Abnormalities Of Gastric Mucosa Research Articles

Clinicopathologic and endoscopic characteristics of ten patients with gastric hamartomatous inverted polyp: a single center case series

BackgroundGastric hamartomatous inverted polyps (GHIPs) are not well characterized and remain diagnostically challenging due to rarity. Therefore, this study aims to investigate the clinicopathologic and endoscopic characteristics of patients with GHIP.MethodsWe retrospectively reviewed clinicopathologic and endoscopic features of ten patients with GHIP who were admitted to Beijing Friendship Hospital from March 2013 to July 2022. All patients were treated successfully by endoscopic resection.ResultsGHIPs were usually asymptomatic and found incidentally during gastroscopic examination. They may be sessile or pedunculated, with diffuse or local surface redness or erosion. On endoscopic ultrasonography, the sessile submucosal tumor-type GHIP demonstrated a heterogeneous lesion with cystic areas in the third layer of the gastric wall. Histologically, GHIPs were characterized by a submucosal inverted proliferation of cystically dilated hyperplastic gastric glands accompanied by a branching proliferation of smooth muscle bundles. Inflammatory cells infiltration was observed in the stroma, whereas only one patient was complicated with glandular low-grade dysplasia. Assessment of the surrounding mucosa demonstrated that six patients (60%) had atrophic gastritis or Helicobacter pylori–associated gastritis, and four patients (40%) had non-specific gastritis. Endoscopic resection was safe and effective.ConclusionsGHIPs often arise from the background of abnormal mucosa, such as atrophic or H.pylori-associated gastritis. We make the hypothesis that acquired inflammation might lead to the development of GHIPs. We recommend to make a full assessment of the background mucosa and H. pylori infection status for evaluation of underlying gastric mucosal abnormalities, which may be the preneoplastic condition of the stomach.

S3738 Agent Orange as a Possible Cause of Helicobacter pylori Negative Gastric Mucosa-Associated Lymphoid Tissue Lymphoma

Introduction: Gastric mucosa-associated lymphoid tissue (MALT) lymphoma was first described in 1983 as the most common extranodal site of non-Hodgkin lymphoma. Helicobacter pylori (H. pylori) infection is implicated in 90% of all gastric MALT lymphoma cases. Agent Orange (AO), with traces of oncogenic 2,3,7,8-tetrachlorodibenzo-p-dioxin, has also been classified as a causative agent in non-Hodgkin lymphoma, which includes gastric MALT lymphoma. Here we report a case of H. pylori negative gastric MALT lymphoma in a patient with history of significant AO exposure. Case Description/Methods: A 75-year-old Caucasian male veteran who served in the Vietnam War with significant AO exposure, as well as history of chronic gastroesophageal reflux disease, was referred for endoscopy to evaluate a reported history of un-staged Barrett’s esophagus 5-years prior but with two subsequent normal endoscopies at an outside facility. He noted symptoms of burning chest pain and dyspepsia following large meals, all of which were worsened with spicy foods and improved with omeprazole. Family history was negative for a history of gastric cancer, and he had a 25-pack year smoking history but quit 20 years prior to presentation.Initial esophagogastroduodenoscopy (EGD) revealed abnormal folds in the gastric fundus and erythema in the gastric antrum, but otherwise normal exam including normal duodenum and esophagus. Random gastric biopsies and biopsies of the abnormal folds were consistent with gastric MALT lymphoma, negative for H. pylori and t(11;18)(q21;q21). Repeat EGD 1 month later for further sampling demonstrated identical findings (Figure 1A). Stool testing for H. pylori antigen was also negative. The patient was referred to oncology and after staging imaging was found to have stage IE gastric MALT lymphoma. He was treated with involved site radiation therapy and EGD 3 months later showed both endoscopic and pathologic resolution (Figure 1B). Discussion: The 10% of cases of H. pylori negative gastric MALT lymphoma have an unclear etiology, although dysregulation of nuclear factor-kappa B (NF-κB) principally via translocations t(11;18)(q21;q21) is thought to be a potentially causative genetic alteration. In this patient, neither H. pylori nor the common t(11,18) genetic alteration were present. Given AO is implicated in non-Hodgkin lymphoma and the most common site of extranodal non-Hodgkin lymphoma is the gastric mucosa, AO exposure should be considered a risk factor for development of gastric MALT lymphoma.Figure 1.: (A) EGD demonstrating abnormal gastric mucosa with prominent gastric fundus folds seen on retroflexion during EGD prior to ISRT (radiation) therapy. (B) Post-radiation EGD demonstrating resolution of the abnormalities seen with the pre-treatment EGD including disappearance of the prominent gastric fundus folds.

