Atrophic Body Gastritis Research Articles

Dynamics of Oxidative Stress in Helicobacter pylori-Positive Patients with Atrophic Body Gastritis and Various Stages of Gastric Cancer.

Gastric cancer is a global health problem. The pathogenesis of this disease remains unclear. This study included 198 H. pylori (+) men aged 45 to 60 years old. Group A included 63 practically healthy men, group B included 45 men with severe atrophic body gastritis, group C included 37 men with epithelial gastric cancer stages I–II according to TNM, and group D included 54 men with epithelial gastric cancer stages III–IV according to the TNM scale. The content of malondialdehyde (MDA), diene conjugates (DCs), superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and glutathione peroxidase (GPO) was detected using an enzyme immunoassay (ELISA) or spectrophotometric methods in the blood plasma. The concentrations of MDA and DC were increased in the patients of group B compared with group A, and in patients of groups C and D compared with groups A and B. The ratio of MDA/SOD and MDA/CAT was decreased in the patients in group D compared with the patients in group C, and was significantly higher compared with group A. The ratios of MDA/GPO and MDA/GST increased linearly and were at a maximum in groups C and D. Our work determined that indicators of oxidative stress may be the biochemical substrate, which brings together the various stages of the Correa cascade, and may explain disease progression. The dynamics of changes in the content of SOD and CAT in the plasma in patients with gastric cancer may be a target of future investigations.

IMPENDING PERICARDIAL TAMPONADE AS THE INITIAL PRESENTATION OF AUTOIMMUNE POLYGLANDULAR SYNDROME 3B

TOPIC: Critical Care TYPE: Fellow Case Reports INTRODUCTION: Autoimmune polyglandular syndromes (APS) are rare polyendocrinopathies characterized by loss of immune tolerance to self-antigens leading to autoimmune destruction of endocrine glands and other tissues. APS is classified into APS types 1, 2, 3 and 4. APS Type 3 is recognized by absence of adrenal insufficiency. APS type 3b (APS3b) specifically comprises of the association of autoimmune thyroid disease with pernicious anemia. CASE PRESENTATION: A 66-year-old female with history of pernicious anemia presented to the emergency department with shortness of breath and lethargy which started on day of arrival. She was diagnosed with pernicious anemia 2 years ago and was receiving intramuscular cyanocobalamin injections. In the emergency department, she was found to be hypoxic with oxygen saturation of 90%. Her physical exam was notable for muffled heart sounds. Her labs on admission were: Hb 11.8 g/dl, HCT 35.8 %, WBC 6.3 K/ul, PLT 166 K/ul, Glucose 106 mg/dl, Sodium 143 mmol/l, BUN 13 mg/dl, Creatinine 1.13 mg/dl, pro-BNP 171 pg/ml, TSH 44.6 UIU/ml, Free T4 0.2 ng/dl, Free T3 0.5 pg/ml and positive thyroid peroxidase antibody >1300 u/ml. Serial troponins were unremarkable. Chest x-ray showed an enlarged cardiac silhouette concerning for pericardial effusion. EKG showed normal sinus rhythm with low voltage QRS complexes. 2D Echo showed a large circumferential pericardial effusion with end diastolic RV collapse suggestive of impending pericardial tamponade. LV ejection fraction was 60%. Pericardiocentesis drained 1700 cc of fluid with relief of patient's symptoms. This was followed by placement of pericardial drain. Her pericardial effusion was attributed to her new diagnosis of hypothyroidism. She was started on low dose levothyroxine given her age above 60 with plan for slowly increasing her dose with close outpatient follow up. DISCUSSION: Pernicious anemia is the most common association with thyroid autoimmune disease in APS type 3 seen in 39% of cases. APS3 is more commonly seen in females. The diagnosis of this condition requires the presence of multiple autoimmune diseases in the same individual, diagnosed in any order and at any age. CONCLUSIONS: A high index of suspicion is required whenever one autoimmune disease is diagnosed to prevent morbidity and mortality from other associated conditions. Here, we describe a patient with known history of pernicious anemia presenting with impending tamponade who was subsequently diagnosed with Hashimoto's thyroiditis. The constellation of these findings represent APS Type 3b. REFERENCE #1: Betterle, Corrado et al. "A rare combination of type 3 autoimmune polyendocrine syndrome (APS-3) or multiple autoimmune syndrome (MAS-3)." Auto- immunity highlights vol. 5,1 27-31. 11 Feb. 2014, doi:10.1007/s13317-013-0055-6 REFERENCE #2: Lahner E, Centanni M, Agnello G, et al. Occurrence and risk factors for autoimmune thyroid disease in patients with atrophic body gastritis. Am J Med. 2008;121(2):136-141. doi:10.1016/j.amjmed.2007.09.025 DISCLOSURES: No relevant relationships by Sana Fatima, source=Web Response No relevant relationships by Shumail Syed, source=Web Response

