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Background: Genetic factors related to DNA repair or xenobiotic pathways might confer different degrees of susceptibility to Helicobacter pylori (H. pylori)-related gastric carcinogenesis. The association between XRCC1 Arg399Gln, and Arg194Trp, GSTP1 Ile104Val, and GSTT1, GSTM1 null polymorphisms with gastric intestinal metaplasia, severity of histological gastritis, and peptic ulcer diseases were evaluated in a Japanese population., Patients and Methods: XRCC1 Arg399Gln and Arg194Trp, GSTP1 Ile104Val and GSTT1, GSTM1 null polymorphisms were genotyped in 280 cancer-free individuals, including 52 gastric and 31 duodenal ulcer patients., Results: Among the five polymorphisms, a significant association between the GSTT1 and GSTM1 null genotypes and increased risk of intestinal metaplasia was found (GSTT1 null: OR=2.42, 95% CI=1.28-4.60, p=0.007, GSTM1 null: OR=2.18, 95% CI=1.15-4.13, p=0.019). When the severity of gastric atrophy was classified into the following three groups: non-atrophy (NA) (atrophy score=0 and metaplasia score=0); severe atrophy (SA) (atrophy score≥2 or metaplasia score≥2) and mild atrophy (MA) (all others), both the GSTT1 and GSTM1 null genotypes held significantly higher risk for developing more severe gastric atrophy (GSTT1 null, SA vs. others: OR=1.95, 95% CI=1.07-3.52, p=0.028, GSTM1 null, NA vs. others: OR=2.57, 95% CI=1.16-5.67, p=0.019, SA vs. others: OR=1.90, 95% CI=1.06-3.42, p=0.032). A significant association was also found between GSTM1 null genotype and increased risk of ulcer diseases (all ulcers: OR=2.42, 95% CI=1.37-4.26, p=0.002, gastric ulcer: OR=2.18, 95% CI=1.11-4.29, p=0.025, duodenal ulcer: OR=2.62, 95% CI=1.15-6.00, p=0.023)., Conclusion: Both the GSTT1 and GSTM1 null genotypes are associated with gastric pre-malignant conditions.

Background: Helicobacter pylori infection is one of the most common infections worldwide and is associated with gastric cancer and peptic ulcer. Bacterial virulence factors such as CagA have been shown to increase the risk of both diseases. Studies have suggested a causal role for CagA EPIYA polymorphisms in gastric carcinogenesis, and it has been shown to be geographically diverse. We studied associations between H. pylori CagA EPIYA patterns and gastric cancer and duodenal ulcer, in an ethnically admixed Western population from Brazil. CagA EPIYA was determined by PCR and confirmed by sequencing. A total of 436 patients were included, being 188 with gastric cancer, 112 with duodenal ulcer and 136 with gastritis., Results: The number of EPIYA C segments was significantly associated with the increased risk of gastric carcinoma (OR=3.08, 95% CI=1.74 to 5.45, p<10-3) even after adjustment for age and gender. Higher number of EPIYA C segments was also associated with gastric atrophy (p=0.04) and intestinal metaplasia (p=0.007). Furthermore, patients infected by cagA strains possessing more than one EPIYA C segment showed decreased serum levels of pepsinogen I in comparison with those infected by strains containing one or less EPIYA C repeat. Otherwise, the number of EPIYA C segments did not associate with duodenal ulcer., Conclusions: Our results demonstrate that infection with H. pylori strains harbouring more than one CagA EPIYA C motif was clearly associated with gastric cancer, but not with duodenal ulcer.Higher number of EPIYA C segments was also associated with gastric precancerous lesions as demonstrated by histological gastric atrophic and metaplastic changes and decreased serum levels of pepsinogen I., (© 2011 Batista et al; licensee BioMed Central Ltd.)

Background and Aim: The distributions and grades of Helicobacter pylori induced gastritis are known to vary among H. pylori-associated diseases. The aim of this study was to investigate the differences in distributions of gastric micromucosal structures observed by magnifying narrow band imaging (NBI) endoscopy among patients with different H. pylori-associated diseases., Methods: Ninety-five patients with active duodenal ulcers (n = 24) and diffuse-type (n = 24) and intestinal-type (n = 47) early gastric cancers were enrolled. The magnified NBI findings were evaluated at the lesser and greater curvatures in the upper gastric corpus and were classified according to the modified A-B classification system. Biopsy specimens were also evaluated., Results: In a total of 190 areas observed with magnifying NBI, histological grading (inflammation, activity, atrophy and intestinal metaplasia) showed significant differences among the classified micromucosal patterns (P < 0.001). Types B-1 and B-2, with mild atrophic changes and few areas of intestinal metaplasia, were seen mostly in the duodenal ulcers group. Types B-3 and A-1, with moderate atrophic changes, were seen in the diffuse-type early gastric cancers at the lesser curvature. Types A-1 and A-2, with severe atrophic change and a high frequency of intestinal metaplasia, were seen in the intestinal-type early gastric cancers at the lesser curvature. The prevalence of micromucosal structures differed significantly among the three groups both at the lesser and greater curvatures (P < 0.001)., Conclusions: Magnifying NBI endoscopy clearly revealed detailed micromorphological differences corresponding to the histology and endoscopic findings among patients with different H. pylori-associated diseases., (© 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd.)

