Antral Ulcers Research Articles

FSSG Scale System in Comparison with GERD Questionnaires in Predicting Endoscopic Findings with Reflux Esophagitis

ABSTRACT Background: Gastroesophageal reflux diseases ( xe GERD) frequently manifests in varied symptoms other than its classics (heartburn and regurgitation), this variation might hinder its diagnostic effort. Several questionnaires based on symptoms filled by the patients themselves may help in diagnosing xe GERD without previous endoscopic examination. This study objects to compare endoscopic findings in patients which previously asked to fill the questionnaires ( xe scale for the symptoms of GERD (FSSG) frequency scale for the symptoms of xe GERD (FSSG)) and xe xe GERD questionnaire GERD questionnaire (GerdQ) in pursuit of reliable and valid instrument to detect xe GERD before endoscopic approaches. Methods: This study was conducted in cross-sectional design involving 72 patients in Adam Malik Hospital, Medan with symptomps of upper abdominal pain or discomfort with or without heartburn/regurgitation. Subjects were asked to fill both FSSG and GerdQ and underwent endoscopy. Diagnoses made were classified as reflux esophagitis, functional dyspepsia, or other diagnoses. Subsequently we conduct a comparison analysis of both questionnaires’ specificity and accuracy using receiver operator curve (ROC) by analyzing the area below the curve. Results: According to endoscopic findings from 72 subjects, we ascertained the following results: 52.8% gastritis, antral ulcer, and esophageal hiatal hernia, 37.5% functional dyspepsia, and reflux esophagitis in 9.7% cases. GerdQ is concluded to be superior in terms of specificity and accuracy compared with FSSG with the following percentages in terms of sensitivity, specificity, accuracy, and p value, respectively: 100%, 23.1%, 61.5%, 0.318 vs. 100%, 73.8%, 86.9%, 0.001. Conclusion: GerdQ is superior compared to FSSG in diagnosing xe GERD GERD based on clinical symptoms in daily practice. Keywords: reflux esophagitis, xe GERD, FSSG, GerdQ, endoscopy, Los Angeles classification, heartburn.

Discovery of Lansoprazole and its Unique Pharmacological Properties Independent from Anti-secretory Activity

The proton pump inhibitors (PPIs) lansoprazole (LPZ) and omeprazole (OPZ) have been widely used for more than 20 years in the treatment of acid-related diseases such as gastro-duodenal ulcers and reflux esophagitis. Both LPZ and OPZ are derivatives of 2-[(2- pyridylmethyl)sulfinyl]-1H-benzimidazole, but LPZ has a trifluoroethoxy group in the molecule which seems to provide unique pharmacological properties in addition to its anti-secretory effect. For example, the anti-secretory effect of LPZ in rats was roughly 2 times greater than that of OPZ but the anti-ulcer effects were more than 10 times stronger than those of OPZ in rat models of reflux esophagitis, indomethacin-induced gastric antral ulcers and mepirizole-induced duodenal ulcers. It has also been reported that LPZ has acidindependent protective effects on the gastrointestinal mucosa, anti-inflammatory effects, and anti-bacterial effects on Helicobacter pylori. In contrast, recent advances in endoscopy have revealed that non-steroidal anti-inflammatory drugs (NSAIDs) often cause ulcers not only in the stomach and duodenum, but also in the small intestine in humans. Anti-secretory drugs such as PPIs and histamine H2-receptor antagonists (H2-RAs) are commonly used for the treatment of upper gastrointestinal mucosal lesions induced by NSAIDs. However, the effects of these drugs on NSAID-induced small intestinal lesions are still not fully understood. In this article, both a brief history of the discovery of LPZ and the unique pharmacological properties of LPZ independent from its anti-secretory action are reviewed, and the effects of PPIs and H2-RAs on NSAID-induced small intestinal lesions are discussed.

