Antral Atrophic Gastritis Research Articles

Epithelial cell proliferation index in patients with atrophic gastritis depending on the presence of complete or incomplete intestinal metaplasia in the gastric antrum

Introduction. There is a debate about the significance of intestinal metaplasia (IM) subtypes for the development of gastric cancer. Therefore, determining the indicators of cellular renewal in individuals with complete and incomplete IM is certainly a topical issue.Aim. To study the proliferative activity of epithelial cells of the gastric antrum in patients with Helicobacter pylori-positive antral atrophic gastritis depending on the subtype of IM.Materials and methods. The study included 20 people with chronic antral non-atrophic gastritis (CNG; group A), 20 patients with chronic antral atrophic gastritis (CAG) without IM (group B), 20 patients with CAG with complete IM (group C) and 20 people with CAG with incomplete IM (group D). The stage of chronic gastritis was assessed by the morphological method in accordance with the modified Sydney classification. Typing of IM foci in the gastric mucosa was performed using the PAS reaction. Proliferation activity was studied by the expression of nuclear protein Ki67 using immunohistochemistry.Results. The proliferation index in the foci of complete BM in group C was 5%, and in group D in the foci of incomplete BM the Ki67 expression index was significantly higher and was 39% (p < 0.001). Outside the foci of metaplasia, the proliferation index was 23.5% in group C and 19% in group D (p = 0.06).Conclusion. We have registered significantly higher proliferation indicators of gastric epithelial cells in foci with incomplete IM compared to foci with complete IM. Determination of proliferation indicators in foci of incomplete intestinal metaplasia may be a marker of an increased risk of developing gastric cancer.

Correlations between Endoscopic and Histopathological Assessment of Helicobacter pylori-Induced Gastric Pathology-A Cross-Sectional Retrospective Study.

Helicobacter pylori (H. pylori) infects about half of the world’s population and can lead to premalignant lesions and gastric cancer. Updated data about the correlation of histopathological diagnostics with endoscopic diagnostics are scarce. The objective of this study was to identify the concordance between endoscopic and histopathologic findings, with a focus on premalignant lesions. We performed a cross sectional, retrospective study over a 4-year period (2017−2021) on adult patients with dyspeptic symptoms and positive RUT (rapid urease test) in a single hospital centre, with a total of 133 patients infected with H. pylori being included in the study. Statistical associations between endoscopic appearance and histopathological results were found for atrophic antral gastritis (p = 0.001), intestinal metaplasia of the antrum (p = 0.018), gastric polyps (p < 0.001) and gastric corpus cancer (p = 0.012). Females were more likely to be diagnosed through endoscopy with gastric atrophy or intestinal metaplasia (p = 0.031), while chronic atrophic gastritis in corpus was more prevalent in patients older than 65 (p = 0.024). Overall, our study reveals only 21% concordance between Giemsa stain and RUT, highlighting the importance of combining rapid testing with endoscopic and histopathological diagnostic methods for a more accurate early diagnosis and prevention of gastric cancer.

Mechanisms for the Sex-Specific Effect of H. Pylori on Risk of Gastroesophageal Reflux Disease and Barrett's Esophagus.

Mechanisms for how Helicobacter pylori infection affects risk of gastroesophageal reflux disease (GERD) and Barrett's esophagus are incompletely understood and might differ by sex. In a case-control study nested in the Melbourne Collaborative Cohort Study with 425 GERD cases and 169 Barrett's esophagus cases (identified at 2007-2010 follow-up), we estimated sex-specific odds ratios for participants who were H. pylori seronegative versus seropositive at baseline (1990-1994). To explore possible mechanisms, we (i) compared patterns of H. pylori-induced gastritis by sex using serum pepsinogen-I and gastrin-17 data and (ii) quantified the effect of H. pylori seronegativity on Barrett's esophagus mediated by GERD using causal mediation analysis. For men, H. pylori seronegativity was associated with 1.69-fold [95% confidence interval (CI), 1.03-2.75] and 2.28-fold (95% CI, 1.27-4.12) higher odds of GERD and Barrett's esophagus, respectively. No association was observed for women. H. pylori-induced atrophic antral gastritis was more common in men (68%) than in women (56%; P = 0.015). For men, 5 of the 15 per 1,000 excess Barrett's esophagus risk from being seronegative were mediated by GERD. Men, but not women, who were H. pylori seronegative had increased risks of GERD and Barrett's esophagus. A possible explanation might be sex differences in patterns of H. pylori-induced atrophic antral gastritis, which could lead to less erosive reflux for men. Evidence of GERD mediating the effect of H. pylori on Barrett's esophagus risk among men supports this proposed mechanism. The findings highlight the importance of investigating sex differences in the effect of H. pylori on risk of GERD and Barrett's esophagus in future studies.

