A1298C Polymorphism 185 Abnormal Color Vision 87 Acetylcysteine 12

Total Page:16

File Type:pdf, Size:1020Kb

A1298C Polymorphism 185 Abnormal Color Vision 87 Acetylcysteine 12 Index A1298C polymorphism 185 aura nofin (AF) 9, 38, 302 abnormal color vision 87 aurocyanide 8, 9 acetylcysteine 12 aurosome 134 ACR20 28, 204 auroth ioglucose 136 ACR20 responder rate 204 aurothi omalate 7- 9 ACR50 28 autoimmune disease 210 ACR70 28 autoimmun e disorders, with anti TNF-a ACR response criteria 179 therapy 272 activator protein 1 (AP-l) 70-72, 75 AV block 86 adalimumab 265 azathioprine 4, 5, 163-1 70, 294 adenosine 177, 178 azathiop rine, and allopurinol 4 adhesion molecule 135 azathioprine, and hypoxanthin e guanine adjuvant arthritis 134 phosphoribosyl transferase 4 adverse reactions, due to sulfasalazine 15 azathiop rine, and 6-mercaptopurine 4, 5 agranulocytosis 150 azathioprine, and thiopurin e methyl­ alcohol intake 192 transferase 4 allopurinol 4 azathiopr ine, and xanthine oxidase 4 alopecia 210 azathioprine, comparison with other aminosalicylate 15, 16 DMARDs 166 amodiaquine 2 azathioprine, metabolism 4, 5 anakinra 279-289 azathioprine, structur e 5 angiogenesis 135 antibody deficiency 134 betamethasone 19 antigen processing 134 bioavailability 83, 175,202,222 antigenicity, anti TNF-a therap y 271 bioavailability, oral or parente ral 175 anti-inflammatory actions of leflunomide 202 biologic agents 69 anti-TNF-a therapy 265-267,270-274 bisdesthylchloroquine 83 AP-l 70- 72,75 bucillamine 12, 13 aplastic anemia 150 apoptosis 178 C677T polymorphism 185 ASPIRE 306 calcineurin 7, 222 337 Index captopril 13 cortisone 19 cardiomyopathy 86 cost of illness (COl) 57 CDI4+ monocyte 134 cost-effectiveness 50,60, 192 chloroquine 1-4, 81, 82,293 cost-effectiveness analysis 50,51,57, 60 chloroquine, and amodiaquine 2 cost-effectiveness ratio 50 chloroquine, and lysosomes 3 cough 191 chloroquine, and mepacrine 1 CTLM-Ig 309 chloroquine, and quinacrine 3 cyclophosphamid e 294 chloroquine, chiral centre 3 cyclosporin 6,7,186,221-231,301,307,310 chloroquine, enantiomers 3, 4 cyclosporin, absorption 6 chloroquine, half life 3 cyclosporin, and calcineurin 7 chloroquine, ionisation 2, 3 cyclosporin, and cyclophilin A 7 chloroquine, lipid solubility cyclosporin, and cytochrome p450 7 chloroquine, log D 2, 3 cyclosporin, and methotrexate 186 chloroquine, log P 3 cyclosporin, structure 6 chloroquine, passive diffusion 2 cyclosporin A (CsA) 77,221,303 chloroquine, tissue binding 3 cyclosporin A, absorption of 222 chloroquine, volume of distribution 3 cyclosporin A, adverse effects of 228, 229 cholesterol 211 cyclosporin A, bioavailability of 222 cholestyramine 203 cyclosporin A, combination therapy with 225, chronic renal impairment 176 230 chrysiasis 150 cyclosporin A, distribution of 223 chrysotherapy 136 cyclosporin A, drug interactions with 223, 224 cirrhosis 190 cyclosporin A, efficacy of 224 clinical efficacy 137, 203 cyclosporin A, hypertension and 228 clinical improvement, with methotrexate 179 cyclosporin A, infection and 229 clinical pharmacology, anti TNF-a therapy 266 cyclosporin A, international guidelines for the clinical practice guidelines 38 use of 224, 230 COBRA 300 cyclosporin A, malignancy and 229 collagen-induced arthritis 134,310 cyclosporin A, monitoring of 230 color vision, abnormal 87 cyclosporin A, monotherapy of 225, 226, 230 combination of infliximab and leflunomide 209 cyclosporin A, nephrotoxicity 224 combination of leflunomide and methotrexate cyclosporin A, renal disfunction with 228 208 cyclosporin A, toxicity of 227,228 combination therapy 168, 186-188,208,209, cytochrome P450 7,223 225,230 cytokine production 133, 134 computer-based decision-support sytem 39 conception, methotrexate 191 DAS28 55 congestive heart failure (CHF), with anti TNF-a decision analysis 49 therapy 273 