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PubMedDate not supplied

Autoimmune gastritis: historical antecedents, outstanding discoveries, and unresolved problems.

The earliest recorded history of autoimmune gastritis can be traced to 1849 in London, when Thomas Addison described "a very remarkable form of anemia" later called pernicious (fatal) anemia (PA). This was followed by the recognition of a gastric mucosal defect suspected to have a nutritional basis, the discovery of the megaloblast that characterized the anemia, the insufficiency of a dietary extrinsic factor characterized as vitamin B12 (cobalamin), and a gastric-secreted intrinsic factor. Treatment with vitamin B12 proved curative. The link between PA and gastritis and atrophy was first confirmed histologically after immediate fixation of the stomach postmortem and later, in the 1940s, by peroral tube biopsy. The causes of gastritis remained enigmatic until the era of autoimmunity, when autoantibodies were detected first to gastric intrinsic factor and then to gastric parietal cells. Hints of a dichotomy in pathogenesis of gastritis were crystallized by the description in 1973 of Type A (Autoimmune) and Type B (later, Bacterial) gastritis. Clarification was enhanced by identification in Type A gastritis of the autoantigen of the parietal cell antibody, by the alpha and beta subunits of gastric H+/K+ ATPase, and by the highly informative experimental murine model of postneonatal thymectomy autoimmune gastritis, and in Type B of the causative role of gastric infection with Helicobacter pylori (H. pylori). A denouement will require a full understanding of (1) the origin and pathogenetic contribution of antibody to intrinsic factor; (2) the connection, if any, between H. pylori infection and Type A autoimmune gastritis; and (3) the genetic contributions to gastritis, whether due to autoimmunity or to H. pylori infection.

Adrenal Cortex Hormones↗
PubMed1995

Helicobacter pylori and atrophic gastritis: importance of the cagA status.

BACKGROUND: Infection with Helicobacter pylori is a major risk factor for the development of atrophic gastritis and gastric cancer. H. pylori strains can differ with respect to the presence of cagA (cytotoxin-associated gene A), a gene encoding a high-molecular-weight immunodominant antigen. H. pylori strains possessing cagA have been associated with enhanced induction of acute gastric inflammation. PURPOSE: We investigated the relationship between cagA status and the development of atrophic gastritis in a cohort of subjects infected with H. pylori. METHODS: Gastrointestinal endoscopy with biopsy sampling was used to study the natural history of gastritis in 58 subjects infected with H. pylori. Biopsy specimens were obtained before and after a mean follow-up period of 11.5 years (range, 10-13 years). The cagA status of each individual was determined at the follow-up visit with the use of an enzyme-linked immunosorbent assay designed to detect the presence of serum immunoglobulin G directed against the CagA protein. Two-sided Fisher's exact tests, McNemar's tests, Student's t tests, and Wilcoxon sum rank tests were used to analyze the data. RESULTS: Twenty-four (41%) of the 58 evaluated subjects had serum antibodies against CagA (i.e., they were cagA positive), and 34 subjects were cagA negative. At the initial visit, moderate to severe atrophic gastritis was observed in eight (33%) of the cagA-positive subjects and in six (18%) of the cagA-negative subjects. At that time, positive cagA status and gastric atrophy were not significantly related (P = .22; Fisher's exact test; odds ratio [OR] 2.33; 95% confidence interval [CI] = 0.58-9.65). During follow-up, 16 (36%) of the 44 initially atrophy-negative subjects developed atrophic gastritis (eight [50%] of 16 cagA-positive subjects versus eight [29%] of 28 cagA-negative subjects; P = .20, Fisher's exact test; relative risk [RR] = 1.75; 95% CI = 0.82-3.76). In six of these 16 subjects (five cagA positive versus one cagA negative), atrophic gastritis was accompanied by the development of intestinal metaplasia (i.e., a change in the type of specialized cells present) (P = .02; Fisher's exact test; RR = 9.06; 95% CI = 1.16-71.0). One of the initially atrophy-negative, cagA-positive subjects developed early gastric cancer. Four (29%) of the 14 subjects initially diagnosed with atrophic gastritis showed regression of atrophy during follow-up (one cagA positive and three cagA negative). Therefore, at the end of follow-up, 15 (62%) of the 24 cagA-positive subjects had atrophic gastritis compared with 11 (32%) of the 34 cagA-negative subjects (P = .02; Fisher's exact test; OR = 3.48; 95% CI = 1.02-12.18). CONCLUSION: Infection with cagA-positive H. pylori strains is associated with an increased risk for the eventual development of atrophic gastritis and intestinal metaplasia.

