Cause Of Peptic Ulcer Research Articles

Beyond the stomach: an updated view of Helicobacter pylori pathogenesis, diagnosis, and treatment.

Helicobacter pylori (H. pylori) is an extremely common, yet underappreciated, pathogen that is able to alter host physiology and subvert the host immune response, allowing it to persist for the life of the host. H. pylori is the primary cause of peptic ulcers and gastric cancer. In the United States, the annual cost associated with peptic ulcer disease is estimated to be $6 billion and gastric cancer kills over 700000 people per year globally. The prevalence of H. pylori infection remains high (> 50%) in much of the world, although the infection rates are dropping in some developed nations. The drop in H. pylori prevalence could be a double-edged sword, reducing the incidence of gastric diseases while increasing the risk of allergies and esophageal diseases. The list of diseases potentially caused by H. pylori continues to grow; however, mechanistic explanations of how H. pylori could contribute to extragastric diseases lag far behind clinical studies. A number of host factors and H. pylori virulence factors act in concert to determine which individuals are at the highest risk of disease. These include bacterial cytotoxins and polymorphisms in host genes responsible for directing the immune response. This review discusses the latest advances in H. pylori pathogenesis, diagnosis, and treatment. Up-to-date information on correlations between H. pylori and extragastric diseases is also provided.

Is there any relationship between Leb antigen expression and Helicobacter pylori infection?

Helicobacter pylori infection is one of the main causes of peptic ulcer. There are some blood groups acting as receptors for the pathogen. Based on this view and previous attempts, we tried to examine the relationship between Lewis blood group and H. pylori infection. Blood and saliva samples were collected from 60 patients with established peptic ulcer induced by H. pylori. Secretory status of each patient was determined by both direct agglutination and saliva tests. Seventy-two percent of the patients were secretor and expressed Lewis B antigen. This rate in control group was 61%. Statistical analysis showed no significant difference between the two groups. This study did not find any correlation between Le(b) antigen expression and presence of H. pylori-induced peptic ulcer. It is now recommended that other factors like Lewis(x) and sialyl Lewis(x) should be investigated in binding, colonization and virulence of H. pylori infection in the future.

The Frey procedure for the treatment of chronic pancreatitis associated with common bile duct stricture: be aware of duct reinsertion into the resection cavity or choledochoduodenostomy

The possible relationship between peptic ulcer disease and the anatomic rearrangement after Roux-en-Y choledochojejunostomy was studied in a series of ninety-seven patients who had undergone this procedure for the treatment of benign extrahepatic biliary obstruction. Peptic ulcer was documented in ten of thirty-nine patients in whom significant complications had developed in the postoperative period. Eight of these had at least one bleeding episode, four had two, and one had three bleeding episodes. Two patients died from the bleeding episodes. Nine of these patients had duodenal ulcers, and one had a gastric ulcer. Four required surgical intervention for complications of the ulcer: three for bleeding and one for perforation. Other complications in this series included fifteen cases of cholangitis, four of infection, and ten of abdominal pain of unknown origin.For comparative purposes, a series of thirty-nine patients who had undergone choledochoduodenostomy at the UCLA and Wadsworth VA Hospitals were reviewed. Of these, twelve had significant postoperative complications: five cases of fistula, three of cholangitis, three of stricture, and one of peptic ulcer.It has been speculated that the cause of peptic ulcer after choledochojejunostomy is secondary to the divergence of alkaline bile secretions from the duodenum. Others have judged that a secondary gastric hypersecretory phenomenon is primarily responsible. In view of our findings, it is believed that a complete preoperative evaluation of peptic ulcer potential is warranted, and postoperative protection of patients with a proclivity to ulcer disease is essential. In high risk patients, vagotomy and pyloroplasty should be considered.