decision-making 26,36,37,49 corneal deposits 87 demyelinating syndrome, with anti TNF-a corticosteroids 18-21 therapy 273 338 Index depression, mood disorder due to sulfasalazine folate supplementation 189 120 folic acid 10,11, 177, 190 dermatitis 149 functional capacity/disability 142 dermatological adverse events 89 functional disability 142,153 desethylchloroquine 83 desethylhydroxychloroquine 83 gastrointestinal adverse events, leflunomide 210 dexamethasone 19 gastrointestinal hyper sensitivity reaction 169 dihydrofolate reductase (DHFR) 175, 177 gastrointestinal side effect, hydroxychloroquine dihydroorotate dehydrogenase 200 85,86 disability 142,153,179,183,184 gastrointestinal toxicity 189 disease models, RA 51 gingival hyperplasia 229 dizziness 86 gold 7-10,133-155,293,304 drug interaction 83 gold, absorption 7, 9 duration of treatment, gold 155 gold, and auranofin 9 gold, and aurocyanide 8, 9 early RA 298 gold, and aurothiomalate 7-9 efficacy 30,84,98,100,101,122,267 gold, and lactoperoxidase 8, 9 efficacy study 30 gold, and myeloperoxidase 8, 9 efficacy, anti-TNF-a therapy 267 gold, aurosomes 8 efficacy, of sulfasalazine 98, 100, 101, 122 gold, mechanism of action 133 elimination, methotrexate 176 gold, metabolism 8, 9 elimination half-life, hydroxychloroquine 83 gold, pharmacology 136 end stage renal failure 203 gold, sodium aurothiomalate 7-9, 134 enterocolitis 151 gold, stereochemistry 7 enterohepatic circulation 176 gold, structure 8, 9 enterohepatic recirculation 202 gold complexes 7-10 eosinophilia 150 gold distribution 136 erosion and joint space narrowing 182 gold dosing 154 c-selccrin 74, 77 gold nephropathy 150 established RA 302 gold treatment, combination with methotrexate established active RA 212 145 etanercept 265, 305-307, 309 gold treatment, history 133 evidence based medicine (EBM) 26, 152 gold treatment, lactation 151 exfoliative dermatitis 149 gold treatment, liver toxicity 151 extracellular signal regulated kinase (ERK) gold treatment, pregnancy 151 70-73 Golgi complex 82 graft rejection 210 Felty's syndrome 210 GSTM (gold sodium thiomalate) 134 fertility, influence of sulfasalazine 121 fibroblast 135 hair bleaching 89 FIN-RACo 300 hair loss 89, 150 fludrocortisone 21 headache 86 339 Index Health Assessment Questionnaire (HAQ) 55, interactions, pharmacological of sulfasalazine 142, 183 97 health-related quality of life 205 interleukin converting enzyme (ICE) 78 hematuria 150 interstitial lung injury 191 hepatotoxicity 187,211 intra-articular methotrexate 176 HLA region 35 intra-articular steroid 301 humoral immunity 134 intracellular folate 177 hydroxychloroquine (HQ) 1-4, 81-89, 187, intracellular signaling molecules 70 295,300 intracellular signaling pathways 69 hydroxychloroquine, and amodiaquine 2 intrahepatic cholestasis 151 hydroxychloroquine, and Iysosomes 3 hydroxychloroquine, and mepacrine 1 Janus kinase (JAK) 77 hydroxychloroquine, and methotrexate 187 joint space narrowing 182 hydroxychloroquine, and quinacrine 3 Jun N-terminal kinase (JNK) 70-73, 75 hydroxychloroquine, chiral centre 3 hydroxychloroquine, dose 87 knockout mouse, ICE 78 hydroxychloroquine, enantiomers 3, 4 hydroxychloroquine, ionisation 2, 3 lab monitoring 89 hydroxychloroquine, lipid solubility 1 lactoperoxidase 8, 9 hydroxychloroquine, log D 2, 3 leflunomide 10,187,199-213,304,307 hydroxychloroquine, log P 3 leflunomide, half life 10, 203 hydroxychloroquine, passive diffusion 2 leflunomide, metabolism 10 hydroxychloroquine, structure 2 leucopenia 119, 150 hypertension 210,228 leucopenia, due to sulfasalazine treatment 119 hypertrichosis 229 liposome encapsulated GSTM 134 hypoxanthine guanine phosphoribosyl liver biopsy 190 transferase 4 liver necrosis 151 long-term efficacy, leflunomide 204 ICE knockout mouse 78 long-term observational study, gold 140 IgM 134 long-term