Severe Chronic Gastritis Research Articles

Immunosuppressive and proinflammatory activities of the VacA toxin of Helicobacter pylori.

20 yr have elapsed since the discovery of the association of the then novel bacterium Helicobacter pylori with different gastroduodenal diseases, including severe active chronic gastritis, gastroduodenal ulcers, adenocarcinoma, and lymphoma ([1][1]). The amount of research performed from the

Depletion of neutrophils in IL-10(-/-) mice delays clearance of gastric Helicobacter infection and decreases the Th1 immune response to Helicobacter.

Gastric infection with Helicobacter induces a lymphocyte-rich mucosal inflammation that contains a minor population of neutrophilic granulocytes. The function of neutrophils in the local immune response to gastric Helicobacter infection remains unknown. To investigate this issue, we conducted experiments in neutrophil-depleted control wild-type (wt) and IL-10(-/-) mice infected with Helicobacter felis by gastric lavage. Infection of wt mice elicited a mild, focal gastritis and a Helicobacter-specific Th1 immune response. In wt mice Helicobacter colonization of the stomach was persistent and progressively increased during the 29 days of observation. Infection of IL-10(-/-) mice with H. felis elicited a severe chronic gastritis and a greatly enhanced Helicobacter-specific Th1 immune response, as compared with wt mice. After initial colonization, the IL-0(-/-) mice completely cleared Helicobacter from the stomach by day 8. The gastric inflammation in wt and IL-10(-/-) mice contained modest numbers of neutrophils. The intensity of gastric inflammation and the extent of Helicobacter colonization were similar in control and in neutrophil-depleted wt mice. In contrast, neutrophil depletion of Helicobacter-infected IL-10(-/-) mice decreased the severity of gastritis, modulated the Helicobacter-specific Th1 immune response, and delayed the clearance of bacteria from the stomach. These studies identify a role for neutrophils in the local and systemic immune response to gastric Helicobacter in IL-10(-/-) mice.

Helicobacter pylori infection in geriatrics.

The prevalence of Helicobacter pylori infection increases with age worldwide. However, the percentage of H. pylori-positive elderly patients who are tested and treated for their infection remains very low. We now have data that demonstrate the benefit of curing H. pylori infection in elderly patients with H. pylori-associated peptic ulcer disease and severe chronic gastritis. Furthermore, the cure of H. pylori may prevent progression of intestinal metaplasia and gastric atrophy. Studies are needed to clarify the role of eradication for elderly patients who have nonulcer dyspepsia, gastroesophageal reflux disease and who use nonsteroidal anti-inflammatory drugs. H. pylori infection may be easily diagnosed by histological evaluation, rapid urease test or culture performed on gastric biopsies taken during endoscopy. However, the biopsy site must be carefully selected in elderly patients. For noninvasive monitoring of H. pylori infection after treatment, the 13C-urea breath test has significantly higher accuracy than serology in the elderly. The role of the H. pylori stool antigen test in old age still needs to be clarified. One-week PPI-based triple therapy regimens including clarithromycin, amoxycillin and/or nitroimidazoles are highly effective and well tolerated in elderly patients. Low doses of both PPIs and clarithromycin (in combination with standard doses of amoxycillin or nitroimidazoles) are sufficient. Antibiotic resistance and low compliance are the main factors related to treatment failure at any age.

Review article: an approach to Helicobacter pylori infection in the elderly.

The prevalence of Helicobacter pylori infection increases with age world-wide, reaching levels of 40-60% in asymptomatic elderly subjects and over 70% in elderly patients with gastroduodenal diseases. However, the percentage of H. pylori-positive elderly patients who are treated for their infection remains very low. Data are now available that demonstrate the benefit of curing H. pylori infection in elderly patients with H. pylori-associated peptic ulcer disease and severe chronic gastritis. Furthermore, the cure of H. pylori may prevent the progression of intestinal metaplasia and gastric atrophy. New studies are needed to clarify the role of eradication in elderly patients with non-ulcer dyspepsia and gastro-oesophageal reflux disease and in those who use non-steroidal anti-inflammatory drugs. H. pylori infection may be easily diagnosed by histological evaluation, rapid urease test or culture performed on gastric biopsies taken during endoscopy. However, the biopsy site must be carefully selected in elderly patients. For non-invasive monitoring of H. pylori infection after treatment, the 13C-urea breath test has significantly higher accuracy than serology in the elderly; further studies are needed to clarify the role of the H. pylori stool antigen test in old age. One-week proton pump inhibitor-based triple therapy regimens, including clarithromycin, amoxicillin and/or nitroimidazoles, are highly effective and well tolerated in elderly patients. Low doses of both proton pump inhibitors and clarithromycin (in combination with standard doses of amoxicillin or nitroimidazoles) are sufficient. Low compliance and antibiotic resistance are the main factors related to treatment failure in old age.

