Pylori-associated Peptic Ulcer Disease Research Articles

Relationship between mucosal TNF-α expression and Th1, Th17, Th22 and Treg responses in Helicobacter pylori infection

Helicobacter pylori (H. pylori)-induced gastric inflammation in the gastric mucosa and significantly increases the risk of developing gastritis and peptic ulcer disease (PUD). The objective of this research is to determine the role of tumor necrosis factor-α (TNF-α) expression in the gastric mucosa of patients with H. pylori-associated gastritis and PUD compared to uninfected patients, and we determined the relation between TNF-α expression and Th1/Th17/Th22, and Treg cells. Fifty-five patients with H. pylori-associated gastritis, 47 patients with H. pylori-associated PUD, and 48 uninfected patients were in this research. Antrum biopsy was used to detect H. pylori, virulence factors and histopathological assessments. Expression of TNF-α in the infected group was significantly higher than the uninfected group. Also, cagA/oipA-positive infected patients induce significantly more TNF-α expression than do cagA/oipA-negative infected patients. Expression of TNF-α was significantly increased in the PUD group than the gastritis group. Notably, TNF-α expression had a significant positive correlation with the frequency of Th1/Th17/Th22 lymphocytes in the PUD group. These findings indicate the importance of increasing TNF-α with Th1, Th17, Th22 responses increase as an important risk factor for PUD in context of H. pylori infection.

Integrative Analysis of Deregulated miRNAs Reveals Candidate Molecular Mechanisms Linking H. pylori Infected Peptic Ulcer Disease with Periodontitis.

Objective Periodontitis is a highly prevalent oral infectious disease and has been increasingly associated with H. pylori infection, gastric inflammation, and gastric cancer but little is known about epigenetic machinery underlying this potentially bidirectional association. The present study is aimed at identifying key deregulated miRNA, their associated genes, signaling pathways, and compounds linking periodontitis with H. pylori-associated peptic ulcer disease. Methods miRNA expression datasets for periodontitis-affected and H. pylori-associated peptic ulcer disease-affected tissues were sought from the GEO database. Differentially expressed miRNA (DEmiRNAs) were identified and the overlapping, shared-DEmiRNA between both datasets were determined. Shared-DEmiRNA-target networks construction and functional analyses were constructed using miRNet 2.0, including shared-DEmiRNA-gene, shared-DEmiRNA-transcription factor (TF), and shared-DEmiRNA-compound networks. Functional enrichment analysis for shared DEmiRNA-gene and shared DEmiRNA-TF networks was performed using the KEGG, Reactome, and Geno Ontology (GO) pathways. Results 11 shared-DEmiRNAs were identified, among which 9 showed similar expression patterns in both diseases, and 7 were overexpressed. miRNA hsa-hsa-mir-155-5p and hsa-mir-29a-3p were top miRNA nodes in both gene and TF networks. The topmost candidate miRNA-deregulated genes were PTEN, CCND1, MDM2, TNRC6A, and SCD while topmost deregulated TFs included STAT3, HIF1A, EZH2, CEBPA, and RUNX1. Curcumin, 5-fluorouracil, and the gallotanin 1,2,6-Tri-O-galloyl-beta-D-glucopyranose emerged as the most relevant linkage compound targets. Functional analyses revealed multiple cancer-associated pathways, PI3K pathways, kinase binding, and transcription factor binding among as enriched by the network-associated genes and TFs. Conclusion Integrative analysis of deregulated miRNAs revealed candidate molecular mechanisms comprising of top miRNA, their gene, and TF targets linking H. pylori-infected peptic ulcer disease with periodontitis and highlighted compounds targeting both diseases. These findings provide basis for directing future experimental research.

Time trends in the prevalence of Helicobacter pylori infection in patients with peptic ulcer disease: a single-center retrospective study in Shanghai.

