Irina N. Bobkova , Elena S. Kamyshova
Abstract
Gout is a systemic disease caused by the deposition of monosodium urate crystals in various tissues and organs with the subsequent development of autoinflammation. The problem of comorbidity in gout has been known for a long time and continues to be actively studied. The gout is associated with cardiovascular diseases, metabolic and metabolic disorders, kidney diseases, and hyperuricemia plays an important role in these associations. Therefore, the elimination of hyperuricemia is the basis of the modern strategy of effective therapy for gout, the main principle of which is “treat-to-target” (serum uric acide concentration <360 μmol/L [6 mg/dL]). Nevertheless, many patients who need treatment for gout still do not receive therapy or receive suboptimal therapy, which significantly increases the risks of overall and cardiovascular mortality. In this regard, it is of great importance that physicians are aware of the indications, optimal timing of initiation and purposes of urate-lowering therapy, as well as strengths and weaknesses of certain urate-lowering drugs, including skin, kidneys, heart, and liver adverse events. The review highlights the modern principles of urate-lowering therapy, including the place of febuxostat in the treatment of patients with gout.
Key words: gout, hyperuricemia, metabolic syndrome, urate-lowering therapy, allopurinol, febuxostat
Key words: gout, hyperuricemia, metabolic syndrome, urate-lowering therapy, allopurinol, febuxostat
About the Author
Irina N. Bobkova 1 , Elena S. Kamyshova 11 Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia
References
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[Eliseev M.S. Podagra. In: Rossiiskie klinicheskie rekomendatsii. Revmatologiia. Ed, E.L. Nasonova. Moscow: GEOTAR-Media, 2020. ISBN: 978-5-9704-5398-8 (in Russian).]
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12. Jing J, Ekici AB, Sitter T et al. Genetics of serum urate concentrations and gout in a high-risk population, patients with chronic kidney disease. Sci Rep 2018; 8 (1): 13184. DOI: 10.1038/s41598-018-31282-z
13. Kuo CF, Grainge MJ, Mallen C et al. Comorbidities in patients with gout prior to and following diagnosis: case-control study. Ann Rheum Dis 2016; 75 (1): 210–7. DOI: 10.1136/annrheumdis-2014-206410
14. Singh JA, Cleveland JD. Gout and the risk of incident atrial fibrillation in older adults: a study of US Medicare data. RMD Open 2018; 4 (2): e000712. DOI: 10.1136/rmdopen-2018-000712
15. Kuo YJ, Tsai TH, Chang HP et al. The risk of atrial fibrillation in patients with gout: a nationwide population-based study. Sci Rep 2016; 6: 32220. DOI: 10.1038/srep32220
16. Clarson LE, Chandratre P, Hider SL et al. Increased cardiovascular mortality associated with gout: a systematic review and meta-analysis. Eur J Prev Cardiol 2015; 22 (3): 335–43. DOI: 10.1177/204748 7313514895
17. Lottmann K, Chen X, Schädlich PK. Association between gout and all-cause as well as cardiovascular mortality: a systematic review. Curr Rheumatol Rep 2012; 14 (2): 195–203. DOI: 10.1007/s11926-011-0234-2
18. Clarson LE, Hider SL, Belcher J et al. Increased risk of vascular disease associated with gout: a retrospective, matched cohort study in the UK clinical practice research datalink. Ann Rheum Dis 2015; 74 (4): 642–7. DOI: 10.1136/annrheumdis-2014-205252
19. Abdul Sultan A, Mallen C, Hayward R et al. Gout and subsequent erectile dysfunction: a population-based cohort study from England. Arthritis Res Ther 2017; 19 (1): 123. DOI: 10.1186/s13075-017-
1322-0
20. Zhang Y, Peloquin CE, Dubreuil M et al. Sleep Apnea and the Risk of Incident Gout: A Population-Based, Body Mass Index-Matched Cohort Study. Arthritis Rheumatol 2015; 67 (12): 3298–302. DOI: 10.1002/art.39330
21. Blagojevic-Bucknall M, Mallen C, Muller S et al. The Risk of Gout Among Patients With Sleep Apnea: A Matched Cohort Study. Arthritis Rheumatol 2019; 71 (1): 154–60. DOI: 10.1002/art.40662
