#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

Current opinions on gout, its diagnosis and treatment


Authors: P. Němec
Authors‘ workplace: Revmatologická ambulance II. interní kliniky Lékařské fakulty MU a FN u sv. Anny Brno, přednosta prof. MUDr. Miroslav Souček, CSc.
Published in: Vnitř Lék 2012; 58(12): 928-937
Category: Review

Overview

Gout is a heterogenous group of metabolic diseases characterized by formation and deposition of sodium urate crystals in various tissues. Gouty arthritis is a rheumatic syndrome occurring in individuals with hyperuricaemia; this is an inflammatory disease of the musculoskeletal system with a presence of sodium urate crystals. Hyperuricaemia, i.e. pathologically increased levels of uric acid in the serum, represents the most important risk factor for the development of gouty arthritis. The causes of hyperuricaemia may include an increased production of uric acid and/or its reduced elimination from the body. Acute gouty arthritis is an early manifestation of gouty arthritis. When deposition of sodium urate crystals in tissues leads to a destruction of musculoskeletal system structures, this is called chronic tophaceous gouty arthritis. To treat chronic tophaceous gout, the uric acid levels must be kept below 360 μmol/l, deposits of sodium urate in tissues dissolved and their further formation prevented. Pharmacological treatment of chronic hyperuricaemia involves administration of uric acid level lowering drugs, particularly xanthine oxidase inhibitors and uricosurics. Hyperuricaemia is an important risk factor not only for the development of chronic tophaceous gout and renal impairment but some data also suggests a risk associated with cardiovascular diseases.

Key words:
gout – hyperuricaemia – uric acid – therapy


Sources

1. Zhang W, Doherty M, Pascual E et al. EULAR evidence based recommendations for gout. Part I: Diagnosis. Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis 2006; 65: 1301–1311.

2. Mikuls TR, Farrar JT, Bilker WB et al. Gout epidemiology: results from the UK General Practice Research Database, 1990–1999. Ann Rheum Dis 2005; 64: 267–272.

3. Annemans L, Spaepen E, Gaskin M et al. Gout in the UK and Germany: prevalence, comorbidities and management in general practice 2000–2005. Ann Rheum Dis 2008; 67: 960–966.

4. Alamanos Y, Drosos AA. Epidemiology of adult rheumatoid arthritis. Autoimmun Rev 2005; 4: 130–136.

5. Arromdee E, Michet CJ, Crowson CS, O‘Fallon WM, Gabriel SE. Epidemiology of gout: is the incidence rising? J Rheumatol 2002; 29: 2403–2406.

6. Pavelka K. Dna (arthritis urica). In: Pavelka K, Rovenský J. Klinická revmatologie. Praha: Galen 2003: 347–358.

7. Nakagawa T, Hu H, Zharikov S et al. A causal role for uric acid in fruktose-induced metabolit syndrome. Am J Physiol Renal Physiol 2006; 290: F625–F631.

8. Enomoto A, Kimura H, Chairoungdua A et al. Molecular identification of a renal urate anion exchanger that regulates blood urate levels. Nature 2002; 417: 447–452.

9. Anzai N, Jutabha P, Amonpatumrat-Takahashi S, Sakurai H. Recent advances in renal urate transport: characterization of candidate transporters indicated by genome-wide association studies. Clin Exp Nephrol 2012; 16: 89–95.

10. Souček M. Metabolický syndrom. Vnitř Lék 2009; 55: 618–621.

11. Mazzali M, Hughes J, Kim YG et al. Elevated uric acid increases blood pressure in the rat by a novel crystal-independent mechanism. Hypertension 2001; 38: 1101–1106.

12. Feig DI, Soletsky B, Johnson RJ. Effect of allopurinol on blood pressure of adolescents with newly diagnosed essential hypertension: a randomized trial. JAMA 2008; 300: 924–932.

13. Siu YP, Leung KT, Tong MK, Kwan TH. Use of allopurinol in slowing the progression of renal disease through its ability to lower serum uric acid level. Am J Kidney Dis 2006; 47: 51–59.

14. Menè P, Punzo G. Uric acid: bystander or culprit in hypertension and progressive renal disease? J Hypertens 2008; 26: 2085–2092.

15. Puig JG, de Miguel E, Castillo MC et al. Symptomatic hyperuricemia: impact of ultrasonography. Nucleosides Nucleotides Nucleic Acids. 2008; 27: 592–595.

16. Richette P, Bardin T. Gout. Lancet 2010; 375: 318–328.

17. Žurek M. Patogeneze, diagnostika a léčba dny. Vnitř Lék 2006; 52: 736–741.

18. Zhang Y, Chen C, Choi H et al. Purine-rich foods intake and recurrent gout attacks. Ann Rheum Dis 2012; 71: 1448–1453.

19. Pavelka K. Doporučení České revmatologické společnosti pro léčbu dnavé artritidy. Čes revmatol 2012; 20: 82–92.

20. Steele TH. Hyperuricemic nephropathies. Nephron 1999; 81: (Suppl. 1): 45–49.

21. Wallace SL, Robinson H, Masi AT et al. Preliminary criteria for the classification of the acute arthritis of primary gout. Arthritis Rheum 1977; 20: 895–900.

