Antrum Of Patients 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.

Gastric function in diabetic gastroparesis assessed by ultrasound and scintigraphy

AbstractBackgroundGastroparesis is a severe diabetes complication characterized by delayed gastric emptying. We examined patients with symptoms of diabetic gastroparesis using gastric emptying scintigraphy and ultrasound drink test. The primary aim was to investigate how ultrasound could provide information about gastric motility features in diabetic gastroparesis.Material and methodsWe prospectively included 58 patients with diabetes (48 type 1) with symptoms of gastroparesis and 30 healthy controls. Patients were examined with ultrasound of the stomach in a seated position after drinking 500 ml low‐caloric meat soup, at the same time recording dyspeptic symptoms. The following day, they were examined with gastric emptying scintigraphy, defining gastroparesis as >10% retention after 4 h.Key ResultsWe found motility disturbances in the proximal stomach measured by ultrasound in patients with diabetic gastroparesis. A linear mixed effects model including repeated ultrasound measurements revealed a slower decrease of the proximal stomach size in gastroparesis compared to healthy controls (p < 0.01), and the proximal diameter at 20 min was correlated to scintigraphy at 4 h (r = 0.510, p = 0.001). The antrum in patients with diabetic gastroparesis was twice as large compared to healthy controls (p = 0.009), and fasting antral size was correlated to gastric emptying scintigraphy (r = 0.329, p = 0.013). Both diabetes patients with and without gastroparesis had impaired accommodation (p = 0.011).Conclusions and InferencesOn ultrasound, we found delayed reduction of proximal stomach size and impaired accommodation after a liquid meal in patients with gastroparesis, emphasizing the role of the proximal stomach. Furthermore, we found antral distention in gastroparesis patients.

Inflammatory microRNAs in gastric mucosa are modulated by Helicobacter pylori infection and proton-pump inhibitors but not by aspirin or NSAIDs.

Gastric carcinogenesis is associated with alterations of microRNAs (miRNAs) and reversal of these alterations may be a crucial element in cancer prevention. Here we evaluate the influence of H. pylori eradication, low-dose aspirin (LDA), non-steroidal anti-inflammatory drugs (NSAIDs) and proton-pump inhibitors (PPI) on modification of inflammatory mucosal miRNAs miR-155 and miR-223 in Helicobacter pylori-infected and non-infected subjects. The study was performed in two parts: 1) interventional study in 20 healthy subjects with and without H. pylori infection or following eradication (each n = 10) where LDA (100 mg) was given daily for 7 days; 2) prospective case-control observational study (n = 188). MiR-155 and miR-223 expression was strongly linked to H. pylori-infection and in short-term view showed a trend for reversal after eradication. Daily LDA as well as regular NSAIDs showed no influence on miRNAs expression both in healthy subjects and patients, while regular PPI intake was associated with lower miR-155 expression in antrum of patients with chronic gastritis independent of density of neutrophils and mononuclear infiltrate. In summary, PPI but not LDA or NSAIDs were associated with modification of inflammatory miRNAs miR-155 and miR-223 in an H. pylori dependent manner. The functional role of inflammatory miR-155 and miR-223 in understanding of H. pylori-related diseases needs further evaluation.

Risk Factors Associated with Helicobacter Pylori Infections in Makurdi Northcentral Nigeria

Background: Helicobacter Pylori (H. pylori) is a microaerophilic bacterium that inhabits the gastric mucosa of the human stomach. Infection with this bacterium leads to chronic gastritis, peptic ulceration, gastric cancers and gastric malt lymphoma. Studies have documented a higher prevalence in Africa and the transmission pathways are still vaque. Methods: Eighty gastric biopsies were collected from the antrum of patients referred for endoscopy. Informed consent was obtained and questionnaires on risk factors such as type of water used, foods and habitswere administered to them. Genomic DNA was extracted from the tissue samples using ReliaPrep genomic DNA miniprep kit (Promega, Southampton UK), and H. pylori DNA was detected using a Singleplex PCR of the 16S rRNA gene. Results: Of all the parameters analyzed, only involvement in milking of cows (OR=3.545, 95% CI: 2.488-5.052; p=0.029) and sharing of spoons and cups (OR=45.00, 95% CI: 8.769-230.936; p <0.001) had significant association with transmission, and patients were at increased risk of infection. Conclusion: Transmission of H. pylori may be associated with the risk factors related to hygiene. Adequate hygiene is advocated to reduce the scourge of the infection.