Demographic, hematologic, and endoscopic differences between predominant corporeal and antral atrophic gastritis: A STROBE-Compliant study.

The study aimed to assess demographic, clinical, and endoscopic parameters in patients with predominant corporeal atrophic gastritis (CAG) and enterochromaffin-like cell hyperplasia suggestive for autoimmune etiology in comparison with patients presenting Helicobacter pylori atrophic gastritis limited to the gastric antrum (AAG).Demographical, clinical, and pathological data of consecutive patients who underwent an upper digestive endoscopy for bleeding screening risk, symptoms, or anemia in a single endoscopy unit were retrieved. The final study group included 63 patients with CAG and enterochromaffin-like cell hyperplasia on histology and a control group of 142 patients with AAG.Female patients were predominant in the group with CAG versus AAG (69.8% vs 46.4%, P = .002). Microcytic anemia (P < .001), but not macrocytic anemia (P = .14) was associated with CAG, the mean corpuscular volume of erythrocyte (MCV) (82.5 vs 86.5 fl, P = .01), the mean value of serum iron (11.8 vs 14.3 μmol/L, P = .02), and hemoglobin level (11.0 vs 12.7 g/dL P < .01) being significantly lower in patients with CAG versus AAG. Upper digestive endoscopies with no visible mucosal lesions (P = .01) were also more frequent in the patients with CAG, but there were not differences regarding digestive symptoms between groups. The linear regression models revealed that the low hemoglobin (P < .001) and low MCV (P = .03) are the independent variables that can predict CAG on histology, but not the serum iron level (P = .77)Consecutive patients investigated on endoscopy with CAG in comparison with those having AAG are more frequent female, they have microcytic anemia, and no mucosal lesions on endoscopy. The decreased hemoglobin level and low MCV, rather than the serum iron level are predictors for CAG versus AAG on histology in endoscopic population.

1210Understanding the effect of Helicobacter pylori infection on gastroesophageal reflux disease and Barrett’s oesophagus

Abstract Background Helicobacter pylori (H.pylori) infection causes atrophic gastritis and gastric cancer. Ironically, decreased gastric acid production in those with atrophic gastritis might reduce harmful gastroesophageal refluxate, thereby reducing gastroesophageal reflux disease (GERD) and Barrett’s oesophagus (BE) risk. Methods In two nested case-control studies with 425 GERD and 169 BE cases, we compared sex-specific GERD and BE risk in H.pylori seronegative participants with seropositive participants. Where seronegativity was associated with increased BE risk, we quantified the effect mediated by GERD using a Monte Carlo simulation-based g-computation approach to estimate interventional effects. Moreover, we classified participants into gastritis types using serum pepsinogen-I and gastrin-17 data. Results For men, H.pylori seronegativity was associated with 1.69-fold (CI:1.03-2.75) and 2.14-fold (CI:1.18-3.88) higher odds for GERD and BE respectively. Five (33%) out of the 15 per 1000 excess BE risk from being seronegative was mediated by GERD. No association was observed for women. Among those seropositive, the proportion with atrophic antral gastritis was higher for men than for women (68% vs 56%; p = 0.015). Conclusions H.pylori seronegativity was associated with increased GERD and BE risk for men but not women, which could be partly explained by the higher proportion of H.pylori-associated atrophic antral gastritis in men. Evidence of GERD mediating seronegativity’s effect on BE supports this explanation. Key messages Whilst H.pylori infection might reduce GERD and BE risk, this is potentially a by-product of atrophic gastritis, a risk factor for gastric cancer. Treating GERD could partly reduce the excess BE risk for seronegative individuals.

