesis being the extent of microvascular injury in the gastric mucosa. The major differences include the fast healing and low probability of transition into chronic gastritis after a single exposure to aspirin. On the other hand, perforated ulcer may develop, especially in the elderly, after chronic aspirin but not ethanol consumption. The main implications of pathogenetic investigations include the relative nature of gastroprotection: that is, initially, the ...

The efficacy of furazolidone and metronidazole in the treatment of chronic gastritis associated with helicobacter (campylobacter) pylori : a randomized double-blind placebo-controlled clinical trial

Abstract: Seventy-two patients with Helicobacter pylori-associated chronic gastritis were randomized to a 3-week oral treatment with furazolidone 0.1g t.i.d. or metronidazole 0.2g t.i.d. or placebo. Endoscopy was performed before and after treatment, and biopsy specimens were taken from the antrum of the stomach for histological examination and culture of Helicobacter pylori. Disappearance rates of Helicobacter pylori in furazolidone, metronidazole and the control groups were 74% (20/27) if considering completion of therapy, the 20/25 or 80%, 33.3% (8/24) and 14.3% (3/21) respectively. There was a significant difference in the disappearance rate of Helicobacter pylori between furazolidone and metronidazole, and between furazolidone and the placebo group (p less than 0.01), but there was no such difference between metronidazole and the placebo group (p greater than 0.05). In the patients receiving furazolidone, the eradication of Helicobacter pylori was accompanied by marked improvement in both inflammatory infiltration in the gastric mucosa and symptoms. These results reasonably suggest that Helicobacter pylori may play an etiological role in the pathogenesis of chronic gastritis, and that furazolidone is effective in the treatment of Helicobacter pylori-associated chronic gastritis.

Peptic ulcer and chronic gastritis: their relation to age and sex, and to location of ulcer and gastritis.

Abstract: The progression, age-behaviour and profiles of chronic gastritis were studied in 460 patients with active gastric or duodenal ulcer, and in 226 patients with ulcer scar. The results were compared with those obtained from a sample of subjects representing the general population. In patients with ulcer or ulcer scar, the progression of chronic gastritis was more rapid in antrum than in body mucosa, and was more rapid in patients with proximal ulcer in those with distal ulcer or in controls. In the body the progression of gastritis was significantly slower in patients with duodenal or juxtapyloric ulcer than in patients with proximal ulcer or in nonulcer controls: body gastritis tended to remain on the same level at all ages whereas it showed a steady progression with age in the nonulcer controls. The degree of gastritis showed a tendency to increase along the shift of ulcer to more proximal in the stomach; the prevalence of gastritis of pure B type (moderate or severe atrophy in antrum, but no atrophy in body mucosa) correspondingly increased along this shift. Severe antral atrophic gastritis was found in 7 per cent of proximal active gastric ulcers and in 20 per cent of proximal ulcer scars. The progression of antral and body gastritis was on the whole more rapid in males than in females irrespectively of the location of ulcer. We conclude that gastritis in different types of ulcers shows characteristic patterns of distribution, dynamics and progression with age. The high prevalence of severe grades of atrophic antral gastritis may also be of significance in regard to the pathogenesis of gastric cancer.

Helicobacter (Campylobacter) pylori infestation and the development and progression of chronic gastritis: results of long-term follow-up examinations of a random sample.

Abstract: One hundred and thirty-nine subjects representing a randomly selected sample of an Estonian urban population examined endoscopically, bioptically and bacteriologically in 1979 was re-examined in 1985. In the antrum the development of superficial gastritis was clearly associated with the appearance or persistence of Helicobacter pylori (HP) infestation. The further progression of superficial gastritis could less clearly be related to HP infestation, although regression and progression of antral superficial gastritis was significantly associated with the disappearance or presence of the bacteria. The progression of atrophic antral gastritis as well as the development and progression of all body gastritis seemed unrelated to the HP infestation. It is concluded, that HP infestation is in some way involved in the appearance of the first stages of chronic gastritis, but is less related or unrelated to its further progression, which is probably determined mainly by factors other than HP.