Adult↗
PubMed1999

Helicobacter pylori gastritis of the gastric cancer phenotype in relatives of gastric carcinoma patients.

OBJECTIVE: Infection with Helicobacter pylori is associated with gastric cancer. However, a hereditary risk of gastric cancer has also been reported. Hence, we decided to evaluate H. pylori gastritis in relatives of gastric cancer patients in comparison with matched controls. DESIGN: Case-controlled study. METHODS: A total of 237 patients with merely H. pylori gastritis (i.e. not associated with either peptic ulcer or gastric malignancy), and either first-degree (93.7%) or second-degree (6.3%) relatives with gastric cancer, were age- and sex-matched with 237 patients with H. pylori gastritis unassociated with a family history of gastric cancer. From each patient, antral and corpus biopsy specimens were obtained and investigated for degree (lymphocyte/plasma cell infiltration) and activity (polymorph infiltration) of gastritis (score: 0-4). Intestinal metaplasia was recorded as present or absent. RESULTS: The results show that relatives of gastric cancer patients have a significantly greater expression of gastritis due to a higher grade of gastritis in the antrum and corpus (P < 0.0001) and a greater activity of gastritis in the corpus (P < 0.0001). Intestinal metaplasia occurs more often in relatives of gastric cancer patients (antrum: P < 0.0001; corpus: P = 0.0237). CONCLUSION: Since the grade of H. pylori gastritis in relatives of gastric cancer patients is significantly higher than in controls, there appears to be a genetic susceptibility influencing the expression of H. pylori gastritis.

Adult↗
PubMed1993

Gastritis in patients on non-steroidal anti-inflammatory drugs.

This study investigated the spectrum of gastric mucosal pathology, including the prevalence of reactive gastritis in patients on non-steroidal anti-inflammatory drugs (NSAIDs). The histological findings were correlated with upper gastrointestinal symptom status and endoscopic findings and were also compared with the histological appearances of the gastric mucosa in a corresponding age-matched control group of 75 patients not receiving NSAIDs or any other drug therapy. Reactive gastritis of the gastric antrum was more common in the NSAID group and was observed in 34 patients (45.3%), as an isolated phenomenon in 24 patients (32%) and with evidence of coexistent chronic gastritis in 10 patients (13.3%). In the control group reactive gastritis of the antrum was seen in 10 patients (13.3%), as an isolated finding in eight cases (10.7%) and with accompanying chronic gastritis in two cases. Chronic antral gastritis of usual type was observed in 36 patients on NSAIDs (48%) and Helicobacter-like organisms were identified histologically in 18 of these (50% carriage rate). These organisms were not seen in any of the patients in whom the picture of reactive gastritis was present. In the control group chronic antral gastritis was seen in 51 patients (68%) with organisms in 34 (66.6% carriage rate). No correlation was found between the presence or absence of upper gastrointestinal symptoms, endoscopic findings and the histological appearances of the gastric mucosa. We conclude that NSAIDs are an independent cause of reactive gastritis in the antrum and do not appear to alter gastric mucosal colonization by Helicobacter-like organisms.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Helicobacter pylori colonization in children with gastritis and peptic ulcer. I. The colonization rate and effects of colonization on mucin content and mucosal inflammation in the antrum.

