Home About us Contact
|
Home About us Contact | ||
|
|
||
Helicobacter Pylori Status (helicobacter + pylori_status)
Selected AbstractsGastroesophageal reflux before and after Helicobacter pylori eradication.DISEASES OF THE ESOPHAGUS, Issue 4 2003A prospective study using ambulatory 24-h esophageal pH monitoring SUMMARY, The aim of this study was to assess prevalence of GERD before and after Helicobacter pylori (HP) eradication utilizing 24-h esophageal pH/manometry studies. Helicobacter pylori status was confirmed by the Campylobacter like organism test. Those testing positive underwent 24-h pH/manometry followed by HP eradication therapy and urea breath test. Patients were followed up at 6 months and then at 1 year when they underwent a repeat 24-h pH/manometry. Twenty patients, 10 with non-ulcer dyspepsia (NUD) and 10 with duodenal ulcer (DU) were enrolled, though only 10 patients attended for a repeat 24-h pH/manometry study. The patients were well matched, though patients with NUD had a significantly higher symptom score at entry compared with the DU group (8.5 vs 5.7, P < 0.05). The pH and esophageal manometry data were similar in the two groups. Overall nine patients (45%; DU = 5, NUD = 4) had evidence of GERD prior to HP eradication and it persisted one year after cure of the infection. The reflux disease occurred in the presence of normal LES pressure (mean 15.6 ± 3.3 mmHg). New onset GERD was uncommon after cure of HP infection, occurring in only one patient with NUD. Overall HP eradication had no impact on percentage of time pH < 4 (4.69 ± 3 vs 4.79 ± 3), episodes > 5 min (9.8 ± 16 vs 15.5 ± 25.3) and Johnson DeMeester Score (16.8 ± 7.5 vs 26.8 ± 18). In addition successful cure of HP produced no significant changes in LES pressure (17.9 ± 3.8 mmHg vs 19.3 ± 4.6 mmHg), and other esophageal manometry data. Half of HP-positive patients with NUD and DU have evidence of GERD before HP eradication. This persists after successful cure of the infection. New onset GERD occurs very uncommonly one year after HP eradication. [source] Usefulness of Non-invasive Tests for Diagnosing Helicobacter pylori Infection in Patients Undergoing Dialysis for Chronic Renal FailureHELICOBACTER, Issue 6 2004Thaďs López ABSTRACT Background.,Helicobacter pylori infection in chronic renal failure patients has been linked to peptic ulcer and gastric neoplasia after kidney transplantation. It may also contribute to the accelerated arteriosclerosis that is usual in this population. Few data are available on the usefulness of noninvasive diagnostic tests for H. pylori infection in dialyzed patients, especially regarding the new fecal antigen detection tests. The objective of this study was to determine the efficacy of a noninvasive test for H. pylori infection in patients with chronic renal failure. Methods., Eighty-six patients were included in a cross-sectional study. Urea breath test, serology and three fecal tests , FemtoLab H. pylori (Connex, Germany), Premier Platinum HpSA (Meridian, USA) and Simple H. pylori (Operon SA, Spain) were performed. Helicobacter pylori status was determined by concordance of the tests. Sensitivity, specificity and positive and negative predictive values were calculated for each test. Results., Sensitivity, specificity, positive and negative predictive values were 94%, 96%, 94% and 96% for the urea breath test; 97%, 64%, 66% and 97% for serology; 86%, 100%, 100% and 91%, for FemtoLab H. pylori; 58%, 96%, 91% and 76% for Premier Platinum HpSA and 61%, 78%, 74% and 67% for Simple H. pylori. Conclusions., The urea breath test seems to be the most reliable diagnostic method for H. pylori infection in patients with chronic renal failure. Serology has a low specificity, and the results of the fecal tests vary widely. [source] The Relationship Between Helicobacter pylori Infection, the Virulence Genotypes of the Infecting Strain and Gastric Cancer in the African SettingHELICOBACTER, Issue 4 2001J. A. Louw Abstract Background. The relationship between Helicobacter pylori infection and gastric carcinoma remains controversial, especially in the African setting where infection is common, while gastric cancer is perceived to be uncommon, the basis of the so called ,African enigma'. This discrepancy between infection and the development of disease is commonly