Evaluation of gastric blood supply in diabetic patients with gastroparesis by contrast-enhanced ultrasound.

Improvement in regional blood flow has been shown to ameliorate diabetic gastroparesis. We compared the gastric blood supply in patients with diabetes with gastroparesis with that in healthy subjects, by using contrast-enhanced ultrasound (CEUS). 30 healthy subjects and 40 patients with diabetic gastroparesis were enrolled. The CEUS parameters of greater curvatures of the antrum (GCOA) and lesser curvatures of the antrum (LCOA), including peak intensity (PI) and the area under the curve (AUC), were compared between the two groups. Intraclass correlation coefficient (ICC) for PI in healthy subjects measured on CEUS were 0.831-0.857 and 0.803-0.823, respectively. Intra-ICC and inter-ICC values for AUC were 0.805-0.823 and 0.813-0.815, respectively. In both groups, no significant difference was observed in PI and AUC values of GCOA and LCOA (p > 0.05). The PI and AUC of GCOA and LCOA in the diabetes group were less than those in the normal group (p < 0.05). CEUS can assess stomach wall vascularity with a high reproducibility. Microcirculation in the antrum of patients with diabetic gastroparesis is poorer than that of normal group, which is consistent with the mechanisms of diabetic neuropathy. CEUS can be used for evaluation of microvascular perfusion in patients with stomach wall disease. Advances in knowledge: This was the first study to use CEUS for assessment of blood supply of the gastric wall and to compare microvascular perfusion between healthy individuals and patients with diabetes with gastroparesis.

The Pulmonary Venous Antrum in Patients with Persistent AF and Heart Failure - Electrophysiologic and Electroanatomic Mapping

The Pulmonary Venous Antrum in Patients with Persistent AF and Heart Failure - Electrophysiologic and Electroanatomic Mapping

EUS-guided FNA biopsy of the muscularis propria of the antrum in patients with gastroparesis is feasible and safe

EUS-guided FNA biopsies of the muscularis propria of the gastric wall in patients with gastroparesis could replace the routine use of surgical full-thickness biopsies for assessing the loss of the interstitial cells of Cajal (ICCs) and cellular infiltrates in the myenteric plexus. We investigated the efficacy and safety of EUS-guided FNA biopsies of the muscularis propria of the gastric antrum in gastroparesis and compared the tissue with a surgically obtained full-thickness biopsy specimen in the same patient. This was a prospective, nonrandomized, feasibility trial. Patients with gastroparesis who were undergoing gastric neurostimulator placement were enrolled. Patients had a gastric wall measurement by radial EUS in the body and antrum of the stomach followed by linear EUS examination and FNA of the muscularis propria in the antrum by using a 19-gauge core needle. Within 24 hours, a full-thickness biopsy specimen of the antrum was obtained surgically during neurostimulator placement. Endoscopic and surgical specimens were compared for tissue morphology, number of ICCs (c-kit stain) and enteric neurons (S-100 stain), and fibrosis (trichome) for each patient. The correlation coefficient of the ICC count per high-power field was used to compare both specimens. Continuous data were compared by using a t test. Eleven patients (10 female, 1 male), with a mean age of 40.6 years, were enrolled in the trial. EUS-guided core biopsies were successful in obtaining sufficient tissue for the histologic assessment of ICCs in 9 patients (81%) and for the myenteric plexus in 6 patients (54%). There was a good correlation coefficient (0.65) when both surgical and endoscopic groups were compared for the loss of ICCs. Mild serosal bruising and/or localized hematoma formations were noted at the sites of EUS biopsies, but there were no serosal tears, perforations, or adverse effects on the hospitalization and outcomes. EUS-guided FNA of the gastric muscularis propria in patients with gastroparesis is safe and provides adequate tissue for full histologic assessment. (Clinical trial registration number: NCT01916460.).