outcome, treatment with sulfasalazine IKK 76 104 Il-1~ 82 Lyell's syndrome 149 immunoglobulin 134 lymphocyte 134 infection 169,210,229,271 lysosome 3, 134 infection , in anti TNF-a therapy 271 infliximab 209,265,306,307 macrophage 134 infusion reactions/injection site reactions, malformations in pregnancy, hydroxy­ anti TNF-a therapy 270 chloroquine 87 inhibition of progression, TNF blockers malignancy, in anti TNF-a therapy 272 153 MAPK activated protein kinase (MAPKAP K) inhibitor of nuclear factor KB inducing kinase 72, 73 (IKB) 75,76 MAPK kinase kinase (MAPKKK) 72 340 Index marrow suppression, azathioprine 168 NF-AT 71 matrix metalloproteinase (MMP) 135,237 NF-KB 71-76,133,134 mechanims of action, anti-TNF-a therap y 265 NF-KB dimer 75 mechanism of action, of sulfasalazine 93 NF-KB inducing kinase (NIK) 75 membranous glomerulonephritis 150 NF-KB inhibitors 76 mepacrine 1 nitritoid reactions 151 mercaptopurine 4, 5 non-steroidal anti-inflammatory drugs (NSAIDs) mesalazine 15, 16 177 methotrexate (MTX) 10, 11, 83, 139, 145, nuclear factor of activated T cells (NFAT) 76, 175-192,208,300-304,307 77 methotrexate, and folic acid 10, 11 number needed to harm (NNH) 29 methotrexate, and cyclosporin 186 number needed to treat (NNT) 29,32 methotrexate, and hydroxychloroquine 187 methotrexate, and leflunomide 187 olsalazine 15 methotrexate, cellular effects 177 oral bioavailability, methotrexate 179 methotrexate, dosage 179 oral folic acid 190 methotrexate, log P 10 osteoclast differentiation 75 methotrexate, polyglutamation 10 oxygen radicals 135 methotrexate induced nodulosis 190 methylprednisolone 20 p38 MAPK 70, 71, 75 methylprednisolone acetate 20 p38 MAPK family 72-75 methylprednisolone sodium succcinate 20 p38 MAPK inhibitor 73-75 metoprolol 83 pancytopenia 150, 273 minocycline 16-18,239 pancytopenia, with anti TNF-a therapy 273 minocycline, half life 18 patient preferences 36, 37 minocycline, ionisation 17-18 penicillamine 11-15 minocycline, log P 18 d-penicillamine 295 minocycline, structure 17 penicillamine pKa 11 minocycline, volume of
Recommended publications
  • Modifying Antirheumatic Drugs in Active Rheumatoid Arthritis: a Japan Phase 3 Trial (HARUKA)
    MODERN RHEUMATOLOGY 2020, VOL. 30, NO. 2, 239–248 https://doi.org/10.1080/14397595.2019.1639939 ORIGINAL ARTICLE Sarilumab monotherapy or in combination with non-methotrexate disease- modifying antirheumatic drugs in active rheumatoid arthritis: A Japan phase 3 trial (HARUKA) Hideto Kamedaa, Kazuteru Wadab, Yoshinori Takahashib, Owen Haginoc, Hubert van Hoogstratend, Neil Grahame and Yoshiya Tanakaf aDivision of Rheumatology, Department of Internal Medicine, Faculty of Medicine, Toho University (Ohashi Medical Center), Tokyo, Japan; bSanofi K.K., Tokyo, Japan; cSanofi, Bridgewater, NJ, USA; dSanofi-Genzyme, Cambridge, MA, USA; eRegeneron Pharmaceuticals, Inc., Tarrytown, NY, USA; fFirst Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Downloaded from https://academic.oup.com/mr/article/30/2/239/6299750 by guest on 01 October 2021 Japan, Kitakyushu, Japan ABSTRACT ARTICLE HISTORY Objectives: To determine long-term safety and efficacy of sarilumab as monotherapy or with non- Received 13 March 2019 methotrexate (MTX) conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) in Accepted 1 July 2019 Japanese patients with active rheumatoid arthritis (RA). KEYWORDS Methods: In this double-blind, randomized study (NCT02373202), patients received subcutaneous sari- Rheumatoid arthritis; lumab 150 mg q2w (S150) or 200 mg q2w (S200) as monotherapy or with non-MTX csDMARDs for 52 sarilumab; Japan; phase III; weeks. The primary endpoint was safety. anti-IL-6 receptor Results: Sixty-one patients received monotherapy (S150, n ¼ 30; S200, n ¼ 31) and 30 received combin- ation therapy (S150 þ csDMARDs, n ¼ 15; S200 þ csDMARDs, n ¼ 15). Rates of treatment-emergent adverse events (TEAEs) were 83.3%/90.3%/93.3%/86.7% for S150/S200/S150 þ csDMARDs/ S200 þ csDMARDs, respectively.
