Risk for gastric neoplasias in patients with chronic atrophic gastritis: A critical reappraisal

Chronic atrophic gastritis (CAG) is an inflammatory condition characterized by the loss of gastric glandular structures which are replaced by connective tissue (non-metaplastic atrophy) or by glandular structures inappropriate for location (metaplastic atrophy). Epidemiological data suggest that CAG is associated with two different types of tumors: Intestinal-type gastric cancer (GC) and type I gastric carcinoid (TIGC). The pathophysiological mechanisms which lead to the development of these gastric tumors are different. It is accepted that a multistep process initiating from Helicobacter pylori-related chronic inflammation of the gastric mucosa progresses to CAG, intestinal metaplasia, dysplasia and, finally, leads to the development of GC. The TIGC is a gastrin-dependent tumor and the chronic elevation of gastrin, which is associated with CAG, stimulates the growth of enterochromaffin-like cells with their hyperplasia leading to the development of TIGC. Thus, several events occur in the gastric mucosa before the development of intestinal-type GC and/or TIGC and these take several years. Knowledge of CAG incidence from superficial gastritis, its prevalence in different clinical settings and possible risk factors associated with the progression of this condition to gastric neoplasias are important issues. This editorial intends to provide a brief review of the main studies regarding incidence and prevalence of CAG and risk factors for the development of gastric neoplasias

Artificial neural networks in the recognition of the presence of thyroid disease in patients with atrophic body gastritis

AIM: To investigate the role of artificial neural networks in predicting the presence of thyroid disease in atrophic body gastritis patients

Unawareness of gastrointestinal symptomatology in adult coeliac patients with unexplained iron-deficiency anaemia presentation

Background Most adults with coeliac disease have a subclinical form of the disease and iron-deficiency anaemia may be the sole presenting symptom. Aim To evaluate demographic, clinical and biochemical characteristics of adult coeliac disease patients presenting with iron-deficiency anaemia. Patients A total of 108 iron-deficiency anaemia patients in whom coeliac disease has been diagnosed were studied. As a control group 108 non-coeliac iron-deficiency anaemia patients, comparable for sex and age, were studied. Results Of the 108 coeliac disease patients, 95 (88%) were female (mean age 34 years, range 19-72) and 13 (12%) were male (mean age 33 years, range 15-65). The median duration of iron-deficiency anaemia before diagnosis was 66 months in coeliac disease patients and 14 months in the iron-deficiency anaemia control group (P = 0.0001). The occurrence of at least one gastrointestinal symptom, not spontaneously reported, was observed in 92 (85%) patients with coeliac disease and in 67 (62%) patients in the control group (P = 0.001). The concomitant presence of diarrhoea, abdominal pain and abdominal bloating was detected in 14% patients with coeliac disease with respect to 3% in the control group (P = 0.005). Conclusions The vast majority of coeliac disease patients with iron-deficiency anaemia presentation were unaware of the gastrointestinal symptoms and this relationship is useful for diet compliance

Pre-endoscopic screening for Helicobacter pylori and celiac disease in young anemic women

AIM: To evaluate the usefulness of pre-endoscopic serological screening for Helicobacter pylori (H pylori) infection and celiac disease in women aged < 50 years affected by iron-deficiency anemia (IDA)

Risk factors for progression to gastric neoplastic lesions in patients with atrophic gastritis

P>Background Atrophic gastritis, involving the gastric body mucosa, predisposes to gastric neoplastic lesions (GNL). However, regular gastroscopic-histological follow-up for GNL is not recommended for patients with atrophic gastritis. Aim To evaluate risk factors for the progression to GNL in a cohort of patients with atrophic gastritis. Methods A total of 300 patients with atrophic gastritis [205 women, aged 54 (18-78) years] underwent gastroscopy with six gastric antrum and body biopsies. All patients had at least one follow-up gastroscopy/histology at an interval of at least 1 year after the atrophic gastritis diagnosis. Baseline clinical and histological features were analysed as risk factors for the development of GNL by Cox-regression. Results During a median follow-up of 4.3 (1-16.5) years, 15 GNL were detected in 14 of the 300 patients with atrophic gastritis: three were gastric cancer, whereas 12 were non-invasive neoplasia. The annual incidence for GNL was 1%. Cox-regression analysis identified the following risk factors: age over 50 years (HR 8.8, 95%CI 1.2-68.4), atrophic pangastritis (HR 4.5, 95% CI 1.5-14.1) and severe intestinal metaplasia in the gastric body (HR 4.0, 95% CI 1.3-11.8). Conclusions Atrophic pangastritis, severe body intestinal metaplasia and/or age over 50 years increase the risk for developing GNL in patients with atrophic gastritis. In this subset of patients, an endoscopic-histological follow-up for GNL surveillance may be worthwhile

HLA-DRB1*03 and DRB1*04 are associated with atrophic gastritis in an Italian population

