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Purpose: Chronic Gastritis is the most common manifestation of infection with Helicobacter pylori. Changes in the gastric mucosa have tendency to progress towards mucosal atrophy, most likely in patients with gastric ulcer. We have explored the frequency of the presence of atrophic gastritis in patients with gastric and duodenal ulcers., Material and Method: We included 175 patients in a prospective study, 119 of whom were patients with duodenal ulcer and 56 suffered from gastric ulcer. The mean age of the patients with duodenal ulcer was 42.27 years, while patients with gastric ulcer had a mean age of 51.87 years. Biopsy was done on all patients with gastric and duodenal ulcer for histopathological examination, in order to confirm the presence of atrophic gastritis. All examined patients were positive for H. Pylori status., Results: The presence of gastritis by type of ulcer, duodenal or gastric, was as follows: type without atrophy 20% and 0%, mild atrophy 61% and 14% and severe atrophy 22% and 86%, respectively., Conclusions: In patients with duodenal ulcers more often occurs mild atrophic gastritis (p < 0001). In the patients with gastric ulcers most often occur alterations with more pronounced gastric atrophy (p < 0.01).

102 tissue samples, resected during treatment of the perforated duodenal ulcers. The most pronounced fibroplastic and acute inflammatory tissue changes were registered in the immediate perforation zone and 0,5 sm above. At a distance of 1,0 sm these changes become less evident. Therefore, in patients with the perforated duodenal ulcer and palpable surrounding infiltrate less than 3,0 sm in diameter, the resection line should be no shorter than 1,0 sm away from the perforation.

Aim: The aim of this investigation is to estimate the role of systemic injuries of lipid metabolism in pathogenesis of ulceration on the model of stress ulcerogenesis., Materials and Methods: There have been assumed as a basis of the work experimental investigations on 60 pubertal white rats of both sexes weighing 200 gr. There was studied the state of macroscopic picture of stomach and small intestine, qualitative and quantitative lipid composition, lipid peroxidation, phospholipase A2, catalase, superoxide dismutase in stomach tissues, small intestine and blood plasma., Results: The facts of the experimental investigations show, that by the effect of ulceration stress there are processes, that underlie modifications of lipid components of cell structures' biomembranes, and registered by qualitative and quantitative changes of lipid composition. Intensification of lipid peroxidation and activation of phospholipase A2 are the key mechanisms of qualitative and quantitative composition of biomembranes' lipid components, and they reduce to beginnings of cascade of pathomorphological and pathophysiological reactions in cell structures, which cause beginnings of membrane destructive processes, that is as a basis of ulcerogenesis., Conclusion: In the result there is broken morphofunctional state of mucous membrane (one of the main factors of protection), that in the end makes it accessible substratum for other aggressive factors and promotes the formation of ulcerous defects.

162 patients with a stomach ulcer were examined, 98 people were with torpid course of a stomach ulcer, and 64 sick people were usual periods of cicatrizing ulcers. 56 sick people (the first group) with torpid course of a stomach ulcer received immunal as a part of complex irradical therapy and comparising group 42 sick people (the second group) with torpid course used only irradical therapy. In estimation of efficiency of therapy, in addition to clinical and endoscopies data, indicators of genotypes Helicobacter pylori and immune system were used. The pathogenetic role of virulent genotypes Helicobacter pylori in the formation of the torpid course of a stomach disease is shown. The information about the dependence of the immune defense from cytotoxic characteristics Helicobacter pylori was received. Inclusion of immunal in complex therapy improves the elimination of Helicobacter pylori and has good clinical effect.

In this article you will find the clinical features of the course of gallstone disease (GSD) and duodenal ulcer (DU) when they are combined and given to their pathogenetic substantiation. There were shown data analysis of the frequency combinations of GSD and DU, depending on age and sex. It was found that at GSD was observed decrease in the frequency of exacerbations of DU until the development of stable remission. The presence of DU, in turn, reduces the frequency of exacerbations of GSD (biliary colic), the severity of its clinical manifestations, which leads to an increase in patients with asymptomatic "stone living". These clinical features are associated with reduced secretion of gastrointestinal hormones (gastrin, cholecystokinin).

In recent years, significant progress in studying the pathogenesis, diagnosis and treatment of gastrointestinal diseases in children and adolescents. However, steady growth of erosive and ulcerative lesions of the mucous membrane of the stomach and duodenum in adolescents. A major role in the formation of chronic diseases of the stomach and duodenum assigned lower sacrificial function of the mucous membrane, which has multifactorial protection against pathogenic effects. The results of the study lektingistohimicheskogo mucus formation in the duodenal ulcer in adolescents.

Was made a clinical-morphological study of elderly patients with a combination of cholelithiasis and duodenal ulcer. Was shown that prolonged ursoterapiya does not adversely affect the clinical course of duodenal ulcer, does not cause exacerbations of her elderly patients. These histological study of gastroesophageal and duodenobioptatov during treatment showed a positive effect of the ursodeoxycholic acid (UDCA) on the mucous membrane of the stomach and duodenum with the partial restoration of its structure, due to its cytoprotective effect.

Background/aims: Double-balloon enteroscopy is a novel endoscopic technique developed to investigate small bowel diseases. The aim of this study was to evaluate the diagnostic and therapeutic impact of double-balloon enteroscopy in patients with suspected or documented small bowel disease who were referred to our tertiary center, which was the first to introduce the double-balloon enteroscopy system in Turkey., Methods: This is a single-center prospective study. A total of 216 double-balloon enteroscopy procedures (168 antegrade, 48 retrograde) were done in 188 patients who were referred to our center for suspected small bowel disease. The main outcome measurements were complications, insertion depth and duration, and diagnostic and therapeutic rates., Results: Indications included obscure gastrointestinal system bleeding, iron deficiency anemia, abnormality on radiographic evaluation, abdominal pain, diarrhea, and suspected celiac disease. A diagnosis was established in 130 (69%) patients. The most common pathologic findings included angiodysplasias (29%), ulcerations (16%) and Crohn's disease (9%). Mean time±standard deviation to perform the examination using the antegrade route was 116.4±7.17 min, and the average±standard deviation insertion length was 310.65±90.3 cm (beyond the pylorus). Therapeutic interventions were performed in 66 patients (56 angiodysplasias, 4 ulcers, 4 strictures, and 2 polyps), and the success rate was 97%. No serious complication was observed, although pancreatitis occurred in 6 of 48 (12.5%) patients who were followed up for post-procedure pancreatic enzyme levels., Conclusions: Our prospective analysis suggests that double-balloon enteroscopy is a feasible and useful technique for the diagnosis as well as treatment of small intestinal disorders.