English

This study was done at Christian Medical College and Hospital, Ludhiana for the period of 5 years from January 2006 to December 2010 in the Department of Microbiology. A total of 306 endoscopic gastric biopsy specimens were collected from the suspected cases of the peptic ulcer and were subjected to rapid urease test for Helicobacter pylori. This test has high sensitivity and cent percent specificity. The prevalence was determined to be 09.48% and male: female ratio was determined to be 68.97:31.03. INTRODUCTION: Helicobacter pylori is a common cause of peptic ulcer. It is gram negative, microaerophilic and motile organism with multiple polar flagella. It associated with 90% of duodenal ulcer and 80% of gastric ulcer¹.H.pylori is also associated with gastric adenocarcinoma. H. pylori infection is mainly acquired through the faeco oral route. Water has been shown to be a source of H. pylori infection by Kleinet al².A study from Bombay reported that H. pylori is present in the dental plaques of 98% patients with dyspepsia³.

Letter: peptic ulcer bleeding in patients with cirrhosis

SIRS, The study by Rudler et al. on the aetiology and outcomes of peptic ulcer bleeding in cirrhotic and noncirrhotic patients has several limitations. First, the study recruited only 203 patients, the majority (85%) of whom were noncirrhotic. These were compared with only 29 (14%) cirrhotic patients, who were loosely defined using clinical, biochemical and radiological parameters. Based on the very small numbers in the cirrhosis group, and as the patients in the two groups were not matched, the study was not sufficiently powered to address the questions they set out to answer. The gold standard test for diagnosing cirrhosis is a liver biopsy, although hepatic elastography is an acceptable alternative. Reliance on tests such as radiology, blood parameters and endoscopic findings can be misleading and lack specificity. For instance, noncirrhotic idiopathic portal hypertension can mimic cirrhosis both clinically and radiologically. Hence, it is conceivable that some of the patients they considered cirrhotic were not. Second, the authors throughout the manuscript refer to ‘idiopathic’ peptic ulcer disease (PUD), meaning those patients who had no evidence of Helicobacter pylori infection or nonsteroidal anti-inflammatory drug (NSAID)/aspirin use. This gives the erroneous impression that these two factors are the only causes of PUD. Before an ulcer can be labelled as idiopathic, one has to exclude other known but rare causes of peptic ulcers (such as other ulcerogenic drugs and diseases including Crohn’s and Zollinger–Ellison syndrome). The authors made no such attempts in their study; hence, it is impossible to know whether other aetiologies were involved. Moreover, recent alcohol intake in cirrhotic patients has been implicated in the pathogenesis of gastroduodenal ulcers; hence, it is misleading to disregard alcohol as a causative factor for ulcers in these patients. Third, the use of H. pylori serology to diagnose H. pylori infection in this study is questionable. It is well known that serological tests for H. pylori are unreliable in patients with cirrhosis and portal hypertension, with high sensitivity but low specificity (83.6 and 55.9, respectively). 5 Gastric biopsies for H. pylori histology and/or rapid urease test would have been preferable due to their higher accuracy in this setting. Thus, the figures they quote for H. pylori infection rate in the study are likely to be inaccurate. Moreover, the authors’ make no mention of whether the patients had received any prior H. pylori eradication therapy, which makes it impossible to determine whether the patients who were positive had current or prior infection, as H. pylori antibodies can take several months to years to disappear following eradication. In addition, noncirrhotic patients were much older than cirrhotic patients, and the differences seen in H. pylori infection rate between the two groups could have been influenced by the age difference. It is well known that the prevalence of H. pylori infection increases with age. Peptic ulcer disease, particularly gastric ulcer, is found more commonly in patients with portal hypertension. Although the exact pathogenetic mechanisms are unknown, it is generally believed that portal hypertension leads to impairment of gastric mucosal defences, hence rendering the gastric lining more susceptible to injury by aggressors such as NSAIDs alcohol and bile salts, culminating in peptic ulcers. Although a high alcohol intake alone has not been unequivocally identified as a risk factor for PUD in noncirrhotic patients, Aurox et al. found that in cirrhotic patients, recent alcohol intake prior to endoscopy was independently associated with gastroduodenal erosions. Almost all cirrhotic patients in this study had a history of excessive alcohol intake. Thus, the only