Functional dyspesia

Dyspepsia is a functional GI disorder consisting in a wide range of symptoms. The main diagnostic challenge has been whether to perform an EGD or an abdominal US in order not to miss organic lesions, but to avoid unnecessary and sometimes invasive tests. Pepsinogen serology has been proposed as an useful non-invasive test to explore the status of the gastric mucosa, suggesting this strategy as an adequate approach in management of dyspepsia. In a primary care setting, 266 dyspeptic patients were investigated to establish the proper diagnosis. The workup included upper GI endoscopy with biopsies, a structured questionnaire including type and severity of symptoms, serological determination of serum pepsinogens, gastrin 17 and IgG against Hp. Inclusion criteria were dyspeptic symptoms (epigastric pain, nausea and/or vomiting, post prandial fullness, early satiation) lasting more than 1 year and the association between symptoms and food ingestion. Helicobacter pylori infection was present in 114 subjects, characterized by high levels of pepsinogen II and IgG against Hp. Twenty subjects were classified according with the diagnosis of chronic body atrophic gastritis. Nausea and post prandial fullness were the most frequent symptoms (48% and 41%, respectively) in the studied population, followed by epigastric pain and early satiation (37% and 26% respectively). A diagnosis of normality by serological diagnosis was found in half of patients experiencing epigastric pain and in about 60% of subjects with the three other symptoms (nausea, post prandial fullness, and early satiation). In conclusion, this experience confirms the clinical usefulness of serology in dyspepsia, contributing to correctly diagnosing CAG and H.p. infection in such patients and providing a good correlation with the clinical picture. (www.actabiomedica.it)

Síndrome Autoinmune Tirogástrico (SAT) . Serie de casos

Un porcentaje importante de pacientes con gastritis crónica atrófica corporal autoinmune, o gastritis tipo A, desarrollan enfermedad autoinmune tiroidea (enfermedad de Graves o de Hashimoto) y viceversa, situación conocida como síndrome autoinmune tirogástrico (SAT), pero no se conoce su prevalencia, por lo que puede pasarse sin el diagnóstico completo. El desarrollo de la gastritis atrófica limita la absorción de la vitamina B12, lo que lleva a alteraciones hematológicas, neurológicas y metabólicas, por tanto, es importante realizar las pruebas necesarias para su diagnóstico y seguir de cerca la evolución de los pacientes. La detección serológica de los autoanticuerpos contra la glándula tiroides y el cuerpo gástrico muestran la etiología autoinmune y un estado inflamatorio con daño tisular. Todo paciente con enfermedad autoinmune debe ser valorado para descartar la presencia de otras patologías de etiología inmunológica.

Tumour type and size are prognostic factors in gastric neuroendocrine neoplasia: A multicentre retrospective study

BackgroundGastric neuroendocrine neoplasias (gNEN) are defined as type I if associated with atrophic body gastritis and type III when tumour is sporadic. This classification, together with grading and size, plays a crucial prognostic role. Nevertheless, the impact of these features on clinical outcome is not clear. AimTo identify factors predicting poor outcome. Patients and methodsAnalysis of type I and type III gNEN. A composite endpoint was defined if tumour-related death or metastases or angioinvasion were observed. Results156 gNENs were evaluated: 137 (87.8%) type I and 19 (12.2%) type III. Among type I, 103 were G1 (75.2%) and 34 (24.8%) were G2. In type III group, 8 were G1 (42.1%), 10 were G2 (52.6%), and 1 was G3 (5.3%). Negative endpoint occurred in 18 patients including 10 type III and 8 type I. Male gender (p = 0.032), tumour type (p = 0.003) and size >10 mm (p = 0.024) were predictors for poor outcome, whereas Ki67 was not confirmed on multivariate analysis (p = 0.192). 5-yr survival rates in type I and type III were 100% and 76.2%, respectively (p = 0.0002). ConclusionsTumour size, tumour type and gender affect clinical outcome in gNENs. In contrast to NENs rising from other sites, Ki67 plays a less important role.

