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Ulcer Disease (ulcer + disease)
Kinds of Ulcer Disease Selected AbstractsA Possible Role for Gap Junctions in Generation of Very Fast EEG Oscillations Preceding the Onset of, and Perhaps Initiating, SeizuresEPILEPSIA, Issue 2 2001Roger D. Traub Summary: ,Purpose: We propose an experimentally and clinically testable hypothesis, concerning the origin of very fast (>,70 Hz) EEG oscillations that sometimes precede the onset of focal seizures. These oscillations are important, as they may play a causal role in the initiation of seizures. Methods: Subdural EEG recordings were obtained from children with focal cortical dysplasias and intractable seizures. Intra- and extracellular recordings were performed in rat hippocampal slices, with induction of population activity, as follows: (a) bath-applied tetramethylamine (an intracellular alkalinizing agent, that opens gap junctions); (b) bath-applied carbachol, a cholinergic agonist; and (c) focal pressure ejection of hypertonic K+ solution. Detailed network simulations were performed, the better to understand the cellular mechanisms underlying oscillations. A major feature of the simulations was inclusion of axon,axon gap junctions between principal neurons, as supported by recent experimental data. Results: Very fast oscillations were found in children before seizure onset, but also superimposed on bursts during the seizure, and on interictal bursts. In slice experiments, very fast oscillations had previously been seen on interictal-like bursts; we now show such oscillations before, between, and after epileptiform bursts. Very fast oscillations were also seen superimposed on gamma (30,70 Hz) oscillations induced by carbachol or hypertonic K+, and in the latter case, very fast oscillations became continuous when chemical synapses were blocked. Simulations replicate these data, when axonal gap junctions are included. Conclusions: Electrical coupling between principal neurons, perhaps via axonal gap junctions, could underlie very fast population oscillations, in seizure-prone brain, but possibly also in normal brain. The anticonvulsant potential of gap-junction blockers such as carbenoxolone, now in clinical use for treatment of ulcer disease, should be considered. [source] cagA gene variants in Malaysian Helicobacter pylori strains isolated from patients of different ethnic groupsFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2 2005Mohamed Ramelah Abstract Helicobacter pylori infection of a distinct subtype of cagA may lead to different pathological manifestation. The aim of this study is to determine the presence of cagA gene and its variants in H. pylori infection among different ethnic groups and its effect on gastroduodenal diseases. Overall detection of cagA among the 205 clinical isolates of H. pylori was 94%. Variations in size of the 3, region of cagA gene were examined among 192 Malaysian H. pylori cagA -positive strains. Results showed that three cagA variants differing in fragment length of PCR products were detected and designated as type A (621,651 bp), type B (732,735 bp) and type C (525 bp). Although there was no association between any of the cagA subtypes with peptic ulcer disease (p > 0.05), an association between cagA subtypes with a specific ethnic group was observed. Specific- cagA subtype A strains were predominantly isolated from Chinese compared to Malays and Indians (p < 0.0005), and cagA subtype B strains were predominantly isolated from Malays and Indians compared to Chinese (p < 0.05). The cagA type A strains of H. pylori is commonly found in the Chinese patients who have a higher risk of peptic ulcer disease, thus indicating that it could be used as an important clinical biomarker for a more severe infection. [source] High relative content of lysophospholipids of Helicobacter pylori mediates increased risk for ulcer diseaseFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 1 2005Tone Tannaes Abstract Helicobacter pylori phospholipase A (OMPLA) degrades bacterial membrane phospholipids to lysophospholipids. High levels of lysophospholipids are associated with higher hemolytic activity, increased release of urease and vacA and better adherence to epithelial cells in vitro. The phospholipase A gene (pldA) displays phase variation due to a slippage in a homopolymeric tract. The aim of this study was to determine if the relative amount of lysophospholipids in the cell wall is associated with ulcer disease, and to further investigate the significance of pldA phase variation. H. pylori isolates of 40 patients were examined. The relative lysophospholipid content of each isolate was determined and the pldA gene was sequenced. The study indicated that H. pylori can regulate its OMPLA activity by phase variation in the pldA gene or by protein level regulation among phase variants in the pldA,ON' status. We found a significant difference between the relative amount of lysophospholipids of the ulcer group and the non-ulcer group (p= 0.022). When the lysophospholipid/phospholipid ratios were compared with outcome, the OR for ulcer disease was 9.0 (95% CI 1.6,49.4; p= 0.014). Isolates with a high OMPLA activity are significantly associated with patients with ulcer disease. [source] The Helicobacter pylori plasticity region locus jhp0947,jhp0949 is associated with duodenal ulcer disease and interleukin-12 production in monocyte cellsFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2 2004Ramon De Jonge Abstract Colonization with Helicobacter pylori always results in chronic gastritis, which is controlled by infiltration of mononuclear cells and the subsequent release of cytokines like interleukin (IL)-12. To identify H. pylori factors involved in inducing cytokine production in mononuclear cells, a random H. pylori mutant library was screened for the inability to induce IL-12 production in monocyte THP-1 cells. Of the 231 random mutants screened, one mutant (M1) showed a consistent twofold decrease in the amount of IL-12 induction compared to the parental strain 1061 (P<0.01). Further characterization of mutant M1 revealed that the kanamycin resistance cassette had integrated in the jhp0945 gene, which is situated in an H. pylori strain-specific plasticity region. Three reference strains possessing this plasticity region induced significantly higher amounts of IL-12 when compared to the H. pylori 26695 reference strain, which does not possess this plasticity region. The role in disease outcome of jhp0945 as well as the neighbouring plasticity region genes jhp0947 and jhp049 was assessed in a Dutch population cohort. Firstly, the presence of jhp0947 was completely linked with that of jhp0949 and was roughly associated with jhp0945 (P=0.072), but not with the cag pathogenicity island (PAI) (P=0.464). The presence of the jhp0947 and jhp0949 genes, but not of jhp0945, was significantly associated with duodenal ulcer disease