    [Show full text]
  • Study Protocol);
    PF-06651600 B7981006 Final Protocol Amendment 1, 26 October 2016 A PHASE 2A, RANDOMIZED, DOUBLE-BLIND, PARALLEL GROUP, PLACEBO-CONTROLLED, MULTI-CENTER STUDY TO ASSESS THE EFFICACY AND SAFETY PROFILE OF PF-06651600 IN SUBJECTS WITH MODERATE TO SEVERE ACTIVE RHEUMATOID ARTHRITIS WITH AN INADEQUATE RESPONSE TO METHOTREXATE Investigational Product Number: PF-06651600 Investigational Product Name: Not Applicable (N/A) United States (US) Investigational New 131274 Drug (IND) Number: European Clinical Trials Database 2016-002862-30 (EudraCT) Number: Protocol Number: B7981006 Phase: 2a Page 1 PF-06651600 B7981006 Final Protocol Amendment 1, 26 October 2016 Document History Document Version Date Summary of Changes and Rationale Amendment 1 26 October 2016 In the Schedule of Activities, and Section 7.2.12, added audiogram testing Rationale: To monitor for potential changes in hearing between baseline [between Visit 1 and Visit 2 (inclusive)] and at the end of the study [between Visit 7 and Visit 9 (inclusive)]. The following exclusion criteria has been added in Section 4.2: Have current or recent history of clinically significant severe or progressive hearing loss or auditory disease. Subjects with hearing aids will be allowed to enter the study provided their hearing impairment is considered controlled/ clinically stable. Rationale: This has been added to ensure that subject hearing for safety is fully evaluated prior to study entry. Several additional minor changes were made to protocol language for the purposes of clarification. Original protocol 31 August 2016 Not applicable (N/A) This amendment incorporates all revisions to date, including amendments made at the request of country health authorities and institutional review boards (IRBs)/ethics committees (ECs).
    [Show full text]
  • Classification of Medicinal Drugs and Driving: Co-Ordination and Synthesis Report
    Project No. TREN-05-FP6TR-S07.61320-518404-DRUID DRUID Driving under the Influence of Drugs, Alcohol and Medicines Integrated Project 1.6. Sustainable Development, Global Change and Ecosystem 1.6.2: Sustainable Surface Transport 6th Framework Programme Deliverable 4.4.1 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Due date of deliverable: 21.07.2011 Actual submission date: 21.07.2011 Revision date: 21.07.2011 Start date of project: 15.10.2006 Duration: 48 months Organisation name of lead contractor for this deliverable: UVA Revision 0.0 Project co-funded by the European Commission within the Sixth Framework Programme (2002-2006) Dissemination Level PU Public PP Restricted to other programme participants (including the Commission x Services) RE Restricted to a group specified by the consortium (including the Commission Services) CO Confidential, only for members of the consortium (including the Commission Services) DRUID 6th Framework Programme Deliverable D.4.4.1 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Page 1 of 243 Classification of medicinal drugs and driving: Co-ordination and synthesis report. Authors Trinidad Gómez-Talegón, Inmaculada Fierro, M. Carmen Del Río, F. Javier Álvarez (UVa, University of Valladolid, Spain) Partners - Silvia Ravera, Susana Monteiro, Han de Gier (RUGPha, University of Groningen, the Netherlands) - Gertrude Van der Linden, Sara-Ann Legrand, Kristof Pil, Alain Verstraete (UGent, Ghent University, Belgium) - Michel Mallaret, Charles Mercier-Guyon, Isabelle Mercier-Guyon (UGren, University of Grenoble, Centre Regional de Pharmacovigilance, France) - Katerina Touliou (CERT-HIT, Centre for Research and Technology Hellas, Greece) - Michael Hei βing (BASt, Bundesanstalt für Straßenwesen, Germany).