attributed to differences in host, environment and bacterial factors. Interest in the bacterial factors has focused on heterogeneity in the so-called ,virulence genes'. Aim. The aim of this prospective, case-controlled study was to establish whether H. pylori infection is significantly associated with gastric cancer and to investigate whether gastric cancer is associated with genotypically distinct (as it relates to the candidate virulence genes) organisms in this population. Methods. Patients with histologically confirmed gastric cancer were matched with nonulcer dyspeptic controls for age (within 5 years), gender and ethnicity. Helicobacter pylori status was determined by RUT, histology, culture and serology (locally validated and used as default determinant of H. pylori status). Tumors were classified according to the Lauren classification. The ,virulence genotype' of 17 paired culture samples was determined by previously described and validated molecular techniques (cagA presence, vacA alleles, structure of the cag pathogenicity island and analysis of the iceA alleles). Categorical variables were analysed by the ,2 test. Results. Forty-eight patients (median age 59 years) could be adequately matched to controls. 39/48 (81%) cases and 43/48 (90%) controls were H. pylori positive (NS). Significant differences in the virulence genotypes of infecting strains were noted: vacAs2-controls 24%, cases 0%, p < .00001; vacAs1 present , cases 100%, controls 76%, p < .05; cagA -3,-length > 650 bp , cases 47%, controls 0%, p < .002; cag pathogenicity island intact , cases 82%, controls 43%, p < .04; iceA1 , cases 53%, controls 6%, p < .005. cagA was found in all subjects. Conclusion. This study indicates that, in this African population at least, there is no difference in the prevalence of H. pylori infection when comparing gastric cancer cases with matched controls. However, the findings suggest that gastric cancer may be associated with infection by organisms that are genotypically different from those not associated with disease. [source] Deregulation of E-cadherin,catenin complex in precancerous lesions of gastric adenocarcinomaJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 5 2003ANNIE ON-ON CHAN Abstract Background and Aim: Decrease in expression of the E-cadherin,catenin complex is an important element in gastric carcinogenesis. However, the expression of the complex in gastric precancerous lesions has not been well studied. The present study aimed to examine the serial change in expression of E-cadherin,catenin complex in the precancerous lesions of gastric cancer patients. Methods: Gastrectomy specimens of 40 patients with gastric cancer were retrieved. Areas with chronic gastritis, atrophic gastritis, intestinal metaplasia and adenocarcinoma were identified and immunostained for ,-catenin, ,-catenin and E-cadherin. The results were scored semiquantitatively by two independent pathologists using a validated scoring system. Results: A significant decrease in score was observed in 5% (1/22) of ,-catenin, 0% (0/22) of ,-catenin and 9% (2/22) of E-cadherin in chronic atrophic gastritis patients, and in 28% (5/18) of ,-catenin, 67% (10/15) of ,-catenin and 57% (8/14) of E-cadherin in intestinal metaplasia patients. The scoring of ,-catenin, ,-catenin and E-cadherin correlated with each other. Forty-three percent of patients had concordant changes of scores along the gastritis,adenocarcinoma sequence. There was no association between Helicobacter pylori status and E-cadherin,catenin complex expression. Conclusion: Deregulation of the E-cadherin,catenin complex was observed in the majority of precancerous lesions in patients with gastric adenocarcinoma, which has potential diagnostic and therapeutic implications. © 2003 Blackwell Publishing Asia Pty Ltd [source] Extending the reading time increases the accuracy of rapid whole blood test for diagnosis of Helicobacter pylori infectionJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2001Tseng-Shing Chen Abstract Background: To evaluate the accuracy of two rapid whole blood tests (the BM-Test Helicobacter pylori and the QuikPac IV One Step H. pylori Whole Blood Test), and compare this to a conventional quantitative ELISA test (HEL-p TEST II). Methods:Helicobacter pylori status in dyspeptic patients was