Immunopathogenesis, diagnosis, and treatment of giant cell arteritis, temporal arteritis, polymyalgia rheumatica, and Takayasu's arteritis

Curr Opin Rheumatol. 1993 Jan;5(1):25-32. doi: 10.1097/00002281-199305010-00005.

Abstract

Although the causes of giant cell arteritis, polymyalgia rheumatica, and Takayasu's arteritis are not known, the immune system participates in the pathogenesis of these disorders. Many reports indicate that cellular immunity is active in giant cell arteritis. The diagnosis of Takayasu's arteritis has been advanced by magnetic resonance imaging and ultrasonography. Neither technique has replaced angiography as the gold standard for diagnosis, but both may help monitor the response of Takayasu's arteritis to therapy. The diagnosis of giant cell arteritis with a low erythrocyte sedimentation rate is unusual but is more frequent in patients with a history of polymyalgia rheumatica or corticosteroid use. One recent retrospective study suggests that 20 mg/d of prednisolone is as effective as higher doses in treating giant cell arteritis. Other preliminary studies indicate that methotrexate may effectively spare corticosteroid use in giant cell arteritis and Takayasu's arteritis. Angioplasty for renal artery stenosis in Takayasu's arteritis initially cures 30% of patients and improves the condition in 70%; however, the long-term success rate is 50%. New studies demonstrate that patients with giant cell arteritis and polymyalgia rheumatica have an increased risk of hypothyroidism.

Publication types

  • Review

MeSH terms

  • Giant Cell Arteritis* / diagnosis
  • Giant Cell Arteritis* / drug therapy
  • Giant Cell Arteritis* / etiology
  • Humans
  • Polymyalgia Rheumatica* / diagnosis
  • Polymyalgia Rheumatica* / drug therapy
  • Polymyalgia Rheumatica* / etiology
  • Takayasu Arteritis* / diagnosis
  • Takayasu Arteritis* / drug therapy
  • Takayasu Arteritis* / etiology