    [Show full text]
  • 24/3 Pag 121 Ok X WENDY
    Treatment continuation rate in relation to efficacy and toxicity in long-term therapy with low-dose methotrexate, sulfasalazine, and bucillamine in 1358 Japanese patients with rheumatoid arthritis M. Nagashima, T. Matsuoka, K. Saitoh, T. Koyama, O. Kikuchi, S. Yoshino Department of Joint Disease and Rheumatism, Nippon Medical School, Japan. Abstract Objective To evaluate the effectiveness of disease-modifying antirheumatic drugs, namely, methotrexate (MTX), sulfasalazine (SSZ) and bucillamine (BUC) at low-doses (4, 6 or 8mg MTX, 500 or1000mg SSZ, and 100 or 200 mg BUC) in 1358 patients with a follow-up of at least 12 months and more than 120 months. Methods Clinical assessments were based on the number of painful joints (NPJ) and that of swollen joints (NSJ), CRP level, erythrocyte sedimentation rate, rheumatoid factor level and morning stiffness before and after treatment. Results were evaluated on the basis of the duration of treatment for each drug with inefficacy or inadequate efficacy as one endpoint for discontinuation and adverse drug reactions (ADRs) as the other in single agent and combination ther- apy. The incidence and nature of ADRs in single and combination treatment are described. Results The effects of MTX, SSZ and BUC on clinical parameters were monitored over the first three months, and in partic- ular, NPJs and NSJs were found to decrease significantly during single agent MTX or BUC treatment over 108 months. CRP levels remained significantly improved for more than 120 months with MTX. In the single and combi- nation long-term treatments, continuation rate with inefficacy or inadequate efficacy as the end point achieved for each of the treatments were 83.1% for MTX, 76.0% for BUC, 68.5% for SSZ, and in the case of the combination treatments, these rates were 83.3% for MTX + BUC and 71.0% for MTX+SSZ.
    [Show full text]
  • Ehealth DSI [Ehdsi V2.2.2-OR] Ehealth DSI – Master Value Set
    MTC eHealth DSI [eHDSI v2.2.2-OR] eHealth DSI – Master Value Set Catalogue Responsible : eHDSI Solution Provider PublishDate : Wed Nov 08 16:16:10 CET 2017 © eHealth DSI eHDSI Solution Provider v2.2.2-OR Wed Nov 08 16:16:10 CET 2017 Page 1 of 490 MTC Table of Contents epSOSActiveIngredient 4 epSOSAdministrativeGender 148 epSOSAdverseEventType 149 epSOSAllergenNoDrugs 150 epSOSBloodGroup 155 epSOSBloodPressure 156 epSOSCodeNoMedication 157 epSOSCodeProb 158 epSOSConfidentiality 159 epSOSCountry 160 epSOSDisplayLabel 167 epSOSDocumentCode 170 epSOSDoseForm 171 epSOSHealthcareProfessionalRoles 184 epSOSIllnessesandDisorders 186 epSOSLanguage 448 epSOSMedicalDevices 458 epSOSNullFavor 461 epSOSPackage 462 © eHealth DSI eHDSI Solution Provider v2.2.2-OR Wed Nov 08 16:16:10 CET 2017 Page 2 of 490 MTC epSOSPersonalRelationship 464 epSOSPregnancyInformation 466 epSOSProcedures 467 epSOSReactionAllergy 470 epSOSResolutionOutcome 472 epSOSRoleClass 473 epSOSRouteofAdministration 474 epSOSSections 477 epSOSSeverity 478 epSOSSocialHistory 479 epSOSStatusCode 480 epSOSSubstitutionCode 481 epSOSTelecomAddress 482 epSOSTimingEvent 483 epSOSUnits 484 epSOSUnknownInformation 487 epSOSVaccine 488 © eHealth DSI eHDSI Solution Provider v2.2.2-OR Wed Nov 08 16:16:10 CET 2017 Page 3 of 490 MTC epSOSActiveIngredient epSOSActiveIngredient Value Set ID 1.3.6.1.4.1.12559.11.10.1.3.1.42.24 TRANSLATIONS Code System ID Code System Version Concept Code Description (FSN) 2.16.840.1.113883.6.73 2017-01 A ALIMENTARY TRACT AND METABOLISM 2.16.840.1.113883.6.73 2017-01
    [Show full text]
  • Efficacy and Toxicity of Methotrexate (MTX)
