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Journal of Immunology Research
Volume 2018, Article ID 5163129, 10 pages
Review Article

Recent Advances in Drug-Induced Hypersensitivity Syndrome/Drug Reaction with Eosinophilia and Systemic Symptoms

Department of Dermatology, Showa University School of Medicine, Tokyo, Japan

Correspondence should be addressed to Hideaki Watanabe;

Received 2 September 2017; Revised 2 December 2017; Accepted 8 February 2018; Published 18 March 2018

Academic Editor: Wichittra Tassaneeyakul

Copyright © 2018 Hideaki Watanabe. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Drug-induced hypersensitivity syndrome (DIHS), also termed as drug reaction with eosinophilia and systemic symptoms (DRESS), is a multiorgan systemic reaction characterized by a close relationship with the reactivation of herpes virus. Published data has demonstrated that among patients with DIHS/DRESS, 75–95% have leukocytosis, 18.2–90% show atypical lymphocytes, 52–95% have eosinophilia, and 75–100% have hepatic abnormalities. Histologically, eosinophils were observed less frequently than we expected (20%). The mainstay of DIHS/DRESS treatment is a moderate dose of systemic corticosteroids, followed by gradual dose reduction. In this review, we will emphasize that elevations in the levels of several cytokines/chemokines, including tumor necrosis factor- (TNF-) α and the thymus and activation-regulated chemokine (TARC/CCL17), during the early stage of disease, are good markers allowing the early recognition of HHV-6 reactivation. TNF-α and TARC levels also reflect therapeutic responses and may be useful markers of the DIHS disease process. Recently, the pathogenic mechanism of T-cell activation triggered by human leukocyte antigen- (HLA-) restricted presentation of a drug or metabolites was elucidated. Additionally, we recently reported that dapsone would fit within the unique subpocket of the antigen-recognition site of HLA-B13:01. Further studies will render it possible to choose better strategies for DIHS prevention and therapy.