The role of disease-modifying antirheumatic drugs in the treatment of giant cell arteritis

Dirk M. Nuenninghoff, Eric L. Matteson

Research output: Contribution to journalReview articlepeer-review

35 Scopus citations

Abstract

Giant cell arteritis (GCA) is a vasculitis of unknown etiology that affects medium-sized and large arteries, and is the most common form of vasculitis in populations of predominantly Northern European ancestry. If left untreated, GCA can lead to significant morbidity including blindness, stroke, aortic aneurysm and dissection, as well as large-artery stenosis. Glucocorticosteroids are in general very effective in the treatment of GCA. Treatment with high dose glucocorticosteroids is associated with considerable morbidity and for some, but not all patients is required for prolonged periods sometimes exceeding several years. Numerous effort have been made over the decades to optimize therapeutic outcomes and reduce the side effects of glucocorticosteroids by enlisting adjuvant and alternative therapies. This review focuses primarily on evidence from randomized controlled trials with the objective of efficacy assessment of the respective drugs and dosing regimens in the treatment of GCA. Various glucocorticosteroid dosing regimens including alternate-day dosing, disease-modifying therapies including methotrexate and azathioprine, and the prospect of using monoclonal anti-cytokine or anti-cytokine receptor antibodies in the treatment of GCA are addressed. Thus far, no disease-modifying antirheumatic drug therapy or alternative to daily glucocorticosteroid therapy has been found to be unequivocally effective in the treatment of GCA.

Original languageEnglish (US)
Pages (from-to)S29-S34
JournalClinical and experimental rheumatology
Volume21
Issue number6 SUPPL. 32
StatePublished - 2003

Keywords

  • Antibodies
  • Antirheumatic agents
  • Azathioprine
  • Glucocorticoids
  • Methotrexate
  • Recombinant proteins
  • Temporal arteritis

ASJC Scopus subject areas

  • Rheumatology
  • Immunology and Allergy
  • Immunology

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