The dupA of Helicobacter pylori has been suggested as a virulence marker associated with the development of duodenal ulcer disease. However, the studies performed in different geographical areas have shown that there are variations in the prevalence of dupA and its association with H. pylori clinical outcomes. Our group did not observe associations between the presence of dupA and H. pylori clinical outcomes in Brazil. On the other hand, we observed 2 mutations in the sequence of dupA that lead to stop codons: a deletion of an adenine at position 1311 and an insertion of an adenine at position 1426 of the gene. Our aim was to evaluate associations of the presence of dupA with duodenal ulcer and gastric cancer, considering dupA-positive only those H. pylori strains that do not have the mutations in the gene sequence. We also evaluated the effect of infection with a strain carrying an intact dupA on the gastric mucosa histology and IL-8 gastric levels. Colonization with strains that had the intact dupA was negatively associated with gastric carcinoma (p=0.001, OR=0.32, 95% CI=0.16-0.66). The presence of dupA was also associated with an increased degree of antral mucosa inflammation (p=0.01) and with decreased corpus atrophy (p<0.01) as well as with increased gastric mucosa IL-8 levels (p=0.04). In conclusion, the infection with a H. pylori strain containing the dupA without the stop codon polymorphisms is associated with a lower risk of development of gastric carcinoma in Brazilian subjects., (Copyright © 2010 Elsevier GmbH. All rights reserved.)

Interleukin-8 (IL-8) plays a central role in the pathogenesis of Helicobacter pylori infection. We used four different H. pylori strains isolated from patients with gastritis or duodenal ulcer disease to examine their differential effects on signaling pathways and IL-8 gene response in gastric epithelial cells. IL-8 mRNA level is elevated in response to high (100) multiplicity of infection (MOI) independent of cagA, vacA, and dupA gene characteristics. By lower MOIs (1 or 10), only cagA ( + ) strains significantly induce IL-8 gene expression. This is based on differential regulation of IL-8 promoter activity. Analysis of intracellular signaling pathways indicates that H. pylori clinical isolates induce IL-8 gene transcription through NF-κB p65, but by a MOI-dependent differential activation of MAPK pathways. Thus, the major virulence factors of H. pylori CagA, VacA, and DupA might play a minor role in the level of IL-8 gene response to a high bacterial load.

Unlabelled: Studying role of duodenogastric reflux (DGR) in pathogenesis and sanogenesis of duodenal ulcer (DU)., Material and Methods: 233 DU patients (92 patients with a mild, 45--with modern and 96--with the complicated current of disease) are surveyed. Control group were 100 healthy volunteers. Clinical research, endoscopy and 24-hours pH-metria was carried out. In a year after eradication Helicobacter pylori (Hp) 30 patients are repeatedly surveyed., Results: at healthy acidity more low, and DGR above and more for a long time, than at DU patients. DU was especially supressed at complicated current DU. Eradication Hp was accompanied by acidity normalization only at mild DU, and at complicated DU--is not present., Conclusion: at healthy people DGR arises in reply to antrum's acidification and has compensative value, and at DU there is the considerable suppression leading to insufficiency of antrum's alkalization. After eradication Hp normalization DGR is marked only at mild current DU.

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.

Helicobacter pylori, discovered 27 years ago, has remained the most prevalent infectious agent in the world. In the author's hypothesis, the increase of peptic ulcer prevalence in the 19-20th century could be attributable to the extended worldwide use of gastric tubes for secretory testing which led to the iatrogenic transmission of pathogenic strains. Helicobacter pylori outer membrane proteins (OMP), and duodenal ulcer promoting (dupA) proteins were identified as novel virulence factors, leading to the production of pro-inflammatory cytokines, which could be future targets of therapy. There is no ideal first-line eradication of the infection and according to expert's opinion, the efficiency of these regimens has fallen gradually in recent years to unacceptably low levels; however, in the author's opinion this is a multifactorial phenomenon which can not be generalized. As alternative drugs, the efficiency of levofloxacin, furazolidone and rifabutin has been proven by meta-analyses. Sequential and bismuth-free quadruple therapies, although highly efficient, are not yet used on a large scale. The recurrence of the infection is 2.27%/year in developed and of 13.0%/year in developing countries. Spontaneous eradication occurred in 8-20% of the children and 5-11% of adults. The prevalence of clarithromycin resistance is increasing worldwide. In Hungary, it has reached 10.9% in county cities, according to a national survey. In a district of Budapest called Ferencváros, the prevalence between 2005 and 2009 was 16-22%, with no increasing trend. The development of enzymatic inhibitors (urease, carbonic anhydrase and gamma-glutamyl transpeptidase), modified antibiotics and efflux pump inhibitors seem promising ways because these compounds do not lead to resistance; however, none have yet been used in humans.

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.)

Helicobacter pylori is a genetically diverse and coevolved pathogen inhabiting human gastric niches and leading to a spectrum of gastric diseases in susceptible populations. We describe the genome sequence of H. pylori 908, which was originally isolated from an African patient living in France who suffered with recrudescent duodenal ulcer disease. The strain was found to be phylogenetically related to H. pylori J99, and its comparative analysis revealed several specific genome features and novel insertion-deletion and substitution events. The genome sequence revealed several strain-specific deletions and/or gain of genes exclusively present in HP908 compared with different sequenced genomes already available in the public domain. Comparative and functional genomics of HP908 and its subclones will be important in understanding genomic plasticity and the capacity to colonize and persist in a changing host environment.

