Atrophic gastritis is associated with increased sucrose permeability related to chronic inflammation

BACKGROUND: Different theories have been presented to explain how atrophic gastritis may lead to gastric cancer development. One contributing factor could be impaired function of the gastric mucosal barrier. The aim of this study was to investigate if there are changes in gastric mucosal permeability to sucrose in atrophic gastritis. METHODS: The study comprised 22 patients with atrophic gastritis and 21 normal controls. Gastritis was classified according to the Sydney system from endoscopic biopsies of the gastric corpus and antrum. All subjects were exposed to oral sucrose load (100 g), and the fraction of sucrose excreted in urine was measured by gas chromatography-mass spectrometry. RESULTS: The fraction of sucrose excreted in urine after oral load was significantly increased in atrophic gastritis compared with controls (median 0.08 vs. 0.04%; p = 0.003). Sucrose excretion was positively related to the degree of chronic inflammation (median fraction excreted: mild inflammation 0.06%, moderate inflammation 0.08%, severe inflammation 0.18%; p = 0.04) rather than to the degree of atrophy in the gastric mucosa. Occurrence of intestinal metaplasia was also associated with significantly higher sucrose excretion. However, in multivariate analysis, including intestinal metaplasia, only the degree of inflammation was positively related to sucrose excretion. CONCLUSION: Atrophic gastritis is associated with increased sucrose permeability, suggesting paracellular leakage of the gastric mucosa. This leakage seems to be related to the degree of inflammation rather than the degree of atrophy. The findings may have implications for the diseases and complications associated with atrophic gastritis.     

Low B12 levels in chronic idiopathic urticaria.

Recent studies suggest that autoimmune mechanisms may be involved in the etiology of chronic idiopathic urticaria (CIU). There is a higher prevalence of B12 deficiency in autoimmune diseases and possibly in gastric Helicobacter pylori (H. pylori) infection. The frequency of B12 deficiency in CIU is unknown. Our objective in this study was to determine the prevalence of B12 deficiency in patients with CIU and also its relationship to gastric H. pylori infection and serologic markers of autoimmunity in these groups. Thirty-three patients with CIU and 27 healthy controls were included in the study. Serum vitamin B12 levels, H. pylori infection and serological markers of autoimmunity (anti-thyroglobulin, thyroid microsomal, gastric parietal cell and antinuclear autoantibodies) were investigated. H. pylori infection was determined according to serology and gastric biopsy in 19 patients, serology and urea breath test in 4 patients and serology alone in the remaining 10 patients. Serum B12 levels were below the normal reference range in 11/33 (33.3%) patients with CIU. The mean serum B12 levels among patients with CIU and the controls were 281+/-127.5 pg/ml and 465.1+/-140.3 pg/ml (p=0.0001), respectively. Anti-thyroid antibodies were positive in 6 of 11 patients (54.5%) with low B12 levels, but only in 4 of 27 (14.8%) healthy controls (p=0.019). Anti-GPC antibodies were positive in 4 of 11 (36.4%) patients with CIU and low B12 levels, but only in 2 of 27 (7.4%) healthy controls (p=0.047). In CIU patients, there was no difference in the frequency of IgG H. pylori antibodies between those with low B12 levels and normal B12 levels. Among the 19 patients who had been performed gastric endoscopy, 15 patients (78.9%) had chronic antral gastritis, 2 patients (10.5%) had atrophic gastritis and there were normal findings in 2 patients (10.5%). In conclusion, serum B12 levels were found to be below the normal reference range in 33% of the patients with CIU. An association between low B12 levels and H. pylori could not be shown. The higher frequency of antithyroid and anti-GPC antibodies in patients with low B12 levels suggest that low B12 levels in CIU may be autoimmune in nature.     