Slow Overmethylation of Housekeeping Genes in the Body Mucosa Is Associated with the Risk for Gastric Cancer

Helicobacter pylori infection increases age-related diverse overmethylation in gene-control regions, which increases the risk of gastric cancer. The H. pylori-associated overmethylation changes subsequently disappear when gastric atrophy and cancer develop. To identify cancer-risk epigenotypes, we traced dynamic methylation changes in the background mucosa of the stomach depending on the extent of gastric atrophy. Paired biopsy specimens were obtained from the noncancerous antrum and body mucosa of 102 patients with cancer and 114 H. pylori-positive and 112 H. pylori-negative controls. The grade of gastric atrophy was evaluated using the endoscopic atrophic border score. The methylation-variable sites at the CpG-island margins and near the transcriptional start sites lacking CpG islands were semiquantitatively analyzed by radioisotope-labeling methylation-specific PCR. We selected eight housekeeping genes adjacent to Alu (CDH1, ARRDC4, PPARG, and TRAPPC2L) or LTR retroelements (MMP2, CDKN2A, RUNX2, and RUNX3) and eight stomach-specific genes (TFF2, PGC, ATP4B, TFF1, TFF3, GHRL, PGA, and ATP4A). Analysis of age-related methylation in the H. pylori-positive controls revealed slow overmethylation in the body and in the LTR-adjacent genes. A high-frequency overmethylation defined based on the slowly overmethylated genes was frequently observed in the body of patients with gastric cancer with open-type atrophy (OR, 12.7; 95% confidence interval, 3.2-49.8). The rapidly changing methylation of Alu-adjacent genes was barely increased in the antrum of patients with gastric cancer. Among diverse methylation changes associated with H. pylori infection, an increase in slowly changing methylation could serve as a cancer-risk marker.

H. pylori infection is associated with DNA damage of Lgr5-positive epithelial stem cells in the stomach of patients with gastric cancer.

H. pylori (Hp) infection is a major risk factor in gastric carcinogenesis leading to epithelial mutagenesis, and may affect gastric epithelial stem cells. To characterize the expression of Lgr5, a marker of epithelial stem cells in human gastric mucosa, to determine whether Hp infection affects Lgr5-positive epithelial cells (LPECs) and whether LPECs are susceptible to DNA damage associated with Hp infection. Lgr5 expression was characterized in non-neoplastic gastric mucosa from 52 patients (34 with and 18 without gastric cancer (GC); 21 Hp-positive (Hp+) and 31 Hp-negative (Hp-)) by immunohistochemical and immunofluorescence staining. To determine the extent of DNA damage in LPECs, nuclear 8-hydroxydeoxyguanosine (8OHdG), a marker of DNA damage associated with oxidative stress, was measured by quantitative spectral image analysis. LPECs were primarily present in gastric antrum. Higher numbers of LPECs were seen in Hp+than in Hp- non-neoplastic mucosa of GC patients, P=.006, but not in patients without GC. 8OHdG levels in LPECs were significantly higher than in Lgr5-negative epithelial cells in Hp+GC patients (P=.012) but not in Hp- cases (P=.414), whereas no difference was seen between Hp+ and Hp- mucosa of patients without GC. The Lgr5-positive epithelial stem cell pool is expanded in Hp-associated gastritis in the antrum of patients with GC. In GC patients with active Hp infection, LPECs may be more susceptible to DNA damage than Lgr5-negative epithelial cells, suggesting that Hp infection may contribute to GC risk by affecting epithelial stem cells in the human stomach.

Helicobacter Pylori Infection in Superficial Gastritis, Erosive Gastritis and Gastric Ulcer

