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Possible enhancement of BP 180 autoantibody production by herpes zoster
Author(s) -
Kamiya Koji,
Aoyama Yumi,
Suzuki Takahiro,
Niwa Haruo,
Horio Ai,
Nishio Eiichi,
Tokura Yoshiki
Publication year - 2016
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/1346-8138.13042
Subject(s) - autoantibody , medicine , pemphigus , antibody , erythema multiforme , acantholysis , virus , histopathology , blisters , erythema , pemphigus foliaceus , immunology , herpes simplex virus , pathology , virology , dermatology
Bullous pemphigoid ( BP ) is an autoimmune blistering disease caused by autoantibodies against type XVII collagen/ BP 180 ( BP 180). Although the mechanisms of autoantibody production remain to be elucidated, herpes virus infections have been identified as a possible triggering factor for pemphigus. We report a case of herpes zoster ( HZ ) having anti‐ BP 180 serum antibodies. The patient developed sudden‐onset, tense blisters and edematous erythema on the right anterior chest, shoulder and upper back. Histopathology showed remarkable degeneration of keratinocytes, acantholysis and blister formation with ballooning cells, indicating herpes virus infection. A polymerase chain reaction analysis of varicella zoster virus ( VZV ) was positive in crusts and effusions from the skin lesions, confirming the definitive diagnosis of HZ . Notably, we found that the patient had anti‐ BP 180 serum antibodies in association with the occurrence of HZ . After successful treatment with valacyclovir hydrochloride for 7 days, the serum levels of anti‐ BP 180 antibodies decreased in accordance with the improvement of skin lesions. These findings suggest that the production of anti‐ BP 180 antibodies could be triggered by the reactivation of VZV .