Morphological features and secretory gastric function in patients with chronic gastritis against the background of B12 deficiency anemia]

As many as 45 patients with chronic atrophic gastritis against the background of B12 and iron-deficiency anemia were examined. Chronic atrophic gastritis combined with B12 deficiency anemia was found to damage in most cases the antral and fundic parts of the stomach simultaneously, while the gastric process combined with iron-deficiency anemia involved the antral part only in most cases. The disease is accompanied by a considerable reduction of acid, pepsinogen and biermerin formation, especially in cases of chronic atrophic gastritis associated with B12 deficiency anemia.     

Duodenogastric reflux: correlations among bile acid pattern, mucus secretion, and mucosal damage

Forty-five patients with bile reflux at endoscopic examination, confirmed by titration of bile acids in gastric juice, were admitted to the study and divided into three groups in accordance with histologic results: normal findings, chronic superficial gastritis, and chronic atrophic gastritis. Bile acid pattern was determined in duodenal samples by high-performance liquid chromatography titration, and the mucoprotein content of gastric juice was assessed. The results of qualitative analysis of bile acid showed an increase of deoxycholic acid in patients with atrophic gastritis (p less than 0.05) in comparison with controls; determination of taurine and glycine conjugates showed an increase of taurodeoxycholic acid in patients with atrophic gastritis (p less than 0.01) compared with controls. The composition of mucus was altered only in patients with atrophic gastritis. Whether the increase in deoxycholic acid in biliary reflux is a factor in the development of chronic atrophic gastritis or is secondary to the increase of gastric pH, detectable in this condition, is still uncertain. However, the increase of deoxycholic acid and its taurine conjugates may be a factor that leads to persistence of mucosal lesions.     

Significance of endoscopically visible blood vessels as an index of atrophic gastritis.

The endoscopic criteria for atrophic gastritis are. 1. pale mucosa; 2. shiny surface and 3. prominent submucosal vessels. To evaluate the diagnostic accuracy of circumscribed atrophic gastritis based on these findings, we studied 184 consecutive upper gastrointestinal endoscopies. The endoscopic diagnosis of atrophic gastritis was made only if two endoscopists both agreed on the findings and interpretation. The location of the atrophic pattern and whether it was circumscribed or diffuse were recorded. Two biopsy specimens were than obtained. Histologic material was interpreted by a pathologist who had no prior knowledge of the endoscopic findings. Twenty-five patients (13%) had atrophic gastritis endoscopically; in four it was diffuse and in 21 it was circumscribed. Utilizing the criteria of Whitehead, et al, atrophic gastritis was diagnosed histologically in three of four patients with diffuse gastritis but in one of those considered to have circumscribed atrophic gastritis. It is concluded from these preliminary data that a circumscribed atrophic mucosal pattern is a frequent endoscopic finding that does not necessarily represent atrophic gastritis histologically.     

Association of tumor necrosis factor genetic polymorphism with chronic atrophic gastritis and gastric adenocarcinoma in Chinese Han population

AIM:To investigate the association of TNF polymorphisms with chronic atrophic gastritis (CAG) and gastric adenocarcin-oma in Chinese Han patients.METHODS:The TNFa-e 5 microsatellites and 3 RFLP sites were typed using PCR technique,followed by high-voltage denaturing PAGE with silver staining and restriction enzyme digestion respectively in specimens from 53 patients with CAG and 56 patients with agstric daenocarcinoma and 164 healthy controls.The PCR products were cloned and sequenced.RESULTS:The frequency of TNF-β Ncol*1/2 genotype was higher in patients with chronic atrophic gastritis than in healthy controls,but no significant difference was observed(60.38% vs 46.34%,p=0.076).The frequency of TNa10 allele was significantly higher in patients with chronic atrophic gastritis than in healthy controls(19.81% vs 11.89%,p=0.04).However,it did not relate to age,gender,atrophic degree or intestinal metaplasin in patients with chronic atrophic gastritis,The frequency of TNF-β Ncol*1/2 and d2/d6 genotypes were significantly higher in patients with gastric adenocarcinoma than in healthy indiveduals(p>0.05).However,TNF-β Ncol*1/2 and d2/d6 genotypes did not relate to age,gender,grade of differentiation and clinicopathologic state in patients with gastric adenocarcinoma.The frequency of TNFa6b5c1 hapolotype homoaygote was significantly lower in patients with gastric adenocarcinoma than in healthy controls (1.79% vs 15.85%,p=0.006).CONCLUSION:TNFa10 allele may be a risk factor for chronic atrophic gastritis ,TNF-β Ncol*1/2 and d2/d6 genotypes are associated with the suscepotibility to gastric adenocarcinoma,whereas TNFa6b5c1 haplotype homozygote may contribute to the resistance against gastric adenocarcinoma.     

