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The Evolving Challenges of Helicobacter pylori Disease, Diagnostics, and Treatment, Part II

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Abstract

Helicobacter pylori infects half of the world's population; is associated with several severe gastric illnesses, including peptic ulcer disease and gastric cancer; and causes significant morbidity in its host. Several trends in the field of H. pylori have evolved recently, drastically changing the way that these infections are managed. Part I of this article reviews the current challenges facing H. pylori disease management and provides both clinicians and laboratorians with a concise overview of its pathogenesis, epidemiology, and testing strategies. Part II of this article will be published in the next issue of Clinical Microbiology Newsletter (Vol. 35, No. 4) and will address treatment strategies and issues concerning medical reimbursement.

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... Colonization may be present, however it may be in its very early stages or the Ab titer may be too low for the assay to detect. Similar findings were reported by Couturier (2013). ...
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UNRAVELING the puzzle of Helicobacter pylori and its pivotal role in gastric disease was not done in isolation. Many of the pieces were already available but dispersed over 100 years in journals of different languages and subspecialties. The prevailing dogma was that the stomach was sterile and that bacteria could not survive in gastric acid, but there were articles describing gastric spiral bacteria as far back as 1886.1 Even after the advent of endoscopy, descriptions of the presence of curved organisms on the surface of the gastric mucosa were ignored by mainstream medicine.REDISCOVERY OF H PYLORI Fourteen years have passed since my work on H pylori began. In 1981, Robin Warren at Royal Perth Hospital in Western Australia first showed me the spiral bacteria he had discovered in patients with gastritis. Together we embarked on an attempt to culture the organisms by taking gastric biopsy specimens from patients
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This article presents a review of the literature on the epidemiology and public health implications of Helico-bacter pylori infection published from April 2008 through March 2009. The authors used MeSH terms ''Helicobacter infections ⁄ epidemiology,'' ''Helicobacter infections ⁄ prevention and control'' to search multiple databases (PubMed, Embase, Cochrane, Cochrane Library, EBMR, BIOSIS), and independently searched PubMed using the term ''Helicobacter'' with ''Epidemi-ology,'' ''Transmission,'' ''Prevalence,'' or ''Environ-ment.'' Papers without topical relevance were excluded. Two additional papers known to the authors were added. The identified literature is summarized below by subtopic: reviews; prevalence; incidence; transmission; risk factors; and public health policy. Reviews The search identified six review papers. Bruce and Maa-roos summarized studies on the epidemiology of H. pylori infection published in peer-reviewed journals [1]. Daugule and Rowland summarized articles on the epi-demiology of H. pylori infection in children [2]. Tan et al. examined the changing H. pylori epidemiology in Asia [3]. All three of these reviews noted that the prev-alence of H. pylori infection was decreasing globally. Goodman et al. reviewed studies of H. pylori infection in Canadian and related Arctic Aboriginal populations, revealing a relatively high prevalence of the infection and occurrence of associated disease in these groups [4]. Zhang et al. summarized 1986–2008 publications on re-infection, recurrence, or recrudescence of H. pylori identified in Medline, concluding that re-infection was not a major concern in clinical settings [5]. A review presenting Asia-Pacific consensus guidelines on gastric cancer prevention concluded that H. pylori screening and treatment strategies aimed at high-risk populations will probably reduce gastric cancer inci-dence and were therefore recommended [6].
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This article presents a review of the literature on the epidemiology and public health implications of Helicobacter pylori infection published from April 2008 through to March 2009. The authors used MeSH terms "Helicobacter infections epidemiology,"Helicobacter infections prevention and control" to search multiple databases (PubMed, Embase, Cochrane, Cochrane Library, EBMR, BIOSIS), and independently searched PubMed using the term "Helicobacter" with "Epidemiology,"Transmission,"Prevalence" or "Environment." Articles without topical relevance were excluded. Two additional papers known to the authors were added. The identified literature is summarized by subtopic: reviews; prevalence; incidence; transmission; risk factors; and public health policy.
