Assessment for varicella zoster virus in patients newly suspected of having giant cell arteritis.


Journal

Rheumatology (Oxford, England)
ISSN: 1462-0332
Titre abrégé: Rheumatology (Oxford)
Pays: England
ID NLM: 100883501

Informations de publication

Date de publication:
01 08 2020
Historique:
received: 31 07 2019
revised: 18 10 2019
pubmed: 30 11 2019
medline: 20 1 2021
entrez: 29 11 2019
Statut: ppublish

Résumé

There is uncertainty if varicella zoster virus (VZV) triggers GCA. This is based on discordant reports of VZV detection in GCA temporal artery biopsies. We conducted a multimodal evaluation for VZV in the inception Giant Cell Arteritis and PET Scan (GAPS) cohort. Consecutive patients who underwent temporal artery biopsy for suspected GCA were clinically reviewed for active and past VZV infection and followed for 6 months. Serum was tested for VZV IgM and IgG. Temporal artery biopsy (TAB) sections were stained for VZV antigen using the VZV Mouse Cocktail Antibody (Cell Marque, Rocklin, CA, USA). A selection of GCA and control tissues were stained with the VZV gE antibody (Santa Cruz Biotechnology, Dallas, TX, USA), which was used in previous studies. A total of 58 patients met inclusion criteria, 12 (21%) had biopsy-positive GCA and 20 had clinically positive GCA. None had herpes zoster at enrolment and only one patient developed a VZV clinical syndrome (zoster ophthalmicus) on follow-up. There was no difference in VZV exposure between GCA and non-GCA patients. None of the 53 patients who had VZV serology collected had positive VZV IgM antibodies. VZV antigen was not convincingly demonstrated in any of the TAB specimens; 57 TABs stained negative and 1 stained equivocally positive. The Santa Cruz Biotechnology VZV antibody exhibited positive staining in a range of negative control tissues, questioning its specificity for VZV antigen. The absence of active infection markers argues against VZV reactivation being the trigger for GCA. Non-specific immunohistochemistry staining may account for positive findings in previous studies.

Identifiants

pubmed: 31776576
pii: 5644422
doi: 10.1093/rheumatology/kez556
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1992-1996

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For permissions, please email: journals.permissions@oup.com.

Auteurs

Anthony M Sammel (AM)

Departments of Rheumatology and Anatomical Pathology, Royal North Shore Hospital, St Leonards, Sydney, New South Wales, Australia.
Northern Clinical School, University of Sydney, St Leonards, Sydney, New South Wales, Australia.
Department of Rheumatology, Prince of Wales Hospital, Randwick, Sydney, New South Wales, Australia.

Susan Smith (S)

Raymond Purves Bone and Joint Research Laboratories, Kolling Institute, St Leonards, Sydney, New South Wales, Australia.

Katherine Nguyen (K)

Departments of Rheumatology and Anatomical Pathology, Royal North Shore Hospital, St Leonards, Sydney, New South Wales, Australia.

Rodger Laurent (R)

Departments of Rheumatology and Anatomical Pathology, Royal North Shore Hospital, St Leonards, Sydney, New South Wales, Australia.
Northern Clinical School, University of Sydney, St Leonards, Sydney, New South Wales, Australia.

Janice Brewer (J)

Departments of Rheumatology and Anatomical Pathology, Royal North Shore Hospital, St Leonards, Sydney, New South Wales, Australia.

Nathan Hall (N)

Departments of Rheumatology and Anatomical Pathology, Royal North Shore Hospital, St Leonards, Sydney, New South Wales, Australia.

Christopher B Little (CB)

Northern Clinical School, University of Sydney, St Leonards, Sydney, New South Wales, Australia.
Raymond Purves Bone and Joint Research Laboratories, Kolling Institute, St Leonards, Sydney, New South Wales, Australia.

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