Atrophic body gastritis patients with enterochromaffin-like cell dysplasia are at increased risk for the development of type I gastric carcinoid.

BACKGROUND/AIMS: In the presence of atrophic body gastritis, gastric carcinoid develops from gastric-body mucosa enterochromaffin-like cells. Few data exist on the prevalence of enterochromaffin-like dysplastic lesions in atrophic body gastritis patients and their presumed risk of evolution to carcinoid has never been assessed prospectively in humans. The aim of the present study was to investigate the prevalence and incidence of dysplastic and neoplastic enterochromaffin-like cell lesions in a consecutive series of patients with atrophic body gastritis. METHODS: A total of 130 atrophic body gastritis patients at diagnosis and 96 atrophic body gastritis patients at follow-up (median 30 months) underwent gastroscopy with multiple biopsies and fasting gastrinaemia evaluation. In patients with enterochromaffin-like cell dysplasia, a more detailed bioptic sampling at follow-up was performed. RESULTS: Of the 130 atrophic body gastritis patients, only one (0.7%) had a gastric carcinoid polyp, whereas enterochromaffin-like cell dysplasia was found in five patients (3.8%). At follow-up only one out of the 96 atrophic body gastritis patients (1%) was diagnosed as having a carcinoid polyp at 41 months. Enterochromaffin-like cell dysplasia was present in four additional patients (4.2%). Two atrophic body gastritis pernicious anaemia patients with enterochromaffin-like cell dysplasia developed a gastric carcinoid in the follow-up. Among nine atrophic body gastritis patients with enterochromaffin-like cell dysplasia, the incidence of carcinoid tumour was 22% compared to 1.1% of atrophic body gastritis patients without dysplasia (odds ratio: 26.00; 95% confidence interval: 2.089-323.52). During the follow-up, fasting gastrin levels increased significantly only in atrophic body gastritis patients with enterochromaffin-like cell dysplasia (mean 677.4 +/- 66.1 vs 1112.2 +/- 185.6; P = 0.0287). CONCLUSION: This study provides the first clinical evidence that, in hypergastrinaemic atrophic body gastritis patients, enterochromaffin-like cell dysplasia carries a markedly increased risk for development of type I gastric carcinoid. This suggests that a more detailed endoscopic/bioptic procedure in this subgroup of atrophic body gastritis patients is able to detect gastric carcinoid at an early stage.     

Relationship between pepsinogen I/II ratio and age or upper gastrointestinal diseases in Helicobacter pylori-positive and -negative subjects]

BACKGROUND/AIMS: Although previous reports suggested that pepsinogen (PG) I/II ratio was the index of gastric atrophy, PG I/II ratio was also related to other factors such as Helicobacter pylori (H. pylori) infection, various gastrointestinal diseases, and aging. The aim of this study was to evaluate the relationship between serum PG I/II ratio and age or upper gastro-intestinal diseases according to H. pylori infection status. METHODS: A total of 529 individuals (307 male; mean age, 57.2 years) were divided into 4 groups (94 gastric ulcers, 35 duodenal ulcers, 105 reflux esophagitis, and 295 atrophic gastritis) according to endoscopic diagnosis. H. pylori infection was determined by H. pylori IgG antibody (ELISA) and PG was measured by latex immunoassay. RESULTS: H. pylori infected patients showed markedly increased serum PG II levels (24.0+/-14.7 ng/mL vs. 13.8+/-16.6 ng/mL, p0.001) and low PG I/II ratio (3.9+/-2.0 vs. 6.0+/-2.5, p0.001) than non-infected subjects. In H. pylori infected patients, mean PG I/II ratios in the gastric ulcer and atrophic gastritis group were significantly lower than those of the duodenal ulcer and reflux esophagitis group (p0.001, ANOVA, Turkey's multiples comparison test). The mean ratio of open type atrophic gastritis was lower than that of close type atrophic gastritis (3.0+/-1.4 vs. 3.8+/-1.7, p0.005). PG I/II ratio gradually decreased with age in H. pylori-infected patients with atrophic gastritis (R(2)=0.9, p=0.005, linear regression analysis). CONCLUSION: Serum PG I/II ratio reflects H. pylori infection and gastric atrophy. In the presence of H. pylori infection, gastric atrophy progresses with age.     

