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Management of Rheumatoid Arthritis: Special Consideration for Biologic Disease-Modifying Antirheumatic Drugs

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Management of Rheumatoid Arthritis: Special Consideration for Biologic Disease-Modifying Antirheumatic Drugs Online - 2455-3891 Vol 11, Issue 11, 2018 Print - 0974-2441 Review Article MANAGEMENT OF RHEUMATOID ARTHRITIS: SPECIAL CONSIDERATION FOR BIOLOGIC DISEASE-MODIFYING ANTIRHEUMATIC DRUGS SALMI ABDUL RAZAK, MOHD MAKMOR-BAKRY, ADYANI MD-REDZUAN* Faculty of Pharmacy, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, 50300 Kuala Lumpur, Federal Territory of Kuala Lumpur. Email: [email protected] Received: 14 June 2018, Revised and Accepted: 13 July 2018 ABSTRACT Rheumatoid arthritis (RA) is a progressive chronic inflammatory disease affecting 0.5–1.0% of the adult population worldwide. Due to the damages caused by this autoimmune disease, new biologic therapies, particularly the biologic disease-modifying antirheumatic drugs (bDMARDs), are now being the treatment of choice in the management of RA. However, special precaution and prescreening before the usage of bDMARDs are needed to ensure better clinical response and avoiding risk of adverse event during treatment with the selected bDMARDs. In this review paper, we will provide overview on the incidence and pathogenesis of the disease, available pharmacological treatment and emphasizing special consideration in need on initiation of bDMARDs among RA patients. A literature review was performed by searching for relevant articles in Medline database through PubMed using medical subject headings terms and keywords: RA, bDMARDs, special consideration, tumor necrosis factor inhibitor, and non-tumor necrosis factor inhibitor. All papers reviewed were from 1999 to 2017 and were written in English. In this article, use of conventional synthetic DMARDs (csDMARDs), bDMARDs and special consideration to be taken upon initiation of biologic therapies in RA will be reviewed. Keywords: Biologic therapy, Non-tumor necrosis factor inhibitors, Precaution, Prescreening, Rheumatoid arthritis, Tumor necrosis factor inhibitor. © 2018 The Authors. Published by Innovare Academic Sciences Pvt Ltd. This is an open access article under the CC BY license (http://creativecommons. org/licenses/by/4. 0/) DOI: http://dx.doi.org/10.22159/ajpcr.2018.v11i11.27953 INTRODUCTION OVERVIEW ON INCIDENCE OF RA Rheumatoid arthritis (RA) is a progressive chronic inflammatory RA is a chronic autoimmune disease causing permanent disability that disease with which, if left untreated, 20–30% of patients would reduces patients’ quality of life overtime of the disease progression. RA become permanently work disabled within 3 years of diagnosis. It is is known to affect 0.5–1.0% of the adult population worldwide [1]. RA known to affect 0.5–1.0% of the adult population worldwide, and the is more prevalent in females than males with female-to-male ratio of overall prevalence of the disease for the adult population of Asia is 3:1 and with increasing age [8]. Studies have shown that the incidence reported between 0.2 and 0.3% [1-3]. This inflammatory autoimmune of RA remained stable or increased over time, and the prevalence of disease is chronic progressive symmetrical polyarticular joint disease, RA is high in the general population [9]. Known as a multifactorial characterized by progressive destructions of the articular cartilage, heterogeneous disease, RA has different incidence rate and prevalence bone, and non-articular muscular structures that can cause joint across different populations and geographical area [2,3]. Studies on deformities. After a mean follow-up of 3.9 years, 47.5% of RA patients prevalence and incidence rates of RA in population of Asia consisting experienced at least one extra-articular or systemic manifestation. New countries from Japan, China, Taiwan, Indonesia, and Philippine reported treatment modalities by the initiation of targeted biologic therapies are a prevalence of the disease between 0.2 and 0.3% [2]. It was observed recommended to for disease control, damage prevention, persevering that the prevalence of RA varies widely from population to population affected joint function, increase in patients’ quality of life, and increase with the highest rate found among Pima Indians (5.3%) and Chippewa the possibilities to achieve complete remission of the disease [4]. The Indians (6.8%) and lowest rate in Asian countries. Prevalence among biologic disease-modifying antirheumatic drugs (bDMARDs) or known population from China and Japan is 0.2–0.3% [10]. The regional as the monoclonal antibody (mAb) therapies, which target directly to the variation of RA prevalence may suggest role of genetic factor underlying specific cytokines cells and molecules of the disease pathophysiology, susceptibility to the disease. In Malaysia, according to the Arthritis can