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Abstract Number: 2159

Human T-Lymphotropic Virus Type 1 Biomarkers in Patients with Rheumatoid Arthritis

Akihiko Okayama1, Masako Iwanaga2, Yasuko Sagara3, Toshihiko Hidaka4, Kunihiko Umekita5, Kazumi Nakano6, Toshiki Watanabe6, Yoshihisa Yamano7, Yoshiro Horai8, Hideki Nakamura9 and Atsushi Kawakami9, 1Department of Rheumatology, Infectious Diseases and Laboratory Medicine, University of Miyazaki, Miyazaki, Japan, 2The Jikei University of School of Medicine, Tokyo, Japan, 3Japanese Red Cross Kyushu Block Blood Center, Fukuoka, Japan, 4Zenjinkai Shimin-No-Mori Hospital, Miyazaki, Japan, 5University of Miyazaki, Miyazaki, Japan, 6Laboratory of Tumor Cell Biology, Department of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, Japan, 7Institute of Medical Science, St. Marianna University School of Medicine, Kanagawa, Japan, 8Departments of Immunology and Rheumatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan, 9Department of Immunology and Rheumatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: Biomarkers, rheumatoid arthritis (RA) and viruses

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Session Information

Title: Infections, Infection-related Biomarkers and Impact of Biologic Therapies

Session Type: Abstract Submissions (ACR)

Background/Purpose: Human T-lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia (ATL). It has been debated recently whether or not immunosuppressive agents for HTLV-1 carriers with a variety of inflammatory/immunological conditions can increase the risk of developing ATL, which is of important in terms of the pros and cons of anti-rheumatic treatment for HTLV-1 positive patients with RA. Through HTLV-1 biomarkers, whether the immunosuppressive medicines or biologics for HTLV-1 positive rheumatoid arthritis (RA) patients may affect adversely to the risk of ATL was speculated.

Methods: HTLV-1 antibody was screened for 808 patients with RA diagnosed in two regions in Japan, Nagasaki and Miyazaki prefectures, endemic areas of HTLV-1 infection. Among those, HTLV-1 positive RA patients treated with anti-rheumatic medicines including biologics (anti-TNFs, tocilizumab, and abatacept) were selected to be subjects for this study and evaluated about the levels in blood samples of HTLV-1 proviral load (PVL) by real-time PCR, antibody titer by particle agglutination assay, and soluble IL-2 receptor (sIL-2R) by enzyme immunoassay. The levels of the biomarkers were compared with those of age and sex matched asymptomatic HTLV-1 carriers (ACs) using Wilcoxon rank sum test.

Results:  The HTLV-1 seroprevalence in patients with RA was 8.2% (66/808). Blood samples were available in 33 among the 66 HTLV-1 positive RA patients. The median HTLV-1 PVL of the 33 patients was 0.52 copies per 100 peripheral blood mononuclear cells (PBMCs), which was lower than that of age and sex matched 99 ACs (1.0 copy per 100 PBMCs) (p=0.08). The median antibody titer of the 33 patients was 28.9, which was lower than that of age and sex matched 99 ACs (29.7) (p=0.03). The level of sIL-2R was not different between 2 groups (p=0.10). 

Conclusion:

The HTLV-1 seroprevalence in patients with RA in the endemic area in Japan was higher than we expected. Both HTLV-1 PVL and antibody titer in HTLV-1 positive RA patients treated with anti-rheumatic medicines showed lower values comparing with those in ACs. These findings, when viewed in light of a previous report that high HTLV-1 PVL is considered as the risk factor for developing ATL, suggest that treatment by anti-rheumatic medicines including biologics may not necessarily increase the risk for ATL development in HTLV-1 positive patients with RA. Further long-term follow-up study can determine the safety of anti-rheumatic treatment in HTLV-1 positive patients with RA.


Disclosure:

A. Okayama,
None;

M. Iwanaga,
None;

Y. Sagara,
None;

T. Hidaka,
None;

K. Umekita,
None;

K. Nakano,
None;

T. Watanabe,
None;

Y. Yamano,
None;

Y. Horai,
None;

H. Nakamura,
None;

A. Kawakami,
None.

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