First prospective European study for the feasibility and safety of magnetically controlled capsule endoscopy in gastric mucosal abnormalities.

BACKGROUNDWhile capsule endoscopy (CE) is the gold standard diagnostic method of detecting small bowel (SB) diseases and disorders, a novel magnetically controlled capsule endoscopy (MCCE) system provides non-invasive evaluation of the gastric mucosal surface, which can be performed without sedation or discomfort. During standard SBCE, passive movement of the CE may cause areas of the complex anatomy of the gastric mucosa to remain unexplored, whereas the precision of MCCE capsule movements inside the stomach promises better visualization of the entire mucosa.AIMTo evaluate the Ankon MCCE system’s feasibility, safety, and diagnostic yield in patients with gastric or SB disorders.METHODSOf outpatients who were referred for SBCE, 284 (male/female: 149/135) were prospectively enrolled and evaluated by MCCE. The stomach was examined in the supine, left, and right lateral decubitus positions without sedation. Next, all patients underwent a complete SBCE study protocol. The gastric mucosa was explored with the Ankon MCCE system with active magnetic control of the capsule endoscope in the stomach, applying three standardized pre-programmed computerized algorithms in combination with manual control of the magnetic movements.RESULTSThe urea breath test revealed Helicobacter pylori positivity in 32.7% of patients. The mean gastric and SB transit times with MCCE were 0 h 47 min 40 s and 3 h 46 min 22 s, respectively. The average total time of upper gastrointestinal MCCE examination was 5 h 48 min 35 s. Active magnetic movement of the Ankon capsule through the pylorus was successful in 41.9% of patients. Overall diagnostic yield for detecting abnormalities in the stomach and SB was 81.9% (68.6% minor; 13.3% major pathologies); 25.8% of abnormalities were in the SB; 74.2% were in the stomach. The diagnostic yield for stomach/SB was 55.9%/12.7% for minor and 4.9%/8.4% for major pathologies.CONCLUSIONMCCE is a feasible, safe diagnostic method for evaluating gastric mucosal lesions and is a promising non-invasive screening tool to decrease morbidity and mortality in upper gastro-intestinal diseases.

S1879 Dysphagia and Odynophagia: Rare Initial Manifestations of Diffuse Large B-Cell Lymphoma

INTRODUCTION: Diffuse large B cell lymphoma (DLBCL) can involve extranodal sites including the gastrointestinal (GI) tract, reportedly occurring in up to 30% of patients. In the GI tract, stomach is the most commonly affected organ. CASE DESCRIPTION/METHODS: A 68-year-old non-obese, immunocompetent male with no history of tobacco and alcohol use presented with six months of progressively worsening solid food dysphagia, odynophagia, and 30 pounds unintentional weight loss. He also mentioned subjective fevers without chills or night sweats. CT imaging showed a 4.4 cm esophageal mass with hilar, mediastinal, supraclavicular, abdominal, iliac, and inguinal lymphadenopathy. Upper endoscopy visualized a circumferential, ulcerated mass from middle to distal esophagus, and a patch of erythematous mucosa in the proximal gastric body. Biopsies of the esophageal mass and abnormal gastric mucosa revealed high grade diffuse large B cell lymphoma with Ki67 proliferative index of >95%, and without evidence of Epstein-Barr Virus. Subsequent FISH studies did not report rearrangements in BCL-2, BCL-6 or MYC. He received 5 cycles of chemotherapy regimen that consisted of rituximab, etoposide, prednisone, vincristine, cyclophosphamide and doxorubicin (R-EPOCH) with excellent treatment response based on subsequent CT imaging that showed significant decrease in size of thoracic, abdominal and pelvic lymphadenopathy. DISCUSSION: With only a handful of cases reported in the literature, esophagus is an infrequent site of extranodal lymphoma. And for esophageal symptoms of dysphagia and odynophagia to be the initial manifestations leading to the diagnosis of DLBCL is rare. Given the widespread lymphadenopathy noted on imaging, we suspect that our patient’s site of origin of DLBCL was in the lymph nodes with a rare secondary spread to the esophagus and stomach, rather than primary DLBCL of the GI tract. Aside from adding to the sparse cases described in the literature, this case highlights the importance of keeping a broad differential diagnosis for esophageal mass particularly in patients who do not have the classic risk factors for esophageal adenocarcinoma and squamous cell carcinoma.Figure 1.: CT chest showed a 4.4 cm esophageal mass with bilateral hilar, mediastinal and left supraclavicular lymphadenopathy, and bilateral pulmonary nodules consistent with metastasis.Figure 2.: Upper endoscopy visualized a circumferential, ulcerated mass from middle to distal esophagus.Figure 3.: Biopsies of the esophageal mass and abnormal gastric mucosa revealed a diffuse infiltrate of large, atypical lymphoid-appearing cells surrounded by a large area of necrosis (A) with stains positive for MUM-1 (B) and BCL-6 (C), consistent with high grade diffuse large B cell lymphoma.