ObjectiveThe present study aimed to investigate the recent trends in Helicobacter pylori infection associated with peptic ulcer disease in a large population in Shanghai.MethodsWe analyzed the medical records of all patients who had undergone upper gastrointestinal endoscopy (EGD) for uninvestigated dyspepsia at Ren Ji Hospital between 2013 and 2019 to determine the prevalence of H. pylori infection in patients with peptic ulcers.ResultsPeptic ulcers were found in 40,385 of the 383,413 patients who underwent EGD during the study period. Over the 7-year study period, the annual prevalence of H. pylori among patients receiving EGD declined from 32.2% to 26.5%. H. pylori was present in 60% of ulcers and the incidence was higher (66.9%) in duodenal compared with gastric ulcers (48.5%). The proportion of H. pylori-associated gastric ulcers declined from 52.2% to 49.3% and that of H. pylori-positive duodenal ulcers declined from 70.0% to 63.9%.ConclusionThe prevalence of H. pylori-positive peptic ulcers, mainly duodenal ulcers, fell from 2013 to 2019. However, the proportion of non-H. pylori-associated peptic ulcer disease increased, especially in elderly people, possibly due to the use of nonsteroidal anti-inflammatory drugs. Further research is needed to confirm this hypothesis.

Clinical factors associated with initial Helicobacter pylori eradication therapy: a retrospective study in China

The eradication rate of Helicobacter pylori (H. pylori) has been decreasing every year, mainly due to the increase in antibiotic resistance. In fact, many other factors may affect H. pylori eradication. To analyze the clinical factors affecting the initial eradication therapy in Chinese patients with H. pylori infection. We conducted a retrospective study on 264 outpatients who were diagnosed with H. pylori-associated chronic gastritis and peptic ulcer disease between January and December 2015 at a large tertiary hospital in China. The patients were divided into three groups: ECA, RCA, and RCM (R: 20 mg rabeprazole, E: 40 mg esomeprazole, C: 0.5 g clarithromycin, A: 1.0 g amoxicillin and M: 0.4 g metronidazole). The patients were treated for 14 days and followed up for 1 year. The 14C-urea breath test (14C-UBT) was performed 4 weeks after the completion of the eradication therapy. The eradication rate was higher in ≥ 40-year-old patients than in < 40-year-old-patients (85.7% vs. 54.7%, p = 0.002). Multivariate analyses revealed only age ≥ 40 years to be significantly associated with a high H. pylori eradication rate [odds ratio (OR) 4.58, p = 0.003]. The H. pylori eradication rate in patients with duodenal ulcers was significantly higher than that in patients with gastric ulcers (79% vs. 60%, p = 0.012). Age could be a predictor of successful H. pylori eradication. Patients with duodenal ulcers had a higher H. pylori eradication rate than those with other lesions.

Up-regulated CCL18, CCL28 and CXCL13 Expression is Associated with the Risk of Gastritis and Peptic Ulcer Disease in Helicobacter Pylori infection

BackgroundHelicobacter pylori (H. pylori) infection causes inflammation and increases the risk of developing peptic ulcer disease (PUD); however, the exact molecular mechanisms of PUD development remain unclear. The aim of this study was to investigate the expression of CCL18, CCL28, and CXCL13 in H. pylori-positive subjects in comparison with H. pylori-negative subjects, and to determine its association with different clinical outcomes and virulence factors. MethodsIn total, 55 H. pylori-positive subjects with gastritis, 47 H. pylori-positive subjects with PUD, and 48 H. pylori-negative subjects were enrolled in this study. CCL18, CCL28, and CXCL13 expression were determined using real time polymerase chain reaction (PCR). The virulence factors of H. pylori such as cytotoxin-associated gene A (cagA), outer inflammatory protein A (oipA), blood group antigen-binding adhesin (babA), and vacuolating cytotoxin A (VacA) genes were evaluated using PCR. ResultsCCL18, CCL28, and CXCL13 expression in H. pylori-positive subjects were significantly higher than H. pylori-negative subjects. CCL18 and CXCL13 expression in H. pylori-positive subjects with oipA+ and babA2+were significantly higher than H. pylori-positive subjects with oipA¯ and babA2¯. CCL18 and CXCL13 expression were found to be significantly elevated in H. pylori-positive subjects with gastritis compared with H. pylori-positive subjects with PUD. CCL28 expression was significantly higher in H. pylori-positive subjects with PUD compared with H. pylori-positive subjects with gastritis. ConclusionsThe increased of CCL18 and CXCL13 may be involved in the pathogenesis of H. pylori-associated gastritis, while the increased of CCL28 may be involved in the pathogenesis of H. pylori-associated PUD.