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Diseases associated with Helicobacter pylori infection, such as peptic ulcer disease and gastric cancer, afflict men more frequently than women. No study, however, has demonstrated any difference in sex-specific rates of H. pylori infection. In a healthy population undergoing multiphasic health evaluations in 1992-1993 as members of the Kaiser Permanente Medical Care Program of Northern California, adults aged 20-39 years were screened for antibodies to H. pylori infection using a serum enzyme-linked immunosorbent assay and were surveyed with regard to their demographic characteristics and health practices. Among 556 African-American, Hispanic, and white men and women, male sex was a significant risk factor for infection. Other risk factors included African-American race and Hispanic ethnicity, increasing age, living with children, birth in a developing country, and lower levels of income and education. Men consistently had a higher prevalence of antibodies across all strata of race/ethnicity, age, education, and income, and in multivariate analysis male sex remained significantly associated with infection (odds ratio = 2.0, 95% confidence interval 1.2-3.1). African-American race, Hispanic ethnicity, increasing age, lower levels of education, and birth in a developing country were also associated with infection in multivariate analysis. Data from previously reported seroprevalence studies support a tendency for men to have a higher risk of infection. The higher prevalence of infection among young males as observed in Northern California may account in part for the increased incidence of H. pylori-related diseases among men in later decades of life.
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To study the prevalence and risk factors of Helicobacter pylori infection in healthy young adults, sera were collected from a nationwide sample of 404 females and 534 males (mean age, 20.2; range, 17-26 years) at induction into the US Army at Fort Jackson, South Carolina, during the fall of 1990. An enzyme-linked immunosorbent assay (PYLORI STAT, BioWhittaker, Inc., Walkersville, MD) was used to detect H. pylori-specific immunoglobulin G antibodies. Demographic data were obtained from a personnel database and by linking US census information to the subject's home address. The observed crude seropositivity rate was 26.3% (95% confidence interval 23.2-28.9). The direct sex-, race-, and geographic region-adjusted seropositivity rate was 20.8% (95% confidence interval 17.9-23.7). Seropositivity rates for blacks, Hispanics, and whites were 44%, 38%, and 14%, respectively, (chi 2, p < 0.001), and rates increased progressively from 24% in the age group 17-18 years to 43% in the age group 24-26 years (chi 2 for trend, p < 0.001). The age trends remained strong after controlling for race Median income was also an important predictive variable for seropositivity (chi 2, p < 0.0001). Sex, the percent urbanization, and population density of the home county were not significant predictors of seropositivity when age and race-ethnic group were controlled in a statistical model. The sharp increase in seroprevalence in this narrow age range suggests that the incidence rates are higher in young adults than previously reported.
Article
We have shown previously that cure of Helicobacter pylori infection leads to the disappearance of acid-neutralizing substances. Also, patients with ulcer after cure may gain weight. The aim of this study was to investigate whether cure of the infection increases the risk of reflux esophagitis. Patients with duodenal ulcer without reflux esophagitis at the time of Helicobacter treatment were followed up prospectively after cure of the infection (n = 244) or after diagnosis of persisting infection (n = 216). All patients underwent endoscopy at 1-year intervals or when upper gastrointestinal symptoms recurred. H. pylori infection was assessed by rapid urease test and histology. The estimated incidence of reflux esophagitis within 3 years was 25.8% after cure of the infection and 12.9% when the infection was ongoing (P < 0.001). Patients who developed reflux esophagitis after the cure had a more severe body gastritis before cure (odds ratio, 5.5; 95% confidence interval [CI], 2.8-13.6), gained weight more frequently after cure (odds ratio, 3.2; 95% CI, 1.2-9.4), and were predominantly men (odds ratio, 3.6; 95% CI, 1.1-10.6). A considerable proportion of patients with duodenal ulcer treated for H. pylori will develop reflux esophagitis; risk factors are male sex, severity of corpus gastritis, and weight gain.
Article
Success in diagnosing a disease depends to a large extent upon the choice of diagnostic techniques. Nowhere is this more obvious than in the case of gastroduodenal infection withHelicobacter pylori. H. pylori had been observed in the gastric mucosa by several independent investigators since the beginning of the twentieth century (Krienitz 1906; Luger and Neuberger 1921; Doenges 1939; Freedberg and Barron 1940), yet its existance was often doubted by the experts of the time. In 1954 Palmer reported a large study of more than 1000 patients undergoing suction biopsies of their stomachs.Palmer had specifically looked for the “spirochetes” observed by others, but found none and concluded that these organisms were just “simple contamination of the mucosal surface by swallowed spirochetes.” Palmer missed the opportunity to discover H. pylori by using an inappropriate diagnostic test. He stained his biopsies with the commonly used H&E stain. This stain is excellent for displaying tissue morphology but can be a relatively poor stain for visualizing H. pylori. Twenty-five years later Warren in Australia was studying gastric mucosa using a Warthin-Starry silver stain (Marshall 1989). This stain shows the bacteria very well, and soon he and Marshall surprised the scientific community by reporting the presence of “unidentified curved bacilli on gastric epithelium in active chronic gastritis” (Warren and Marshall 1983).