when compared to gastritis (P=0.027). Therefore, the jhp0947,jhp0949 locus may be a novel putative H. pylori marker for disease outcome independent of the cag PAI. [source] Role of Mucin Lewis Status in Resistance to Helicobacter pylori Infection in Pediatric PatientsHELICOBACTER, Issue 4 2010Sara Lindén Abstract Background:,Helicobacter pylori causes gastritis, peptic ulcer and is a risk factor for adenocarcinoma and lymphoma of the stomach. Gastric mucins, carrying highly diverse carbohydrate structures, present functional binding sites for H. pylori and may play a role in pathogenesis. However, little information is available regarding gastric mucin in children with and without stomach diseases. Materials and Methods:, Expression of mucins and glycosylation was studied by immunohistochemistry on gastric biopsies from 51 children with and without H. pylori infection and/or peptic ulcer disease. Results:, In all children, MUC5AC was present in the surface epithelium and MUC6 in the glands. No MUC6 in the surface epithelium or MUC2 was detected in any section. The Leb and Lea blood group antigens were present in the surface epithelium of 80% and 29% of children, respectively. H. pylori load was higher in Leb negative children than in Leb positive individuals (mean ± SEM 17.8 ± 3.5 vs 10.8 ± 1.5; p < 0.05), but there was no correlation between Lea or Leb status and gastritis, nodularity, and gastric or duodenal ulcer (DU). Expression of sialyl-Lex was associated with H. pylori infection, and DU. Conclusions:, Mucin expression and glycosylation is similar in children and adults. However, in contrast to adults, pediatric H. pylori infection is not accompanied by aberrant expression of MUC6 or MUC2. Furthermore, the lower H. pylori density in Leb positive children indicates that H. pylori is suppressed in the presence of gastric mucins decorated with Leb, the binding site of the H. pylori BabA adhesin. [source] High Level of Antimicrobial Resistance in French Helicobacter pylori IsolatesHELICOBACTER, Issue 1 2010Josette Raymond Abstract Background: Helicobacter pylori is a human pathogen responsible for serious diseases including peptic ulcer disease and gastric cancer. The recommended triple therapy included clarithromycin but increasing resistance has undermined its effectiveness. It is therefore important to be aware of the local prevalence of antimicrobial resistance to adjust treatment strategy. Materials and Methods: Overall, 530 biopsies were collected between 2004 and 2007. The antimicrobial susceptibility of H. pylori was determined by E-test and molecular methods. Results: Among these, 138/530 (26%) strains were resistant to clarithromycin, 324/530 (61%) to metronidazole and 70/530 (13.2%) to ciprofloxacin. Whereas no resistance against amoxicillin and tetracycline was observed, only one strain was resistant to rifampicin. Compared to the patients never treated for H. pylori infection, the prevalence of resistance was significantly higher in patients previously treated (19.1% vs 68% for clarithromycin; 13.2% vs 53.3% for both clarithromycin and metronidazole). The trend analysis revealed an increase of primary resistance to ciprofloxacin between 2004 and 2005 (7.3%) vs 2006,2007 (14.1%) (p = .04) and the secondary resistance reached 22.7% in 2007. Interestingly, 27 biopsies (19.6%) contained a double population of clarithromycin-susceptible and -resistant strains. Conclusions: The reported high prevalence of clarithromycin and multiple resistances of H. pylori suggest that the empiric therapy with clarithromycin should be abandoned as no longer pretreatment susceptibility testing has assessed the susceptibility of the strain. As culture and antibiogram are not routinely performable in most clinical laboratories, the use of molecular test should be developed to allow a wide availability of pretreatment susceptibility testing. [source] Four Modes of Adhesion are Used During Helicobacter pylori Binding to Human Mucins in the Oral and Gastric NichesHELICOBACTER, Issue 2 2008Sara K. Lindén Abstract Background:,Helicobacter pylori causes peptic ulcer disease and gastric cancer, and the oral cavity is likely to serve as a reservoir for this pathogen. We investigated the binding of H. pylori to the mucins covering the mucosal surfaces in the niches along the oral to gastric infection route and during gastric disease and modeled the outcome of these interactions. Materials and Methods:, A panel of seven H. pylori strains with defined binding properties was used to identify binding to human mucins from saliva, gastric juice, cardia, corpus, and antrum of healthy stomachs and of stomachs affected by gastritis at pH 7.4 and 3.0 using a microtiter-based method. Results:,H. pylori binding to mucins differed substantially with the anatomic site, mucin type, pH, gastritis status, and H. pylori strain all having effect on binding. Mucins from saliva and gastric juice displayed the most diverse binding patterns, involving four modes of H. pylori adhesion and the MUC5B, MUC7, and MUC5AC mucins as well as the salivary agglutinin. Binding occurred via the blood-group antigen-binding adhesin (BabA), the sialic acid-binding adhesin (SabA), a charge/low pH-dependent mechanism, and a novel saliva-binding adhesin. In the healthy gastric mucus layer only BabA and acid/charge affect binding to the mucins, whereas in gastritis, the BabA/Leb -dependent binding to MUC5AC remained, and SabA and low pH binding increased. Conclusions:, The four H. pylori adhesion modes binding to mucins are likely to play different roles during colonization of the oral to gastric niches and during long-term infection. [source] Molecular Epidemiology and Outcome of Helicobacter pylori Infection in Thailand: a Cultural Cross RoadsHELICOBACTER, Issue 5 2004Ratha-Korn Vilaichone ABSTRACT Background., Thailand is at the cultural cross roads between East and South Asia. It has been suggested that this is also the region where the predominant Helicobacter pylori (H. pylori) genotype changes from East Asian to South Asian. Methods., We compared the molecular epidemiology and outcome of H. pylori infections among different ethnic groups in Thailand (Thai, Thai-Chinese and Chinese). H. pylori isolates were genotyped by polymerase chain reaction based on cagA, cag right end junction and vacA genotypes. Results., Ninety-eight isolates from 38 ethnic Thai, 20 ethnic Chinese and 40 Thai-Chinese were categorized into East Asian (45%), South/Central Asian (26%), Western (1%) or mixed type (29%). The East Asian genotype was the most common among Chinese (85%) and Thai-Chinese (55%) (p < .01 compared to ethnic Thai). The ethnicity of the mother among mixed Thai-Chinese marriages predicted the genotype of the child's H. pylori (e.g. when the mother was Chinese, 84% had East Asian type vs. 29% when the mother was Thai) (p < .001). Gastric cancer was common among ethnic Chinese with East Asian genotype (e.g. all Chinese with gastric cancer or peptic ulcer disease had East Asian genotype, whereas only 40% of Chinese with gastritis had this genotype). Conclusions., Immigration, intermarriage and the variety of H. pylori genotypes in Thailand suggest that Thailand is an ideal site for epidemiological studies attempting to relate H. pylori genotypes and host factors to outcome. Our data also support the hypothesis that the primary caretaker of the children is most likely the source of the infection. [source] Improvement of Reflux Symptoms 3 Years After Cure of Helicobacter pylori Infection: A Case-Controlled Study in the Japanese PopulationHELICOBACTER, Issue 4 2002Hiroto Miwa Abstract Background. Development of reflux esophagitis is one of the adverse effects that cause concern in relation to curative treatment of Helicobacter pylori infection. However, recent studies present a rather negative association between curative treatment and development of reflux esophagitis or reflux symptoms. Therefore, this issue has remained controversial. Accordingly, we investigated the long-term adverse effects of H. pylori eradication treatment in special reference to development of reflux symptoms. Patients and Methods. We conducted a case controlled study by mailing structured questionnaires on past (before curative treatment or 3 years previously) and current status. A case was an endoscopically confirmed peptic ulcer patient with confirmed cure of the infection after eradication treatment 3 years previously and a control was one who had not undergone the eradication treatment during the same period. We studied 241 pairs who matched for age, gender, and type of ulcer disease (GU, DU or GDU). Of these pairs, 81.3% were male and the mean age was 52.6 ± 9.6 year (range 23,76). Results. The rates of patients with improved reflux symptoms in the case and control groups were 65.4% and 30.4%, respectively, with the rate being significantly greater in the case group. On the contrary, the rates of those with worsened reflux symptoms were similar (5.1% and 7.6%). Regarding general events, the rate of patients with decreased frequency of hospital visits and of those who regularly used antiacid medications were significantly decreased in the case group. Furthermore, the case group experienced significantly fewer hospital admissions for various diseases in this 3-year period. However, a significantly greater number of case group patients than control subjects gained weight. Conclusion. Reflux symptoms as well as general well-being were significantly improved after cure of H. pylori infection. [source] Is Eradication of Helicobacter pylori With Colloidal Bismuth Subcitrate Quadruple Therapy Safe?HELICOBACTER, Issue 2 2001Rosemary H. Phillips ABSTRACT Background. When standard triple therapy fails to eradicate Helicobacter pylori, quadruple ,rescue' therapy is often used which, in Europe, generally comprises colloidal bismuth subcitrate (CBS) based triple therapy and a proton pump inhibitor. Since hypochlorhydria could greatly increase absorption of the toxic bismuth ion from CBS, we investigated the bismuth status of patients receiving anti- H. pylori quadruple therapy. Materials and Methods. In a prospective open label study 34 patients with nonulcer dyspepsia or peptic ulcer disease, who had failed to eradicate H. pylori with standard triple therapy, were subsequently treated with CBS, omeprazole, amoxycillin and metronidazole (BOAM). A further 35 patients received triple therapy for the eradication of H. pylori: CBS, amoxycillin and metronidazole (BAM) (n = 18); placebo bismuth, amoxycillin and metronidazole (AM) (n = 9); or omeprazole, amoxycillin and metronidazole (OAM) (n = 8). Whole blood bismuth levels were determined before and within 24 hours of completing treatment. Analysis of bismuth was by inductively coupled plasma mass spectrometry, and concentrations were compared between groups and with the Hillemand ,alarm level' for blood bismuth (50,100 µg/l). Results. BOAM gave higher blood bismuth levels than BAM (difference in means 13.1, CI 6.0,20.2, p < .001); three (8.8%) patients taking BOAM had concentrations within the Hillemand alarm level at 54.2, 64.7 and 91.8 µg/l. OAM and AM did not alter baseline blood bismuth levels. Conclusions. Caution should be observed in prescribing CBS with gastric acid suppression, and alternative bismuth preparations should be considered. [source] Negative Association Between Helicobacter pylori Infection and Reflux Esophagitis in Older Patients: Case-Control Study in JapanHELICOBACTER, Issue 1 2000Ken Haruma Background. Recent studies have clarified a close association between H. pylori infection and gastritis, peptic ulcer disease, and gastric cancer, but there is little information concerning the relationship between H. pylori infection and reflux esophagitis (RE). We investigated the relationship between H. pylori, RE, and corpus gastritis. Subjects and Methods. Ninety-five patients with RE and 190 sex- and age-matched asymptomatic healthy controls demonstrating no localized lesions in the upper GI tract were studied and evaluated for H. pylori infection, histologic gastritis, serum gastrin, and pepsinogens (PGs). Results.H. pylori infection was significantly lower in RE patients than in asymptomatic controls (41% vs. 76%, p < .01). Histologic gastritis of both the antrum and corpus was significantly less frequent (antrum; p < .01, corpus; p < .01), and serum levels of PGI and the PG I/II ratio were significantly higher in RE patients than in controls (PGI; p < .05, PG I/II ratio; p < .01). When the subjects were divided into two age groups (59 years of age and younger and 60 years of age and older), a significant difference was found only among patients over 60 years of age (29% vs. 85%, p < .01). Among subjects in this age group, gastritis in both the antrum and corpus were significantly milder in RE patients than in controls. Although the prevalence of H. pylori infection was similar between the two groups of patients under 59 years of age, corpus gastritis was significantly milder in patients than in controls (p < .05). Conclusions. A significantly low prevalence of H. pylori infection was found in RE patients over 60 years of age but not in those under 59 in comparison with sex- and age-matched controls. The relative lack of corpus gastritis might play a role in the pathogenesis of RE in our population through preservation of the acid secretion area. [source] Disease-specific Helicobacter pylori Virulence Factors: The Unfulfilled PromiseHELICOBACTER, Issue S1 2000David Y. Graham A number of putative virulence factors for Helicobacter pylori have been identified including cagA, vacA and iceA. The criteria for a true virulence factor includes meeting the tests of biologically plausibility with the associations being both experimentally and epidemiologically consistent. Although disease-specific associations have