Gastroesophageal reflux symptoms and microscopic esophagitis in a cohort of consecutive patients affected by atrophic body gastritis: a pilot study

Aim: In patients affected by atrophic body gastritis (ABG) gastro-oesophageal reflux (GER) related symptoms have been reported, despite the presence of hypochlorhydria.Objective: Objectives of this single-centre study was to assess in ABG the occurrence of GER-related symptoms and their relationship with histopathologic oesophageal findings.Materials and methods: Fifty-four consecutive patients (20.4%male, 57.6 ± 14 years) undergoing to follow-up for ABG, underwent assessment of GER-related symptoms and gastroscopy with multiple gastric and oesophageal biopsies to investigate the presence of microscopic esophagitis (ME).Results: At least one typical GER symptoms were reported in 24.1% with 9.2% of patients complaining of heartburn and 18.5% regurgitation. One or more atypical GERD symptoms were reported in 44.4% of patients. Two symptomatic ABG patients presented oesophageal lesions at endoscopy (one with erosive esophagitis (LA-C) and one with Barrett’s oesophagus (C2M2)), 49% reported a mild ME and 24.5% a severe ME. No significant differences regarding GERD prevalence were found among patients with or without ME, but cough was the only symptom significantly more frequent in patients with ME (38.95% vs. 7.7%, p = .042).Conclusions: These data showed that GERD is present in a quarter of ABG patients, suggesting that hypochlorhydria not exclude per se arising of oesophageal symptoms. In ABG we found that ME is a frequent finding but its clinical relevance remains to be investigated with further studies.

Atrophic Body Gastritis: Clinical Presentation, Diagnosis, and Outcome

Atrophic body gastritis is a chronic disorder characterised by atrophy of the oxyntic glands leading to reduced gastric acid and intrinsic factor secretion. Serological studies reported yearly prevalence and incidence rates between 3–9% and 0–11%, respectively. In atrophic body gastritis, the presence of parietal cells and/or intrinsic factor autoantibodies, and autoimmune diseases, such as autoimmune thyroid disease or Type 1 diabetes mellitus, are often observed. These cases are often diagnosed as autoimmune gastritis. This association has been included as part of the autoimmune polyendocrine syndrome. A frequent clinical presentation of atrophic body gastritis is pernicious anaemia, considered an autoimmune condition, arising from vitamin B12 malabsorption as a consequence of intrinsic factor deficiency. Another presentation may be an otherwise unexplained iron deficiency anaemia, as a result of iron malabsorption and consequence of reduced gastric acid secretion. To date, no universally accepted criteria are available to define autoimmune gastritis and to distinguish this clinical entity from chronic, Helicobacter pylori-driven, multifocal atrophic gastritis. In contrast with the classical perception of a silent condition, patients with atrophic body gastritis may complain of a spectrum of gastrointestinal symptoms, ranging from dyspepsia as early satiety, postprandial fullness, and epigastric pain, to gastro-oesophageal reflux symptoms such as regurgitation and heartburn. The timely diagnosis of atrophic body gastritis is important, as this condition puts patients at an increased risk of gastric cancer and other Type 1 carcinoids that may lead to micronutrient deficiencies crucial for erythropoiesis. The present review provides an update on epidemiological and clinical aspects as well as diagnosis and outcome of the disease.

Time trend occurrence of duodenal intraepithelial lymphocytosis and celiac disease in an open access endoscopic population.

Duodenal intraepithelial lymphocytosis (DIL) is a histological finding characterized by the increase of intraepithelial CD3T-lymphocytes over the normal value without villous atrophy, mostly associated to coeliac disease (CD), Helicobacter pylori (Hp) gastritis and autoimmune diseases. To assess the occurrence of DIL, CD and Hp gastritis in an endoscopic population over a 13 year period. From 2003 to 2015 we included adult patients who consecutively underwent oesophago-gastro-duodenoscopy (OGD) with duodenal biopsies assessing the overall and annual occurrence of DIL and CD and the prevalence of Hp gastritis. 160 (2.3%) patients with DIL and 275 (3.9%) with CD were detected among 7001 patients. CD occurrence was higher from 2003 to 2011, while since 2012 DIL occurrence gradually increased significantly compared to CD (p = 0.03). DIL patients were more frequently female (p = 0.0006) and underwent OGD more frequently for dyspepsia (p = 0.002) and for indications not related to gastrointestinal symptoms than CD patients (p = 0.0003). Hp gastritis occurred similarly in CD and DIL patients but the latter had higher frequency of atrophic body gastritis (p = 0.005). DIL is a condition increasing in the general endoscopic population mainly diagnosed by chance. Concomitant gastric histological evaluation is able in one third of DIL patients to identify associated possible causes of DIL, such as Hp and atrophic gastritis.