Background: Although gastric cancer (GC) and duodenal ulcer (DU) are both strongly associated with Helicobacter pylori infection, a DU is negatively associated with the risk of GC. The aim of the study is to evaluate histologic risk factors for GC among patients with a DU., Materials and Methods: A total of 541 consecutive patients with GC were prospectively evaluated for the presence of a DU. Control patients with only a DU (n = 89) were recruited from health screening population. Histologic grading was assessed using the updated Sydney system for six gastric biopsies from three regions. GC risk among patients with a DU was evaluated using logistic regression analysis., Results: Among patients with GC, 7.6% (41/541) had a concomitant DU or an ulcer scar. Corpus-predominant/pangastritis were more frequently found in concomitant GC patients with a DU (90%) than in patients with a DU alone (62%) (p = .001). In patients with a DU, moderate-severe chronic inflammation at the lesser and greater curvatures of corpus was associated with GC risk (OR, 3.70; 95% CI, 1.46-9.36, and OR, 7.72; 95% CI, 3.18-18.7, respectively). Additionally, moderate-severe intestinal metaplasia (IM) at the antrum and corpus lesser curvature was associated with GC risk (OR, 7.52; 95% CI, 3.06-18.5, and OR, 9.25, 95% CI, 2.39-35.8, respectively)., Conclusions: A DU is not rare in patients with GC in a high-risk region of GC. Patients with a DU with chronic corpus gastritis and IM have an increased risk of GC, thus those patients should be followed up for GC development., (© 2010 Blackwell Publishing Ltd.)

Aim: To search the independent factors determining gastric juice acidity and to investigate the acidity of gastric juices in various benign and malignant upper gastrointestinal diseases., Methods: Fasting gastric juice acidity of 165 healthy subjects and 346 patients with esophageal ulcer (n = 21), gastric ulcer (n = 136), duodenal ulcer (n = 100) or gastric cancer (n = 89) were measured and compared. Additionally, gastric specimens were taken from the antrum and body for rapid urease test and histological examination., Results: Multivariate analysis revealed that bile stain of gastric juice, high acute inflammatory score of the corpus, and atrophy of the corpus were independent risk factors for the development of gastric hypoacidity with odds ratios of 3.1 (95% CI: 1.3-7.3), 3.1 (95% CI: 1.2-7.9) and 3.5 (95% CI: 1.3-9.2). Esophageal ulcer and duodenal ulcer patients had a lower pH level (1.9 and 2.1 vs 2.9, both P < 0.05) of gastric juices than healthy subjects. In contrast, gastric ulcer and gastric cancer patients had a higher pH level (3.4 and 6.6 vs 2.9, both P < 0.001) than healthy controls. Hypoacidity existed in 22%, 5%, 29%, 5% and 88% of healthy subjects, esophageal ulcer, gastric ulcer, duodenal ulcer and gastric cancer patients, respectively., Conclusion: Bile reflux, atrophy and dense neutrophil infiltrate of the corpus are three independent factors determining the acidity of gastric juice.

Macrophage migration inhibitory factor (MIF) is a key proinflammatory mediator, which plays a pivotal role in inflammatory and immune diseases. We attempted to clarify the association of functional polymorphisms of MIF gene promoter with the development of gastro-duodenal ulcer. The study was performed in 471 stocked DNAs obtained from the subjects, including 93 healthy volunteers, with no evidence of gastric malignancy. We employed the PCR-SSCP method to detect gene polymorphisms. In all 471 DNAs, 92 and 43 were obtained from gastric and duodenal ulcer patients, respectively. By an unadjusted analysis, infection with Helicobacter pylori (H. pylori), male gender and non-steroidal anti-inflammatory drug (NSAID/aspirin) use were significantly associated with a risk for developing a gastric ulcer, whereas MIF promoter polymorphisms were not. On the other hand, infection with H. pylori, male gender and 7-CATT repeat at position -794 were significantly associated with the development of a duodenal ulcer, whereas NSAID/ aspirin use was not. By the analysis after adjustment for age, gender, NSAID/aspirin use and H. pylori infection status, 7/7-CATT homozygote had a significantly increased risk for the development of duodenal ulcers (OR, 6.31; 95% CI, 1.50-26.6; p=0.012). No factors were significantly associated with the development of peptic ulcers in NSAID/aspirin users. Our results suggested that tetranucleotide repeat polymorphism of MIF gene promoter might be associated with the development of duodenal ulcers.

Aims: We aimed to determine differences in gastroduodenal damage related to the presence of Helicobacter pylori (Hp) in patients starting long-term NSAID therapy. Seventy-one candidates for chronic NSAIDs therapy (33 Hp negative and 38 Hp positive) entered the study and underwent upper GI endoscopy before, and 8 and 16 weeks after, continuous NSAID therapy., Results: Lanza score increased in both Hp positive and negative patients in the course of NSAID therapy (P < 0.001), being significantly higher in Hp positive than Hp negative (4.31 ± 1.33 vs 3.15 ± 1.95, P < 0.05) after 16 weeks of follow-up. In gastric mucosa, no significant difference in mean Lanza score was observed between the two groups. Duodenal ulcer was diagnosed in 18 (36.8%) Hp positive and 1 (3%) Hp negative patient (P < 0.05)., Conclusions: Hp is more closely related to duodenal than gastric mucosal injury in NSAID users. Risk for duodenal ulcer in Hp-infected individual increases after 4 months of NSAID therapy.