Evaluation of Invasive and Non-Invasive Methods for the Diagnosis of H. pylori in Dyspepsia Patients

Background: H. pylori has been established as the major causative agent of chronic gastritis, and represents the main etiological cause of other gastroduodenal diseases such as peptic ulceration, gastric lymphoma, and gastric cancer. Therefore, screening and treatment of the bacterium is an important strategy for preventing gastric cancer. Objective: To compare some invasive classical histological tests to non-invasive serological antibody and stool antigen tests for the diagnosis of H. pylori infections. Patients and Methods:The study population comprised of 171 patients with symptoms of dyspepsia and other gastritis related symptoms. Three biopsy specimens were taken and collected from the stomach and sent for histopathologic study. H and E staining and modified Giemsa staining were performed on tissue sections of each case. Serology antibody and Stool antigen tests were also used as nan-invasive tests in this study. Results: Four tests had been done to detect the presence of H. pylori Bacteria. The mean age (+ SD) of the studied sample was 43.8 + 14.7 years, ranging from 20 to 74 years. The median was 44 years. The total agreement between the serum Ab test and the stool Ag test was 88.3%. Significant differences were detected between the two tests (p < 0.001). It is evident that the serum Ab test is highly sensitive (sensitivity = 98.4%), but the Predictive value positive (76.3%) was not so high. The Giemsa test was highly specific (specificity = 98.2%), and highly sensitive (sensitivity = 93.5%). Conclusion: The main advantage of histopathology tests is not only restricted to detection purpose, it also can detect any abnormalities of gastric mucosa by bacteria such as peptic ulcer bleeding, atrophic gastritis, intestinal metaplasia, and gastric cancer. The modified Giemsa staining method could be used as a method of choice for the detection of H. pylori due to its sensitivity, simplicity and consistency.

Low Yield and High Cost of Gastric and Duodenal Biopsies for Investigation of Symptoms of Abdominal Pain During Routine Esophagogastroduodenoscopy

Esophagogastroduodenoscopy (EGD) referrals for symptoms of abdominal pain are common. Current guidelines for dyspepsia recommend biopsies of gastric mucosa for Helicobacter pylori in all patients referred for EGD. Our study aimed to determine the clinical yield and cost-effectiveness of gastric and duodenal biopsy in EGDs performed for abdominal pain. Three hundred and ninety-one outpatient EGDs performed at a single academic tertiary care center were studied. For each procedure, endoscopic as well as pathologic findings from the stomach and duodenum were then recorded. Charge of biopsy was calculated using the increased charges for professional fees, forceps, and pathology fees when a biopsy was performed. Gastric biopsies were obtained on 304 EGDs performed with 13 (4.2%) patients diagnosed with H. pylori. In patients with abnormal gastric mucosa on EGD, 11 of 167 (6.5%) were positive for H. pylori compared to 2 of 137 (1.4%) with normal appearing mucosa (p=0.02). Charge per diagnosis of H. pylori for normal mucosa was calculated to be $43,073. Duodenal biopsies were performed in 263 cases. Celiac disease was diagnosed in 4 of 263 cases (1.5%). Of patients with abnormal duodenal mucosa on EGD, 1 of 36 (2.7%) were positive for celiac disease compared to 3 of 227 (1.3%) with normal mucosa (p=0.57). Charge per diagnosis of celiac disease for normal mucosa was calculated to be $47,580. Routine biopsy during EGD for symptoms of abdominal pain has low yield with high costs. Practice of routine biopsies of normal appearing tissue and the present guidelines should be reconsidered in the investigation of abdominal pain with EGD.

