Giant cell arteritis and polymyalgia rheumatica: pathophysiology and management
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Updated: Jul 20, 2026

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
Published on: February 8, 2019
Miguel A Gonzalez-Gay1, Carlos Garcia-Porrua, Jose A Miranda-Filloy
1Division of Rheumatology, Hospital Xeral-Calde, Lugo, Spain. miguelaggay@hotmail.com
Abstract:
Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are common and often concurrent diseases in Western countries in individuals aged >50 years. Clinical features of GCA are mainly due to involvement of the cranial arteries. PMR is clinically characterised by pain, aching and morning stiffness involving the neck, shoulder and hip girdles. Both conditions are generally associated with elevation of erythrocyte sedimentation rate and C-reactive protein. A temporal artery biopsy is the gold standard test for the diagnosis of GCA. Some diseases may mimic PMR or present with polymyalgic symptoms. Corticosteroids are the cornerstone of the management of GCA and PMR. An initial dosage of prednisone 10-20 mg/day yields a dramatic improvement of PMR symptoms in most cases. In GCA, the initial prednisone dosage required is higher (40-60 mg/day). However, once established, visual loss, which is the most feared complication of GCA, does not usually improve following corticosteroid therapy. Some patients exhibit a chronic-relapsing course and may need low doses of corticosteroids for several years. Alternative corticosteroid-sparing therapies and some therapeutic agents aimed at restoring balanced bone cell activity in patients taking corticosteroids are potentially useful in the management of GCA and PMR.
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