The diagnosis of a DRESS syndrome has been sufficiently established on the basis of typical clinical features and viral reactivations

Abstract

Conflicts of interest: none declared. Sir, We read with great interest the article entitled ‘Variability in the clinical pattern of cutaneous side‐effects of drugs with systemic symptoms: does a DRESS syndrome really exist?’ by Peyrière et al.1 Based on data collected retrospectively from the French Pharmacovigilance database, the authors concluded that the acronym ‘DRESS’ is both inaccurate and quite imprecise with no clear definition regarding both cutaneous and systemic signs. We believe, however, that many of the authors’ considerations are in contrast to the current knowledge about this syndrome and may be based on misinterpretations of these data probably due to their unawareness of several important findings uniquely observed in this syndrome. Thirty years ago, the rules concerning the diagnosis of this syndrome had for the most part been formulated by nondermatologists who defined this disease in terms of each organ involvement. As a result, sufficient attention had not been paid to the cutaneous features of this syndrome. In 1996, Bocquet et al.2 coined the term ‘drug rash with eosinophilia and systemic symptoms’ (DRESS) for this syndrome to encompass these diverse clinical presentations. Subsequently, during the past 10 years, the clinical spectrum of this syndrome was defined: there have been no significant differences in the clinical findings of these cases reported under the name of DRESS. The lack of a specific and sensitive diagnostic test, however, was a major obstacle to correct identification of all patients with this syndrome. In this regard, my group and Hashimoto's group independently demonstrated that human herpesvirus 6 (HHV‐6) can be reactivated at a particular time point, namely 2–3 weeks after onset of rash in the vast majority of patients with this syndrome, despite the diverse clinical presentations at onset: HHV‐6 reactivation as evidenced by the rise in HHV‐6 IgG titres and HHV‐6 DNA levels commonly occurs 2–3 weeks after onset regardless of treatment.3–6