Helicobacter pylori and Different Topographic Types of Gastritis

Background: Helicobacter pylori gastritis is usually a lifelong disease which can cause different topographical inflammatory reactions and induce divergent effects on acid secretion in humans. High acid output and antrum-predominant gastritis are associated with duodenal ulcer disease, whereas corpuspredominat gastritis has been associated with low acid output and risk of gastric carcinoma. The objective of this study was to evaluate the role of different gastritis subtypes in the long-term treatment response of H. pylori -positive functional dyspepsia. Methods: The gastric biopsies from 143 H. pylori- positive patients with functional dyspepsia were classified in accordance with the Sydney System as antrumpredominant gastritis, pangastritis or corpus-predominant gastritis. The patients were randomized to receive either eradication therapy or placebo antibiotics. Moreover, to standardize acid suppression every patient received omeprazole therapy for the first 3 months. Dyspeptic symptoms were evaluated from a questionnaire and the follow-up time was 12 months. In addition, delta-over-baseline (DOB) values of the 13C-urea breath test (UBT) were analysed from a subgroup of 36 patients to measure urease activity of the stomach. Results: After 1 year, the dyspepsia symptom score was 7.4 ± 3.0 (95% CI 6.6-8.2) in successfully H. pylori -eradicated patients and 7.6 ± 3.1 (95% CI 6.9-8.4) in controls ( P = ns). Among patients with antrum-predominant gastritis, dyspepsia score was reduced more in subjects whose H. pylori was eradicated than in controls with ongoing infection (-3.6 ± 2.9 versus-1.7 ± 2.9; P = 0.05). High urease activity of the stomach was associated with severe or moderate chronic antrum-predominant gastritis. Conclusions: Patients with antrum-predominant H. pylori -positive chronic gastritis and functional dyspepsia get symptom improvement after successful eradication therapy. A high DOB value of UBT is associated with these patients.

Low prevalence of latently Epstein-Barr virus-infected cells in chronic gastritis.

The association of Epstein-Barr virus (EBV) with a proportion of gastric carcinomas is well established. The role of EBV in conditions predisposing to carcinoma such as chronic gastritis has remained undefined, however. We used in situ hybridization with radioactive and nonradioactive single-stranded RNA probes specific for the EBV small latent nuclear transcripts, EBER1 and EBER2, to analyze biopsy specimens from 242 patients with mild to severe chronic gastritis of Sydney classification types A, B, and C. A small number of EBV infected lymphocytes was detected in only nine cases, even in biopsies investigated with radioactive probes. Labeling of epithelial or stromal cells was not observed. The paucity of latently EBV-infected cells in chronic gastritis biopsies differs from the previously reported higher prevalence of virus carrying cells in inflammatory conditions at other sites of the gastrointestinal tract. These findings argue against a direct involvement of EBV in the pathogenesis of chronic gastritis. The low prevalence of EBV-positive cells suggests that local factors do not favor the entry and retention of circulating EBV-infected lymphocytes in gastric mucosa. Moreover, our findings indicate that EBV infection of gastric epithelial cells is not an early event in gastric carcinogenesis.

Helicobacter pylori infection: mechanism of colonization and functional dyspepsia Reduced colonization of gastric mucosa by Helicobacter pylori in mice deficient in interleukin-10.