Discovery of Lansoprazole and its Unique Pharmacological Properties Independent from Anti-secretory Activity

The proton pump inhibitors (PPIs) lansoprazole (LPZ) and omeprazole (OPZ) have been widely used for more than 20 years in the treatment of acid-related diseases such as gastro-duodenal ulcers and reflux esophagitis. Both LPZ and OPZ are derivatives of 2-[(2- pyridylmethyl)sulfinyl]-1H-benzimidazole, but LPZ has a trifluoroethoxy group in the molecule which seems to provide unique pharmacological properties in addition to its anti-secretory effect. For example, the anti-secretory effect of LPZ in rats was roughly 2 times greater than that of OPZ but the anti-ulcer effects were more than 10 times stronger than those of OPZ in rat models of reflux esophagitis, indomethacin-induced gastric antral ulcers and mepirizole-induced duodenal ulcers. It has also been reported that LPZ has acid-independent protective effects on the gastrointestinal mucosa, anti-inflammatory effects, and anti-bacterial effects on Helicobacter pylori. In contrast, recent advances in endoscopy have revealed that non-steroidal anti-inflammatory drugs (NSAIDs) often cause ulcers not only in the stomach and duodenum, but also in the small intestine in humans. Anti-secretory drugs such as PPIs and histamine H(2)-receptor antagonists (H(2)-RAs) are commonly used for the treatment of upper gastrointestinal mucosal lesions induced by NSAIDs. However, the effects of these drugs on NSAID-induced small intestinal lesions are still not fully understood. In this article, both a brief history of the discovery of LPZ and the unique pharmacological properties of LPZ independent from its anti-secretory action are reviewed, and the effects of PPIs and H(2)-RAs on NSAID-induced small intestinal lesions are discussed.

B Cell Lymphoma Manifesting as Gastric and Colonic Ulcers

Purpose: A 46-year-old African American female with history of AIDS on HAART with CD4 count of 80/mm3, syphilis was referred by her RUQ physician for abdominal pain and worsening distension. An abdominal ultrasonogram showed the presence of numerous hepatic masses in the left and right lobes concerning for malignancy. Her viral hepatitis B and C serologies were negative. In view of the newly diagnosed hepatic lesions endoscopy was undertaken and it showed the presence of an 8 mm ulcer with heaped edges and clean-base in the ascending colon (which was biopsied) and numerous 3-4 mm nodules suspicious for lymphoid follicles, were seen in the transverse and descending colon. An esophagogastrodoudenoscopy (EGD) showed monilial esophagitis and a 10 mm gastric antral ulcer and a 6 mm gastric body ulcer, both with heaped edges and a clean base. Biopsy of the gastric and ascending colon ulcers each showed patchy foci of large B cell lymphoma staining positive for CD20 (B-lymphoid marker) and negative for CD3, CD43, CD30 and CD15. Immunostain for BCL-2 was weakly positive in a few neoplastic cells. The nodules of the transverse and descending colon showed lymphoid aggregates without cytological atypia which were reactive in nature. A core liver biopsy od the hepatic masses was performed. Flow-cytometric analysis of cells obtained showed the presence of homogenous population of monoclonal lymphoid cells with immune-phenotype of CD20, CD45, CD19, CD10 and CD25 positive consistent with large B cell lymphoma. A final diagnosis of diffuse large B cell lymphoma with colonic, gastric and hepatic involvement was made. Discussion: Diffuse large B-cell lymphoma (DLBCL) commonly involves the gastro-intestinal (GI) tract. The most common site for primary GI lymphoma is the stomach (35-75%), followed by the small intestine (30%) and rarely, the large intestine (10%). However, rectal involvement of lymphoma occurs very rarely and in a large multi centric trial, only 4 of a total of 371 patients had rectal lymphoma. HIV co-infection is uncommon in patients with primary GI lymphomas with a reported incidence of 4.6%. Our patient had a history of HIV and presented with involvement of the rectum, stomach and liver.Figure: Antral ulcer with heaped edges.

Helicobacter pylori–Associated Antral Gastritis and Ulcer Disease

Helicobacter pylori–Associated Antral Gastritis and Ulcer Disease

Analysis of alarming signals for the progression of atrophic gastritis to dysplasia

