Abstract
We thank de Hollander and Kuipers for their comments on our article, in which we demonstrated in a randomised clinical trial (RCT), that simvastatin as adjuvant therapy to the standard triple therapy improves the eradication rate of Helicobacter pylori infection. We agree with de Hollander and Kuipers in noting that the treatment groups were small and we did not provide clinical information, especially on gastrointestinal pathology. On the subject of whether H. pylori eradication treatment is more effective in patients with peptic ulcer disease (PUD) than in those with non-ulcer dyspepsia (NUD) or other non-ulcer gastric diseases this remains controversial. 4 Huang et al. in a systematic review including 22 studies showed that there is no convincing evidence to suggest that NUD patients respond to H. pylori eradication treatments differently from those with PUD. However, there was a trend for patients with PUD who received the classical triad of proton pump inhibitor, clarithromycin and amoxicillin for 7 days. Regarding the underlying mechanisms involved in H. pylori eradication, we proposed a number of speculative mechanisms. One of these speculative mechanisms is the anti-inflammatory effect of statins. We agree with de Hollander and Kuipers that statins, by exerting anti-inflammatory effects, may play a significant role in H. pylori eradication. In contrast, statins have not been proven to reduce the progression of gastritis to gastric cancer. More RCTs are needed to assess the efficacy of statins in H. pylori eradication focusing on the impact of 10–14 days treatment, and the role of long-term statin use in preventing or reducing the risk of progression to neoplasia in Barrett's oesophagus and gastric cancer.
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