    Extended report Ann Rheum Dis: first published as 10.1136/ard.2008.099861 on 3 December 2008. Downloaded from Efficacy and toxicity of methotrexate (MTX) monotherapy versus MTX combination therapy with non-biological disease-modifying antirheumatic drugs in rheumatoid arthritis: a systematic review and meta-analysis W Katchamart,1,2 J Trudeau,3 V Phumethum,1 C Bombardier4,5 c Additional figures and ABSTRACT combination DMARD therapy be used: initially or appendixes are published online Objective: To evaluate the efficacy and toxicity of only after a trial of MTX monotherapy? Finally, only at http://ard.bmj.com/ which is the preferred combination DMARD content/vol68/issue7 methotrexate (MTX) monotherapy compared with MTX combination with non-biological disease-modifying anti- strategy? These questions are particularly salient 1 Rheumatology Division, rheumatic drugs (DMARDs) in adults with rheumatoid as formularies in many countries require the use of Department of Medicine, University of Toronto, Toronto, arthritis. MTX mono and MTX combo therapies before Ontario, Canada; Method: A systematic review of randomised trials reimbursing for the more expensive biological 2 Rheumatology Division, comparing MTX alone and in combination with other non- drugs. The objective of this paper was to system- Department of Medicine, Siriraj biological DMARDs was carried out. Trials were identified atically review randomised trials that compared Hospital, Mahidol University, MTX monotherapy with MTX in combination Bangkok, Thailand; 3 Hoˆspital in Medline, EMBASE, the Cochrane Library and ACR/ Notre-Dame, Department of EULAR meeting abstracts. Primary outcomes were with other non-biological DMARDs. This manu- Rheumatology, Montreal, withdrawals for adverse events or lack of efficacy.
    [Show full text]
  • Alphabetical Listing of ATC Drugs & Codes
    Alphabetical Listing of ATC drugs & codes. Introduction This file is an alphabetical listing of ATC codes as supplied to us in November 1999. It is supplied free as a service to those who care about good medicine use by mSupply support. To get an overview of the ATC system, use the “ATC categories.pdf” document also alvailable from www.msupply.org.nz Thanks to the WHO collaborating centre for Drug Statistics & Methodology, Norway, for supplying the raw data. I have intentionally supplied these files as PDFs so that they are not quite so easily manipulated and redistributed. I am told there is no copyright on the files, but it still seems polite to ask before using other people’s work, so please contact <[email protected]> for permission before asking us for text files. mSupply support also distributes mSupply software for inventory control, which has an inbuilt system for reporting on medicine usage using the ATC system You can download a full working version from www.msupply.org.nz Craig Drown, mSupply Support <[email protected]> April 2000 A (2-benzhydryloxyethyl)diethyl-methylammonium iodide A03AB16 0.3 g O 2-(4-chlorphenoxy)-ethanol D01AE06 4-dimethylaminophenol V03AB27 Abciximab B01AC13 25 mg P Absorbable gelatin sponge B02BC01 Acadesine C01EB13 Acamprosate V03AA03 2 g O Acarbose A10BF01 0.3 g O Acebutolol C07AB04 0.4 g O,P Acebutolol and thiazides C07BB04 Aceclidine S01EB08 Aceclidine, combinations S01EB58 Aceclofenac M01AB16 0.2 g O Acefylline piperazine R03DA09 Acemetacin M01AB11 Acenocoumarol B01AA07 5 mg O Acepromazine N05AA04
    [Show full text]
  • Small Molecule DMARD Therapy and Its Position in RA Treatment
