Acute necrotizing gastritis associated with adult T-cell leukemia in the course of chemotherapy

A 63-year-old man with smoldering adult T-cell leukemia (ATL) which became acute was admitted. During chemotherapy, he experienced epigastric pain and fever due to neutropenia. The combination therapy of antimicrobials and rhG-CSF was ineffective and he died. Autopsy revealed systemic invasion of ATL cells. The stomach findings resembled those of phlegmonous gastritis, a rare form of bacterial gastritis, along with diffuse, mucosal necrosis with hemorrhage. The pathogenesis of necrotizing gastritis remains to be elucidated. The patient had also received histamine H2 antagonist for gastric ulceration, which might have influenced the gastric bacterial flora.     

Emphysematous gastritis secondary to ingestion of large amounts of Coca Cola

Acute emphysematous gastritis (AEG) is a life-threatening disease in which gas-forming bacteria invade the gastric wall and cause acute inflammation of it. The clinical presentation of the patient with AEG is stormy: severe sepsis which usually leads to an early death. Presented herein is a case of a 16-yr-old boy with AEG. There were no predisposing factors to the condition in this case. Gas invaded the stomach wall and portal venous system, as well as the duodenal wall, a finding that has not been reported previously. The clinical course was very severe but, in contrast to previously reported cases, recovery was very rapid and left no sequelae.     

Management of nevus spilus

BACKGROUND: Granulomatous gastritis is a rarely observed pathological diagnosis. This condition often mimics gastric adenocarcinoma clinically, resulting in gastric resection. However, granulomatous gastritis has long been viewed as a benign process not observed in association with adenocarcinoma of the stomach. This article describes a patient with granulomatous gastritis occurring in close proximity to an area of superficially invading gastric adenocarcinoma. METHODS: Acid-fast stains, fungal stains, standard cultures, tuberculosis cultures, and a VDRL serum test were all obtained. Both upper endoscopy and colonoscopy were performed. Chest radiographs were taken and pulmonary consultation was obtained. RESULTS: The gastric samples obtained from resection showed no evidence of foreign body reaction. The acid-fast stains, fungal stains, cultures, and VDRL were all negative. Endoscopic exams did not show granulomatous inflammation in any other part of the gastrointestinal tract. No pulmonary disease was evident on radiographic or pulmonary exam. CONCLUSION: Isolated granulomatous gastritis is a diagnosis of exclusion. The findings in this patient do not support a diagnosis of Crohn's disease, tuberculosis, sarcoidosis, syphilis, histoplasmosis, berylliosis, or foreign-body reaction. This is a unique case suggesting an association between isolated granulomatous gastritis and metaplastic mucosal changes.     

Healthy cats are commonly colonized with "Helicobacter heilmannii" that is associated with minimal gastritis

Gastric Helicobacter infection in healthy pet cats is not well characterized. We performed endoscopy with gastric biopsy on 15 healthy pet cats that were rigorously screened to exclude underlying or concurrent diseases that might affect Helicobacter colonization. Gastric mucosa biopsy specimens were examined by histology, culture, and PCR for the presence of Helicobacter infection and by histology for the presence of gastritis. Of 15 cats, all but 1 had gastric Helicobacter-like organisms (GHLOs) on examination by light microscopy, and in the one histologically negative cat, GHLOs were detected by PCR. Gastric inflammation was mild or was absent for all cats. No Helicobacter species were identified by culture. Analysis of the 16S rRNA sequence from Helicobacter strains from 10 cats showed that all bacteria were closely related to Helicobacter felis, although there was heterogeneity among the sequences. These results suggest that the gastric mucosa of healthy pet cats is commonly colonized with an uncultivated Helicobacter that is closely related to H. felis, is associated with little or no gastritis, and shows heterogeneity in its 16S rRNA sequence. The epithet "Helicobacter heilmannii" continues to be an appropriate working designation for these bacteria.     