assessed by culture, histology, and rapid urease tests on biopsies from the antrum and corpus. The optimal cut-off value of the reading time for the rapid blood tests was determined by using the receiver characteristics operative (ROC) curves. Results: In the 141 patients examined, 89 were infected, 51 were not infected, and one was indeterminate (only positive in either urease test or histology). Areas under ROC curves were greater in the BM-Test compared with the QuikPac IV (0.948 vs 0.840, P < 0.01), with their most appropriate cut-off reading times at 360 and 395 min, respectively, rather than 10 min as suggested by the manufacturer. The sensitivity and specificity were 94.4% and 94.1% at 360 min, and 74.2 and 96.1% at 10 min for the BM-Test; 80.9, 76.5 at 395 min and 3.4 and 100% at 10 min for the QuikPac IV. The antibody titer of the quantitative ELISA test was negatively correlated with the reaction time of the two rapid blood tests in H. pylori -infected patients (P < 0.05, r = ,0.3). Conclusions: The BM-Test is an appropriate office-based test for diagnosing H. pylori infection in Chinese patients. Extending the reading time would facilitate the readability of rapid blood tests with a resultant increase in accuracy. [source] Determination of the optimal cut-off value for the [13C]-urea breath test based on a Helicobacter pylori -specific polymerase chain reaction assayJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2 2000Haruhiko Yoshida Abstract Background: This study was conducted to determine the optimal cut-off value and breath sample collection time for the [13C]-urea breath test based on the assessment of Helicobacter pylori status with a gastric juice-based polymerase chain reaction (PCR) assay. Methods and Results: A total of 104 patients took 100 mg [13C]-urea orally and breath samples were collected at 5, 10, 20, 30 and 60 min. The increment of 13CO2: 12CO2 ratio from the baseline (,13C) was measured using a laser spectroanalyser. The PCR assay was positive in 63 and negative in 41 patients. The optimal cut-off value of ,13C was calculated for each sample collection time so that the distance from the geometric mean value among Helicobacter pylori -positive patients and that from the arithmetic mean value among negative patients were simultaneously maximized. The cut-off value of 2.7, at 20 min had the longest distance, being separated by 3.16 SD from the two mean values. Using this cut-off value, the urea breath test showed 100% specificity and 98% sensitivity for the diagnosis of Helicobacter pylori infection. [source] Chronic Atrophic Gastritis and Metachronous Gastric Cancer in Japanese Alcoholic Men With Esophageal Squamous Cell CarcinomaALCOHOLISM, Issue 5 2009Akira Yokoyama Background:, The risk of metachronous gastric cancer is high in Japanese with esophageal squamous cell carcinoma (SCC), especially in alcoholic men, suggesting a common background underlying the gastric and esophageal cancers. Methods:, Endoscopic follow-up ranging from 7 to 160 months (median, 47 months) after the initial diagnosis was performed in 99 Japanese gastric-cancer-free alcoholic men (56.8 ± 6.4 years) with esophageal SCC detected by an endoscopic screening examination. Chronic atrophic gastritis (CAG) assessed by the serum pepsinogen test and Helicobacter pylori status was compared between 90 of the 99 esophageal SCC cases and 180 age-matched Japanese gastric- and esophageal-cancer-free alcoholic men. Results:, The serum pepsinogen test showed a higher seroprevalence of severe CAG among the cases than among the age-matched controls (35.4% vs. 14.2% for H. pylori -seropositive, 71.4% vs. 7.7% for H. pylori -indeterminate, and 17.1% vs. 9.8% for H. pylori -negative, respectively; H. pylori status-adjusted p = 0.0008), whereas their H. pylori status was similar. The accelerated progression of severe CAG observed in the Japanese alcoholic men with esophageal SCC suggests the existence of common mechanisms by which both esophageal SCC and H. pylori -related severe CAG develop in this population. Metachronous gastric adenocarcinoma was diagnosed in 11 of the 99 gastric-cancer-free patients, and the cumulative rate of metachronous gastric cancer within 5 years was estimated to be 15% according to the Kaplan,Meier method. The age-adjusted hazard ratios