    Chapter 8 Small Molecule DMARD Therapy and Its Position in RA Treatment Hiroaki Matsuno Additional information is available at the end of the chapter http://dx.doi.org/10.5772/53320 1. Introduction Small molecule disease-modifying antirheumatic drugs (DMARDs) played a central role in drug therapy for rheumatoid arthritis (RA) before biological preparations (biologics) came into extensive use for the treatment of this disease. Unlike non-steroidal anti-inflammatory drugs (NSAIDs) and steroids, which primarily alleviate the symptoms of RA such as pain and inflammation, DMARDs are known to suppress the progression of RA through their ac‐ tion against immunological abnormalities. To review the history of the clinical positioning of DMARD therapy, until the beginning of the 1990s, DMARDs were used only in patients showing signs of disease progression (e.g., bone erosion) after NSAIDs or steroid treatment within the framework of pyramid therapy [1]. During the 1990s through the 2000s, the strategy and goals of RA therapy have under‐ gone marked changes following the introduction of methotrexate (MTX) as another treat‐ ment option, the expansion of MTX as an anchor drug [2,3,4], endorsement of the usefulness of combined drug therapy involving DMARDs [5], the introduction of biologics into RA treatment [6,7,8], and other advances. In 2002, the American College of Rheumatology (ACR) released its Guidelines on RA Management, clearly indicating DMARDs as first-line drugs for the treatment of RA. As a result, NSAIDs and steroids came to be positioned as auxiliary means of treating RA [9]. The small molecule DMARDs that have been used frequently in Western countries are MTX, sulphasalazine (SASP), hydroxychloroquine (HCQ), leflunomide (LFN), and minocycline (MIN).
    [Show full text]
  • Mechanisms of Action of Second-Line Agents and Choice of Drugs in Combination Therapy
    Mechanisms of action of second-line agents and choice of drugs in combination therapy E. Choy, G. Panayi Department of Rheumatology, Division ABSTRACT stimulation of IL-2 receptor (IL-2R) of Medicine, GKT School of Medicine, Second-line agents are used commonly positive lymphocytes and monocytes. King’s College, London. for the treatment of rheumatoid arthritis The latter release monokines, including Dr. Ernest Choy, MD, MRCP, Consultant (RA). They suppress inflammation and IL-1, IL-6, and tumour necrosis factor a and Senior Lecturer in Rheumatology; ameliorate symptoms but often fail to (TNFa ) that stimulate mesenchymal Professor Gabriel Panayi, MD, DSc, substantially improve long-term disease cells such as fibroblasts, as well as en- FRCP, Arthritis Research Campaign outcome. Their use in RA was discov- dothelial cells. Activated fibroblasts, mo- Professor of Rheumatology. ered serendipitously and their modes of nocytes, and macrophages release ma- Please address correspondence and action were largely unknown. Recent re- trix metalloproteinases, such as collagen- reprint requests to: Dr. E. Choy, searches have identified some of their ases and stromelysin, that degrade con- Department of Rheumatology, GKT mechanisms of action. Most of them have nective tissues and result in tissue dam- School of Medicine, King’s College antiinflammatory properties and some age. Stimulated endothelial cells up-re- Hospital (Dulwich), East Dulwich are immunomodulators. Traditionally, gulate surface vascular adhesion mole- Grove, London SE22 8PT, U.K. second-line agents are used as mono- cule expression. These include selectins Clin Exp Rheumatol 1999; 17 (Suppl. 18): therapy, but recent evidence suggests and integrins such as intercellular adhe- S20 - S28.
