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Longitudinal analysis of antibody profiles against plakins in severe drug eruptions: emphasis on correlation with tissue damage in drug‐induced hypersensitivity syndrome and drug reaction with eosinophilia and systemic symptoms
Author(s) -
Takehara A.,
Aoyama Y.,
Kurosawa M.,
Shirafuji Y.,
Umemura H.,
Kamiya K.,
Ushigome Y.,
Kano Y.,
Shiohara T.,
Iwatsuki K.
Publication year - 2016
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/bjd.14677
Subject(s) - toxic epidermal necrolysis , medicine , autoantibody , immunology , drug , systemic disease , dermatology , antibody , immunopathology , pharmacology
Summary Background The evidence for severe drug eruption as a trigger for autoimmune disease has recently increased. No information is available on how tissue damage in severe drug eruptions can induce autoimmune responses. Objectives To investigate whether the generation of autoantibodies (autoAbs) against plakin family proteins could be the cause or result of tissue damage in patients with severe drug eruptions and whether the generation of autoAbs could be prevented by systemic corticosteroids during the acute stage. Methods We retrospectively analysed alterations of serum levels of autoAbs against plakin family proteins in patients with Stevens–Johnson syndrome ( SJS )/toxic epidermal necrolysis ( TEN ) and drug‐induced hypersensitivity syndrome (Di HS )/drug reaction with eosinophilia and systemic symptoms ( DRESS ) during the acute stage and long after resolution over a period of more than 10 years. Results AutoAbs against plakin family proteins were detected in patients with either SJS / TEN or Di HS / DRESS regardless of the epidermal damage in the acute stage, and were sustained even long after resolution in Di HS / DRESS , indicating that those autoAbs are neither the cause nor the consequence of epidermal damage, at least in Di HS / DRESS . Severe liver damage and noncorticosteroid therapy during the early and acute stages of Di HS / DRESS were associated with the subsequent generation of these autoAbs. Conclusions These autoAbs are neither necessarily the cause nor the result of epidermal damage in Di HS / DRESS , because the presence of these autoAbs was not restricted to patients with SJS / TEN but was also observed in those with Di HS / DRESS , which is characterized by lack of epidermal damage. Severe liver damage and/or immune responses that could be prevented by corticosteroids in the acute stage of Di HS / DRESS are among the causal factors contributing to the generation of autoimmune responses.