Open AccessYKL‐40 in giant cells and macrophages from patients with giant cell arteritis
Author(s) -
Johansen Julia S.,
Baslund Bo,
Garbarsch Charly,
Hansen Michael,
Stoltenberg Michael,
Lorenzen Ib,
Price Paul A.
Publication year - 1999
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/1529-0131(199912)42:12<2624::aid-anr17>3.0.co;2-k
Subject(s) - giant cell arteritis , polymyalgia rheumatica , prednisolone , cd68 , gastroenterology , liter , medicine , pathogenesis , pathology , biopsy , giant cell , adventitia , immunohistochemistry , vasculitis , immunology , disease
Objective YKL‐40, a mammalian member of the family 18 glycosyl hydrolases, is secreted by activated macrophages at a late stage of differentiation. Macrophages are present in inflammation of the arterial wall and are thought to participate in the pathogenesis of giant cell arteritis (GCA). The aim of this study was to evaluate whether macrophages and giant cells of patients with GCA produce YKL‐40, and whether serum YKL‐40 concentrations are elevated in these patients. Methods Serum YKL‐40 was determined by radioimmunoassay in 19 patients with GCA and 8 patients with polymyalgia rheumatica (PMR) who were followed up prospectively during 1 year of treatment with prednisolone. Immunohistochemical staining for YKL‐40 was performed in temporal artery biopsy samples that were obtained before treatment. Results In the arteritic vessels of patients with GCA, positive staining for the YKL‐40 antigen was found in CD68+ giant cells and mononuclear cells located in the media. Macrophages located in the adventitia and intima were negative for YKL‐40. At the time of diagnosis, patients with GCA had an increased median serum level of YKL‐40 (256 μg/liter; P < 0.01) compared with healthy age‐matched controls (median 118 μg/liter), and the serum level of YKL‐40 decreased to normal levels during prednisolone treatment (–38% after 1 month; P < 0.001). Most patients with PMR had normal serum YKL‐40 levels (median 158 μg/liter) and had no changes in the serum YKL‐40 levels during prednisolone treatment. The observed changes in serum YKL‐40 did not always parallel the changes in serum C‐reactive protein levels and erythrocyte sedimentation rate during the 1‐year study period. Conclusion YKL‐40 is found in CD68+ giant cells and mononuclear cells in the media of arteritic vessels of patients with GCA, and the concentration of serum YKL‐40 may reflect the local activity of these cells in the inflamed artery.