Unlabelled: There are no solid figures of the frequency of ulcer disease during childhood in Europe. We assessed its frequency and analyzed known risk factors., Patients and Methods: Ulcers, erosions, indications, and risk factors were recorded in all children undergoing an upper gastrointestinal endoscopy in a prospective study carried out during 1-month simultaneously in 19 centers among 14 European countries., Results: Ulcers and/or erosions were observed in 56 out of 694 children. Children with ulcers/erosions were significantly older than those without lesions (10.3+/-5.5 vs. 8.1+/-5.7 years, P=0.002). Helicobacter pylori infection was present in 15 of 56 children (27%) where NSAIDs were used in eight, steroids in five, immune-suppressive drugs in five, antibiotics in six, antacids in one, H2-blockers in six and proton pump inhibitors in eight children (more than one risk factor was detected in 32 of 56 children). No risk factors were observed in 24 of 56 children (43%). The main indications for endoscopy were epigastric or abdominal pain (24%) and suspicion of gastroesophageal reflux disease (15%). Similarly, epigastric tenderness, hematemesis, melena, and weight stagnation were significantly associated with ulcers/erosions, whereas sex, H. pylori infection, socioeconomic and lifestyle factors were equally distributed., Conclusion: Although limited by the short-time duration and the heterogeneity of the patients included throughout the 19 centers, our study shows a frequency of 8.1% of ulcers and/or erosions in children, occurring mainly in the second decade of life. H. pylori infection and gastrotoxic medications were less frequently implicated than expected.

Background: Ghrelin is a hormone produced by neuroendocrine cells of gastric mucosa. Its concentration changes in cases of Helicobacter pylori (H. pylori) infection of stomach, but the relation between the expression of plasma and mucosal ghrelin content and H. pylori infection is not completely defined. This study was designed to determine the changes in plasma and gastric mucosa ghrelin concentrations in diseases of gastric mucosa depending upon the H. pylori infection., Material/methods: The following groups were included; Group 1. patients with gastric cancer and concomitant H. pylori infection (N=25); Group 2. patients with antral gastritis with H. pylori infection and concomitant duodenal peptic ulcer (N=18); Group 3. patients with atrophic gastritis of both the fundus and the body of the stomach without H. pylori infection (N=10); Group 4. control group consisting of patients without morphological and histological lesions of gastric mucosa and without H. pylori infection (n=25). Endoscopic biopsies of gastric mucosa of fundus, body and pyloric region were obtained in all tested groups. In patients suffering from gastric cancer biopsies of tumor were also taken. The ghrelin concentrations were measured by specific RIA. Biopsy specimens were examined to assess ghrelin mRNA expression in intact gastric mucosa and gastric cancer., Results: The study showed significant influence of H. pylori infection on ghrelin plasma concentrations. The highest ghrelin concentrations were found in patients of the group 2 (average 503 pg/mL (95% CI: 285-886). Ghrelin concentrations were found to fall to the lowest values in the group 3 (average 144 pg/mL (95% CI: 93-222). In the group 1, the ghrelin concentration averaged 203 pg/mL (95% CI: 161-257), while in the group 4 (control group) - 255 pg/mL; 95% (CI: 160-406). The study proved that gastric cancer does not exert any ghrelin-production activity, as confirmed by RT-PCR examination of biopsy specimens of the cancer., Conclusions: This study shows that the presence of H. pylori in the stomach with peptic ulcer increases plasma ghrelin levels, whereas in gastric cancer and atrophic gastritis it is accompanied by a marked decrease in plasma and cancer tissue levels of ghrelin.

Many drugs are known to have adverse effects on the gastrointestinal tract. The consequences can range from asymptomatic histological lesions in the gastrointestinal mucosa to fatal complications such as haemorrhage or perforation. On the biopsies (or on surgical specimens), there is a limited number of injury pattern that should suggest drug-induced pathology. They are mostly non specific (ex: ulcer). However, some drugs may induce pathognomonic histological lesions. For this reason, the diagnosis of a drug-induced gastrointestinal pathology depends on a clinicopathological correlation and implies a good communication between the pathologist and the clinician. In this review, we focus on the most common and well-described drug-related clinico-pathological conditions of the gastrointestinal tract using an organ and lesion based approach.

Purpose: To evaluate, for the first time, the efficacy of copper-indomethacin in the inhibition of aberrant crypt foci formation using the azoxymethane-induced adenocarcinoma model, to examine cell viability in the HCT-116 colorectal cancer cell line, gastrointestinal permeability, mitochondrial oxidative damage, and renal toxicity in rat models., Methods: Azoxymethane-induced adenocarcinoma rats were dosed with indomethacin and copper-indomethacin for 28 days and aberrant crypt foci were evaluated. HCT-116 colorectal cancer cells were exposed to indomethacin and copper-indomethacin at 0-250 microg/mL (0-698 microM for indomethacin, and 0-147 microM for copper-indomethacin), and cell viability was measured. Acute gastrointestinal toxicity was measured using gastrointestinal permeability markers, gastrointestinal ulceration and bleeding, and measurement of an acute-phase protein haptoglobin. Effects of acute and chronic administration of indomethacin and copper-indomethacin on urinary electrolyte concentrations were examined., Results: Both indomethacin and copper-indomethacin resulted in a significant reduction in aberrant crypt foci in azoxymethane-treated rats. In parallel, high concentrations of indomethacin and copper-indomethacin also reduced cell viability in HCT-116 colorectal cancer cells. However, copper-indomethacin was considerably safer in all measures of gastrointestinal toxicity compared to indomethacin. In addition, indomethacin reduced urinary electrolytes at an ulcerogenic dose of 10 mg/kg acutely and chronically at 3.0 mg/kg for 28 days, whereas copper-indomethacin at equimolar doses of indomethacin affected urine electrolytes after acute dosing but not after chronic dosing for 28 days., Conclusions: Copper-indomethacin has both gastrointestinal and renal sparing properties while maintaining efficacy in experimental adenocarcinoma.