Introduction: The scheme proton pump inhibitor/amoxicillin/clarithromycin (PPI/AC) is still the first-line treatment for Helicobacter pylori (H. pylori) infections despite evidence suggesting its failure in up to 20% to 30% of patients., Methodology: This study involved 493 patients who were prescribed omeprazole (20 mg twice a day) or another proton pump inhibitor in equivalent dosage, amoxicillin (1 g twice a day), and clarithromycin (500 mg twice a day) for seven days. Efficacy was determined by negative urease test and absence of H. pylori on gastric biopsy samples twelve weeks after the end of treatment. Safety was defined according to the adverse effects reported. Mean age of the patients was (± SD) 48.96 ± 13, and demographic and clinical data were recorded for correlation with treatment outcomes., Results: Out of 493 patients, 316 (64.1%) presented duodenal ulcer, 111 (22.5%) gastric ulcer, and 66 (14.4%) simultaneous gastric and duodenal ulcers. Additionally, 267 (54.2%) patients had at least one risk factor for peptic ulcer disease, smoking being the most common (99 [36.5%]). Successful eradication was achieved in 408 patients. The eradication rates per protocol, and according to the intention to treat, were 88.8% and 82.7%, respectively.  Of 164 (35.5%) patients who presented adverse effects, 100 (61%) reported them as mild and only six (3.7%) patients had to discontinue treatment. Previous use of tobacco and non-steroid anti-inflammatory drugs was the only risk factor for treatment failure (P = 0.00)., Conclusion: PPI/AC is still a valuable and remarkably tolerable option for first-line H. pylori eradication in Brazil.

Helicobacter pylori plays an essential role in the development of various gastroduodenal diseases; however, only a small proportion of people infected with H. pylori develop these diseases. Some populations that have a high prevalence of H. pylori infection also have a high incidence of gastric cancer (for example, in East Asia), whereas others do not (for example, in Africa and South Asia). Even within East Asia, the incidence of gastric cancer varies (decreasing in the south). H. pylori is a highly heterogeneous bacterium and its virulence varies geographically. Geographic differences in the incidence of gastric cancer can be explained, at least in part, by the presence of different types of H. pylori virulence factor, especially CagA, VacA and OipA. However, it is still unclear why the pathogenicity of H. pylori increased as it migrated from Africa to East Asia during the course of evolution. H. pylori infection is also thought to be involved in the development of duodenal ulcer, which is at the opposite end of the disease spectrum to gastric cancer. This discrepancy can be explained in part by the presence of H. pylori virulence factor DupA. Despite advances in our understanding of the development of H. pylori-related diseases, further work is required to clarify the roles of H. pylori virulence factors.

Article presents the results of medical treatment after peptic ulcer surgery. I group--59 patients with late complications after peptic ulcer surgery and II group--16 patients with complications of peptic ulcer disease, operated in presence of absolute indications. 13C-UBT and RUT of biopsy material were used to diagnose Hp infection. Hp positive patients received antibacterial treatment. After 1 month from the end of therapy and 1 year after Hp eradication control investigations by 13C-UBT and endoscopy were performed. 77.3% of all and 84.4% of early non treated patients were Hp positive. All patients (of I and II gr.), who followed control testing after antibacterial treatment were finally detected as Hp negative. In I group, control endoscopy revealed epitelization or scarring of ulcer and reduction of inflammatory changes in gastric and duodenal mucosa in all 44 cases of eradication of Hp infection (in 2 patients with peptic ulcer of GEA ulcer relapsed in later). In II group, in 8 patients, who received antibacterial treatment additionally to surgical method, any late complications after surgery were not revealed. In other 6 Hp positive patients: 2--ulcer recurrence and 2--development of chronic gastritis of operated stomach were noted, which required the treatment of Hp infection in future. It is concluded that 1)surgery does not change Hp-status of patients and Hp infection retains in more than 80% of cases; 2) ulcer recurrence, chronic gastritis of operated stomach or its stump are associated with Hp and regress after Hp eradication; 3) progression of gastritis into atrophic remain after surgery, which increases risk of cancer development and there is possibility of its regression after antibacterial treatment of Hp infection. The recommendations were worked out: 1) perforated, bleeding or stenosing ulcer must be treated only by ulceroraphy, suturing or pyloroplasty respectively, added with subsequent Hp eradication therapy for the prevention of late complications after peptic ulcer surgery; 2) vagotomy or partial gastrectomy must be a forced intervention in cases of decompensate pylorostenosis, resistant to treatment ulcers, as ulcers non-healing or recurring after adequate conservative treatment. Subsequent verification and eradication of Hp infection are necessary.

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.

Background and Aim: The aim of this study is to determine the incidence of Helicobacter pylori (H. pylori) in patients operated on for duodenal ulcer perforation and to evaluate the late results of a simple closure technique in patients positive and negative for H. pylori., Methods: The data of 84 patients who underwent simple closure for duodenal ulcer between 2003-2007 were retrospectively studied. Antral biopsy material taken from all patients during laparotomy was studied with the rapid urease test and the patients were then separated into 2 groups. Group 1 (H. Pylori positive) received postoperative H. pylori eradication treatment, and Group 2 (H. pylori negative) received only lansaprasol treatment after surgery. All patients were evaluated with upper gastrointestinal endoscopy on the 6th and 14th postoperative weeks. Primary treatment failure was considered in patients who had non-healing ulcers after 14 weeks. Patients with healed ulcers were scheduled for annual examinations. The results were compared between the groups., Results: The rate of H. pylori infection in duodenal ulcer perforation was found to be 80.9%. Ulcer healing rates on the postoperative 6th and 14th weeks were 88.2% and 97.5% in the first group, and 68.8% and 81.2% in the second group, respectively. Mean postoperative follow-up was 41.28 +/- 17.63 (range 17-73) months. Ulcer recurrence rate was found to be 4.54% in Group 1 and 30.76% in group 2 (p = 0.012)., Conclusions: All patients with a perforated peptic ulcer should be treated with simple closure of the perforation followed by medical therapy aimed at healing the ulcer. We believe that H. pylori negative patients have more risk of recurrence and such patients require close postoperative follow-up.