Effect of Outpatient Status on Practice Management of H. pylori-associated Peptic Ulcer Disease

Introduction:Helicobacter pylori infection remains an important cause of peptic ulcer disease (PUD). The 2007 and updated 2017 American College of Gastroenterology guidelines indicate that patients with H. pylori-associated PUD should receive eradication therapy followed by confirmation testing to prove H. pylori eradication. The latter is relevant because initial H. pylori treatment is often only 70-85% successful and persistent H. pylori infection may be associated with recurrent ulcers and gastric malignancy. Despite guidelines, confirmation testing rates are modest (30-40%) for largely unexplored reasons. The aim was to identify barriers and predictors of receiving guideline-concordant confirmation testing. Methods: We performed a retrospective cohort study of patients with active H. pylori-associated PUD diagnosed in 2007-2015, who received standard eradication therapy and had follow-up within one year. Our primary outcome of interest was the effect of outpatient vs. inpatient status (at time of peptic ulcer diagnosis) on confirmation testing rates. We also compared confirmation testing rates in patients with vs. without repeat endoscopy and patients with vs. without gastroenterology follow-up. We used logistic regression models with propensity scores to control for age, sex, race, comorbidity status, insurance status, ulcer location and symptom persistence. Results: 67/152 (44%) patients received guideline-concordant confirmation testing. Outpatients (OR 3.9, 95% CI 1.8-8.8, p=0.0009) and patients who had gastroenterology follow-up (OR 9.7, 95% CI 3.2-29.0, p=0.0009) were significantly more likely to receive confirmation testing than their counterparts (Table 1). Repeat endoscopy was not a significant independent predictor of receiving confirmation testing.Table: Table. Independent predictors of receiving confirmation testing to prove H. pylori eradication in patients with H. pylori-associated peptic ulcer diseaseConclusion: This study provides some insight into the discrepancy between recommended and practiced management of H. pylori-associated PUD following eradication therapy. We identified outpatient status and gastroenterology follow-up as independent predictors of receiving guideline-concordant confirmation testing. These findings suggest a potential role for quality improvement initiatives, particularly during the transition of care from inpatient to outpatient setting, in order to optimize adherence to best practices.

Helicobacter pylori infection and nonmalignant diseases.

A substantial decrease in Helicobacter pylori-associated peptic ulcer disease has been observed during the last decades. Drug-related ulcers as well as idiopathic ulcers are becoming predominant and are more refractory to treatment; however, H. pylori infection still plays an important role in ulcer bleeding and recurrence after therapy. The effect of H. pylori eradication upon functional dyspepsia symptoms has been reviewed in this article and generally confirms the results of previous meta-analyses. Additional evidence suggests a lack of impact upon the quality of life, in spite of improvement in symptoms. The association of H. pylori with gastroesophageal reflux disease and Barrett's esophagus remains controversial with a majority of published studies showing a negative association. Furthermore, a strong inverse relationship between the presence of H. pylori and the esophageal eosinophilia was also reported. Several studies and a review addressed the role of H. pylori in autoimmune gastritis and pernicious anemia. The association of the above still remains controversial. Finally, the necessity of routine endoscopy and H. pylori eradication before bariatric surgery is discussed. Several studies suggest the rationale of preoperative upper endoscopy and H. pylori eradication prior to surgery. However, the prevalence of H. pylori infection prior to surgery in these studies generally reflects the overall prevalence of the infection in the particular geographic area. In addition, results on the role of H. pylori in developing postoperative complications remain controversial.