22. Zhang W, Doherty M, Bardin T et al. EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis 2006; 65: 1312–1324.

23. Pavelka K. Terapie dny. In: Pavelka K et al. Farmakoterapie revmatických onemocnění. Praha: Grada Publishing 2005: 345–351.

24. Emmerson BT. Regimen of indomethacin therapy in acute gouty arthritis. Br Med J 1967; 2: 272–274.

25. Arnold MH, Preston SJ, Buchanan WW. Comparison of the natural history of untreated acute gouty arthritis vs acute gouty arthritis treated with non-steroidal-anti-inflammatory drugs. Br J Clin Pharmacol 1988; 26: 488–489.

26. Martínez RV, Reval M, Campos MD et al. Involvement of peripheral cyclooxygenase-1 and cyclooxygenase-2 in inflammatory pain. J Pharm Pharmacol 2002; 54: 405–412.

27. Yeomans ND, Tulassay Z, Juhász L et al. A comparison of omeprazole with ranitidine for ulcers associated with nonsteroidal antiinflammatory drugs. Acid Suppression Trial: Ranitidine versus Omeprazole for NSAID-associated Ulcer Treatment (ASTRONAUT) Study Group. N Engl J Med 1998; 338: 719–726.

28. Silverstein FE, Graham DY, Senior JR et al. Misoprostol reduces serious gastrointestinal complications in patients with rheumatoid arthritis receiving nonsteroidal anti-inflammatory drugs. A randomized, double-blind, placebo-controlled trial. Ann Intern Med 1995; 123: 241–249.

29. Hawkey C, Laine L, Simon T et al. Comparison of the effect of rofecoxib (a cyclooxygenase 2 inhibitor), ibuprofen, and placebo on the gastroduodenal mucosa of patients with osteoarthritis: a randomized, double-blind, placebo--controlled trial. The Rofecoxib Osteoarthritis Endoscopy Multinational Study Group. Arthritis Rheum 2000; 43: 370–377.

30. Okamoto K, Eger BT, Nishino T et al. An extremely potent inhibitor of xanthine oxidoreductase. Crystal structure of the enzyme-inhibitor complex and mechanism of inhibition. J Biol Chem 2003; 278: 1848–1855.

31. Okamoto K, Nishino T. Crystal structures of mammalian xanthine oxidoreductase bound with various inhibitors: allopurinol, febuxostat, and FYX-051. J Nippon Med Sch 2008; 75: 2–3.

32. SPC Adenuric

33. Khosravan R, Kukulka MJ, Wu JT, Joseph--Ridge N, Vernillet L. The effect of age and gender on pharmacokinetics, pharmacodynamics, and safety of febuxostat, a novel nonpurine selective inhibitor of xanthine oxidase. J Clin Pharmacol 2008; 48: 1014–1024.

34. Schumacher HR Jr, Becker MA, Wortmann RL et al. Effects of febuxostat versus allopurinol and placebo in reducing serum urate in subjects with hyperuricemia and gout: a 28-week, phase III, randomized, double-blind, parallel-group trial. Arthritis Rheum 2008; 59: 1540–1548.

35. Becker MA, Schumacher HR Jr, Wortmann RL et al. Febuxostat compared with allopurinol in patients with hyperuricemia and gout. N Engl J Med 2005; 353: 2450–2461.

36. Becker MA, Schumacher HR, MacDonald PA, Lloyd E, Lademacher C. Clinical efficacy and safety of successful long term urate lowering with febuxostat or allopurinol in subjects with gout. J Rheumatol 2009; 36: 1273–1282.

37. Schumacher HR Jr, Becker MA, Lloyd E, MacDonald PA, Lademacher C. Febuxostat in the treatment of gout: 5-year findings of the FOCUS efficacy and safety study. Rheumatology (Oxford) 2009; 48: 188–194.

38. Becker MA, Schumacher HR Jr, Wortmann RL et al. Febuxostat, a novel nonpurine selective inhibitor of xanthine oxidase: a twenty-eight-day, multicenter, phase II, randomized, double-blind, placebo-controlled, doseresponse clinical trial examining safety and efficacy in patients with gout. Arthritis Rheum 2005; 52: 916–923.

39. Warring WS, McKnight JA, Webb DJ, Maxwell SR. Uric acid restores endothelial function in patient with type 1 diabetes and regular smoker. Diabetes 2006; 55: 3127–3132.

40. Waring WS, Convery A, Mishra V et al. Uric acid reduces exercise-induced oxidative stress in healthy adults. Clin Sci (Lond) 2003; 105: 425–430.

Labels
Diabetology Endocrinology Internal medicine
Login
Forgotten password

Enter the email address that you registered with. We will send you instructions on how to set a new password.

Login

Don‘t have an account?  Create new account

#ADS_BOTTOM_SCRIPTS#