Frequency of Helicobacter Pylori Infection on Histopathology in Patients with Dyspepsia

Objective: To determine the frequency of Helicobacter Pylori infection on histopathology in patients presenting with dyspepsia. Background: Helicobacter Pylori is associated with dyspepsia in patients who have gastric mucosal abnormalities and this infection can be diagnosed by invasive and non invasive test. Histology of endoscopically taken biopsy, for exploration of this organism is used in this study. Study Design: Cross-sectional, observational study. Place and Duration of Study: Department of Emergency Medicine, Ziauddin University Hospital, Karachi for Six months from March 2013 to August 2013. Methodology: A total of 362 cases with dyspeptic symptoms were underwent an upper gastrointestinal endoscopy after fulfilling the selection criteria. H. Pylori infection would be defined by the presence of dyspeptic symptoms with detection of the bacterium on histopathology. All the data was collected by using a proforma and different parameters were assessed for a minimum follow-up period of one month. Data was analyzed by descriptive statistics using SPSS software version 19. Result: Out of 362 cases of dyspepsia 218 (60.2%) males and 144 (39.8%) females (Male: Female was 1.5: 1). Two fifty one (69.3%) patients with dyspepsia were H. Pylori positive on histopathology. Out of 251 cases having H. Pylori infection 165 (75.7%) were male and 86 (59.7%) female. High percentage was found in the age between 31 – 50 years, 160 (77.3%). Conclusion: In this study 69.3% of the patients examined were H. Pylori positive on histopathology. Male sex and older age (> 30 years) are independent risk factor of H. Pylori infection in dyspeptic patients.

GI Sarcoidosis

Purpose: A 42-year-old African-American male with PMH of recently diagnosed hereditary hemochromatosis presented to a GI clinic complaining of abdominal pain, cramps, associated diarrhea and dyspepsia but denied any bloody stools, fever, weight loss or nausea/vomiting. Vital signs were stable and physical exam was benign. There was no palpable adenopathy, breath sounds were clear bilaterally, no murmurs on cardiovascular auscultations, no abdominal tenderness, no joint abnormalities and no appreciable skin rashes on examination. CMP showed mildly elevated AST/ALT, and stool analysis for fecal leukocytes, ova and parasites, culture and Clostridium difficile were negative. Upper GI endoscopy was positive for hiatus hernia, gastric mucosal abnormalities characterized by congestion, erythema and erosions and duodinitis. No ulcerations, nodular irregularities, segmental mucosal thickening, non distensibility mimicking linitis plastic or mucosal polyps were seen. Biopsies of these areas were sent to pathology. Colonoscopy performed revealed erythematous transverse colon and rectum, but was otherwise unremarkable. Biopsies were also sent to pathology. Biopsy report revealed chronic inflammatory changes and non-caseating granulomas involving the stomach, terminal ileum, colon and rectum. There was no evidence of acid-fast bacilli, fungi or H. pylori. Although the patient had not lived in an endemic area, histoplasma urine antigen was measured and negative. Liver biopsy from months earlier was negative for non-caseating granulomas, but consistent with changes associated with Hemochromatosis. CT chest showed no acute or chronic pulmonary disease. There were no hilar adenopathy and the lungs were clear bilaterally without infiltrates, volume loss or mass lesions. CT abdomen and pelvis was significant for hepato-splenomegaly, but negative for retroperitoneal mesenteric or pelvic lymphadenopathy. Sedimentation rate was within normal limits, but angiotensin converting enzyme was elevated. Chrohn's disease was ruled out because there was no evidence of perianal disease, fistulas or strictures, normal ESR and CRP and elevated ACE levels. Gastric Sarcoidosis was highly suspected in this patient and he is pending an appointment with Rheumatology for management of sarcoidosis.Figure

Delayed gastric emptying determined using the 13C–octanoic acid breath test in patients with systemic sclerosis