On the importance of developing a new generation of breath tests for Helicobacter pylori detection

State-of-the-art methods for non-invasive detection of the Helicobacter pylori (H. pylori) infection have been considered. A reported global tendency towards a non-decreasing prevalence of H. pylori worldwide could be co-influenced by the functional limitations of urea breath tests (UBTs), currently preferred for the non-invasive recognition of H. pylori in a clinical setting. Namely, the UBTs can demonstrate false-positive or false-negative results. Within this context, limitations of conventional clinically exploited H. pylori tests have been discussed to justify the existing need for the development of a new generation of breath tests for the detection of H. pylori and the differentiation of pathogenic and non-pathogenic strains of the bacterium. This paper presents the results of a pilot clinical study aimed at evaluating the development and diagnostic potential of a new method based on the detection of the non-urease products of H. pylori vital activity in exhaled gas. The characteristics of breath of adolescents with H. pylori-positive and H. pylori-negative functional dyspepsia, together with a consideration of the cytotoxin-associated gene A (CagA) status of H. pylori-positive subjects, have been determined for the first time using innovative point-contact nanosensor devices based on salts of the organic conductor tetracyanoquinodimethane (TCNQ). The clinical and diagnostic relevance of the response curves of the point-contact sensors was assessed. It was found that the recovery time of the point-contact sensors has a diagnostic value for differentiation of the H. pylori-associated peptic ulcer disease. The diagnostically significant elongation of the recovery time was even more pronounced in patients infected with CagA-positive H. pylori strains compared to the CagA-negative patients. Taking into account the operation of the point-contact sensors in the real-time mode, the obtained results are essential prerequisites for the development of a fast and portable breath test for non-invasive detection of cytotoxic CagA strains of H. pylori infection. The relaxation time of the point-contact nanosensors could be selected as a diagnostic criterion for non-invasive determination of H. pylori-associated destructive lesions of the gastroduodenal area in adolescents, using the point-contact spectroscopic concept of breath analysis. This can subsequently be implemented into a ‘test-and-treat’ approach for the management of uninvestigated dyspepsia in populations with a high prevalence of H. pylori (according to the Maastricht III and IV Consensus recommendations).

Effect of Acid Pump Antagonist (Revaprazan, Revanex®) on the Result of13C Urea Breath Test in the Patients withHelicobacter pyloriAssociated Peptic Ulcer Disease

Effect of Acid Pump Antagonist (Revaprazan, Revanex®) on the Result of13C Urea Breath Test in the Patients withHelicobacter pyloriAssociated Peptic Ulcer Disease

Interval hypoxic training in complex treatment of Helicobacter pylori-associated peptic ulcer disease.

This study was aimed to demonstrate the efficacy of interval hypoxic training (IHT) in complex treatment of Helicobacter pylori-associated duodenal peptic ulcer disease (DPUD) by parameters of aerobic metabolism and indexes of heart rate variability (HRV). Eighty patients with H. pylori-associated DPUD were included into the study, mean age 32+/-1.8 yrs, duration of the disease up to 10 years (66.3 %). IHT was modulated using Frolov's hypoxicator (TDI-01) for 30 days after standard eradication therapy. Daily hypoxic sessions consisted of three one-minute sessions, one two-minute, and one three-minute sessions separated by one-minute intervals of room-air breathing. Use of IHT resulted in more efficient elimination of clinical symptoms, histological hallmarks of inflammation and signs of oxidative stress in glandulocytes of the gastric mucosa as determined by 4-hydroxynonenal accumulation. Moderate prooxidant activity of IHT was demonstrated by the increased level of TBARS and oxidatively modified products, normalization of hydroperoxides, middle mass molecules and atherogenic beta-lipoproteins with simultaneous increase in catalase activity and mild decline of SOD activity. Therefore, IHT appeared to be accompanied by higher intensity of redox reactions and enhanced regeneratory processes in cells and tissues. Significant increase in HRV was also noted. Such changes were associated with reduction of inflammation signs and modulation of the autonomic homeostasis in DPUD patients. In general, use of IHT in complex treatment of H. pylori in DPUD patients can be recommended to increase resistance to oxidative stress and to modulate autonomic balance and oxidative homeostasis.