Animal models of bacterial gastritis: the role of host, bacterial species and duration of infection on severity of gastritis

Gastric bacteria from cheetahs with gastritis were used to inoculate specific-pathogen free kittens and conventional mice. Helicobacter sp. and Gastrospirillum sp. colonized kittens, while only Gastrospirillum sp. colonized mice. In kittens, both bacterial species induced mild lymphofolliclar gastritis which did not change over the course of the 11 months observation period. In mice, Gastrospirillum sp. induced lymphoplasmacytic and follicular gastritis which increased in severity over 6 months and persisted for the 12 month observation period. Gastric ulcers and gastric mucosal hypertrophy were present in chronically infected mice. These results indicate that host but not bacterial factors influence the severity of gastritis, and that in mice, bacterial gastritis increases in severity with time and may lead to gastric ulceration in some individuals.     

Evaluation of CD23 expression in paraffin-embedded gastric lymphomas of mucosa-associated lymphoid tissue

The CD23 antigen is expressed in a normal subset of B lymphocytes and in some non-Hodgkin's lymphomas. Reactivity for anti-CD23 (BU38) is present in paraffin-embedded tissue in the large majority of nodal small lymphocytic lymphomas, as well as in follicular center cell lymphomas. Most studies of gastric lymphomas of mucosa-associated lymphoid tissue (MALT) reported a lack of CD23, but these studies were performed on frozen tissue. We evaluated CD23 staining in paraffin-embedded tissue in a large series of gastric MALT lymphomas, as well as in cases of chronic gastritis. We assayed 49 well-characterized gastric lymphomas (9 high-grade non-MALT and 40 MALT [20 low grade, 13 mixed low and high grade, and 7 high grade]). High-grade MALT lymphomas without a low-grade component were distinguished from high-grade non-MALT lymphomas by the presence of lymphoepithelial lesions composed of large cells. In addition, we studies nine cases of chronic gastritis containing B-cell aggregates. We used anti-CD23 (BU38) in formalin-fixed, paraffin-embedded tissue. All of our low-grade gastric MALT lymphomas lacked CD23 immunoreactivity. One of the 13 mixed low-grade and high-grade lesions showed CD23 expression in the high-grade component. All of the high-grade MALT and high-grade non-MALT lesions lacked CD23. All of the nine cases of chronic gastritis lacked CD23. CD23 highlighted residual follicular dendritic cells and gastric epithelium. We concluded that gastric MALT lymphomas lacked CD23 (BU38) in paraffin-embedded tissue, with rare exceptions. This lack of CD23 expression might represent a useful feature in small or partially crushed biopsy specimens, particularly in the differential diagnosis with follicular small cleaved cell lymphoma presenting in the gastrointestinal tract.     

Dopamine receptor D2 Ser/Cys311 variant associated with disorganized symptomatology of schizophrenia

AIMS: To investigate the prevalence of lymphocytic gastritis in patients with coeliac disease. METHODS: Gastric biopsies from 70 patients with coeliac disease were examined by light microscopy for the presence of lymphocytic gastritis, defined as 25 or more intraepithelial lymphocytes/100 gastric columnar epithelial cells. RESULTS: Lymphocytic gastritis was found in seven cases. Positive cases had a mean of 32.1 intraepithelial lymphocytes/100 columnar cells, compared with a mean of 13.9 in negative cases, and 5.15 in noncoeliac controls. No differences were found for age, sex, gastric corpus or antrum, or degree of inflammation in the gastric lamina propria. All intraepithelial lymphocytes were of T cell lineage. Cases not showing lymphocytic gastritis did however show significantly increased gastric intraepithelial lymphocytes compared with non-coeliac controls. Eighteen of 70 cases were positive for Helicobacter pylori, and four of seven cases of lymphocytic gastritis were H pylori positive; no significant difference was observed between H pylori positive and negative patients. Three cases had concomitant ulcerative enteritis, of which none showed lymphocytic gastritis, while five cases had concomitant enteropathy associated T cell lymphoma, of which one showed lymphocytic gastritis. CONCLUSIONS: Lymphocytic gastritis occurred in 10% of patients with coeliac disease. Cases without lymphocytic gastritis nevertheless showed increased gastric intraepithelial lymphocytes. Coeliac disease may on occasion be a diffuse lymphocytic enteropathy occurring in response to gluten. Lymphocytic gastritis outside coeliac disease may involve an immune response to luminal antigens, such as H pylori, not unlike the response to gluten in patients with coeliac disease.     