were 7.87 (95% confidence interval: 1.43 to 43.46) and 4.84 (1.16 to 20.21), respectively, in the patients with severe CAG in comparison with those without CAG and those without severe CAG. Inactive heterozygous aldehyde dehydrogenase-2, a very strong risk factor for esophageal SCC in the alcoholics, was not associated with an increased risk of metachronous gastric cancer. Conclusions:, Accelerated development of severe CAG at least partially explained the very high frequency of development of metachronous gastric cancer in this population. [source] Gastritis OLGA-staging and gastric cancer risk: a twelve-year clinico-pathological follow-up studyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 10 2010M. RUGGE Aliment Pharmacol Ther,31, 1104,1111 Summary Background, Intestinal-type gastric cancer (GC) still ranks among the high-incidence, highly lethal malignancies. Atrophic gastritis is the cancerization field in which GC develops. The current histological reporting formats for gastritis do not include any (atrophy-based) ranking of GC risk. Aim, To test the gastritis OLGA-staging (Operative Link for Gastritis Assessment) in prognosticating neoplastic progression. Methods, Ninety-three Italian patients were followed up for more than 12 years (range: 144,204 months). Clinical examinations, pepsinogen serology, endoscopy and histology (also assessing Helicobacter pylori status) were performed both at enrolment (T1) and at the end of the follow-up (T2). Results, All invasive or intra-epithelial gastric neoplasia were consistently associated with high-risk (III/IV) OLGA stages. There was a significant inverse correlation between the mean pepsinogen ratio and the OLGA stage (test for trend; P < 0.001). OLGA-staging at T1 predicted both the OLGA stage (Kaplan,Maier log-rank test, P = 0.001) and the neoplasia at T2 (Kaplan,Maier log-rank test, P = 0.001). Conclusions, This long-term follow-up study provides the first evidence that gastritis OLGA-staging conveys relevant information on the clinico-pathological outcome of gastritis and therefore for patient management. According to OLGA-staging and H. pylori- status, gastritis patients could be confidently stratified and managed according to their different cancer risks. [source] Predictors of gastroduodenal erosions in patients taking low-dose aspirinALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2010J. HART Summary Background, Gastroduodenal ulcers are common in patients taking low-dose aspirin. However, the factors predisposing to mucosal erosions, the precursor lesions, are not well known. Aims, To examine the potential risk factors for the development of erosions in patients chronically taking low-dose aspirin. Methods, Patients included were taking aspirin 75,325 mg daily for >28 days. Exclusion criteria included use of nonsteroidal anti-inflammatory and ulcer-healing drugs. Demographic data were collected at baseline, prior to endoscopy to determine the frequency and number of erosions and Helicobacter pylori status. In those without ulcer or other exclusions, endoscopy was repeated at 3 months. Results, Fewer patients had gastric erosions if they were H. pylori +ve (48.5% vs. 66.4% in H. pylori,ve patients at baseline, P = 0.17; 40.0% vs. 64.1% at 3 months, P = 0.029). If gastric erosions were present, they were also less numerous in H. pylori +ve patients (3.61 ± 0.83 vs. 4.90 ± 0.53 at baseline, P = 0.026; 2.17 ± 0.68 vs. 5.68 ± 0.86 at 3 months, P = 0.029). There was a trend (0.1 > P > 0.05) for more gastric erosions in those taking >100 mg/day aspirin. Males had more duodenal erosions at baseline (25.2% vs. 7.5%, P = 0.016). Patient age did not affect the presence or number of erosions. H. Pylori was not significantly associated with duodenal erosion numbers. Conclusions,Helicobacter pylori infection may partially protect against low-dose aspirin-induced gastric erosions; damage to the stomach appears weakly dose-related; and older age does not increase the risk of erosions. [source] Clinical trial: factors associated with resolution of heartburn in patients with reflux oesophagitis , results from the EXPO studyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 9 2009J. LABENZ Summary Background, The ability to predict symptom response to reflux oesophagitis-healing therapy may