P.02.4: Efficacy of Bismuth-Based Helicobacter Pylori Treatment in Patients with Atrophic Body Gastritis

P.02.4: Efficacy of Bismuth-Based Helicobacter Pylori Treatment in Patients with Atrophic Body Gastritis

P.01.3: Gastro-Esophageal Reflux (GER) Symptoms and Esophageal Lesions in Patients with Atrophic Body Gastritis

P.01.3: Gastro-Esophageal Reflux (GER) Symptoms and Esophageal Lesions in Patients with Atrophic Body Gastritis

Gut microbiota and pancreatic diseases.

Changes in diet, lifestyle, and exposure to environmental risk factors account for the increased incidence of pancreatic disorders, including acute and chronic pancreatitis, and pancreatic cancer. The role of the microbiota in the development of pancreatic disorders is increasingly acknowledged. The translocation of gut bacteria and endotoxins following gut barrier failure is a key event contributing to the severity of acute pancreatitis, while small intestine bacterial overgrowth is common in patients with chronic pancreatitis and further worsens their symptoms and malnutrition. Specific molecular mimicry link the microbiota and Helicobacter pylori with autoimmune pancreatitis. Changes in the oral microbiota typical of periodontitis seem to be associated with an increased risk of developing pancreatic cancer. The composition of the gut microbiota is also unbalanced in the presence of risk factors for pancreatic cancer, such as obesity, smoking and diabetes. Helicobacter pylori infection, atrophic body gastritis and related decreased gastric acid secretion also seem associated with the risk of pancreatic cancer, although this area needs further research. The link between dysbiosis, immune response and proinflammatory status is most likely the key for these associations. The present review article will discuss current available evidence on the role of gut microbiota in pancreatic disorders, highlighting potential areas for future research.

Luminescent Immunoprecipitation System (LIPS) for Detection of Autoantibodies Against ATP4A and ATP4B Subunits of Gastric Proton Pump H+,K+-ATPase in Atrophic Body Gastritis Patients.

Objectives:Circulating autoantibodies targeting the H+/K+-ATPase proton pump of gastric parietal cells are considered markers of autoimmune gastritis, whose diagnostic accuracy in atrophic body gastritis, the pathological lesion of autoimmune gastritis, remains unknown. This study aimed to assess autoantibodies against ATP4A and ATP4B subunits of parietal cells H+, K+-ATPase in atrophic body gastritis patients and controls.Methods:One-hundred and four cases with atrophic body gastritis and 205 controls were assessed for serological autoantibodies specific for ATP4A or ATP4B subunits using luminescent immunoprecipitation system (LIPS). Recombinant luciferase-reporter-fused-antigens were expressed by in vitro transcription-translation (ATP4A) or after transfection in Expi293F cells (ATP4B), incubated with test sera, and immune complexes recovered using protein-A-sepharose. LIPS assays were compared with a commercial enzyme immunoassay (EIA) for parietal cell autoantibodies.Results:ATP4A and ATP4B autoantibody titers were higher in cases compared to controls (P<0.0001). The area under the receiver-operating characteristic curve was 0.98 (95% CI 0.965–0.996) for ATP4A, and 0.99 (95% CI 0.979–1.000) for ATP4B, both higher as compared with that of EIA: 0.86 (95% CI 0.809–0.896), P<0.0001. Sensitivity-specificity were 100–89% for ATP4A and 100–90% for ATP4B assay. Compared with LIPS, EIA for parietal cell autoantibodies showed a lower sensitivity (72%, P<0.0001) at a similar specificity (92%, P=0.558).Conclusions:Positivity to both, ATP4A and ATP4B autoantibodies is closely associated with atrophic body gastritis. Both assays had the highest sensitivity, at the cost of diagnostic accuracy (89 and 90% specificity), outperforming traditional EIA. Once validated, these LIPS assays should be valuable screening tools for detecting biomarkers of damaged atrophic oxyntic mucosa.