22. Huang CC, Huang PH, Chen JH et al. An Independent Risk of Gout on the Development of Deep Vein Thrombosis and Pulmonary Embolism: A Nationwide, Population-Based Cohort Study. Medicine (Baltimore) 2015; 94 (51): e2140. DOI: 10.1097/MD.0000000000002140
23. Li L, McCormick N, Sayre EC et al. Trends of venous thromboembolism risk before and after diagnosis of gout: a general population-based study. Rheumatology (Oxford) 2020; 59 (5): 1099–7. DOI: 10.1093/rheumatology/kez398
24. Kok VC, Horng JT, Wang MN et al. Gout as a risk factor for osteoporosis: epidemiologic evidence from a population-based longitudinal study involving 108,060 individuals. Osteoporos Int 2018; 29 (4): 973–85. DOI: 10.1007/s00198-018-4375-2
25. Tzeng HE, Lin CC, Wang IK et al. Gout increases risk of fracture: A nationwide population-based cohort study. Medicine (Baltimore) 2016; 95 (34): e4669. DOI: 10.1097/MD.0000000000004669
26. Roughley M, Sultan AA, Clarson L et al. Risk of chronic kidney disease in patients with gout and the impact of urate lowering therapy: a population-based cohort study. Arthritis Res Ther 2018; 20 (1): 243. DOI: 10.1186/s13075-018-1746-1
27. Singh JA, Cleveland JD. Gout is associated with a higher risk of chronic renal disease in older adults: a retrospective cohort study of U.S. Medicare population. BMC Nephrol 2019; 20 (1): 93. DOI: 10.1186/s12882-019-1274-5
28. Shimizu T, Hori H. The prevalence of nephrolithiasis in patients with primary gout: a cross-sectional study using helical computed tomography. J Rheumatol 2009; 36 (9): 1958–62. DOI: 10.3899/jrheum.081128
29. Nakagawa T, Cirillo P, Sato W et al. The conundrum of hyperuricemia, metabolic syndrome, and renal disease. Intern Emerg Med 2008; 3 (4): 313–18. DOI: 10.1007/s11739-008-0141-3
30. King C, Lanaspa MA, Jensen T et al. Uric Acid as a Cause of the Metabolic Syndrome. Contrib Nephrol 2018; 192: 88–02. DOI: 10.1159/000484283А
31. Trevisan M, Liu J, Bahsas FB, Menotti A. Syndrome X and mortality: a population-based study. Risk Factor and Life Expectancy Research Group. Am J Epidemiol 1998; 148 (10): 958–966. DOI: 10.1093/oxfordjournals.aje.a009572
32. Ford ES. Risks for all-cause mortality, cardiovascular disease, and diabetes associated with the metabolic syndrome: a summary of the evidence. Diabetes Care 2005; 28 (7): 1769–78. DOI: 10.2337/diacare.28.7.1769
33. Rho YH, Choi SJ, Lee YH et al. The prevalence of metabolic syndrome in patients with gout: a multicenter study. J Korean Med Sci 2005;
20 (6): 1029–33. DOI: 10.3346/jkms.2005.20.6.1029
34. Vázquez-Mellado J, García CG, Vázquez SG et al. Metabolic syndrome and ischemic heart disease in gout. J Clin Rheumatol 2004; 10 (3): 105–9. DOI: 10.1097/01.rhu.0000129082.42094.fc
35. Choi HK, Ford ES. Prevalence of the metabolic syndrome in individuals with hyperuricemia. Am J Med 2007; 120 (5): 442–7. DOI: 10.1016/j.amjmed.2006.06.040
36. Барскова В.Г. Метаболический синдром и кардиоваскулярные нарушения при подагре. Международный эндокринологический журнал. 2007; 6 (12). www.mif-ua.com/archive/article/3768
[Barskova V.G. Metabolicheskii sindrom i kardiovaskuliarnye narusheniia pri podagre. Mezhdunarodnyi endokrinologicheskii zhurnal. 2007; 6 (12). www.mif-ua.com/archive/article/3768 (in Russian).]
37. Richette P, Doherty M, Pascual E et al. 2016 updated EULAR evidence-based recommendations for the management of gout. Ann Rheum Dis 2017; 76 (1): 29–42. DOI: 10.1136/annrheumdis-2016-
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[Chikina M.N., Zheliabina O.V., Eliseev M.S. Vliianie uratsnizhaiushchei terapii na pokazateli kachestva zhizni u patsientov s podagroi. Sovremennaia revmatologiia. 2021; 15 (3): 62–8 (in Russian).]
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For citation:Bobkova I.N., Kamyshova E.S. The many faces of gout: modern treatment concepts. Clinical review for general practice. 2021; 10: 14–19. DOI: 10.47407/kr2021.2.10.00113
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