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10.1097/QCO.0000000000000258

http://scihub22266oqcxt.onion/10.1097/QCO.0000000000000258
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C5134838!5134838!26871403
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suck abstract from ncbi

pmid26871403      Curr+Opin+Infect+Dis 2016 ; 29 (3): 275-9
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  • Varicella zoster virus and giant cell arteritis #MMPMID26871403
  • Gilden D; Nagel MA
  • Curr Opin Infect Dis 2016[Jun]; 29 (3): 275-9 PMID26871403show ga
  • Purpose of review: Giant cell arteritis (GCA) is a serious disease and the most common cause of vasculitis in the elderly. Here, studies describing the recent discovery of varicella zoster virus (VZV) in the temporal arteries (TA) of patients with GCA are reviewed. Recent findings: GCA is characterized by severe headache/head pain and scalp tenderness. Many patients also have a history of vision loss, jaw claudication, polymyalgia rheumatica, fever, night sweats, weight loss and fatigue. ESR and CRP are usually elevated. Diagnosis is confirmed by TA biopsy which reveals vessel wall damage and inflammation, with multinucleated giant cells and/or epithelioid macrophages. Skip lesions are common. Importantly, TA biopsies are pathologically negative in many clinically suspect cases. This review highlights recent virological findings in TAs from patients with pathologically-verified GCA and in TAs from patients who manifest clinical and laboratory features of GCA but whose TA biopsies are pathologically negative for GCA. Virological analysis revealed that VZV is present in most GCA-positive and GCA-negative TA biopsies, particularly in skip areas that correlate with adjacent GCA pathology. Summary: The presence of VZV in GCA-positive and GCA-negative TAs reflects the possible role of VZV in triggering the immunopathology of GCA and indicates that both groups of patients should be treated with antivirals in addition to corticosteroids. Whether oral antiviral agents and steroids are as effective as intravenous acyclovir and steroids, as well as the dosage and duration of treatment, remain to be determined.
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