To determine the prevalence of delayed gastric emptying using the 13C-octanoic acid breath test in unselected patients with systemic sclerosis (SSc), to evaluate whether findings of the 13C-octanoic acid breath test are associated with clinical digestive manifestations, gastric mucosal abnormalities detected by gastroscopy, motor activity dysfunction detected by antroduodenal manometry, and esophageal motor impairment and extradigestive manifestations of SSc, and to develop a risk prediction score of gastric emptying in SSc. Consecutive patients with SSc (n=57) underwent the 13C-octanoic acid breath test. All of the patients with SSc completed a questionnaire on digestive symptoms, and a global symptom score (GSS) was calculated. The prevalence of delayed gastric emptying was 47.4% in patients with SSc. A marked correlation was observed between a GSS of digestive symptoms≥5 and the presence of delayed gastric emptying (P<0.00001). The sensitivity of a GSS≥5 for predicting delayed gastric emptying was as high as 0.93, while the specificity was 0.73. Moreover, a GSS≥5, mucosal gastric abnormalities, severe esophageal motor impairment, and interstitial lung disease were factors that were independently associated with the presence of delayed gastric emptying, and these variables were used to create a risk prediction score. The area under the receiver operating characteristic curve for the risk prediction score was 0.90; the sensitivity of this score for the prediction of delayed gastric emptying was 0.93, while the specificity was 0.77. The results indicate that delayed gastric emptying occurs often in patients with SSc. Interestingly, using risk models with routine clinical characteristics, a simple risk prediction score can be calculated, allowing prediction of the occurrence of delayed gastric emptying in patients with SSc.

Gastric Cancer: Clinical Aspects, Epidemiology and Molecular Background

The validity and usefulness of the 7th edition of the UICC tumor node metastasis classification in the context of clinical management of gastric cancer are discussed. The most relevant new agent in gastric cancer therapy is trastuzumab for HER2-positive gastric carcinomas. This marks the success of continuous effort of translational research. Trastuzumab, initially applied in palliative settings, is currently being evaluated also in neoadjuvant treatment regimens. Several new meta-analyses support the carcinogenic effect of high salt intake and smoking in the context of Helicobacter pylori infection. Further data have become available on the efficacy of protective agents, acetyl salicylic acid/nonsteroidal anti-inflammatory drugs, and antioxidants. In search for a successful prevention strategy, the focus is on the identification of individuals at high risk who demand screening (testing) and surveillance. Serological assessment of gastric mucosal abnormalities with increased risk for gastric cancer development is extensively studied, and new data are presented from Asia as well as from Europe. New high-throughput techniques combined with bioinformatic vector analysis open the gate to the identification of new potential diagnostic and therapeutic targets. Furthermore, these approaches allow us to elucidate the interplay of bacterial virulence factors and the host's immune response as well as H. pylori-associated alterations of mucosal gene expression.

Incidental Gastric Eosinophils in Patients With Eosinophilic Esophagitis: Do They Matter?

Some patients with eosinophilic esophagitis (EE) (>15 eosinophils/high-power field on esophageal mucosal biopsies and lack of response to acid suppression and/or normal pH probe study) demonstrate incidental eosinophilic inflammation of the gastric mucosa. It is unclear whether patients with EE and normal gastric biopsies (EE-N) are phenotypically different from patients with EE and gastric mucosal abnormalities (EE-A) (ie, >10 eos/hpf on gastric biopsies). The aim of the study was to compare the clinical features and response to therapy among patients with EE-N and EE-A. Medical records of all of the EE-A and a random group of patients with EE-N diagnosed during an 8-year period were reviewed. A subgroup analysis of patients treated with swallowed fluticasone with a repeat esophagogastroduodenoscopy within 6 months of starting therapy was also performed. During the study period, 41 patients had EE-A. When compared to 50 random patients with EE-N, no clinical differences were noted, including sex, age, presenting symptoms, esophageal histology, and atopy history. Eleven (27%) of the 41 EE-A and 14 (28%) of the 50 EE-N patients were treated with swallowed fluticasone, and the response was similar among the groups. The mean esophageal eosinophils/high-power field among the EE-A group dropped from 47 to 8 compared with a 46 to 7 drop among the EE-N group treated with fluticasone therapy (P = 0.91). In 9 (82%) of the 11 patients with EE-A treated with fluticasone, there was resolution (7 of 9) or significant improvement (2 of 9) of gastric eosinophilia. Patients with EE-A and EE-N have similar clinical presentations. Incidental gastric inflammation does not predict a worse response of esophageal inflammation to fluticasone and should not exclude its use in patients with EE-A. In fact, gastric inflammation responded to swallowed fluticasone in the majority of patients with EE-A. This observation should foster further investigation into pathogenesis of EE and presumed esophagogastric inflammatory axis.