There is a rise in the rates of acute erosive gastropathies in patients with cardiovascular and other somatic diseases. The role of acute erosive gastropathy-induced hemorrhages in the tanatogenesis of these diseases is underestimated; the problems of their prevention, diagnosis, and treatment remained unsolved. Many factors, mainly acute or chronic ischemia of the gastroduodenal mucosa, as well as its age-related involution, Helicobacter pylori infection, reflux gastritis, multiple organ dysfunction, drug-induced damage, etc., which are implicated in the pathogenesis of acute erosive gastropathies in patients with cardiovascular and other somatic diseases, are summarized.

A total of 4684 autopsies made at Moscow multidisciplinary hospitals in 2002-2008 were studied to reveal the incidence and morphological features of acute gastroduodenal erosions and ulcers in coronary heart disease (CHD), cerebrovascular disease (CVD), and chronic obstructive pulmonary disease (COPD). Cases with combined, background, and concomitant diseases that could be independent causes of gastroduodenal lesions were excluded. Patients older than 60 years with infarctions of the myocardium or brain, a concurrence of CHD, CVD, and COPD, and various diseases with chronic heart failure syndrome, particularly in the presence of arterial hypertension and diabetes mellitus should be referred to as a risk group for acute gastroduodenal erosions and ulcers and their induced hemorrhages.

Background and Aims: Low-dose aspirin is used as a preventive treatment for ischemic heart disease and ischemic cerebrovascular disease, on the other hand gastrointestinal injuries are an adverse effect of aspirin. We reported that endoscopic surveillance reveals a high risk of gastroduodenal ulcer and erosion in aspirin users of ischemic heart disease. But risk of gastroduodenal injuries may be different among pre-existing disease. In the present study, endoscopic examination was performed to investigate the frequency of gastroduodenal injuries associated with low-dose aspirin in patients with cerebrovascular disease., Methods: Routine examination using upper gastrointestinal tract endoscopy was prospectively performed for all patients admitted to Sasson Hospital for rehabilitation after cerebral infarction from April 2005 to September 2007. Endoscopic findings such as ulcers and flat erosions were assessed as mucosal injuries., Results: Endoscopic examination was performed for 142 successive patients, divided into three groups: 70 patients as low-dose aspirin users (aspirin group); 61 as non-aspirin users (non-aspirin group); and 11 as multi-drug users of aspirin plus other anti-platelet drugs (combination group). The aspirin group without anti-ulcer drugs (A(-) group) comprised 47 patients and the non-aspirin group without anti-ulcer drugs (NA(-) group) 31 patients. Mucosal injuries were detected in 29.8% of the A(-) group and in 6.4% of the NA(-) group (P < 0.05). The frequency of ulcer was similar between the A(-) group (6.4%) and NA(-) group (3.2%)., Conclusion: Endoscopy reveals low-dose aspirin-induced gastroduodenal injuries in patients with cerebral infarction.

Background and Aims: Enteroscopic observation has clearly demonstrated that non-steroidal anti-inflammatory drugs/low-dose aspirin (usually enteric-coated) induces hemorrhagic lesions, including ulcers and bleeding, in the small intestine of patients at a high incidence. Such intestinal lesions induced by NSAIDs have been confirmed in animal experiments. With aspirin, however, it has long been believed that it is difficult to induce any damage in the intestinal mucosa of laboratory animals. Therefore, we established a new method of inducing intestinal hemorrhagic lesions in rats by injecting aspirin into the proximal duodenum., Methods: Under ether anesthesia, aspirin (50-200 mg/body), suspended in 2% methylcellulose (with or without 0.1 N HCl), was injected into the proximal duodenum of normally fed or 20-h non-fed rats (male Sprague-Dawley, 9 weeks old). At 1 h after treatment, the animals were killed with ether and the entire small intestine was removed for histological examination. In some experiments, 1% Evans blue was injected (i.v.) into the rats 1 h after aspirin treatment to visualize the lesions. An image analyzer determined the total area of the intestinal lesions. Oral proton pump inhibitors and histamine H(2)-receptor blockers were given 1 h before aspirin injection. 16,16-dimethyl prostaglandin E(2) (dmPGE(2)) was given s.c. 30 min before aspirin injection., Results: Aspirin alone clearly induced severe lesions (including bleeding and ulcers) mainly in the jejunum at 100% incidence. Total score of lesions per rat obtained by histological examination was similar to the damaged area quantified with the dye method. Dose-related induction of lesions by aspirin was confirmed both by the histological and dye methods. The irritable effect of aspirin suspended in 0.1 N HCl solution was the same as that of aspirin alone; 0.1 N HCl alone induced only minor lesions in the intestine. Both proton pump inhibitors and histamine H(2)-receptor blockers, at doses that inhibit gastric acid secretion, had no or little effect on aspirin-induced intestinal lesions. Pretreatment with dmPGE(2) (3, 10, 30 microg/kg) showed significant prevention of both aspirin- and HCl/aspirin-induced intestinal lesions., Conclusion: This new aspirin lesion model will be useful for screening defensive drugs against aspirin-induced intestinal lesions and to elucidate the underlying mechanism.

Background: Cancer of unknown primary (CUP) is defined as histologically confirmed metastases in the absence of an identifiable primary tumor. Patients with solely liver metastases from adenocarinomas represent the most frequent subgroup with an unfavourable prognosis. The medium survival averages 6 to 9 months. No chemotherapheutic standard has been established., Case: We present a patient with hepatic CUP. After cycles of chemotherapy and hemihepatectomy the tumor returned and showed hepatic progression. The patient was evaluated for selective internal radiation therapy (SIRT). Three years after diagnosis she is still alive and tumorfree. Despite a good result and disease control our patient suffered radiation-induced ulceration in the oesophagus, stomach, and duodenum. This side effect appears in up to 12 % of patients, often very late after treatment, is refractory to pharmacotherapy and persistent over a long time., Conclusions: SIRT is a new, effective treatment in patients with hepatic CUP. Because of the anticipated increase of this therapy, adverse side effects such as ulcerations in the upper-GI tract secondary to ectopic implantation of microspheres may be seen more commonly. Awareness of this and the recognition of microspheres in biopsies is cardinal for appropriate management and maintenance of the patient's quality of life.