A study of the changes in the cause of peptic ulcer bleeding

To clarify the frequency of and changes in the cause of peptic ulcer bleeding. This study retrospectively evaluated the out- and inpatients who underwent endoscopy between 2002 to 2008. The subjects were patients presenting with peptic ulcer bleeding. The details of these patients were obtained from their endoscopic reports and medical records. The rates of Helicobacter pylori (H. pylori) infection were significantly low (P = 0.039), while the proportion of nonsteroidal antiinflammatory drugs (NSAIDs) users and vascular disease significantly increased over the period studied (P = 0.034 and P = 0.04, respectively). However, there was no significant difference in the proportion of low-dose aspirin users (P = 0.832). It's found that the primary cause of peptic ulcer bleeding changed from H. pylori infection to use of NSAIDs over the 7-year period of study. It seems that the number of low-dose aspirin users has increased with the increase in the proportion of vascular disease. It is necessary to take measures to prevent peptic ulcer bleeding among NSAIDs and low dose aspirin users.

Culture Method and PCR for the Detection ofHelicobacter pyloriin Drinking Water in Basrah Governorate Iraq

Helicobacter pylori is recognized by the World Health Organization to be the primary cause of peptic ulcers, chronic gastritis, and stomach cancer, though the source of human infection is not well understood. One of the problems in understanding the source of human contamination is the difficulty in isolating the organism from the environment. However, the combination of PCR results with those of culturing of 471 drinking water samples can provide a more accurate picture of H. pylori detection. In this method 78 presumptive H. pylori colonies out of 266 tap water samples were obtained in the preliminary detection on modified Columbia agar (MCUA) slant relying on urease positivity with a rate of 29.3%. However, only 11 out of them were confirmed by Gram staining and biochemical tests reducing the rate to 4.13% whereas only 3 (1.46%) from 205 reverse osmosis (RO) water samples. Furthermore, only 6 (54.5%) out of the 11 isolates from tap water and 1 (33.3%) of the 3 RO isolates were confirmed by 16SrRNA PCR. Thus PCR confirmation reduced the rate to 2.2%. In addition, only 4 (4%) of 100 tap water samples negative for H. pylori by culture method were H. pylori positive by 16SrRNA. Water samples were collected from 24 districts of Basrah Governorate from February–December 2009. The direct recovery of H. pylori from drinking water is both alarming and scientifically exciting in terms of the investigation of its epidemiology.

PA01.62. Mukta-sukti bhasma; nectar for acid peptic disorders, w.s.r to its anti-ulcer activity - an experimental study

Purpose: Mukta Shukti (Pearl oyster shell); a sudha varga dravya, attains better therapeutic properties with proper sodhana and marana processes. It is indicated in Amlapitta, Parinamashoola and Annadravashoola. Acharya Susruta mentioned; Amla is the property of Vidagdha Pitta. The term Amlapitta may be correlated with Acid reflux syndrome which comprises of various types of Gastro esophageal reflux diseases like Gastritis, Peptic ulcer etc. A peptic ulcer is a sore on the lining of the stomach or duodenum, the beginning of the small intestine. A bacterium called Helicobacter pylori is a major cause of peptic ulcers. An attempt was made in this regard to establish standards to assure quality and to assess antiulcer activity of Mukta Sukti Bhasma. Method: Mukta sukti Bhasma prepared as per Rasatarangini and subjected to Atomic absorption spectroscopy (AAS) and X ray diffraction (XRD). Anti ulcer activity of Mukta sukti Bhasma in Albino rats by Aspirin induced gastric ulcer. Sucralfate as standard group and normal food water as control group used for the comparison. Result: Mukta sukti Bhasma showed highly significant Anti ulcer activity than control group. The alkaline pH and chemical components might have contributed by inhibiting secretions, neutralizing the acidity and reducing size of the ulcerative lesions. Presence of Calcium (Ca), Magnesium (Mg), Manganese (Mn), Iron (Fe), Potassium (K), Aluminum (Al), Copper (Cu), Sodium (Na) and Zinc (Zn) were detected in raw Mukta sukti and Mukta sukti Bhasma. X ray diffraction shown face centered Cubic, hexagonal, tetragonal and monoclinic crystal structures. Conclusion: In aspirin induced model, the Mukta sukti Bhasma and standard group (Sucralfate) showed highly significant Anti ulcer activity than control group (food water). The Mukta sukti Bhasma showed highly significant Anti ulcer activity than standard group (Sucralfate) when compared. This experimental study has given scientific evidence for the claim in the ancient text regarding the Anti ulcer property of Mukta sukti Bhasma which gives scope for conducting clinical study.