Serum gastrin concentration and changes in G and D cell densities in gastric antrum in children with chronic gastritis

Elevated gastrin concentration leading to gastritis is explained as the effect of change in the density of D and G cells. The aim of the study was to determine and compare fasting serum gastrin concentrations, G and D cell densities in gastric antrum mucosa in children with chronic gastritis and in children with no gastritis or Helicobacter pylori infection. A total of 184 patients aged 6-18 years, with chronic abdominal pain underwent endoscopic examination. We created three groups: I--patients with chronic gastritis and H. pylori infection; II--patients with chronic gastritis but no H. pylori infection; III--patients with neither gastric mucosal abnormalities nor H. pylori infection. G and D cell densities were determined in the biopsy specimens (using Rbalpha H Gastrin & Somatostatin antibodies). Fasting serum gastrin concentrations were measured using a Beckmann gamma-counter and a GASK-PR kit. The mean serum gastrin concentration in group I was higher when compared with group II (p = 0.04) and group III (p = 0.019). No statistically significant differences were found between groups II and III (p = 0.91). There were no statistically significant differences in G and D cell densities between groups. The mean G/D cell ratios in groups I and III were almost identical. The mean fasting serum gastrin concentration was higher in children with both chronic gastritis and H. pylori infection compared with patients without infection or without antral inflammation. No difference in the G cell density or D cell density in children was found, regardless of the presence or absence of gastritis or H. pylori infection.

Portal hypertensive duodenal polyp: A case report

Abnormalities of gastric mucosa in patients with portal hypertension are well documented. Manifestations of portal hypertension in small bowel and colon are less common. Colonic polypoid lesions microscopically consisting of a normal mucosa, with dilatation of submucosal vessels, have been described. We here report the first case of portal hypertensive duodenal polyp, responsible for gastro-intestinal bleeding. Endoscopic treatment turned out to be successful.

Portal hypertension and portal hypertensive gastropathy in patients with liver cirrhosis: a haemodynamic study.

The relationships between the levels of portal hypertension and the morphologic alterations of gastric mucosa in patients with liver cirrhosis--generally described as portal hypertensive gastropathy--are poorly defined. In total, 62 patients with cirrhosis of different aetiologies, were examined by endoscopy and measurement of portal hypertension by hepatic venous pressure gradient. Portal hypertensive gastropathy was observed in 49 cases; six patients showed gastric antral vascular ectasia always associated with gastric lesions described as severe portal hypertensive gastropathy with different localizations. Hepatic venous pressure gradient showed severe portal hypertension in 37 cases, and averaged 17.7 +/- 4.3 mmHg. It was much higher in patients with severe lesions (p=0.0004). Hepatic venous pressure gradient in patients with endoscopic signs of isolated antral gastropathy was lower (p=0.04) than in those with isolated lesions in body-fundus. No relationship was found between hepatic function, as assessed by the Child-Pugh score, and portal hypertensive gastropathy. The present data suggest that the severity of portal hypertensive gastropathy is related to portal hypertension, but portal hypertension is not the sole determinant of the occurrence of endoscopic abnormalities of gastric mucosa. The derangement of liver function does not appear to play any role in the occurrence of portal hypertensive gastropathy.

Early Gastric Cancer

Early Gastric Cancer (EGC) is a carcinoma limited to the gastric mucosa or submucosa without the involvement of any lymph node. In Indonesia, the prevalence of EGC in 1980 was 2.2% and 1.7% for Jakarta and Medan, respectively. From 1980-1987 in Surabaya, the prevalence was 9.1% from all gastric cancers. Gastric mucosal abnormalities include atrophic gastritis, which is frequently accompanied by achlorhidria or hipochlorhidria and pernicious anemia, and the presence of an ulcer or polyp were believed to be precarcinogenic factors. Environmental factors, life style, age, sex, genetic factors, race, as well as dietary factors, especially intake of foods containing N-nitrosa (N-nitrosa compound) might play a role as risk factors for EGC. H.pylori infection also causes an increased risk for EGC. The diagnosis of EGC is based on physical examination, occult blood in stool sample, cytology, double contrast roentgenologic examination, gastroscopy, gastrobiopsy, and radioactive phosphor. There are no tumor markers specific for EGC. Histologically, EGC is classified into intestinal and diffuse infiltrative EGC. In 1962, the Japanese Research Society for Gastric Cancer made a classification for EGC based on gastroscopy, fluoroscopy, histopathology and microscopic examinations. In Japan, detection for EGC was performed by spraying the gastric mucosa with methylen blue during endoscopy, which will stain intestinal mucosa and spare normal mucosa. Early detection of EGC in Japan was performed through mass screening of people ages 40-50 years with recent dyspepsia, by means of endoscopy, biopsy, and upper GI tract radiological examinations. Endoscopic Ultrasonography (EUS) is the most accurate tool to determine EGC staging, particularly those with non-ulcerative lessions. The choices of treatment for EGC are surgical therapy or Endoscopic Mucosal Resection (EMR). EMR is a localized therapy, and it is indicated for EGC without metastases, for patients unwilling to undergo operation, or for those who are bad candidates for operation. The prognosis for EGC does not depend upon microscopic classification, but mostly on the depth of gastric mucosal invasion, spread to regional lymph nodes, and the presence of distant metastases. By establishing the diagnosis of EGC, the prognosis is usually better, for the treatment can be given at an earlier stage. Key words: Early gastric cancer, diagnosis, treatment