Tumour Necrosis Factor (TNF) and Heat Shock Protein 70 (HSP70) are important molecules in inflammatory, infectious and tumoral processes. The genes codifying these molecules are polymorphic and certain alleles have been associated with susceptibility to disease. Gastric cancer is associated with an Helicobacter pylori-induced chronic inflammatory response. The aim of this work was to analyze whether polymorphisms in inflammation-related genes are associated with the development of gastric cancer. We studied 447 Mexican adult patients including 228 with non-atrophic gastritis, 98 with intestinal metaplasia, 63 with gastric cancer and 58 with duodenal ulcer, and 132 asymptomatic individuals as well. DNA from peripheral white blood cells was typed for the Single Nucleotide Polymorphisms (SNPs) -308 of TNF-alpha, +252 of TNF-beta, +190 of HSP70-1, +1267 of HSP70-2 and +2437 of HSP70-HOM. Compared with the asymptomatic group, we found a significant association of TNF-beta*A and HSP70-1*C alleles with gastric cancer (OR 5.69 and 3.76, respectively) and HSP70-1*C with duodenal ulcer (OR 3.08). Genotype TNF-beta G/G showed a significant gene-dose effect with gastric cancer (OR 0.09); whereas HSP70-1 C/G showed significant association with both, gastric cancer (OR 13.31) and duodenal ulcer (OR 16.19). Polymorphisms in TNF and HSP70 showed a significant severity-dose-response as risk markers from preneoplastic lesions to gastric cancer in Mexican population, probably because of their association with an intense and sustained inflammatory response.

Ethnopharmacological Relevance: Cinnamomum tamala T. Nees & Eberm (Family Lauraceae) is used traditionally in Indian System of Medicine as carminative, anthelmintic, diuretic, and used in colic, dyspepsia, and diarrhea., Aim of the Study: This study was aimed to evaluate the gastroprotective effects of Cinnamomum tamala leaves., Methods: Cinnamomum tamala leaves extract (CTE; 50,100 and 200mg/kg body weight) was administered orally, twice daily for 5 days for prevention from ethanol (EtOH)-, cold-restraint stress (CRS)- and pylorus ligation (PL)-induced ulcers. Estimation of H(+)K(+)ATPase activity and gastric wall mucous were performed in EtOH-induced ulcer model, antioxidant enzyme activities was carried out in CRS-induced ulcer model, and various gastric secretion parameters like volume of gastric juice, acid output, and pH value were estimated in PL-induced ulcer model., Results: A significant reduction in lesion index was observed in ulcer-induced animals treated with CTE at different doses when compared with ulcerated rats in all models. A significant decrease occurred in the level of H(+)K(+)ATPase, volume of gastric juice, and acid output. Simultaneously the level of gastric wall mucus and pH were increased significantly. These showed dose-dependent action of CTE. The antioxidant enzyme levels of LPO and SOD were decreased while administering CTE at different doses, compared with their control values. Contrary to this the level of CAT enzyme showed significant increase., Conclusions: The results of our study showed that Cinnamomum tamala possess significant gastroprotective activity, probably due to its free radical scavenging activity., (Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.)

Objectives: To evaluate the clinical, epidemiological and endoscopic characteristics of the Helicobacter pylori (Hp) negative peptic ulcer disease., Methods: In this cross sectional study we included 651 patients diagnosed of peptic ulcer disease between January 2000 and December 2005. The diagnosis of Hp infection was established by histology. Clinical and epidemiological characteristics of patients with and without Hp infection were compared., Results: Males prevailed (69%). Hp negative ulcers were older (57.73 +/- 19.44 years old vs 50.26 +/- 18, 64 years old, P < 0.001). Clinical characteristics did not differ among both groups. Duodenal ulcer prevailed in Hp positive patients (56.5%) and gastric ulcer in Hp negative patients (53.5%). Multiple ulcers and intestinal metaplasia were more frequently found in Hp negative cases [9.3% vs 4.5% (P = 0.015) and 34.5% vs 22.1% (P = 0.001), respectively]. CONCLUSION. Hp negative peptic ulcer disease is found in older patients, with a higher frequency of gastric ulcers, multiple lesions and intestinal metaplasia.

We investigated the levels of proinflammatory and antiinflammatory cytokines in experimental gastric and duodenal ulcers. Precedence shown an increase of pro-inflammatory cytokine TNF-a level in the isolated simulation of gastric ulcers and duodenal ulcers and preferential increase in cytokine IL-4 level in a prior administration of serotonin. The development of chronic diseases of the gastrointestinal tract is largely mediated by immunological reactions and the activation of the serotonergic system. Diversion of functional activity of the immune system plays a big role in the pathogenesis of ulcer disease, particularly T-helper lymphocytes and cytokines produced by them. The formation of the ulcer was accompanied by massive apoptosis of epithelial cells, development of vascular reactions--a plethora of vessels, edema and development of fibrinoid necrosis and infiltration of the mucosa by neutrophils, plasma cells and proliferation of fibroblasts. These processes significantly induced and regulated by cytokines, particularly interleukin IL-1beta, TNF-alpha, IL-4, -6, -8, -12 [4-7]. The purpose of the study was to identify the role of serotonin in the development of immunological reactions during experimental gastric and duodenal ulcers.

On the basis of results of research the pathomorphology severe blood loss and haemorrhagic shock at 38 patients who have died from ulcer gastroduodenal of bleedings, with the purpose of preventive maintains of relapses of bleedings am established by authors necessity of carrying out of the general, and also local metabolic rehabilitation during the endoscopic haemostasis at massive bleedings at the patients with high risk of surgical treatment.

