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Clinical Manifestations of Human T Lymphotropic Virus Type I-Infected Patients with Systemic Lupus Erythematosus MASAKI AKIMOTO, KAKUSHI MATSUSHITA, YUKIO SURUGA, NORIKO AOKI, ATSUO OZAKI, KIMIHARU UOZUMI, CHUWA TEI, and NAOMICHI ARIMA
ABSTRACT. Methods. Eighty-nine patients with SLE were screened for antibodies to HTLV-I by electrochemiluminescence immunoassay. The presence of HTLV-I proviral sequences in peripheral blood mononuclear cells (PBMC) was determined by real-time polymerase chain reaction (PCR) quantification and Southern blotting analysis. The differences in clinical manifestations between HTLV-I-seropositive and seronegative patients with SLE were analyzed statistically. Results. Fourteen of 89 (15.7%) patients were HTLV-I seropositive. All PBMC samples from 11 patients tested by PCR and 3 samples from 10 patients tested by Southern blotting analysis were positive for HTLV-I-related sequences. The age of HTLV-I-seropositive patients with SLE was significantly higher than that of seronegative patients (median 60 vs 42 yrs; p < 0.0005). The age at onset of SLE in HTLV-I-seropositive patients was also significantly higher than that of seronegative patients (median 45.5 vs 30 yrs; p < 0.0005). The lymphocyte count in HTLV-I-seropositive SLE patients was significantly higher than that of seronegative patients (median 1740 vs 1066/µl; p = 0.027). The maintenance dose of prednisolone in HTLV-I-seropositive patients with SLE was significantly lower than that in seronegative patients (median 5 vs 9 mg/day; p = 0.012). Conclusion. This is the first report of the differences in clinical manifestations between SLE patients with and without HTLV-I infection. Our results suggest some involvement of HTLV-I in the pathogenesis of SLE. (First Release August 1 2007; J Rheumatol 2007;34:1841-8) Key Indexing Terms:
HUMAN T LYMPHOTROPIC VIRUS TYPE I
From the Department of Hematology and Immunology, Kagoshima University Hospital; and the Division of Host Response, Center for Chronic Viral Diseases, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan. M. Akimoto, MD; K. Matsushita, MD; Y. Suruga, MD; N. Aoki, MD; A. Ozaki, MD, Department of Hematology and Immunology, Kagoshima University Hospital; K. Uozumi, MD, Assistant Professor; N. Arima, MD, Professor, Division of Host Response, Center for Chronic Viral Diseases, Kagoshima University Graduate School of Medical and Dental Sciences; C. Tei, MD, Professor, Department of Cardiovascular, Respiratory and Metabolic Medicine, Kagoshima University Graduate School of Medical and Dental Sciences. Address reprint requests to Dr. M. Akimoto, Department of Hematology and Immunology, Kagoshima University Hospital, 8-35-1 Sakuragaoka, Kagoshima, 890-8520, Japan. E-mail: akimoto@m3.kufm.kagoshima-u.ac.jp Accepted for publication May 3, 2007. |
