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Vol. 20. Núm. 1.
Páginas 33-39 (enero - febrero 2013)
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Vol. 20. Núm. 1.
Páginas 33-39 (enero - febrero 2013)
Open Access
Canakinumab: un anticuerpo monoclonal prometedor en el tratamiento de enfermedades cardiovasculares
Canakinumab: a promising monoclonal antibody in the treatment of cardiovascular diseases
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5268
Fernando Manzur1,2,
Autor para correspondencia
fmanzur1954@hotmail.com

Correspondencia.
, Carlos Moneriz1,
Autor para correspondencia
cmonerizpretel@yahoo.com

Correspondencia.
1 Universidad de Cartagena. Cartagena, Colombia
2 Nuevo Hospital Bocagrande. Cartagena, Colombia
Este artículo ha recibido

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El canakinumab es un anticuerpo monoclonal anti-IL-1β totalmente humano desarrollado por Novartis, cuyo mecanismo de acción se basa en la neutralización de la señalización IL-1β, lo cual conduce a la supresión de la inflamación en pacientes con trastornos de origen autoinmune. La IL-1β actúa como un mediador de la respuesta inmune periférica durante la infección y la inflamación. Mediante la unión antígeno-anticuerpo el canakinumab inhibe la acción de la IL1-β evitando sus efectos pro-inflamatorios. En la actualidad, está en evaluación como un nuevo posible agente dirigido frente a la IL-1β, con el objetivo de reducir la tasa de eventos cardiovasculares y la diabetes de aparición reciente (estudio CANTOS).

Palabras clave:
factores de riesgo cardiovascular
biomarcadores
diagnóstico

Canakinumab is a totally human monoclonal antibody anti-IL-1β developed by Novartis, whose mode of action is based on the neutralization of IL-1β signaling, which leads to suppression of inflammation in patients with autoimmune disorders. The IL-1β acts as a mediator of the peripheral immune response during infection and inflammation. By the antigen-antibody binding, canakinumab inhibits the action of IL1-β avoiding its pro-inflammatory effects. Currently, it is being evaluated as a new possible agent directed against IL-1β, with the goal of reducing the rate of cardiovascular events and new onset diabetes (study CANTOS).

