Open AccessTemporal artery biopsy: A diagnostic tool for systemic necrotizing vasculitis
Author(s) -
Généreau Thierry,
Lortholary Olivier,
Pottier MarieAntoinette,
MichonPasturel Ulrique,
Ponge Thierry,
De Wazières Benoît,
Liozon Eric,
Pinède Laurent,
Hachulla Eric,
Roblot Pascal,
Barrier JacquesHenri,
Herson Serge,
Guillevin Loïc
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<2674::aid-anr25>3.0.co;2-a
Subject(s) - medicine , giant cell arteritis , polyarteritis nodosa , vasculitis , systemic vasculitis , biopsy , arteritis , necrotizing vasculitis , rheumatology , retrospective cohort study , skin biopsy , systemic disease , pathology , dermatology , disease
Abstract Objective To describe the clinical, biologic, and histologic features of temporal artery biopsy (TAB)–localized systemic necrotizing vasculitides (SNV), and to assess their frequency among elderly patients undergoing TAB for suspected giant cell (temporal) arteritis (GCA). Methods The frequency of a TAB localization of SNV was prospectively assessed in a multicenter study of elderly patients undergoing TAB for suspected GCA. All patients with SNV fulfilling the American College of Rheumatology criteria for a specific vasculitic syndrome and with evidence of vasculitis on TAB were included in a retrospective, descriptive study. Results SNV was diagnosed based on the TAB in 1.4% of the patients with suspected GCA and in 4.5% of the positive (inflamed) TAB specimens. We retrospectively selected 27 patients (18 female, 9 male; mean ± SD age 62 ± 15 years, range 22–79 years) with SNV and TAB‐localized vasculitis. Only 2 of these patients were known to have SNV before TAB localization. Twenty‐two patients (81%) had cephalic symptoms, including jaw claudication in 33%, clinically abnormal temporal arteries in 33%, and neuro‐ophthalmologic symptoms in 11%. All patients had systemic symptoms suggestive of SNV and histologically proven NV in the TAB specimens (70%) or elsewhere in other biopsy sites (74%). Abnormal biologic results suggestive of SNV were present in 17 patients (63%). For 4 patients, the TAB‐documented involvement led to initial misdiagnoses of GCA, and systemic manifestations that developed under steroid therapy revealed the correct diagnosis. The final diagnoses of the patients were polyarteritis nodosa (PAN) (n = 11), Churg‐Strauss syndrome (n = 6), micropolyangiitis (n = 3), Wegener's granulomatosis (n = 3), hepatitis B virus–related PAN (n = 2), hepatitis C virus–related cryoglobulinemic vasculitis (n = 1), and rheumatoid vasculitis (n = 1). Conclusion TAB‐localized SNV presents a major diagnostic dilemma because it can mimic GCA. Careful analysis of clinical, biologic, and histologic data should lead to the correct diagnosis and help guide the clinician's choice of appropriate therapy.