H. pylori eradication therapy: impact of gastric mucosa atrophy on transport of amoxicillin to H. pylori colonization area

AIM: The aim was to assess systemic transport of amoxicillin, the most common antibiotic in H. pylori eradication regimens to the gastric in atrophic gastritis.&#x0D; MATERIALS AND METHODS: Systemic transport of amoxicillin to the gastric lumen of rats was evaluated in washes from the gastric mucosa in the model of atrophic gastritis after intravenous drug infusion. Transport of amoxicillin from bloodstream to the gastric lumen was also assessed in patients with atrophic and non-atrophic gastritis in aspirated via nasogastric probe gastric juice after oral drug administration. Amoxicillin concentration was measured in samples using liquid chromatography-mass spectrometry.&#x0D; RESULTS: In rats with induced atrophic gastritis, hyperemia and acute erosions of the gastric mucosa, as well as microscopic signs of non-active chronic body gastritis and non-active antral atrophic gastritis were found. Amoxicillin concentration in washes from the gastric mucosa was significantly (p 0.01) higher in rats of experimental group than in control group at all time points (30, 60, 120, 240 min after drug infusion). The lowest mean amoxicillin concentration in gastric juice was observed in patients with antral atrophy (p 0.01). The maximum amoxicillin concentration in gastric secretion was found at the 180th min of aspiration in patients with atrophy of gastric mucosa, while in patients of the group of comparison it was found at 30-120th min of aspiration.&#x0D; CONCLUSIONS: Acute gastric mucosa erosions enhance amoxicillin delivery to gastric lumen in rats. Atrophy of antral mucosa more than in the corpus is characterized by decreased amoxicillin transfer from systemic bloodstream to gastric lumen in patients after oral amoxicillin intake. The gastric mucosa atrophy should be taken into consideration while predicting the efficacy of H. pylori eradication therapy in patients with chronic gastritis.

A rare gastric polyp: MANET

A 79-year-old woman with a medical history of type 2 diabetes, hypertension, and chronic heart and kidney failure was admitted to the hospital because of cholangitis. She underwent ERCP, which incidentally showed a 25 × 10 mm pedunculated polyp with eroded tip located on the greater gastric curvature (Paris endoscopic classification of polyps 0-Ip) (A, B). Subsequent gastroscopy showed atrophic antral gastritis. The polyp was electroresected. Histologic analysis indentified a mixed neuroendocrine-noneuroendocrine neoplasm (MiNEN) composed of neuroendocrine tumor and tubular adenoma (MANET), with growth in the deeper part of the mucosa and submucosa.

Amoxicillin secretion by gastric mucosa in Chernobyl nuclear power plant accident recovery workers with atrophic and nonatrophic gastritis undergoing eradication therapy

Relevance. Today gastric cancer is still one of the oncologic diseases most often leading to death. H. pylori eradication reduces risk of gastric cancer, but its efficacy depends on gastric mucosa state. Atrophy of gastric mucosa is more common in Chernobyl nuclear power plant (CNPP) accident recovery workers than in patients who have not been involved in CNPP accident recovery works. It seems especially important to investigate the features of antibiotics transport to H. pylori colonization area in this contingent.Intention – to determine the features of amoxicillin secretion by gastric mucosa in CNPP accident recovery workers with atrophic and nonatrophic gastritis undergoing H. pylori eradication.Methodology. 65 CNPP accident recovery workers were divided into groups depending on state of gastric mucosa according to endoscopic and histological examination, immunosorbent assay of pepsinogens I and II and gastrin-17 basal serum levels. On the first day of eradication therapy, gastric secretion samples were obtained via nasogastric probe 30, 60, 120, 180 and 240 minutes after oral amoxicillin administration. Drug concentrations in gastric secretion were assessed via liquid chromatography-mass spectrometry.Results and discussion. Amoxicillin concentrations in gastric secretion samples were lower (р &lt; 0.01) in patients with atrophic antral gastritis than in patients with normal gastric mucosa and atrophic fundal gastritis. Patients with fundal atrophy were characterized by lower amoxicillin concentrations 30 and 60 (p = 0.02) minutes after drug intake than in patients with normal gastric mucosa, and higher concentration in the 120th (p &lt; 0.01) and 180th (p = 0.02) minute than in patients with antral atrophy. Amoxicillin concentrations in patients with antral atrophy were lower (p &lt; 0.01) than in non-atrophy group in the 30th, 60th and 120th minute. In the 240th minute, amoxicillin concentrations in patients with fundal atrophy exceeded concentrations in both other groups (p &lt; 0.01). Amoxicillin concentration peak was registered in patients with fundal and antral atrophy in the 180th minute, in patients without atrophy – from the 30th to 120th minute.Conclusion. Atrophy of gastric mucosa is characterized by decreased transport of orally administered amoxicillin from bloodstream to gastric lumen. Depending on gastric mucosa state, amoxicillin concentrations in gastric secretion should be evaluated at different time points after drug administration: in patients with atrophic gastritis – in the 180th minute, in patients without atrophy – in the 120th minute. While predicting the efficacy and choosing H. pylori eradication regimen, morphological and functional state of gastric mucosa should be taken into account.