The incidence of Helicobacter pylori infection and effects of H. pylori colonization on mucin content and mucosal inflammation of the antral mucosa were studied quantitatively in 55 Japanese children with suspected gastritis and peptic ulcers (aged 6-16 years, mean 12.3 years). H. pylori was detected, using Warthin-Starry stain, in nine of the 22 cases (41%) with antral histological gastritis, but in none of the 33 histologically normal cases. Five out of seven duodenal ulcer cases showed histological gastritis, and all five cases were H. pylori positive. Severity of gastritis, evaluated by means of gastritis score, was significantly higher in H. pylori positive gastritis cases than in H. pylori negative gastritis cases (5.4 +/- 1.0 vs 3.1 +/- 0.3, P < 0.001). A PAS-AB index, a proportion of the periodic acid Schiff-alcian blue (PAS-AB) positive mucin area to the total epithelial area, was significantly lower in H. pylori positive cases than in H. pylori negative cases, irrespective of the existence of histological gastritis (23.5 +/- 7.6% vs 40.4 +/- 5.5%, 43.5 +/- 4.2%, P < 0.001). The decreased mucin content of gastric mucosa is likely to lead to weakening of an important defensive factor of gastric mucosa. These findings suggest that H. pylori plays an important role in gastritis and peptic ulcers in children, especially in cases with duodenal ulcer.

Adolescent↗
PubMed1996

Serum and gastric luminal epidermal growth factor in Helicobacter pylori-associated gastritis and peptic ulcer disease.

BACKGROUND: Helicobacter pylori is the cause of chronic (type B) gastritis, duodenal ulceration (DU), and gastric ulceration (GU). Smoking is associated with delayed ulcer healing. Epidermal growth factor (EGF) is produced in the salivary and Brunner's glands of the upper gastrointestinal tract, inhibits gastric acid secretion, and is a powerful mitogen. MATERIALS AND METHODS: We sought to determine gastric luminal EGF (GL-EGF) in smokers and patients with Hp-associated DU and the effects of Hp eradication. Our aim was to determine GL-EGF in patients with GU and the effect of ulcer healing and to measure serum EGF in patients with Hp gastritis with or without DU disease. RESULTS: GL-EGF was reduced in smokers compared to controls (p = .008). Subjects with HP gastritis had reduced GL-EGF compared to controls (p = .0002). There was no difference in GL-EGF between Hp-positive subjects who had DU and those with chronic gastritis alone. Eradication of Hp from those patients with DU had no effect on the low levels of GL-EGF. There was no difference between GL-EGF in Hp gastritis alone and in Hp-associated active GU. GL-EGF fell after ulcer healing (p = .04), a difference confirmed by analysis of paired samples from patients before and after ulcer healing (p = .03). There was no difference in serum EGF between controls and subjects with Hp infection. There was no difference in serum EGF in subjects with DU associated and non-ulcer-associated gastritis. CONCLUSIONS: Subjects with Hp gastritis, or those who smoke, had low concentrations of GL-EGF regardless of whether DU was present. Eradication of Hp did not return the concentrations of GL-EGF to normal in DU subjects. Individuals and Hp gastritis and inactive GU had low levels of GL-EGF compared to non-ulcer Hp infection. The relative increase in GL-EGF that occurred with ulceration of the gastric mucosa may have resulted from the development of an ulcer-associated cell lineage. Serum EGF did not play a role in the pathogenesis of Hp gastritis or of associated DU ulcer disease.

Adult↗
PubMed2003

Helicobacter pylori-associated chronic gastritis and unexplained iron deficiency anemia: a reliable association?