Background: Helicobacter pylori (H. pylori) infection leads to inflammation of the gastric mucosa. It damages the gastric epithelium and related to the risk of developing gastric cancer. Over time, it may develop into the development of glandular atrophy and intestinal metaplasia. This study was aimed to evaluate the histological features of gastric mucosa, including H. pylori infection in patients with endoscopically found superficial gastritis, erosive gastritis and gastric ulcer. Method: Subjects with abdominal complaints who underwent consecutive upper gastrointestinal endoscopy were prospectively selected at Tugurejo Hospital between November 2004 and December 2010. Eligible subjects were those with endoscopic diagnosis of superficial gastritis, erosive gastritis or gastric ulcer. The biopsy specimens were taken from the corpus, angulus and antrum of all the patients. Giemsa and hematoxylin-eosin staining were used for the histological diagnosis H. pylori and gastric mucosa inflammation. Results: The overall prevalence of H. pylori infection in superficial gastritis, erosive gastritis and gastric ulcer were 24.3%. There was significant difference between H. pylori infection rate in antrum of patients with superficial gastritis 19.4%, erosive gastritis 26.3%, and gastric ulcer 34.7%. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H. pylori- positivity was 12.5%, 14.0%; erosive gastritis 26.3%, 16.6%; and of gastric ulcer 38.9%, 29.3%; respectively. However, there was no significant difference. Conclusion: Patients with gastric ulcer have H. pylori infection, atrophic gastritis and metaplasia intestinal more than superficial gastritis and erosive gastritis. Progression of the gastric ulcer to atrophic gastritis and intestinal metaplasia is related to H. pylori infection. Keywords : Helicobacter pylori infection, superficial gastritis, erosion and ulcer

Family history of gastric cancer correlates with decreased expression of HINT1 tumor suppressor gene in gastric mucosa of dyspeptic patients

Gastric cancer (GC) is the fourth most common cancer and the second most common cause of cancer-associated mortality worldwide. Approximately 10% of gastric cancers are hereditary and a small percentage of these cases (1-3%) have been classified as a single hereditary syndrome (hereditary diffuse gastric cancer). We previously demonstrated that a family history of gastric cancer (FHGC) contributes to a predisposition towards the development of gastric cancer. Our data revealed that for dyspeptic patients whose first-degree relative(s) succumbed to GC, the levels of the fragile histidine triad pro-apoptotic protein in gastric mucosa were decreased. Another member of the histidine triad protein superfamily is histidine triad nucleotide-binding protein 1 (HINT1), a novel tumor suppressor that plays an inhibitory role in the control of gene transcription. The study comprised 38 ethnically homogeneous patients with dyspeptic symptoms without concomitant chronic diseases (18 controls/20 patients with FHGC). The results showed that the samples from the control patients predominantly exhibited non-atrophic changes (approximately 90%), whereas atrophic changes occurred more frequently in patients with FHGC. Notably, the expression levels of the HINT1 gene were markedly higher in the samples with atrophy taken from the antrum of FHGC patients compared to the non-atrophic samples. Moreover, the levels of HINT1 mRNA in samples obtained from the antrum of patients with FHGC were lower compared to analogous samples from the control individuals. The decreased levels of HINT1 mRNA in the antrum samples of patients with the FHGC indicate that it is a factor predisposing those patients to the development of gastric cancer.

Allergic Eosinophilic Gastroenteritis With Protein-Losing Enteropathy: Intestinal Pathology, Clinical Course, and Long-term Follow-up

