Treatment of giant cell arteritis - Interleukin-6 as a biologic marker of disease activity

Objective. To determine the value of the erythrocyte sedimentation rate (ES R) and plasma interleukin-6 (IL-6) as biologic markers for monitoring disea se activity in giant cell arteritis (GCA). Methods. Twenty-five patients with biopsy-proven GCA were enrolled into a p rospective treatment study. Therapy was initiated with prednisone, 60 mg/da y, followed by a predetermined tapering schedule. Patients were monitored m onthly for clinical signs of active vasculitis and laboratory parameters in dicative of inflammation, including elevated ESR (>30 mm/hour) and elevated plasma IL-6 concentrations (>6.1 pg/ml). Results. Upon initiation of corticosteroid treatment, clinical signs of GCA disappeared in all patients; however, 60% of the patients developed sympto ms of recurrent disease, on 1 or more occasions, while the prednisone dosag e was being reduced. These 31 disease flares diagnosed over 550 days were a ssociated with symptoms of systemic inflammation but did not result in vasc ular complications. The ESR was elevated in 76% of the patients prior to in itiation of treatment (median 65 mm/hour) and normalized by day 28 of thera py (median 6 mm/hour). The median ESR remained in the normal range during t he followup period. Plasma IL-6 levels, which were abnormal in 92% of untre ated patients (median 16 pg/ml), were partially responsive to the initial h igh doses of corticosteroids by day 28 (median 6 pg/ml), but levels did not completely normalize with continued therapy. Elevation of the ESR was seen during only 58% of all disease flares, but 89% of disease recurrences were associated with increased plasma IL-6 levels (P = 0.03). Conclusion. Plasma IL-6 is more sensitive than ESR for indicating disease a ctivity in untreated and treated GCA patients. Standard corticosteroid regi mens only partially suppress vascular inflammation. Smoldering disease acti vity may expose GCA patients to the risk of progressive vascular disease (e .g., formation of aortic aneurysms) and chronic systemic complications such as IL-6-mediated osteopenia.