BACKGROUND AND AIM: About 35% of iron deficiency anemia cases remain unexplained after a gastrointestinal evaluation. An association between Helicobacter pylori and iron malabsorption has been suggested. The aim of this study was to determine whether H. pylori-associated chronic gastritis is linked to unexplained iron deficiency anemia in adults. METHODS: From 1996 to 2001, we identified 105 patients with unexplained iron deficiency anemia after upper endoscopy, colonoscopy, small bowel radiographic examination and duodenal biopsies. Two biopsies were obtained from the gastric antrum and two from the corpus of each patient. Gastritis status was described according to the Sydney System and H. pylori infection was assessed by an immunohistochemical test on biopsy specimens. This group was compared to a control group matched for sex and age. RESULTS: There were 76 women and 29 men (mean age 57.4 +/- 21.4 years) examined in the study. A H. pylori-associated chronic gastritis was identified in 63 cases (60%) vs. 45 cases (43%) cases in the control group (p <.01). Atrophic gastritis was significantly associated with iron deficiency anemia compared with the control group [16 (15%) vs. 6 (6%); p <.03]. In the unexplained iron deficiency anemia group, (1) patients with chronic gastritis were significantly younger (52 +/- 22 vs. 64 +/- 20 years; p <.005), and (2) chronic gastritis was not linked to sex [sex ratio (male/female): 0.5 vs. 0.34, p =.34]. The prevalence of H. pylori infection was similar between premenopausal and postmenopausal women [28 (27%) vs. 26 (25%); p =.7] with iron deficiency anemia. CONCLUSION: H. pylori infection and chronic gastritis, especially atrophic gastritis, are significantly associated with unexplained iron deficiency anemia. Relationships between H. pylori-associated chronic gastritis and unexplained iron deficiency anemia should be considered.

Adult↗
PubMed2005

Is there a possible relation between atrophic gastritis and premature atherosclerosis?

BACKGROUND: In this study, we have aimed to show the possible relation between atrophic gastritis and premature atherosclerosis via hyperhomocysteinemia. MATERIALS AND METHODS: Thirty-four patients with atrophic gastritis were enrolled to the study. The control group consisted of 35 patients with non-atrophic gastritis. Classical cardiovascular disease risk factors did not significantly differ between atrophic gastritis and control subjects. The presence and degree of atrophic gastritis were assessed histologically and Helicobacter pylori infection was determined by both histologic and serologic methods. Body mass index was measured by standard technique blood fasting glucose, serum creatinine, total cholesterol, triglyceride, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, vitamin B12, folic acid, and homocysteine levels were measured by biochemical methods. Carotid intima-media thickness was measured by B-mode ultrasonography to examine the premature atherosclerosis. RESULTS: Plasma vitamin B12 levels were significantly lower (p = .00) and homocysteine levels were significantly higher (p = .01) in the atrophic gastritis group. There was no statistically significant difference in plasma folic acid levels between the two groups (p = .728). Carotid intima-media thickness was higher in the atrophic gastritis group than in the control group (0.516 mm versus 0.465 mm), but this difference did not show any statistical significance (p = .062). CONCLUSION: Our results showed that atrophic gastritis may cause hyperhomocysteinemia, which is an independent risk factor for atherosclerosis and cardiovascular diseases. However, when compared with controls, carotid intima-media thickness of the atrophic gastritis patients was found to be higher but did not reach statistically significant levels.

Atherosclerosis↗
PubMed1999

Helicobacter pylori infection inhibits reflux esophagitis by inducing atrophic gastritis.

OBJECTIVE: Although it is widely accepted that Helicobacter pylori (H. pylori) infection is an important cause of atrophic gastritis, few studies have examined the relationship between H. pylori-induced atrophic gastritis and the occurrence of reflux esophagitis. The present study was aimed to examine the relationship between H. pylori infection, atrophic gastritis, and reflux esophagitis in Japan. METHODS: A total of 175 patients with reflux esophagitis were compared with sex- and age-matched 175 control subjects. Diagnosis of H. pylori infection was made by gastric mucosal biopsy, rapid urease test, and serum IgG antibodies. Severity of atrophic gastritis was assessed by histology and serum pepsinogen I/II ratio. RESULTS: H. pylori infection was found in 59 (33.7%) patients with reflux esophagitis, whereas it was found in 126 (72.0%) control subjects. The grade of atrophic gastritis was significantly lower in the former than in the latter. Among the H. pylori-positive patients, atrophic gastritis was milder in the patients with reflux esophagitis than in the patients without it. CONCLUSIONS: These findings suggest that most cases of reflux esophagitis in Japan occur in the absence of H. pylori infection and atrophic gastritis, and it may also tend to occur in patients with milder gastritis even in the presence of H. pylori infection. Therefore, H. pylori infection may be an inhibitory factor of reflux esophagitis through inducing atrophic gastritis and concomitant hypoacidity.