Low prevalence of idiopathic peptic ulcer disease: An Italian endoscopic survey

Background Peptic ulcer disease (PUD) represents a common condition, although its incidence is decreasing. Previous studies reported a high rate of idiopathic PUD prevalence. Aim To investigate prevalence, relative distribution of etiologic factors and prevalence of complication of PUD in an Italian endoscopic series. Materials and methods All gastroscopies performed in adult patients during 3 years were considered. Patients with PUD, with antral and corporal histology, were included in the study. Helicobacter pylori infection was assessed by histology. Idiopathic PUD was defined as an ulcer without evidence H. pylori infection or prior exposure to NSAIDs. Results 300 patients with PUD out of 11,148 gastroscopies were included in our study accounting for a prevalence of 2.7%. H. pylori-associated PUD was diagnosed in 62.3%, NSAID/aspirin-associated PUD in 22%, H. pylori/NSAID/aspirin-associated PUD in 11.6%, and idiopathic PUD in the remaining 4% of cases. Regarding ulcer complications the logistic regression analysis identified the following significant risk factors for GI bleeding: NSAIDs and/or aspirin use, age >65 years and coexistent gastric and duodenal ulcers. Conclusion Our data found a low endoscopic prevalence of peptic ulcer. Both H. pylori infection and NSAIDs and/or aspirin use remain the main determinants and idiopathic ulcer prevalence is very low.

Systematic review: the global incidence and prevalence of peptic ulcer disease

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. To evaluate the current global incidence and prevalence of PUD by systematic review of the literature published over the last decade. Systematic searches of PubMed, EMBASE and the Cochrane library. 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. 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.

Helicobacter pylori in children and adolescents.

There is now considerable evidence that suggests that the H. pylori organism isa human pathogen. The strong association between H. pylori and gastroduodenal disease is well documented. A number of hypotheses have been suggested for the pathogenic mechanisms of H. pylori-induced gastroduodenal disease, including the presence of bacterial virulence factors, the production of inflammatory mediators, disregulation of acid secretion, and the host immune response. At the present time, treatment with a combination of a proton pump inhibitor and antimicrobial agents continues to be recommended for the treatment of H. pylori-associated peptic ulcer disease.

Aging and upper gastrointestinal disorders

The prevalence of upper gastrointestinal (GI) diseases is increasing in subjects aged 65 years and over. Pathophysiological changes in esophageal functions that occur with aging may, at least in part, be responsible for the high prevalence of gastro-esophageal reflux disease (GERD) in old age. GERD symptoms are different in the elderly compared to young or adult patients; moreover, esophagitis is a more severe disease in the elderly than in young subjects, relapse occurring in a high percentage of cases in those elderly patients who are not in maintenance therapy with antisecretories. In old age, PPIs are more effective than H2-blockers in healing and reducing the relapse of esophagitis; PPI therapy is well tolerated and very effective even in elderly subjects with concomitant diseases and treatments. Discontinuing maintenance treatment with PPIs after 6 months is associated with a significant increase in the relapse rate. The incidence of gastric and duodenal ulcers and their bleeding complications is increasing in old-aged populations worldwide. Approximately 53-73% of elderly peptic ulcer patients are Helicobacter pylori positive; however, the percentage of H. pylori-positive elderly patients who are treated for their infection remains very low. We now have data that demonstrate the benefit of curing H. pylori infection in elderly patients with H. pylori-associated peptic ulcer disease and severe chronic gastritis. One-week PPI-based triple therapy regimens including clarithromycin, amoxycillin and/or nitroimidazoles are highly effective and well tolerated in elderly patients. Low doses of both PPIs and clarithromycin (in combination with standard doses of amoxycillin or nitroimidazoles) are sufficient. Almost 40% of GU and 25% of DU in the elderly patients are associated with the use of NSAID and/or aspirin. Several strategies are available to prevent NSAID-related peptic ulcers, i.e. the use of low doses and/or less damaging NSAIDs, the use of coxibs, gastroprotection with antisecretory drugs, the eradication of H. pylori infection in infected patients as well as educational programs to reduce inappropriate prescriptions. Strategies for subgroups of patients that will take account of the GI and non-GI risks, i.e. disability, co-morbidity and friality of patients, according to a comprehensive geriatric assessment are recommended.