been hypothesized/claimed, there are now sufficient data to conclusively state that none of these putative virulence factors have disease specificity. CagA has been claimed to be associated with increased mucosal IL-8 and inflammation, increased density of H. pylori in the antrum, duodenal ulcer (DU), gastric cancer, and protection against Barrett's cancer. Only the increase in IL-8/inflammation is direct and substantiated. Different H. pylori strains with functional cag pathogenicity islands do not vary in virulance as it has been shown that mucosal IL-8 levels are proportional to the number of cagA +H. pylori independent of the disease from which the H. pylori were obtained. It is now known that the density of either cagA + and cagA,H. pylori in the antrum of patients with H. pylori gastritis is the same. In contrast, the mean density of H. pylori in the antrum in DU is greater than in the antrum of patients with H. pylori gastritis. Of interest, the density of H. pylori is higher in the corpus of patients with H. pylori gastritis than those with DU, suggesting that acid secretion plays a critical role in these phenomena. The presence of a functional cag pathogenicity island increases inflammation and it is likely that any factor that results in an increase in inflammation also increases the risk of a symptomatic outcome. Nevertheless, the presence of a functional cag pathogenicity island has no predictive value for the presence, or the future development of a clinically significant outcome. The hypothesis that iceA has disease specificity has not been confirmed and there is currently no known biological or epidemiological evidence for a role for iceA as a virulence factor in H. pylori -related disease. The claim that vacA genotyping might prove clinically useful, e.g. to predict presentation such as duodenal ulcer, has been proven wrong. Analysis of the worldwide data show that vacA genotype s1 is actually a surrogate for the cag pathogenicity island. There is now evidence to suggest that virulence is a host-dependent factor. The pattern of gastritis has withstood the test of time for its relation to different H. pylori -related diseases (e.g. antral predominant gastritis with duodenal ulcer disease). The primary factors responsible for the different patterns of gastritis in response to an H. pylori infection are environmental (e.g. diet), with the H. pylori strain playing a lesser role. Future studies should work to eliminate potential bias before claiming disease associations. Controls must exclude regional or geographic associations related to the common strain circulation and not to the outcome. The authors must also control for both the presence of the factor and for the disease association. The study should be sufficiently large and employ different diseases and ethnic groups for the results to be robust. The findings in the initial sample (data derived hypothesis) should be tested in a new group (hypothesis testing), preferably from another area, before making claims. Finally, it is important to ask whether the results are actually a surrogate for another marker (e.g. vacA s1 for cagA) masquerading for a new finding. Only the cag pathogenicity island has passed the tests of biological plausibility (increased inflammation) and experimental and epidemiological consistency. [source] Should Non-Invasive Helicobacter pylori Testing Replace Endoscopy in Investigation of Dyspepsia?HELICOBACTER, Issue S1 2000Kenneth McColl Our knowledge of Helicobacter pylori infection is now changing the way in which we investigate patients presenting with dyspepsia, with noninvasive H. pylori testing replacing endoscopy. Non-invasive H. pylori testing has been shown to be useful in predicting the underlying diagnosis in patients presenting with dyspepsia. Several studies have shown that 20,50% of dyspeptic patients with a positive H. pylori test will have evidence of underlying ulcer disease or duodenitis. In contrast, less than 5% of dyspeptic patients with a negative H. pylori test will have evidence of ulcer disease and in these subjects, the likeliest diagnosis is gastroesophageal reflux disease. This has led to many groups recommending that noninvasive H. pylori testing should be used in place of endoscopy, with all those testing positive being given anti- H. pylori therapy and those testing negative being treated symptomatically. One concern about nonendoscopic management of dyspeptic patients is the possibility of missing underlying malignancy but studies have shown that in western countries this is rare in patients less than 55 years of age presenting with dyspepsia in the absence of sinister symptoms. There is increasing evidence supporting eradication of H. pylori infection in dyspeptic patients without ulcer disease. Meta-analysis of four prospective randomized trials indicates that such treatment is superior to placebo in about 10% of subjects. H. pylori -positive dyspeptic patients are also recognized to have an increased risk of developing ulcer disease in the future which will be removed by treating the infection. Another justification for eradicating the infection in the absence of ulcer disease is the fact that H. pylori infection is now proven to be a risk factor for gastric cancer. Prospective randomized studies comparing endoscopy with noninvasive H. pylori testing in the management of dyspeptic patients indicate that managing dyspepsia by noninvasive H. pylori testing is at least as effective as endoscopic-based management in producing symptomatic resolution and saves a substantial number of endoscopic procedures. There is therefore now substantial evidence indicating that noninvasive H. pylori testing should be used in place of endoscopy to determine the management of younger dyspeptic patients without sinister symptoms and who are not taking nonsteroidal anti-inflammatory drugs. [source] The risk of pancreatic cancer in patients with gastric or duodenal ulcer diseaseINTERNATIONAL JOURNAL OF CANCER, Issue 2 2007Juhua Luo Abstract Although Helicobacter pylori (H. pylori) seropositivity is linked to an excess risk of pancreatic cancer, the biologic mechanism is unknown. Gastric ulcer is primarily associated with corpus colonization of H. pylori, atrophic gastritis and formation of N -nitrosamines. Duodenal ulcer is a marker of antral colonization, hyperacidity and uninhibited secretin release. We estimated relative risks for pancreatic cancer among patients with gastric or duodenal ulcer, based on a register-based retrospective cohort study with 88,338 patients hospitalized for gastric ulcer and 70,516 patients for duodenal ulcer recorded in the Swedish Inpatient Register between 1965 and 2003. Following operation, the 14,887 patients who underwent gastric resection and 8,205 with vagotomy were analyzed separately. Multiple record-linkages allowed complete follow-up and identification of all incident cases of pancreatic cancer until December 31, 2003. Standardized incidence ratios (SIRs) estimated relative risks. During years 3,38 of follow-up, we observed a 20% excess risk (95% confidence interval [CI] 10,40%) for pancreatic cancer among unoperated gastric ulcer patients. The excess increased to 50% (95% CI 10,110%) 15 years after first hospitalization (p for trend = 0.03). SIR was 2.1 (95% CI 1.4,3.1) 20 years after gastric resection. Unoperated duodenal ulcer was not associated with pancreatic cancer risk, nor was vagotomy. Our results lend indirect support to the nitrosamine hypothesis, but not to the hyperacidity hypothesis in the etiology of pancreatic cancer. © 2006 Wiley-Liss, Inc. [source] Unspecified abdominal pain in primary care: the role of gastrointestinal morbidityINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 10 2007M.