Adult↗
PubMed2001

Cure of Helicobacter pylori infection and resolution of gastritis by adoptive transfer of splenocytes in mice.

Vaccination suppresses Helicobacter pylori colonization but does not cure infection. Furthermore, postvaccination gastritis, likely induced by enhanced host response to residual colonization, may exacerbate disease. The goal of this study was to determine if adoptive transfer of C57BL/6 splenocytes to C57BL/6scid/scid (severe combined immunodeficient [SCID]) mice cures infection without exacerbating gastritis. H. pylori-infected and uninfected C57BL/6 mice and SCID recipients of normal splenocytes were killed at intervals between 5 and 51 weeks after infection. Colonization and gastritis were quantified, humoral immune responses were determined by enzyme-linked immunosorbent assay, and cellular immune responses were determined by delayed-type hypersensitivity response and by a proliferative response of cultured splenocytes to H. pylori sonicate. In infected C57BL/6 mice, gastritis developed gradually and bacterial colonization diminished but persisted throughout the experiment. In contrast, gastritis in infected recipient SCID mice developed rapidly and bacterial colonization decreased precipitously. Gastritis in those mice peaked 9 weeks after adoptive transfer, however, and began to resolve. By 45 weeks after transfer, gastritis had returned to background levels and bacteria were no longer detectable. Resolution of gastritis and elimination of infection were associated with a cellular but not humoral immune response to H. pylori antigens. These results demonstrate that although the host response fails to clear bacterial colonization in normal mice, enhanced cellular immune responses in recipient SCID mice are capable of clearing H. pylori infection and allowing resolution of gastritis. Thus, immune mechanisms of cure exist, and effective and safe vaccination protocols may be feasible.

Adoptive Transfer↗
PubMed1990

Helicobacter pylori and gastritis in patients with peptic ulcer and non-ulcer dyspepsia: ethnic differences in Singapore.

Peptic ulcer occurs with different frequencies in the three main racial groups in Singapore. This study aimed firstly to determine the prevalence of Helicobacter pylori in peptic ulcer and non-ulcer dyspepsia patients of the different races and secondly, to assess the relation between H pylori, histological gastritis, patient diagnosis, and race. Gastric antral biopsy specimens from 1502 patients undergoing gastroduodenoscopy were studied and 892 (59%) were positive for H pylori. H pylori was strongly associated with gastritis: 873 of 1197 (73%) patients with gastritis were positive compared with 19 of 305 (6%) without gastritis (p less than 0.0001). The prevalences of H pylori and gastritis were similar in peptic ulcer patients of different races. Malay patients with non-ulcer dyspepsia, however, were less likely to be positive for H pylori (10 of 46 (22%] or to have antral gastritis (17 of 46 (37%] than Chinese (292 of 605 (48%) were positive for H pylori and 421 of 605 (70%) had gastritis) and Indians (35 of 61 (57%) were H pylori positive and 42 of 61 (69%) had gastritis). Patients with duodenal ulcer were more likely to be positive for H pylori than those with non-ulcer dyspepsia, even when subjects with gastritis were considered separately. While our results do not help to explain the observed racial differences in peptic ulcer frequency it may be that the pathophysiology of non-ulcer dyspepsia is different in the different races in Singapore.

