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We read with interest the recent paper comparing 1 and 2 weeks of triple therapy for Helicobacter pylori infection in patients with duodenal ulcer disease. (Gut 2007;56:475–9) H pylori is an infectious disease and the goal of treatment is to cure the infection. In 2007, one would hope to be able to reliably cure 95% of the treated patients (discussed by Graham et al).1 In 1989, a successful treatment has been defined as one that cures >80% of the patients.2 By 1995, it seemed that 90% was achievable.3 The Maastricht consensus conferences defined a useful therapy as the one with an intention to treat (ITT) cure rate of >80%, which is a relatively low hurdle (ie, those with cure rates of 80% would be unacceptable).5 Although the authors concluded that 7 and 14 days therapy provided essentially equivalent results, the focus should have been on the fact that the cure rates obtained were unacceptably low with either duration (eg, ITT of 79.7 for 7 days and 81.7 for 14 days), especially among patients with duodenal ulcer disease where the cure rates are typically higher than among patients without ulcers.5,6,7,8
Their results are not unexpected as large studies of this legacy triple therapy (proton‐pump inhibitor (PPI), amoxicillin and clarithromycin) have recently yielded unacceptably low eradication rates in Europe and the US, and have only infrequently achieved the minimum 80% success rate (table 11).10,11,12,13,14,15,16,17 Overall, these results suggest that traditional triple therapy should no longer be used in Western populations unless pretreatment susceptibility is confirmed and then it should be used for 14 days.18,19
H pylori is a serious, chronic, transmissible infectious disease that causes damage to gastric structure and function, and is a major cause of morbidity and mortality worldwide. All the patients in this study had H pylori‐related ulcer disease, and untreated 10–25% would be expected to develop complications such as haemorrhage. We are concerned about the inclusion of the dual therapy arm of omeprazole and amoxicillin in the trial. The dual therapy at these doses typically yields a cure rate of 50% and is listed under the category of “not recommended”. The manuscript states that the protocol was approved by institutional review boards, and all patients gave informed consent. What was the nature of the informed consent? How was a known ineffective therapy justified to the patients with duodenal ulcer disease and to the review boards? We believe that the information given to patients and the justifications must be described in detail in the publication including what the patients were told, and that they entered the trial knowing that they would have a high chance of treatment failure. Finally, what was done to ensure that the large number of patients with failed treatment subsequently receive appropriate therapy for H pylori‐related duodenal ulcer disease? It may also be good time to rethink current approaches to H pylori treatment.
This material is based upon work supported in part by the Office of Research and Development Medical Research Service Department of Veterans Affairs and by Public Health Service grant DK56338, which funds the Texas Gulf Coast Digestive Diseases Center.
Competing interests: DYG has received small amounts of grant support and/or free drugs or urea breath tests from Meretek, Jannsen/Eisai, TAP, and BioHit for investigator initiated and completely investigator controlled research in the area of H pylori infections. In addition, DYG is a paid consultant for Otsuka Pharmaceuticals and a member of the Board of Directors of Meretek, Diagnostics, the manufacturer of the 13C‐urea breath test. He is also a consultant to Novartis with regards to H pylori vaccine development and also receives royalties on the Baylor College of Medicine patent covering the serologic test, HM‐CAP. YY has no potential conflicts of interest to declare.