Rheumatoid arthritis

Czech version

Authors: Ladislav Šenolt
Authors‘ workplace: Revmatologický ústav, Praha
Published in: Vnitř Lék 2018; 64(2): 98-106
Category: Reviews

Overview

Rheumatoid arthritis is an autoimmune disease manifested by a persistent inflammation of synovial joints, bone destruction, loss of cartilage and increased risk of cardiovascular and other intercurrent diseases. The treatment of rheumatoid arthritis should be based on the strategy of treat to target therapy which is achieving remission, in some cases low activity of the disease. Essential to the treat to target therapy are more frequent checkups and optimization of treatment based on disease activity. Methotrexate continues to be the essential medicine from the group of disease modifying antirheumatic drugs for rheumatoid arthritis treatment. At the start are frequently added glucocorticoids. If the effect is insufficient, biological therapy or use of targeted synthetic drugs can be considered. In this overview, the author will focus on epidemiology and risk factors, pathophysiology and in particular on the diagnostics, evaluation of activity and treatment of rheumatoid arthritis.

Key words:
diagnostics – disease activity – rheumatoid arthritis – treatment

Sources

1. Smolen JS, Aletaha D, Mc Innes IB. Rheumatoid arthritis. Lancet 2016; 388(10055): 2023–2038. Dostupné z DOI: <http://dx.doi.org/10.1016/S0140–6736(16)30173–8>.

2. Smolen JS, Breedveld FC, Burmester GR et al. Treating rheumatoid arthritis to target: 2014 update of the recommendations of an international task force. Ann Rheum Dis 2016; 75(1): 3–15. Dostupné z DOI: <http://dx.doi.org/10.1136/annrheumdis-2015–207524>.

3. Frisell T, Hellgren K, Alfredsson L t al. Familial aggregation of arthritis-related diseases in seropositive and seronegative rheumatoid arthritis: a register-based case-control study in Sweden. Ann Rheum Dis 2016; 75(1): 183–189. Dostupné z DOI: <http://dx.doi.org/10.1136/annrheumdis-2014–206133>.

4. Okada Y, Wu D, Trynka G et al. Genetics of rheumatoid arthritis contributes to biology and drug discovery. Nature 2014; 506(7488): 376–381. Dostupné z DOI: <http://dx.doi.org/10.1038/nature12873>.

5. Viatte S, Plant D, Han B et al. Association of HLA-DRB1 haplotypes with rheumatoid arthritis severity, mortality, and treatment response. JAMA 2015; 313(16): 1645–1656. Dostupné z DOI: <http://dx.doi.org/10.1001/jama.2015.3435>.

6. Ospelt C, Gay S, Klein K Epigenetics in the pathogenesis of RA. Semin Immunopathol 2017; 39(4): 409–419. Dostupné z DOI: <http://dx.doi.org/10.1007/s00281–017–0621–5>.

7. Filková M, Jüngel A, Gay RE et al. MicroRNAs in rheumatoid arthritis: potential role in diagnosis and therapy. BioDrugs 2012; 26(3): 131–141. <http://dx.doi.org/10.2165/11631480–000000000–00000>.

8. Baka Z, Buzás E, Nagy G. Rheumatoid arthritis and smoking: putting the pieces together. Arthritis Res Ther 2009; 11(4): 238. Dostupné z DOI: <http://dx.doi.org/10.1186/ar2751>.

9. Damgaard D, Senolt L, Nielsen MF et al. Demonstration of extracellular peptidylarginine deiminase (PAD) activity in synovial fluid of patients with rheumatoid arthritis using a novel assay for citrullination of fibrinogen. Arthritis Res Ther 2014; 16(6): 498. Dostupné z DOI: <http://dx.doi.org/10.1186/s13075–014–0498–9>.

10. Wegner N, Wait R, Sroka A et al. Peptidylarginine deiminase from Porphyromonas gingivalis citrullinates human fibrinogen and α-enolase: implications for autoimmunity in rheumatoid arthritis. Arthritis Rheum 2010; 62(9): 2662–2672. Dostupné z DOI: <http://dx.doi.org/10.1002/art.27552>.

11. Maeda Y, Kurakawa T, Umemoto E et al. Dysbiosis Contributes to Arthritis Development via Activation of Autoreactive T Cells in the Intestine. Arthritis Rheumatol 2016; 68(11): 2646–2661. Dostupné z DOI: <http://dx.doi.org/10.1002/art.39783>.

12. McInnes IB, Schett G. The pathogenesis of rheumatoid arthritis. N Engl J Med 2011; 365(23): 2205–2219. Dostupné z DOI: <http://dx.doi.org/10.1056/NEJMra1004965>.

