%0 Journal Article
%T Oral Janus Kinase Inhibitor for the Treatment of Rheumatoid Arthritis: Tofacitinib
%A Han Ni
%A Soe Moe
%A Kay Thi Myint
%A Aung Htet
%J ISRN Rheumatology
%D 2013
%R 10.1155/2013/357904
%X Since the introduction of immune modulators in the treatment of rheumatoid arthritis (RA), there has been hope that orally effective biologic agents would be developed. Tofacitinib, a Janus kinase inhibitor, has become the first oral biologic to receive approval for use in active RA patients. This paper reviews the efficacy and safety profile of Tofacitinib at dosages of 5£¿mg and 10£¿mg twice daily. Remarkable improvement in terms of ACR 20 response and HAQ-DI score was noted at month 3 and month 6. DAS 28-4 ESR < 2.6 achievement was noticeably obvious at month 6 for both dosages. No significant serious adverse events, serious infections, neutropenia, or anaemia were observed compared to placebo. In fact, Tofacitinib 5£¿mg was even found to have significant protective effect of anaemia in the meta-analysis ( ). Tofacitinib has a noticeable efficacy in controlling disease activity in RA with a manageable safety profile. However, longer studies are needed for its long-term safety profile. 1. Introduction Rheumatoid arthritis (RA) is a common immune-mediated systemic disorder, characterized by inflammatory polyarthritis affecting synovium of joints, tendons, and extra-articular sites. It is progressive and leads to joint erosions and deformities, causing premature mortality, functional impairment, and reduced quality of life [1]. The prevalence of RA remains constant at 0.5¨C1.0% among various population group [2, 3]. The prevalence is generally lower in developing countries [4]. In 2005, 1.5 million adults of more than 18 years (0.6%) in the United States were estimated to have RA [5]. HLA DRB1 allele is the major genetic risk factor of RA around the world [2]. Conventionally, RA was treated with ¡°Pyramid¡± approach, where disease modifying antirheumatic drug (DMARD) was deferred until advanced stage. In 1960s and 1970s, gold and penicillamine were the only DMARDs used for RA [6]. However, in 1980s, methotrexate was found to retard or even prevent bone erosions [7]. This has led to dramatic changes in the treatment of RA, with early aggressive use of DMARDs within the first few months of diagnosis, and methotrexate becomes the first line DMARD in RA [6]. In the pathogenesis of rheumatoid arthritis, various inflammatory mediators are found to be involved, among which tumour necrosis factor (TNF) ¦Á is the main agent. New drugs targeting these inflammatory mediators have changed the prognosis and outcome of this chronic debilitating disease. Early initiation of DMARDs, either nonbiologic or biologic, has decreased the morbidity of this condition [8, 9]. Thus,
%U http://www.hindawi.com/journals/isrn.rheumatology/2013/357904/