atrophic gastritis (AG) and dysplasia are precancerous lesions, with which early surveillance of disease progression is particularly important for patients. The present study aimed to explore potential alarming signals for atrophic gastritis progression towards dysplasia. clinical data for patients with AG in the Digestive Endoscopy Center of Guangzhou Nanfang Hospital between 2001 and 2011 were retrospectively reviewed. Survival analysis, dichotomous logistic regression analysis and rank correlation analysis were carried out. in 234 patients with atrophic gastritis, after follow up of 0.5, 1, 2, 5 and 10 years, the occurrence rates of dysplasia were respectively 2.3, 4.4, 9.6, 19.3, and 42.4%. Patients with AG combined with antral ulcer or gastric angle ulcer, had a higher risk for dysplasia than patients with simple AG (OR = 2.427, 95%Cl 1.069 ~ 5.511, p = 0.034; OR = 2.961, 95%Cl 1.336 ~ 6.564, p = 0.008). The constituent ratios of moderate to severe dysplasia were respectively 8.6, 2.7 and 1.2% (p = 0.000) in three patient groups: AG combined with antral ulcer/gastric angle ulcer (n = 255), antral ulcer/gastric angle ulcer alone (n = 1,389), and AG alone (n = 3,106). The Spearman correlation coefficients between a) Hp infection; and b) atrophy, intestinal metaplasia and dysplasia were -0.114 (p = 0.078), -0.169 (p = 0.009) and 0.064 (p > 0.05), respectively. long follow-up interval and gastric ulcer may be alarming signals for the progression of AG to dysplasia. But in patients with atrophy, intestinal metaplasia or dysplasia, Hp infection may not be a risk factor for these lesions aggravated, further studies are required to confirm it.

Evaluation of Gastric Ulcerogenic and Healing Impairment Effects of Bisphosphonates: Adverse Gastric Reactions of Bisphosphonate

Bisphosphonates (BPPs) were developed as antiresorptive drugs capable of treating diseases related to bone remodeling; however, they have untoward effects including ulceration in the upper gastrointestinal tract and worsen the healing-impairment action of nonsteroidal anti-inflammatory drugs, prescribed in patients with arthritis or osteoporosis. We produced ulcers in the antrum by administering BPPs to fasted rats, followed by refeeding, and confirmed their healing-impairment action on pre-existing gastric ulcers; the ulcerogenic effect is due to direct mucosal irritation and decrease in the mucosal anti-oxidative system, while the latter effect is due to dysregulation of growth factor expression, such as vascular endothelial growth factor and basic fibroblast growth factor, and angiogenesis in the ulcerated mucosa. In this article, we describe these two animal models for investigating BPP-related adverse reactions, including methods for the induction of antral ulcers and healing impairment of gastric ulcers, as well as measurement of pathogenic functional and biochemical changes.

Giant gastric ulcer penetrating into the pancreas

A 57-year-old man developed haematemesis and was referred to our institution. His discomfort had begun 3weeks earlier and localised to the upper abdomen.Abdominal CT showed a defect of gastric mucosa and gastric wall thickening. Oesophagogastroduodenoscopy showed that he had an active gastric ulcer, 40mm in diameter, on the lesser curvature in the upper third of the corpus and the presence of a pancreatic body at the ulcer base, penetration to the pancreas. Open gastrectomy was performed with a preoperative diagnosis of localised peritonitis caused by penetration of the stomach into the pancreas. Histopathology of resected specimens showed a benign peptic ulcer, 40×40mm in size, was found on the lesser curvature in the antrum, and this had penetrated through the pancreas. The most serious complications of PUD include haemorrhage, perforation, penetration, and gastric outlet obstruction.Approximately 7% of patients experience perforation, which occurs when an ulcer erodes through the wall and leaks air and digestive contents into the peritoneal cavity. Antral and duodenal ulcers can penetrate into the pancreas. We report a case of gastric ulcer penetrating into the pancreas.

PMO-190 Investigating the prevalence and cause of iron deficiency in a faecal occult blood positive, colonoscopy negative patients from the UK Colorectal Cancer Screening Programme

IntroductionFaecal occult blood test (FOBT) is a simple test, which detects small amounts of blood released from the gastrointestinal tract. Recently it has been adopted as discriminator test for the...

Endoscopic and clinical features of gastric ulcers in Japanese patients with or without Helicobacter pylori infection who were using NSAIDs or low-dose aspirin

