Leg Ulcers Associated With Giant Cell Arteritis Relapse

Abstract

Giant cell arteritis (GCA) is a granulomatous vasculitis of the aorta and its major branches, with a predilection for the extracranial branches of the carotid artery. In June 2012, an 81-year-old Caucasian woman was referred to our dermatology service because of nonhealing ulcers on the right leg. The patient has a personal history of GCA diagnosed in 1991 and was treated with methotrexato and prednisone. She did not complain of asthenia, jaw claudication, and headache. On admission, her inflammatory markers were elevated: erythrocyte sedimentation rate was 52 mm/h and C-reactive protein level was 1.16 mg/dL. The rest of the laboratory tests and coagulative screening were within normal limits. On admission, she resumed methotrexate 5 mg/ week, folic acid 5 mg/week, prednisone 5 mg/day, and pantoprazole 40 mg/day. On physical examination, we found 3 crusted leg ulcers surrounded with a zone of erythema (Figure 1). The patient underwent to a 3-mm punch biopsy of the lesions and an arteriovenous echo color Doppler of the leg. After debridement, the wound was dressed with medicated bandage. The histological finding was atypical for leg ulcers (Figure 2). We observed ulceration; granulation tissue; sparse, perivascular, interstitial mixed mostly lymphocytes; neutrophils; intraluminal thrombi; extravasated erythrocytes; and granulomatous infiltrate made up of histiocytes in the mid and reticular dermis. The ultrasonographic examination showed preserved vascular function and atherosclerosis of the right femoropopliteal arteries, even without significant stenosis. We made the diagnosis of leg ulcers associated with GCA relapse. After treatment with higher doses of systemic glucocorticoids, the ulcers improved in about 1 month. The histological features of GCA were first recognized in 1932 by Horton et al, and so is also called “Horton’s giant cell arteritis.” GCA usually occurs in individuals aged 50 years and older, more often in women. Genetic or ambient factors probably contribute to the development of GCA, but the etiology is still unknown. GCA is responsible for a broad spectrum of manifestations due to the inflammatory involvement of vessel wall with lymphocytic and macrophagic infiltrates in the tunica media that can extend from the tunica intima to the avventitia and sometimes involving internal elastic lamina. Giant cells can be present. Granulomas and fibrinoid necrosis are seen infrequently. Acute-phase 476518 IJLXXX10.1177/1534734613476518The International Journal of Lower Extremity WoundsMisciali et al © The Author(s) 2011