Effects of medical treatment on gastric mucosal abnormalities in gastroduodenal ulcer disease.

The development of carcinoma in cases of gastric ulcer disease during long-term H(2)-blocker treatment is slowly increasing, and ulcers that require such treatment exhibit the characteristics of intractable conditions, including linear ulcers, simultaneous gastric and duodenal ulcers, immature intestinal metaplasia of the gastric epithelium, and atrophic gastritis accompanied with multiple ulcer cicatrices. The incomplete form of intestinal metaplasia resembling Filipe's type III lesions and showing structural atypia developed in the background gastric mucosa in such cases, and the characteristics of this metaplasia included structural atypia, a residuum of gastric-type mucous cells, rapid proliferative activity, and in some areas abnormal expression of P53 protein. In addition, in rat studies it was demonstrated that prolonged administration of H(2)-blockers while gastric ulcers were present accelerated cell proliferation in the background gastric mucosa in the long term. Accordingly, it was considered possible that the development of the incomplete form of intestinal metaplasia, which was strongly suggested to have some relation to the sites where intestinal-type gastric carcinoma appeared, was accelerated by mucosal injury due to chronic ulcers and by persistent elevation in intragastric pH. The results of the present study of gastric carcinoma as a complication of peptic ulcer disease indicated the possibility that Helicobacter pylori was a major contributory factor to the development of the incomplete form of intestinal metaplasia from damage to the background mucosa, but it was unclear whether H. pylori made any direct contribution to carcinogenesis.

S20-2 - Functional and morphological abnormality of gastric mucosa in histamine H2 receptor-deficient mice

S20-2 - Functional and morphological abnormality of gastric mucosa in histamine H2 receptor-deficient mice

Characterization of gastric mucosal lesions in patients with celiac disease: a prospective controlled study

OBJECTIVE: Several studies have demonstrated that chronic exposure to gluten may damage the structure and function of the gastric mucosa in gluten-sensitive patients. However, until now, these abnormalities have been incompletely studied. Our purpose in the present study was to characterize, in a prospective controlled study, the endoscopic and histological appearance of the gastric mucosa in a large cohort of patients with celiac disease with and without Helicobacter pylori ( H. pylori) infection. METHODS: We evaluated biopsy specimens taken from the gastric body and antrum of 218 individuals who underwent upper endoscopy for small bowel biopsy. One hundred-four patients had celiac disease (80 of them at the time of diagnosis-untreated). In 114 subjects celiac disease was excluded. RESULTS: Endoscopic findings did not show a difference between the groups. The prevalence of cases with normal gastric mucosa, chronic superficial gastritis, and atrophic gastritis was similar in patients and controls. Similarly, presence of metaplasia, inflammatory activity, and lymphoid follicles and aggregates did not show differences between the groups. Histological or serological evidence of H. pylori infection was detected in 86% of patients (82% of untreated celiacs and 95% of those on those taking treatment). The infection was highly prevalent in patients (89%) and controls (97%) diagnosed with chronic gastritis. Untreated patients had a significant greater IEL count in the antrum and corpus than controls ( p < 0.0001 and p < 0.001, respectively). A global analysis of the data on intraepithelial lymphocyte (IEL) counts in the different populations suggest that the inflammatory state may represent the cumulative effect of H. pylori infection and gluten sensitivity. Only three patients had IEL infiltration compatible with diagnosis of lymphocytic gastritis (count >25%) and three other patients had borderline counts. CONCLUSIONS: According to our results, celiac disease patients presented a similar prevalence of gastric mucosal abnormalities compared with the control population. Evidence of H. pylori infection was very high compared with the prevalence in the general Argentine population. As a particular observation in our celiac population, the disease was rarely associated with lymphocytic gastritis. We suggest that the chronic inflammatory state evidenced by a gastric mucosal lymphocyte infiltration may be secondary to the combination of H. pylori infection and chronic gluten ingestion in gluten-sensitive subjects.

