Although thrombosis caused by giant cell arteritis may theoretically affect all medium- and large-sized arteries [1, 2], thrombosis of the pulmonary artery is rare [3, 4]. We report a case of pulmonary infarction secondary to segmentary thrombosis of the pulmonary artery in a patient treated for giant cell arteritis. Pneumonia was suspected in an 86-year-old woman who had been successfully treated for 3 months with prednisone for histologically confirmed giant cell arteritis. A chest radiograph showed infiltration of the upper left lobe of the lung with areas of cavitation.

Laboratory findings included a leukocyte count of 22 000 cells/mm³ and an erythrocyte sedimentation rate of 74 mm/h. Bronchoscopy results were normal. Bacteriologic samples were negative for bacteria, fungi, and acid-fast bacilli. The patient's serum was negative for antinuclear antibodies, antineutrophil cytoplasmic autoantibodies, and circulating anticoagulant antibodies. A computed tomographic scan showed proximal thrombosis of the left pulmonary artery, which was confirmed by pulmonary angiogram (Figure 1). Results of tests for deep venous thrombosis were negative. We suspected a pulmonary infarction had occurred that was secondary to inflammatory thrombosis of the pulmonary artery, which was caused by giant cell arteritis. The prednisone dose was increased to 50 mg daily, and this dose had a rapid and long-lasting (1-year follow-up) favorable effect on all symptoms.

View larger version (140K): [in this window] [in a new window]   Figure 1. Pulmonary angiography. Obstruction of the left pulmonary artery is associated with multiple cavitary lesions of the left upper lobe.

The diagnosis in our patient of pulmonary artery thrombosis that was secondary to giant cell arteritis was supported by 1) the pulmonary angiogram anomalies, 2) the absence of other identified causes [tumor; infection; or other vasculitis, such as Wegener granulomatosis], and 3) complete resolution of all symptoms with steroids (without any associated anticoagulant therapy). To our knowledge, pulmonary vasculitis lesions in giant cell arteritis have only been shown in two previously reported cases [3, 4], including one postmortem biopsy specimen. In our patient, the rapid improvement of the pulmonary lesions with steroids should be emphasized. This clinical course suggests that the hypothesis of a predominant inflammatory thrombosis that is secondary to vasculitis might be valid and should perhaps be studied.