Adult↗
PubMed1995

Interferon gamma and interleukin 4 secreting cells in the gastric antrum in Helicobacter pylori positive and negative gastritis.

Little is known of the function of the T cells in the inflammatory infiltrate in Helicobacter pylori associated gastritis. This study thus measured T cell in vivo activation by enumerating the frequency of interferon gamma (IFN gamma) and interleukin 4 (IL 4) secreting cells isolated from the gastric antral mucosa in patients with or without gastritis and in H pylori positive and negative gastritis. Fifty four samples were examined for cytokine secretion. Four antral biopsy specimens from each patient (n = 51) were taken during diagnostic endoscopy. One was used to estimate histological gastritis and the presence of H pylori, and three of the samples were used to isolate T cells by enzymatic digestion. IFN gamma and IL 4 secreting cells were enumerated by ELISPOT. Thirty four samples had gastritis and 79% of those were H pylori positive. None of the samples from non-inflamed mucosa had H pylori. The numbers of IFN gamma secreting cells per 10(5) T cells were higher in gastritis than in normal mucosa (145 v 20 IFN gamma spots, p < 0.01), and higher in H pylori negative than H pylori positive gastritis (371 v 110 IFN gamma spots, p < 0.05). The frequencies of IL 4 secreting cells did not differ between gastritis and non-inflamed mucosa. In conclusion, there is an increase in IFN gamma secreting cells but not in IL 4 secreting cells in H pylori positive and negative gastritis. It is not known if this TH1 type reaction has a pathogenetic or protective role.

Adult↗
PubMed1995

Lymphocytic gastritis and Helicobacter pylori infection in gastric lymphoma.

Lymphocytic gastritis and primary gastric lymphoma are rare conditions with unknown aetiology. It has recently been suggested that Helicobacter pylori has a role in the pathogenesis of both of them. The occurrence of lymphocytic gastritis and H pylori was studied in a series of patients with primary gastric lymphoma. The cases of primary gastric lymphomas (n = 35) diagnosed in years 1970-1993 were identified. The specimens of 22 cases contained gastric mucosa sufficiently so that the number of intra-epithelial lymphocytes, severity of gastritis, and occurrence of H pylori could be studied. Lymphocytic gastritis was detected in seven of 22 patients (32%), and in most cases both in antral and body mucosa. Atrophy of the body glands was significantly more severe in lymphocytic gastritis patients. H pylori was detected in 13 of all 22 patients (59%); two of seven lymphocytic gastritis patients (29%), and 11 of 15 (73%) of patients without lymphocytic gastritis were H pylori positive. Patients with gastric lymphoma have significantly increased prevalence of lymphocytic gastritis. Rarity of H pylori in these patients might be connected with atrophic changes in body mucosa. Further studies are needed to show the significance of lymphocytic gastritis as a precursor of gastric lymphoma.

Adult↗
PubMed1994

Relation between IgG and IgA antibody titres against Helicobacter pylori in serum and severity of gastritis in asymptomatic subjects.

AIMS: To investigate whether the absorbance index of IgG and IgA antibodies against Helicobacter pylori is related to a semiquantitative assessment of the density of H pylori colonisation in gastric biopsy specimens and to the severity of gastritis. METHODS: The grade of gastritis was scored separately for antral and fundic mucosa using three different classifications. Serum IgA and IgG antibodies against H pylori were measured by ELISA. The density of gastric H pylori colonisation was graded semiquantitatively from 0 to 3. RESULTS: Among 48 healthy volunteers studied, 17 were found to have gastritis according to Whitehead's criteria. H pylori was present in the biopsy specimens of 14 of 17 subjects with gastritis. The IgG H pylori antibody absorbance index was significantly (p < 0.05) correlated not only with the density of antral H pylori colonisation, but also with the degree of gastritis of the antrum, as assessed by the Whitehead score, activity, and the Sydney system (p < 0.05). The IgA H pylori antibody absorbance index was significantly correlated with the Whitehead score and Sydney system, but not with the activity score of the antrum or with the density of antral gastric H pylori infection. There were no significant correlations between the IgG H pylori antibody absorbance index and the gastritis scores of the fundus mucosa and the density of H pylori infection of the gastric body. The IgA H pylori antibody absorbance index was only significantly (p < 0.05) correlated with the density of H pylori colonisation and the Sydney system gastritis score of the corpus. CONCLUSIONS: The serological absorbance index of IgG antibodies against H pylori is related to the severity of antral gastritis and the density of antral H pylori colonisation. Thus a high absorbance index of IgG antibodies against H pylori points to severe antral gastritis and dense H pylori colonisation of the antrum.