Article
The living conditions of many aboriginal communities in Canada may place their residents at risk for H. pylori infection. Our aims were to determine: (1) the seroprevalence of H. pylori in a traditional Indian community, (2) the clinical relevance of H. pylori infection in this population, and (3) if H. pylori could be identified by polymerase chain reaction from the local water. A demographic questionnaire was administered, and blood was collected from subjects in an Indian community in northwestern Manitoba. The serum was analyzed by ELISA for IgG to H. pylori and to CagA. ABO and Lewis antigens were tested. Age-adjusted incidence of gastric cancer and of hospitalizations associated with diagnoses of peptic ulcer were determined for the Indian and non-Indian Manitoba population in the years 1989-1993. Nested PCR was performed on lake water using H. pylori-specific primers and the amplicons probed with an internal Dig-labeled probe. Three hundred six (59%) of approximately 518 individuals who were resident in the community at the time of the study were enrolled. The ELISA for H. pylori was positive in 291 (95%). There was no association between H. pylori seropositivity and age, sex, gastrointestinal complaints, medications, housing characteristics, and ABO or Lewis antigen status. CagA was positive in 84.5% of infected subjects. The average annual age-adjusted incidence of hospitalizations associated with diagnoses of peptic ulcer disease in Manitoba was higher for treaty-status Indians (394.3/100,000) than for non-Indians (203.8/100,000), but gastric cancer rates were similar (11.2/100,000 vs 11.6/100,000). No H. pylori DNA was detected in the lake water. In conclusion, the seroprevalence of CagA-positive H. pylori is high in this representative Manitoban Indian community. This may be associated with an increased risk for peptic ulcer disease but is not associated with an increased risk for gastric cancer.
Article
In previous studies an exaggerated effect of proton pump inhibitors (PPIs) on intragastric pH in Helicobacter pylori-infected patients was observed. Because healing and improvement of symptoms in patients with gastroesophageal reflux disease (GERD) is directly associated with an increase of intragastric pH during treatment, we hypothesized that the response to treatment with a PPI in patients with reflux esophagitis would be better in H. pylori-infected patients than in patients without H. pylori infection. We recruited 971 patients with endoscopically verified reflux esophagitis grades II and III (Savary/Miller). At study entry, H. pylori status was assessed by a 13C-urea breath test and baseline characteristics were recorded. Physicians and patients were not notified about the results of the breath test until completion of the study. All patients underwent treatment with pantoprazole, 40 mg orally once daily for 4 weeks. Healing was verified by endoscopy after 4 or 8 weeks of treatment. If the esophagitis had not completely healed at this time, treatment was continued for a further 4-week period. Healing rates and symptom relief were compared for patients with and without H. pylori infection. The prevalence of H. pylori was 39.9% (95% confidence interval [CI], 36.9-42.9), and neither gender, smoking, nor alcohol consumption were associated with the H. pylori infection (P > 0.4). The trial was completed by 846 patients without protocol violation. Overall healing rates of reflux esophagitis were 80.4% (95% CI, 77.7-83.1) and 93.6% (95% CI, 91.8-95.2) after 4 and 8 weeks, respectively. In H. pylori-positive patients, healing rates were significantly higher after 4 (86.6% vs. 76.3%; P = 0.0005) and 8 weeks (96.4% vs. 91.8%; P < 0.004). Relief of symptoms after 4 weeks was also significantly (P < 0.05) better in H. pylori-infected patients than in uninfected patients. Patients with reflux esophagitis and H. pylori infection respond significantly better than H. pylori-negative patients to the PPI pantoprazole.
