Abstract:We found evidence of Helicobacter infection in a significant number of patients presenting for colonoscopy but no specific association between the presence of these bacteria and colon disease. Our finding of disparity between molecular and serological techniques to detect Helicobacter species suggests that future studies should not rely on serology alone to detect these bacteria in the human colon.
“…Additionally, there was no statistical correlation between H. pylori PCR positivity and CRC. This finding was further confirmed in a later study on a separate population (Keenan et al, 2010).…”
“…Additionally, there was no statistical correlation between H. pylori PCR positivity and CRC. This finding was further confirmed in a later study on a separate population (Keenan et al, 2010).…”
“…Of 100 patients, 22 showed H. pylori DNA, while only 15 patients had a positive H. pylori serology, without a good correlation between the two. Thirteen others appeared to harbor Helicobacter species other than H. pylori in the colon [26].…”
If we had to give a general view of the articles published in the year 2010, we should conclude that the evidence in the year 2010 suggests that, also in Helicobacter pylori diagnosis, "the devil is in the details". In this sense, different studies suggested that skipping citric acid pretreatment or local validation or reducing the (13) C-urea dose markedly decreases the accuracy of the urea breath test. The studies also implied that, even between monoclonal stool tests, there are large differences between the marketed tests. Finally, even histology does not work adequately in patients with gastric cancer or extensive areas of intestinal metaplasia. In these cases, specific gastric sites should be biopsied to improve the reliability of histology.
“…The controls had undergone colonoscopy for a variety of reasons, but their assessment demonstrated a macroscopically and microscopically normal colon. Keenan et al (2008) investigated colonic mucosal DNA for Helicobacter from 100 patients in New Zealand (of whom 14 had IBD, 18 had adenomatous polyps, 34 had no macroscopic or microscopic abnormalities, and the remaining 34 can be presumed to have other colonic pathologies including lipoma and diverticulosis, but they are not described in detail). The IBD groups were both significantly higher in prevalence than the control cohort (P = 0.013 and 0.004, respectively).…”
The discovery of Helicobacter pylori sparked a revolution in the understanding and management of peptic ulcer disease and gastric cancer. Other Helicobacter species are recognized as important pathogenic agents in colitic diseases of rodents and primates, in particular Helicobacter bilis, Helicobacter fennelliae, Helicobacter hepaticus and Helicobacter trogontum. Helicobacter bilis and H. hepaticus are now routinely used to initiate rodent models of inflammatory bowel disease (IBD), particularly in immunocompromised hosts. Molecular evidence exists linking various non-pylori Helicobacter spp. with human IBD; however, attempts to culture organisms in this disease cohort have proved unsuccessful to date. Attributing causation has therefore proved elusive. Seven enterohepatic, non-pylori Helicobacter organisms have been successfully cultured from humans, namely Helicobacter canadensis, Helicobacter canis, Helicobacter cinaedi, H. fennelliae, Helicobacter pullorum, Helicobacter winghamensis and Helicobacter sp. flexispira taxon 8 (now classified as H. bilis). Of these, H. cinaedi and H. fennelliae are the closest to fulfilling Koch's postulates as causative agents in homosexual proctitis. The possibility that novel Helicobacter organisms have a role in the initiation of human IBD warrants further consideration and targeted investigations.
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