Keywords:
cardiovascular risk factors
biomarkers
diagnosis
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Bibliografía
[1.]
E. Dhimolea.
Canakinumab. MAbs, 2 (2010), pp. 3-13
[2.]
M.P. Curran.
Canakinumab: in patients with cryopyrin-associated periodic syndromes.
[3.]
I. Kone-Paut, H.J. Lachmann, J.B. Kuemmerle-Deschner, E. Hachulla, K.S. Leslie, R. Mouy, et al.
Sustained remission of symptoms and improved health-related quality of life in patients with cryopyrin-associated periodic syndrome treated with canakinumab: results of a double-blind placebo-controlled randomized withdrawal study.
Arthritis Res Ther, 13 (2011), pp. R202
[4.]
J.B. Kuemmerle-Deschner, E. Hachulla, R. Cartwright, P.N. Hawkins, T.A. Tran, B. Bader- Meunier, et al.
Two-year results from an open-label, multicentre, phase III study evaluating the safety and efficacy of canakinumab in patients with cryopyrinassociated periodic syndrome across different severity phenotypes.
Ann Rheum Dis, 70 (2011), pp. 2095-2102
[5.]
S. Yokota, M. Kikuchi, T. Nozawa, T. Kizawa, T. Kanetaka, T. Miyamae, et al.
An approach to the patients with cryopyrin-associated periodic syndrome (CAPS): a new biologic response modifier, canakinumab.
Nihon Rinsho Meneki Gakkai Kaishi, 35 (2012), pp. 23-29
[6.]
S.M. Mueller, P. Itin, P. Haeusermann.
Muckle-Wells syndrome effectively treated with canakinumab: is the recommended dosing schedule mandatory?.
Dermatology, 223 (2011), pp. 113-118
[7.]
J.R. Yu, K.S. Leslie.
Cryopyrin-associated periodic syndrome: an update on diagnosis and treatment response.
Curr Allergy Asthma Rep, 11 (2011), pp. 12-20
[8.]
O. Toker, P.J. Hashkes.
Critical appraisal of canakinumab in the treatment of adults and children with cryopyrin-associated periodic syndrome (CAPS).
Biologics, 4 (2010), pp. 131-138
[9.]
A. So, M. De Meulemeester, A. Pikhlak, A.E. Yucel, D. Richard, V. Murphy, et al.
Canakinumab for the treatment of acute flares in difficult-to-treat gouty arthritis: Results of a multicenter, phase II, dose-ranging study.
Arthritis Rheum, 62 (2010), pp. 3064-3076
[10.]
N. Schlesinger, E. Mysler, H.Y. Lin, M. De Meulemeester, J. Rovensky, U. Arulmani, et al.
Canakinumab reduces the risk of acute gouty arthritis flares during initiation of allopurinol treatment: results of a double-blind, randomised study.
Ann Rheum Dis, 70 (2011), pp. 1264-1271
[11.]
R. Alten, J. Gomez-Reino, P. Durez, A. Beaulieu, A. Sebba, G. Krammer, et al.
Efficacy and safety of the human anti-IL-1beta monoclonal antibody canakinumab in rheumatoid arthritis: results of a 12-week, phase II, dose-finding study.
BMC Musculoskelet Disord, 12 (2011), pp. 153
[12.]
I. Mitroulis, P. Skendros, A. Oikonomou, A.G. Tzioufas, K. Ritis.
The efficacy of canakinumab in the treatment of a patient with familial mediterranean fever and longstanding destructive arthritis.
Ann Rheum Dis, 70 (2011), pp. 1347-1348
[13.]
N. Ruperto, P. Quartier, N. Wulffraat, P. Woo, A. Ravelli, R. Mouy, et al.
A phase II, multicenter, open-label study evaluating dosing and preliminary safety and efficacy of canakinumab in systemic juvenile idiopathic arthritis with active systemic features.
Arthritis Rheum, 64 (2012), pp. 557-567
[14.]
N. Schlesinger, M. De Meulemeester, A. Pikhlak, A.E. Yucel, D. Richard, V. Murphy, et al.
Canakinumab relieves symptoms of acute flares and improves health-related quality of life in patients with difficult-to-treat Gouty Arthritis by suppressing inflammation: results of a randomized, dose-ranging study.
Arthritis Res Ther, 13 (2011), pp. R53
[15.]
J.B. Kuemmerle-Deschner, E. Ramos, N. Blank, J. Roesler, S.D. Felix, T. Jung, et al.
Canakinumab (ACZ885, a fully human IgG1 anti-IL-1beta mAb) induces sustained remission in pediatric patients with cryopyrin-associated periodic syndrome (CAPS).
Arthritis Res Ther, 13 (2011), pp. R34
[16.]
Y. Ogura, F.S. Sutterwala, R.A. Flavell.
The inflammasome: first line of the immune response to cell stress.
[17.]
K. Rajamaki, J. Lappalainen, K. Oorni, E. Valimaki, S. Matikainen, P.T. Kovanen, et al.
Cholesterol crystals activate the NLRP3 inflammasome in human macrophages: a novel link between cholesterol metabolism and inflammation.
[18.]
H.J. Lachmann, P. Quartier, A. So, P.N. Hawkins.
The emerging role of interleukin- 1beta in autoinflammatory diseases.
Arthritis Rheum, 63 (2011), pp. 314-324
[19.]
I. Fabreguet, A. So.