Adjuvant therapy with a glycoprotein IIb-IIa inhibitor (abciximab) in coronary angioplasties with a high thrombotic risk

OBJECTIVES/DESIGN: Chronic inflammation is increasingly being linked to ischaemia, but the mechanism is poorly understood, and little is known about its effect on local gastric endothelial microvessels. We aimed at studying the number and surface area of gastric mucosal endothelial microstructures in the presence or absence of chronic gastritis. METHODS: Immunohistochemical assessments were carried out on gastric antral and body biopsies taken from patients with chronic gastritis and others with normal histology. The primary antibody (QB-END/10) was raised against CD34 antigen within the endothelial cell membranes. A computer attached to a microscope was used to count the number and measure the surface area of mucosal endothelial entities. RESULTS: In patients with Helicobacter pylori gastritis (n = 19), the median number of endothelial microstructures per section was 43 in the antrum and 86 in the gastric body, compared with 205 (P = 0.00004) and 165 (P = 0.002), respectively, in subjects with normal gastric histology (n = 11). The median surface area of the endothelial microstructures was also reduced in patients with gastritis. The normal gastric antrum had more endothelial entities than the normal body (median of 205 vs 165; P = 0.007). CONCLUSIONS: Within the normal stomach, the antrum is more richly vascularized than the gastric body. However, active chronic gastritis is associated with reduction in both the number and surface area of mucosal endothelial microstructures, with the reduction being more marked in the antrum. This is different from acute inflammation, and is relevant to our understanding of the natural history of mucosal defence, particularly the greater susceptibility of the gastric antrum to ulceration, compared with the gastric body.     

Fatal invasive gastric mucormycosis occurring with emphysematous gastritis: case report and literature review

Emphysematous gastritis is an often lethal, rare clinical entity referring to air bubbles in the wall of the stomach produced by gas-forming bacteria. Invasive gastrointestinal mucormycosis is an unusual clinical presentation of this invasive fungal disease. We report the first case of invasive gastric mucormycosis occurring with emphysematous gastritis, and review the literature regarding both of these clinical entities.     

Consistent improvement in sphincterotome orientation with manual grooming

AIMS: To determine the prevalence of lymphoid follicles in Helicobacter pylori positive and negative gastritis in antral and body type gastric mucosa in patients with non-ulcer dyspepsia (NUD), duodenal ulcer, or gastric ulcer; to correlate follicle presence with patient age; to evaluate the correlation between the prevalence of lymphoid follicles and active and inactive gastritis and its severity; and to assess the positive predictive value of lymphoid follicle prevalence with respect to H pylori infection. METHODS: Gastric biopsy specimens, graded according to the Sydney system, from 337 patients were studied. RESULTS: Lymphoid follicles occurred more often in antral mucosa (78%) than in body type mucosa (41%) and were observed in 85% of patients with H pylori positive gastritis. There was no significant difference between NUD and gastric and duodenal ulcer disease with regard to the presence of lymphoid follicles. The positive predictive value of the presence of lymphoid follicles in H pylori infection was 96%. Lymphoid follicles were more commonly observed in patients aged between 10 and 29 years. Lymphoid follicles were more frequently found in pangastritis of all subtypes than in antral gastritis and also in active gastritis than in inactive gastritis. The presence of lymphoid follicles correlated strongly with the degree and severity of gastritis. CONCLUSION: Lymphoid follicles are a constant morphological feature of H pylori associated gastritis.     

