401 General Military Hospital of Athens, Greece; Aristotle University of Thessaloniki, Macedonia, Greece; Ippokration Hospital, Aristotle University of Thessaloniki, Macedonia, Greece; University of Zurich, Switzerland
aDepartment of Gastroenterology, 401 General Military Hospital of Athens, Greece (Apostolis Papaefthymiou); bFirst Laboratory of Pharmacology, School of Medicine, Aristotle University of Thessaloniki, Macedonia, Greece (Apostolis Papaefthymiou, Michael Doulberis, Stergios A. Polyzos); cDepartment of Internal Medicine, Second Medical Clinic, Ippokration Hospital, Aristotle University of Thessaloniki, Macedonia, Greece (Apostolis Papaefthymiou, Michael Doulberis, Jannis Kountouras); dDepartment of Gastroenterology and Hepatology, University of Zurich, Switzerland (Michael Doulberis)
The Hellenic Society of Gastroenterology  recently published the National consensus on Helicobacter pylori (H. pylori) infection, following the necessity of a uniform approach to yield optimal eradication rates. As implied by the recent Maastricht V/Florence consensus , an “add-on” strategy regarding antibiotics was adapted to overleap the increasing antibiotic resistance, combined with the absence of bismuth-containing drugs, thus perpetuating a “vicious circle” and emerging novel approaches in treatment models with a targeted pathophysiological perspective. Importantly, parameters connected with the multidrug resistance include the formation of H. pylori-related biofilms, suggesting the introduction of novel anti-biofilm therapeutic approaches using anti-biofilm agents .
A unanimous suggestion (Statement 10) proposed that H. pylori culture or molecular techniques should be conducted to evaluate the antimicrobial susceptibility. Nevertheless, those methods are characterized by limited availability in most regions. On the other hand, recent data imply a potential benefit of vitamin D (vitD) for H. pylori infection treatment, related to the vitD-receptor’s (VDR) antimicrobial role [4-6]. VDR, stimulated by the active H. pylori infection, induces human β-defensins, which in high concentrations suppress H. pylori biofilm activity ; subtle or strong activation of VDR, due to vitD absence or adequacy, could contribute or not to H. pylori acclimatization, morbidity, resistance, and survival . Additionally, vitD seems to act directly as an antibacterial agent through stimulation of defensins and cathelicidins, and vitD upregulated protein 1 (VDP1). possesses an H. pylori-specific antimicrobial ability, indicating a promising therapeutic potential [7,8]. Moreover, studies in mouse models revealed a protective role of a VDP1 against H. pylori-related gastric cancer . Clinical studies concluded that vitD had a protective role against H. pylori infection and suggested its deficiency as a distinct risk factor in the failure of eradication treatment, while a recent meta-analysis concluded that vitD supplementation could change the effectiveness of eradication regimens . Therefore, a National multicenter study has recently been inaugurated to elucidate the relationship between vitD and H. pylori infection and the potential beneficial effect of vitD supplementation during eradication treatment.
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