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Submitted May 4, 2026
Published 2026-08-28

Artículos Originales

Vol. 46 No. 2 (2026): Revista médica de Panamá

Polymyalgia rheumatica and giant cell arteritis


DOI https://doi.org/10.48204/medica.v46n2.a9909

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References
DOI: 10.48204/medica.v46n2.a9909

Published: 2026-08-28

How to Cite

Guerra, G. (2026). Polymyalgia rheumatica and giant cell arteritis. Revista médica De Panamá, 46(2), 33–44. https://doi.org/10.48204/medica.v46n2.a9909

Abstract

Introduction: Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are closely related inflammatory diseases that are considered part of the same clinical spectrum of large-vessel vasculitis, predominantly affecting older adults. Both conditions share immunopathological mechanisms, epidemiological characteristics, and overlapping clinical manifestations, which explains their frequent coexistence.                                                                                                   Objective: To review the current epidemiological, pathophysiological, clinical, diagnostic, and therapeutic aspects of giant cell arteritis and polymyalgia rheumatica, emphasizing their relationship within the same disease spectrum and recent advances in their diagnosis and treatment.

Methods: A narrative review of the medical literature available in international biomedical databases was conducted, including observational studies, clinical trials, and recent reviews on giant cell arteritis and polymyalgia rheumatica.

Results: Giant cell arteritis is the most common systemic vasculitis in older adults and can manifest in three main clinical phenotypes: cranial, extracranial, and mixed. Polymyalgia rheumatica is characterized by pain and stiffness in the shoulder girdle and pelvis, with frequent elevation of acute-phase reactants, although up to 20% of patients may have normal erythrocyte sedimentation rate and C-reactive protein levels. The development of advanced imaging techniques such as vascular ultrasound, magnetic resonance angiography, computed tomography angiography, and positron emission tomography (PET) has significantly improved the detection of vascular involvement. Glucocorticoids remain the mainstay of treatment; however, new targeted therapies such as tocilizumab, upadacitinib, and sarilumab have demonstrated efficacy in reducing cumulative steroid exposure. In settings where these therapies are not available, methotrexate can be used as a glucocorticoid-sparing agent.

Conclusions: GCA and PMR represent manifestations of the same inflammatory process related to immunological aging. Early recognition of their clinical manifestations and the appropriate use of modern diagnostic tools and targeted therapies allow for improved clinical management and a reduction in complications associated with prolonged glucocorticoid treatment.

 

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