Background: Atrophic gastritis (AG) is often considered an autoimmune disorder and is associated with other autoimmune diseases. HLA-DRB1 alleles are often associated with autoimmune diseases, however HLA-DRB1 genotyping data in AG patients are lacking. The objective of the study was to evaluate the prevalence of HLA-DRB1 in AG patients. Methods: The occurrence of HLA-DRB1 alleles was assessed in 89 Italian AG patients (69.1% female) and 313 controls (47.3% females). Genomic DNA was extracted from peripheral venous blood, PCR-coamplified for HLA-DRB1 and typed using a reverse line-blot assay. Results: Compared to controls, prevalence of HLA-DRB1*03 (28.1% vs. 15.9%, p = 0.01) and HLA-DRB1*04 (25.8% vs. 14.4%, p = 0.01) was greater in AG patients, conferring an OR of 2.05 and 2.07, respectively. HLA-DRB1*01 occurred more frequently in controls than in AG patients (11.5% vs. 3.4%, p = 0.01) conferring an OR of 0.27. AG patients carrying the HLA-DRB1*03 or *04 alleles were characterised by having more frequently autoimmune thyroid disease (70.4% vs. 42.2%, p = 0.01) and intestinal metaplasia (86.4% vs. 62.2%, p = 0.01). Conclusions: In our population, over 50% of AG patients carry the HLA-DRB1*03 or *04 alleles associated with autoimmune diseases, suggesting that this subset of AG patients has a genetic predisposition to autoimmunity. (C) 2010 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved

Reassessment of Intrinsic Factor and Parietal Cell Autoantibodies in Atrophic Gastritis With Respect to Cobalamin Deficiency

OBJECTIVES: Atrophic body gastritis (ABG) is an autoimmune condition eventually manifesting itself as pernicious anemia (PA). Parietal cell autoantibodies (PCAs) and intrinsic factor autoantibodies (IFAs) are considered characteristics of these conditions. Recent studies on IFA and PCA frequency with respect to cobalamin deficiency in biopsy-proven ABG patients are lacking. We addressed this issue using new enzyme-linked immunosorbent assay (ELISA)-based assays. METHODS: Sera from 165 patients with histologically diagnosed ABG and 113 controls were tested for IFA and PCA using ELISA. A total of 81 ABG patients had cobalamin deficiency and macrocytic anemia (Group 1-PA), 36 had cobalamin deficiency without macrocytic anemia (Group 2), and 48 had normal cobalamin levels (Group 3). RESULTS: IFAs were detected in 44/165 ABG patients (27% sensitivity) and in 0/113 controls (100% specificity). PCAs were detected in 134 ABG patients (81% sensitivity) and in 11 controls (90% specificity). In Group 1, IFAs showed 37% sensitivity and 100% specificity, whereas PCAs showed 81% sensitivity and 90% specificity. Combining IFA and PCA testing increased the sensitivity to 61% in all ABG patients and to 73% in Group 1, while maintaining 100% specificity. CONCLUSIONS: IFAs are 100% specific for biopsy-proven ABG and occurred in 27% of patients. PCAs occurred in 81% of ABG patients and in 10% of controls. Combining IFA and PCA testing significantly increases their diagnostic performance for ABG and PA, yielding a 73% sensitivity for PA. The non-invasive combined PCA and IFA assessment may be useful in selecting patients at risk for autoimmune gastritis to be confirmed by gastroscopic-histologic examination

Occurrence and Risk Factors for Autoimmune Thyroid Disease in Patients with Atrophic Body Gastritis

Purpose: To investigate the occurrence of and risk factors for autoimmune thyroid disease in atrophic body gastritis patients. Methods: Cross-sectional study on 401 consecutive outpatients with atrophic body gastritis. Diagnostic work-up of thyroid disease was completed in 319 atrophic body gastritis patients (225 women, median age 55.5 years [range 17-95 years]). Data on anagraphics, lifestyle, family history, and biochemical and histological items were obtained at baseline, and associations between atrophic body gastritis and autoimmune and nonautoimmune thyroid diseases were explored through descriptive statistics and logistic regression analyses. Results: Of the 319 atrophic body gastritis patients, 169 (53%) had an associated thyroid disorder, and 89 (52.7%) of these were unaware of it. The thyroid disease was autoimmune in 128 patients (75.7%) and nonautoimmune in 41 patients. Logistic regression showed that risk factors for having autoimmune thyroid disease in atrophic body gastritis patients were female sex (odds ratio [OR] 5.6, 95% confidence interval [CI], 2.6-12.1), presence of parietal cell antibodies (OR 2.5, 95% CI, 1.1-5.5), and presence of metaplastic atrophy (OR 2.2, 95% CI, 1.0-5.0). Conclusions: Autoimmune thyroid disease and atrophic body gastritis occur in a closely linked fashion, suggesting that atrophic body gastritis patients should be investigated for an occult autoimmune thyroid disease, in particular women and those with positive parietal cell antibodies. © 2008 Elsevier Inc. All rights reserved