13. Perry E, Kelly C, Eggleton P et al. The lung in ACPA-positive rheumatoid arthritis: an initiating site of injury? Rheumatology (Oxford) 2014; 53(11): 1940–1950. Dostupné z DOI: <http://dx.doi.org/10.1093/rheumatology/keu195>.

14. Scher JU, Littman DR, Abramson SB Review: microbiome in inflammatory arthritis and human rheumatic diseases. Arthritis Rheumatol 2016; 68(1): 35–45. Dostupné z DOI: <http://dx.doi.org/10.1002/art.39259>.

15. Nielen MM, van Schaardenburg D, Reesink WH et al. Specific autoantibodies precede the symptoms of rheumatoid arthritis: a study of serial measurements in blood donors. Arthritis Rheum 2004; 50(2): 380–386.

16. Harre U, Georgess D, Bang H et al. Induction of osteoclastogenesis and bone loss by human autoantibodies against citrullinated vimentin. J Clin Invest 2012; 122(5): 1791–1802. Dostupné z DOI: <http://dx.doi.org/10.1172/JCI60975>.

17. van de Sande MG, de Hair MJ, van der Leij C et al. Different stages of rheumatoid arthritis: features of the synovium in the preclinical phase. Ann Rheum Dis 2011; 70(5): 772–777. Dostupné z DOI: <http://dx.doi.org/10.1136/ard.2010.139527>.

18. Feldmann M, Maini SR. Role of cytokines in rheumatoid arthritis: an education in pathophysiology and therapeutics. Immunol Rev 2008; 223(1): 7–19. Dostupné z DOI: <http://dx.doi.org/10.1111/j.1600–065X.2008.00626.x>.

19. Korb-Pap A, Bertrand J, Sherwood J et al. Stable activation of fibroblasts in rheumatic arthritis-causes and consequences. Rheumatology (Oxford) 2016; 55(Suppl 2): ii64-ii67. Dostupné z DOI: <http://dx.doi.org/10.1093/rheumatology/kew347>.

20. Redlich K, Hayer S, Ricci R et al. Osteoclasts are essential for TNF-α-mediated joint destruction. J Clin Invest 2002; 110(10): 1419–1427. Dostupné z DOI: <http://dx.doi.org/10.1172/JCI15582>.

21. Martel-Pelletier J, Welsch DJ, Pelletier JP. Metalloproteases and inhibitors in arthritic diseases. Best Pract Res Clin Rheumatol 2001; 15(5): 805–829. Dostupné z DOI: <http://dx.doi.org/10.1053/berh.2001.0195>.

22. Klareskog L, Catrina AI, Paget S. Rheumatoid arthritis. Lancet 2009; 373(9664): 659–672. Dostupné z DOI: <http://dx.doi.org/10.1016/S0140–6736(09)60008–8>.

23. Turesson C, McClelland RL, Christianson T et al. Clustering of extraarticular manifestations in patients with rheumatoid arthritis. J Rheumatol 2008; 35(1): 179–180.

24. Roubille C, Haraoui B. Interstitial lung diseases induced or exacerbated by DMARDS and biologic agents in rheumatoid arthritis: a systematic literature review. Semin Arthritis Rheum 2014; 43(5): 613–626. Dostupné z DOI: <http://dx.doi.org/10.1016/j.semarthrit.2013.09.005>.

25. Rozin A, Hoffman R, Hayek T et al. Felty’s syndrome without rheumatoid arthritis? Clin Rheumatol 2013; 32(5): 701–704. Dostupné z DOI: <http://dx.doi.org/10.1007/s10067–012–2157–3>.

26. Buckley CD, Pilling D, Lord JM et al. Fibroblasts regulate the switch from acute resolving to chronic persistent inflammation. Trends Immunol 2001; 22(4): 199–204.

27. Arnett FC, Edworthy SM, Bloch DA et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 1988; 31(3): 315–324.

28. Aletaha D, Neogi T, Silman AJ et al. 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Ann Rheum Dis 2010; 69(9): 1580–1588. Dostupné z DOI: <http://dx.doi.org/10.1136/ard.2010.138461>.

29. van Nies JA, Tsonaka R, Gaujoux-Viala C et al. Evaluating relationships between symptom duration and persistence of rheumatoid arthritis: does a window of opportunity exist? Results on the Leiden early arthritis clinic and ESPOIR cohorts. Ann Rheum Dis 2015; 74(5): 806–812. Dostupné z DOI: <http://dx.doi.org/10.1136/annrheumdis-2014–206047>.