-A. Wallander Summary Background:, Many patients with abdominal pain have no obvious cause for their symptoms and receive a diagnosis of unspecified abdominal pain. Aim:, The objective of this study was to ascertain risk factors and consequences of a diagnosis of unspecified abdominal pain in primary care. Methods:, A population-based, case,control study was conducted using the UK General Practice Research Database. We identified 29,299 patients with a new diagnosis of abdominal pain, and 30,000 age- and sex-matched controls. Only diagnostic codes that did not specify the type or location of abdominal pain were included. Results and discussion:, The incidence of newly diagnosed unspecified abdominal pain was 22.3 per 1000 person-years. The incidence was higher in females than in males, and 29% of patients were below 20 years of age. Prior gastrointestinal morbidity was associated with abdominal pain, but high body mass index, smoking and alcohol intake were not. Patients newly diagnosed with abdominal pain were 16 to 27 times more likely than controls to receive a subsequent new diagnosis of gallbladder disease, diverticular disease, pancreatitis or appendicitis in the year after the diagnosis of abdominal pain. The likelihood of receiving other gastrointestinal diagnoses such as peptic ulcer disease, hiatus hernia, gastro-oesophageal reflux disease (GERD), irritable bowel syndrome (IBS) or dyspepsia was increased three- to 14-fold among patients consulting for abdominal pain. Conclusion:, When managing abdominal pain in primary care, morbidities such as GERD and IBS should be considered as diagnoses once potentially life-threatening problems have been excluded. [source] Changing epidemiology of Helicobacter pylori in AsiaJOURNAL OF DIGESTIVE DISEASES, Issue 4 2008Huck J TAN As in developed societies, the prevalence of Helicobacter pylori has declined rapidly in Asia. This has been shown in both seroprevalence-based and endoscopy-based studies. While the decline in the incidence of gastric cancer has now been observed, a decrease in peptic ulcer disease has not been so clearly evident. This apparent paradox can be explained by an increase in non- H. pylori associated ulcers , such as those related to non-steroidal anti-inflammatory drugs or idiopathic ulcers. The increase of gastroesophageal reflux disease in Asia has been widely observed and commented on and its relationship to the decline in H. pylori speculated upon. However there have been few conclusive studies from Asia on this subject. While the improved diagnosis and elimination of H. pylori has contributed to its decline, a more basic change involving large segments of the Asian population must be responsible. An improvement in hygiene and living conditions that results from more affluent Asian societies is thought to be a possible cause. [source] Phytoceuticals: Mighty but ignored weapons against Helicobacter pylori infectionJOURNAL OF DIGESTIVE DISEASES, Issue 3 2008Sun-Young LEE Helicobacter pylori (H. pylori) infection causes peptic ulcer disease, mucosa-associated lymphoid tissue (MALT) lymphomas and gastric adenocarcinomas, for which the pathogenesis of chronic gastric inflammation prevails and provides the pathogenic basis. Since the role of H. pylori infection is promoting carcinogenesis rather than acting as a direct carcinogen, as several publications show, eradication alone cannot be the right answer for preventing H. pylori -associated gastric cancer. Therefore, a non-antimicrobial approach has been suggested to attain microbe-associated cancer prevention through controlling H. pylori -related chronic inflammatory processes and mediators responsible for carcinogenesis. Phytoceutical is a term for plant products that are active on biological systems. Phytoceuticals such as Korean red ginseng, green tea, red wine, flavonoids, broccoli sprouts, garlic, probiotics and flavonoids are known to inhibit H. pylori colonization, decrease gastric inflammation by inhibiting cytokine and chemokine release, and repress precancerous changes by inhibiting nuclear factor-kappa B DNA binding, inducing profuse levels of apoptosis and inhibiting mutagenesis. Even though further unsolved issues are awaited before phytoceuticals are accepted as a standard treatment for H. pylori infection, phytoceuticals can be a mighty weapon for either suppressing or modulating the disease-associated footprints of H. pylori infection. [source] Changing trends in gastrointestinal disease in the Asia,Pacific regionJOURNAL OF DIGESTIVE DISEASES, Issue 4 2007KL GOH The new millennium has seen distinct changes in the pattern of gastrointestinal disease in the Asia,Pacific region. These changes are important as more than half of the world's population come from the region and therefore impact significantly on the global disease burden. The highest incidence of gastric cancer (GCA) has been reported from Asia and GCA remains a very important cancer. However time-trend studies have shown a decrease in GCA incidence in several countries in Asia. A rise in cardio-esophageal cancers as seen in the West has not been reported. On the other hand, colorectal cancer has been steadily increasing in Asia with age-standardized incidence rates of some countries approaching that of the West. The pattern of acid-related diseases has also changed. Gastroesophageal reflux disease is a fast emerging disease with an increasing prevalence of reflux esophagitis and reflux symptoms. The prevalence of peptic ulcer disease has at the same time declined in step with a decrease in H. pylori infection. Many of the changes taking place mirror the Western experience of several decades ago. Astute observation of the epidemiology of emerging diseases combined with good scientific work will allow a clearer understanding of the key processes underlying these changes. With rapid modernization, lifestyle changes have been blamed for an increase in several diseases including gastroesophageal reflux disease, nonalcoholic fatty liver disease and colorectal cancer. A worrying trend has been the increase in obesity among Asians, which