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CD64 on Neutrophils Is a Sensitive and Specific
Marker for Detection of Infection in Patients with Rheumatoid Arthritis
TOSHIHIRO MATSUI, KAYOKO OHSUMI, NAOKO OZAWA, KOTA SHIMADA, SHUJI SUMITOMO, KENICHI SHIMANE, MISATO KAWAKAMI, HISANORI NAKAYAMA, SHOJI SUGII, YOSHINORI OZAWA, and SHIGETO TOHMA ABSTRACT. Objective. In inflammatory diseases, differentiation between infection and disease flares is often clinically difficult because of similar signs and symptoms, such as fever and elevation of inflammatory markers. In rheumatoid arthritis (RA), infection is not only one of the major complications but also one of the frequent causes of death. Use of biologic agents such as tumor necrosis factor-a blockers has been reported to increase the incidence of tuberculosis or opportunistic infections. We examined the utility of CD64 (FcgRI) expressed on neutrophils as a marker for detection of infection complicated with RA. Methods. We measured the expression level of CD64 per neutrophil quantitatively by flow cytometry in 279 samples from 237 patients with RA with various levels of disease activity or types of infection, and in 52 samples from 36 controls including subjects with infection. Results. CD64 expression was significantly higher among RA patients with infection (median 4156 molecules per neutrophil, interquartile range 2583–8587) than in those without infection (884, IQR 670–1262) (p < 0.001). The sensitivity of CD64 on neutrophils for the diagnosis of infection (using a cutoff value of 2000 molecules per cell) was 92.7% and specificity was 96.5%. CD64 expression was not affected by the disease activity of RA or the use of corticosteroids, disease modifying antirheumatic drugs, and biologic agents. CD64 was upregulated in infection by bacteria, viruses, fungi, and mycobacteria. Conclusion. Our results suggest that quantitative measurement of CD64 expression on neutrophils can be used as a sensitive and specific marker to detect infection complicating RA. (First Release Oct 15 2006; J Rheumatol 2006;33:2416–24) Key Indexing Terms:
RHEUMATOID ARTHRITIS From the Department of Rheumatology; the Division of Rheumatology, Clinical Research Center for Allergy and Rheumatology; and the Department of Rehabilitation, Sagamihara National Hospital, National Hospital Organization, Kanagawa, Japan. Supported in part by grants from the National Hospital Organization and the Manabe Foundation. T. Matsui, MD, PhD, Department of Rheumatology; K. Ohsumi, Research Assistant; N. Ozawa, Research Assistant; K. Shimada, MD, PhD, Division of Rheumatology, Clinical Research Center for Allergy and Rheumatology; S. Sumitomo, MD; K. Shimane, MD; M. Kawakami, MD; H. Nakayama, MD, Department of Rheumatology; S. Sugii, MD, Department of Rehabilitation; Y. Ozawa, MD, Department of Rheumatology; S. Tohma, MD, Division of Rheumatology, Clinical Research Center for Allergy and Rheumatology, Sagamihara National Hospital. Address reprint requests to Dr. T. Matsui, Department of Rheumatology, Sagamihara National Hospital, National Hospital Organization, 18-1, Sakuradai Sagamihara City, Kanagawa, 228-8522, Japan. E-mail: t-matsui@sagamihara-hosp.gr.jp Accepted for publication August 8, 2006.
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