Manifestation of В&lt;sub&gt;12&lt;/sub&gt; deficiency in the oral cavity

A clinical case of pathological state of oral cavity caused by B 12 deficiency is presented. The patient (25 y.o.) was diagnosed with atrophy of the oral mucosa (Hunter glossitis), hyperchromic microcytic anemia, gastroesophageal reflux disease, and atrophic antral gastritis. A course of injections of cyanocobalamin was prescribed. At the control examination after three months, laboratory and clinical symptoms of disease relapse were not detected.

Endoscopic and histological evaluation of the mucous membrane of the stomach in relatives of people suffering from cancer of the stomach

The condition of gastric mucosa was assessed in relatives of patients with gastric cancer (RPGC). The study included 108 RPGC (main group) and 102 patients with no family history of gastric cancer who were screened for dyspepsia. All study participants were subjected to clinical examination, questioning and esophagogastroduodenoscopy (EGDS) with a biopsy, in which the gastric mucosa state was assessed according to the modified Sydney system, the OLGA and OLGIM systems, and the definition of Helicobacter pylori (H. pylori) infection. It was established that the prevalence of H. pylori infection in the main group was 58.3 % (95 % CI 48.8–67.7), in the control group – 56.0 % (95 % CI 46.1–65.6). At RPGC, atrophy of any localization (46.3 % (95 % CI 39.4–53.2) versus 26.5 % (95 % CI 20.4–32.6), respectively, was found more often than in the control group, respectively, p = 0.002), antral atrophic gastritis (41.6 % (95 % CI 34.8–48.4) versus 26.5 % (95 % CI 20.4–32.6), respectively, p = 0.020), and isolated atrophy in the stomach body (4.6 % (95 % CI 1.7–7.4) versus 0 % ( p = 0.03). In RPGC, atrophy developed at a younger age (48.0 years (95 % CI 44.0–52.0) versus 53.0 years in the control group (95 % CI 48.3–57.8) p = 0.000). There were no significant differences between the groups in the incidence of metaplasia and dysplasia. The following risk factors for development of atrophy were identified in the factor analysis: age over 6f0 years (odd ratio (OR) 53.0; 95 % CI 12.2–390.1; p &lt; 0.001), age over 40 years (OR 4.0; 95 % CI 2.0–8.2; p &lt; 0.001), heredity burdened by gastric cancer (OR 2.7; 95 % CI 1.4–5.7; p = 0.006) and the use of strong alcoholic beverages (OR 5.5; 95 % CI 1.6–21.6; p = 0.009). The frequency of the atrophy development of the gastric mucosa is increased in RPGC, and atrophic gastritis develops at a younger age in comparison with individuals without a burdened hereditary history. In addition to the hereditary factor, the risk of atrophy is associated with age and alcohol use.

Gastroesophageal reflux disease in an area with low Helicobacter pylori infection prevalence.