Metaplasia represents the process of transforming a well-differentiated adult tissue into another type of adult tissue. Pancreatic metaplasia of the gastric mucosa represents the process in which the normal mucosa of the stomach is replaced with pancreatic formations, which mimic the structure of pancreatic acini. We describe the case of a male patient aged 39 who was admitted for abdominal pain, vomiting, hematemesis, melena, pale teguments, intense perspiration and nausea. The patient underwent surgery for suturing a perforated duodenal ulcer five years prior to this episode (2002). A gastric ulcer complicated with superior digestive bleeding and a chronic duodenal ulcer complicated with partial stenosis and perivisceritis were found during surgery. Gastric wall fragments were harvested and underwent usual histological techniques and immunohistochemistry. We found an ulceration from the gastric mucosa to the submucosa, covered by fibrino-leukocytic detritus. In the mucosal chorion we found numerous round or oval shaped nested formations which occupied the lower two thirds of the chorion, to the muscularis mucosae. Some metaplasic acini contain cells variable in shape, color and immunophenotype. Surrounding the nested acini we found tubular formations, formed of cubic shaped cells, representing excretory canals which were continued by gastric glands or opened directly in the crypts of the gastric epithelium.

Exacerbation of duodenal ulcer disease (DUD) is associated with elevated number of Ki-67 and Bcl-2 positive endtotheliocytes and apoptotic activity. Inhibition of endotheliocyte proliferation and apoptotic activity in gastric mucosa (GM) upon eradication of Hp in DUD patients promotes ulcer healing. Combination of eradication with melaxen therapy substantially enhances efficiency of Hp elimination and reduces cicatrization time. Antirelapse treatment with melaxene and omeprazole normalizes endotheliocyte homeostasis on GM to a greater degree than omeprazole monotherapy.

Aim: to study the specific features of working conditions in workers from the chemical plants manufacturing nitrogen compounds by the groups under study and by the time course of changes in the serum levels of gastrin-17 (G-17) and pepsinogen-1 (P-1) in relation to the chemical composition of noxious substances, the length of service, the stage of the disease, and the performed therapy., Subjects and Method: A test GastroPanel was used to study the serum levels of G-17 and P-1 in 54 patients with duodenal peptic ulcer (DPU) who worked at the chemical plants manufacturing nitrogen compounds (a study group) and in 15 healthy individuals (a control group)., Results: The objective data on the time course of changes in the functional characteristics (G-17 and P-1) of the gastric mucosa (GM) in patients with DPU vary with the chemical composition of noxious substances and the length of service in chemical industry. The basic therapy for PDU contributes to a positive change in the functional parameters reflecting the state of GM., Conclusion: In patients with DPU, the working conditions at the chemical plants manufacturing nitrogen compounds result in changes in the functional parameters reflecting the state of GM

Background/aims: It is controversial whether pretreatment with a proton pump inhibitor (PPI) before Helicobacter pylori eradication treatment decreases the eradication rate. To determine the effects of pretreatment with lansoprazole alone, followed by an H. pylori eradication regimen (lansoprazole 30 mg, amoxicillin 750 mg and clarithromycin 200 mg twice daily for 1 week), on the eradication rate and quality of life (QoL) of the patient., Methods: Patients with H. pylori-positive peptic ulcer were randomly assigned to two groups. The patients received either lansoprazole (30 mg) once daily for 6-8 weeks before H. pylori eradication (group A), or eradication treatment and then lansoprazole (30 mg) for 6-8 weeks (group B). To assess the QoL of the patients, the Gastrointestinal Symptom Rating Scale (GSRS) questionnaire was evaluated., Results: A total of 116 patients were enrolled. The cure rates were 78.9% in group A and 78.0% in group B. In both groups, GSRS analysis showed a significant improvement of the overall GSRS score at the assessment of eradication efficacy, compared to baseline; there was no difference between the groups., Conclusion: With this H. pylori eradication regimen, there was no difference in the cure rates and QoL associated with PPI pretreatment.

The p53 gene has been referred to as 'the guardian of the genome' because it controls apoptosis and cell cycle arrest. The purpose of this study was to evaluate the association of p53 codon 72 genetic polymorphism and the p53 immunohistochemistry with Helicobacter pylori-associated gastroduodenal diseases, including gastric cancer. This study included 1,852 subjects: controls and patients with gastric cancer, dysplasia, benign gastric ulcers, and duodenal ulcers (DU). Biallelic polymorphism was genotyped by restriction fragment length polymorphism. Immunohistochemical analysis for the detection of mutant type p53 expression was performed. The frequency of the Pro/Pro allele of the p53 codon 72 was higher in the patients with H. pylori-positive dysplasia than in controls (OR: 2.3, 95% CI: 1.3-4.3), but it was less frequent among patients with a H. pylori-positive DU (OR: 0.5, 95% CI: 0.3-0.8). However, there was no significant association with gastric cancer, including the location, stage, or histological type of gastric cancer. Expression of a mutant type of p53 protein was detected in 6.3% of dysplastic tissues and 26.5% of cancerous tissues compared 0% in the controls. Positive expression was higher in the intestinal type of cancer (34.9%) than in the diffuse type (15.0%; P = 0.001). These results suggest that genetic polymorphism of p53 codon 72 played a role in the determination of H. pylori-associated gastroduodenal diseases, but p53 immunostaining did not correlate with those of the p53 genetic polymorphism analysis.

Background: Recent advances in endoscopy have revealed that non-steroidal anti-inflammatory drugs (NSAIDs) often cause ulcers in the human small intestine. However, the mechanism of intestinal ulcer formation is still unclear., Aims: The role of dietary fibre (DF), intestinal motility and leukotrienes (LTs) in the formation of small intestinal ulcers induced by indomethacin (IND) was investigated in cats., Methods: Several types of diets containing DF at various percentages were given to animals twice daily during the experiment. IND was administered orally once daily after the morning meal for 3 days, and the area of mucosal lesions in the intestine was measured. Gastrointestinal motility was measured using a telemetry system in conscious cats implanted with force transducers., Results: In cats fed regular dry food containing 2.8% DF, IND (3 mg/kg, p.o.) significantly increased the motility of the lower half of the small intestine and produced many severe lesions; the total lesion area was 7.7 (SEM 2.0) cm(2) (n = 5). The lesions were markedly decreased with the low-DF diet (0.4%) and increased with the high-DF diet (7.2%). The lesion area was 0.1 (SEM 0.1) cm(2) (p<0.05) and 18.2 (SEM 4.1) cm(2) (p<0.05), respectively. Supplementation with insoluble DF (6% cellulose), but not soluble DF (pectin), in the low-DF diet increased the lesion area significantly. The hypermotility and lesion formation in the small intestine induced by IND were significantly (p<0.05) inhibited by AA-861 (a 5-lipoxygenase inhibitor), pranlukast (a LT receptor antagonist) or atropine., Conclusions: Insoluble DF, intestinal hypermotility, leukotrienes and cholinergic pathways are implicated in the pathogenesis of small intestinal ulcers induced by NSAIDs.