Progress in the pathology of gastritis and duodenitis.

Abstract: Although for many years a simple classification of ‘non-specific’ gastritis into acute, chronic superficial and chronic atrophic categories has sufficed in routine histopathological practice, the clinical significance of the latter diagnoses is uncertain. While acute gastritis has well established and consistent clinical associations (a recent history of drug ingestion or alcohol excess leading to haemorrhagic erosions), the clinical features of chronic gastritis are much more nebulous. The finding of chronic gastritis in ‘healthy volunteers’ (Kreuning et al. 1978) and in random population surveys (Villako et al. 1976) has led some to conclude that the condition is a normal aging process of no clinical consequence. While this is a minority view, even those who believe it to be a pathological process have difficulty in recognising at what point the density of the inflammatory cell infiltration becomes ‘abnormal’, and the relationship between this inflammatory process, symptomatology and associated pathology.

[Human chronic gastritis associated with non-Helicobacter pylori spiral organisms (Gastrospirillum hominis). Four cases and review of the literature].

Abstract: Four cases of human active chronic gastritis associated with Gastrospirillum hominis, a recently described spiral shaped organism are presented. These 4 cases originated from a series of 1976 consecutive gastric biopsies, i.e. a prevalence of 0.25 percent in our material, are compared with Helicobacter pylori prevalence of 45 percent. Histopathological findings were chronic active gastritis with mild or no atrophy. Electron microscopy showed spiral bacteria with terminal flagellae, identical to those previously described in the literature. These bacteria have not yet been cultured; similar organisms are found in many animal species, and it seems that they do not provoke gastric inflammation. Gastrospirillum hominis could be responsible for cases of Helicobacter pylori negative chronic gastritis in man, but its pathogenicity remains to be demonstrated.

Association of Helicobacter pylori with acid peptic disease in Karachi.

Abstract: The prevalence of H. pylori infection in 200 dyspeptic patients undergoing upper G.I. endoscopy was investigated by histology and rapid urease test. H. pylori was associated with 86% cases of chronic gastritis, 84.6% cases of duodenal ulcers and 78.5% of gastric ulcers. None of the 15 histologically normal gastric biopsies showed H. pylori.

Campylobacter pylori interactions with gastric cell tissue culture.

Abstract: Many investigators have reported that gastric mucosal biopsies of patients with chronic gastritis and peptic ulcer disease show the presence of Campylobacter pylori in a large majority of cases. Histologic examinations of such tissues indicate a close approximation of C. pylori with gastric surface epithelial cells. A recent report has described both adherence and cell invasion of gastric cells by C. pylori. Using a transmission electron microscope, we have examined the interaction between C. pylori, C. jejuni, and E. coli in vitro with a gastric cancer cell line, Kato III. Our results indicate marked toxicity of E. coli and moderate toxicity of C. jejuni for Kato III cells. C. pylori had only a minor effect on tissue culture viability. C. pylori was found to have a strong association with the Kato III cell membranes and evidence of occasional cell invasion. Both C. jejuni and E. coli showed no attachment or association with the Kato III cells. We interpret these findings as indicating that C. pylori may have a specific adhesion for gastric cells.

Chronic gastritis and ulcer risk.

Abstract: (1990). Chronic Gastritis and Ulcer Risk. Scandinavian Journal of Gastroenterology: Vol. 25, No. 3, pp. 193-196.

Exocrine and Endocrine Epithelial Changes in Types A and B Chronic Gastritis

Abstract: Gastritis-associated epithelial changes are known to have a major role in the pathogenesis of gastric diseases such as peptic ulcer and exocrine or endocrine cell neoplasia [1, 26, 27, 31, 33]. Thus, a careful cytologic characterization of these epithelial changes at the light and electron microscopy level should prove helpful in understanding the cause and evolution of such diseases.

Acridine orange fluorescence, Campylobacter pylori, and chronic gastritis.