Aim: To investigate Helicobacter pylori (H. pylori) CagA diversity and to evaluate the association between protein polymorphisms and the occurrence of gastric pathologies., Methods: One hundred and twenty-two clinical isolates of H. pylori cultured from gastric biopsies obtained from Colombian patients with dyspepsia were included as study material. DNA extracted from isolates was used to determine cagA status, amplifying the C-terminal cagA gene region by polymerase chain reaction. One hundred and six strains with a single amplicon were sequenced and results were used to characterize the 3' variable region of the cagA gene. To establish the number and type of tyrosine phosphorylation motifs Glutamine acid-Proline-Isoleucine-Tyrosine-Alanine (EPIYA) bioinformatic analysis using Amino Acid Sequence Analyzer-Amino Acid Sequence Analyzer software was conducted. Analysis of the association between the number of EPIYA motifs and the gastric pathology was performed using chi(2) test and analysis of the presence of EPIYA-C motifs in relation to the pathology was made by logistic regression odds ratios. Comparisons among EPIYA types found and those reported in GenBank were performed using a proportion test in Statistix Analytical Software version 8.0., Results: After amplification of the 3' of the cagA gene, 106 from 122 isolates presented a single amplicon and 16 showed multiple amplicons. As expected, diversity in the size of the cagA unique fragments among isolates was observed. The 106 strains that presented a single amplicon after 3' cagA amplification came from patients with gastritis (19 patients), atrophic gastritis (21), intestinal metaplasia (26), duodenal ulcer (22) and gastric cancer. DNA sequence analysis showed that the differences in size of 3' cagA unique fragments was attributable to the number of EPIYA motifs: 1.9% had two EPIYA motifs, 62.3% had three, 33.0% had four and 2.8% had five motifs. The majority of tested clinical strains (62.3%) were found to harbor the ABC combination of EPIYA motifs and a significant statistical difference was observed between the frequencies of ABCC tyrosine phosphorylation motifs and Western strains sequences deposited in GenBank., Conclusion: The present report describes a lack of association between H. pylori CagA-protein polymorphisms and pathogenesis. ABCC high frequency variations compared with Western-strains sequences deposited in GenBank require more investigation.

Background: This study investigated if the H. pylori dupA genotype and certain host single nucleotide polymorphisms (SNPs) of matrix metalloproteinases (MMPs) and their inhibitors (TIMPs), including MMP-3, MMP-7, MMP-9, TIMP-1 and TIMP-2, might correlate with ulcer risk of H. pylori-infected Taiwanese patients., Results: Of the 549 H. pylori-infected patients enrolled, 470 patients (265 with gastritis, 118 with duodenal ulcer, and 87 with gastric ulcer) received SNPs analysis of MMP-3-1612 6A > 5A, MMP-7-181 A > G, MMP-9exon 6 A > G, TIMP-1372 T > C and TIMP-2-418 G > C by PCR-RFLP. The 181 collected H. pylori isolates were detected for the dupA genotype by PCR. The rates of dupA-positive H. pylori infection were similar among patients with duodenal ulcer (22.8%), gastric ulcer (20.0%), and gastritis (25.5%) (p > 0.05). Males had higher rates of duodenal ulcer and gastric ulcer than females (p < 0.01). Of H. pylori-infected patients, the MMP-3 6A6A genotype were more common in patients with duodenal ulcers than in those with gastritis (87.7% vs. 74.9%, p < 0.05) in females. This genotype had a 2.4-fold (95% CI: 1.02-5.66) increased risk of duodenal ulcer, compared to those with the 5A carrier. Combining the MMP-3/TIMP-1 genotype as 6A6A/CC, the risk of duodenal ulcer increased up to 3.6 fold (p < 0.05) in H. pylori-infected females., Conclusions: The MMP-3 promoter polymorphism, but not the dupA-status, may correlate with susceptibility to duodenal ulcer after H. pylori infection in Taiwanese females.

Background: Gastric (GU) and duodenal ulcers (DU) are in most instances either induced by Helicobacter pylori infection or by nonsteroidal anti-inflammatory drugs (NSAIDs). Whether eradication of H. pylori is beneficial in NSAID users for preventing NSAID induced GU and DU has been the focus of different studies., Materials and Methods: Mechanisms shared by both H. pylori and NSAIDs for the induction of GU and DU were reviewed and randomized controlled trials on H. pylori eradication for prevention and healing of GU and DU in patients requiring NSAID therapy were identified by a PubMed search., Results: Key factors in the induction of GU and DU for both H. pylori and NSAIDs are a decrease in pH, imbalance between apoptosis and proliferation, reduction in mucosal blood flow, and recruitment of polymorphonucleates in distinct compartments. For primary ulcer prevention, H. pylori eradication before starting an NSAID therapy reduces the risk of NSAID induced GU and virtually abolishes the risk of DU. H. pylori eradication alone is not sufficient for secondary prevention of NSAID induced GU and DU. H. pylori infection appears to further increase the protective effects of proton-pump inhibitors (PPI) to reduce the risk of ulcer relapse. H. pylori eradication does not influence the healing of both GU and DU if NSAID intake is discontinued., Conclusions: Duodenal ulcer is more closely related to H. pylori infection than GU in NSAID users. H. pylori eradication is recommended for primary prevention of GU and DU in patients requiring NSAID therapy. PPI therapy is mandatory for secondary prevention of gastroduodenal ulcers, and appears to further reduce the risk of ulcer relapse in the presence of H. pylori.