Article
Many North American arctic communities are characterized by risk markers associated with Helicobacter pylori (H. pylori) infection, including overcrowded housing and inadequate water supply and sanitation systems. Our aim was to determine the seroprevalence of H. pylori infection in two traditional Inuit communities in the central Canadian arctic and to test for the presence of H. pylori, by polymerase chain reaction (PCR), in local water supplies. Samples of venous whole blood from adults and capillary blood from children were collected and analyzed by enzyme immunoassay and Helisal Rapid Test, respectively, for IgG antibody to H. pylori. Antibodies to CagA were detected by enzyme immunoassay, and ABO and Lewis antigens were also determined. Demographic and clinical information were collected by questionnaire. Water samples from each community were tested for H. pylori by PCR. One hundred-thirty (50.8%) of 256 subjects from the two communities were positive for H. pylori IgG antibodies. Seropositive subjects were more likely to be male, compared with seronegative individuals (p = 0.01). Antibody status did not differ with respect to age, community, alcohol or cigarette use, number of persons per household, gastrointestinal complaints or previous investigations, medications, or presence of blood group O, Lewis a-b+. CagA antibodies were detected in 78 (61.9%) of 126 H. pylori-seropositive subjects tested; however, 41 (35.3%) of 116 H. pylori-seronegative subjects were also CagA positive. Water samples taken from the water delivery truck in Chesterfield Inlet and two lakes near Repulse Bay were positive for H. pylori. The seroprevalence of H. pylori in the study group was higher than rates in southern Canadian populations, but lower than the seroprevalence previously documented in a Canadian subarctic Indian (First Nations) community. The detection of H. pylori in local water supplies may indicate a natural reservoir for the organism or possible contamination from human sewage.
Article
Helicobacter pylori infection can be diagnosed by invasive (that is, endoscopy and biopsy) and non-invasive techniques. The choice of a diagnostic test should depend on the clinical circumstances, the pre-test probability of infection, sensitivity and specificity of the test (or more correctly the likelihood ratio of a positive and negative test), the cost effectiveness of the testing strategy, and the availability of the test. Some clinical circumstances warrant invasive studies: patients who have failed eradication therapy may need culture and antimicrobial sensitivity testing to help determine an appropriate regimen, older patients with new onset dyspepsia, and those with “alarm” symptoms (bleeding, weight loss, etc) that raise the concern of malignancy. Non-invasive studies are preferable in epidemiological studies and in young children. Recent studies have also demonstrated that a strategy to test and treat H pylori in uninvestigated young (<50 years) dyspeptic patients in primary care is safe and reduces the need for endoscopy.1 Until recently, only two non-invasive methods of testing for H pylori have been available: (1) the13C or 14C labelled urea breath test (UBT), which is based on detection of 13C or 14C labelled CO2 in expired air as a result of H pylori urease activity2-4and (2) serology (which is based on detection of a specific anti- H pylori IgG antibody in the patient's serum.5 6 Several new methods of detecting H pylori have recently been described and include detection of antibodies in saliva7 and urine,8 and detection of antigens in stool. ### SEROLOGY There are a number of different techniques for antibody detection in serum, including enzyme linked immunosorbant assay (ELISA), agglutination tests, and western blotting but ELISA is the most widely used clinically. Antibody levels persist in the blood for long periods of time. Not surprisingly, …
Article
The 14C-urea breath test is an accurate means of identifying the presence of H. pylori infection before and after antimicrobial therapy. Several issues, including out of office analysis, the need for a support structure to perform the test, concerns regarding radiation exposure, and inconsistent reimbursement, have slowed the widespread acceptance of the 14C-urea breath test in clinical practice. Despite these problems, the 14C-urea breath test is simple, rapid, and relatively inexpensive compared with the currently available version of the 13C-urea breath test. As such, the 14C-urea breath test provides an attractive, nonendoscopic means of identifying active H. pylori infection.
Article
Gastroduodenal disease associated with Helicobacter pylori infection are reviewed as well as the diagnostic approach. Generally, there are by and large two ways in which a diagnosis of infection by Helicobacter pylori can be made: by using either an invasive or non-invasive procedure. The invasive procedures involve endoscopy and biopsy Biopsy is essential since the mucosa may often appear macroscopically normal but, nevertheless, be inflamed. Once a biopsy is obtained histological examination, culture, polymerase chain reaction, detection of the presence of urease activity can be detected. The non-invasive tests that can be used to diagnose the infection are: serology, detection of labelled metabolic products of urea hydrolysis either in the breath (13CO2, 14CO2), the urine or the blood, detection of Helicobacter pylori antigen in stool specimen. At present, no single test is sufficiently reliable to definitely detect colonisation by Helicobacter pylori, and a combination of two is recommended, if feasible. Choice of the test to be used is not straightforward and relies on a series of situations, i. e., clinical setting and local expertise and availability, that the clinician must consider to obtain the best diagnostic yeld. The challenge of Helicobacter pylori eradication is not very easy to obtain. The possible scenario and the use of a new proton pump inhibitor (esomeprazole) are reviewed and discussed.
Article
Gastro-oesophageal reflux disease (GERD) and Helicobacter pylori infection are common conditions that frequently coexist. Controversy continues regarding the role of H. pylori infection in GERD. The results of some studies suggest that eradication of H. pylori may increase the risk for developing GERD, and some experts have suggested that chronic H. pylori infection may be of benefit. This article reviews the data on H. pylori infection and GERD and its treatment.