Helicobacter pylori infection in patients with acquired immune deficiency syndrome

A controlled study was conducted on patients with human immunodeficiency virus (HIV) infection referred for upper endoscopy to evaluate the prevalence of Helicobacter pylori (H. pylori) infection. Four different stains and culture for H. pylori were performed on biopsy specimens from the gastric antrum. Sixteen (40%) of 40 patients with acquired immune deficiency syndrome (AIDS) or AIDS-related complex (ARC) were diagnosed to be infected with H. pylori versus 14 (39%) of 36 age-matched control patients. Eight of 15 AIDS/ARC patients without AIDS-related esophagogastroduodenal findings (53%) were infected with H. pylori versus 8/25 (32%) with endoscopic findings typical of AIDS. No invasion of the lamina propria by H. pylori was noted in any patient. Active chronic gastritis was present in 60% of AIDS/ARC patients and 61% of controls. Fifty-eight and 59%, respectively, of active chronic gastritis cases were infected with H. pylori. All the H. pylori infections, except one, were found in patients with chronic gastritis. In AIDS/ARC patients, H. pylori infection and active chronic gastritis are as common as in other patients referred for upper endoscopy. They may play a pathogenic role, especially when endoscopic AIDS-related findings are lacking. Cell-mediated immune deficiency does not appear to increase the risk of infection with H. pylori.     

Study of gastrointestinal polypeptides controlling gastric acid secretion in patients with primary antibody deficiency.

BACKGROUND: Gastric abnormalities are a common feature in patients with primary antibody deficiency. The most important problem is the high incidence of stomach cancer found in these patients. Chronic atrophic gastritis with pernicious anemia is also a common finding that predisposes to gastric adenocarcinoma. The aim of the present study was to identify factors predictive of high risk for developing gastric cancer in patients with primary antibody deficiency. PATIENTS AND METHODS: We studied gastric hormones (gastrin, somatostatin and gastrin-releasing peptide, GRP) in 47 patients (23 children and 24 adults) with primary antibody deficiency. In accordance with the World Health Organization (WHO) classification, patients were diagnosed as having X-linked agammaglobulinemia (Bruton disease) in 13 cases, common variable immunodeficiency in 28, and hypogammaglobulinemia with hyperIgM in 6. Gastric biopsy was performed in 22 patients (16 children and 6 adults). Hormone determinations were carried out by radioimmunoassay. RESULTS: Baseline serum gastrin levels were normal or increased compared with controls, but the response to stimulation with a hyperproteic diet was delayed in 18 patients and lower than in controls in 7. In 4 adult patients, all with pernicious anemia, gastric biopsy revealed chronic atrophic gastritis involving the stomach corpus and antrum (type B gastritis). The absence of a normal response of gastrin secretion to stimulation with a hyperproteic diet may be explained by this finding. Serum somatostatin and GRP levels were higher than in controls. No correlations were found between these findings and patient age, type of immunodeficiency or duration of clinical manifestations.     