Adult↗
PubMed2000

Cell proliferation in type C gastritis affecting the intact stomach.

AIMS: Type C gastritis caused by bile reflux has a characteristic appearance, similar to that seen in other forms of chemical gastritis, such as those associated with NSAIDs or alcohol. An increase in mucosal cell proliferation increases the likelihood of a neoplastic clone of epithelial cells emerging, particularly where there is chronic epithelial injury associated with bile reflux. It has been shown previously that type C gastritis is associated with increased cell proliferation in the postsurgical stomach. The aim of this study was to determine cell proliferation in type C gastritis caused by bile reflux affecting the intact stomach. METHODS: Specimens from 15 patients with a histological diagnosis of type C gastritis on antral biopsy were obtained from the pathology archives between 1994 and 1997. A control group of nine normal antral biopsies was also selected and all underwent MIB-1 immunostaining. The gastric glands were divided into three zones (zone 1, gastric pit; zone 2, isthmus; and zone 3, gland base) and the numbers of positively staining nuclei for 500 epithelial cell nuclei were counted in each zone to determine the percentage labelling index (LI%). RESULTS: Cell proliferation was significantly higher in all three zones of the gastric glands with type C gastritis compared with controls as follows: zone 1, median LI% in type C gastritis 64.7 (range, 7.8-99.2), controls 4.7 (range, 2.0-11.3); zone 2, median LI% in type C gastritis 94.7 (range, 28.8-98.7), controls 40.2 (range, 23.1-70.3); and zone 3, median LI% in type C gastritis 20.0 (range, 1.3-96.0), controls 2.6 (range, 0.9-8.7). CONCLUSIONS: Bile reflux is thought to act as a promoter of gastric carcinogenesis in the postsurgical stomach. The same may be true in the intact stomach.

Adult↗
PubMed1999

Resolution of gastritis induced by Helicobacter pylori 4-5 weeks after successful eradication of infection using a triple therapy regimen of pantoprazole, amoxycillin and clarithromycin for one week.

UNLABELLED: This open-label study was designed to determine the extent of histological resolution of gastritis induced by Helicobacter pylori infection 4-5 weeks after successful eradication of the infection. Eradication was achieved using a triple therapy regimen consisting of a twice daily dose of pantoprazole 40 mg, clarithromycin 500 mg, and amoxicillin 1,000 mg taken for 1 week only. No other medications were given thereafter. Four biopsies were processed for histological examination of each patient, two from the antral and two from the corporeal mucosa, first at the start of the study and then again 4 weeks after cessation of the medication trial. Scoring for H. pylori colonization and the severity of gastritis was determined for each patient according to the Sydney system. 53 of 57 patients in this study had their H. pylori infection successfully eradicated by the regimen mentioned and could be histologically evaluated. According to the severity of gastritis in the antral mucosa, patients were studied in 3 groups: mild, moderate and severe gastritis. 17 of 19 cases with mild gastritis showed complete resolution of the inflammation, with residual inflammatory changes persisting in 2 cases only. 22 of the 26 cases with moderate gastritis showed almost complete recovery except for minor residual inflammatory changes as judged by irregularity of intracytoplasmic mucine storage. Persistent residual inflammatory changes in the lamina propria were detected in 4 cases. Of the 8 cases with severe gastritis 5 showed subsidence of the inflammatory changes, but the mucosa in these cases revealed some scarring, distortion of the glandular epithelium and atrophy. In 3 cases residual inflammation persisted. CONCLUSION: One-week therapy with a twice daily dose of pantoprazole 40 mg, clarithromycin 500 mg and amoxicillin 1,000 mg, used to eradicate H. pylori causing active inflammation of the gastric mucosa, has led to subsidence of the acute inflammatory changes in all the cases with residual inflammation persisting in 17%. Severe gastritis may cause irreparable damage to the gastric mucosa. The density of H. pylori colonization does not appear to be related to the severity of gastritis, nor to the successful eradication achieved.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1997

