Helicobacter pylori Infection REPLY

Division of Cardiovascular and Medical Sciences, University of Glasgow, Gardiner Institute, Glasgow, United Kingdom.
New England Journal of Medicine (Impact Factor: 54.42). 04/2010; 362(17):1597-604. DOI: 10.1056/NEJMcp1001110
Source: PubMed

ABSTRACT A 29-year-old man presents with intermittent epigastric discomfort, without weight loss or evidence of gastrointestinal bleeding. He reports no use of aspirin or nonsteroidal antiinflammatory drugs (NSAIDs). Abdominal examination reveals epigastric tenderness. A serologic test for Helicobacter pylori is positive, and he receives a 10-day course of triple therapy (omeprazole, amoxicillin, and clarithromycin). Six weeks later, he returns with the same symptoms. How should his case be further evaluated and managed?

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    ABSTRACT: Background. Helicobacter pylori (H. pylori) was linked with several extragastrointestinal diseases, including preeclampsia and intrauterine growth restriction of fetus. One of the signals which can be transferred from mother to fetus is the H. pylori IgG antibody. Aims. We utilized a commercial immunochromatographic kit to detect the antibody in maternal and cord serum. Methods. Three hundred and forty-six females were enrolled and the blood samples were collected on antenatal examination and on delivery. The maternal H. pylori infection was determined by stool H. pylori antigen test. Results. One hundred and five females (30.3%) were H. pylori-infected, and the prevalence was higher in immigrants (43.5%) than in Taiwanese (28.7%, P = 0.058). The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of the kit were 77.1%, 88.0%, 73.6%, 89.8%, and 84.7%, respectively. This kit also had similar performance in cord serum. Comparing to the maternal result on delivery, this kit offered a consistent performance in antenatal maternal serum (kappa coefficient 0.92) and in cord serum (kappa coefficient 0.88). Conclusions. H. pylori IgG antibody can be transferred through the placenta into the fetal circulation. However, accuracy of the test kit needs to be evaluated before utilization in screening.
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    ABSTRACT: Helicobacter pylori (H pylori) infection is one of the most common chronic bacterial infections worldwide. International guidelines recommend H pylori eradication in several scenarios: patients with peptic ulcer disease, patients who have had endoscopic resection of early gastric cancer, and patients with a gastric mucosa-associated lymphoid tissue lymphoma (MALToma). There is variability among the guidelines for other conditions. Treatment options for H pylori infection include triple, quadruple, and sequential therapy. Ideally, patients in whom previous eradication attempts failed and those suspected to have resistant strains should be considered for antimicrobial sensitivity testing, which requires culture of gastric mucosal biopsies; such testing, however, has limited availability in the United States. Resistance rates vary by location depending on local antibiotic usage rates. As such, the success rates associated with different regimens vary throughout the world. Many patients with H pylori infection are asymptomatic, whereas others are diagnosed with the infection during evaluation of dyspeptic symptoms or following a diagnosis of peptic ulcer. Symptoms may not be an accurate indicator of treatment success. The American College of Gastroenterology (ACG) endorses the carbon 13-labeled urea breath test ((13)C-UBT) as the most reliable test to confirm H pylori eradication. This clinical roundtable monograph begins with an overview of H pylori infection and then discusses treatment, antibiotic resistance, management of patients with antibiotic resistance, and posttreatment testing, with a focus on the ACG guidelines.
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    ABSTRACT: Metronidazole resistance is a key factor associated with Helicobacter pylori treatment failure. Although resistance is mainly associated with mutations in rdxA and frxA genes, metronidazole resistance caused by inactivation of frxA alone is still debated. Furthermore, it is unclear whether there are other mutations in addition to the two genes associated with resistance. A metronidazole-resistant strain was cultured from the metronidazole-susceptible H. pylori strain 26695 by exposure to low concentrations of metronidazole. The genome sequences of both susceptible and resistant H. pylori were determined by Illumina next-generation sequencing, from which putative candidate resistance mutations were identified. Natural transformation was used to introduce PCR products containing candidate mutations into the susceptible parent strain 26695, and the metronidazole MIC was determined for each strain. Mutations in frxA (hp0642), rdxA (hp0954), and rpsU (hp0562) were confirmed by Sanger's method. The mutated sequence in rdxA was successfully transformed into strain 26695 and the transformants showed resistance to metronidazole. The transformants containing single mutation in rdxA showed a low MIC (16 mg/L), while those containing mutations in both rdxA and frxA showed a higher MIC (48 mg/L). No transformants containing single mutation in frxA or rpsU were obtained. Next-generation sequencing was used to identify mutations related to drug resistance. We confirmed that the mutations in rdxA are mainly associated with metronidazole resistance, and mutations in frxA are able to enhance H. pylori resistance only in the presence of rdxA mutations. Moreover, mutation in rpsU may play a role in metronidazole resistance. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
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