optimize treatment decisions. Aim, To identify factors associated with heartburn resolution in patients receiving acid-suppressive therapy for reflux oesophagitis. Methods, In this multicentre, randomized, double-blind trial (EXPO; AstraZeneca study code: SH-NEG-0008), patients with endoscopically confirmed reflux oesophagitis and reflux symptoms received once-daily proton pump inhibitor therapy [esomeprazole 40 mg (n = 1562) or pantoprazole 40 mg (n = 1589)] for ,4 weeks. Factors associated with heartburn resolution after 4 weeks were identified by multiple logistic regression analysis. Results, Esomeprazole therapy, positive Helicobacter pylori status and greater age were associated with an increased likelihood of heartburn resolution [odds ratio (95% confidence interval): 1.31 (1.12, 1.54), 1.44 (1.19, 1.74) and 1.013 (1.007, 1.019) per year, respectively; all P < 0.001]. Men and patients with no acid regurgitation or epigastric pain pre-treatment were also more likely to achieve heartburn resolution (all P < 0.05). Conclusions, The use of esomeprazole rather than pantoprazole increases the probability of achieving resolution of heartburn during reflux oesophagitis-healing therapy. Other factors, including H. pylori status, age, gender and symptom profile may be helpful in determining the likelihood of heartburn resolution in such patients. [source] Symptoms in patients on long-term proton pump inhibitors: prevalence and predictorsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 4 2009A. S. RAGHUNATH Summary Background, Symptom control in primary care patients on long-term proton pump inhibitor (PPI) treatment is poorly understood. Aim, To explore associations between symptom control and demographics, lifestyle, PPI use, diagnosis and Helicobacter pylori status. Methods, A cross-sectional survey (n = 726) using note reviews, questionnaires and carbon-13 urea breath testing. Determinants of symptom control [Leeds Dyspepsia Questionnaire (LDQ), Carlsson and Dent Reflux Questionnaire (CDRQ), health-related quality-of-life measures (EuroQoL: EQ-5D and EQ-VAS)] were explored using stepwise linear regression. Results, Moderate or severe dyspepsia symptoms occurred in 61% of subjects (LDQ) and reflux symptoms in 59% (CDRQ). Age, gender, smoking and body mass index had little or no influence upon symptom control or PPI use. Average symptom scores and PPI use were lower in patients with non-ulcer dyspepsia and gastro-protection than gastro-oesophageal reflux disease (GERD) and uninvestigated dyspepsia. H. pylori infection was associated with lower reflux symptom scores only in patients with GERD and uninvestigated dyspepsia. EQ-5D was not able to discriminate between diagnostic groups, although the EQ-VAS performed well. Conclusions, A majority of patients suffered ongoing moderate or severe symptoms. GERD and uninvestigated dyspepsia were associated with poorer long-term symptom control; H. pylori appeared to have a protective effect on reflux symptoms in these patients. [source] Influence of risk factors on endoscopic and clinical ulcers in patients taking rofecoxib or ibuprofen in two randomized controlled trialsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 10 2001C. J. Hawkey Background: Highly selective inhibitors of the inducible cyclooxygenase-2 enzyme (coxibs) have been associated with less gastrotoxicity than nonselective NSAIDs in clinical studies. Aim: To evaluate the influence of risk factors for NSAID-induced gastrotoxicity on endoscopic and clinical ulcers in patients taking rofecoxib or ibuprofen. Methods: We analysed pooled data from two identical double-blind, randomized, 12-week endoscopy studies which compared the gastroduodenal toxicity of placebo (n=371), rofecoxib 25 mg (n=390), rofecoxib 50 mg (n=379), and ibuprofen 2400 mg daily (n=376) in patients with osteoarthritis. The potential risk factors evaluated were: age (< 65, , 65 years), sex, race (white, nonwhite), Helicobacter pylori status, presence of gastroduodenal erosions at baseline, a history of upper gastrointestinal disease, prior NSAID use within 30 days of study entry, and smoking. We also evaluated these factors for possible association with the development of clinically-evident gastrointestinal perforations, ulcers or bleeds over 12 weeks. Results: Across all treatment