The association between gastroesophageal reflux disease (GERD) prevalence and its risk factors in an area with low Helicobacter pylori prevalence is important to clarify. We analyzed the prevalence of GERD and risk factors in an area of Indonesia with low prevalence of H. pylori infection. We recruited 104 dyspeptic patients who underwent endoscopy in Surabaya. Patients were diagnosed with GERD based on the Los Angeles classification. We evaluated gastric biopsy specimens and measured serum pepsinogen levels. Interleukin polymorphisms were evaluated by polymerase chain reaction-restriction fragment length polymorphism. Of 104 patients, 56 (53.8%) were endoscopically found to have GERD, with most categorized as grade A; 48 (46.2%) were classified as non-GERD. Higher economic status, smoking, and a history of proton-pump inhibitor use significantly increased the risk of GERD. GERD Questionnaire scores showed a positive correlation with GERD (P < 0.001). An association was found between antral atrophic gastritis and GERD (P = 0.030), and patients with GERD more frequently had severe antral atrophy than nonerosive reflux disease (P = 0.018). We found an association between pepsinogen I/II levels and GERD (P = 0.047), but with low accuracy. IL-1β -511 TT and CT were predominant among the IL-1β -511 genotypes, and IL-8–251 AT and TT were predominant among the IL-8–251 genotypes. In conclusion, we found a high prevalence of GERD in an area with low prevalence of H. pylori infection, which could be associated with acid reflux. Smoking, history of proton-pump inhibitor use, and higher economic group significantly increased the risk of GERD.

Serological Criteria for Mild, Moderate and Severe Atrophy in Atrophic Gastritis

The study was carried out in a group of 360 dyspeptic Helicobacter pylori-infected patients. These patients were tested for markers of atrophy of the mucous membrane of the antrum section (gastrin-17) and corpus of stomach (pepsinogen-1). The markers were detected via the test panel for immune-enzyme analysis - GastroPanel. All the 360 patients underwent the upper gastrointestinal endoscopy with subsequent biopsy of the antral and corpus mucosa. These markers were identified for a group of patients with severe atrophic gastritis and for a group of patients with mild and moderate atrophy. The level of the gastrin-17 was determined for the number of patients with mild, moderate and severe antral atrophic gastritis, which was identified with the use of upper gastrointestinal endoscopy followed by a biopsy of the antral mucosa. The level of the gastrin-17 in the serum was: mild antral atrophy - 7 ≤ pmol/L 0 10, moderate antral atrophy – 4 ≤ pmol/L <7, severe antral atrophy - 0 ≤ pmol/L < 4, no atrophy - 10 ≤ pmol/L. The level of the pepsinogen-1 was determined for the number of patients with mild, moderate and severe corpus atrophic gastritis, which was identified with the use of upper gastrointestinal endoscopy followed by a biopsy of the corpus mucosa. The bounds of the pepsinogen-1 level in the serum were: mild corpus atrophy - 15 ≤ µg/L <25, moderate corpus atrophy – 9 ≤ µg/L <15, severe corpus atrophy - 0 ≤ µg/L <9, no corpus atrophy - 25 ≤ µg/L. Rising of the effectiveness of serological screening considering the lines of serological markers severe atrophy and detected patients with high risk gastric cancer allows to avoid the upper gastrointestinal endoscopy

Risk factors of atrophic gastritis and intestinal metaplasia in first-degree relatives of gastric cancer patients compared with age-sex matched controls.

Background:To identify whether first-degree relatives (FDRs) of gastric cancer (GC) patients have increased risk for atrophic gastritis (AG) and intestinal metaplasia (IM) in relation to other risk factors of GC.Methods:The study cohort consisted of 224 pairs of age-sex matched controls and FDRs. AG and IM in the gastric mucosa were scored histologically using the updated Sydney classification. Risk of having AG and IM was studied by comparing FDRs to controls. Impacts of age, H. pylori infection, smoking, dietary and socioeconomic factors on the presence of AG and IM were studied.Results:In multivariate regression analysis, FDRs had adjusted OR of 2.69 (95% CI 1.06–6.80, P=0.037) for antral IM in male population. Adjusted OR for antral AG and IM were 9.28 (95% CI 4.73–18.18, P<0.001) and 7.81 (95% CI 3.72–16.40, P<0.001) for the H. pylori infected subjects in total population. Getting old by 5 years increased the ORs of having AG and IM by approximately 1.25 fold (P<0.001). Spicy food increased the OR of antral IM by 2.28 fold (95% CI 1.36–3.84, P=0.002).Conclusions:Family history of GC was an independent risk factor for antral IM in male in our study, which could be one reason for the increase of gastric cancer in the family member of gastric cancer. It could be an evidence for the necessity of frequent endoscopy in the presence of family history of GC compared to general population in male.