Chehade M, Magid MS, Mofidi S, Nowak-Wegrzyn A, Sampson HA, Sicherer SH. J Pediatr Gastroenterol Nutr. 2006;42:516–521 PURPOSE OF THE STUDY. To identify gross and/or histologic distinguishing features of antral and duodenal biopsy specimens as well as clinical response to various treatment regimens in the subset of patients with eosinophilic gastroenteritis (AEG) with protein-losing enteropathy (PLE). STUDY POPULATION. The experimental group consisted of 6 children with anemia and hypoalbuminemia and biopsy-proven AEG identified retrospectively from a series of 93 patients with AEG who were evaluated at Mount Sinai Medical Center (New York, NY) over a 7.5-year period. METHODS. Two comparison groups were used in addition to the experimental group. The first included 6 randomly selected patients from the series of 93 patients with AEG without anemia and/or hypoalbuminemia. The second comparison group included 5 patients who presented with symptoms consistent with possible AEG yet normal gross findings and histology after endoscopy. Causes of eosinophilia other than AEG were ruled out. The diagnoses of AEG required the presence of &amp;gt;20 eosinophils per high-power field in antral biopsy specimens and &amp;gt;50 in the duodenum. Hematoxylin/eosin staining and immunohistochemical staining of tryptase were used for identification of eosinophils and mast cells, respectively. The cell count was taken from the high-power field with maximum infiltration. RESULTS. Various therapies were attempted in the experimental group including oral corticosteroids, cromolyn sodium, 6-mercaptopurine, food-elimination diets, and montelukast. They were, at best, partially or temporarily beneficial. All experimental patients received an exclusive amino acid–based formula diet at some point in their care; this formula was associated with rapid improvement of anemia and hypoalbuminemia as well as clinical symptoms. These patients eventually tolerated the addition of various foods to their diet. In duodenal biopsy specimens, mast cells were significantly increased in patients with AEG and PLE compared with those with AEG only, whereas eosinophil numbers were comparable. This was not seen in the antral samples. Eosinophilia was more prominent in the antrum of patients with AEG and PLE compared with those with AEG only. Patchy duodenal villous blunting was seen in 1 patient with AEG and PLE and 1 with AEG. CONCLUSIONS. As in the treatment of eosinophilic esophagitis, amino acid–based formulas seem to be the most effective form of therapy. After improvement on an amino acid–based formula diet, many patients eventually tolerate expanded diets. Malabsorption and villous blunting do not seem to be the cause of hypoalbuminemia and anemia in those patients with AEG and PLE. Increased intestinal mast cells seen in the patients with AEG with PLE may be the source of the intestinal protein loss. REVIEWER COMMENTS. Although the sample size in this study was small, these data provide additional insight into the specific role of mast cells in patients with AEG and PLE.

Prevalência da infecção por Helicobacter pylori e das lesões precusoras do câncer gástrico em pacientes dispéticos

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

Hyperplastic Polyps of the Gastric Antrum in Patients with Gastrointestinal Blood Loss

The significance of hyperplastic polyps of the gastric antrum in anemic patients with suspected gastrointestinal bleeding has not been determined. The aim of this study is to evaluate the prevalence and prognosis of such polyps in this patient group. Clinical records of patients referred to our endoscopy lab from November 1999 to February 2003 for the evaluation of iron deficiency anemia or suspected gastrointestinal bleeding were reviewed. There were 987 patients. Fourteen patients (1.4%) had hyperplastic polyps in the gastric antrum. Five of the patients reported melena, but the rest were asymptomatic. Multiple antral polyps were present in seven cases. The largest polyp measured 5.0 cm. Helicobacter pylori infection was present in one patient. All patients were anemic and nine had documented iron deficiency. No follow-up information was available in four patients. Hyperplastic polyps of the gastric antrum are a rare but significant cause of gastrointestinal blood loss in older patients. Removal of the polyps using endoscopic or surgical methods may be required for resolution of the blood loss along with iron supplementation. Gastroenterologists should be aware that hyperplastic polyps of the gastric antrum might result in gastrointestinal blood loss and iron deficiency anemia.

H pyloriinfection and reflux oesophagitis: A case-control study

To examine the relationship between H. pylori and gastro-oesophageal reflux disease (GORD) in Iran. In this study 51 GORD patients (referred to endoscopy at Taleghani hospital) were compared with 49 age-sex matched controls. Diagnosis of H. pylori was made by gastric mucosal biopsy and rapid urease test (positive if the result of one or both diagnostic methods was positive). Updated Sydney system was used to report histopathological changes. The frequency of H. pylori infection based on rapid urease test and histology was 88.2% (45) in patients and 77.6% (38) in controls, which showed no significant difference. The frequency of H. pylori infection was significantly higher in the antrum than in the corpus and cardia. The mean activity, inflammation, and gastritis scores were also higher in the antrum of patients than in the antrum of controls. The mean scores were significantly higher in the corpus of controls than in the corpus of patients. Diffuse active gastritis was observed in a significantly larger number of controls, while the frequency of diffuse chronic gastritis was higher in patients. There was no significant difference in the frequency of other histological findings between patients and controls. H. pylori infection cannot prevent GORD in this region.

