Buscar en
Revista Colombiana de Reumatología
Toda la web
Inicio Revista Colombiana de Reumatología Gota: nuevos conceptos patogénicos y nuevos agentes terapéuticos
Información de la revista
Vol. 18. Núm. 3.
Páginas 163-174 (Septiembre 2011)
Descargar PDF
Más opciones de artículo
Vol. 18. Núm. 3.
Páginas 163-174 (Septiembre 2011)
DOI: 10.1016/S0121-8123(11)70051-2
Acceso a texto completo
Gota: nuevos conceptos patogénicos y nuevos agentes terapéuticos
Gout: New pathogenic concepts and new therapeutic agents
José A. Gómez-Puerta1,
Autor para correspondencia

Correspondencia: Villarroel 170, 08036, Barcelona, España. Correo electrónico:.
Información del artículo

La gota es una artropatía inflamatoria caracterizada por brotes autolimitados de artritis con marcado dolor como consecuencia de los depósitos de cristales de urato monosódico (UMS) en los tejidos articulares y periarticulares. En algunas ocasiones se puede desarrollar una gota tofácea crónica que puede conducir a una importante destrucción articular y por ende una marcada discapacidad. La gota es la causa más común de artritis inflamatoria entre hombres y mujeres post-menopáusicas.

Durante los últimos años se han dado pasos importantes en la patogenia de la gota, tanto a nivel de estudios genéticos, como la participación del inflamosoma, comportándose la gota como una enfermedad auto-inflamatoria.

Adicionalmente, se han desarrollado nuevos agentes farmacológicos incluyendo anti-IL1 (anakinra, rinolacept y canakinumab) e inhibidores de xantina oxidasa (febuxostat) los cuales han demostrado ser útiles en términos de reducción de las concentraciones séricas de ácido úrico (AU) en pacientes resistentes o con intolerancia a las terapias hipouricemiantes convencionales.

Palabras clave:

Gout is an inflammatory arthritis characterized by selflimiting but excruciatingly painful acute attacks. These are a consequence of monosodium urate crystal deposition within articular or periarticular tissue. After years of acute intermittent gout, chronic tophaceous gout can develop. Gout is the most frequent cause of inflammatory arthritis in men and postmenopausic women.

Several important advances had been developed during last years in terms of pathogenic mechanisms, including genetic and inflammatory aspects such as the participation of inflammosome. In that sense, the gout can follow a course similar than othe autoinflammatory disorders.

Additionally, new therapeutic agents had been developed, including anti-IL1 antibodies (anakinra, rinolacept and canakinumab) and xanthine oxidase inhibitors such as febuxostat. Those treatments had demonstrated efficacy in term of lowering serum urate concentrations in refractory patients to conventional treatments.