Abstract: Endoscopic gastric biopsy specimens from 230 consecutive patients in a North Liverpool District were histologically studied by routine light microscopy and ultraviolet fluorescence after acridine orange staining. Eighty patients with chronic gastritis were further studied with regard to type of gastritis and its activity, presence of Campylobacter pylori (CP), and degree of colonization of the gastric mucosa. Miscellaneous gastritis, gastric ulcers, erosions, neoplasms, and histologically normal specimens were excluded from the study. The results show statistically significant correlation between chronic gastritis and CP (P = 0.01, Mann-Whitney test). The activity of gastritis correlated well with CP, but there was no statistical significance between the density of neutrophils and degree of CP colonization (P greater than 0.5, Mann-Whitney test). In a small sample of CP-positive specimens acridine orange stain was compared with Warthin-Starry, Giemsa (modified), cresyl fast violet, and haematoxylin and eosin stains. Acridine orange stain in the histologic identification of CP has been used only once before in a large study.

Epidemiology and treatment of gastric Campylobacter pylori infection: more questions than answers.

Abstract: Two-hundred and ten consecutive patients undergoing routine gastroscopy were additionally investigated for evidence of Campylobacter pylori (C.p.). 106 patients were positive in one or more tests: 99.1% using a rapid urease detecting test (CLO-test), 80.2% histology, 78.3% cytology and 60% culture. We found no difference between the CLO-test results from biopsies taken from different parts of the stomach in individual patients. C.p. was found in 100% of patients with significant chronic antral gastritis, 67.7% with gastric ulcers, 65% with duodenal ulcers and in 12.1% of normal individuals. The C.p. infection was apparently eliminated in 50% of cases treated with bismuth subsalicylate (BSS) for four weeks. The combination of BSS with amoxicillin, tinidazole or an H2-receptor antagonist offered no advantage over BSS alone. Treatment with BSS led to improvement in symptoms and histological findings including healing of ulcers in patients with or without persistent C.p. infection. The recurrence of C.p. infection after apparently successful treatment was, however, 75% in 4 weeks. In conclusion, C.p. infection correlates strongly with the presence of chronic gastritis, and significantly with gastric and duodenal ulceration. The best diagnostic approach is the combination of a rapid urease detecting test and histology. C.p. infection is of long duration and difficult to eliminate. The most effective treatment for C.p. infection remains BSS as single agent.

Peptic Ulcer Disease in Children

Abstract: Chronic gastroduodenal ulceration is the end product of an imbalance between acid levels, peptic hostile factors, and mucosal defenses. This condition differs significantly from stress ulceration, in which the primary factor is decreased mucosal blood flow, and from nonsteroidal anti-inflammatory drug-induced injury, in which there is local vascular injury and inhibition of prostaglandin synthesis. The identification of H pylori as a cause of chronic gastritis, duodenitis, and peptic ulcer is required for specific antibacterial therapy.

Association of Helicobacter pylori with Gastritis, Duodenitis and Peptic Ulcer Diseases

Abstract: Helicobacter pylori occurs worldwide and there is a close relationship between its occurrence and histologically proven gastritis. The evidence that intake of H. pylori induces active gastritis and that eradication of H. pylori reverses the established gastritis suggests that the causative agent is H. pylori. H. pylori is frequently observed in patients with peptic ulcer diseases, and it may be associated with gastritis or duodenitis, which often accompany the ulcer diseases. Eradication of H. pylori, however, accelerates ulcer healing and diminishes ulcer relapse, suggesting, in part, an association of H. pylori with peptic ulcer diseases. We have attempted to facilitate the visual detection of H. pylori with endoscopy, to improve the diagnostic capability of this procedure.

The first cases of Helicobacter pylori (Campylobacter pylori) reported from Costa Rica.

Abstract: Two gastric antrum biopsies of each of 92 consecutive patients undergoing gastroendoscopy were studied. The first biopsy was cultured for Helicobacter (Campylobacter) pylori. The second specimen was fixed and processed for histopathological analysis. The bacteria were isolated from 34 (81%) of 42 patients with nonspecific chronic gastritis, 19 (90%) of 21 cases of duodenal or gastric peptic ulcer, and from 3 (23%) of 13 normal patients. The overall frequency of isolation was 62 (67%) of the 92 cases.