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Attending Physician Department of Medicine Sun Yat-Sen Cancer Center 125 Lih-Der Road Taipei, Taiwan 112 fax 011886-2-2897-2233 ticheng{at}mail.kfcc.org.tw
Professor Institute of Occupational Medicine and Industrial Hygiene College of Public Health National Taiwan University Taipei
Clinical Coordinator Department of Pharmacy Sun Yat-Sen Cancer Center
Published Online, November 9, 2004. www.theannals.com, DOI 10.1345/aph.1E156
Case Report.
A 75-year-old man was diagnosed with Parkinson's disease in July 1997; aspirin 100 mg daily was started one month later since a computed tomographic scan of the brain showed lacunar stroke. No baseline eosinophil count was obtained at that time. In March 1999, he was admitted because of altered mental status due to the adverse effects of trihexyphenidyl for Parkinson's disease. After this medicine was discontinued, the patient did well without any sequelae. On that admission, his laboratory tests revealed a leukocyte count of 5.40 x 103 cells/mm3 with 2% eosinophils (absolute eosinophil count [AEC] 108 cells/mm3). He had a health screening in October 2002, and laboratory tests showed a leukocyte count of 7.89 x 103 cells/mm3 with 60% eosinophils (AEC 4734 cells/mm3) (Table 1). Besides aspirin, the medications the man was taking included levodopa 100 mg and pergolide mesylate 0.25 mg 3 times daily, docusate sodium 100 mg and the laxative Sterculia 7 g once daily, and finasteride 5 mg at bedtime.
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The studies for eosinophilia did not reveal evidence of bronchial asthma, allergic rhinitis, eczema, urticaria, collagen vascular diseases, or helminthic infection. The patient underwent chest X-ray, abdominal ultrasound, esophagogastroduodenoscopic examinations, and a whole body positron emission tomographic scan. All studies for possible malignancy were unrevealing.
A search of databases including Micromedex, Iowa Drug Information System, MEDLINE, and EMBASE indicated that aspirin and levodopa have been linked to drug-induced eosinophilia.1-6 Levodopa was critical for the control of our patient's Parkinson's disease. Aspirin was therefore withheld first. The AEC reduced dramatically at that time to 900 cells/mm3 in 2 weeks and 365 cells/mm3 in 10 weeks. During this period, all other medications were continued. The Naranjo probability scale rated the adverse drug reaction at the level of highly possible.7
Discussion.
Previous studies have shown a relationship between aspirin use and tissue infiltration of eosinophils in patients with bronchial asthma, nasal polyps, or hypereosinophilic syndrome.1-4 However, the evidence showing an association between aspirin use and peripheral eosinophilia has been limited. Zeitz2 described peripheral eosinophilia as one of the clinical features in aspirin-induced Samter's syndrome, and its onset may be slow. However, our patient with peripheral eosinophilia did not have other associated clinical features. In the literature, the association of eosinophilia with hypersensitivity vasculitis secondary to levodopa is also listed.5 This association seems to be weak in our case because the AEC dropped after withholding aspirin, while levodopa was continued. Previous studies have shown that eosinophilia is related with the overexpression of interleukin-5.4,6 However, the relevance between aspirin-induced eosinophilia and a systemic level of interleukin-5 remains to be determined. Based on our case, eosinophilia in the absence of clinical symptoms is a highly possible adverse event caused by aspirin, and monitoring of the patient's complete blood cell count needs to be considered.
Footnotes
We thank Dr. Steven M Holland for his valuable discussion.
References
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