Histopathological features of mucosa atrophy in atrophic body gastritis

Introduction: Gastric mucosa atrophy became a major issue in gastric pathology because of its connection with risk lesions for gastric cancer. Although gastric atrophy is frequently associated with different diseases, it has been included in many studies simply as a generic pathological condition, and different causes of gastric atrophy are omitted. Objective: To study the histopathological features of gastric mucosa atrophy inH. pylori- negative patients with atrophic body gastritis (ABG). Material and methods: Consecutive cases of patients diagnosed with ABG, and presenting normal or just lightly inflamed antral mucosa, were studied. Patients with gastrointestinal cancer and those with history of prior gastrointestinal surgery were excluded. The presence of intestinal metaplasia and pseudoantral (PSA) metaplasia in atrophic body mucosa was assessed. Results: During the period of 2004-2006 a total of 7,309 patients underwent gastroesophageal endoscopy with biopsies of the gastric mucosa; 3,556 (48.6%) were males, and 3,713 (51.4%) females. Among them, 105 had the diagnosis of ABG confirmed, with 32 (30.5%) males, and 73 (69.5%) females (p < 0.001). Intestinal metaplasia and/or PSA metaplasia were identified in all patients. As isolated lesions, PSA metaplasia was more frequent than intestinal metaplasia, respectively 42 (40%) vs. four (3.8%) cases. In most patients (56.2%) both types of metaplasia occurred simultaneously, and no differences were observed among genders (p = 0.67). Conclusion: Gastric mucosa atrophy in ABG shows distinctive histopathological features which should be considered in studies on the relationship between gastric mucosa atrophy and gastric cancer.

ATPase4A Autoreactivity and Its Association With Autoimmune Phenotypes in the Type 1 Diabetes Genetics Consortium Study.

Autoantibodies targeting the H+/K+-ATPase proton pump of the gastric parietal cell (parietal cell antibodies [PCA]) are diagnostic of atrophic body gastritis (ABG) leading to pernicious anemia (PA). PCA, ABG, and PA occur in increased frequency in patients with type 1 diabetes and their relatives and are considered “minor” components of forms of autoimmune polyglandular syndrome (APS). A customized radioimmunoprecipitation assay was applied to 6,749 samples from the Type 1 Diabetes Genetics Consortium to measure ATP4A autoreactivity. Autoantibody prevalence was correlated with variants in HLA class II, PTPN22, and CTLA4 genes. With an ATP4A radioimmunoprecipitation assay, PCA were detected in sera from 20.9% of affected individuals. PCA prevalence increased with age and was greater in females (25.3%) than males (16.5%) and among Hispanics (36.3%) and blacks (26.2%) compared with non-Hispanic whites (20.8%) and Asians (16.7%). PCA and other organ-specific autoantibodies GAD65, IA-2, thyroid peroxidase (TPO), 21-hydroxylase (21-OH), and transglutaminase (TG) clustered within families with heritability estimates from 71 to 95%. PCA clustered with TPO, 21-OH, and persistent GAD65 autoantibodies but not with celiac (TG) or IA-2 autoantibodies. PCA-positive subjects showed an increased frequency of DRB1*0404, DPB1*0201, and PTPN22 R620W (rs2476601-T) and a decreased frequency of DRB1*0101, DPB1*0301, and CTLA4 CT60 (rs3087243-T). Genetic variants accounted for 4–5% of the heritable risk for PCA. The same alleles were associated with other autoantibody phenotypes in a consistent pattern. Whereas most of the heritable risk for PCA and other antibodies reflects genetic effects that are tissue specific, parietal cell autoimmunity is a major pathogenetic contributor in APS2.