groups, the likelihood of detecting endoscopic ulcers, or of clinical presentation with a bleed, over 12 weeks was increased approximately 4,5-fold in patients with previous upper gastrointestinal disease (relative risk [95% confidence interval] of 4.2 [2.5, 7.1] for endoscopic ulcers; 3.8 [1.4, 10.6] for bleeds), or those with gastroduodenal erosions at baseline endoscopy (relative risk of 4.4 [2.6, 7.5] for endoscopic ulcers; 5.0 [1.9, 13.5] for bleeds). H. pylori infection did not increase the risk of endoscopic ulcers or bleeds (relative risk of 1.1 [0.8, 1.6] for endoscopic ulcers; 0.3 [0.1, 0.9] for bleeds). The risk factor sub-group effects were constant across all treatment groups, and the significantly higher incidence of ulcers with ibuprofen as compared to rofecoxib and placebo was maintained in all risk factor subgroups. Conclusions: Gastroduodenal erosions at baseline and a clinical history of upper gastrointestinal disease, but not H. pylori colonization, increased the risk for endoscopically-detected ulcers and clinical bleeds. Rofecoxib did not magnify the risk in any of the patient subgroups studied. [source] Diagnosis of Helicobacter pylori after triple therapy in uncomplicated duodenal ulcers,a cost-effectiveness analysisALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 4 2000Gené Background: The cost-effectiveness of determining Helicobacter pylori status after treatment remains to be established. Aim: To determine the benefit of post-treatment assessment of H. pylori eradication in patients with uncomplicated duodenal ulcer. Materials and methods: A decision analysis was performed in patients with uncomplicated duodenal ulcer who were H. pylori -positive and had received eradication therapy. A decision tree was devised to compare the costs per patient of two different strategies: (a) systematic performance of post-treatment urea breath test and new treatment if positive; and (b) clinical follow-up, 13C-urea breath test if dyspeptic symptoms recurred and eradication treatment if the test was positive. Results: Post-eradication 13C-urea breath test was notably more expensive than clinical follow-up, both in a low-cost per care setting (197 vs. 132 Euros) and in a high-cost per care (614 vs. 340 US $) scenario. This conclusion remained stable for a wide range of variations of the variables included in the decision tree (e.g. cure rates of eradication treatment, cost of the urea breath test or sensitivity, and specificity of urea breath test to detect eradication). Conclusion: In patients with uncomplicated duodenal ulcer, evaluation of eradication after H. pylori treatment markedly increases costs with no clear improvement in results and therefore should not be performed routinely. [source] U-shaped Effect of Drinking and Linear Effect of Smoking on Risk for Stomach Cancer in JapanCANCER SCIENCE, Issue 9 2002Shogo Kikuchi A case-control study was conducted to evaluate the relationship between smoking or drinking doses and risk for stomach cancer, and to clarify whether the relationship is dose-dependent or U-shaped. Smoking dose was categorized as 0,1,399, 400,799, or 800+ cigarette-years, and drinking dose as 0, occasional/0.1,134.9, 135,1349.9, or 1350+ alcohol-years (ml of pure alcohol intake per day multiplied by years of drinking). Helicobacter pylori status was determined by serology for adjustment. Using logistic regression, the adjusted effects of smoking and drinking doses on risk for stomach cancer were calculated for both genders. Among male subjects, the odds ratios (95% confidence intervals (CIs)) were 1.29 (0.76, 2.18) for 1,399, 1.71 (1.05, 2.80) for 400,799 and 2.46 (1.49, 4.07) for 800+ cigarette-years compared with never-smokers, and 1.89 (0.97, 3.69) for never-drinkers, 2.82 (1.63, 4.86) for 135,1349.9 and 2.84 (1.97, 4.83) for 1350.0+, compared with occasional/0.1,134.9 alcohol-years. Among female subjects, they were 0.44 (0.20, 1.00) for 1,399 and 2.471 (0.91, 6.68) for 400+ cigarette-years compared with never-smokers, and 1.54 (0.90, 2.63) for never-drinkers and 1.39 (0.66, 2.93) for 135.0+ alcohol-years. Smoking seems to exert a linear effect and drinking, a J- or U-shaped effect on risk for stomach cancer, although there might be a dip of risk in light smokers among female subjects. [source] | ||||||||||