Rationale in diagnosis and screening of atrophic gastritis with stomach-specific plasma biomarkers

Background and aims. Atrophic gastritis (AG) results most often from Helicobacter pylori (H. pylori) infection. AG is the most important single risk condition for gastric cancer that often leads to an acid-free or hypochlorhydric stomach. In the present paper, we suggest a rationale for noninvasive screening of AG with stomach-specific biomarkers. Methods. The paper summarizes a set of data on application of the biomarkers and describes how the test results could be interpreted in practice. Results. In AG of the gastric corpus and fundus, the plasma levels of pepsinogen I and/or the pepsinogen I/pepsinogen II ratio are always low. The fasting level of gastrin-17 is high in AG limited to the corpus and fundus, but low or non-elevated if the AG occurs in both antrum and corpus. A low fasting level of G-17 is a sign of antral AG or indicates high intragastric acidity. Differentiation between antral AG and high intragastric acidity can be done by assaying the plasma G-17 before and after protein stimulation, or before and after administration of the proton pump inhibitors (PPI). Amidated G-17 will rise if the antral mucosa is normal in structure. H. pylori antibodies are a reliable indicator of helicobacter infection, even in patients with AG and hypochlorhydria. Conclusions. Stomach-specific biomarkers provide information about the stomach health and about the function of stomach mucosa and are a noninvasive tool for diagnosis and screening of AG and acid-free stomach.

Chronic atrophic antral gastritis and risk of metaplasia and dysplasia in an area with low prevalence of Helicobacter pylori

The Northeastern region of Peninsular Malaysia is an area with exceptionally low prevalence for Helicobacter pylori infection. The risk of intestinal metaplasia and dysplasia in patients with chronic atrophic gastritis (CAG) and its association with Helicobacter pylori is unknown in this region. This was a cross-sectional study on gastric biopsies from 234 consecutive patients (mean age 53.5 [14.8] years) who underwent upper gastrointestinal endoscopy between January 2006 and December 2006. There were 137 (59%) men and 185 (79%) Malay patients. Among 234 biopsies, CAG was found in 99 and non-atrophic gastritis in 135. Intestinal metaplasia and dysplasia were detected in 8 and 6 atrophic gastritis biopsies, respectively, and in 10 and 3 of non-atrophic gastritis biopsies, respectively. H. pylori were detected in 16 (9 Malays, 7 non- Malays) biopsies (p=0.024); intestinal metaplasia was detected in 4 biopsies (p=0.3) and dysplasia in 5 biopsies (p=0.3). Of the 218 biopsies negative for H. pylori, intestinal metaplasia was found in 14 and dysplasia in 4. The risk of intestinal metaplasia as well as dysplasia was associated with presence of H. pylori infection (p=0.029 and p<0.001 respectively). Even in a setting of low prevalence of H. pylori, intestinal metaplasia and dysplasia were significantly associated with H. pylori infection. The frequency of intestinal metaplasia and dysplasia was similar different between biopsies with atrophic gastritis and non-atrophic gastritis.

Non-invasive tests in gastric diseases

Although the gastric cancer incidence is decreasing, this neoplasia remains one of the major causes of oncological mortality. Because of an insidious development, gastric cancer is often diagnosed in an advanced stage and consequently with a poor prognosis. Accurate non-invasive tests should be extremely useful in order to detect gastric neoplasm in an early phase. In clinical practice, there is no reliable bio-marker for detecting this malignant disease. However, intestinal as well as diffuse types of gastric cancer are preceded by gastric mucosa inflammation. Furthermore, the intestinal type of the neoplasia is, generally, related to chronic atrophic gastritis, especially if associated with intestinal metaplasia. In particular, the risk of the neoplasm is linked to both extension and severity of gastric atrophy. Serological parameters such as serum pepsinogens I (PGI) and II (PGII), gastrin-17 (G-17) cytokines (e.g. IL-8), antiparietal cells, IgG anti-Hp and CagA antibodies and lastly ghrelin supply information about either atrophic or inflammatory conditions characterising gastric mucosa. Low PGI and PGI/PGII ratio levels, especially if combined with high G-17 levels, are recognised bio-markers of corpus atrophic gastritis. Low G-17 levels could be, also, suggestive of antral atrophic gastritis. Furthermore, plasmatic ghrelin levels seem to be also a bio-marker of corpus atrophy. Anti-Hp IgG and CagA antibodies as well as PGII levels are able to detect gastric inflammation. Serological parameters could select subjects at risk for gastric mucosa alterations such as inflammation or atrophy, rather than gastric cancer itself. This review analyses the information derived from serological bio-markers as well as the involved clinical studies.