has been associated with an increase in metabolic diseases and various gastrointestinal cancers. Conversely, an improvement in living conditions has been closely linked to the decrease in GCA and H. pylori prevalence. [source] Construction and identification of a recombinant live attenuated Salmonella typhimurium vaccine strain carrying Helicobacter pylori heat shock protein subunit B geneJOURNAL OF DIGESTIVE DISEASES, Issue 4 2003Guo Qing LI OBJECTIVE: Because Helicobacter pylori is the principal cause of chronic active gastritis and peptic ulcer disease, the present study explored the possibility of constructing a recombinant live attenuated S. typhimurium vaccine strain carrying H. pylori heat shock protein subunit B (HspB) gene. METHODS: A 1640-bp HspB gene was cloned into a prokaryotic expression plasmid pTrc99A. After sequence analysis, the result was compared with the sequence of H. pylori -HspB gene and protein provided by the Genebank using BLAST analysis. The identified recombinant plasmid was then introduced into a live attenuated S. typhimurium strain SL3261. RESULTS: Using polymerase chain reaction (PCR) and restriction enzyme digestion, a recombinant prokaryotic expression plasmid pTrc99A-HspB harboring the HspB gene was constructed and successfully introduced into a live attenuated S. typhimurium strain SL3261. Most of the H. pylori -HspB in the recombinant plasmid pTrc99A-HspB was consistent with the H. pylori -HspB sequence provided by the Genebank. The exchange of A/T or C/G in the cloned sequence hardly changed the encoded amino acids; the homology for both the genes and proteins of H. pylori SS1 strain was 97%; the homology with other common H. pylori strains J99 and 26695 was 96% for both. CONCLUSION: A recombinant live attenuated S. typhimurium vaccine strain harboring H. pylori -HspB gene was successfully constructed and verified, which may help in the development of an oral vaccine against H. pylori infection. [source] Geographical difference in antimicrobial resistance pattern of Helicobacter pylori clinical isolates from Indian patients: Multicentric studyJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2003SP THYAGARAJAN Abstract Aim:, To assess the pattern of antimicrobial resistance of Helicobacter pylori isolates from peptic ulcer disease patients of Chandigarh, Delhi, Lucknow, Hyderabad and Chennai in India, and to recommend an updated anti- H. pylori treatment regimen to be used in these areas. Methods:, Two hundred and fifty-nine H. pylori isolates from patients with peptic ulcer disease reporting for clinical management to the Post Graduate Institute of Medical Education and Research, Chandigarh; All India Institute of Medical Sciences, New Delhi; Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow; Deccan College of Medical Sciences and Allied Hospitals, Hyderabad; and hospitals in Chennai in collaboration with the Dr ALM Post Graduate Institute of Basic Medical Sciences were analyzed for their levels of antibiotic susceptibility to metronidazole, clarithromycin, amoxycillin, ciprofloxacin and tetracycline. The Epsilometer test (E-test), a quantitative disc diffusion antibiotic susceptibility testing method, was adopted in all the centers. The pattern of single and multiple resistance at the respective centers and at the national level were analyzed. Results:, Overall H. pylori resistance rate was 77.9% to metronidazole, 44.7% to clarithromycin and 32.8% to amoxycillin. Multiple resistance was seen in 112/259 isolates (43.2%) and these were two/three and four drug resistance pattern to metronidazole, clarithromycin, amoxycillin observed (13.2, 32 and 2.56%, respectively). Metronidazole resistance was high in Lucknow, Chennai and Hyderabad (68, 88.2 and 100%, respectively) and moderate in Delhi (37.5%) and Chandigarh (38.2%). Ciprofloxacin and tetracycline resistance was the least, ranging from 1.0 to 4%. Conclusion:, In the Indian population, the prevalence of resistance of H. pylori is very high to metronidazole, moderate to clarithromycin and amoxycillin and low to ciprofloxacin and tetracycline. The rate of resistance was higher in southern India than in northern India. The E-test emerges as a reliable quantitative antibiotic susceptibility test. A change in antibiotic policy to provide scope for rotation of antibiotics in the treatment of H. pylori in India is a public health emergency. [source] Risk of gastric cancer is not increased after partial gastrectomyJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 7 2000R Bassily Abstract Background: It has been suggested that there is an increased risk of gastric cancer following partial gastrectomy. This question has not been studied in an Australian population. Methods: The records of a total of 569 patients who had a partial gastrectomy for peptic ulcer disease at Repatriation General Hospital, Heidelberg, between 1957 and 1976 were reviewed. All were followed to date of death or 31 December 1996. The expected rate of gastric cancer for this population was estimated from published Australian age-and sex-specific gastric cancer mortality rates over this period, and a standardized incidence ratio was calculated. Results: The mean age at surgery was 53.5 years (range 27,83 years). There were 547 male (96.4%) and 22 female (3.6%) patients. Five hundred and seven (83.5%) had a Billroth II procedure. Thirty-eight patients (6.3%) were lost to follow up and were not included in the analysis. From the records of the Department of Veterans' Affairs, it was established that 125 (20.6%) were alive in December 1996, a mean survival after surgery of 18.8 years. The mean documented duration of follow up was 17.3 years (range 1,41 years). Nine patients developed cancer in the gastric remnant. The expected number of cancers in this population was 6.5. Assuming all survivors were free of gastric cancer, the standardized incidence ratio was 1.39 (95% confidence intervals 0.64,2.65, P = 0.313). Conclusion: The risk of gastric cancer was not increased after partial gastrectomy in this Australian population. [source] Prospective peer-review audit of paediatric upper gastrointestinal endoscopyJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 7-8 2007Edward V O'Loughlin Aim: To describe the findings of paediatric upper gastrointestinal endoscopy (UGE) and to reduce the rate of normal findings in children undergoing diagnostic UGE. Methods: Upper gastrointestinal endoscopy were performed at a single tertiary referral children's hospital over a 3-year period by four endoscopists. Patients were subgrouped into diagnostic categories (recurrent abdominal pain syndrome (RAP), oesophagitis, coeliac disease and enteropathy/inflammatory bowel disease) and endoscopists recorded their clinical diagnosis as above before each procedure. Endoscopic and biopsy findings were compared with clinical diagnosis. After the first year of audit each endoscopist was appraised of