Article
Although gastric adenocarcinoma is associated with the presence of Helicobacter pylori in the stomach, only a small fraction of colonized individuals develop this common malignancy. H. pylori strain and host genotypes probably influence the risk of carcinogenesis by differentially affecting host inflammatory responses and epithelial-cell physiology. Understanding the host-microbial interactions that lead to neoplasia will improve cancer-targeted therapeutics and diagnostics, and provide mechanistic insights into other malignancies that arise within the context of microbially initiated inflammatory states.
Article
The relationship between previous antimicrobial treatments and infection with drug-resistant Helicobacter pylori is unknown. To determine whether previous use of antimicrobial agents predicts subsequent antibiotic resistance of H. pylori and whether resistance affects treatment outcome. Retrospective cohort analysis of adults recruited sequentially from a clinical practice. A referral hospital in Anchorage, Alaska. 125 adults infected with H. pylori. Medical records were reviewed for antimicrobial agents prescribed in the 10 years before diagnosis with H. pylori infection. Antimicrobial susceptibility of H. pylori isolates obtained from endoscopic gastric biopsy was determined by using agar dilution. Cure was determined by using the urea breath test 2 months after antimicrobial treatment. Among the 125 patients, 37 (30%) were found to have H. pylori isolates resistant to clarithromycin and 83 (66%) were found to have H. pylori isolates resistant to metronidazole. Resistance to clarithromycin was associated with previous use of any macrolide antibiotic (P < 0.001), and resistance to metronidazole was associated with previous use of metronidazole (P < 0.001). The odds of isolates being resistant to clarithromycin increased in relation to the number of courses of macrolides received (P < 0.001). Among 53 persons treated with clarithromycin-based regimens, treatment failed in 77% of those carrying clarithromycin-resistant H. pylori (10 of 13) and 13% of those with clarithromycin-susceptible strains (5 of 40) (relative risk, 6.2 [95% CI, 1.9 to 37.1]; P < 0.001). Previous use of macrolides and metronidazole is associated with H. pylori resistant to these antimicrobial agents. Clarithromycin resistance is associated with a greater risk for failure with clarithromycin-based treatments.
Article
The cultivation of Helicobacter pylori and the recognition of its clinical significance have served to stimulate interest in bacteria associated with the gastrointestinal and hepatobiliary tracts. Many novel Helicobacter species have been identified and are increasingly recognized in association with human disease, most of which is likely acquired as a zoonosis. Because their identification can be difficult by use of routine methods available in the clinical laboratory, awareness of methods for diagnosis and treatment of these Helicobacter species is important, particularly in the evaluation of immunocompromised patients.
Article
The urea breath test is a non-invasive, simple and safe test which provides excellent accuracy both for the initial diagnosis of Helicobacter pylori infection and for the confirmation of its eradication after treatment. Some studies have found no differences between urea breath test performed under non-fasting conditions. The simplicity, good tolerance and economy of the citric acid test meal probably make its systematic use advisable. The urea breath test protocol may be performed with relatively low doses (<100 mg) of urea: 75 mg or even 50 mg seem to be sufficient. With the most widely used protocol (with citric acid and 75 mg of urea), excellent accuracy is obtained when breath samples are collected as early as 10–15 min after urea ingestion. A unique and generally proposed cut-off level is not possible because it has to be adapted to different factors, such as the test meal, the dose and type of urea, or the pre-/post-treatment setting. Fortunately, because positive and negative urea breath test results tend to cluster outside of the range between 2 and 5‰, a change in cut-off value within this range would be expected to have little effect on clinical accuracy of the test.
Article
Secreted proteins are of general interest from the perspective of bacteria-host interaction. The gastric bacterial pathogen Helicobacter pylori uses a set of secreted and translocated proteins--including outer membrane adhesins, secreted extracellular enzymes and translocated effector proteins--to adapt to its extraordinary habitat, the gastric mucosa. Two major virulence factors of H. pylori are the vacuolating cytotoxin (VacA) and the cag type-IV secretion system and its translocated effector protein, cytotoxin-associated antigen A (CagA). VacA targets not only epithelial cells, but also cells of the immune system and induces immunosuppression. CagA has been shown to interact with a growing set of eucaryotic signaling molecules in phosphorylation-dependent and -independent ways.