Histological identification ofH. pyloristained by hematoxylin-eosin and Giemsa: review for quality control

Introduction: Several special staining methods are available for H. pylori (Hp) identification in histological sections of chronic gastritis (CG), including the routine hematoxylin-eosin (HE) method. Some reports suggest that ancillary stains are not always needed to establish the diagnosis of Hp infection. In addition, the benefit of using them, when biopsies show minimal inflammation, is not clear. Objective: We performed a retrospective study to compare the usefulness of HE with Giemsa method for the histopathological diagnosis of Hp in tissue sections. Methods: Histological sections from 390 consecutive patients were reviewed. The patients were registered in the histopathology laboratory of Instituto Alfa de Gastroenterologia, Hospital das Clinicas da Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brasil. They were divided in 4 groups according to the gastric inflammatory changes as follows: Group I, gastric mucosa with normal morphology or minimal inflammatory changes (n = 146); Group II, chronic gastritis (CG) with mild inflammatory activity (n = 101); Group III, CG with patent inflammatory activity (n = 123); Group IV, patients with atrophic body gastritis (n = 20). All histological sections were carefully evaluated by 2 examiners at the oil immersion objective (1000×). Results: The identification of Hp was positive by Giemsa and HE, respectively at: Group III, 111 (90.2%) and 93 (75.6%) patients (p < 0.01); Group II, 43 (42.6%) and 29 (28.7%) patients (p < 0.05). Hp was negative in Groups I and IV. Conclusion: The results show that Giemsa stain is superior to HE for histological identification of Hp in CG. Although Hp could be identified by HE stain in the majority of CG cases, a significant number of infected patients may be neglected, regardless the intensity of the inflammatory response.

Persistent Type I Gastric Microcarcinoid in a Patient With Pernicious Anemia

Introduction: An interesting presentation of pancytopenia caused by type 1 gastric carcinoid. Case Report: A 56-year-old male with distant history of type 1 gastric carcinoid presented to the emergency department with complaints of left-sided chest and exertional dyspnea for several months. Hemogram demonstrated pancytopenia. Pancytopenia was attributed to extreme pernicious anemia due to marked B12 deficiency. Upon admission, the patient was found to have a macrocytic anemia (MCV 106) with Hb of 5.3, methylmalonic acid, and homocysteine levels were both elevated. The patient’s chest pain was presumed to be secondary to symptomatic anemia. Upper endoscopy was performed as part of the anemia work-up and demonstrated flattened folds within the fundus and the body of the stomach. Random biopsies of the fundus were performed to rule out atrophic gastritis. Histopathology revealed gastric microcarcinoid in the setting of atrophic gastritis, negative for Helicobacter pylori organisms. Discussion: Gastric carcinoid can be divided into 3 types: type I (in the presence of atrophic body gastritis, ABG), type II (in the presence of Zollinger-Ellison/multiple endocrine neoplasia type I syndrome), and type III (sporadic carcinoids without any background pathology). This patient’s biopsies of the fundus revealed micro-carcinoid, which is a rarely described entity. There are no specific surveillance guidelines for type 1 gastric carcinoid tumors. Conclusion: Further data needs to be gathered, as well as long-term follow-up, to understand the pathologic potential of gastric micro-carcinoid. When encountering a patient with pernicious anemia, it is important to entertain a diagnosis of type 1 gastric carcinoid and perform upper endoscopy.

ATP4A autoimmunity and Helicobacter pylori infection in children with type 1 diabetes.

Persistent presence of ATP4A autoantibodies (ATP4AA) directed towards parietal cells is typical for atrophic body gastritis (ABG), an autoimmune disease associated with type 1 diabetes. We assessed whether Helicobacter pylori (Hp) infection might be associated with positivity for ATP4AA in children with type 1 diabetes. Sera were collected from 70 (38♀) type 1 diabetes children [aged 13·2 ± 4·5 years, age at diagnosis 8·8 ± 4·3 years, diabetes duration 4·5 ± 3·8 years, mean HbA1c 7·8 ± 1·6% (62 ± 17·5 mmol/mol)] seen at the regional diabetes clinic in Katowice, Poland. Patients were tested concurrently for Hp infection by means of a 13C urea breath test. ATP4AA were measured using a novel radioimmunoprecipitation assay developed at the Barbara Davies Center for Childhood Diabetes, University of Colorado. ATP4AA were present in 21 [30%, 95% confidence interval (CI) = 19-41%] and Hp infection was detected in 23 (33%, 95% CI = 22-44%) children. There was no statistically significant association between ATP4AA presence and Hp status. ATP4AA presence was not associated with current age, age at type 1 diabetes diagnosis, diabetes duration or current HbA1c. ATP4AA were more prevalent in females [42% (26-58%)] than males [16% (3-28%)], P = 0·016. ATP4A are found in nearly one-third of children with type 1 diabetes and more common among females. In this cross-sectional analysis, Hp infection was not associated with autoimmunity against parietal cells.