The evolution of drug-eluting stents (DES), effective periprocedural antithrombotic therapy, and advanced interventional techniques have fueled the surge of percutaneous coronary interventions. Stent thrombosis remains a serious complication of coronary artery stent implantation. Long-term antiplatelet therapy is required to prevent stent thrombosis, especially following DES implantation. Discontinuation of antiplatelet therapy (particularly clopidogrel) is the strongest independent risk factor for the development of stent thrombosis. Bleeding complications, most of which arise from the upper gastrointestinal (GI) tract, are the major limiting factors for antiplatelet therapy. The association of aspirin with the increased risk of upper GI bleeding has been well established. Peptic ulcer bleeding and Helicobacter pylori infection are the 2 most important risk factors for aspirin-associated GI bleeding complications. Endoscopy (for both surveillance and potential intervention), performed either emergently or semi-electively, is the primary tool for definitive management of GI bleeding. Considering the increase in GI bleeding risk seen with prolonged antiplatelet therapy, adjunctive proton pump inhibitor therapy and/or eradication of H. pylori infection might be beneficial for DES patients on long-term antiplatelet therapy.

The background of this research is to study morphological and functional microcirculatory channel condition with duodenum ulcer in the period of rehabilitation against the background of regular antiulcer therapy (1 group) and further treatment using Vazonit (2 group) in clinical conditions. EDU in animals results in marked microcirculatory disease in duodenum depending on the time of ulcer process development. Hypoxia is to be the significant factor associated with capillary stases, venous congestion. Blood flow impairment in organ results in metabolic damages of tissue structures. The results obtained are evidence of significant correction of microcirculatory channel state, improvement of regeneration and reparation processes. Vazonit improves the disorder of microcirculation and theological blood properties, restoring of macro and microangiopathy changes of hemocirculatory channel.

Background: We have previously demonstrated that Helicobacter pylori infection is associated with an increased number of CD4(+)CD25(high) regulatory T cells in the gastric and duodenal mucosa. In this study, we determined the number and localization of CD4(+) cells expressing the regulatory T-cell-specific transcription factor FOXP3 in the antrum and duodenum of duodenal ulcer patients, asymptomatic carriers, and uninfected individuals. We also determined gene expression levels of FOXP3 as well as anti- and proinflammatory cytokines before and after H. pylori eradication., Methods: Cellular FOXP3 expression was studied by immunofluorescence and flow cytometry, and transcription levels of FOXP3, interleukin (IL)-10, transforming growth factor-beta, CD4, and interferon-gamma were analyzed by real-time reverse transcription-polymerase chain reaction., Results: We found an increased (6-fold) frequency of CD4(+)FOXP3(+) T cells in H. pylori-infected gastric mucosa; interestingly 26% of these cells did not co-express CD25. The increase of FOXP3-expressing T cells in the antrum of infected individuals was dependent on the presence of H. pylori, since eradication therapy resulted in 4-fold lower levels of FOXP3 and IL-10 mRNA in the antrum. Furthermore, higher numbers of CD4(+)FOXP3(+) T cells were found in areas of duodenal gastric metaplasia in the duodenum of duodenal ulcer patients compared to duodenal gastric metaplasia of asymptomatic individuals and healthy mucosa in both patient groups. In duodenal ulcer patients, the CD4(+)FOXP3(+) T cells were more highly associated to aggregates in the duodenal mucosa., Conclusion: The numbers of CD4(+)FOXP3(+) T cells are increased and localized in CD4(+) T-cell aggregates in areas of duodenal gastric metaplasia in duodenal ulcer patients.

Cysteamine induces perforating duodenal ulcers in rats within 24-48 h. This reducing aminothiol generates hydrogen peroxide in the presence of transition metals (e.g., ferric iron), producing oxidative stress, which may contribute to organ-specific tissue damage. Since most intestinal iron absorption takes place in the proximal duodenum, we hypothesized that cysteamine may disrupt regulation of mucosal iron transport, and iron may facilitate cysteamine-induced duodenal ulceration. We show here that cysteamine-induced ulceration was aggravated by pretreatment of rats with Fe(3+) or Fe(2+) compounds, which elevated iron concentration in the duodenal mucosa. In contrast, feeding rats an iron-deficient diet was associated with a 4.6-fold decrease in ulcer formation, accompanied by a 34% decrease (P < 0.05) in the duodenal mucosal iron concentration. Administration of deferoxamine inhibited ulceration by 65%. We also observed that the antiulcer effect of H2 receptor antagonist cimetidine included a 35% decrease in iron concentration in the duodenal mucosa. Cysteamine-induced duodenal ulcers were also decreased in iron-deficient Belgrade rats (P < 0.05). In normal rats, cysteamine administration increased the iron concentration in the proximal duodenal mucosa by 33% in the preulcerogenic stage but at the same time decreased serum iron (P < 0.05). Cysteamine also enhanced activation of mucosal iron regulatory protein 1 and increased the expression of divalent metal transporter 1 mRNA and protein. Transferrin receptor 1 protein expression was also increased, although mucosal ferroportin and ferritin remained almost unchanged. These results indicate an expansion of the intracellular labile iron pool in the duodenal mucosa, increasing its susceptibility to oxidative stress, and suggest a role for iron in the pathogenesis of organ-specific tissue injury such as duodenal ulcers.