Relation of atrophic gastritis with Helicobacter pylori -CagA+ and interleukin-1 gene polymorphisms

To determine the association of Helicobacter pylori (H pylori) CagA(+) infection and pro-inflammatory polymorphisms of the genes interleukin (IL)-1RN and IL-1B with the risk of gastric atrophy and peptic ulcers in a dyspeptic population in Costa Rica, a country with high incidence and mortality of gastric cancer. Seven biopsy specimens, a fasting blood sample and a questionnaire concerning nutritional and sociodemographic factors were obtained from 501 consecutive patients who had undergone endoscopy for dyspeptic symptoms. A histopathological diagnosis was made. Pepsinogen concentrations were analyzed by enzyme linked immunosorbent assay (ELISA). Infection with H pylori CagA(+) was determined by serology and polymerase chain reaction (PCR). IL-1B and IL-1RN polymorphisms genotyping was performed by PCR-restriction fragment length polymorphism (PCR-RFLP) and PCR respectively. In this dyspeptic population, 86% were H pylori positive and of these, 67.8% were positive for CagA. Atrophic antral gastritis (AAG) was associated with CagA(+) status [odd ratio (OR) = 4.1; P < 0.000] and fruit consumption (OR = 0.3; P < 0.00). Atrophic body gastritis (ABG) was associated with pepsinogen PGI/PGII < 3.4 (OR = 4.9; P < 0.04) and alcohol consumption (OR = 7.3; P < 0.02). Duodenal ulcer was associated with CagA(+) (OR = 2.9; P < 0.04) and smoking (OR = 2.4; P < 0.04). PGI < 60 microg/L as well as PGI/PGII < 3.4 were associated with CagA(+). In a dyspeptic population in Costa Rica, H pylori CagA(+) is not associated with ABG, but it is a risk factor for AAG. The pro-inflammatory cytokine polymorphisms IL-1B + 3945 and IL-1RN are not associated with the atrophic lesions of this dyspeptic population.

Screening of atrophic gastritis and gastric cancer by serum pepsinogen, gastrin‐17 and Helicobacter pylori immunoglobulin G antibodies

Currently the screening and diagnosis of gastric cancer and atrophic gastritis are mainly made by endoscopy and biopsy. The aim of this study was to evaluate the use of serum tests: serum pepsinogen I (PGI pepsinogen I/II ratio (PGR), gastrin-17 (G-17) and H. pylori-immunoglobulin G (IgG) antibodies to screen atrophic gastritis and gastric cancer. A total of 458 patients were recruited, and each underwent endoscopy with biopsies before the serum tests were performed. These patients were divided into five groups based on the endoscopic and histological findings: 92 patients in the atrophic gastritis group, 58 in the gastric ulcer group, 90 in the duodenal ulcer group, 141 in the gastric cancer group (40 early gastric cancer and 101 advanced gastric cancer) and 77 (including mild non-atrophic gastritis) served as a control group. Serum samples for PGI and II, G-17, and H. pylori-IgG antibodies estimation were analyzed by ELISA. PGI and PGR values decreased significantly both in atrophic gastritis and gastric cancer groups (P<0.01). For the best discrimination of atrophic gastritis, the cut-off values of PGI and PGR were 82.3 microg/L and 6.05, respectively. The PGI, PGR and G-17 values were related significantly with the grades and/or sites of atrophic gastritis (P<0.01). Patients with atrophic corpus gastritis had low PGI and PGR values and high G-17 level, and patients with atrophic antral gastritis had low G-17 level. G-17 increased significantly in the gastric cancer group (P<0.01). PGI and PGR values were significantly lower in patients with advanced gastric cancer than in patients with early gastric cancer, while there was no difference in G-17 level between them. The positivity rate of H. pylori-IgG antibodies was 54.55% in the control group. The PGI level was higher in H. pylori positive patients than in H. pylori negative ones (P<0.001), while there was no difference in G-17 level between them. The positivity rates of H. pylori-IgG antibodies were over 85% in all other four groups. Low serum PGI, PGR and G-17 values are biomarkers of atrophic antral gastritis. Atrophic be screened by serum PGI and PGR values. Gastric cancer can be screened on the basis of increased serum G-17 and remarkedly low serum PGI and PGR values. The H. pylori infection is related to the change of PG level.