Detection of 16S r RNA gene of Helicobacter pylori in patients with peptic ulcer and gastric carcinoma: molecular and bacteriological study

Objective and background: It is well document Helicobacter pylori, has been a major causes of peptic ulcer, gastric ulcer, duodenal ulcer disease and is an early risk factor for gastric carcinoma. This study has been undertaken forisolation of Helicobacter pylori form clinical specimens using culture technique and detection the role of this technique in the investigation of H. pylori infection. Also detection of anti -H. pylori IgG using enzyme linked immune sorbent assay (ELISA), further molecular detection of H. pylori genome by amplification of 16s r-ribonucleic acid gene with 520 pb by polymerase chain reaction PCR. Patients and Methods: Atotal of Eighty five adult patient attending the gastro endoscopy unit of Al- Ramadi Teaching Hospital to undergo selective esophageal gastroduodenoscopy (OGD) were studied. They were all suffering from clinical manifestation of duodenal ulcer (DU), gastric ulcer (GU), peptic ulcer (PU) and nonulcer dyspepsia (NUD). Culture and ELISA technique were used. Further molecular detect of 16 s r RNA gene was performed by PCR. Results: A total 7(8.23%) with GU, 5 (5.91%) with PU, 10 (11.75%) with DU and 28 (32.94%) patients with NUD were positive by urease test (UT). A total 3 (3.52%) patients with GU, 4 (4.71%) patients with PU and 3 (3.52%) patients with DU were positive by culture while no one of the patients of NUD was positive by culture. By using ELISA technique 18 (21.2%) patients were positive by ELISA. In the present study, the presence of Helicobacter DNA was investigated using a Helicobacter species-specific 16srRNA PCR amplification.DNA extracted from human blood and bacterial colonies. PCR showed 20(100%) of cases positive result from human blood while 6 (60%) of cases were positive result of PCR from bacterial colonies. Conclusions: The study concludedthat urease test was useful as preliminary screening test and important in give indicate for H. pylori presence. Further, the role of culture was very important in the detection of H. pylori in clinical samples. Furthermore, the immunologically bases serological test, detection of anti-H pyloriIgG by ELISA technique was undependable serological test. It can be used as preliminary screening test for detection of H. pylori in association with the other tests. FurtherPCR was sensitive and specific test for diagnosis of H. pyloriinfection.

