A case of drug-induced hypersensitivity syndrome showing transient immunosuppression before viral reactivation during treatment for pemphigus foliaceus

• Published in: Clinical and experimental dermatology Vol. 31; no. 1; pp. 33 - 35
• Main Authors: Takahashi, H., Tanaka, M., Tanikawa, A., Toyohara, A., Ogo, Y., Morimoto, A., Harato, R., Kobayashi, M., Amagai, M.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.01.2006; Blackwell; Oxford University Press
• Subjects: Administration, Oral; Adult; Anti-Infective Agents - administration & dosage; Anti-Infective Agents - adverse effects; Biological and medical sciences; Bullous diseases of the skin; Cytomegalovirus - immunology; Dapsone - administration & dosage; Dapsone - adverse effects; Dermatology; Desmoglein 1 - immunology; Drug Hypersensitivity - blood; Drug Hypersensitivity - immunology; Drug Hypersensitivity - virology; Herpesvirus 4, Human - immunology; Herpesvirus 6, Human - immunology; Herpesvirus 6, Human - physiology; Humans; Immunoglobulin G - blood; Immunoglobulin M - blood; Lymphocyte Count; Male; Medical sciences; Pemphigus - blood; Pemphigus - drug therapy; Pemphigus - immunology; Virus Activation; Bullous dermatosis; Human; Drug; Skin disease; Reactivation; Dermatology; Pemphigus foliaceous; Autoimmune disease; Infection; Case study; Immunosuppression; Treatment; Viral disease
• ISSN: 0307-6938; 1365-2230
• DOI: 10.1111/j.1365-2230.2005.01913.x

Summary Drug–induced hypersensitivity syndrome (DIHS) is one of the most severe drug adverse reactions, with characteristic biphasic symptoms. Reactivation of human herpesvirus‐6 (HHV‐6) is frequently observed, although the cause of DIHS is still unknown. A patient developed DIHS during treatment with diaminodiphenylsulphone for pemphigus foliaceus. The number of lymphocytes in his peripheral blood, and titres of serum total IgG and IgM and anti‐desmoglein1 antibody transiently decreased just before reactivation of HHV‐6, cytomegalovirus and Epstein–Barr virus. This observation suggests that transient suppression of both cellular and humoral immunity may trigger viral reactivation, which leads to the development of the second phase of DIHS.