Potential implications of Helicobacter pylori-related neutrophil-activating protein

Helicobacter pylori （H. pylori） virulence factors pro- mote the release of various chemoattractants/inflam- matory mediators, including mainly the neutrophil- attractant chemokine interleukin-8 and neutrophil- activating protein （NAP）, involved in H. pylor/-induced gastric pathologies. Co-administration of Chios mastic gum （CMG）, which inhibits H. pylor/NAP, with an H. pylori eradication regimen might add clinical benefits against H. pylori-related gastric pathologies, but pos- sibly not CMG as main therapy. Although H. pylori NAP and other H. pylori-related cytotoxins [i.e., vaculating cytotoxin （VacA）] appear to play a major role in gener- ating and maintaining the H. pylori-associated gastric inflammatory response and H. pylor/NAP is a promising vaccine candidate against H. pylori infection （H. pylori-1）, concerns regarding its potential drawbacks, particularly neurogenic ones, due to possible cross- mimicry, should be considered. Possible cross-mimicry between H. p, vlor/ NAP and/or bacterial aquaporin （AQP） and neural tissues may be associated with the anti-AQP-4 antibody-related neural damage in multiple sclerosis （MS）/neuromyelitis optica patients. Moreover, the sequence homology found between H. pylori VacA and human Na＋/K＋-ATPase A subunit suggests that antibodies to VacA involve ion channels in abaxonal Schwann cell plasmalemma resulting in demyelination in some patients. A series of factors have been im- plicated in inducing blood-brain barrier （BBB） disrup- tion, including inflammatory mediators （e.g., cytokines and chemokines induced by H. pylor/-I） and oxidative stress. BBB disruption permits access of AQP4-specific antibodies and T lymphocytes to the central nervous system, thereby playing a major role in multiple sclero- sis pathogenesis. Relative studies show a strong asso- ciation between H. pylori-I and MS. H. pylor/-I induces humoral and cellular immune responses that, owing to the sharing of homologous epitopes （molecular mim- icry）, cross-react with components of nerves, thereby contributing and perpetuating neural tissue damage. Finally, H. pylori NAP also plays a possible pathoge- netic role in both gastric and colon oncogenesis.

Comparison of a monoclonal antigen stool test (Hp StAR) with the ^(13)C-urea breath test in monitoring Helicobacter pylori eradication therapy

AIM： To evaluate the agreement between a mAb-based stool test （HP STAR） and the urea breath test （UBT） in monitoring （H pylon） infection after eradication therapy. METHODS： Patients with discordant results on UBT and Hp STAR underwent endoscopy with biopsies for rapid urease test, culture, and histology to confirm H pylori status. RESULTS： Among 250 patients （50±14 years）, 240 （96.0%） had concordant UBT and Hp STAR tests with a significant correlation between DOB and A values （R = 0.87; P〈0.0001）. The remaining 10 （4.0%） patients had discordant tests （positive Hp STAR and negative UBT） with the Hp STAR inaccurate in five cases （false positive） and UBT inaccurate in the other five cases （false negative）. The “maximal expected” sensitivity, specificity, ＋PV, -PV, ＋LR, and -LR were 91%, 100%, 100%, 97.4%, ∞, and 8.2 respectively, for the UBT, and 100%, 97.4%, 91%, 100%, 38.8, and 0, respectively, for the Hp STAR. Overall accuracy for both tests was 98%. CONCLUSION： Both the UBT and the Hp StAR are equally accurate in monitoring H pylori infection. Nowadays, the choice of the “best” non-invasive H pylori test in the post-treatment setting should be done not only in terms of diagnostic accuracy but also in view of cost and local facilities.