High prevalence of duodenal ulcer in a tertiary care hospital in the city of São Paulo, SP, Brazil

In spite of Helicobacter pylori infection being the etiological cause of peptic ulcer and its high prevalence in Brazil, the prevalence of peptic ulcer disease has been poorly studied. To verify the peptic ulcer disease prevalence in patients of a tertiary care hospital. Diagnostic findings from 1,478 consecutive endoscopies were correlated with the urease test results for H. pylori infection diagnosis and demographic data in a total of 3,779 endoscopies performed in 2005. The mean age of the patients was 51.14 ± 16.46, being 613 (41.5%) men. Peptic ulcer was diagnosed in 494 (33.4%) patients with a mean age of 54.86 ± 14.53, 205 (52%) were men, being 391 (26.5%) duodenal ulcer and 103 (7%) gastric ulcer. Normal endoscopy was found in 272 (18.4%) patients with a mean age of 38.4 ± 15.22, being 49 (18%) men. The comparison of peptic ulcer group with the patients that had normal endoscopy revealed that H. pylori infection [P = 0.005; OR = 1.70; 95% CI = 1.17-2.47], male gender [P<0.0001; OR = 5.53; 95%CI = 3.67-8.34] and older age [P<0.0001; OR = 1.08; 95%CI = 1.06-1.09] increased the risk of peptic ulcers. The overall H. pylori prevalence was 53% (786). Prevalence of duodenal ulcer is high in a Brazilian population that had H. pylori infection associated with older age and male gender as important determinants to gastrointestinal diseases outcome. Future prospective studies should confirm these findings.

Medication-Induced Acute Abdominal Pain: Evaluation with CT Imaging

A variety of medications can produce severe abdominal pain simulating an acute abdomen and, in some cases, a surgical abdomen. Nonsteroidal anti-inflammatory drugs are a well-established cause of peptic ulcer. Hemorrhage is the most serious complication of antithrombotic therapy. Pseudomembraneous colitis after use of antibiotics or chemotherapeutic agents can result in acute abdominal pain. Neutropenic enterocolitis or cytomegalovirus enterocolitis often occurs in immunocompromised patients after chemotherapy. Some other medications are associated with acute pancreatitis, biliary sludge, angioedema, pneumatosis intestinalis, renal stones, and hemorrhagic cystitis. The diagnosis of medicationinduced diseases can be suggested by combinations of clinical information including acute onset of abdominal pain, medication history, laboratory data and characteristic imaging findings. Therefore, recognizing CT findings of the medicationinduced acute abdomen and knowledge of the clinical significance of each entity are important for establishing a correct diagnosis and for guiding appropriate management. Keywords: Abdomen, acute conditions, CT, Drugs, side effects, medications, anti-inflammatory drugs, Disease, angiotensin

Host immunological conditions that determine status of Helicobacter pylori as pathogenic or commensal bacterium (166.26)

Abstract H. pylori is a leading cause of peptic ulcer, gastric lymphoma and adenocarcinoma. In spite of being a highly prevalent bacterium in the gastric mucosa, only 15 % of carriers develop overt disease. Bacterial pathogenesis is believed to arise from an interaction of strain-specific immunity-mediating capabilities and the host susceptibility. To investigate the mechanisms of immune modulation by H. pylori we have created a mathematical model of immune cells of the gastric mucosa, gastric lymph nodes and their response to H. pylori. A local sensitivity analysis suggests that, in a healthy host, the H. pylori strains that are asymptomatically tolerated are those with the ability to invade the mucous layer as well as those that inhibit the ability of epithelial cells to secrete defensin and chemoattractants. Interestingly, our model also indicates that persistence of H. pylori in the gastric mucosa is facilitated by a strain’s ability to induce secretion of inflammatory mediators in the gastric epithelium. However, H. pylori strains that induce a tolerogenic phenotype in APCs or induce cytoskeletal changes in epithelial cells are likely to elicit a pathological inflammatory response. A global sensitivity analysis revealed novel context-dependent functional interactions occurring between the host and H. pylori.