30. Šenolt L, Mann H, Herle P. Revmatologie: Doporučení pro včasný záchyt nejčastějších zánětlivých revmatických onemocnění. Doporučené diagnostické a terapeutické postupy pro všeobecné praktické lékaře. Společnost všeobecného lékařství ČLS JEP: Praha 2014.ISBN 978–80–86998–74–9.

31. Farheen K, Agarwal SK. Assessment of disease activity and treatment outcomes in rheumatoid arthritis. J Manag Care Pharm 2011; 17(9 Suppl B): S09-S13.

32. Smolen JS, Aletaha D. Scores for all seasons: SDAI and CDAI. Clin Exp Rheumatol 2014; 32(5 Suppl 85): S75-S79.

33. Felson DT, Smolen JS, Wells G et al. American College of Rheumatology/European League against Rheumatism provisional definition of remission in rheumatoid arthritis for clinical trials. Ann Rheum Dis 2011; 70(3): 404–413. Dostupné z DOI: <http://dx.doi.org/10.1136/ard.2011.149765>.

34. Smolen JS, van der Heijde D, Machold KP et al. Proposal for a new nomenclature of disease-modifying antirheumatic drugs. Ann Rheum Dis 2014; 73(1): 3–5. Dostupné z DOI: <http://dx.doi.org/10.1136/annrheumdis-2013–204317>.

35. Singh JA, Saag KG, Bridges jr. SL et al. 2015 American College of Rheumatology Guideline for the Treatment of Rheumatoid Arthritis. Arthritis Rheumatol 2016; 68(1): 1–26. Dostupné z DOI: <http://dx.doi.org/10.1002/art.39480>.

36. Smolen JS, Landewé R, Bijlsma J et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2016 update. Ann Rheum Dis 2017; 76(6): 960–977. Dostupné z DOI: <http://dx.doi.org/10.1136/annrheumdis-2016–210715>.

37. Šenolt L, Mann H, Závada J t al. Doporučení České revmatologické společnosti pro farmakoterapii revmatoidní artritidy 2017. Čes Revmatol 2017; 25(1): 8–24.

38. Hoes JN, Jacobs JW, Buttgereit F et al. Current view of glucocorticoid co-therapy with DMARDs in rheumatoid arthritis. Nat Rev Rheumatol 2010; 6(12): 693–702. Dostupné z DOI: <http://dx.doi.org/10.1038/nrrheum.2010.179>.

39. O’Dell JR, Haire CE, Erikson N et al. Treatment of rheumatoid arthritis with methotrexate alone, sulfasalazine and hydroxychloroquine, or a combination of all three medications. N Engl J Med 1996; 334(20): 1287–1291. Dostupné z DOI: <http://dx.doi.org/10.1056/NEJM199605163342002>.

40. Yamaoka K. Janus kinase inhibitors for rheumatoid arthritis. Curr Opin Chem Biol 2016; 32: 29–33. Dostupné z DOI: <http://dx.doi.org/10.1016/j.cbpa.2016.03.006>.

41. Smolen JS, Burmester GR, Combe B. Head-to-head comparison of certolizumab pegol versus adalimumab in rheumatoid arthritis: 2-year efficacy and safety results from the randomised EXXELERATE study. Lancet 2016; 388(10061): 2763–2774. Dostupné z DOI: <http://dx.doi.org/10.1016/S0140–6736(16)31651–8>.

42. Emery P, Gottenberg JE, Rubbert-Roth A et al. Rituximab versus an alternative TNF inhibitor in patients with rheumatoid arthritis who failed to respond to a single previous TNF inhibitor: SWITCH-RA, a global, observational, comparative effectiveness study. Ann Rheum Dis 2015; 74(6): 979–984. Dostupné z DOI: <http://dx.doi.org/10.1136/annrheumdis-2013–203993>.

43. Ramiro S, Sepriano A, Chatzidionysiou K et al. Safety of synthetic and biological DMARDs: a systematic literature review informing the 2016 update of the EULAR recommendations for management of rheumatoid arthritis. Ann Rheum Dis 2017; 76(6): 1101–1136. Dostupné z DOI: <http://dx.doi.org/10.1136/annrheumdis-2016–210708>.

44. Schett G, Emery P, Tanaka Y et al. Tapering biologic and conventional DMARD therapy in rheumatoid arthritis: current evidence and future directions. Ann Rheum Dis 2016; 75(8): 1428–1437. Dostupné z DOI: <http://dx.doi.org/10.1136/annrheumdis-2016–209201>.

45. Aletaha D, Smolen J. The Simplified Disease Activity Index (SDAI) and the Clinical Disease Activity Index (CDAI): A review of their usefulness and validity in rheumatoid arthritis. Clin Exp Rheumatol 2005; 23(5 Suppl 39): 100–108.