Autofluorescence imaging for predicting development of metachronous gastric cancer after Helicobacter pylori eradication

Background and Aims: Although Helicobacter pylori eradication decreases the incidence of metachronous gastric cancer after endoscopic treatment for early gastric cancer (EGC), metachronous cancer still develops after successful eradication, particularly in patients with severe corpus gastritis. We investigated whether the extent of atrophic fundic gastritis diagnosed by autofluorescence imaging (AFI) videoendoscopy is predictive of development of metachronous gastric cancer after H. pylori eradication in patients treated with endoscopic submucosal dissection (ESD) for EGC. Patients and Methods: A total of 82 patients who underwent ESD for EGC from 2003 to 2006, who received eradication therapy participated in this study. The extent of chronic atrophic fundic gastritis was evaluated by AFI and categorized into closed and open type. The main outcome was the incidence of metachronous gastric cancer detected by annual surveillance endoscopy. Results: During a median observation period of 55 months, metachronous gastric cancer developed in 12 of 82 patients (14.6%). Multivariate Cox's proportional hazard analysis revealed that open‐type, atrophic fundic gastritis diagnosed by AFI was significantly associated with development of metachronous gastric cancer (hazard ratio: 4.88, 95% confidence interval [CI]: 1.32–18.2, P = 0.018) after adjustment for age, sex, histological intestinal metaplasia, serum pepsinogen level, and H. pylori status. Conclusions: Metachronous EGC developed after successful H. pylori eradication, and extensive atrophic fundic gastritis diagnosed by AFI was a significant predictor, thus it could identify patients undergoing ESD for EGC who still required intensive surveillance after eradication.     

Prevalence of Helicobacter pylori infection and gastric cancer precursor lesions in patients with dyspepsia

BACKGROUND: Helicobacter pylori infection has been considered to play significant role in gastric carcinogenesis, but only a minority of people who harbor this organism will develop gastric cancer. H. pylori infection first causes chronic non atrophic gastritis. Chronic non atrophic gastritis may evolve to atrophic gastritis and intestinal metaplasia and finally to dysplasia and adenocarcinoma. AIMS: To estimate the prevalence of H. pylori infection and the precancerous gastric lesions and their relationship, in patients with dyspeptic symptoms who underwent upper gastrointestinal endoscopy at a reference center in the central region of Rio Grande do Sul state, Brazil. METHODS: We analyzed gastric biopsies taken from corpus and antrum of patients who underwent upper gastrointestinal endoscopy for H. pylori detection, between 1994 and 2003. According to Sydney system, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed by histological examination (H-E stain). The histological diagnoses were related to H. pylori infection status. RESULTS: Biopsies from 2,019 patients were included in the study. Patients mean age was 52 (+/-15) and 59% were female. Seventy six percent had H. pylori infection. Normal mucosa, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed in 5%, 77%, 3% and 15%, respectively. The OR for any degree of gastric mucosa lesion in infected patients was 10 (CI95% 6.50 - 17%). The OR for infected patients had chronic non atrophic gastritis was 3 (CI95% 2,2 - 3,4). The OR for infected patients had atrophic gastritis or intestinal metaplasia was less than 1. CONCLUSIONS: The prevalence of H. pylori infection in this population was high (76%) and infected individuals had the probability 10 folds greater than non infected individuals to have any lesion of gastric mucosa. The prevalence of precancerous lesions was 77% for non atrophic chronic gastritis, 3% for atrophic gastritis and 15% for intestinal metaplasia. Infected patients had risk 3 folds greater than non-infected for the occurrence of non atrophic chronic gastritis. H. pylori infection did not show risk for occurrence of atrophic gastritis and intestinal metaplasia, suggesting that other risk factors should be involved in the carcinogenesis process.     

Folic acid malabsorption in atrophic gastritis. Possible compensation by bacterial folate synthesis

Folic acid absorption was studied in 12 elderly subjects with atrophic gastritis and 10 elderly normal controls using tritium-labeled pteroylmonoglutamic acid. Two folic acid absorption tests were carried out on each subject with 120 ml of either water or 0.1 N HCl. Folic acid absorption was significantly lower in subjects with atrophic gastritis than in normal controls (31% vs. 51%, respectively; p less than 0.01). In subjects with atrophic gastritis, folic acid absorption rose significantly to 54% (p less than 0.001) when administered with acid, but did not change in normal controls (50%). Serum folate levels were normal in all subjects. Proximal small intestinal pH was higher in atrophic gastritis subjects than in normal controls (7.1 vs. 6.7, respectively; p less than 0.05), as were bacterial counts of small intestinal fluid (p less than 0.01). Bacteria cultured from the aspirates of subjects with atrophic gastritis were able to synthesize folate in vitro when incubated in a folate-free medium. Atrophic gastritis results in folic acid malabsorption but not in folate deficiency, possibly due to increased bacterial synthesis of folate in the small intestine.     