The ulcer sleuths: The search for the cause of peptic ulcers

The search for the cause or causes of peptic ulcers has been a long one. It was recognised as early as the 19th Century that damage to the stomach or duodenal bulb was likely to result if the resistance of their mucosae to luminal acid was for some reason impaired. An early theory suggested microscopic vascular occlusion leading to local infarction could be the initiating event but evidence was lacking. Excessive acid secretion is seen in some patients but not in many so is implausible as the main factor in most ulcers. Cigarette smoking is a risk factor and chronic life difficulties has been shown to sometimes play a part, but we would now think that they play only minor roles to possibly tip the balance when a major etiologic factor is already present. The overwhelming evidence now is that the major etiologic factors in chronic peptic ulcer are ingestion of nonsteroidal anti-inflammatory drugs (NSAIDs) and infection with Helicobacter pylori. Understanding the mechanism of the first, and the discovery and demonstration of Koch's postulates for the second, have been instrumental in the award of two Nobel prizes.

778 Treatment of Gastric Outlet Obstruction Due to Peptic Ulcer in Four Children

Background: Peptic ulcer disease complicated with gastric outlet obstruction (GOO) is rare in children. The experience in management of such patients is limited. The purpose of this study is to review the etiology, clinical manifestations, treatment and outcome of the patients in two tertiary referral centers. Material and methods: From 2005 to 2008, all the pediatric patients admitted to National Cheng Kung University Hospital and Kaohsiung Veterans General Hospital, Taiwan due to pyloric stenosis were reviewed. Infantile hypertrophic pyloric stenosis (IHPS) and anatomical anomalies, such as atresia, web were excluded. Four patients were enrolled into the study. The diagnosis of all the patients were confirmed by panendoscopy and barium meal study in all the patients. Results: There were 3 boys and one girl. The mean age was 32 months (15-71 months). Two patients had ulcer over the pre-pyloric area and the other two had duodenal ulcer. The etiology of peptic ulcers included non-steroid anti-inflammation drugs (NASIDs) ingestion (2), Helicobacter pylori and unknown (1). All patients manifested as post-prandial vomiting. Three patients received conservative treatment including proton pumping inhibitor succeβfully. Only one patient received operation with Billroth I +vagotomy due to pyloric complete obstruction. No recurrent gastric outlet obstruction was noted in all the patients Conclusions: NSAIDs ingestion was an important cause of peptic ulcer in children. Conservative treatment including PPI should be first line therapy for the gastric outlet obstruction due to peptic ulcer in children. Surgical treatment should be reserved for the patients with failed medical treatment.

Contribution of Specific Amino Acid Changes in Penicillin Binding Protein 1 to Amoxicillin Resistance in ClinicalHelicobacter pyloriisolates

Amoxicillin is commonly used to treat Helicobacter pylori, a major cause of peptic ulcers, stomach cancer, and B-cell mucosa-associated lymphoid tissue lymphoma. Amoxicillin resistance in H. pylori is increasing steadily, especially in developing countries, leading to treatment failures. In this study, we characterize the mechanism of amoxicillin resistance in the U.S. clinical isolate B258. Transformation of amoxicillin-susceptible strain 26695 with the penicillin binding protein 1 gene (pbp1) from B258 increased the amoxicillin resistance of 26695 to equal that of B258, while studies using biotinylated amoxicillin showed a decrease in the binding of amoxicillin to the PBP1 of B258. Transformation with 4 pbp1 fragments, each encompassing several amino acid substitutions, combined with site-directed mutagenesis studies, identified 3 amino acid substitutions in PBP1 of B258 which affected amoxicillin susceptibility (Val 469 Met, Phe 473 Leu, and Ser 543 Arg). Homology modeling showed the spatial orientation of these specific amino acid changes in PBP1 from 26695 and B258. The results of these studies demonstrate that amoxicillin resistance in the clinical U.S. isolate B258 is due solely to an altered PBP1 protein with a lower binding affinity for amoxicillin. Homology modeling analyses using previously identified amino acid substitutions of amoxicillin-resistant PBP1s demonstrate the importance of specific amino acid substitutions in PBP1 that affect the binding of amoxicillin in the putative binding cleft, defining those substitutions deemed most important in amoxicillin resistance.