The endoscopic characteristics of gastric ulcers in patients who were using non-steroidal anti-inflammatory drugs (NSAIDs) or low-dose aspirin (LDA) and were infected with Helicobacter pylori remain unclear. We elucidated the endoscopic characteristics of gastric ulcers that occurred in the presence or absence of H. pylori infection and were associated with the use of these drugs. A total of 379 patients with active-stage gastric ulcer were divided into three groups: H. pylori-positive patients using neither NSAIDs nor LDA (control group, n = 216), H. pylori-positive or -negative patients using NSAIDs (NSAIDs group, n = 100), and H. pylori-positive or -negative patients using LDA (LDA group, n = 63). The differences among these groups in endoscopic characteristics of the ulcers (site, multiplicity, and morphology) were determined. The influence of an antacid drug, i.e., a proton pump inhibitor (PPI) or a histamine H(2) receptor antagonist (H(2)RA), was also investigated. The NSAIDs group, regardless of H. pylori infection status, had higher incidences of antral, multiple, and irregularly shaped ulcers. The LDA group had a higher incidence of antral ulcers in H. pylori-negative patients and, regardless of H. pylori infection status, a higher incidence of multiple ulcers. However, the incidence of irregularly shaped ulcers in the LDA group did not differ from that in the control group. Neither the concomitant use of an antacid nor the dosing period of NSAIDs affected the results. Our study elucidated the morphological characteristics of gastric ulcers in persons taking NSAIDs or LDA in the presence and absence of H. pylori infection. Our results may be clinically useful for inferring the causes of ulcers from their morphological characteristics.

Expressions of MMPs and TIMP-1 in Gastric Ulcers May DifferentiateH. pylori-Infected from NSAID-Related Ulcers

Background. Two major causes of gastric ulcers are Helicobacter pylori (H. pylori) infection and nonsteroidal anti-inflammatory drug (NSAID) use. Aims. This study aimed to determine if there were different expressions of matrix metalloproteinases (MMPs) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) between H. pylori-infected and NSAID-related ulcers. Methods. The 126 gastric ulcer patients (H. pylori infected n = 46; NSAID related n = 30; combined with two factors n = 50) provided ulcer and nonulcer tissues for assessment of MMP-3, -7, and -9 and TIMP-1 expression by immunohistochemical staining. Results. Gastric ulcer tissues had significantly higher MMP-3, -7, and -9 and TIMP-1 expressions than nonulcer tissues (P < 0.05). H. pylori-infected gastric ulcers had even higher MMP-7, MMP-9, and TIMP-1 expressions in epithelial cells than NSAID-related gastric ulcers (P < 0.05). In patients with the two combined factors, gastric ulcers expressed similar proportions of antral ulcers and MMP-7 and MMP-9 intensities to NSAID-related gastric ulcers, but lower MMP-9 and TIMP-1 than H. pylori-infected gastric ulcers (P < 0.05). Conclusions. H. pylori-infected gastric ulcers express higher MMP-7, MMP-9, and TIMP-1 than NSAID-related ulcers. In patients with the two combined factors, ulcer location and MMP-7 and MMP-9 intensities are similar to NSAID use.

Implication on Bariatric Surgery by Disregarded Neural Related Structures in the Hepato-Bilio-Pancreas-Gastro-Intestinal Tract in the Rat

Purpose: The aim of this report is to describe essentially macroscopic anatomical findings; secondarily, some microscopic details, of an evaluation carried out in 300 Wistar rats. This approach was restricted primarily to the neural autonomic innervation of the hepato-bilio-pancreato-gastro-intestinal tract. Methods: In male animals, body weight 150 to 600 g, under eter or tiopental anesthesia, with delicate instruments and the support of a dissecting microscope (Wild), a microscopic analysis (linear neuronal counting) of the submucous and the myenteric ganglionated plexus was performed, respectively, in the duodenal and the stomach antral segment. Results:Table 1. Emphasis was put on several structures, unexpectedly disregarded in the literature, like, e.g, the diagonal antral band (DAB), a connective nervous band extended from the antral-fundic-junction(AFJ) up to the pylorus; the pre-bile duct-nodular-plexus(PBDNP); the neural fibers that jump the duodeno-pancreatic-cleft-plexus (DPCP), first described in the literature by our group in the sixties; the peri-Vaterian-Center (PVC), with its rich neural density, considered a real autonomic -neural-brain (ANB), and a main starting trigger of autonomic-arc-reflexes, primarily upon the pancreatic “revolver”, pivotal background of a model to mimick human biliary acute pancreatitis; the peculiar arrangement of the celiac ganglia and their linking with the PVC through the perivascular neural network of the inferior pancreatico-duodenal-artery(IPDA). In the PVC and the AFJ a greater linear neuronal counting, respectively, of the submucous and myenteric ganglia when compared with their adjacent zones.Table 1: Oral glucose tolerance test- cumulative value 60 minConclusion: The section and reanastomosis at the level of the AFJ is an inducer of antral peptic ulcers that mimick the human one. The PBDNP and the DAB constitute a “carrrefour” of nerve fibers coming from different sources. Neural impulses, either sympathetic and/or peptidergic, starting from them, the same as those originated from th or the DPCP, modulate, at the level of the neural plexuses of the biliary tract and the hepatic gland, their autonomic neural tone background. The surgical interruption of this modulation, e.g, through a “cicatricial barrier” in what we have called the enteric neural plexus freeway (ENPF), induce trophic changes of the pancreatic gland, and, through an enhancement of the hepatic cholinergic tone an increased release of the Lautt postulated factor (hepatic-insulin-sensitizing-substance, HISS) and, consequently, an improved response of the insulin receptors primarily in the skeletal muscle. The latter, if confirmed in humans, might undoubtedly constitute a much simpler and less dangerous approach to the treatment of morbid obesity in the field of bariatric surgery.