Background: Helicobacter pylori infection is associated with several gastro-duodenal inflammatory diseases of various levels of severity. To determine whether certain combinations of genetic markers can be used to predict the clinical source of the infection, we analyzed well documented and geographically homogenous clinical isolates using a comparative genomics approach., Results: A set of 254 H. pylori genes was used to perform array-based comparative genomic hybridization among 120 French H. pylori strains associated with chronic gastritis (n = 33), duodenal ulcers (n = 27), intestinal metaplasia (n = 17) or gastric extra-nodal marginal zone B-cell MALT lymphoma (n = 43). Hierarchical cluster analyses of the DNA hybridization values allowed us to identify a homogeneous subpopulation of strains that clustered exclusively with cagPAI minus MALT lymphoma isolates. The genome sequence of B38, a representative of this MALT lymphoma strain-cluster, was completed, fully annotated, and compared with the six previously released H. pylori genomes (i.e. J99, 26695, HPAG1, P12, G27 and Shi470). B38 has the smallest H. pylori genome described thus far (1,576,758 base pairs containing 1,528 CDSs); it contains the vacAs2m2 allele and lacks the genes encoding the major virulence factors (absence of cagPAI, babB, babC, sabB, and homB). Comparative genomics led to the identification of very few sequences that are unique to the B38 strain (9 intact CDSs and 7 pseudogenes). Pair-wise genomic synteny comparisons between B38 and the 6 H. pylori sequenced genomes revealed an almost complete co-linearity, never seen before between the genomes of strain Shi470 (a Peruvian isolate) and B38., Conclusion: These isolates are deprived of the main H. pylori virulence factors characterized previously, but are nonetheless associated with gastric neoplasia.

Background: Many drugs increase the risk for gastroduodenal ulcer bleeding. The aim of this study was to investigate Helicobacter pylori infection and drug use in patients who had gastroduodenal ulcer bleeding in 2002 or 2007, and possible differences between the periods., Material and Methods: Patients with gastroduodenal ulcer bleeding were prospectively included in the periods 1.1 - 31.12. 2002 and 1.1 - 31.12. 2007. Information was recorded about Helicobacter pylori infection and intake of NSAIDs (non steroidal anti-inflammatory drugs), acetylsalicylic acid, warfarin, clopidogrel, low-molecular heparine, SSRIs (selective serotonin reuptake inhibitors), corticosteroids, paracetamol and proton pump inhibitors. Inhabitants in Oslo age >or= 60 years in 2007, were used as a control for drug use., Results: 78.2 % of patients in 2002 and 90.7 % of those in 2007 used at least one of the drugs (p = 0.01). In 2002, 25.7 % of patients used non-selective NSAIDs and in 2007 46.1 % used such drugs (p = 0.001). In 2002, 36.7 % of patients used more than one of the studied drugs, versus 50.9 % in 2007 (p = 0.02). Compared to controls, the patients used more NSAIDs, acetylsalicylic acid, clopidogrel, low- molecular heparine, SSRIs and corticosteroids. Helicobacter pylori infection was diagnosed in 51.0 % of patients in 2002, versus 41.1 % in 2007 (p = 0.11)., Interpretation: Most patients with gastroduodenal ulcer bleeding use drugs that have a known risk of adverse effects such as ulcer and/or gastrointestinal bleeding.

Background and Aim: The prevalence of Helicobacter pylori-negative duodenal ulcer (DU) is increasing in Western countries but is rare in Japan. We aimed to examine the prevalence of H. pylori infection and the characteristics in DU and gastro-duodenal ulcer (GDU) diseases in Taiwan., Study: All patients with an endoscopic diagnosis of DU or GDU from September 2003 to May 2004 at Taipei Veterans General Hospital were included. Rapid urease test was done for all patients, while urea breath test was carried out on those with negative rapid urease tests. A patient was considered infected if either test was positive., Results: The prevalence of H. pylori was 88.7% (555/626) in DU and 90.5% (95/105) in GDU patients. There was no difference in sex and prevalence of H. pylori between the two groups but age was higher in the GDU patients (60.1 +/- 15.5 vs. 55.4 +/- 15.5, P = 0.005). Of H. pylori-negative DU patients, 28.2% (20/71) reported using non-steroidal anti-inflammatory drugs (NSAIDs)/aspirin, which were used by all 10 H. pylori-negative GDU patients (100%) (P < 0.001). There was no difference in sex and age between H. pylori-positive and negative DU patients. The prevalence rate of H. pylori in DU was not statistically different among outpatients, inpatients, and physical check-up subjects (86.8% vs. 93.3% vs. 90.7%, P = 0.163)., Conclusion: The prevalence of H. pylori infection in DU appears to be decreasing in Taiwan. Thus, eradication therapy without confirming the presence of H. pylori in DU patients cannot be recommended. NSAIDs/aspirin is the major risk factor for H. pylori-negative DU patients, especially those with co-morbid gastric ulcer.

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.

Complex examination and surgical treatment, using various organ-preserving operations, was done in 54 patients, suffering recurrent postoperative complicated duodenal ulcers. Performance of pathogenetically unsatisfactory volume of the first operation, technical faults, absence of pathogenetically substantiated therapy in postoperative period had constituted the causes of unsatisfactory results of the first operation. Reconstructive organ preserving intervention, consisting of impact on all chains of recurrent ulcerogenesis, with subsequent pathogenetically substantiated rehabilitation of patients, were consider the operation of choice.

Introduction: It is now well established that Helicobacter pylori eradication can significantly modify the natural history of peptic ulcer disease. The aim of this study was to assess the frequency of duodenal ulcer among patients endoscopically examined for dyspeptic symptoms and analyse the disease time trend during two ten-year long distinctive retrospective periods (1987-2006)., Material and Methods: Data were obtained through retrospective analysis of outpatients upper endoscopy reports. Full reports were available for 58,515 patients which were analysed for selected clinicopathological features in two clearly defined time periods. The first one, starting from 1987 to 1996 in which Helicobacter pylori infection was not assessed and treated accordingly and the second period from 1997 to 2006 during which the presence of Helicobacter pylori infection in certain diseases was routinely assessed and then treated with PPI based triple therapy., Results: Symptoms of dyspepsia appeared to be approximately the same as the indication for endoscopy in both periods (65.1%:63.3%). The frequency of duodenal ulcer disease significantly decreased in the second period of analysis (t=14761; p < 0.01). In both periods men had more often duodenal ulcer comparing to women (chi2 = 218.53, p < 0.01; chi2 = 21.7, p < 0.01). During the second examined period the number of women who had duodenal ulcer significantly increased comparing to the first ten-year period (chi2=17232; p < 0.01)., Conclusion: The test-and-treat strategy and the implementation of consensus on diagnosis and treatment of Helicobacter pylori infection resuited in a significant decrease in the frequency of duodenal ulcer disease.