Helicobacter pylori and uremic gastritis: a histopathologic study and a correlation with endoscopic and bacteriologic findings.

In this work 70 asymptomatic uremic patients under maintenance hemodialysis in our institution underwent upper-gastrointestinal endoscopy as part of a routine investigation prior to kidney transplantation. Their endoscopic findings were scored and antral mucosal biopsies were obtained and subjected to histopathologic and bacteriologic assessment. Bacteriologic examination included culture, rapid urease test, and microscopic examination for detection of Helicobacter pylori. Histopathologic examination of the gastric mucosa showed chronic superficial gastritis in 52%, atrophic gastritis in 5.7% and intestinal metaplasia in 37% of the cases. Of the cases with superficial gastritis, 5 showed in addition gastric mucosal dysplastic changes. There was no correlation between the histopathologic and endoscopic findings. Nevertheless, there was a significant association between histopathologic changes and H. pylori infection (p = 0.0001). All cases with atrophic gastritis showed H. pylori, and of 24 cases with chronic active superficial gastritis. H. pylori was detected in 18, while it was detected in only 2 of 13 cases with chronic inactive superficial gastritis and in 4 of 29 cases with normal antral mucosal biopsies. Among different variables in dialysis patients, only patients' ages were found to have significant association with H. pylori infection (p < 0.03). We have concluded that in asymptomatic uremic patients under maintenance hemodialysis, relying only on endoscopy for critical assessment of the upper gastrointestinal tract is unsatisfactory and histopathologic examination of the antral mucosal biopsies is mandatory. Chronic superficial gastritis and atrophic gastritis should be expected in up to 60% of the patients, and there is a strong association between H. pylori infection and gastritis.

Adult↗
PubMed2005

Trichomonad gastritis in rhesus macaques (Macaca mulatta) infected with simian immunodeficiency virus.

In a retrospective study, 51 cases of gastritis (14%) were identified from among 341 necropsies performed on simian immunodeficiency virus (SIV)-infected rhesus macaques (Macaca mulatta) at the New England Primate Research Center from 1993 to 2001. Protozoa were seen in the stomach of 13 monkeys (25%) with gastritis. Two histopathologic manifestations of gastritis were observed: seven cases of lymphoplasmacytic gastritis with trichomonad trophozoites within lumens of gastric glands and four cases of necrosuppurative gastritis containing intralesional periodic acid-Schiff-positive protozoa; two cases of gastritis had morphologic features of both types of gastritis. In instances of necrosuppurative and combined lymphoplasmacytic and necrosuppurative gastritis, protozoa were 4-35 microm in diameter and round to tear-shaped. Because of the unusual morphology of the protozoa in these latter cases, transmission electron microscopy and polymerase chain reaction (PCR) were used to further identify these organisms. The protozoa were definitively identified as Tritrichomonas in all cases on the basis of ultrastructural characteristics (flagella and undulating membranes) and amplification of a 347-bp product of the 5.8S ribosomal RNA gene of Tritrichomonas foetus, Tritrichomonas suis and Tritrichomonas mobilensis by PCR using DNA extracted from stomach tissue. On the basis of these observations, we conclude that Tritrichomonas can be a significant cofactor in the development of necrosuppurative gastritis in SIV-infected rhesus macaques.

Animals↗