Giant Cell Arteritis

Journal/Book: Z Rheumatol 1998; 57 Suppl. 1: 14 (V 58). 1998;

Abstract: Mayo Clinic Rochester Giant. cell arteritis occurs within an increasing frequency in persons over the age of 50 years and 90 % are over 60 years at onset. the cranial branches of the arteries originating from the arch of the aorta are involved most prominently but the arteritis may be more generalized. Some studies have shown an increasing incidence of this disease. We and others have noted variations in disease frequency. Hypotheses regarding pathogenesis of giant cell arteritis have included the internal elastic lamina as a potential autoantigen an ethnic or genetic predisposition and immune abnormality related to the significant association with HLA-DR4. A sequence polymorphism within the second hypervariable region of the HLA-DRB1 gene in giant cell arteritis and polymyalgia rheumatica has been identified with maps to the antigen-binding cleft of the HLA-DR molecule. Qtherr immunologic alteration include alterations in peripheral blood CD8 cell populations and elevated plasma interleukin-6 which is related to disease activity. Short-term withdrawal of corticosteroids even after several months of therapy was followed by an immediate increase in plasma interleukin-6 concentrations along with the return of symptoms. Monocytes in peripheral blood and macrophages in the inflamed artery cell walls both produce this cytokine. Wagner and co-workers found expression of interleukin-6 and interleukin-1 beta in 60 to 80 percent of circulating monocytes in patients with untreated giant cell arteritis or polymyalgia rheumatica but not rheumatoid arthritis. In temporal arteries positive for giant cell arteritis twenty percent of macrophagias showed interleukin-6 and interleukin-1 synthesis. The latter cells were dispersed throughout the temporal artery wall. Some of these cells also produced collagenase. However collagenase synthesis was not found in circulating cells. ... le

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