their practice and strategies implemented to reduce the normal UGE. In years 2 and 3 all endoscopists were audited by their peers on a monthly basis. Results: A total of 1172 UGE were performed over a 3-year period. Ninety per cent were diagnostic procedures, of which 48% were normal, 16% identified oesophagitis, 11% coeliac disease, 6% gastritis, 3%Helicobacter pylori and 1% peptic ulcer disease. Peer-review audit significantly reduced the number of normal findings in coeliac disease, RAP and overall (P < 0.01) but not in the groups with presumed oesophagitis or investigation of enteropathy/inflammatory bowel disease. Conclusions: A high proportion of patients undergoing UGE have normal procedures. Peer-review audit can reduce the number of normal procedures particularly in RAP and in the diagnosis of coeliac disease. [source] Dyspepsia and irritable bowel syndrome in China: a population-based endoscopy study of prevalence and impactALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 4 2010Y. Zhao Aliment Pharmacol Ther 2010; 32: 562,572 Summary Background, Dyspepsia and irritable bowel syndrome (IBS) are common in Western populations. Aim, To determine the epidemiology of dyspepsia and IBS in China. Methods, A representative sample of 18 000 adults from five regions of China were asked to complete the modified Rome II questionnaire; 20% were asked to complete the 36-item Short Form Health Survey (SF-36). Participants from Shanghai were invited to provide blood samples and undergo oesophagogastroduodenoscopy. Odds ratios (ORs) and 95% confidence intervals (CIs) were determined using a multivariate logistic regression model. Results, The survey was completed by 16 091 individuals (response rate: 89.4%). Overall, 387 participants (2.4%) had dyspepsia and 735 (4.6%) had IBS. All SF-36 dimension scores were at least five points lower in individuals with than without dyspepsia or IBS (P , 0.001). In Shanghai, 1030 (32.7%) of the 3153 respondents agreed to endoscopy; neither dyspepsia nor IBS was found to be associated with reflux oesophagitis, peptic ulcer disease or Helicobacter pylori infection. Conclusions, Prevalence estimates for dyspepsia and IBS in China are lower than in Western populations. In China, dyspepsia or IBS symptoms are generally not associated with underlying organic disease. [source] Clinical trial: prolonged beneficial effect of Helicobacter pylori eradication on dyspepsia consultations , the Bristol Helicobacter ProjectALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2010R. F. Harvey Aliment Pharmacol Ther 2010; 32: 394,400 Summary Background, Chronic infection of the stomach with Helicobacter pylori is widespread throughout the world and is the major cause of peptic ulcer disease and gastric cancer. Short-term benefit results from community programmes to eradicate the infection, but there is little information on cumulative long-term benefit. Aim, To determine whether a community programme of screening for and eradication of H. pylori infection produces further benefit after an initial 2-year period, as judged by a reduction in GP consultations for dyspepsia. Methods, A total of 1517 people aged 20,59 years, who were registered with seven general practices in Frenchay Health District, Bristol, had a positive 13C-urea breath test for H. pylori infection and were entered into a randomized double-blind trial of H. pylori eradication therapy. After 2 years, we found a 35% reduction in GP consultations for dyspepsia (previously reported). In this extension to the study, we analysed dyspepsia consultations between two and 7 years after treatment. Results, Between two and 7 years after treatment, 81/764 (10.6%) of participants randomized to receive active treatment consulted for dyspepsia, compared with 106/753 (14.1%) of those who received placebo, a 25% reduction, odds ratio 0.84 (0.71, 1.00), P = 0.042. Conclusions, Eradication of H. pylori infection in the community gives cumulative long-term benefit, with a continued reduction in the development of dyspepsia severe enough to require a consultation with a general practitioner up to at least 7 years. The cost savings resulting from this aspect of a community H. pylori eradication programme, in addition to the other theoretical benefits, make such programmes worthy of serious consideration, particularly in populations with a high prevalence of H. pylori infection. [source] Review article: Helicobacter pylori -negative duodenal ulcer diseaseALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2009J. P. GISBERT Aliment Pharmacol Ther,30, 791,815 Summary Background,Helicobacter pylori infection rates in duodenal ulcer (DU) patients may be lower than previously estimated. Aim, To review the real prevalence of H. pylori -negative DUs and its possible causes. Methods, Bibliographical searches in MEDLINE looking for the terms ,H. pylori' and ,duodenal ulcer'. Results, Mean prevalence of H. pylori infection in DU disease, calculated from studies published during the last 10 years including a total of 16 080 patients, was 81%, and this figure was lower (77%) when only the last 5 years were considered. Associations with H. pylori -negative DU were: (1) False negative results of diagnostic methods, (2) NSAID use (21% in studies with <90% infection rate), (3) Complicated DU (bleeding, obstruction, perforation), (4) Smoking, (5) Isolated H. pylori duodenal colonization, (6) Older age, (7) Gastric hypersecretion, (8) Diseases of the duodenal mucosa, (9) Helicobacter,heilmanii' infection and (10) Concomitant diseases. Conclusion, In patients with H. pylori -negative DU disease, one should carefully confirm that the assessment of H. pylori status is reliable. In truly H. pylori -negative patients, the most common single cause of DU is, by far, the use of NSAIDs. Ulcers not associated with H. pylori, NSAIDs or other obvious causes should, for the present, be viewed as ,idiopathic'. True idiopathic DU disease only exceptionally exists. [source] Bleeding peptic ulcer , time trends in incidence, treatment and mortality in SwedenALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 4 2009J. SADIC Summary Background, The incidence of peptic ulcer disease was expected to decrease following the introduction of acid inhibitors and Helicobacter pylori eradication. Aim, To analyse possible changes in the incidence of bleeding peptic ulcer, treatment and mortality over time. Methods, Residents of Malmö hospitalized for bleeding gastric or duodenal ulcer disease during 1987,2004 were identified in hospital databases (n = 1610). The material was divided into 6-year periods to identify changes over time. All patients who had been submitted to emergency surgery (n = 137) were reviewed. Results, The incidence rate for bleeding gastric or duodenal ulcers decreased by one half in males and by one-third in females and emergency operations decreased significantly (9.2%, 7.5% and 5.7% during the