Does cholecystectomy affect antral mucosa? Endoscopic, histopathologic and DNA flow cytometric study

BACKGROUND/AIMS: Although cholecystectomy is still the "gold standard" for treatment of gallstones, this operation may be followed by gastric disorders. The aim of this study is to detect the effects of cholecystectomy on gastric antral mucosa. METHODOLOGY: This prospective study has been carried out on 46 patients (20 M & 26 F) with mean age 41.7 +/- 0.2 years for whom simple cholecystectomy for gallstones was decided. Prior to the operation and 1 year after, patients were subjected to the following: clinical assessment, upper gastrointestinal endoscopy, histopathology of antral mucosa, detection of H. pylori and DNA flow cytometry. RESULTS: There was an increase in the number of patients presenting suggestive symptoms of reflux gastritis: patients experiencing epigastric pain increased from 8 (17.4%) to 11 (23.39%) patients, nausea increased from 6 (13%) to 12 (26.1%) patients and bilious vomiting increased from 3 (6.5%) to 11 (23.9%) patients. Mild antral gastritis increased from 20 (43.5%) to 27 (58.7%) patients. Antral gastritis and antral erosions were detected only after the operation in 8 (17.4%) and 2 (4.3%) patients, respectively. The incidence of active chronic superficial gastritis decreased from 23 (50%) to 13 (28.2%) patients while the inactive form increased from 15 (32.6%) to 23 (50%) patients. Chronic atrophic gastritis, intestinal metaplasia and dysplasia were only detected postoperatively in 2 (4.3%) patients each. There was a decrease in the incidence of H. pylori infection from 32 (69.6) to 19 (41.3%) patients. DNA aneuploid pattern increased from 1 (2.2%) to 4 (8.7%) patients and there was a significant increase of DNA index from 1.01 (+/- 0.03) to 1.03 (+/- 0.05) (P < 0.005). CONCLUSIONS: Changes in clinical, endoscopic and histopathologic findings suggest that cholecystectomy may affect gastric antral mucosa due to duodenogastric reflux. Flow cytometry may be used as an objective method for detection and evaluation of postcholecystectomy reflux gastritis.     

Role of tissue kallikrein in chronic gastritis

Tissue kallikrein could be specifically demonstrated in the human gastric mucosa using sandwich-type enzyme-linked immunosorbent assay. Eighty-five patients with chronic gastritis were then studied to investigate the relationship of tissue kallikrein to endoscopic and pathologic findings. The endoscopic Congo red method was used to classify the atrophic pattern of each patients gastric mucosa into the normal, closed or open type. Tissue kallikrein increased significantly in the closed type compared with the normal type (P less than 0.01) and in the open type compared with the closed type (P less than 0.001). Pathological findings were classified into three groups: (A) normal surface epithelium, with slight infiltration by inflammatory cells; (B) atrophic surface epithelium, with marked infiltration by inflammatory cells; and (C) atrophic surface epithelium, with marked infiltration by inflammatory cells and intestinal metaplasia. Tissue kallikrein significantly increased in the B group compared with the A group (P less than 0.01) and in the C group compared with the B group (P less than 0.001). Tissue kallikrein markedly increased with the appearance of intestinal metaplasia in the open type rather than in the closed type. An immunohistological study demonstrated that tissue kallikrein was present in the cells showing intestinal metaplasia and goblet cells. These findings suggest that chronic gastritis is a process of reconstruction of gastric mucosa.     