Non-healing Gastric Ulcer: Rare Presentation of Metastatic Seminoma

Purpose: Introduction: Metastatic seminoma presenting as gastric ulcer and hemorrhage is rare. Liver, lung, and bones are the most common locations of metastasis. Case Description: 39-year-old Hispanic male with history of end stage renal disease (ESRD) requiring hemodialysis and hypertension that presented to the hospital with hematemesis. Esophagogastroduodenoscopy (EGD) showed 2 large cratered antral ulcers ranging from 12 mm to 15mm. The ulcers were actively oozing and were treated with epinephrine and bipolar electrocoagulation (BICAP). A second look EGD to re-evaluate the ulcer was performed. Multiple biopsies were taken at this time to rule out a malignant ulcer. The pathology returned negative for malignancy, but presence of some atypical cells on the cautery end. The patient re-presented to the emergency room 6 months and 8 months later with continued episodes of hematemesis. Repeat endoscopy were performed and showed chronic large gastric ulcer with raised irregular borders with visible vessel. The ulcers were again treated with epinephrine, endoclips, and BICAP. Computed tomography (CT) scan of the abdomen and pelvis were performed. Findings showed an enlarged pelvic mass, retroperitoneal lymph node, and large bilateral inguinal hernias. He underwent laprascopic pyloromyotomy and gastric wedge resection for non-healing gastric ulcer as well as pelvic mass resection. Pathology returned metastatic poorly differentiated seminoma. He was found to have metastasis to stomach and retroperitoneal perigastric lymph nodes. It is suspected that the seminoma originated from the pelvic mass, which may actually be an undescended testis. It is suspected that due to his inguinal hernias, he actually had large bowel in his scrotum. Alpha-fetoprotein and lactated dehydrogenase were normal, but had a mildly elevated beta- human chorionic gonadotropin (HCG). He is scheduled to undergo chemotherapy. Discussion: Upper gastrointestinal bleeding as a presentation of metastatic seminoma is quite rare. Only 2.5% of seminomas are metastatic on initial presentation. Liver, lung and bones are the most common locations of metastasis. The reported incidence of metastases to the stomach has ranged from 0.2% to 0.7%. There have been reports of a “burned-out” phenomenon where a metastatic germ cell tumor is present with a regressed testicular primary. This may be a variant of that situation as the pelvic mass is suspected to be an undescended testis, but was not confirmed by pathology.

Effect of anthocyanins on expression of matrix metalloproteinase-2 in naproxen-induced gastric ulcers

Non-steroidal anti-inflammatory drugs cause gastric ulceration through a number of mechanisms including inhibition of PG synthesis, generation of reactive oxygen species (ROS) and induction of apoptosis. Recently, matrix metalloproteinases (MMP) have been suggested to play a crucial role in these mechanisms. The present study investigated the protective effect of anthocyanins isolated from black rice bran (Heugjinjubyeo) against naproxen-induced gastric mucosal injury in rats. The oral administration of anthocyanins (5, 25 or 50mg/kg body weight) showed significant protection against naproxen (80mg/kg body weight)-induced gastric ulcer and inhibited lipid peroxidation in the gastric mucosa. In addition, pretreatment with anthocyanins resulted in a significant increase in the activities of radical-scavenging enzymes such as superoxide dismutase, catalase and glutathione peroxidase. Also biochemical and zymographic analyses suggested that the administration of anthocyanins gives a significant protection against naproxen-induced gastric antral ulcer through scavenging ROS and regulation of matrix metalloproteinase-2 (MMP-2) activity. The results of intracellular radical activation show that anthocyanins suppress the generation of intracellular ROS and attenuate the suppression of MMP-2 activity by naproxen. These results suggest that anthocyanins extracted from black rice may offer potential remedy of gastric antral ulceration.