The effect of Helicobacter pylori on asthma and allergy

Current evidence indicates an inverse association between Helicobacter pylori and asthma and allergy. H. pylori is a Gram-negative bacterium which represents the major cause of peptic ulcer and gastric cancer, and preferentially elicits a T helper (Th)-1 response. Many H. pylori factors, such as the neutrophil-activating factor of H. pylori (HP-NAP), are able to drive Th-1 polarization and to display a powerful inhibition of allergic Th-2 response. This article proposes an overview of the actual knowledge about the effects of H. pylori on asthma and allergy. Special attention has been drawn to HP-NAP as a potential novel strategy for the prevention and treatment of asthma and atopy.

Management of Helicobacter pylori infection

Helicobacter pylori is the cause of peptic ulcer, gastric cancer and gastric lymphoma. Diagnosis of H. pylori infection can be made using invasive and noninvasive tests. Invasive tests based on endoscopy, such as histology, are recommended when a gastric malignancy is suspected. Alternatively, noninvasive tests, such as the urea breath test and stool tests are useful for H. pylori diagnosis and follow-up. Triple therapy with either amoxicillin or metronidazole, clarithromycin and proton pump inhibitor given twice daily for 7–14 days is the recommended first-line treatment, after having checked the individual clarithromycin antimicrobial susceptibility. A triple therapy with levofloxacin, amoxicillin and proton pump inhibitor for 10–14 days should be used as second-line treatment, where the strains are susceptible to fluoroquinolone. Alternatively, bismuth-based quadruple therapy is recommended.

Clinical Relevance and Diversity of Two Homologous Genes Encoding Glycosyltransferases in Helicobacter pylori

Helicobacter pylori is known to be a major cause of peptic ulceration. The jhp0562 gene, encoding a glycosyltransferase involved in the synthesis of the lipopolysaccharide, was associated with peptic ulcer disease (PUD) in children. The beta-(1,3)-galactosyltransferase [beta-(1,3)GalT] gene (jhp0563), involved in Lewis (Le) antigen expression, is highly similar to jhp0562. The clinical significance and diversity of both genes were examined by PCR and sequencing of clinical strains (n = 117) isolated from children with PUD (n = 57) and nonulcer dyspepsia (NUD; n = 60). The prevalence of the jhp0562 gene was significantly higher in strains with a more-virulent profile (strains positive for the cag pathogenicity island [PAI], vacA sl allele, babA, homB, phase-variable gene oipA "on" [i.e., functional], and hopQ I allele). The distribution of genotypes according to clinical outcome showed that the presence of jhp0562 represented one of the greatest risks for the development of PUD. Moreover, the triple-positive genotype for the cag PAI, jhp0562, and homB provided the best discriminatory model for distinguishing PUD and NUD outcomes in children. Sequence and in vitro expression analyses of jhp0562 showed the presence of a complete open reading frame, while the beta-(1,3)GalT gene was shown to be a phase-variable gene. The regular presence of jhp0562 in strains with a truncated beta-(1,3)GalT gene suggests that jhp0562 may also be implicated in the regulation of Le antigen expression. Overall, the results of this study suggest that the jhp0562 gene is of great clinical relevance, being a useful comarker for severe H. pylori-related disease and contributing to host adaptation.

Overview of 50 years' progress in upper gastrointestinal diseases

There have been numerous and dramatic advances in our understanding of the mechanisms, causes and treatments of upper gastrointestinal diseases in the past 50 years. This review focuses on a few, not dealt with elsewhere in this special issue of the Journal. The early history of the recognition that nonsteroidal anti-inflammatory drugs are a major cause of peptic ulcer is described, with particular attention to the work of the pioneering Australian investigators. The story of the development of the histamine H(2)-receptor antagonists and the proton pump inhibitors is also outlined.

Fifty years of Australian gastroenterology and hepatology: A golden era of contributions to the region

Fifty years of Australian gastroenterology and hepatology: A golden era of contributions to the region