    [Show full text]
  • Assessment Report
    26 January 2017 EMA/CHMP/853224/2016 Committee for Medicinal Products for Human Use (CHMP) Assessment report Xeljanz International non-proprietary name: tofacitinib Procedure No. EMEA/H/C/004214/0000 Note Assessment report as adopted by the CHMP with all information of a commercially confidential nature deleted. 30 Churchill Place ● Canary Wharf ● London E14 5EU ● United Kingdom Telephone +44 (0)20 3660 6000 Facsimile +44 (0)20 3660 5520 Send a question via our website www.ema.europa.eu/contact An agency of the European Union Table of contents 1. Background information on the procedure .............................................. 9 1.1. Submission of the dossier ..................................................................................... 9 1.2. Steps taken for the assessment of the product ...................................................... 10 2. Scientific discussion .............................................................................. 11 2.1. Problem statement ............................................................................................. 11 2.2. Quality aspects .................................................................................................. 16 2.3. Non-clinical aspects ............................................................................................ 24 2.4. Clinical aspects .................................................................................................. 36 2.5. Clinical efficacy .................................................................................................
    [Show full text]
  • Serum Matrix Metalloproteinase-3 As Predictor of Joint Destruction in Rheumatoid Arthritis, Treated with Non-Biological Disease Modifying Anti-Rheumatic Drugs
    Kobe J. Med. Sci., Vol. 56, No. 3, pp. E98-E107, 2010 Serum Matrix Metalloproteinase-3 as Predictor of Joint Destruction in Rheumatoid Arthritis, Treated with Non-biological Disease Modifying Anti-Rheumatic Drugs AKIRA MAMEHARA1,2, TAKESHI SUGIMOTO1, DAISUKE SUGIYAMA1, SAHOKO MORINOBU1, GOH TSUJI1, SEIJI KAWANO1, AKIO MORINOBU1, and SHUNICHI KUMAGAI1,* 1 Department of Clinical Pathology and Immunology, Kobe University Graduate School of Medicine, Kobe, Japan; 2 Department of Medicine, Kasai Civic Hospital, Hyogo, Japan; Received 20 January 2010/ Accepted 22 January 2010 Key Words: Matrix metalloproteinase-3; Rheumatoid arthritis; Radiographic progression; Disease modifying anti-rheumatic drugs, Background: Rheumatoid factor (RF), anti-citrullinated peptide antibody (ACPA), C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) have been studied extensively as prognostic markers of rheumatoid arthritis (RA). However, despite the fact that matrix metalloproteinase-3 (MMP-3) is linked to RA activity, few studies have evaluated MMP-3 as prognostic marker. Objective: To evaluate the performance of MMP-3 as predictor of joint destruction in RA treated with non-biological disease modifying anti-rheumatic drugs. Methods: In a retrospective study of 58 early to moderate stage RA patients who consulted the Department of Clinical Pathology and Immunology, Kobe University Hospital between May 2002 and April 2009, we evaluated the performance of MMP-3 and other biomarkers as predictors of joint destruction, by comparing them between radiographically progressive and non-progressive group. Results: Serum levels of RF at entry and ACPA, but not MMP-3 at entry, were significantly higher for the progressive group. Ratios of patients with MMP-3 levels higher than healthy control were not significantly different for the two groups.
    [Show full text]
  • WO 2012/175518 Al 27 December 2012 (27.12.2012) P O P C T
    (12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2012/175518 Al 27 December 2012 (27.12.2012) P O P C T (51) International Patent Classification: (72) Inventor; and A61K 39/39 (2006.01) A61K 39/205 (2006.01) (75) Inventor/Applicant (for US only): PETROVSKY, A61K 31/715 (2006.01) A61K 39/29 (2006.01) Nikolai [AU/AU]; 11 Walkley Avenue, Warradale, A d A61K 39/145 (2006.01) elaide, South Australia 5046 (AU). (21) International Application Number: (74) Agent: WRIGHT,, Andrew John; POTTER CLARKSON PCT/EP2012/061748 LLP, Park View House, 58 The Ropewalk, Nottingham Nottinghamshire NG1 5DD (GB). (22) International Filing Date: 19 June 2012 (19.06.2012) (81) Designated States (unless otherwise indicated, for every kind of national protection available): AE, AG, AL, AM, (25) English Filing Language: AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, (26) Publication Language: English CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, (30) Priority Data: HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, KR, 61/498,557 19 June 201 1 (19.06.201 1) US KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, (71) Applicant (for all designated States except US): VAXINE MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, PTY LTD [AU/AU]; Endocrinology Department, Room OM, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SC, SD, 6D313, Flinders Medical Centre, Bedford Park, South SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, Australia 5042 (AU).
    [Show full text]