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.

Background and Aim: Gastroduodenal disease is more common among adults and children with cagA+ Helicobacter pylori infection, but disease severity varies among those infected with cagA+ strains. We examined whether cagA in situ expression can predict disease manifestations among H pylori-infected children., Patients and Methods: Fifty-one children were selected from 805 patients with abdominal symptoms who underwent esophagogastroduodenoscopy with gastric biopsies. Endoscopic and histologic gastritis were scored and H pylori colonization was quantified by Genta stain and in situ hybridization expression of 16S rRNA and cagA., Results: Endoscopy was either normal (n = 14) or demonstrated nodularity (n = 18), gastric ulcer (n = 8) or duodenal ulcer (n = 11). H pylori was present in 7, 18, 6, and 10 children, respectively. Expression of 16S rRNA and cagA were significantly higher in children with ulcer compared with normal children. The fraction of H pylori bacteria expressing cagA in situ was higher in children with ulcer compared to those with endoscopic nodularity (P < 0.05)., Conclusions: Thus, cagA in situ expression is increased in H pylori-infected children with peptic ulcers and may play a role in the pathogenesis of peptic ulcer disease during childhood. Determination of in situ expression of cagA complements traditional isolation and in vitro testing of single-colony isolates.

Background/aim: Resistance to metronidazole is one of the most common reasons for Helicobacter pylori treatment failure with the classic triple therapy. The clarithromycin-based regimen is not cost-effective for use in developing countries. Though furazolidone is a great substitute it has many side effects. Decreasing the duration of treatment with furazolidone to 1 week may help decrease the drug's side effects., Aim: To study the efficacy and side effects of furazolidone when given for 1 week in combination with bismuth subcitrate, amoxicillin, and omeprazole., Materials and Methods: One hundred and seventy-seven patients with duodenal ulcer were randomly divided into two groups. Group I received omeprazole 2 Chi 20 mg + amoxicillin 2 Chi 1 g + bismuth subcitrate 4 Chi 120 mg for 2 weeks, with furazolidone 2 Chi 200 mg in the first week only. Group II received the same regimen, except that 1 week of furazolidone was followed by 1 week of metronidazole in the second week. Control endoscopy was performed after 6 weeks. Three biopsies from the antrum and three from the corpus were taken for urease testing and histology. Eradication was concluded if all tests were negative for H pylori., Results: One hundred and fifty-seven patients completed the study. Two subjects from group I and three from group II did not tolerate the regimen and were excluded from the analysis. No serious complication was detected in any patient. The eradication rates by per-protocol (PP) analysis and intention-to-treat (ITT) analysis were 89% and 79.3% in group I and 86.6% and 74.4% in group II, respectively., Conclusion: One week of furazolidone in combination with 2 weeks of amoxicillin, omeprazole, and bismuth subcitrate is a safe and cost-effective regimen for the eradication of H pylori. Adding metronidazole to the above regimen does not increase the eradication rate.

Helicobacter pylori putative virulence factors can undergo a continuously evolving mechanism as an approach to bacterial adaptation to the host changing environment during chronic infection. oipA, vacA and dupA genetic diversity among isolates from multiple biopsies (niches) from the antrum and corpus of 40 patients was investigated. A set of 229 isolates was examined. Direct DNA sequence analysis of amplified fragments was used to study oipA 'on/off' expression status as well as the presence of C or T insertion in jhp0917 that originates a continuous (jhp0917-jhp0918) dupA gene. vacA alleles were identified by multiplex PCR. Different inter-niches oipA CT repeat patterns were observed in nine patients; in six of these, 'on' and 'off' mixed patterns were found. In three of these nine patients, different vacA alleles were also observed in a single host. Inter-niche dupA differences involved the absence and presence of jhp0917 and/or jhp0918 or mutations in dupA, including those that may originate a non-functional gene, and they were also present in two patients with mixed oipA CT patterns and in another seven patients. Evidence of mixed infection was observed in two patients only. In conclusion, oipA and dupA genes showed similar inter-niche variability, occurring in approximately 1/4 patients. Conversely, vacA allele microevolution seemed to be a less common event, occurring in approximately 1/10 patients, probably due to the mechanism that this gene evolves 'in vivo'.

Unlabelled: The aim was to study the relationship duodenogastral reflux (DGR) and Helicobacterpylori infection (Hp) at duodenal ulcer (DU)., Material and Methods: Group 1-50 patients with uncomplicated course of DU, Group 2-75 patients with destructive complications of DU; Group 3-40 "healthy" volunteers. It was performed daily EGDS, pH meter, semi-quantitative assessment of contamination of the Hp., Results: The acidity in the body of the stomach was highest in group 2, and lowest--in group 3, patients diagnosed DU night rush giperatsidnosti. In the night period patients from the 1st and 3rd groups were recorded an increase of antral pH, including the expense of growth duration of DGR, while in group 2 reflux was extremely short. The maximum Hp dissemination was in a bulb at fetomaternal of DU., Conclusions: in healthy individuals DGR intragastral involved in the regulation of pH, in patients with uncomplicated DU while reducing the duration of this resonance persists compensation of antral alkalization, and complications throughout the DGR sharply depressed, which is accompanied by severe decompensation alkalization of antrum. Bulbs semination with Hp inversely proportional to the intensity of this resonance.