Appendicular skeletal muscle mass: prediction from multiple frequency segmental bioimpedance analysis

The presence of Helicobacter pylori (H. pylori) in the stomach is closely associated with histological signs of chronic active gastritis and peptic ulcer. Another spiral organism named Gastrospirillum hominis (G. hominis) has led to further interest in the bacterial pathogenesis of gastritis. Due to the low prevalence of G. hominis, it is difficult to evaluate its biological behavior. Recently 16 cases of G. hominis-associated gastritis were found in 257 Thai individuals, which made it possible to study the biological characteristics of G. hominis and its relationship with gastric mucosal inflammation. The results showed that H. pylori and G. hominis could be easily observed in the lower third of the mucous layer and in the mucosa of the gastric pits by means of toluidine blue staining. Both bacteria immunostained positive. Helicobacter pylori were usually in the shape of curved bacillary while G. hominis often appeared in spiral configuration. In 257 cases of Thai subjects, 169 cases were found to be H. pylori positive, the detection rate was 65.7%, and 16 cases were G. hominis positive, with a 6.2% detection rate. In G. hominis infection, 43.6% of cases had normal gastric mucosa. Superficial, erosive and atrophic gastritis cases were 13.2, 10.9 and 12.5%, respectively. Mucosal inflammation was usually severe in H. pylori, but neutrophil polymorph infiltration was often mild and focal in G. hominis infection. Although no G. hominis infection with carcinoma was shown in our cases, the occurrence of mucosal atrophy, metaplasia and dysplasia was higher in both bacterial infections compared with H. pylori- and G. hominis-negative cases. It is suggested that G. hominis may be partly responsible for the mucosal inflammation and some malignant-associated lesions.     

Temporal stability of antisocial personality disorder: blind follow-up study at 8 years

We studied the relation between Helicobacter pylori and residual gastritis in 28 patients with gastric cancer on whom distal partial gastrectomy with Billroth I reconstruction was performed over a 13-month period. They were subjected to serologic testing along with endoscopic and histologic examinations before operation and at 3, 6, and 12 months after operation. Anti-H. pylori immunoglobulin G (IgG) and serum gastrin levels were measured by serologic tests. The presence or absence of gastritis was determined endoscopically, and gastric mucosal hexosamine levels were determined. Gastritis was measured quantitatively by histologic examination in specimens taken from the gastric mucosa using Rauws' score. After the initial histologic evaluation we divided the H. pylori-positive patients into two groups: those with a Rauws' score of 0 to 3 ("weak" gastritis group), and those with a Rauws' score of 4 to 10 ("strong" gastritis group), allowing us to compare the results of our three postoperative histologic examinations of the two groups for possible significant differences. Our endoscopic examinations showed gastric mucosal inflammatory changes in both H. pylori-positive and H. pylori-negative patients at 3, 6, and 12 months after operation, but there was no significant difference between these two groups at any point. During the histologic examinations, however, anti-H. pylori IgG assay had become negative in several patients in the "weak" gastritis group at 3 months after operation and was found to have become negative in 78% of all patients in that group 12 months after operation. In contrast, in the "strong" gastritis group H. pylori infection was still evident in the patients 12 months after operation, suggesting that "strong" histologic gastritis may have some connection to H. pylori infection, whereas "weak" histologic gastritis has no such connection. The gastric mucosal hexosamine level was higher in the "weak" gastritis group than in the "strong" gastritis group both before operation and at 6 and 12 months, indicating some relation between gastric inflammatory changes and hexosamine levels in gastric mucosa. It further suggested the possibility that H. pylori plays a role in destroying gastric mucosa by depleting mucin, thus acting as one (though not the only) cause of residual gastritis after distal partial gastrectomy. In conclusion, we found evidence that there is a relation between residual gastritis and H. pylori infection, but H. pylori is not the sole cause of residual gastritis after gastric surgery. A causal relation is difficult to detect by simple analysis of histologic findings or by endoscopic observation or clinical symptoms alone.     