Article
Detection of Helicobacter pylori antigen in faeces is a valid method to diagnose H. pylori infection. Presently available stool tests are performed in the laboratory, and diagnostic report is delayed. To evaluate a new rapid stool test in a pre-treatment setting and to compare it with a validated laboratory stool test. A total of 105 patients underwent gastroscopy with brush cytology, and biopsies for histology and rapid urease test, to assess H. pylori presence. Helicobacter pylori-status was considered positive if at least two tests were positive; negative if all tests were negative; indeterminate if one test was positive and two negative. Stool specimens were tested using either a rapid immunoassay kit (ImmunoCard STAT) or a laboratory enzyme immunoassay kit (Hp StAR). Sixty patients were infected with H. pylori, 44 non-infected, one indeterminate. The sensitivity and specificity of ImmunoCard STAT were 85 and 93%; those of Hp StAR were 88 and 100% (not significant). ImmunoCard STAT seems a reliable method for detecting H. pylori in untreated patients. It could replace laboratory stool tests, as it is easy and can be performed quickly. These characteristics might be a breakthrough for diagnosing H. pylori in the doctor's office.
Article
As an update to previously published recommendations for the management of Helicobacter pylori infection, an evidence-based appraisal of 14 topics was undertaken in a consensus conference sponsored by the Canadian Helicobacter Study Group. The goal was to update guidelines based on the best available evidence using an established and uniform methodology to address and formulate recommendations for each topic. The degree of consensus for each recommendation is also presented. The clinical issues addressed and recommendations made were: population-based screening for H. pylori in asymptomatic children to prevent gastric cancer is not warranted; testing for H. pylori in children should be considered if there is a family history of gastric cancer; the goal of diagnostic interventions should be to determine the cause of presenting gastrointestinal symptoms and not the presence of H. pylori infection; recurrent abdominal pain of childhood is not an indication to test for H. pylori infection; H. pylori testing is not required in patients with newly diagnosed gastroesophageal reflux disease; H. pylori testing may be considered before the use of long-term proton pump inhibitor therapy; testing for H. pylori infection should be considered in children with refractory iron deficiency anemia when no other cause has been found; when investigation of pediatric patients with persistent or severe upper abdominal symptoms is indicated, upper endoscopy with biopsy is the investigation of choice; the 13C-urea breath test is currently the best noninvasive diagnostic test for H. pylori infection in children; there is currently insufficient evidence to recommend stool antigen tests as acceptable diagnostic tools for H. pylori infection; serological antibody tests are not recommended as diagnostic tools for H. pylori infection in children; first-line therapy for H. pylori infection in children is a twice-daily, triple-drug regimen comprised of a proton pump inhibitor plus two antibiotics (clarithromycin plus amoxicillin or metronidazole); the optimal treatment period for H. pylori infection in children is 14 days; and H. pylori culture and antibiotic sensitivity testing should be made available to monitor population antibiotic resistance and manage treatment failures.
Article
Dyspepsia is a chronic or recurrent pain or discomfort centered in the upper abdomen; patients with predominant or frequent (more than once a week) heartburn or acid regurgitation, should be considered to have gastroesophageal reflux disease (GERD) until proven otherwise. Dyspeptic patients over 55 yr of age, or those with alarm features should undergo prompt esophagogastroduodenoscopy (EGD). In all other patients, there are two approximately equivalent options: (i) test and treat for Helicobacter pylori (H. pylori) using a validated noninvasive test and a trial of acid suppression if eradication is successful but symptoms do not resolve or (ii) an empiric trial of acid suppression with a proton pump inhibitor (PPI) for 4-8 wk. The test-and-treat option is preferable in populations with a moderate to high prevalence of H. pylori infection (> or =10%); empirical PPI is an initial option in low prevalence situations. If initial acid suppression fails after 2-4 wk, it is reasonable to consider changing drug class or dosing. If the patient fails to respond or relapses rapidly on stopping antisecretory therapy, then the test-and-treat strategy is best applied before consideration of referral for EGD. Prokinetics are not currently recommended as first-line therapy for uninvestigated dyspepsia. EGD is not mandatory in those who remain symptomatic as the yield is low; the decision to endoscope or not must be based on clinical judgement. In patients who do respond to initial therapy, stop treatment after 4-8 wk; if symptoms recur, another course of the same treatment is justified. The management of functional dyspepsia is challenging when initial antisecretory therapy and H. pylori eradication fails. There are very limited data to support the use of low-dose tricyclic antidepressants or psychological treatments in functional dyspepsia.