Low serum vitamin B12 is common in coeliac disease and is not due to autoimmune gastritis

OBJECTIVE: Although coeliac disease is a disorder of the proximal small bowel, associated vitamin B12 deficiency has been reported. This study aimed to assess the prevalence of B12 deficiency in a large series of coeliac patients, and to exclude the possibility that it is due to associated autoimmune gastritis. DESIGN: Prospective routine measurement of serum B12 in coeliac patients, with investigations for pernicious anaemia/autoimmune gastritis in B12-deficient patients. SETTING: Gastroenterology department of a large district general hospital. INTERVENTIONS: If they were not taking vitamin B12 supplements already, patients had serum B12 measured before starting dietary gluten exclusion. Those with low levels also had gastric biopsies taken and plasma gastrin and serum gastric parietal cell and intrinsic factor antibodies measured. MAIN OUTCOME MEASURES: Prevalence of low serum B12, and presence or absence of indicators of pernicious anaemia/autoimmune gastritis in patients with low serum B12. RESULTS: Of 159 patients, 13 had low serum B12 at diagnosis. A further six had been receiving B12 replacement therapy for 3-37 years before diagnosis, giving an overall prevalence of 12% (19 patients). Only 2/19 patients had gastric corpus atrophy, one with intrinsic factor antibodies and the other with hypergastrinaemia. There was no relationship between low B12 and clinical characteristics. CONCLUSIONS: Low B12 is common in coeliac disease without concurrent pernicious anaemia, and may be a presenting manifestation. B12 status should be known before folic acid replacement is started.     

Helicobacter pylori--is it a novel causative agent in Vitamin B12 deficiency?

BACKGROUND: Evidence for vitamin B12 deficiency usually involves combinations of low serum vitamin B12 levels, clinical and metabolic abnormalities, and therapeutic response. Identification of the underlying cause is important in the diagnosis of vitamin B12 deficiency that is usually attributed to malabsorption. Helicobacter pylori is one of the most common causes of peptic ulcer disease worldwide and a major cause of chronic superficial gastritis leading to atrophy of gastric glands. It is suggested that there may be a casual relationship between H. pylori and food-cobalamin malabsorption. OBJECTIVES: To evaluate the H. pylori incidence in patients with vitamin B12 deficiency prospectively and to assess whether treatment for H pylori infection could correct this deficiency over time. PATIENTS AND METHODS: We performed a prospective cohort study involving 138 patients who had anemia and vitamin B12 deficiency. An upper gastrointestinal endoscopy was performed to assess the severity of atrophic gastritis and biopsy specimens for Campylobacter-like organisms tests and histological examination for H pylori were obtained at the time of diagnosis. The diagnosis of H. pylori prompted a combination treatment. RESULTS: Helicobacter pylori was detected in 77 (56%) of 138 patients with vitamin B12 deficiency and eradication of H pylori infection successfully improved anemia and serum vitamin B12 levels in 31 (40 %) of 77 infected patients. CONCLUSIONS: Helicobacter pylori seems to be a causative agent in the development of adult vitamin B12 deficiency. Eradication of H. pylori infection alone may correct vitamin B12 levels and improve anemia in this subgroup of patients.     

Clinical usefulness of gastric-juice analysis in 2007: the stone that the builders rejected has become the cornerstone