Interleukin-10 (IL-10) is a potent anti-inflammatory and immunoregulatory cytokine. Mice deficient in IL-10 production (IL-10-/-mice) develop a spontaneous chronic enterocolitis, suggesting that IL-10 is an important regulator of the mucosal immune response in vivo. The objective of this study was to determine the role of endogenous IL-10 in the host defense against gastric colonization by Helicobacter pylori by using IL-10-deficient mice. The IL-10-/-mice were inoculated intragastrically with a mouse-adapted H. pylori isolate (Sydney Strain 1). Gastric colonization by H. pylori (biopsy urease test and bacterial colony counts), serum levels of H. pylori-specific immunoglobulin (Ig) M, A, G, isotypes of IgG, and the gastric mucosal inflammatory scores were determined 6 weeks after inoculation. Results were compared with those obtained from H. pylori-infected control mice (IL-10+/-mice). The colonization of gastric mucosa by H. pylori was reduced approximately 100-fold (P < 0.0001) in IL-10-/-mice (log10 4.87 +/- 0.26CFU/g tissue) as compared to IL-10+/-mice (log10 6.64 +/- 0.22 CFU/g tissue). Furthermore, IL-10-/-mice infected with H. pylori had significantly higher H. pylori-specific IgA and IgG antibodies in serum (P < or = 0.01), and developed much more severe chronic active gastritis than infected IL-10+/-mice. The median scores of the infiltration of gastric mucosa by mononuclear cells and neutrophils were up to threefold higher in IL-10-/-mice than they were in IL-10+/-mice. Our studies suggest that endogenous IL-10 is an inhibitor of the protective immune response to H. pylori infection. Interleukin-10 participates in the downregulation of H. pylori-induced gastric inflammatory responses, which apparently confers a survival advantage to the organism promoting more effective colonization of gastric mucosa.

Histological analysis of gastritis and Helicobacter pylori infection in patients with early gastric cancer: a case-control study.

Infection with Helicobacter pylori is associated with an increased risk of gastric adenocarcinoma. However, most patients with H. pylori infection will not develop gastric cancer. The aims of the present study were to examine which histological features, including H. pylori infection, would increase the risk of gastric cancer using a case-control study. Three gastric biopsy specimens were taken from 72 patients with early gastric cancer and 72 age- and sex-matched control subjects. The grade of gastritis was examined according to the updated Sydney System. The presence of H. pylori infection was determined by serology and histology. Odds ratio (OR) of developing gastric cancer was calculated for H. pylori positivity and histological features using conditional logistic regression. For patients with H. pylori infection, histological features in cancer patients and control subjects were compared. The OR of the presence of mononuclear cell infiltration in the corpus and intestinal metaplasia in the angulus were significantly elevated. The grade of mononuclear cell infiltration in the corpus and antrum was significantly higher in both types of cancer patients than controls. Glandular atrophy and intestinal metaplasia were increased in patients with intestinal-type cancer in the angulus and antrum. Bacterial density in the corpus and polymorphonuclear cell infiltration in the antrum were increased in patients with diffuse-type cancer. Severe chronic gastritis induced by H. pylori infection seems to be associated with diffuse-type gastric cancer. Glandular atrophy and intestinal metaplasia, which occur in gastric mucosa with chronic inflammation, are significantly associated with intestinal-type cancer.

S6–6 - Helicobacter pylori infection induces gastric cancer in Mongolian gerbils

Background & Aims: Although epidemiological studies have indicated that Helicobacter pylori infection plays a crucial role in gastric carcinogenesis in humans, there is no direct proof that H. pylori is actually associated with gastric carcinogenesis. The purpose of this study was to elucidate the relationship between H. pylori infection and gastric carcinogenesis using an animal model of long-term H. pylori infection. Methods: Mongolian gerbils were orally inoculated with H. pylori, and the sequential morphological changes in the stomach were examined for up to 62 weeks. Results: H. pylori was constantly detected in all infected animals throughout the study. At the 26th week, severe active chronic gastritis, ulcers, and intestinal metaplasia could be observed in infected animals. By the end of the study, adenocarcinoma had developed in the pyloric region of 37% of the infected animals. All tumors consisted of well-differentiated intestinal-type epithelium, and their development seemed to be closely related to intestinal metaplasia. Conclusions: We have successfully demonstrated that long-term infection with H. pylori induces adenocarcinoma in Mongolian gerbils. The observations are thus highly suggestive of the involvement of H. pylori infection in gastric carcinogenesis in humans.