Gastric Ulcerogenic and Healing Impairment Actions of Alendronate, A Nitrogen- Containing Bisphosphonate - Prophylactic Effects of Rebamipide

Alendronate, a nitrogen containing bisphosphonate (BPP), when given p.o., decreases the transmucosal potential difference by direct irritating action, resulting in non-hemorrhagic lesions in both the corpus and antrum of fasted rats, and after re-feeding produces large ulcers in the antrum with increased vascular permeability and submucosal edema. The pathogenesis of these ulcers may be explained by the impairment of the mucosal anti-oxidative system and does not involve acid digestion as well as a deficiency of prostaglandins (PGs). Alendronate, although does not affect cyclooxygenase/ PGE(2) production in the ulcerated mucosa, but impairs the healing of gastric ulcers in rats, and this effect may be related to the down-regulation of vascular endothelial growth factor and basic fibroblast growth factor (bFGF), the important growth factors for the vascularization/granulation as well as the suppression of the stimulatory action of epidermal growth factor on the epithelial proliferation/migration. Rebamipide, a mucosal protective and antiulcer drug, does not affect the direct irritating action of alendronate in the gastric mucosa but prevents the alendronate-induced antral ulceration, probably due to anti-oxidative and anti-inflammatory actions. In addition, this agent also antagonizes the healing impairment action of alendronate by counteracting the down-regulation of bFGF expression in the ulcerated mucosa. It is assumed that rebamipide is a promising drug that can be used as a prophylactic against the adverse effects of BPPs in the stomach.

Gastrointestinal Mantle Cell Lymphoma—A Tale of Two Endoscopies

A 52-year-old male with a 2-year history of typical gastroesophageal reflux symptoms and concomitant weight loss despite good appetite is presented in this paper. Endoscopy showed hypertrophic gastric folds and multiple antral ulcers which were considered benign both histologically and macroscopically. The diagnosis at the time of presentation was moderate chronic gastritis. Eighteen months later, the patient presents with overt adenopathy in all peripheral lymph nodes and was subsequently diagnosed with mantle cell lymphoma (MCL). On second presentation, the patient underwent a repeat endoscopy with biopsy and immunohistochemical (IHC) testing of gastrointestinal and lymph node tissue. The gastrointestinal endoscopy showed multiple polypoid nodules in the first and second parts of the duodenum and multiple sessile polypoid masses carpeting the colon. Gastric and lymph node biopsies were consistent with a diagnosis of MCL and MLP showing immunoperoxidase staining positive for cyclin D1, CD20 and bcl-2. A repeat IHC testing of the gastrointestinal tissue collected on initial endoscopy also showed a positive expression of the IHC markers consistent with MCL. In retrospect, an earlier detection of MCL was possible when the patient had first presented.

Helicobacter pylori induces human dendritic cell maturation and duodenal ulcer promoting gene a (dupA) enhances dendritic cell cytokine expression

<h3>Introduction</h3> <i>Helicobacter pylori</i> is the leading cause of peptic ulceration worldwide and possession of duodenal ulcer promoting gene A (<i>dupA</i>) increases ulcer risk. In vitro, <i>dupA</i> increases production of pro-inflammatory cytokines by monocytes, but these cells are not present in gastric mucosal tissue. However, isolation and characterisation of immune cells from human gastric biopsy samples has shown the presence of myeloid dendritic cells. Dendritic cells are antigen-presenting cells with a unique ability to initiate a primary immune response from naïve T-cells. We therefore investigated whether <i>Helicobacter pylori</i> is able to induce dendritic cell maturation and pro-inflammatory cytokine expression and whether this is influenced by the <i>dupA</i> gene. <h3>Methods</h3> Human dendritic cells were derived from circulating monocytes from healthy donors. These cells were co-cultured with <i>H pylori</i> strains AB21 and AB31 and their isogenic <i>dupA</i> knockout mutants. The activation status of dendritic cells was assessed by flow cytometry; cytokine production was quantified by ELISA. <h3>Results</h3> In their resting state the monocyte derived dendritic cells expressed MHC class II, but very low levels of co-stimulatory molecules CD80, CD83 and CD86. Upon culture with <i>H. pylori</i>, the cells expressed significantly higher levels of these co-stimulatory molecules, demonstrating maturation (&gt;25 fold increase in percentage of positive events for CD80, CD83, CD86 on flow cytometry; p&lt;0.01). There were no differences between the responses to wild type and <i>dupA</i> knockout mutant strains, or following stimulation with lipopolysaccharide (LPS). The <i>H. pylori-</i>matured dendritic cells secreted high levels of IL-12p40, IL-12p70, IL-10 and IL-23. The concentrations induced by the <i>dupA</i>+ strains were significantly higher than those induced by the <i>dupA</i> mutants (1.5 fold increase in IL-12p40 production, p&lt;0.05; 1.4 fold increase in IL-12p70, p&lt;0.05). <h3>Conclusion</h3> <i>H pylori</i> induces dendritic cell maturation and secretion of pro-inflammatory cytokines. <i>dupA</i> increases IL-12 production from these dendritic cells. This may explain the enhanced antral gastritis and ulcer risk associated with <i>dupA</i> + <i>H pylori</i> strains.