Key words:
El Texto completo está disponible en PDF
T. Neogi.
Clinical practice Gout.
N Engl J Med, 364 (2011), pp. 443-452
E. Pascual, F. Sivera.
Diagnóstico de artropatía microcristalina.
Reumatol Clin, 4 (2008), pp. 45-49
E. Pascual, F. Sivera.
Therapeutic advances in gout.
Curr Opin Rheumatol, 19 (2007), pp. 122-127
S. Li, R. Micheletti.
Role of diet in rheumatic disease.
Rheum Dis Clin North Am, 37 (2011), pp. 119-133
A. Iglesias-Gamarra, G. Quintana, J.F. Restrepo Suárez.
Prehistoria, historia y arte de la Reumatología Gota y espondilitis anquilosante.
Rev Col Reumatol, (2006), pp. 120-141
N.N. Kohn, R.E. Hughes, C.D. Mc Jr., J.S. Faires.
The significance of calcium phosphate crystals in the synovial fluid of arthritic patients: the “pseudogout syndrome” II. Identification of crystals.
Ann Intern Med, 56 (1962), pp. 738-745
J.T. Scott.
Comparison of allopurinol and probenecid.
Ann Rheum Dis, 25 (1966), pp. 623-626
R.O. Day, D.J. Birkett, M. Hicks, J.O. Miners, G.G. Graham, P.M. Brooks.
New uses for allopurinol.
Drugs, 48 (1994), pp. 339-344
N. Dalbeth, A. So.
Hyperuricaemia and gout: state of the art and future perspectives.
Ann Rheum Dis, 69 (2010), pp. 1738-1743
J. Graessler, A. Graessler, S. Unger, S. Kopprasch, A.K. Tausche, E. Kuhlisch, et al.
Association of the human urate transporter 1 with reduced renal uric acid excretion and hyperuricemia in a German Caucasian population.
Arthritis Rheum, 54 (2006), pp. 292-300
M. Kolz, T. Johnson, S. Sanna, A. Teumer, V. Vitart, M. Perola, et al.
Meta-analysis of 28,141 individuals identifies common variants within five new loci that influence uric acid concentrations.
PLoS Genet, 5 (2009), pp. e1000504
H.M. Hoffman, A.A. Wanderer.
Inflammasome and IL- 1beta-mediated disorders.
Curr Allergy Asthma Rep, 10 (2010), pp. 229-235
T.R. Merriman, N. Dalbeth.
The genetic basis of hyperuricaemia and gout.
Joint Bone Spine, 78 (2010), pp. 35-40
E. Peñaranda-Parada, S-BN, J.F. Restrepo, F. Rondón- Herrera, A. Millán, A. Iglesias Gamarra.
Enfermedades Autoinflamatorias.
Rev Col Reumatol, 17 (2010), pp. 85-95
P.I. Sidiropoulos, G. Goulielmos, G.K. Voloudakis, E. Petraki, D.T. Boumpas.
Inflammasomes and rheumatic diseases: evolving concepts.
Ann Rheum Dis, 67 (2008), pp. 1382-1389
F. Martinon, V. Petrilli, A. Mayor, A. Tardivel, J. Tschopp.
Gout-associated uric acid crystals activate the NALP3 inflammasome.
Nature, 440 (2006), pp. 237-241
C.A. Dinarello.
Blocking interleukin-1beta in acute and chronic autoinflammatory diseases.
J Intern Med, 269 (2011), pp. 16-28
A. So, T. De Smedt, S. Revaz, J. Tschopp.
A pilot study of IL-1 inhibition by anakinra in acute gout.
Arthritis Res Ther, 9 (2007), pp. R28
R. Terkeltaub, J.S. Sundy, H.R. Schumacher, F. Murphy, S. Bookbinder, S. Biedermann, et al.
The interleukin 1 inhibitor rilonacept in treatment of chronic gouty arthritis: results of a placebo-controlled, monosequence crossover, non-randomised, single-blind pilot study.
Ann Rheum Dis, 68 (2009), pp. 1613-1617
A. So, D.M.M. Shamim T.
Canakinumab (ACZ885) vs. triamcinolone acetonide for treatment of acute flares and prevention of recurrent flares in gouty arthritis patients refractory to or contraindicated to NSAIDs and/or colchicine.
Arthritis Rheum, 60 (2009), pp. LB4
C.M. Burns, R.L. Wortmann.
Gout therapeutics: new drugs for an old disease.
E.W. Campion, R.J. Glynn, L.O. DeLabry.
Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study.
Am J Med, 82 (1987), pp. 421-426
F. Perez-Ruiz.
Treating to target: a strategy to cure gout.
Rheumatology (Oxford), 48 (2009), pp. ii9-ii14
E. de Miguel.
Papel de la ecografía en las artritis microcristalinas.
Reumatol Clin, (2008), pp. 50-54
F. Perez-Ruiz, I. Martin, B. Canteli.
Ultrasonographic measurement of tophi as an outcome measure for chronic gout.
J Rheumatol, 34 (2007), pp. 1888-1893
A. Shah, R.T. Keenan.
Gout, hyperuricemia, and the risk of cardiovascular disease: cause and effect?.
Curr Rheumatol Rep, 12 (2010), pp. 118-124
M. Doherty.
New insights into the epidemiology of gout.
Rheumatology (Oxford), 48 (2009), pp. ii2-ii8
E. Krishnan, Inflammation.
oxidative stress and lipids: the risk triad for atherosclerosis in gout.