Helicobacter pylori binds von Willebrand factor and interacts with GPIb to induce platelet aggregation

Background & Aims: Clinical studies have suggested an association between cardiovascular disease and infection with Helicobacter pylori. We examined the effect of H. pylori on platelets and the mechanism of the interaction. Methods: Three of 5 strains of H. pylori induced platelet aggregation with a lag time of 5 ± 2 minutes that was independent of the toxigenic genes cagA and vacA. Aggregation was inhibited completely by aspirin and a glycoprotein (GP) IIb/IIIa antagonist. Aggregation also was inhibited by monoclonal antibodies that prevented the von Willebrand factor (vWF) interaction with GPIb. vWF-coated H. pylori bound to cells transfected with GPIbα but not to mock transfected cells and this was inhibited by an antibody to GPIb. Results: The interaction with platelets appeared to be mediated by vWF because platelet aggregation was blocked by an antibody to vWF. Moreover, a strain of H. pylori that induced platelet aggregation bound vWF to a greater extent than a nonaggregating strain. Aggregation also required IgG and could be inhibited by an antibody to the platelet IgG receptor (FcγRIIA). Conclusions: Some strains of H. pylori induce platelet activation mediated by H. pylori-bound vWF interacting with GPIb, and supported by IgG. These platelet- H. pylori interactions may contribute to the pathogenesis of H. pylori-associated peptic ulcer disease and to the association between H. pylori infection and cardiovascular disease, whereas local platelet effects may contribute to the pathogenesis of H. pylori-associated peptic ulcer disease.

Antigen stool test for assessment of Helicobacter pylori infection in patients with upper gastrointestinal bleeding.

Re-bleeding of Helicobacter pylori-associated peptic ulcer disease is reduced by H. pylori eradication. To validate a non-invasive test, the Premium Platinum HpSA stool test, in patients with upper gastrointestinal bleeding. Stool samples of consecutive patients with relevant bleeding from gastric or duodenal ulcers or erosions were collected at initial endoscopy and during the following week. Samples were assessed using the HpSA test. H. pylori status was defined by three biopsy-based reference methods: culture, rapid urease test and histology. It was positive if culture was positive or if rapid urease test and histology were positive. One hundred and fourteen patients (mean age, 66 years) were included. In accordance with the definition, 56 (49%) were H. pylori positive. The sensitivity and specificity of the first stool sample were 84% and 90%, respectively. The respective values for two samples from consecutive days were 91% and 86%. In comparison with a serum immunoglobulin G antibody enzyme-linked immunoabsorbent assay, the HpSA test showed superior specificity. The diagnostic accuracy, in particular the sensitivity, of the HpSA stool test is reduced by upper gastrointestinal bleeding. The positive predictive value of 89%, however, justifies the initiation of eradication therapy on the basis of a positive stool test. A negative test result should be confirmed by a further diagnostic method.

Helicobacter pylori infection in geriatrics.

The prevalence of Helicobacter pylori infection increases with age worldwide. However, the percentage of H. pylori-positive elderly patients who are tested and treated for their infection remains very low. We now have data that demonstrate the benefit of curing H. pylori infection in elderly patients with H. pylori-associated peptic ulcer disease and severe chronic gastritis. Furthermore, the cure of H. pylori may prevent progression of intestinal metaplasia and gastric atrophy. Studies are needed to clarify the role of eradication for elderly patients who have nonulcer dyspepsia, gastroesophageal reflux disease and who use nonsteroidal anti-inflammatory drugs. H. pylori infection may be easily diagnosed by histological evaluation, rapid urease test or culture performed on gastric biopsies taken during endoscopy. However, the biopsy site must be carefully selected in elderly patients. For noninvasive monitoring of H. pylori infection after treatment, the 13C-urea breath test has significantly higher accuracy than serology in the elderly. The role of the H. pylori stool antigen test in old age still needs to be clarified. One-week PPI-based triple therapy regimens including clarithromycin, amoxycillin and/or nitroimidazoles are highly effective and well tolerated in elderly patients. Low doses of both PPIs and clarithromycin (in combination with standard doses of amoxycillin or nitroimidazoles) are sufficient. Antibiotic resistance and low compliance are the main factors related to treatment failure at any age.

Review article: an approach to Helicobacter pylori infection in the elderly.

