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FRI0365 Limited Evidence of Active Varicella Zoster Virus (VZV) Infection in A Cohort of Acute Giant Cell Arteritis (GCA) Patients
  1. A.M. Sammel1,2,
  2. K. Rosettenstein2,
  3. J.J. Post1,3,
  4. J.V. Bertouch2
  1. 1Prince of Wales Clinical School, University of New South Wales
  2. 2Rheumatology
  3. 3Infectious Diseases, Prince of Wales Hospital, Randwick, Australia

Abstract

Background Recent studies have identified a high prevalence of VZV antigen in temporal artery biopsy specimens from patients with GCA. The clinical implication of this finding is uncertain. Some researchers have proposed that reactivation of VZV infection may have a role in inducing arteritis and have promoted antiviral therapy as adjunctive therapy to corticosteroids in cases of biopsy negative and positive GCA. While not currently recommended in GCA, antiviral therapy is used in the clinically distinct condition of VZV vasculopathy which is associated with angiographic abnormalities in the anterior and middle cerebral arteries.

Objectives We aimed to assess if there was clinical, serological or imaging evidence of active VZV in patients with acute GCA. Positive findings may have supported a role for antiviral therapy.

Methods We prospectively assessed the clinical, serological and angiographic profile of all 13 patients referred for assessment of acute GCA to our tertiary referral rheumatology service from June to December 2015 to identify evidence of active VZV infection.

Results 10 patients with an average age of 77 years (range 66 to 87 years) were ultimately diagnosed with GCA. Nine met the American College of Rheumatology 1990 criteria for the classification of GCA, three had positive and one had an equivocal biopsy. Eight were female. All ten had visual disturbance and three had evidence of acute ischaemic optic neuropathy on fundoscopy.

One patient had an episode of cutaneous herpes zoster affecting the right sixth thoracic dermatome two months after onset of GCA headache. This was treated with a five day course of valaciclovir and resolved three weeks before referral to our service. GCA symptoms progressed despite valaciclovir. Seven patients recalled an episode of primary VZV infection in childhood but no other patients had a history of herpes zoster.

VZV serology was performed in all ten patients within 24 days of referral. Time from GCA symptom onset to serology ranged from 15 days to five months. All patients had positive VZV IgG indicating past exposure to the virus. Nine had negative IgM serology. IgM was equivocally elevated in the patient with recent herpes zoster.

Six patients underwent magnetic resonance imaging or computer tomographic cererbral angiography and there was no evidence of VZV vasculopathy of the anterior or middle cerebral arteries.

Patients were treated with pulse intravenous methylprednisolone 500 mg to 1000 mg for three days plus an antiplatelet agent with subsequent oral prednisone. We did not add antiviral therapy. All demonstrated rapid clinical improvement with normalization of inflammatory markers and no progression of visual loss.

Conclusions We did not find clinical, serological or imaging evidence of active VZV infection contributing to acute GCA to support routine adjunctive antiviral therapy.

  1. Nagel MA et al. Analysis of Varicella-Zoster Virus in Temporal Arteries Biopsy Positive and Negative for Giant Cell Arteritis. JAMA Neurol. 2015; 72: 1281–7.

  2. Gilden D et al. Prevalence and distribution of VZV in temporal arteries of patients with giant cell arteritis. Neurology. 2015; 84: 1948–55

Disclosure of Interest None declared

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