Helicobacter pylori infection and gastric cancer. A nested case-control study in a rural area of Japan

We conducted a seroepidemiological nested case-control study to determine the association of gastric cancer with Helicobacter pylori infection and atrophic gastritis. A cohort of 2858 participants in an annual multiphasic health check-up were followed for eight years. Data for 45 gastric cancer cases and 225 sex-, age-, and address-matched control subjects were analyzed. Helicobacter pylori infection was determined by IgG antibodies, and atrophic gastritis was diagnosed by both serum pepsinogen I level (< or = 70 ng/ml) and the pepsinogen I/II ratio (< or = 3.0). Univariate analysis showed that Helicobacter pylori and atrophic gastritis were significantly associated with gastric cancer. In a multivariate analysis, atrophic gastritis was associated with significantly increased risk of cancer (odds ratio, 3.38; 95% confidence interval, 1.54-7.42); however, Helicobacter pylori was not associated with cancer (odds ratio, 1.84; 95% confidence interval, 0.59-5.72). These results suggest that Helicobacter pylori infection alone is not directly associated with gastric carcinogenesis but has an indirect relation to gastric cancer through the development of atrophic gastritis.     

Treatment of gastritis in cheetahs (Acinonyx jubatus)

Three cheetahs (Acinonyx jubatus) had a clinical history of chronic spiral bacteria-associated gastritis and three cheetahs had no clinical history of gastritis. Gastric biopsies were obtained from all six cheetahs prior to treatment for gastritis and 3 wk and 1 yr posttreatment. The cheetahs were treated with tetracycline hydrochloride 500 mg p.o. q.i.d., metronidazole 250 mg p.o. q.i.d., and bismuth subsalicylate 300 mg p.o. q.i.d. Each drug was administered concurrently for 7 days. Following this treatment, each cheetah was maintained on 300 mg bismuth subsalicylate p.o. s.i.d. for 1 yr. The three cheetahs with a history of gastritis were culture positive for Helicobacter acinonyx and remained positive during the entire study. The three cheetahs with no clinical history of gastritis were culture negative for H. acinonyx, but gastric biopsies revealed Gastrospirillum-like bacteria (tentatively named Helicobacter heilmannii) pretreatment. Gastric biopsies were negative for H. heilmannii on subsequent examinations. Although the treatment did not eradicate H. acinonyx, it did provide symptomatic relief from the vomiting, anorexia, and weight loss associated with clinical gastritis. The use of endoscopically guided gastric mucosal biopsies for urease testing and histopathologic examination of Warthin-Starry-stained sections is a sensitive and specific method of diagnosing spiral bacteria-associated gastritis. Treatment of spiral bacteria-associated gastritis in cheetahs should include the rational use of antibiotics (tetracycline or amoxicillin and metronidazole), bismuth compounds, and omeprazole and evaluation of husbandry methods to reduce stress.     

In vitro cytotoxic effects of vacuolating cytotoxin produced by clinical isolates of Helicobacter pylori

