Abstract

We thank Dr Molina-Infante, Dr Moawad and Dr Rhijn for their thoughtful editorial.1 In our study,2 oesophageal basophil infiltration was significantly higher in patients with eosinophilic oesophagitis (EoE) and those with proton pump inhibitor-responsive oesophageal eosinophilia (PPI-REE) compared with individuals with a normal oesophagus or patients with gastro-oesophageal reflux disease (GERD). Basophil infiltration was co-localised with thymic stromal lymphopoietin (TSLP)-positive oesophageal epithelium, and decreased after steroid swallowing therapy in patients with EoE. These results suggest that TSLP-basophils play an important role in the pathogenesis of EoE, which is consistent with the findings of the outstanding basic study by Noti et al.3 Our unpublished data revealed that PPI therapy significantly reduced oesophageal basophil infiltration from 1.4 (0–2.8) to 0 (0–0.8) in patients with PPI-REE (data were median with interquartile range, P < 0.01). Therefore, PPI-REE might have a similar pathogenesis to that of EoE, but the role of epithelial barrier dysfunction4, 5 caused by acid reflux, or the responsiveness to any anti-inflammatory effects of PPI6, 7 might be different between the two diseases. As shown in the table of the editorial by Molina-Infante,1 several studies attempted to find markers to distinguish EoE from PPI-REE. We observed a significant difference in oesophageal basophil, but not mast cell, infiltration between EoE and PPI-REE.2 It is not known whether oesophageal basophil count is a novel marker, because of the small difference due to the small number of samples. Furthermore, larger prospective studies are needed to determine whether oesophageal basophils have a clinically useful role in distinguishing EoE from PPI-REE. Finally, we totally agree with the ‘PPI-responsive EoE’ concept proposed by Molina-Infante et al.1 The authors’ declarations of personal and financial interests are unchanged from those in the original article.2

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