Posttreatment Follow-Up of Helicobacter pylori Infection Using a Stool Antigen Immunoassay

Abstract

The Helicobacter pylori stool antigen enzyme immunoassay (HpSA) was evaluated during posttreatment follow-up of patients in a country with a very high prevalence of H. pylori infection. From among 273 dyspeptic individuals (18 to 55 years) initially recruited from a shantytown in Lima, Peru, 238 participants who met the inclusion criteria and were suspected to be H. pylori positive based on 14 C urea breath test (UBT) results underwent endoscopy. Participants with endoscopy-proven infections received standard eradication therapy and were monitored by UBT and HpSA at 1 month following treatment and at 3-month intervals for 9 months posttreatment. A second endoscopy was performed if UBT results showed evidence of treatment failure or H. pylori recurrence. Biopsy results were considered the "gold standard" in all analyses. Among patients who underwent endoscopy, HpSA had a pretreatment sensitivity of 93%. Two-hundred thirty patients completed the treatment regimen, of whom 201 (93%) were considered to have had successful treatment outcomes based on a negative follow-up UBT. Thirty-two patients with UBT-defined treatment failures or H. pylori recurrences at any point during the 9-month follow-up underwent a second endoscopy. In the posttreatment setting, HpSA had an overall sensitivity of 73% and a specificity of 67%. Agreement between UBT and HpSA diminished throughout the follow-up. Among 14 participants in whom HpSA remained positive at 1 month following treatment despite UBT evidence of treatment success, 12 (86%) became HpSA negative within 3 months posttreatment. Although this study confirmed the validity of the HpSA in the initial assessment of dyspeptic patients, the test demonstrated a reduced overall accuracy in the detection of treatment failures and H. pylori recurrences during 9 months of posttreatment follow-up. Furthermore, in some patients it may take up to 3 months after successful eradication for antigen shedding to diminish to levels within the negative HpSA range.Helicobacter pylori was first linked with gastritis in 1975 and was subsequently shown to be associated with peptic ulcer in 1985. Since then, the detection of the spiral bacterium in the gastric mucosa has become a principal aspect of the diagnostic investigation of patients with upper gastrointestinal symptoms suggestive of peptic ulcer disease (7). Chronic superficial gastritis due to infection with H. pylori is responsible for up to 95% of duodenal ulcers and 80% of gastric ulcers throughout the world (25). Perhaps the most convincing evidence for the pathogenic role of H. pylori is the dramatic effect of antibiotic therapy. Current treatment regimens combining at least two antibiotics and a proton pump inhibitor can eradicate H. pylori infections in greater than 90% of patients (21), and they significantly reduced ulcer recurrence in long-term follow-up studies (29). The organism has also been classified as a class I carcinogen due to its pathogenic role in intestinal-type gastric adenocarcinoma and has further been linked to diffus...

Detection of Helicobacter pylori DNA in human faeces and water with different levels of faecal pollution in the north-east of Spain

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Efficacy of enzyme immunoassay for the detection of Helicobacter pylori antigens in frozen stool specimens: local validation

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Stool Antigen Test for the Diagnosis of Helicobacter pylori Infection: a Systematic Review

“…Eighty‐nine studies, including 10,858 patients, fulfilled the inclusion criteria and evaluated the accuracy of the stool antigen test for the diagnosis of H. pylori in untreated patients (Table 1) [14–95]. Some of the studies reviewed included, in the same protocol, patients before and after therapy, without separating them depending on the time at which the H. pylori stool antigen test was performed, thus preventing us from calculating the true diagnostic accuracy in each circumstance [96–100].…”