TO THE EDITOR: We read the recent article by Kim et al1 with great interest. This study adds to a body of literatures supporting the hypothesis that eradication of Helicobacter pylori leads to improvement in symptoms of functional dyspepsia (FD), at least in the context of Asia. The authors further suggest that inflammation mediates FD, a conclusion that sparks more controversies than answers. The Western data have been less convincing in this regard when compared to the data from Asia, mainly from China, Korea, Japan and Singapore.2 A recent report from India, with a robust study design and sample size, did not find eradication of H. pylori as being useful in resolving symptoms of FD despite the healing of gastritis.3 Our experience in the ethnic Malays, known to have an extremely low prevalence of H. pylori infection did not suggest a less common prevalence of FD.4,5 At this juncture, available data suggest a wide divide in the role and mechanism of H. pylori in FD.
The results of this study suffer from a number of limitations most of which had been mentioned in their paper. The low sample size, the non-randomized not double-blind design and non-masking of results of H. pylori eradication have considerable influence on eventual study outcome. Multivariable analysis is not suitable in the face of low sample size and multiple variables, which explain the wide confidence intervals. In addition, the measures for outcome assessment used in this study may not be sensitive enough.6 Regardless of the above limitations, this study does give a hint that the Rome III criteria for FD is not ideal for the Asian population at least in the presence of H. pylori.7 And that the role of H. pylori in FD is more complex than what available data can explain in particular with regards to the gut-brain axis, an assessment that should be considered in future studies.8
Footnotes
Conflicts of interest: None.
References
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