Eosinophilic Gastritis: A Rare Cause of Non Healing Chronic Antral Ulcer

Purpose: Gastric ulcers are highly unusual manifestation of eosinophilic gastroenteritis (EG). We describe a rare case of a non healing gastric ulcer occurring in patient with EG. Methods: 63-year-old male underwent follow up EGD for non healing antral ulcer. At the time of EGD, he was taking oral prednisone 60 mg for acute contact dermatitis. Prior EGD findings were ringed esophagus, 1 cm antral ulcer and gastritis and duodenitis. He was first referred to us with low ferritin (20) without GI symptoms. No history of NSAIDs/ ASA usage, smoking, cocaine or alcohol abuse. Biopsies revealed chronic inflammation in esophagus with marked eosinophilic infiltration (> 25 eosinophil /HPF) and moderate eosinophilia with chronic inflammation in antrum and duodenum; H. pylori was not seen on gastric biopsies; no malignancy or granulomas present. Special stain for CMV was negative. Patient was treated with PPI twice a day followed by additional sucralfate twice a day. Normal CBC with differential; ESR & CRP, IgE and gastrin were normal; negative stool for ova & parasites. Normal colonoscopy with negative random biopsies. Follow-up EGD showed partially healing 5 mm antral ulcer with scattered surrounding erosions compared with prior EGD. There were a markedly reduced number of eosinophils on biopsies. Results: Fortuitously, this patient was placed on steroid for a dermatologic condition prior to his repeat EGD with findings of significant healing of gastric ulcer and resolution of eosinophilic infiltration. Conclusion: EG is defined as a disorder that selectively affects the gastrointestinal tract with eosinophilic inflammation in the absence of known causes for eosinophilia, e.g., drug reactions, parasitic infections, malignancy. Clinical manifestations of disease depend on site of histologic involvement: 1) Diarrhea, iron deficiency anemia and protein-losing enteropathy in predominant mucosal disease; 2) obstruction/ motility disorder in predominant muscle layer disease; 3) ascites in predominant serosal disease. The cause of EG is unknown and the pathogenesis is poorly understood. Typical endoscopic findings in mucosal disease include nodular or polypoid gastric mucosa, erythema, or erosions; ulcer formation is unusual. The definitive finding of Eosinophilic Esophagitis (EE) in our patient supports the diagnosis of eosinophilic gastritis as the cause of our patient's gastric ulcer. The role of food allergy as a stimulus to EG has not been as clearly defined as in EE. It is conceivable that this is not one, but several disorders that manifest as similar histologic end points. Steroids are the mainstay of therapy in patients who fail to respond to dietary manipulation.