Characterization of gastric mucosal lesions in patients with celiac disease: a prospective controlled study.

Several studies have demonstrated that chronic exposure to gluten may damage the structure and function of the gastric mucosa in gluten-sensitive patients. However, until now, these abnormalities have been incompletely studied. Our purpose in the present study was to characterize, in a prospective controlled study, the endoscopic and histological appearance of the gastric mucosa in a large cohort of patients with celiac disease with and without Helicobacter pylori (H. pylori) infection. We evaluated biopsy specimens taken from the gastric body and antrum of 218 individuals who underwent upper endoscopy for small bowel biopsy. One hundred-four patients had celiac disease (80 of them at the time of diagnosis-untreated). In 114 subjects celiac disease was excluded. Endoscopic findings did not show a difference between the groups. The prevalence of cases with normal gastric mucosa, chronic superficial gastritis, and atrophic gastritis was similar in patients and controls. Similarly, presence of metaplasia, inflammatory activity, and lymphoid follicles and aggregates did not show differences between the groups. Histological or serological evidence of H. pylori infection was detected in 86% of patients (82% of untreated celiacs and 95% of those on those taking treatment). The infection was highly prevalent in patients (89%) and controls (97%) diagnosed with chronic gastritis. Untreated patients had a significant greater IEL count in the antrum and corpus than controls (p < 0.0001 and p < 0.001, respectively). A global analysis of the data on intraepithelial lymphocyte (IEL) counts in the different populations suggest that the inflammatory state may represent the cumulative effect of H. pylori infection and gluten sensitivity. Only three patients had IEL infiltration compatible with diagnosis of lymphocytic gastritis (count >25%) and three other patients had borderline counts. According to our results, celiac disease patients presented a similar prevalence of gastric mucosal abnormalities compared with the control population. Evidence of H. pylori infection was very high compared with the prevalence in the general Argentine population. As a particular observation in our celiac population, the disease was rarely associated with lymphocytic gastritis. We suggest that the chronic inflammatory state evidenced by a gastric mucosal lymphocyte infiltration may be secondary to the combination of H. pylori infection and chronic gluten ingestion in gluten-sensitive subjects.

Prevalence of Helicobacter pylori infection and gastric mucosal abnormalities in chronic pancreatitis

Objective: Chronic pancreatitis is often associated with abnormal gastric acid secretion. However, previous studies have taken into consideration neither the potential role of Helicobacter pylori ( H. pylori) infection nor histological features of the gastric mucosa in this context. The aim of this study was to analyze the prevalence of H. pylori infection as well as the pattern of gastritis in patients with chronic pancreatitis. Methods: Forty patients with chronic alcoholic pancreatitis were included in the study: 40 patients with alcoholic liver cirrhosis and normal exocrine pancreatic function and 40 asymptomatic nonalcoholic subjects matched for age and sex used as control subjects. Endoscopy was performed in all patients, and five biopsy specimens from the antrum (three from the gastric body and two from the cardia) were taken for histological grading of gastritis and H. pylori assessment. Results: Prevalence of H. pylori infection was similar in subjects with chronic pancreatitis (38%), asymptomatic subjects (28%) and liver cirrhosis (30%). Topography and expression of H. pylori-associated chronic gastritis was also not different among the three groups of subjects. In H. pylori-negative subjects, the presence of moderate to severe chronic antral gastritis was significantly more common in patients with chronic pancreatitis (40%) than in subjects with liver cirrhosis (18%) and in asymptomatic subjects (14%) ( p < 0.05). No difference was found among the three groups of patients with regard to gastritis activity, atrophy, and intestinal metaplasia in the various gastric regions. The chronicity grade of gastritis did not correlate with the severity of pancreatic insufficiency. Conclusion: Prevalence of H. pylori infection is not different in patients with chronic pancreatitis as compared with subjects alcoholic liver cirrhosis and asymptomatic subjects. A severe H. pylori-negative chronic gastritis is more common in patients with chronic pancreatitis. This chronic inflammation of the gastric mucosa could contribute to determining the changes in gastric physiology described in patients with chronic pancreatitis.