Possible enhancement of BP180 autoantibody production by herpes zoster

• Published in: Journal of dermatology Vol. 43; no. 2; pp. 197 - 199
• Main Authors: Kamiya, Koji, Aoyama, Yumi, Suzuki, Takahiro, Niwa, Haruo, Horio, Ai, Nishio, Eiichi, Tokura, Yoshiki
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 01.02.2016; Wiley Subscription Services, Inc
• Subjects: Aged, 80 and over; Autoantibodies - biosynthesis; Autoantibodies - blood; autoantibody; Autoantigens - immunology; BP180 antibody; bullous pemphigoid; Collagen Type XVII; Female; herpes zoster; Herpes Zoster - complications; Herpes Zoster - immunology; Herpes Zoster - pathology; Herpesviridae; Herpesvirus; Herpesvirus 3, Human - pathogenicity; Humans; Non-Fibrillar Collagens - immunology; Pemphigoid, Bullous - etiology; Pemphigoid, Bullous - immunology; Pemphigoid, Bullous - pathology; Varicella-zoster virus; varicella zoster virus; bullous pemphigoid; autoantibody; herpes zoster; BP180 antibody
• ISSN: 0385-2407; 1346-8138
• DOI: 10.1111/1346-8138.13042

Bullous pemphigoid (BP) is an autoimmune blistering disease caused by autoantibodies against type XVII collagen/BP180 (BP180). 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‐BP180 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‐BP180 serum antibodies in association with the occurrence of HZ. After successful treatment with valacyclovir hydrochloride for 7 days, the serum levels of anti‐BP180 antibodies decreased in accordance with the improvement of skin lesions. These findings suggest that the production of anti‐BP180 antibodies could be triggered by the reactivation of VZV.