Gastric mucosal mast cells are increased in Helicobacter pylori-negative functional dyspepsia

Background & Aims : Mast cells might be involved in pathogenesis of functional dyspepsia because they can release a wide range of potent mediators, capable of altering gastric nerve and muscle function. This study aimed to determine whether mast cell numbers were increased in the gastric mucosa of patients with functional dyspepsia compared to control subjects. Methods : Biopsy samples were taken from the antrum and corpus of 111 patients: 20 asymptomatic control subjects, 62 patients with Rome criteria functional dyspepsia (33 Helicobacter pylori positive, 29 H. pylori negative), and 29 inflammatory control subjects ( H. pylori positive). Mast cells were detected immunohistochemically by using a mouse monoclonal antibody specific for tryptase. Quantification was performed with light microscopy, and results were expressed as mast cells/mm 2 ± standard error of mean. Results : Mast cells were significantly increased in H. pylori negative functional dyspepsia samples compared to normal control samples in the antrum (230.1 ± 11.3 vs. 94.8 ± 8.4, P < 0.001) and corpus (264.1 ± 27.1 vs. 123.9 ± 11.5, P = 0.001). Mast cells were also significantly increased in the antrum of patients with H. pylori positive functional dyspepsia compared to asymptomatic control subjects (166.5 ± 17.0 vs. 94.8 ± 8.4, P < 0.03). However, there was no significant difference between mast cell numbers in patients with H. pylori positive functional dyspepsia compared to inflammatory control subjects. Conclusions : Mast cells are increased in functional dyspepsia, independently of inflammation. This might contribute to the pathogenesis of functional dyspepsia by altering signaling in the brain-gut axis.

Hyperplastic polyps of the gastric antrum in patients with gastrointestinal blood loss

Hyperplastic polyps of the gastric antrum in patients with gastrointestinal blood loss

Helicobacter pylori genotypes, host factors, and gastric mucosal histopathology in peptic ulcer disease

From 183 patients undergoing upper gastrointestinal endoscopy, we used antral and corpus gastric biopsies for bacterial culture and histopathologic examination, blood samples to detect immunoglobulin G antibodies against Helicobacter pylori, and H pylori genomic DNA to analyze cytotoxin-associated gene A (cagA) and vacuolating cytotoxin (vacA) genotypes. As expected, among H pylori biopsy-positive patients, those with duodenal ulcer (DU) (n = 34) had significantly more severe chronic and acute inflammation (P <.001) and epithelial degeneration (P =.004) in the gastric antrum than in the gastric corpus. Each of those 3 parameters and H pylori density were significantly higher in the antrum of patients with DU than in patients with gastric ulcer (GU) or no ulcer. Colonization with vacA s1/cagA-positive strains of H pylori was associated with inflammation and epithelial degeneration in gastric mucosa and increased risk for peptic ulcer disease (PUD), whereas colonization with vacA s2m2/cagA-negative strains was associated with mild gastric histopathology and was not associated with any significant risk for PUD. The predominant H pylori strains in African Americans were vacA s1bm1/cagA-positive, whereas all genotypes were well represented in non—Hispanic-Caucasians. By multivariate analysis, H pylori colonization was significantly associated with DU (Adjusted odds ratio [AdjOR] = 3.2 [1.4-7.2]) and nonsteroidal anti-inflammatory drugs (NSAID) use was inversely associated (AdjOR = 0.3 [0.2-0.7]). NSAID use (AdjOR = 4.3 [1.02-18.5]) and African-American ethnicity (AdjOR = 10.9 [2.6-50]) were significantly associated with GU. Smoking and age were not significantly associated with either DU or GU. These data indicate that DU is associated with an antral-dominant gastritis, and H pylori genotype and NSAID use independently contribute to the pathogenesis of PUD. HUM PATHOL 32:264-273. This is a US Government work. There are no restrictions on its use.

2214 Peroral intubation of self-expanding metal stents for palliation of inoperable gastric cancer with antral obstruction.