Rheumatology (Oxford), 49 (2010), pp. 1229-1238
H.K. Choi, G. Curhan.
Independent impact of gout on mortality and risk for coronary heart disease.
Circulation, 116 (2007), pp. 894-900
D.I. Feig, D.H. Kang, R.J. Johnson.
Uric acid cardiovascular risk.
Engl J N. Med, 359 (2008), pp. 1811-1821
D.H. Kang, T. Nakagawa, L. Feng, S. Watanabe, L. Han, M. Mazzali, et al.
A role for uric acid in the progression of renal disease.
J Am Soc Nephrol, 13 (2002), pp. 2888-2897
D.I. Feig, B. Soletsky, R.J. Johnson.
Effect of allopurinol on blood pressure of adolescents with newly diagnosed essential hypertension: a randomized trial.
Jama, 300 (2008), pp. 924-932
S.A. Wright, E. Filippucci, C. McVeigh, A. Grey, M. McCarron, W. Grassi, et al.
High-resolution ultrasonography of the first metatarsal phalangeal joint in gout: a controlled study.
Ann Rheum Dis, 66 (2007), pp. 859-864
S.D. Anker, W. Doehner, M. Rauchhaus, R. Sharma, D. Francis, C. Knosalla, et al.
Uric acid and survival in chronic heart failure: validation and application in metabolic, functional, and hemodynamic staging.
Circulation, 107 (2003), pp. 1991-1997
K. Nagahama, K. Iseki, T. Inoue, T. Touma, Y. Ikemiya, S. Takishita.
Hyperuricemia and cardiovascular risk factor clustering in a screened cohort in Okinawa Japan.
Hypertens Res, 27 (2004), pp. 227-233
S.Y. Kim, J.P. Guevara, K.M. Kim, H.K. Choi, D.F. Heitjan, D.A. Albert.
Hyperuricemia and coronary heart disease: a systematic review and meta-analysis.
Arthritis Care Res (Hoboken), 62 (2010), pp. 170-180
M. Elisaf, V. Tsimichodimos, E. Bairaktari, K.C. Siamopoulos.
Effect of micronized fenofibrate and losartan combination on uric acid metabolism in hypertensive patients with hyperuricemia.
J Cardiovasc Pharmacol, 34 (1999), pp. 60-63
W. Zhang, M. Doherty, T. Bardin, E. Pascual, V. Barskova, P. Conaghan, 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, 65 (2006), pp. 1312-1324
A. Whelton.
Current and future therapeutic options for the management of gout.
Am J Ther, 17 (2010), pp. 402-417
F. Perez-Ruiz, F. Liote.
Lowering serum uric acid levels: what is the optimal target for improving clinical outcomes in gout?.
Arthritis Rheum, 57 (2007), pp. 1324-1328
E. Pascual, F. Sivera.
Time required for disappearance of urate crystals from synovial fluid after successful hypouricaemic treatment relates to the duration of gout.
Ann Rheum Dis, 66 (2007), pp. 1056-1058
T.G. Rider, K.M. Jordan.
The modern management of gout.
Rheumatology (Oxford), 49 (2010), pp. 5-14
B.L. Love, R. Barrons, A. Veverka, K.M. Snider.
Uratelowering therapy for gout: focus on febuxostat.
Pharmacotherapy, 30 (2010), pp. 594-608
F.D.N. Perez-Ruiz, N. Schlesinger.
Febuxostat, a novel drug for the treatment of hyperuricemia of gout Future Rheumatol, 5 (2008), pp. 421-427
N.L. Edwards.
Febuxostat: a new treatment for hyperuricaemia in gout.
Rheumatology (Oxford), 48 (2009), pp. ii15-ii19
M.A. Becker, H.R. Schumacher, L.R. Espinoza, A.F. Wells, P. MacDonald, E. Lloyd, et al.
The urate-lowering efficacy and safety of febuxostat in the treatment of the hyperuricemia of gout: the CONFIRMS trial.
Arthritis Res Ther, 12 (2010), pp. R63
H.R. Schumacher Jr., M.A. Becker, R.L. Wortmann, P.A. Macdonald, B. Hunt, J. Streit, 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, parallelgroup trial.
Arthritis Rheum, 59 (2008), pp. 1540-1548
M.A. Becker, H.R. Schumacher Jr., R.L. Wortmann, P.A. MacDonald, D. Eustace, W.A. Palo, et al.
Febuxostat compared with allopurinol in patients with hyperuricemia and gout.
N Engl J Med, 353 (2005), pp. 2450-2461
H.R. Schumacher Jr., M.A. Becker, E. Lloyd, P.A. MacDonald, C. Lademacher.
Febuxostat in the treatment of gout: 5-yr findings of the FOCUS efficacy and safety study.
Rheumatology (Oxford), 48 (2009), pp. 188-194
M.S.H. Becker, P.A. MacDonald.
Urate-lowering therapy in subjects with gout: interim results from the febuxostat comparative extension long-term study (EXCEL).
Ann Rheum Dis, 66 (2007), pp. 230

Unidad de Artritis, Servicio de Reumatología. Hospital Clínic, Barcelona.

El autor declara no presentar ningún conflicto de interés al momento de la redacción del manuscrito.

Copyright © 2011. Asociación Colombiana de Reumatología
Opciones de artículo