be initiated either alone as monotherapy or as combination therapy Foundation Malaysia 2007, RA affects 5 in 1000 Malaysians. The with the conventional synthetic DMARDs (csDMARDs) therapy within Rochester Epidemiology Project provides the most recent US data on the first 3 months of early RA diagnosis [5-7]. This review will provide the incidence of RA. It is observed that in a period of time from 1995 to an overview of the RA disease, the use of new mAb therapies in addition 2007, it was estimated 1.5 million of the United States (US) adults age to the csDMARDs used in the management of RA, as well as suggestive more than 18 years old had RA and the RA incidence increased among prescreening test based on disease history or concurrent condition on women compared to men [8]. Published data showed that prevalence selection of biologic treatment initiation in RA patient. rate of RA is generally 2–3 times higher in female than male, and the prevalence increases with increasing age up to about eighth decade of METHODOLOGY life and peaks at around age of sixties. The incidence peaked earlier for women than men at about ages 55–64 years for women, compared with Relevant articles were searched in Medline database through PubMed 75–84 years for men [11,12]. using medical subject headings terms and keywords: RA, bDMARDs, special consideration, tumor necrosis factor inhibitor, and non-tumor Pathogenesis and extra-articular manifestation of RA necrosis factor inhibitor. All papers reviewed were written in English, Basically, the first affected joint structure in RA is the synovium. from 1999 to 2017. The articles focused on descriptive information on Synovium is the synovial membrane lines within the joint capsule RA disease, treatment used in the management of RA including biologic and produces the synovial fluid. The inner layer of the synovial mAb and prescreening on biologic treatment initiation. membrane consists of two synoviocytes which are the macrophage-like Razak et al. Asian J Pharm Clin Res, Vol 11, Iss1e 11, 2018, 47-53 synoviocytes and fibroblast-like synoviocytes, and both are capable or all conditions and symptoms which are not directly related to the of expressing cytokines and degenerative enzymes. In the case of locomotor system [13,15]. A retrospective analysis done by Hochberg joint inflammation, the inflammatory arthritis leukocytes migrate et al. on the incidence and prevalence of extra-articular and systemic from the blood vessels into the synovial lining and trigger release of manifestations in a cohort of newly diagnosed patients with RA in inflammatory mediators and enzymes by cellular interactions. This the US, 47.5% of 16,752 patients with RA experienced at least one synovial immunologic process and inflammation will lead to synovitis, extra-articular or systemic manifestation with a mean follow-up of irreversible damage to the cartilage and bone and contributes to 3.9 years diagnosis [16]. Extra-articular manifestations identified were systemic consequences of the disease [1,13]. rheumatoid nodules, vasculitis, pericarditis, keratoconjunctivitis sicca, uveitis, Felty’s syndrome, scleritis, pericarditis, and rheumatoid lung It is suggestive that the development of RA is related to trauma, disease [17]. Whereas, for systemic manifestations identified include degeneration, abnormalities in biochemical pathways, autoimmunity, non-specific features such as asthenia, fatigue, muscle weakness, inflammation, and genetic polymorphisms. Environmental factors fever, anorexia, anemia, osteoporosis, weight loss, acute-phase protein were found to trigger the disease, as well as social factors [13]. The production, cardiovascular disease (CVD), and depression [18]. interaction of genetics and environmental factors such as cigarette smoking, infection, or trauma can cause a breakdown of immune Epidemiologic studies of comorbidities and extra-articular manifestations tolerance and synovial inflammation in a characteristic symmetric in RA patients have emphasized that both were associations and pattern [10]. The T-cells, B-cells, and coordinated interaction of pro- predictors to increased morbidity and premature mortality in RA inflammatory cytokines play important roles in the pathophysiology of patients [19-21]. A cross-sectional, international, and multicenter RA. CD4 T-cells are activated to secrete interleukin (IL)-2 and interferon study, COMORA (Comorbidities in RA) of 3920 RA patients recruited from 17 countries on five different continents, revealed high prevalence synovial membrane. These cells later activate synovial macrophages associated comorbidities were psychiatric disorder, mainly depression, andgamma fibroblasts (tumor andnecrosis hence factorlose responsiveness [TNF]-γ) for toinfiltration T-cell activities into the in gastrointestinal diseases, pulmonary diseases, especially chronic the course of RA. The B-cells may serve as
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