The prevalence of Helicobacter pylori infection increases with age world-wide, reaching levels of 40-60% in asymptomatic elderly subjects and over 70% in elderly patients with gastroduodenal diseases. However, the percentage of H. pylori-positive elderly patients who are treated for their infection remains very low. Data are now available that demonstrate the benefit of curing H. pylori infection in elderly patients with H. pylori-associated peptic ulcer disease and severe chronic gastritis. Furthermore, the cure of H. pylori may prevent the progression of intestinal metaplasia and gastric atrophy. New studies are needed to clarify the role of eradication in elderly patients with non-ulcer dyspepsia and gastro-oesophageal reflux disease and in those who use non-steroidal anti-inflammatory drugs. H. pylori infection may be easily diagnosed by histological evaluation, rapid urease test or culture performed on gastric biopsies taken during endoscopy. However, the biopsy site must be carefully selected in elderly patients. For non-invasive monitoring of H. pylori infection after treatment, the 13C-urea breath test has significantly higher accuracy than serology in the elderly; further studies are needed to clarify the role of the H. pylori stool antigen test in old age. One-week proton pump inhibitor-based triple therapy regimens, including clarithromycin, amoxicillin and/or nitroimidazoles, are highly effective and well tolerated in elderly patients. Low doses of both proton pump inhibitors and clarithromycin (in combination with standard doses of amoxicillin or nitroimidazoles) are sufficient. Low compliance and antibiotic resistance are the main factors related to treatment failure in old age.

Recurrent abdominal pain.

1. Paul N. Thiessen, MD* 1. *Editorial Board. Clinical Professor of Pediatrics, B.C. Children’s Hospital, Vancouver, B.C., Canada After completing this article, readers should be able to: 1. Characterize the epidemiology and classification of recurrent abdominal pain. 2. List the major clinical conditions that manifest with recurrent abdominal pain. 3. Describe the most important findings in the history and physical examination of the child who has recurrent abdominal pain that suggest an organic medical condition. 4. Outline a targeted approach to ordering investigations that will confirm or disprove suspected organic disease. 5. Delineate the prognosis of recurrent abdominal pain. Recurrent abdominal pain (RAP) is a frequent and troublesome complaint in childhood and adolescence, and the search for a cause and a credible approach to management can be taxing for both family and physician. The term “recurrent abdominal pain” was coined by the British pediatrician John Apley, who first published on the subject in 1958. His definition included at least three attacks of pain occurring over a period of 3 months that were severe enough to affect activities and for which no organic cause was identified. In practice, the definition may include any child or adolescent who has RAP for which the family seeks medical attention and explanation, even if the duration of the pain does not adhere strictly to the Apley definition. The definition explicitly excludes the many causes of acute abdominal pain, which lie outside the scope of this review. There is wide variation in the threshold of severity and frequency that must be crossed before a family will seek medical attention for a child who has RAP. Inevitably, parents want a clear explanation and reassurance that no sinister causes lurk undetected, and the clinician wants to oblige but often lacks the conviction that organic causes have been excluded. The most difficult challenge for the clinician is to determine to what extent diagnostic studies should be employed before the label “recurrent abdominal …

H. pylori eradication: new role for the pharmacist?

The American Society of Health-System Pharmacists (ASHP) has published therapeutic position statements on a select group of disease states. The ASHP directors created an advisory body called the Commission on Therapeutics to be concerned with societal drug use and therapeutic issues. The ASHP therapeutic position statement on the identification and treatment of Helicobacter pylori-associated peptic ulcer disease in adults was developed by this organization after an extensive review of the available literature and consensus panel guidelines. The purpose of the article is to summarize testing options for identifying H. pylori infection, effective treatment regimens for eradicating H. pylori infection, and the role and impact of antimicrobial resistance, and to stress the importance of pharmacists’ involvement in identifying and treating patients with H. pylori-associated disease. The complexity of treatment regimens heightens the importance of patient education and monitoring to ensure compliance and optimal response to therapy. The article is divided into several sections, beginning with an informative background review of H. pylori infection including incidence, complications, and relationship to peptic ulcer disease. The first major topic addressed is testing for H. pylori infection. This section is followed by a review of six treatment regimens. The last two sections include a review of the impact of antimicrobial resistance and the role of the pharmacist as a resource in managing the H. pylori-infected patient.