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Pulmonary Artery Obstruction and Giant Cell Arteritis
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TO THE EDITOR:
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.
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.
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
