Helicobacter pylori cagE is not associated with clinical outcomes in the Kurdistan region of Iraq.

We have read with interest the article entitled “cagE as a biomarker of the pathogenicity of Helicobacter pylori" by Ramis et al.1. In this study, with a sample size of 57, the authors suggested that cagE is an important prognostic indicator for developing lesions during Helicobacter pylori infection. This suggestion was based on the fact that a statistically signifi cant association was found between cagE and gastric erosion, but not between cagA and gastric erosion. With reference to this study, we conducted a study in the Kurdistan region of Iraq to examine relationships between H. pylori virulence factors and clinical outcomes. Antral Biopsies were collected from 105 patients visiting the Endoscopy Department at the Azadi Teaching Hospital for diagnostic upper gastric endoscopy. Deoxyribonucleic acid (DNA) was extracted directly from the biopsy samples, and the presence of H. pylori was confi rmed by polymerase chain reaction (PCR) amplifi cation of the ureA gene. We amplifi ed the cagA, cagE, vacAs1/m1, vacA, iceA1, iceA2, and babA2 genes and found a statistically signifi cant association between cagA and gastric and duodenal ulcerations (p = 0.005), but no statistically signifi cant association between cagE and gastric and duodenal ulcerations (p = 0.659). In addition, no association was found between other genes and clinical outcomes. cagA is a part of a 40-kb DNA insertion cassette designated as the cag pathogenicity island (cagPAI), which may have a nonHelicobacter origin. The cagPAI contains 31 putative genes, 6 of which are thought to encode components of a bacterial type IV secretion system. cagE, is a homolog of the virB4 gene from Agrobacterium tumefaciens2 and also is a part of the cagPAI