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Editor,—We thank Dr Grigg for his interest in our work.1 We agree that the asthma attacks may have resolved spontaneously in some cases, which was precisely why we stated that the markers fell in association with steroid therapy, and nowhere implied causality. Nevertheless, the statistical analysis suggests that the chances this occurred at random are extremely low.
We agree that corticosteroids do not inhibit, except at very high concentrations, degranulation of the eosinophils induced by incubation with opsonised particles, such as Sepharose beads in vitro.2 However, there is overwhelming evidence that cytokines such as IL-5 prime eosinophils for increased release of granule proteins in this situation,3 4 and that they inhibit cytokine-mediated prolongation of eosinophil survival.5 These observations, coupled with the abundant evidence that corticosteroids reduce the expression of eosinophil-active cytokines, such as IL-5, provide a convincing chain of evidence linking the clinical use of corticosteroids with reduced release of eosinophil granule proteins in vivo.
With regard to the controls in this study the ratio of atopic to non-atopic asthmatics was 4:1 and of atopic to non-atopic controls was 3:1. These differences are not significant by chi-squared testing. Whilst we agree that more controls might have strengthened our conclusions, nonetheless the evidence of unresolved inflammation after an apparently clinically adequate course of prednisolone, as shown by the elevated levels of IL-5 and sCD25, remains strong.
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