A Woman with Black Spheres in Her Stomach

Purpose: Selective internal radiation therapy (SIRT) delivers targeted, high dose intra-arterial radiation to liver tumors via beta radiation-emitting Yttrium-90 microspheres, sparing contiguous hepatic parenchyma and adjacent viscera. However, inadvertent radiation injury to abdominal organs may occur. We report a case of radiation-induced gastric ulceration to alert clinicians to the diagnostic difficulties and diverse clinical spectrum associated with this underappreciated and potentially catastrophic complication of SIRT. A 57 year-old woman with stage IV breast cancer including liver and lung metastases presented in Jan. 2010 complaining of 2 months of worsening nausea and vomiting. She had received chemotherapy in Nov. 2009, consisting of 5-FU, gemcitabine, cyclophosphamide and trastuzumab; that month she also received SIRT with Yttrium-90 microspheres, a targeted radioembolization treatment aimed at her liver metastases. She was hospitalized elsewhere in early Dec. 2009 for nausea and vomiting, treated symptomatically with ondansetron, and discharged. On exam, vital signs were normal, physical exam was unremarkable. CBC and basic chemistries were normal. Abdominal CT scan: diffuse gastric antral thickening. A GI consultant performed UGI endoscopy: diffuse, severe gastritis and extensive, circumferential antral ulceration. Overlying blood clots and duodenal bulb ulcerations were also present; biopsies were taken. On histologic examination, black, spherical foreign bodies, consistent with Yttrium-90 microspheres, were visualized, documenting radiation gastritis and extrahepatic dissemination of radioactive particles. She received IV omeprazole and steroids, which improved symptoms. The patient was discharged home on a steroid taper, liquid hydromorphone, lorazepam, and ondansetron. GI complications of SIRT involving Yttrium-90 microspheres have been reported to be as high as 8%. Diverse sequelae of radiation damage may occur, including esophagitis, gastroduodenal ulceration, acute cholecystitis, pancreatitis, and small bowel obstruction or perforation. Mechanisms of unintended microsphere spread may include unrecognized vascular variants, collateral circulation, or changes in flow dynamics during infusion. Misdiagnosis and diagnostic delay of these potentially fatal complications of SIRT are common, as this case illustrates. Reasons for delay include non-specific, diverse symptoms which may be immediate, early or delayed as long as a year. These complaints may be attributed to widespread malignancy or chemotherapy. Clinicians must consider radiation-associated toxicity in SIRT-treated patients developing abdominal symptoms.

An Unusual Duodenal Mass with GI Bleeding: Gastroduodenal Artery Pseudoaneurysm

Purpose: Pseudoaneurysm of the gastroduodenal artery is a rare and potentially lethal complication of chronic pancreatitis. A 44 yo man with a history of chronic alcoholic pancreatitis complicated by pseudocysts of the pancreatic head (4 × 5 cm and 2.5 × 2 cm) presented with a 2 week history of fatigue and black stools. Physical examination revealed pallor, normal vital signs and cardiopulmonary examination, and abdominal tenderness in the epigastrium. Laboratory tests showed Hg 4.1 g/dL, others were normal. EGD demonstrated mild esophagitis, 2 small antral ulcers without stigmata of hemorrhage, and an area of edematous and erythematous mucosa in the duodenal bulb. There were no varices and urease test was negative. Colonoscopy was normal. The patient was transfused, treated with PPI and discharged. Two weeks later he was re-admitted with the same symptoms. Laboratory evaluation showed Hg 6.9 g/dL, lipase 2,472 U/L. EGD revealed normal esophagus, mild antral erythema and a 2 cm friable mass in the duodenal bulb with mild oozing from its surface. Biopsy was obtained and oozing was successfully treated with injection of epinephrine. CT scan, ordered for further evaluation, demonstrated near complete resolution of the pancreatic pseudocysts but discovered a 1.7 × 1.9 × 1.2 cm gastroduodenal artery pseudoaneurysm (PA). Coil embolization of the PA was performed successfully. Splanchnic aneurysms and PAs are seen in 10% of autopsy studies; however, they remain asymptomatic in most individuals. In pancreatitis, splanchnic aneurysms form from enzymatic injury to the vascular wall, often within a pseudocyst. A PA develops when the wall of the aneurysm further enzymatically erodes and ruptures into the pseudocyst. Most cases involve the splenic (30-50%) or gastroduodenal (10-15%) artery. Occasionally a PA may erode into adjacent structures or other vessels. When a patient with PA presents with hemorrhage mortality reaches 50%. When suspected, the presence of PA is confirmed by IV contrast enhanced CT and/or angiogram. Therapy by percutaneous transcatheter arterial embolization or vascular stenting are treatments of choice. Surgery is reserved for complicated cases when endovascular intervention is unsuccessful. Splanchnic PAs are rare but important causes of GI bleeding in patients with acute and chronic pancreatitis. This potentially lethal complication should be considered in the differential diagnosis when treating a patient with GI bleeding and a history of chronic or acute pancreatitis. Caution should be taken during endoscopic evaluation in these cases, as the presence of a mass may be a manifestation of a PA and acute hemorrhage could be provoked by endoscopic manipulations.