Helicobacter pylori infection induces gastric cancer in Mongolian gerbils

Background & Aims: Although epidemiological studies have indicated that Helicobacter pylori infection plays a crucial role in gastric carcinogenesis in humans, there is no direct proof that H. pylori is actually associated with gastric carcinogenesis. The purpose of this study was to elucidate the relationship between H. pylori infection and gastric carcinogenesis using an animal model of long-term H. pylori infection. Methods: Mongolian gerbils were orally inoculated with H. pylori, and the sequential morphological changes in the stomach were examined for up to 62 weeks. Results: H. pylori was constantly detected in all infected animals throughout the study. At the 26th week, severe active chronic gastritis, ulcers, and intestinal metaplasia could be observed in infected animals. By the end of the study, adenocarcinoma had developed in the pyloric region of 37% of the infected animals. All tumors consisted of well-differentiated intestinal-type epithelium, and their development seemed to be closely related to intestinal metaplasia. Conclusions: We have successfully demonstrated that long-term infection with H. pylori induces adenocarcinoma in Mongolian gerbils. The observations are thus highly suggestive of the involvement of H. pylori infection in gastric carcinogenesis in humans. GASTROENTEROLOGY 1998;115:642-648

Prevalence of Helicobacter pylori infection and gastric mucosal abnormalities in chronic pancreatitis

Objective: Chronic pancreatitis is often associated with abnormal gastric acid secretion. However, previous studies have taken into consideration neither the potential role of Helicobacter pylori ( H. pylori) infection nor histological features of the gastric mucosa in this context. The aim of this study was to analyze the prevalence of H. pylori infection as well as the pattern of gastritis in patients with chronic pancreatitis. Methods: Forty patients with chronic alcoholic pancreatitis were included in the study: 40 patients with alcoholic liver cirrhosis and normal exocrine pancreatic function and 40 asymptomatic nonalcoholic subjects matched for age and sex used as control subjects. Endoscopy was performed in all patients, and five biopsy specimens from the antrum (three from the gastric body and two from the cardia) were taken for histological grading of gastritis and H. pylori assessment. Results: Prevalence of H. pylori infection was similar in subjects with chronic pancreatitis (38%), asymptomatic subjects (28%) and liver cirrhosis (30%). Topography and expression of H. pylori-associated chronic gastritis was also not different among the three groups of subjects. In H. pylori-negative subjects, the presence of moderate to severe chronic antral gastritis was significantly more common in patients with chronic pancreatitis (40%) than in subjects with liver cirrhosis (18%) and in asymptomatic subjects (14%) ( p < 0.05). No difference was found among the three groups of patients with regard to gastritis activity, atrophy, and intestinal metaplasia in the various gastric regions. The chronicity grade of gastritis did not correlate with the severity of pancreatic insufficiency. Conclusion: Prevalence of H. pylori infection is not different in patients with chronic pancreatitis as compared with subjects alcoholic liver cirrhosis and asymptomatic subjects. A severe H. pylori-negative chronic gastritis is more common in patients with chronic pancreatitis. This chronic inflammation of the gastric mucosa could contribute to determining the changes in gastric physiology described in patients with chronic pancreatitis.

Epidemiology of intestinal and diffuse types of gastric carcinoma a time-trend study in finland with comparison between studies from high- and low-risk areas

The incidence of gastric cancer has declined markedly in Finland during the last 4 decades. To document the changes caused by that in the ratio of the intestinal type (IT) to the diffuse type (DT) of gastric carcinoma we compared the 367 cases diagnosed from southwestern Finland at the Department of Pathology, Turku University, from 1950-1959 and 1076 cases from 1980-1989. IT virtually disappeared in the male and female populations younger than 50 years, and in patients younger than 60 years, DT became more common than IT (P < 0.001). The transitional age, the time at which IT exceeds DT in frequency, shifted by 20 years to older age groups. In patients older than 60 years, IT remained the dominant type, but the ratio of IT to DT (IT:DT) decreased in men from 3.8 to 2.1 (P < 0.05) and in women from 4.4 to 2.1 (P < 0.001). No decrease in the frequency of DT could be demonstrated in the material studied. The disappearance of the male-dominant IT in the younger male population changed the male-to-female ratio of patients reported to the Finnish Cancer Registry. When the ratio IT:DT in Finland was compared with the ratios reported by the authors in data from other continents and by other investigators, regional variations in basal level of IT:DT emerged. This phenomenon seems to be based on the differing genetic susceptibility to DT of various races. The decrease of IT, seen in reports from regions with declining incidence of gastric carcinoma, seems to be connected to a diminished rate of severe chronic gastritis.

