Assessment for varicella zoster virus in patients newly suspected of having giant cell arteritis
| Autor: | Janice Brewer, Nathan Hall, Rodger Laurent, Anthony M. Sammel, Christopher B. Little, Katherine Nguyen, Susan M. Smith |
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| Rok vydání: | 2019 |
| Předmět: |
Male
0301 basic medicine Herpesvirus 3 Human Pathology medicine.medical_specialty viruses Giant Cell Arteritis medicine.disease_cause Serology 03 medical and health sciences 0302 clinical medicine Rheumatology Biopsy Humans Medicine Pharmacology (medical) Aged Aged 80 and over Chickenpox integumentary system biology medicine.diagnostic_test business.industry Varicella zoster virus virus diseases Middle Aged biochemical phenomena metabolism and nutrition medicine.disease eye diseases Temporal Arteries Giant cell arteritis 030104 developmental biology Immunoglobulin M Varicella Zoster Virus Infection biology.protein Female Antibody business Vasculitis 030217 neurology & neurosurgery |
| Zdroj: | Rheumatology. 59:1992-1996 |
| ISSN: | 1462-0332 1462-0324 |
| DOI: | 10.1093/rheumatology/kez556 |
| Popis: | Objectives 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. Methods 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. Results 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. Conclusion 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. |
| Databáze: | OpenAIRE |
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