The vacuolating cytotoxin produced by Helicobacter pylori is considered to be one virulence factor causing peptic ulceration. In this study, we examined the activity of vacuolating cytotoxin in induction of intracellular vacuolation of rabbit gastric epithelial cells (RGECs). We used culture supernatants of H. pylori as a source of vacuolating cytotoxin and quantitated cytotoxic activity by the MTT method. Intracellular vacuolation of RGECs was observed in the presence of 36 of 57 (63%) clinically isolated H. pylori strains. However, there were no differences in the incidence of H. pylori strains with positive vacuolating cytotoxin (Tox+) among patients with gastritis, gastric ulcers or duodenal ulcers. The MTT assay showed that the cytotoxic activity of H. pylori supernatants obtained from patients with gastric ulcers was significantly higher than in patients with gastritis (p < 0.01), but was not different to duodenal ulcer patient supernatants. Similar results were also observed in Tox+ isolates, however, there were no significant differences between patients with regard to the incidence of vacuolating cytotoxin-negative isolates. Although our data may not indicate a clear correlation between prevalence of vacuolating cytotoxin and clinical manifestations, they suggest that H. pylori harboring vacuolating cytotoxin may particularly induce damage to the gastric epithelium in patients with gastric ulcers.     

Higher incidence of Gastrospirillum sp. in swine with gastric ulcer of the pars oesophagea

Gastric ulcer in swine is characterized by an area of acid-peptic digestion, occurs usually in the pars oesophagea of the stomach, and has unknown etiopathogenesis. The present work was carried out to investigate the prevalence of the newly described spiral-shaped microorganism Gastrospirillum sp. ("Gastrospirillum suis") in stomachs of abattoir pigs with and without gastric ulcer. Stomachs were removed from 32 consecutive pigs presenting apparently normal mucosa and from 32 additional consecutive pigs presenting frank, chronic gastric ulcer of the pars oesophagea. Fragments of antral, oxyntic, cardiac and pars oesophagea regions were taken from each stomach and processed for histology and for identification of Gastrospirillum sp. in tissue sections. The microorganisms were identified mainly in the mucous layer and in gastric foveolas of the antral and oxyntic mucosa. Forty pigs (62.5%) were positive for Gastrospirillum sp.; among them, 27 (67.5%) had gastric ulcer, and 13 (32.5%) had no ulcer. Twenty-four pigs (37.5%) were negative for Gastrospirillum sp.; among them, five (20.8%) presented with gastric ulcer, and 19 (79.2%) had no ulcer. There was a significant difference between pigs with and without gastric ulcer in regard to the presence of Gastrospirillum sp. (P < 0.01). The spiral-shaped microorganism Gastrospirillum sp. that inhabits the stomach of pigs should be considered a possible factor connected with the etiopathogenesis of swine gastric ulcer.     

The modified Steiner stain: a new use for an old stain? Staining cytomegalovirus-infected cells in gastrointestinal biopsies

The modified Steiner stain is a non-specific silver stain for identifying bacteria in formalin-fixed, paraffin-embedded tissues. The principle behind its use is that bacteria are first sensitized using uranyl nitrate solution, making them able to precipitate silver from a silver nitrate solution. It is used routinely for staining gastric biopsies to identify Helicobacter pylori. Upon staining a gastric biopsy from a patient with acquired immunodeficiency syndrome (AIDS) and cytomegalovirus gastritis, we recognized that this technique also stains the viral inclusions of cytomegalovirus-infected cells. We then proceeded to stain 43 consecutive cytomegalovirus-positive gastrointestinal biopsies from 33 immunocompromised patients based on positive cytomegalovirus immunohistochemistry (DAKO-cytomegalovirus monoclonal antibody, clones DDG9 and CCH2). We also stained eight cytomegalovirus-infected, non-gastrointestinal tissues, including lung, adrenal gland, ovary, skin and neural tissue, to ensure that the stain was staining the cytomegalovirus-infected cells and not argyrophilic or argentaffin neuroendocrine cells of the gastrointestinal tract. In 40 of the 43 cytomegalovirus-infected gastrointestinal biopsies, we saw positive staining with the modified Steiner stain (93% sensitivity). The cytomegalovirus-infected, non-gastrointestinal tissues all stained positively with the modified Steiner stain. Because the modified Steiner stain is frequently used to identify Helicobacter pylori in gastric biopsies, we propose that it be studied further for possible use either as a screen or as a confirmatory tool, or both, for cytomegalovirus inclusions in gastrointestinal biopsies.     

