Abstract
Objective: This study aims to determine the clinical, laboratory, and ultrasonographic findings of giant cell arteritis in patients with Herpes Zoster. Methods: The study included 36 consecutive patients (median age 59.0 years; range 19 to 76 years) who were admitted to the Dermatology Outpatient Clinic with the diagnosis of Herpes Zoster. Demographic and clinical features of the patients were recorded. The presence of ultrasonographic characteristics of giant cell arteritis such as halo sign, compression sign, occlusion, and stenosis was also recorded using ultrasound. The patients were evaluated at baseline and 6 months. Results: A total of 36 patients were assessed. 4 patients had jaw claudication (11.1%), 5 patients had scalp tenderness (13.9%), 11 patients had a new-onset headache (30.6%) and, 23 patients had post-herpetic neuralgia (63.9%). No patients had elevated erythrocyte sedimentation rate and ultrasonographic findings of Giant cell arteritis. Conclusion: Our data show that a small proportion of patients with Herpes Zoster may have clinical findings suggesting Giant cell arteritis. However, they do not have elevated erythrocyte sedimentation rate and sonographic findings of Giant cell arteritis.
Highlights
Varicella zoster virus (VZV) is a member of the Herpes viridae family and results in two different clinical conditions
Our data show that a small proportion of patients with Herpes Zoster may have clinical findings suggesting Giant cell arteritis
Shingles or herpes zoster (HZ) is a recurrent infection of latent VZV following the primary infection of the organism [1]
Summary
Varicella zoster virus (VZV) is a member of the Herpes viridae family and results in two different clinical conditions. Shingles or herpes zoster (HZ) is a recurrent infection of latent VZV following the primary infection of the organism [1]. Giant cell arteritis (GCA) is a type of vasculitis diagnosed frequently in patients older than 50 years, which affects medium-to-large-sized arteries. It may produce a wide spectrum of clinical symptoms. Diagnosis is usually made with clinical symptoms with additional diagnostic methods such as ultrasonography (USG) and other imaging techniques, laboratory parameters, and temporal artery biopsy. USG is shown to have a higher sensitivity and specificity rate in GCA diagnosis when compared with biopsy and is proven to be much more cost-effective [6]
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