Eosinophil infiltration and degranulation inHelicobacter pylori-associated chronic gastritis

Eosinophil granules contain cationic proteins, including the major basic protein, which are toxic to mammalian tissue. While eosinophils have been observed to comprise part of the inflammatory reaction in acute Helicobacter pylori gastritis, the role of the eosinophil in the pathogenesis of chronic gastritis is unknown. We evaluated whether eosinophil infiltration and degranulation are associated with chronic gastritis and H. pylori infection. We studied eight patients with chronic H. pylori antral gastritis, three with chronic antral gastritis in the absence of H. pylori, 11 healthy age-matched volunteers without antral gastritis, and eight patients with H. pylori-negative chronic specific gastritis (three Crohn's antral gastritis and five Ménétrier's disease). Serial sections were stained with hematoxylin and eosin, with Giemsa, and by a specific indirect immunofluorescence technique for eosinophil granule major basic protein. Specimens were graded independently by three observers and scores of 0-3 were given for eosinophil infiltration and degranulation (0 = none to 3 = confluent infiltration and/or degranulation). In H. pylori antral gastritis, significantly greater eosinophil infiltration and degranulation were found compared to the normal group, Ménétrier's disease, and chronic H. pylori-negative gastritis. There was no significant difference between gastric Crohn's disease and H. pylori gastritis. The severity of chronic gastritis was significantly correlated with the eosinophil score. Eosinophil degranulation did not appear to be greater at or near sites of bacterial colonization in the H. pylori gastritis specimens. The results suggest that eosinophil infiltration and degranulation may be associated with H. pylori gastritis. We postulate that the release of toxic cationic proteins from eosinophils contributes to the inflammatory changes present in H. pylori gastritis.

The Occurrence and Extent ofHelicobacter pyloriColonization and Antral and Body Gastritis Profiles in an Estonian Population Sample

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

Atrophic gastritis as a premalignant condition.

Chronic (atrophic) gastritis is a progressive disease which in a small proportion of patients leads to severe (total) atrophy (severe grade of chronic gastritis) of the antral or body mucosa or both. Chronic gastritis is a premalignant condition which favours the development of gastric cancer. Chronic gastritis precedes gastric cancer and shows a severalfold increase in the risk of gastric cancer compared to subjects with histologically normal stomach. Several tentative modifications to the estimate of the risks may be presented: (i) a severe risk of developing gastric cancer is restricted to subjects with a severe grade of chronic gastritis (ii) the risk of gastric cancer is increased in subjects who have either severe antral or body chronic gastritis, the risk being approximately three to five times higher in the antral chronic gastritis (B-type of gastritis) than in the body chronic gastritis (A type of gastritis); (iii) the antral and body chronic gastritis are independent risk factors for gastric cancer, the joint risks being multiplicands of the marginal risks i.e., the estimated risk is highest in those subjects who show severe chronic gastritis in both the antrum and the body (AB type of gastritis); (iiii) the chronic gastritis mediated gastric cancer risk is limited to gastric cancers of the intestinal type, and thus covers only a proportion of all cases of gastric cancer. In the highest risk groups it may be estimated that the probability of a subject developing gastric cancer in subsequent decades is up to 30% if the subject is a young man who has severe chronic gastritis in his antrum, or who has it coexistently in the antrum and body.

The altered expression of MHC-class II determinants on monocytes of cancer patients.