Canakinumab: a promising treatment in rheumatology.
Rev Med Suisse, 8 (2012), pp. 57-60
[20.]
J.P. Drenth, J.W. van der Meer.
The inflammasome -a linebacker of innate defense.
N Engl J Med, 355 (2006), pp. 730-732
[21.]
S.R. Kingsbury, P.G. Conaghan, M.F. McDermott.
The role of the NLRP3 inflammasome in gout.
J Inflamm Res, 4 (2011), pp. 39-49
[22.]
A. Stutz, D.T. Golenbock, E. Latz.
Inflammasomes: too big to miss.
J Clin Invest, 119 (2009), pp. 3502-3511
[23.]
C.A. Dinarello.
Immunological and inflammatory functions of the interleukin-1 family.
Annu Rev Immunol, 27 (2009), pp. 519-550
[24.]
C.A. Dinarello.
The role of the interleukin-1-receptor antagonist in blocking inflammation mediated by interleukin-1.
N Engl J Med, 343 (2000), pp. 732-734
[25.]
P.M. Ridker, T. Thuren, A. Zalewski, P. Libby.
Interleukin-1beta inhibition and the prevention of recurrent cardiovascular events: rationale and design of the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS).
Am Heart J, 162 (2011), pp. 597-605
[26.]
K. Ren, R. Torres.
Role of interleukin-1beta during pain and inflammation.
Brain Res Rev, 60 (2009), pp. 57-64
[27.]
C.A. Dinarello.
Therapeutic strategies to reduce IL-1 activity in treating local and systemic inflammation.
Curr Opin Pharmacol, 4 (2004), pp. 378-385
[28.]
H.J. Lachmann, P. Lowe, S.D. Felix, C. Rordorf, K. Leslie, S. Madhoo, et al.
In vivo regulation of interleukin 1beta in patients with cryopyrin-associated periodic syndromes.
J Exp Med, 206 (2009), pp. 1029-1036
[29.]
P. Libby, P.M. Ridker, G.K. Hansson.
Inflammation in atherosclerosis: from pathophysiology to practice.
J Am Coll Cardiol, 54 (2009), pp. 2129-2138
[30.]
C.A. Dinarello.
Interleukin-1beta and the autoinflammatory diseases.
N Engl J Med, 360 (2009), pp. 2467-2470
[31.]
W.F. Fearon, D.T. Fearon.
Inflammation and cardiovascular disease: role of the interleukin-1 receptor antagonist.
Circulation, 117 (2008), pp. 2577-2579
[32.]
P. Duewell, H. Kono, K.J. Rayner, C.M. Sirois, G. Vladimer, F.G. Bauernfeind, et al.
NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals.
Nature, 464 (2010), pp. 1357-1361
[33.]
E. Galkina, K. Ley.
Immune and inflammatory mechanisms of atherosclerosis (*).
Annu Rev Immunol, 27 (2009), pp. 165-197
[34.]
A. Tedgui, Z. Mallat.
Cytokines in atherosclerosis: pathogenic and regulatory pathways.
Physiol Rev, 86 (2006), pp. 515-581
[35.]
G.S. Abela, K. Aziz, A. Vedre, D.R. Pathak, J.D. Talbott, J. Dejong.
Effect of cholesterol crystals on plaques and intima in arteries of patients with acute coronary and cerebrovascular syndromes.
Am J Cardiol, 103 (2009), pp. 959-968
[36.]
B. Vicenova, V. Vopalensky, L. Burysek, M. Pospisek.
Emerging role of interleukin-1 in cardiovascular diseases.
Physiol Res, 58 (2009), pp. 481-498
[37.]
P.M. Ridker.
C-reactive protein and the prediction of cardiovascular events among those at intermediate risk: moving an inflammatory hypothesis toward consensus.
J Am Coll Cardiol, 49 (2007), pp. 2129-2138
[38.]
P.M. Ridker, E. Danielson, F.A. Fonseca, J. Genest, A.M. Gotto Jr., J.J. Kastelein, et al.
Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein.
N Engl J Med, 359 (2008), pp. 2195-2207
[39.]
P.M. Ridker, C.P. Cannon, D. Morrow, N. Rifai, L.M. Rose, C.H. McCabe, et al.
Creactive protein levels and outcomes after statin therapy.
N Engl J Med, 352 (2005), pp. 20-28
[40.]
M.Y. Donath, S.E. Shoelson.
Type 2 diabetes as an inflammatory disease.
Nat Rev Immunol, 11 (2011), pp. 98-107
[41.]
M.Y. Donath.
Inflammation as a sensor of metabolic stress in obesity and type 2 diabetes.
Endocrinology, 152 (2011), pp. 4005-4006
[42.]
A. Kastrati, W. Koch, P.B. Berger, J. Mehilli, K. Stephenson, F.J. Neumann, et al.
Protective role against restenosis from an interleukin-1 receptor antagonist gene polymorphism in patients treated with coronary stenting.
J Am Coll Cardiol, 36 (2000), pp. 2168-2173
[43.]
G. Patti, A. D’Ambrosio, A. Dobrina, G. Dicuonzo, C. Giansante, N. Fiotti, et al.
Interleukin-1 receptor antagonist: a sensitive marker of instability in patients with coronary artery disease.
J Thromb Thrombolysis, 14 (2002), pp. 139-143
[44.]
D.L. Mann.
Inflammatory mediators and the failing heart: past, present, and the foreseeable future.
Circ Res, 91 (2002), pp. 988-998
Copyright © 2013. Sociedad Colombiana de Cardiología y Cirugía Cardiovascular
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