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.

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.

The effects of Helicobacter pylori genotypes on clinical prognosis in the Cukurova region of Turkey were investigated by PCR. The prevalence of type I strains carrying the s1c allele, unlike in neighboring regions and countries, was found to be significantly higher in patients with gastritis and/or gastric ulcers (P = 0.001), and that of type I strains carrying the s1a allele was found to be significantly higher in patients with duodenal ulcers (P < 0.001). The cagA gene was strongly associated with the more virulent vacA genotypes (P < 0.001).

Background: Effective medical management of peptic ulcer disease (PUD) has reduced the incidence of gastric outlet obstruction (GOO) as a complication, but perforation especially in the elderly remains unchanged and is in fact on the increase. There is a changing trend in emergency surgery for perforated duodenal ulcer (PDU) from definitive anti ulcer surgery to simple closure followed by Helicobacter pylori eradication., Objective: To present our experience in managing PDU with simple closure followed by Helicobacter pylori eradication., Methods: This was a chart review of patients managed for PDU over a nine year period (Jan 1999 to Dec 2007) using information obtained from ward admission registers, theatre operation registers, and patients case files from the medical records department. The patients biodata, clinical, and operative findings as well as treatment outcome were extracted for analysis., Results: Of 55 patients eligible for analysis, 44 (80%) were males and 11(20%) females (M to F, 4:1). Their ages ranged between 18 and 65 years with a mean(SD) of 39.9 (13.5) years. Most of the patients, 34 (61.8%), were below 40 years of age and majority 39(71.0%) had a history suggestive of chronic peptic ulcer disease. Twenty six (47.3%) patients presented within 24 hours of perforation, while nine (16.4%) presented more than 72 hours afterwards. The latter group accounted for most, five(55.6%), of the mortality. All the perforations were anterior pyloroduodenal and all except one had simple closure with omental patch followed by a course of a proton pump inhibitor and Helicobacter pylori eradication therapy., Conclusion: Simple closure with omental patch followed by Helicobacter pylori eradication is effective in managing PDU with low morbidity and mortality despite patients late presentation in our center. This technique is recommended in place of a definitive ulcer surgery.

The hom family of Helicobacter pylori outer-membrane proteins, especially the homB gene, has been suggested as a novel virulence factor; however, the clinical association and function of this gene are still unclear. We evaluated the presence of the homA, homB, and cagA genes in 286 strains isolated from patients in the U.S. and Colombian populations (126 with gastritis, 96 with duodenal ulcer, and 64 with gastric cancer) by PCR. The results were compared with the clinical presentation and gastric injury. The prevalence of the homB gene was significantly higher in strains isolated from gastric-cancer patients (71.9%) than in those from duodenal ulcer patients (52.1%) (P = 0.012). In a multivariate analysis, the presence of the cagA gene significantly increased the risk for developing gastric cancer and duodenal ulcer, with the presence of the homB gene acting as a factor that could distinguish gastric cancer from duodenal ulcer (adjusted odds ratio, 3.033; 95% confidence interval, approximately 1.37 to approximately 6.73). cagA status was correlated with homB status (r = 0.323; P < 0.01). A histological analysis showed that cagA status was associated with inflammation and atrophy both in the antrum and in the corpus, while homB status was associated with inflammation and atrophy in the corpus. homB gene status might be susceptible to gastric-cancer development such that the homB gene is used as a factor for discriminating the risk of gastric cancer from that of duodenal ulcer.

Background: Helicobacter pylori is the primary cause of peptic ulcer disease and an etiologic agent in the development of gastric cancer. A high frequency of H. pylori infection has been reported from resource-poor regions. H. pylori infection is curable with regimens of multiple antimicrobial agents. However, antibiotic resistance is a leading cause of treatment failure. In Africa, there are very little data concerning the susceptibility of H. pylori isolates to antibiotics., Methodology: H. pylori isolates from gastric biopsies from outpatients > or = 18 years old affected by a gastro-duodenal ulcer were used in this study. Susceptibility testing was performed for amoxicillin, ciprofloxacin and metronidazole by using the Epsilometer test (E-test) method., Results: H. pylori strains were isolated from 40 patients of whom 36 were diagnosed as having duodenal ulcer, two with gastric ulcer, and two with gastro-duodenal ulcer. Thirty-six (90%) of the isolates were resistant to metronidazole (MICs > or = 8 microg/l), whereas all isolates were susceptible to amoxicillin (MICs < or = 0.5 microg/ml) and ciprofloxacin (MICs < or = 1 microg/ml)., Conclusion: These data suggest that metronidazole should not be used therapeutically among Senegalese patients in first-line therapy, while ciprofloxacin could be recommended in association with amoxicillin and a proton pump inhibitor in Senegal.

Background: The vacuolating cytotoxin and the cytotoxinassociated protein, encoded by vacA and cagA, respectively, are important virulence determinants of Helicobacter pylori., Objective: The aim of this study was to perform vacA genotyping and evaluate its association with cagA genotype and clinical outcome., Methods: One hundred and twenty H. pylori strains were isolated from dyspeptic patients (29 with peptic ulcer, 91 with non-ulcer dyspepsia). Genotype was determined by PCR., Results: Seventy-nine (66%) of 120 strains had the vacA signal sequence genotype s1 and 41 (34%) had the type s2. The vacA middle-region types m1 and m2 were detected in 56 (47%) and 64 (53%) strains, respectively. The combinations s1-m1 (n=56 [47%] and s2-m2 (41 [34%]) occurred more frequently than s1-m2 (23 [19.2%]; p=0.001). No strain with the combination s2-m1 was found. All patients with peptic ulcers harbored type s1 strains compared to 75 (82.4%) of 91 patients with non-ulcer dyspepsia (p=0.01). The vacA genotype s1 was associated with the presence of cagA (p <0.0001). The cagA gene was detectable in 38 (31.6%) of 120 isolates and present in all 29 patients with ulcer compared to nine of 91 with non-ulcer dyspepsia (p <0.001)., Conclusion: Helicobacter pylori strains of vacA type s1 and the combination of s1-m1 were associated with peptic ulceration and the presence of cagA gene.