Background and Methods: Upper endoscopy records from 1998 to 2003 were reviewed. The demographic data, endoscopic diagnosis, results of rapid urease test and the absence or presence of intestinal metaplasia (IM) in histology were reviewed, to evaluate the prevalence of IM and Helicobacter pylori (Hp) infection over time in Hong Kong., Results: Among 1805 endoscopies performed, 1751 had both rapid urease test and histology available. A significant drop in the prevalence of duodenal ulcers from 17.9% in 1998 to 9.8% in 2003 was found (P = 0.015). Prevalence of IM was 13.9%, 5.9% and 9.4% in Hp positive, Hp negative and overall respectively (P < 0.05). The prevalence of IM increased with age, and the patterns were similar amongst subjects in 1998-2000 and those in 2001-2003. There was progressive decrease in Hp prevalence from 58% in 1998 to 40% in 2001 (P = 0.014), but no further decrease was seen in 2002-3. There was no corresponding decrease in IM prevalence. Instead IM prevalence in 2002-2003 was significantly higher than the prevalence in previous few years (P = 0.04)., Conclusion: The prevalence of IM did not change in the period from 1998 to 2003 despite a drop in the prevalence of Hp infection since 1994.

Background and Aim: The relationship between blood group antigens and peptic ulcer disease has been widely evaluated in the past. Data concerning the same association with upper gastrointestinal bleeding are very limited. We aimed to evaluate this association and we thought it was worthwhile to try to determine whether these components take some part in this complication., Methods: The study population consisted of 1,098 adults (364 patients and 734 volunteer blood donors as controls). Demographic features, comorbid illnesses, and use of aspirin/nonsteroidal anti-inflammatory drugs (NSAIDs) were recorded. Blood groups were examined by gel centrifugation method. We included only patients with bleeding from peptic ulcer disease and erosive gastropathy. Ulcers were classified by using Forrest's classification system in terms of rebleeding risk. Helicobacter pylori was examined by histology., Results: The gender distribution was similar in both groups. The ABO blood group phenotype distribution in patients and controls (respectively) was as follows: 46.2% versus 34.9% for group O, 32.4% versus 39.5% for group A, 15.7% versus 18.4% for group B, and 5.8% versus 7.2% for group AB. Blood group O was found to have higher frequency in the patient group than in the control group (P=0.004). Rh positivity was also higher in patients than in controls (P=0.007). H. pylori positivity was similar between blood groups among patients. The rebleeding and mortality rates between blood groups were also similar., Conclusion: ABO blood group O had an important role in patients with upper gastrointestinal bleeding. The impact of blood group on rebleeding and mortality may be a focus for further studies.

Aim: To investigate the association of gastric histological and endoscopic findings in patients with Helicobacter pylori (H. pylori), according to presence of seropositivity to 12 bacterial virulence antigens., Methods: This is a cross-sectional single-center study of 360 consecutive outpatients referred in the period of one year to upper gastrointestinal endoscopy because of dyspeptic complaints. Patients sera were tested by Western blot method to determine the presence of serum antibodies to bacterial virulence antigens--p120 (CagA--cytotoxin-associated antigen), p95 (VacA - vacuolating cytotoxin), p67 (FSH--flagellar sheath protein), p66 (UreB--urease enzyme heavy subunit), p57 (HSP homologue--heath shock protein homologue), p54 (flagellin), p33, p30 (OMP--outer membrane protein), p29 (UreA--urease enzyme light subunit), p26, p19, and p17. Upper gastrointestinal endoscopy was performed, endoscopic diagnosis recorded, and 4 mucosal biopsy samples were obtained and assessed according to Updated Sydney protocol., Results: The sera of 207 patients were analyzed. Thirty patients had gastric adenocarcinoma, 126 peptic ulcers, and 51 normal finding. p120 (CagA) seropositivity was significantly more often present in patients with higher activity grade in the antrum (P = 0.025), p30 in patients with greater inflammation in the antrum (P = 0.025) and the corpus (P = 0.010), p33 in patients with greater inflammation in the corpus (P = 0.050), and p19 (OMP) in patients with lower intestinal metaplasia grades in the corpus (P = 0.025). Seroreactivity to all other bacterial proteins showed no association with the histological status of the stomach mucosa. Except for the seropositivity to protein p95 (VacA), which was more often present in patients with duodenal ulcer (P = 0.006), there was no difference in seroreactivity to other bacterial proteins and upper gastrointestinal endoscopic findings., Conclusions: p120 (CagA), p33, p30 (OMP), and p19 (OMP) seropositivity was more often present in patients with higher grades of the histological parameters of gastritis and seropositivity to protein p95 (VacA) with endoscopic presence of duodenal ulcer. Histological parameters of gastritis are more associated with bacterial virulence than endoscopic findings.

Background and Aim: We compared endoscopic findings of the frequency scale for the symptoms of gastroesophageal reflux disease (FSSG), a written questionnaire developed in Japan, to that for the questionnaire for the diagnosis of reflux esophagitis (QUEST) for the diagnosis of reflux esophagitis., Methods: We registered 475 patients with untreated symptoms of upper abdominal pain (male/female: 252/223, average age 52.4 +/- 17.8 years). Subjects were assessed first with the FSSG and QUEST questionnaires, then by endoscopy, before allocation to a gastric ulcer (GU), duodenal ulcer (DU), gastroesophageal reflux disease (GERD) or functional dyspepsia (FD) group., Results: On the basis of the endoscopic findings the diagnoses for the 475 subjects were as follows: FD 52.2%, DU 7.6%, GU 7.8%, and GERD 32.4% (Grade M 10.1%, Grade A + B 20.2%, Grade C + D 2.3%). There was no difference between the FSSG and QUEST in sensitivity, specificity or accuracy for any condition. The FSSG score rose with increasing endoscopic severity of GERD, but there was no correlation between the QUEST score and endoscopic severity. The FSSG total score was inferior to QUEST in terms of distinguishing GERD from other conditions, but when only the questions relating to reflux symptoms were used, the FSSG was able to distinguish GERD from other conditions as well as QUEST., Conclusions: The FSSG score reflects the severity of the endoscopic findings of GERD.