title: Clinical and pathological evolution of giant cell arteritis: a prospective study of follow-up temporal artery biopsies in 40 treated patients.
abstract: Although clinical signs and symptoms of giant cell arteritis improve promptly after starting glucocorticoid therapy, reports have suggested that the vascular inflammation may persist. To assess the duration and quality of histopathologic changes in treated patients, we prospectively obtained second temporal artery biopsies in patients treated for 3 to 12 months after their first diagnostic biopsy. Forty patients (28 women, 12 men, median age 77 years) agreed to have a second temporal artery biopsy randomly assigned to 3, 6, 9, or 12 months subsequent to the first. Clinical and laboratory evaluation of the patient cohort revealed a typical rapid response and continued suppression of clinical manifestations as a result of glucocorticoid treatment. Histopathologic findings, evaluated in a blinded manner by a cardiovascular pathologist, showed unequivocal findings of vasculitis in 7/10 patients with second temporal artery biopsy at 3 months, 9/12 at 6 months, 4/9 at 9 months, and 4/9 at 12 months. Lymphocytes were present in all positive initial biopsies and remained the dominant cell population in chronically treated patients. Granulomatous inflammation decreased in a time-dependent manner from 78 to 100% at initial biopsy to 50% at 9 months and 25% at 12 months. The increased medial fibrosis noted in the second biopsies (60 vs 33% in primary temporal artery biopsies) suggested that the finding may represent a chronic finding in arteritis. In summary, the response to glucocorticoids in giant cell arteritis was frequently discordant. Clinical manifestations were readily suppressed, but vascular changes were gradual and often incomplete.
authors.affiliation: Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.
authors.forename: Joseph J
authors.initials: JJ
authors.lastname: Maleszewski
authors.affiliation: Department of Ophthalmology, Mayo Clinic, Rochester, MN, USA.
authors.forename: Brian R
authors.initials: BR
authors.lastname: Younge
authors.affiliation: School of Medicine, University of Kansas, Kansas City, KS, USA.
authors.forename: John T
authors.initials: JT
authors.lastname: Fritzlen
authors.affiliation: Division of Rheumatology, Mayo Clinic, Rochester, MN, USA.
authors.forename: Gene G
authors.initials: GG
authors.lastname: Hunder
authors.affiliation: Division of Immunology and Rheumatology, Stanford University, Stanford, CA, USA.
authors.forename: Jorg J
authors.initials: JJ
authors.lastname: Goronzy
authors.affiliation: Division of Rheumatology, Mayo Clinic, Rochester, MN, USA.
authors.forename: Kenneth J
authors.initials: KJ
authors.lastname: Warrington
authors.affiliation: Division of Immunology and Rheumatology, Stanford University, Stanford, CA, USA.
authors.forename: Cornelia M
authors.initials: CM
authors.lastname: Weyand
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001706:Biopsy; D005260:Female; D005355:Fibrosis; D013700:Giant Cell Arteritis / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology*; D005938:Glucocorticoids / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011241:Prednisone / Q000627:therapeutic use*; D011446:Prospective Studies; D011897:Random Allocation; D013699:Temporal Arteries / Q000187:drug effects* / Q000276:immunology / Q000473:pathology*; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D005938:Glucocorticoids; D011241:Prednisone