Background: Peroral intubation of self-expanding metal stent(SEMS) seems to be faster and more durable than other nonsurgical modalities in malignant gastrointestinal obstruction. However, it is very difficult in malignant obstruction of the gastric antrum in patients with inoperable gastric cancer due to the curved anatomic structure of the gastroduodenal axis. Methods: Placement of 18 endocoil stents( In stent Inc., Eden Prairie, Minn., U.S.A), 11 modified Gianturco Z-stent(Choo stent, Sooho Medi-Tech Co., Ltd., Seoul, Korea) and 66 nitinol through-the-scope(TTS) stents (Niti- S, Taewoong Inc., Seoul, Korea) were attempted in 95 consecutive patients suffering from intractable vomiting due to inoperable gastric cancer with antral obstruction. Results: Technical success was achieved in 83.3%(15/18)of endocoil stent group, 90.9%(10/11) of modified Z-stent group and 100%(66/66) of TTS stent group. Procedure-related complications included bowel injury by the tip of the guide wire in 2 of modified Zstent group and 3 of TTS stent group, who were managed with conservative treatment. After SEMS placement, restoration of oral food intake and relief of vomiting was achieved in 93.3%(14/15)of endocoil stent group, 80.0%(8/10) of modified Z-stent group and 96.9%(63/66), respectively. Early complications included stent migration into the stomach in 1 of modified Zstent group. During the follow-up, stent occlusion occurred in each one of endocoil and TTS stent group by food materials, in 9 of TTS stent group by tumor ingrowth, and in 2 of TTS stent group by tumor overgrowth. There were no delayed serious complications, such as stent migration or GI bleeding. Conclusion: These results suggest that peroral intubation of SEMSs, especially nitinol TTS stent, is effective non-surgical palliation for inoperable gastric cancer with antral obstuction.

Disease-specific Helicobacter pylori virulence factors: the unfulfilled promise.

A number of putative virulence factors for Helicobacter pylori have been identified including cagA, vacA and iceA. The criteria for a true virulence factor includes meeting the tests of biologically plausibility with the associations being both experimentally and epidemiologically consistent. Although disease-specific associations have been hypothesized/claimed, there are now sufficient data to conclusively state that none of these putative virulence factors have disease specificity. CagA has been claimed to be associated with increased mucosal IL-8 and inflammation, increased density of H. pylori in the antrum, duodenal ulcer (DU), gastric cancer, and protection against Barrett's cancer. Only the increase in IL-8/inflammation is direct and substantiated. Different H. pylori strains with functional cag pathogenicity islands do not vary in virulance as it has been shown that mucosal IL-8 levels are proportional to the number of cagA + H. pylori independent of the disease from which the H. pylori were obtained. It is now known that the density of either cagA + and cagA-H. pylori in the antrum of patients with H. pylori gastritis is the same. In contrast, the mean density of H. pylori in the antrum in DU is greater than in the antrum of patients with H. pylori gastritis. Of interest, the density of H. pylori is higher in the corpus of patients with H. pylori gastritis than those with DU, suggesting that acid secretion plays a critical role in these phenomena. The presence of a functional cag pathogenicity island increases inflammation and it is likely that any factor that results in an increase in inflammation also increases the risk of a symptomatic outcome. Nevertheless, the presence of a functional cag pathogenicity island has no predictive value for the presence, or the future development of a clinically significant outcome. The hypothesis that iceA has disease specificity has not been confirmed and there is currently no known biological or epidemiological evidence for a role for iceA as a virulence factor in H. pylori-related disease. The claim that vacA genotyping might prove clinically useful, e.g. to predict presentation such as duodenal ulcer, has been proven wrong. Analysis of the worldwide data show that vacA genotype s1 is actually a surrogate for the cag pathogenicity island. There is now evidence to suggest that virulence is a host-dependent factor. The pattern of gastritis has withstood the test of time for its relation to different H. pylori-related diseases (e.g. antral predominant gastritis with duodenal ulcer disease). The primary factors responsible for the different patterns of gastritis in response to an H. pylori infection are environmental (e.g. diet), with the H. pylori strain playing a lesser role. Future studies should work to eliminate potential bias before claiming disease associations. Controls must exclude regional or geographic associations related to the common strain circulation and not to the outcome. The authors must also control for both the presence of the factor and for the disease association. The study should be sufficiently large and employ different diseases and ethnic groups for the results to be robust. The findings in the initial sample (data derived hypothesis) should be tested in a new group (hypothesis testing), preferably from another area, before making claims. Finally, it is important to ask whether the results are actually a surrogate for another marker (e.g. vacA s1 for cagA) masquerading for a new finding. Only the cag pathogenicity island has passed the tests of biological plausibility (increased inflammation) and experimental and epidemiological consistency.