three time periods, respectively (P < 0.05). The post-operative mortality tended to decrease (9.7, 2.4 and 3.7%, respectively) and the 30-day mortality rates in the whole material were 1.2%, 3.6% and 3.4% during the different time periods. Conclusion, The incidence of bleeding gastric and duodenal ulcer disease has decreased markedly. Operative treatment has been replaced by endoscopic treatment. The bleeding ulcer-related mortality was less than 4% and has not changed over time. [source] Systematic review: the global incidence and prevalence of peptic ulcer diseaseALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 9 2009J. J. Y. SUNG Summary Background, Peptic ulcer disease (PUD) is most commonly associated with Helicobacter pylori infection and the use of acetylsalicylic acid (ASA) and nonsteroidal anti-inflammatory drugs (NSAIDs). The management of H. pylori infection has improved radically in recent years; however, the prescription of ASA and NSAIDs has increased over the same period. Aim, To evaluate the current global incidence and prevalence of PUD by systematic review of the literature published over the last decade. Methods, Systematic searches of PubMed, EMBASE and the Cochrane library. Results, The annual incidence rates of PUD were 0.10,0.19% for physician-diagnosed PUD and 0.03,0.17% when based on hospitalization data. The 1-year prevalence based on physician diagnosis was 0.12,1.50% and that based on hospitalization data was 0.10,0.19%. The majority of studies reported a decrease in the incidence or prevalence of PUD over time. Conclusions, Peptic ulcer disease remains a common condition, although reported incidence and prevalence are decreasing. This decrease may be due to a decrease in H. pylori -associated PUD. [source] Systematic review: the epidemiology of gastro-oesophageal reflux disease in primary care, using the UK General Practice Research DatabaseALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 5 2009H. EL-SERAG Summary Background, Gastro-oesophageal reflux disease (GERD) is a common diagnosis in primary care; however, there has been no comprehensive review of the epidemiology of GERD in this setting. Aim, To review systematically articles that used the General Practice Research Database to study the epidemiology of GERD. Methods, Systematic literature searches. Results, Seventeen articles fulfilled the inclusion criteria. The incidence of GERD in primary care was 4.5 new diagnoses per 1000 person-years in 1996 (95% CI: 4.4,4.7). A new diagnosis of GERD was associated with being overweight, obese or an ex-smoker. Prior diagnoses of ischaemic heart disease, peptic ulcer disease, nonspecific chest pain, nonspecific abdominal pain, chronic obstructive pulmonary disease and asthma were associated with a subsequent new GERD diagnosis. A first diagnosis of GERD was associated with an increased risk of a subsequent diagnosis of oesophageal adenocarcinoma, oesophageal stricture, chronic cough, sinusitis, chest pain, angina, gallbladder disease, irritable bowel syndrome or sleep problems. Mortality may be higher in patients with a GERD diagnosis than in those without in the first year after diagnosis, but not long term. Conclusion, The General Practice Research Database is an effective way of studying the epidemiology of GERD in a large population-based primary care setting. [source] Recurrence of peptic ulcer in uraemic and non-uraemic patients after Helicobacter pylori eradication: a 2-year studyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2007G.-Y. TSENG Summary Background The role of Helicobacter pylori in the pathogenesis of peptic ulcer disease in patients with uraemia remains unclear. Aim To evaluate the long-term effect of H. pylori eradication in these patients. Methods Uraemic and non-uraemic patients with peptic ulcer were enrolled in this study. Patients having history of non-steroidal anti-inflammatory drugs use or cardiovascular disease that need aspirin use were excluded. After confirmation of H. pylori infection, they received a triple therapy and were followed up for 2 years. Results Between September 1999 and December 2005, 34 patients (41%) of the end-stage renal disease [H. pylori (+) group] and 67 (84%) of the non-uraemic patients with peptic ulcer disease (PU group) received anti- H. pylori therapy. After triple therapy, 32 (94%) from the end-stage renal disease group and 64 (96%) from the peptic ulcer group obtained successful eradication. During the 2-year follow-up, three patients in the end-stage renal disease group were excluded because of the presence of cardiovascular disease and aspirin use in two cases and died of heart failure in one case; two patients in peptic ulcer group refused follow-up. Finally, 29 uraemic and 62 non-uraemic patients had achieved the follow-up. Recurrence of peptic ulcer was more in the end-stage renal disease group than in the peptic ulcer group with intention-to-treat analysis (eight of 32, 25% vs. two of 64, 3%, P = 0.001, OR: 10.0, 95% CI: 1.979,50.540) or per-protocol analysis (eight of 29, 28% vs. two of 62, 3%, P < 0.001, OR: 11.4, 95% CI: 2.245,58.168). Conclusions Peptic ulcer recurrence after H. pylori eradication is higher in end-stage renal disease patients with peptic ulcer than in peptic ulcer patients without renal disease. Factors aside from H. pylori play an important role in peptic ulcer recurrence in end-stage renal disease patients. [source] Review article: From gastrin to gastro-oesophageal reflux disease , a century of acid suppressionALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2006P. MALFERTHEINER Summary To commemorate Edkins' discovery of gastrin in 1905, we review a century of progress in the physiology and pathobiology of gastrin and acid secretion especially as it pertains to clinical aspects of gastro-oesophageal reflux disease. Although initially ignored, Edkins' observations eventually led to the enthusiastic investigation of gastrin and acid regulation in peptic ulcer disease, culminating in important therapeutic advances in the management of acid peptic disease. Following the improved understanding of gastric secretory physiology, and the development of acid suppressants with increasing efficacy, the use of surgical intervention for peptic ulcer disease was almost eliminated. Surgery became obsolete with the discovery of Helicobacter pylori. Three other advances are also influencing modern practice: the gastrotoxicity of aspirin and non-steroidal anti-inflammatory drugs is now increasingly appreciated, the role of endoscopy in the diagnosis and therapy of upper gastrointestinal bleeding, and the use of intravenous acid-suppressive agents. The major issue for the future resides within the epidemic of gastro-oesophageal reflux disease. How to diagnose, categorize and treat this condition and how to identify and prevent neoplasia, are the challenges of the new century. [source] | ||||||||||||||||||||||||||||