BACKGROUND: Gastric juice is usually discarded during upper-GI endoscopy. OBJECTIVE: By using a novel device, the Mt 21-42, we evaluated the potential of this important organic fluid in clinical practice, exploring its contribution to the diagnosis of Helicobacter pylori infection and atrophic gastritis of the oxyntic mucosa (AGOM). DESIGN AND PATIENTS: A multicenter study (17,907 patients; 10 endoscopy units) estimated the frequency of diagnosis of AGOM and H pylori infection in routine endoscopic practice. A prospective study (216 patients) at 1 of these units aimed to determine the real prevalence of these conditions and the possible benefits of gastric juice analysis. We considered gastric juice pH and ammonium concentration, endoscopic and histologic features, serologic parameters for atrophy and H pylori, gastric acid secretion, and costs. RESULTS: We found that H pylori infection and, even more markedly, AGOM were greatly underdiagnosed in routine endoscopic practice (20.1% and 0.8% vs 49.1% and 12.5% in the prospective study, respectively), because of the intrinsic limitations of the conventional tests and lack/inappropriateness of biopsy planning. Gastric-juice analysis proved to be a cheap, simple, and effective way to prevent such underdiagnosis and allowed detection of atrophic gastritis and H pylori in 96% and 98% of cases, and saved costs (cost-effectiveness ratio 209 vs 274-5047). CONCLUSIONS: Gastric juice provided a valuable source of clinicopathologic information that, properly analyzed, allowed detection of the main risk factors for gastric cancer (H pylori and atrophic gastritis), overcoming the diagnostic limitations associated with these conditions and also producing time and cost savings.     

Phospholipid composition of human gastric mucosa: a study of endoscopic biopsy specimens.

Gastric mucosal phospholipids, and in particular those of the surface layer, play an important part in mucosal barrier function. This study examined whether the phospholipid composition of the full thickness gastric mucosa is changed in peptic ulcer disease and gastritis. The phospholipid composition of gastric mucosa from endoscopic biopsy specimens in 28 subjects (eight healthy controls, 12 patients with duodenal ulcer, and eight with chronic atrophic gastritis) was studied. In addition, the phospholipid composition of gastric mucosa was compared with that of duodenal mucosa in 10 patients with duodenal ulcer. As expected phosphatidylcholine and phosphatidylethanolamine prevailed in all three groups. Lysolecithin was the smallest component in the duodenal ulcer and chronic atrophic gastritis groups. The phosphatidylethanolamine value was higher in duodenal ulcer and lower in chronic atrophic gastritis compared with the control group. In chronic atrophic gastritis there was an appreciable amount of phosphatidylglycerol that was not present in patients with duodenal ulcer or in the control group. There was no significant difference in phospholipid composition between antral and duodenal sites in duodenal ulcer patients. In conclusion, the phospholipid composition of gastric mucosa changes in human gastrointestinal diseases but its relation to cellular functions needs further study.     

Fundic atrophic gastritis in an elderly population. Effect on hemoglobin and several serum nutritional indicators

The ratio of pepsinogen I to pepsinogen II in the circulation decreases progressively with increasing severity of atrophic gastritis of the fundic gland mucosa. Fasting blood was obtained from 359 free-living and institutionalized elderly people (age range, 60 to 99 years). A pepsinogen I/pepsinogen II ratio less than 2.9, indicating atrophic gastritis, was found in 113 (31.5%) subjects. The prevalence of atrophic gastritis increased significantly with advancing age (P less than .05). Within the atrophic gastritis group, 84 had a pepsinogen I level greater than or equal to 20 micrograms/L, indicating mild to moderate atrophic gastritis, and 29 had a pepsinogen I level less than 20 micrograms/L, indicating severe atrophic gastritis or gastric atrophy. A significant increase in the prevalences of elevated serum gastrin levels (P less than .005), low serum vitamin B12 levels (P less than .005), circulating intrinsic factor antibody (P less than .005), and anemia (P less than .025) was observed with stepwise increases in severity of atrophic gastritis. Subjects with atrophic gastritis exhibited a lower mean serum vitamin B12 level (P less than .05) and a higher mean folate level (P less than .05), but no difference was detected in mean hemoglobin levels or serum levels of iron, ferritin, retinol or alpha-tocopherol. It is concluded that serum pepsinogen I and pepsinogen II levels can be used to determine the prevalence and severity of atrophic gastritis, that atrophic gastritis is common in an elderly population, and that atrophic gastritis is associated with vitamin B12 deficiency and anemia. Further, higher folate levels in atrophic gastritis may be related to an accumulation of 5-methyl tetrahydrofolate in serum due to vitamin B12 deficiency and/or greater folate synthesis by the intestinal flora resulting from bacterial overgrowth secondary to hypo- or achlorhydria.