Gastric cancer in patients with type I gastric carcinoids.

Atrophic body gastritis (ABG) is associated with both type I gastric carcinoids (T1-GCs) and intestinal-type gastric cancer. The occurrence of gastric cancer in ABG patients with type I gastric carcinoids has not yet been described. To describe the occurrence at follow-up of gastric cancer in ABG patients with type I gastric carcinoid in a retrospective case series in a single tertiary referral center. Between 1994 and 2012, 17 new cases of T1-GCs were diagnosed among a cohort of ABG patients in a single tertiary referral center for ABG. The clinical charts of these 17 T1-GC patients were retrospectively evaluated for the occurrence of gastric cancer at follow-up (median 4.2years, range 0.5-13). In 4 (23.5%)/17 T1-GCs patients (3 females, age 40-78years), gastric cancer occurred (median follow-up 5.9years, range 5.1-13). Three cases were intestinal-type adenocarcinomas and one a signet-ring cell diffuse gastric cancer, localized in three cases in the antrum. In two patients, it was detected on random biopsies during follow-up gastroscopy; in the other two, gastroscopy was performed because of new symptoms. All patients with gastric cancer had associated autoimmune features (pernicious anemia, autoimmune thyroid disease and a spared antrum) compared to 77, 46 and 54% of those without gastric cancer, although statistical significance was not reached. This case series shows that in patients with T1-GCs, gastric cancer may frequently occur at long-term follow-up. Thus, these patients should be monitored by a long-term surveillance program, including an accurate bioptic sampling of the antral mucosa.

Pernicious Anemia: Non - Gastroscopic Diagnosis of Autoimmune Atrophic Gastritis with Positive Serological Marker

For the last many decades pernicious anemia has been treated as a separate clinical feature. Pernicious anemia is also known as macrocytic anemia which originates due to the lack of vitamin B12 (cobalamin). A protein called intrinsic factor which helps vitamin B12 for its absorption through terminal ileum so, the deficiency of intrinsic factor result in a lack of vitamin B12 absorption, which, in turn, causes pernicious anemia. The gastric parietal cell normally produces chlorhydric acid and intrinsic factor. Atrophic body gastritis (ABG) is a condition which cause the destruction of the oxyntic mucosa and the reduction of the parietal cell hence result in the deficiency of intrinsic factor . Pernicious anemia can present in many different clinical patterns like fatigue (tiredness), headache, dizziness, shortness of breath, pale or yellowish skin, coldness in your hands and feet, and chest pain. Presentation of Case: We report a case of a 55 year old male who presented with one month history of fatigue ness, dizziness, abdominal pain and short of breath on exertion. On further investigation, it is turnout to be atrophic gastritis which is treated conservatively.

Development of a novel autoantibody assay for autoimmune gastritis in type 1 diabetic individuals

Autoimmune atrophic body gastritis (ABG) and pernicious anaemia are prototypical, organ-specific autoimmune diseases whose prevalence in the general population is 2.0 vs 2 and 0.15-1%, respectively. The incidence of disease increases with age and is frequently associated with other autoimmune disorders such as type 1 diabetes mellitus (T1DM). Early diagnosis of ABG/pernicious anaemia is essential for the prevention and/or treatment before manifestations of chronic disease become irreversible. Parietal cell autoantibody detection via enzyme-linked immunosorbent assay is currently the most widely used biomarker of disease with diagnosis confirmed by subsequent immunohistochemistry via biopsy. To improve the assay we designed a specific, molecularly defined radioimmunoprecipitation assay for early detection of ABG, targeting its major antigen, the gastric H+/K+ ATPase 4A subunit ATP4A. The major antigenic domain in ATP4A was tested against a panel of sera from new onset patients with T1DM which tested positive for the gold standard T1DM autoantibodies (IAA, IA2A, GAD65A, and ZnT8A). Significant immunoreactivity to ATP4A was measured (25%) while 6% of first-degree relatives of subjects with T1DM who were sero-negative for T1DM autoantigens were positive for ATP4A autoantibodies. ATP4A antibody prevalence increased with age of onset of T1DM, which is atypical of other T1DM autoantibodies. Immunoreactivity to ATP4A, unlike that of T1DM antigens, demonstrates a significant gender bias in newly diagnosed individuals with T1DM. Although the utility of the assay as a biomarker for T1DM is likely limited, it may serve as an improved indicator of ABG.