The occurrence of spiral-shaped bacteria in the abomasum of cattle

The goal of this study was to determine whether Helicobacter pylori or similar bacteria are present in the abomasum of cows. The abomasa of 112 clinically healthy cows were examined at slaughter. Prior to macroscopic examination, samples for bacteriological and histological examination were obtained from the fundus and from the pylorus. Bacteriological examination of the abomasal mucosa included the urease test, the microscopic examination of a Gram's stained smear, and culture on various solid media. Samples from the pylorus (63) were more often positive in the urease test than those from the fundus (35). Examination of Gram's stained smears revealed two groups of suspicious microorganisms; spiral-shaped and rod-shaped bacteria, whereby the latter could not be differentiated morphologically from Helicobacter pylori. Spiral-shaped bacteria were more often isolated from the pylorus (101 samples) than from the fundus (30 samples). The bacteria that resembled Helicobacter pylori were found in seven samples from the pylorus and in seven samples from the fundus. Helicobacter pylori was not cultured in any of the abomasal samples. Tissue samples from the fundus and pylorus were stained with hemalum and eosin and with silver according to Warthin-Starry. All but one abomasum had diffuse infiltration of lymphocytes and plasma cells. Lymphocytic follicles were observed in 109 abomasa. Neutrophils were seen in four abomasa, eosinophils in 37 and parasitic lesions in 20. As in the Gram's stained smears, spiral-shaped and rod-shaped bacteria were seen in silver-stained smears. Spiral-shaped bacteria were found in the pylorus of 96 abomasa and in the fundus and pylorus of one abomasum. The rod-shaped bacteria could not be differentiated from Helicobacter pylori by light microscopy. They were seen in glandular lumina of the superficial region of the mucosa in 97 abomasa. They were limited to the pylorus and fundus in 16 and 59 cases, respectively, and occurred in both these areas in 23 cases. The results of this study indicate that spiral-shaped bacteria may be found frequently in the bovine abomasum. Further investigations are required to determine whether these bacteria are associated with the inflammatory lesions that were observed and whether they play a role in the pathogenesis of abomasal ulcers.     

Dose uniformity of ferromagnetic seed implants in tissue with discrete vasculature: a numerical study on the impact of seed characteristics and implantation techniques

There is evidence of a two-way interaction between gastric acid secretion and H. pylori-associated gastritis. Gastric acid secretion influences the density of H. pylori colonisation, its distribution within the stomach and the severity of the mucosal inflammatory response to the infection. In addition, H. pylori gastritis alters gastric acid secretion. In subjects with a predominant antral gastritis, it increases acid secretion predisposing to duodenal ulcer, whereas in others with predominant body gastritis, acid secretion is impaired and the subjects have an increased risk of gastric cancer. The two-way interaction between acid secretion and H. pylori gastritis is observed when H. pylori-positive subjects are treated with proton pump inhibitor agents. The inhibition of acid secretion induces a body gastritis and this inflammation of the body mucosa inhibits acid secretion thus augmenting the anti-secretory effect of the drug. In this article, we discuss the interaction between gastric acid secretion and H. pylori gastritis and its importance in determining disease outcome.     

Severe metabolic alkalosis

In the rat, hypergastrinaemia induced by drug treatment with omeprazole or potent H2-receptor antagonists leads to the development of gastric enterochromaffin-like cell carcinoids. In man, gastric carcinoids induced by hypergastrinaemia have been described only in patients with chronic atrophic gastritis type A and in patients with the multiple endocrine neoplasia syndrome type 1. This patient with Zollinger-Ellison syndrome without gastric mucosal atrophy and without evidence of the multiple endocrine neoplasia syndrome developed an argyrophil gastric carcinoid tumour. This observation indicates that hypergastrinaemia in the sporadic Zollinger-Ellison-syndrome may induce gastric carcinoids.