Article
Recently, several new diagnostic methods aimed to detect Helicobacter pylori stool antigens have been developed. Our aim was to evaluate the accuracy of 3 different stool tests to confirm H. pylori eradication. Patients and methods: Twenty-six patients received H. pylori eradication treatment. Eradication was confirmed with 13C-urea breath test 6-8 weeks later, when stool samples were analyzed by polyclonal (Premier-Platinum-HpSATM), monoclonal (Amplified-IDEIATM-HpStARTM), and rapid test (ImmunoCard-STAT-HpSATM). H. pylori was eradicated in 85% of the cases. Sensitivity, specificity, positive predictive value and negative predictive value with the polyclonal test were: 25%, 91%, 33% and 87%. Corresponding results with the monoclonal test, using the cut-off point recommended by the manufacturer, were 100%, 46%, 25% and 100%. However, the best cut-off point in our study had 100% sensitivity and 91% specificity. The area under ROC curve for the polyclonal and the monoclonal tests was 0.65 and 0.95. Diagnostic accuracy with the rapid test was 75%, 90%, 60% and 95%. Neither the polyclonal stool antigen test nor the rapid stool antigen test can be recommended to confirm H. pylori eradication after treatment. The monoclonal test has better diagnostic accuracy, although more studies are necessary to definitively recommend its use for the confirmation of H. pylori eradication success.
Article
The prevalence and persistence of antibodies against cytomegalovirus (CMV), herpes simplex virus types 1 (HSV1) and 2 (HSV2), Helicobacter pylori and Chlamydia pneumoniae were determined in Alaskan Eskimos. The study included 610 individuals (mean age 43 +/- 15 years; 45% males) participating in the Genetics of Coronary Artery Disease in Alaska Natives (GOCADAN) study. Archived serum samples and those collected during the GOCADAN study were analysed for antibodies against the above pathogens by ELISA. The current prevalence of antibody seropositivity was 94% to CMV, 90% to HSV1, 38% to HSV2, 80% to H. pylori, and 42% to C. pneumoniae. The persistence of antibodies (in both archived and current samples) against CMV, HSV1 and H. pylori was high (83%, 84% and 67%, respectively) compared with those against HSV2 (26%) and C. pneumoniae (29%). Moreover, the seroconversion rates to these organisms were low. Most individuals acquired CMV, HSV1 and H. pylori antibodies by the age of 24 years (94%, 90% and 72%, respectively), and >50% carried HSV2 and C. pneumoniae antibodies by the age of 45 years. There were gender differences in antibody seropositivity rates. Over 70% of individuals had antibodies to at least three of the five pathogens tested. The study demonstrated the high prevalence and lifelong persistence of multiple antibodies, suggesting chronic infections among Alaskan Eskimos.
Article
Limited information exists regarding risk factors for reinfection after cure of Helicobacter pylori infection. To determine the 2-year reinfection rate of H. pylori in a cohort of urban Alaska Natives. Participants over 18 years of age undergoing oesophagogastroduodenoscopy had (13)C urea breath test, culture, CLOtest and histology performed. Those diagnosed with H. pylori who tested urea breath test-negative at 8 weeks after treatment were followed prospectively at 4 months, 6 months, 1 year and 2 years. Subjects experiencing H. pylori reinfection as defined by a positive urea breath test were compared with those who did not become reinfected using univariable and multivariable analysis. Risk of reinfection over time was estimated by the Kaplan-Meier method. Helicobacter pylori reinfection occurred in 14 of 98 subjects successfully treated. The cumulative reinfection rate was 5.1% (95% CI: 0.7%-9.5%) at 4 months, 7.2% (2.0-12.3%) at 6 months, 10.3% (4.2-16.3%) at 1-year and 14.5% (7.5-21.6%) at 2 years. In multivariable analysis, a history of previous peptic ulcer disease or presence of ulcer at time of study oesophagogastroduodenoscopy were the only risk factors associated with reinfection (P = 0.01). Based on the findings from our study, subjects with a history of or current peptic ulcer disease should be followed, after successful treatment for H. pylori, with periodic urea breath test to detect reinfection, as reinfection would put them at high risk for ulcer recurrence.