The expression of MHC class II determinants Ia.7 (detected by cross reactive mouse anti-Iak antibody) and HLA-DR on monocytes (MO) of gastric and colorectal cancer patients was examined. An increased proportion of MO bearing the Ia.7 determinant was found, while the number of MO expressing DR was not elevated. In gastric cancer patients the increased expression of the Ia.7 determinant was most pronounced in advanced cancer (stage IVA and IVB). The increased expression of this determinant was related to the presence of the tumour as the number of MO expressing Ia.7 decreased 6 months following surgical resection of the tumour. Further, the increased expression of Ia.7 on MO correlated with the tumour infiltration of the serosa. The Ia.7 determinants were mainly expressed on MO which also expressed the receptor for the Fc part of immunoglobulin. Immunostaining in cellular infiltrates surrounding the tumour revealed that Ia.7+ macrophages (MO) were more numerous than in normal gastric mucosa and severe chronic gastritis and were mostly present in close proximity to tumour cells, while DR+MO were mainly localized within the stromal tissue of the tumour and their number was not increased in cancer infiltrates. These observations indicate that the Ia.7+ subpopulation of MO may be involved in the anti-tumour response of the host.

Toxicity, tissue distribution, and excretion of benzyl chloride in the rat.

The tissue distribution and excretion of [14C]benzyl chloride was investigated in adult male and female Fischer 344/N rats after administration of a single oral dose of [14C]benzyl chloride in corn oil at 25 mg/kg, data was correlated with histopathologic and toxicity findings elicited from a 27-37-wk repeated-dose oral toxicity study of benzyl chloride. Radioactivity was detected in all tissues selected for examination. Elimination of the isotope occurred predominantly in the urine. Female rats excreted the isotope at a faster rate than the males and also maintained slightly lower tissue concentrations (with the exception of the blood and kidneys). Isotope recovery was achieved at 90% in the urine and feces of female rats at 24 h, compared with an 80% recovery rate in males. Concentrations of radioactivity were high in the gastrointestinal tract, reflecting the route of administration; however, the squamous stomach and the small intestine consistently retained higher concentrations of isotope than the glandular stomach. Results of acute toxicity and organ histopathology studies in animals dosed with benzyl chloride for 27-37 wk are compatible with the organ distribution and excretion of [14C]benzyl chloride. Histopathologic findings included severe acute and chronic gastritis, hyperkeratosis and hyperplasia of the squamous stomach, and progressive lesions of the heart ranging from proliferation of interstitial cells to acute necrosis of myocardial fibers. Both of these studies suggest that the squamous stomach is a target organ for benzyl chloride or one of its metabolites.

Gastritic glandularis et cystica profunda

Three cases of gastritis glandularis et cystica profunda are presented, two associated with severe chronic gastritis and the other with invasive gastric carcinoma and chronic gastritis. This poorly known entity consists of benign downgrowths of deep gastric glands through the muscularis mucosae into the submucosa. The pattern is primarily adenomatous with secondary cyst formation, which varies in extent and severity. The lesion is related to the chronic gastritis but why it should occur so rarely in such a common condition as chronic gastritis remains obscure. More documented cases are needed before a meaningful analysis can be attempted.

Cryptosporidium in Snakes with Hypertrophic Gastritis

Fourteen captive snakes of three genera and four species had severe chronic hypertrophic gastritis. Persistent postprandial regurgitation and firm midbody swelling were the most common clinical signs. Fecal smears had many roughly spherical organisms confirmed by ultrastructural study to be oocysts of Cryptosporidium. Pathologic changes included hypertrophy of gastric mucosa and atrophy of granular cells. There were cystic changes in gastric glands and focal mucosal necrosis. Many Cryptosporidium lined microvillar surfaces. All developmental forms were identified by ultrastructure. Characteristic oocysts were found in abundance.

Gastric parietal cell antibodies in young men with alcoholism and with non-ulcer dyspepsia.

A series of 101 young men comprising alcoholics, patients presenting with non-ulcer dyspepsia (NUD) and healthy controls was investigated for incidence of antibodies against gastric parietal cells, thyroglobulin and thyroid microsomes and for chronic gastritis as revealed by gastric biopsy. Alcohol is shown to be a cause of chronic gastritis. The incidence of parietal cell antibody (PCA) was unrelated to either the alcohol intake or to the incidence and severity of chronic gastritis. Subjects with PCA showed no increased incidence of thyroid antibodies. There is thus no evidence for the involvement of an autoimmune process in the genesis of alcohol-induced chronic gastritis. The incidence of PCA is significantly less in non-ulcer dyspeptics than in either control subjects or in the remainder of the series as a whole. The interpretation of this finding is not clear. Chronic gastritis is no more or less common among NUD patients than among healthy controls.