Giant cell arteritis (GCA) is a systemic inflammatory vasculitis affecting medium and large vessels with potentially sight and life-threatening complications. Early diagnosis and prompt treatment are imperative in order to prevent vision loss and progression of the disease. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are inflammatory markers which are elevated in the majority of patients and support the diagnosis of GCA among patients who present with typical symptoms. GCA is confirmed with superficial temporal artery biopsy which demonstrates characteristic pathological findings. Treatment of suspected ophthalmic involvement must be initiated urgently, even when diagnostic studies are pending. High dose corticosteroid therapy is the mainstay of treatment and is administered either intravenously or orally to prevent further vision loss and treat systemic vasculitis. Oral corticosteroid therapy is required for months to years with careful follow-up and periodic laboratory evaluations with ESR and CRP. Corticosteroids are tapered gradually over months and may be associated with complications such as hypertension, diabetes mellitus, osteoporosis, psychosis, peptic ulcer disease, and infection. Supplementation with calcium, vitamin D, bisphosphonate therapy, antimicrobial prophylaxis, and initiation of a proton pump inhibitor or Histamine H2-receptor antagonist should be considered. Recurrence of inflammation is common in GCA and necessitates an escalation of corticosteroid dose. Adjunctive immunomodulatory therapy may be considered in patients experiencing relapsing inflammation despite high doses of corticosteroids or those with corticosteroid-induced complications. Emerging evidence for adjunctive therapy with tocilizumab, methotrexate, aspirin, angiotensin receptor blockers, and statins is encouraging and may lead to a more mainstream role for these therapies among patients with GCA.
Keywords: Corticosteroids; Giant cell arteritis; Immunosuppression; Ischemic optic neuropathy; Tocilizumab.