ANTIBODIES TO CARDIOLIPIN AND BETA2 GLYCOPROTEIN-I IN PATIENTS WITH POLYMYALGIA-RHEUMATICA AND GIANT-CELL ARTERITIS

IgG antibodies to cardiolipin and beta 2-glycoprotein I were looked fo r using an enzyme-linked immunosorbent assay (ELISA) in 19 patients wi th giant cell arteritis (meeting 1990 American College of Rheumatology criteria), including 16 with concomitant polymyalgia rheumatica (meet ing Bird's criteria) and in three patients with isolated polymyalgia r heumatica, IgG anti-cardiolipin antibodies were demonstrated in eight patients (36%) and IgG anti-beta 2-glycoprotein I antibodies in two pa tients (9%) including one without anti-cardiolipin antibodies. Titers of anti-cardiolipin antibodies ranged from 27 to 190 units of IgG anti phospholipid antibodies (UGPL) (mean 71 UGPL). Of the eight patients w ith anti-cardiolipin antibodies, two had giant cell arteritis without polymyalgia rheumatica and six had polymyalgia rheumatica with clinica l (n=2) or histologic (n=4) evidence of giant cell arteritis, None of the three patients with polymyalgia rheumatica but no giant cell arter itis had anticardiolipin or anti-beta 2 glycoprotein I antibodies, The VDRL was negative in the 14 patients who had this test, Tests for lup us anticoagulant were performed routinely, always with negative result s. Among giant cell arteritis patients, those who tested positive for anticardiolipin antibody had significantly higher values for the eryth rocyte sedimentation rate (p<0.006) and for serum C-reactive protein ( p<0.03) and fibrinogen values (p=0.05), and a trend toward higher plat elet counts, as compared to those who tested negative for anticardioli pin antibody. The mean daily prednisone dose at the time of sampling w as significantly lower in giant cell arteritis patients with anti-card iolipin antibodies (p<0.05); this difference may account for the appar ent correlation between anti-cardiolipin antibodies and laboratory mar kers for inflammation. These data, as well as findings from serial mea surements, suggest that anticardiolipin antibodies are present early i n the course of giant cell arteritis and disappear within a few weeks of initiation of corticosteroid therapy in a dose of more than 25 mg p rednisone per day. In this study, only one patient without anticardiol ipin antibodies developed a cerebrovascular accident, Positive tests f or anticardiolipin antibody or anti-beta 2 glycoprotein I antibody in a patient with polymyalgia rheumatica suggest a diagnosis of concomita nt giant cell arteritis, which is usually symptomatic.