Authors' reply.

We read with great interest the letter by Papaefthymiou et al [1] concerning the Greek National Consensus on Helicobacter pylori (H. pylori) infection [2]. We certainly agree with the authors that over the past years in order to overcome the fast-growing antibiotic resistance of H. pylori infection worldwide, an “add-on” strategy has been adapted, and that this is more obvious in countries like Greece, where bismuth salts are not commercially available. Thus, novel H. pylori eradication regimens, with a more targeted pathophysiological approach, are under evaluation and we are awaiting with great interest the results of the ongoing clinical trials.

Eradication of H. pylori infection has traditionally relied on empiric therapeutic regimens, since the need for endoscopy and the limited availability of culture, in most countries including Greece, have rendered the susceptibility-guided treatment option impractical or even unfeasible. Moreover, a recent randomized study showed that susceptibility-guided therapy in a high-resistance area was equally effective as a local empirical regimen [3], while another randomized study failed to reveal superiority of genotypic resistance-guided therapy over a properly designed empirical treatment for eradication of refractory H. pylori infection [4]. For these reasons, the Greek consensus has stated (Statement 26) that culture and antimicrobial susceptibility testing is not recommended before first-line therapy, and that susceptibility-guided therapy should be provided as a rescue treatment, especially after second-line treatment has failed.

On the other hand, the effect of vitamin D (vitD) on H. pylori infection and eradication rates has been widely investigated recently [5]. VitD, apart from its well-known role in calcium and phosphorus metabolism, has been proven to be potent immune modulator of the adaptive immune system, stimulating the innate immune response upon infection [6]. Based on these data, several clinical studies have illustrated that vitD analogs may have anti-H. pylori antimicrobial effects. Cytological research has also found that vitD3 decomposition product 1 can lyse H. pylori bacterial cells by inducing the collapse of the cell membrane [7]. However, the correlation with vitD has not been fully clarified and studies of the impact of serum vitD levels on H. pylori eradication were mostly observational or retrospective and of small sample size [8-10]. Therefore, well-designed randomized controlled prospective studies with a large sample size are needed. We were delighted to hear that a national multicenter study on the relationship between vitD and H. pylori was recently launched and we are awaiting the results.