Remarkable efficacy of tocilizumab for treating rheumatoid arthritis in patients with high platelet counts

被引:14
作者
Matsuno, Hiroaki [1 ,2 ]
机构
[1] Matsuno Clin Rheumat Dis, Toyama 9300138, Japan
[2] Tokyo Med Univ, Inst Med Sci, Tokyo 1608402, Japan
关键词
Bone destruction; Disease activity score; Hemoglobin; Platelet count; Rheumatoid arthritis; Tocilizumab; JOINT DAMAGE; CRITERIA; CLASSIFICATION; INFLAMMATION; PROGRESSION; LEAGUE; MICE;
D O I
10.3109/14397595.2014.915073
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objectives. To optimize the efficacy of treatment with tocilizumab for rheumatoid arthritis (RA), we comparatively analyzed the outcome of tocilizumab treatment in patients with normal background changes associated closely with IL-6. Patients and Methods. The study involved 87 patients with RA satisfying the diagnostic criteria of the American College of Rheumatology (ACR) and receiving continuous tocilizumab treatment for 24 weeks or longer. The outcome of tocilizumab treatment in these patients was comparatively analyzed in relation to the baseline platelet count (the high platelet count group and the normal group), pretreatment hemoglobin levels (the low group and the normal platelet count group), and speed of bone destruction (the rapid progression group and slow progression group). Results. Treatment with tocilizumab significantly improved the 28-joint disease activity score using the erythrocyte sedimentation rate (DAS28-ESR) and Clinical Disease Activity Index (CDAI), regardless of baseline platelet count, hemoglobin level, or annual speed of bone destruction (Delta TSS). The margins of improvement in DAS28-ESR and CDAI did not differ depending on baseline hemoglobin level or Delta TSS, but the improvement was significantly greater in the high platelet count group than in the normal platelet count group. Conclusions. These results suggest that in patients with high platelet count, IL-6 is a more important factor involved in RA pathogenesis and that tocilizumab is suitable as a first-line biologic for the treatment of RA patients with high platelet count.
引用
收藏
页码:38 / 42
页数:5
相关论文
共 15 条
[1]  
Aletaha D, 2005, CLIN EXP RHEUMATOL, V23, pS100
[2]  
Aletaha D, 2010, ANN RHEUM DIS, V69, P1580, DOI [10.1136/ard.2010.138461, 10.1002/art.27584]
[3]   THE AMERICAN-RHEUMATISM-ASSOCIATION 1987 REVISED CRITERIA FOR THE CLASSIFICATION OF RHEUMATOID-ARTHRITIS [J].
ARNETT, FC ;
EDWORTHY, SM ;
BLOCH, DA ;
MCSHANE, DJ ;
FRIES, JF ;
COOPER, NS ;
HEALEY, LA ;
KAPLAN, SR ;
LIANG, MH ;
LUTHRA, HS ;
MEDSGER, TA ;
MITCHELL, DM ;
NEUSTADT, DH ;
PINALS, RS ;
SCHALLER, JG ;
SHARP, JT ;
WILDER, RL ;
HUNDER, GG .
ARTHRITIS AND RHEUMATISM, 1988, 31 (03) :315-324
[4]  
Campbell Ken, 2004, Nurs Times, V100, P40
[5]   Access to the next wave of biologic therapies (Abatacept and Tocilizumab) for the treatment of rheumatoid arthritis in England and Wales Addressing treatment outside the current NICE guidance [J].
Chiu, Yee ;
Ostor, Andrew J. K. ;
Hammond, Anthony ;
Sokoll, Katharina ;
Anderson, Marina ;
Buch, Maya ;
Ehrenstein, Michael R. ;
Gordon, Patrick ;
Steer, Sophia ;
Bruce, Ian N. .
CLINICAL RHEUMATOLOGY, 2012, 31 (06) :1005-1012
[6]   IL-6 receptor inhibition with tocilizumab improves treatment outcomes in patients with rheumatoid arthritis refractory to anti-tumour necrosis factor biologicals: results from a 24-week multicentre randomised placebo-controlled trial [J].
Emery, P. ;
Keystone, E. ;
Tony, H. P. ;
Cantagrel, A. ;
van Vollenhoven, R. ;
Sanchez, A. ;
Alecock, E. ;
Lee, J. ;
Kremer, J. .
ANNALS OF THE RHEUMATIC DISEASES, 2008, 67 (11) :1516-1523
[7]   Hepcidin, a key regulator of iron metabolism and mediator of anemia of inflammation [J].
Ganz, T .
BLOOD, 2003, 102 (03) :783-788
[8]  
ISHIBASHI T, 1989, BLOOD, V74, P1241
[9]   Anti-interleukin 6 (IL-6) receptor antibody suppresses Castleman's disease like symptoms emerged in IL-6 transgenic mice [J].
Katsume, A ;
Saito, H ;
Yamada, Y ;
Yorozu, K ;
Ueda, O ;
Akamatsu, K ;
Nishimoto, N ;
Kishimoto, T ;
Yoshizaki, K ;
Ohsugi, Y .
CYTOKINE, 2002, 20 (06) :304-311
[10]   The role of TNF-α in the pathogenesis of inflammation and joint destruction in rheumatoid arthritis (RA):: a study using a human RA/SCID mouse chimera [J].
Matsuno, H ;
Yudoh, K ;
Katayama, R ;
Nakazawa, F ;
Uzuki, M ;
Sawai, T ;
Yonezawa, T ;
Saeki, Y ;
Panayi, GS ;
Pitzalis, C ;
Kimura, T .
RHEUMATOLOGY, 2002, 41 (03) :329-337