Long‐term follow‐up in atrophic body gastritis patients: atrophy and intestinal metaplasia are persistent lesions irrespective of Helicobacter pylori infection

Long-term outcome of atrophic body gastritis has not yet been defined. To investigate at long-term follow-up the behaviour of atrophy and intestinal metaplasia and the occurrence of neoplastic lesions in atrophic body gastritis patients. Overall 106 atrophic body gastritis patients with > or = 4-year follow-up were studied; 38 were Helicobacter pylori-positive at histology + serology and cured of infection (group A), 36 were positive at serology and not treated (group B) and 32 were H. pylori-negative (group C). Patients underwent gastroscopy with antral (n = 3) and body (n = 3) biopsies for histology according to the Sydney System. At 6.7-year follow-up body atrophy and intestinal metaplasia remained unchanged in all 106 patients irrespective of H. pylori status. Antral atrophy was significantly increased at follow-up only in group C, whereas antral intestinal metaplasia was unchanged in all three groups. During follow-up eight (8%) patients developed neoplastic lesions (one adenocarcinoma, one adenoma with low-grade dysplasia and six low-grade dysplasia without endoscopic lesions). Antral atrophic gastritis was present at baseline in all but one (88%) of the eight patients with neoplastic lesions, but only in 15 (15%) of the 98 patients without (P < 0.0001, RR = 26.7). Atrophy and intestinal metaplasia persist at 6.7-year follow-up and atrophic body gastritis patients with panatrophic gastritis are at increased risk of developing neoplastic lesions.

Clinical usefulness of serum pepsinogens I and II, gastrin-17 and anti- Helicobacterpylori antibodies in the management of dyspeptic patients in primary care

Background. Several tests have been proposed for evaluating dyspeptic symptoms and their relationship to the underlying gastric disease. Serum pepsinogens and gastrin-17 are known to be useful biomarkers for the detection of gastric pathologies. Aim. To evaluate the capability of screening dyspeptic patients in the primary care by analyses of serum pepsinogens I (sPGI) and II (sPGII), gastrin-17 (sG-17) and the IgG anti- Helicobacter pylori antibodies (IgG-Hp). Patients and methods. Three hundred and sixty-two consecutive patients with dyspeptic symptoms (208 females, mean age 50.6 ± 16 years, range 18–88 years) referred by general practitioners for upper gastrointestinal endoscopy were enrolled. A blood sample was taken from each subject for IgG-Hp, sPGI, sPGII and sG-17 analyses. Results. Two hundred and eighty-seven patients had a complete screening; of these, 132 resulted positive for Hp infection. Patients with atrophic chronic gastritis showed significantly lower serum pepsinogen I levels and sPGI/sPGII ratio than patients with non-atrophic chronic gastritis. Moreover, by calculating the values of sPGI by sG-17 and sG-17 by sPGII/sPGI, subjects with atrophic chronic gastritis could be distinguished from those with non-atrophic chronic gastritis and from those with normal mucosa, respectively. sG-17 levels were found to be a useful biomarker for the detection of antral atrophic gastritis, while the combination of sPGI, the sPGI/sPGII ratio and sG-17 was found effective in identifying corpus atrophy. Conclusion. A panel composed of PGI, PGII, G-17 and IgG-Hp could be used as a first approach in the ‘test and scope’ and/or ‘test and treat’ strategy in the primary care management of dyspeptic patients.