SUMMARYThe aim of this study was to validate the rapid lateral flow Helicobacter pylori stool antigen test (One step H. pylori antigen test, ACON laboratories, San Diego, USA; Prime diagnostics, São Paulo), using 13 C-Urea Breath Test as the gold standard for H. pylori infection diagnosis. A total of 98 consecutive patients, asymptomatic or dyspeptic, entered the study. Sixty-nine were women, with a mean age of 45.76 ± 14.59 years (14 to 79 years). In the H. pylori-positive group, the rapid stool antigen test detected H. pylori antigen in 44 of the 50 positive patients (sensitivity 88%; 95% CI: 75.7-95.5%), and six false-negative; and in the H. pylori-negative group 42 presented negative results (specificity 87.5%; 95% CI: 74.7-95.3%), and six false-positive, showing a substantial agreement (Kappa Index = 0.75; p < 0.0001; 95% CI: 0.6-0.9). Forty four of fifty patients that had positive stool antigen were H. pylori-positive, the PPV of the stool antigen test was 88% (95% CI: 75.7-95.5%), and 42 patients with negative stool antigen test were H. pylori-negative, the NPV of the stool antigen test was 87.5% (95% CI: 74.7-95.3%). We conclude that the lateral flow stool antigen test can be used as an alternative to breath test for H. pylori infection diagnosis especially in developing countries.

The purpose of this study was to verify whether the presence of any of the Helicobacter pylori cagPAI genes or segments -cagA, cagA promoter, cagE, cagM, tnpB, tnpA, cagT and the left end of the cag II (LEC) region -would be a useful marker for the risk of peptic ulcer disease development. H. pylori DNA extracted from positive urease tests of 150 peptic ulcer patients and 65 dyspeptic controls was analysed by PCR. Duodenal ulcers were present in 110, gastric ulcers in 23 and both gastric and duodenal ulcers in 17 patients. A significant association (P <0.001) was found between a conserved cagPAI and peptic ulcer disease (34 %). The positivity of the cagA gene varied according to the region of the gene that was amplified. The region near to the promoter was present in almost all of the H. pylori isolates (97.2 %). The segment from nt 1764 to 2083 and the extreme right end were frequently deleted in the isolates from the controls (P <0.01). The positivity of the promoter region of cagA and cagT, cagE, cagM and LEC showed a significant difference between the isolates from peptic ulcer patients and from the controls (P <0.01). Patients usually had moderate gastritis; however, the intensity of the active inflammation was higher in the peptic ulcer group (P <0.001). cagT, cagM, LEC and the right end terminus of the cagA-positive H. pylori isolates were associated with a 27-fold, 8-fold, 4-fold and 4-fold risk of peptic ulcer disease, respectively, and may be useful markers to identify individuals at higher risk of peptic ulcer disease development in Brazil. INTRODUCTIONHelicobacter pylori colonizes the human stomach causing chronic gastritis. A small number of individuals progress to peptic ulcer or gastric cancer. Multiple bacterial and/or host factors are involved in disease development (Backert et al., 2004;Peek, 2005).H. pylori clinical isolates are classified into two types according to their degree of pathogenicity. Type I, associated with severe disease pathology, expresses functional VacA (vacuolating cytotoxin A) and contains an insertion of 40 kb of foreign DNA, the cag (cytotoxin-associated gene) pathogenicity island (cagPAI). Type II lacks cagPAI, harbours a non-toxic form of VacA and is regarded as less virulent (Censini et al., 1996;Backert et al., 2004).The cagPAI may be divided into two regions, cag I and cag II, by a novel insertion sequence (IS605). There are approximately 16 and 15 open reading frames in cag I and cag II, respectively (Censini et al., 1996; Akopyants et al., 1998). The cagPAI encodes a type IV secretion system, which delivers CagA into the cytosol of gastric epithelial cells (Covacci & Rappuoli, 2000) through a rigid needle structure covered by Cag7 or CagY, a VirB10-homologous protein, and CagT, a VirB7-homologous protein, at the base (Rohde et al., 2003). CagA is tyrosine-phosphorylated by Src-family kinases (Selbach et al., 2002), triggering the elongated hummingbird phenotype (Higashi et al., 2005) similar to that of hepatocyte growth factor (Segal et al., 1999). Numerous phosp...

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ObjectiveTo verify whether the variable number of tandem repeat (VNTR) polymorphism in the IL-1RN gene that encodes the interleukin (IL)-1 receptor antagonist (IL-1Ra) plays a role in the outcome of gastrointestinal diseases associated with Helicobacter pylori (H. pylori) infection.MethodsPatients with normal endoscopy (n = 71), inflammation of the upper gastrointestinal tract only (n = 196), gastric ulcer (n = 28), duodenal ulcer (n = 76), and gastric cancer (n = 19) were studied. H. pylori infection was diagnosed by the urease test, histological examination, and polymerase chain reaction. The IL-1 receptor antagonist gene (IL-1RN intron 2 VNTR) was analyzed by polymerase chain reaction. Gastritis was scored according to the updated Sydney system of classification.ResultsH. pylori infection was an independent risk factor for mild (odds ratio [OR] = 5.53 [95% confidence interval [CI] = 2.63–11.64; P < 0.05]), moderate (OR = 83.93 [95% CI = 29.7–237.18; P < 0.05]) and marked (OR = 47.47 [95% CI = 5.39–418.05; P < 0.05]) gastritis. The carriage of IL-1RN*2/*2 had a significant protective effect of H. pylori infection (OR = 0.31 [95% CI = 0.17–0.57; P < 0.05]). H. pylori infection was identified as an independent risk of inflammation, duodenal ulcer, and gastric ulcer. The carriage of IL-1RN*2/*2 was an independent risk factor for gastric cancer (OR = 5.81 [95% CI = 1.06–31.98; P < 0.05]); nonetheless, the carriage of allele 2 (IL-1RN*2/*2 plus IL-1RN*L/*2) had an independent protective effect on duodenal ulcer (OR = 0.45 [95% CI = 0.22–0.91; P < 0.05]).ConclusionsAllele 2 of the VNTR IL-1RN polymorphism had a protective effect against duodenal ulcer and H. pylori infection; however, it increased the risk of gastric cancer.