Article
Many bacteria carry the urease enzyme in different human ecosystems, but Helicobacter pylori is the only known bacterium showing urease activity in gastric ecosystems. For this reason, the rapid urease test (RUT) on gastric biopsies and urea breath test (C-UBT) are used to detect H. pylori infection. The aim of this study was to evaluate the presence of urease-positive bacteria other than H. pylori in gastric juice and mucosa in hypochlorhydric subjects. Twenty-five hypochlorhydric and 10 normochlorhydric patients were analyzed for the presence of H. pylori and bacterial overgrowth both in gastric juice and on the mucosa. During upper gastrointestinal endoscopy at 8.00 a.m. gastric juice samples and biopsy specimens were taken from the antrum and corpus. All samples were analyzed using standard microbiological procedures like aerobic/anaerobic growth, gram-staining, gas chromatography, API test, 96-clone method, and selective medium to search for specific bacteria. In addition, all strains isolated were screened for urease activity using the CP-test. Urease positive strains were tested for the capacity to survive in an acid environment with or without urea (10 mM/L), at pH 7, 4, 3, and 2, respectively, at different times (0, 20, 30, and 60 min). Six hypochlorhydric patients had 10 strains of urease-positive non-H. pylori bacteria among which Staphylococcus capitis urealiticum showed the strongest urease activity. Hypochlorhydric patients present many urease-positive bacteria other than H. pylori. The strong urease activity may be responsible for false positive results at RUT or UBT test in patients with suspected H. pylori infection.
Article
The relationship between prior fluoroquinolone use and levofloxacin resistance in Helicobacter pylori infection is unknown. Among 125 enrolled patients, 8.8% had H. pylori isolates that were resistant to levofloxacin. Levofloxacin resistance was associated with any prior fluoroquinolone use over the previous 10 years and with the total number of fluoroquinolone courses prescribed (P < .001).
Article
During evolution microorganisms have developed several immune modulating strategies. The Helicobacter pylori neutrophil-activating protein (HP-NAP) is a virulence factor that attracts and activates neutrophils, and promotes their endothelial adhesion and the production of oxygen radicals and chemokines, including CXCL8, CCL3 and CCL4. HP-NAP, a TLR2 agonist, is an immune modulator able to induce the expression of interleukin-12 (IL-12) and IL-23 by human neutrophils and monocytes. In fact, HP-NAP has the potential to shift antigen-specific T-cell responses from a predominant Th2 to a polarized Th1 cytotoxic phenotype, characterized by high levels of interferon-gamma and tumor necrosis factor-alpha production. Thus, HP-NAP is a key factor driving Th1 inflammation in H. pylori infection and may be a new tool for future therapeutic strategies aimed at redirecting Th2 into Th1 responses, for example in atopy, vaccinology and cancer immunotherapy.
Article
Helicobacter pylori (H. pylori) remains a prevalent, worldwide, chronic infection. Though the prevalence of this infection appears to be decreasing in many parts of the world, H. pylori remains an important factor linked to the development of peptic ulcer disease, gastric malignanc and dyspeptic symptoms. Whether to test for H. pylori in patients with functional dyspepsia, gastroesophageal reflux disease (GERD), patients taking nonsteroidal antiinflammatory drugs, with iron deficiency anemia, or who are at greater risk of developing gastric cancer remains controversial. H. pylori can be diagnosed by endoscopic or nonendoscopic methods. A variety of factors including the need for endoscopy, pretest probability of infection, local availability, and an understanding of the performance characteristics and cost of the individual tests influences choice of evaluation in a given patient. Testing to prove eradication should be performed in patients who receive treatment of H. pylori for peptic ulcer disease, individuals with persistent dyspeptic symptoms despite the test-and-treat strategy, those with H. pylori-associated MALT lymphoma, and individuals who have undergone resection of early gastric cancer. Recent studies suggest that eradication rates achieved by first-line treatment with a proton pump inhibitor (PPI), clarithromycin, and amoxicillin have decreased to 70-85%, in part due to increasing clarithromycin resistance. Eradication rates may also be lower with 7 versus 14-day regimens. Bismuth-containing quadruple regimens for 7-14 days are another first-line treatment option. Sequential therapy for 10 days has shown promise in Europe but requires validation in North America. The most commonly used salvage regimen in patients with persistent H. pylori is bismuth quadruple therapy. Recent data suggest that a PPI, levofloxacin, and amoxicillin for 10 days is more effective and better tolerated than bismuth quadruple therapy for persistent H. pylori infection, though this needs to be validated in the United States.
Methods for antimicrobial dilution and disk susceptibility testing of infrequently isolated or fastidious bacteria; approved guideline –
CLSI. 2010. Methods for antimicrobial dilution and disk susceptibility testing of infrequently isolated or fastidious bacteria; approved guideline – 2nd ed. Clinical Laboratory Standards Institute, Wayne, PA.