Background: A higher body mass index (BMI) may lead to a more adverse outcome of reflux esophagitis. The study aimed to determine whether increased BMI after H. pylori eradication in duodenal ulcer patients predisposes to erosive reflux esophagitis., Methods: Four hundred fifty-nine patients with Helicobacter pylori-positive duodenal ulcers but without reflux esophagitis were evaluated. Serial BMIs were collected before therapy and on the 2nd, 6th, and 12th months after H. pylori eradication. New-onset reflux esophagitis was recorded., Results: In 350 patients with complete follow-up, mean BMI increased from the second month after H. pylori eradication (P<0.001). H. pylori eradication also led to a net increase of BMI >1.5 kg/m in nearly 20% of patients in the 12-month follow-up, whereas new-onset of reflux esophagitis was noted in 16.3% (57/350). Baseline BMI, prevalence rate of hiatus hernia, and net increase of BMI were higher in patients with new-onset reflux than in those without (P<0.05). Multiple logistic regression confirmed higher baseline BMI, hiatus hernia, and net BMI increase >1.5 kg/m after H. pylori eradication were independently associated with new-onset reflux esophagitis (P<0.05)., Conclusions: Eradication of H. pylori may lead to a significant net increase of BMI in patients with duodenal ulcers. Such BMI gain, as well as higher baseline BMI and hiatus hernia, predisposes to new-onset reflux esophagitis after H. pylori eradication.

Disseminated histoplasmosis is an AIDS-defining illness which usually involves the liver and gastrointestinal tract, most commonly the small bowel. Abdominal pain, diarrhea, GI bleeding, hepatosplenomegaly and small bowel obstruction are well described presentations. Still gastrointestinal histoplasmosis often results in either vague symptomatology or no symptoms. Pancreaticobiliary disease related to disseminated histoplasmosis is not well characterized. We report the case of a young female with advanced HIV infection and biliary obstruction and a periampullary duodenal ulcer due to disseminated histoplasmosis.

Unlabelled: Helicobacter pylori (H. pylori) is the main etiologic factor for duodenal ulcer (DU). Bleeding is still a frequent and sometimes severe complication, with unacceptable mortality despite modern therapeutic modalities. The importance of diagnosing and treating H. pylori infection in bleeding DU is underlined by the fact that eradication therapy is effective in preventing recurrent bleeding. The aim of this study was to evaluate the prevalence of H. pylori infection by means of 13C urea breath test (13C-UBT) in patients with bleeding DU., Material and Method: Thirty-nine patients (25 men, 14 women) hospitalized with bleeding DU underwent emergency endoscopy and treated with intravenous proton pump inhibitors (PPIs), and a 13C-UBT was performed the day after the resuming oral feeding., Results: Twenty-seven patients (19 men, 8 women) (69.3%) had a positive 13C-UBT. All patients received intravenous PPIs (22 pantoprazole, 17 esomeprazole) after emergency endoscopy (80 mg bolus + 8 mg/hour infusion/day) for 3-4 days. The time elapsed between admission and performance of 13C-UBT did not differ significantly between patients having a positive or negative 3C-UBT (5.6 vs 6.1 days). Eight of the twelve patients (66.6%) with a negative 13C-UBT had a repeated test two month later, and five of them became positive; therefore, H. pylori infection was finally detected in 32 (82%) out of 39 patients with bleeding DU., Conclusion: Most patients with bleeding DU have a positive 13C-UBT although they were taking PPIs.

The most important clinical point for dyspeptic H pylori-negative NSAID-absent negative ulcers is to adequately ensure that these common risk factors are indeed absent. Once that is done, further investigations to include the rare causes of ulcer disease need to be performed and exclusion of underlying malignancy ensured. The possibility of the Zollinger Ellison syndrome should be considered, remembering that proton pump inhibitor therapy will mitigate its classical, clinical features.

Helicobacter pylori is the most prevalent human pathogen and although, it remains silent in most individuals for lifetime, colonization may develop into severe gastric and duodenal conditions. Rapidly developing resistance to antibiotic treatment urgently calls for the development of effective vaccines. We determined the ANTIGENome of two clinical isolates of H. pylori, KTH-Ca1 and KTH-Du, derived from patients with gastric cancer and duodenal ulcer, respectively. Using disease-relevant human sera from well-characterized donors we identified 124 annotated ORFs and 54 non-annotated peptides as antigens. Through in vitro validation assays we selected the 20 most promising vaccine candidates. Importantly, two candidates represent proteins that were previously shown to provide protection in models of H. pylori infection. One of the most frequently selected and conserved protein, the siderophore-dependent transporter HP1341, was confirmed to show high reactivity with human serum IgGs. These analyses provide the means to identify novel antigens for the selection of vaccine candidates, as well as disease associated biomarkers.

Bloodstream infections are associated with high morbidity and mortality. Accurate identification of blood isolates to the species level and identification of the source of infection and/or the portal of entry are crucial for optimal management of these infections. These investigations-in addition to clinical findings and laboratory and imaging studies-are central to informing and directing efficient and effective diagnostic examinations and to choosing the optimal antimicrobial regimen. Four case studies that demonstrate the importance of identifying the causative agents and the source of infection are discussed to illustrate the central importance of microbiological findings in the diagnosis of bacteremia and bloodstream infections associated with infections at other sites.

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.