metricas
covid
Buscar en
Enfermedades Infecciosas y Microbiología Clínica
Toda la web
Inicio Enfermedades Infecciosas y Microbiología Clínica Perfil lipídico de atazanavir
Información de la revista
Vol. 26. Núm. S17.
Atazanavir
Páginas 34-40 (diciembre 2008)
Compartir
Compartir
Descargar PDF
Más opciones de artículo
Vol. 26. Núm. S17.
Atazanavir
Páginas 34-40 (diciembre 2008)
Acceso a texto completo
Perfil lipídico de atazanavir
Lipid profile of atazanavir
Visitas
2372
Esteban Martínez Chamorro
Autor para correspondencia
esteban@fundsoriano.es

Correspondencia: Dr. E. Martínez. Servicio de Infecciones. Hospital Clínic. Villarroel, 170. 08036 Barcelona. España.
Servicio de Infecciones. Hospital Clínic-Institut d’Investigaciones Biomèdiques August Pi i Sunyer. Universidad de Barcelona. España
Este artículo ha recibido
Información del artículo
Resumen
Bibliografía
Descargar PDF
Estadísticas

En la actualidad se sabe que la exposición al tratamiento antirretroviral, particularmente a los inhibidores de proteasa clásicos, se asocia con un incremento del riesgo de presentar enfermedad cardiovascular, aunque la interrupción del tratamiento antirretroviral puede ocasionar un riesgo aún mayor. Se han emitido recomendaciones sobre la intervención ante la dislipidemia y el riesgo cardiovascular en personas seropositivas. Estas recomendaciones se semejan a las de la población general, pero incluyen el carácter particular de considerar incluir un tratamiento antirretroviral benigno con los lípidos en la medida de lo posible.

Atazanavir presenta unas características diferentes de las de otros inhibidores de la proteasa en cuanto a sus efectos sobre el tejido adiposo y el metabolismo en general. Atazanavir no se ha asociado con los aumentos de las concentraciones de colesterol total, colesterol unido a lipoproteínas de baja densidad (cLDL) o triglicéridos que han presentado otros inhibidores de la proteasa en pautas de inicio, rescate o simplificación. Los resultados de los estudios in vitro y clínicos son claros y contundentes.

Estas características le confieren un papel singular muy atractivo a la hora de decidir el tratamiento antirretroviral más adecuado para una proporción de pacientes infectados por el virus de la inmunodeficiencia humana (VIH) en los que la reducción del riesgo cardiovascular constituya una prioridad.

Palabras clave:
Atazanavir
Hiperlipidemia
Riesgo cardiovascular

It is currently known that exposure to antiretroviral treatment, particularly to the classic protease inhibitors, is associated with an increased risk of suffering from cardiovascular disease, although stopping antiretroviral treatment can cause an even greater risk. Recommendations have been made on how to deal with dyslipaemia and cardiovascular risk in seropositive patients. These recommendations are similar to those for the general population, but include the particular feature of considering including benign treatment with lipids wherever possible.

Atazanavir has different characteristics from other protease inhibitors as regards its effects on adipose tissue and metabolism in general. Atazanavir is not associated with increases in total cholesterol, LDL-cholesterol or triglycerides as with other PI in initial, rescue or simplification therapy. The results of in vitro studies and clinical studies are clear and convincing. These characteristics give it a particular role that is very attractive when deciding the most suitable antiretroviral treatment for a proportion of HIV-infected patients in whom the reduction in cardiovascular risk is seen as a priority.

Key words:
Atazanavir
Hyperlipaemia
Cardiovascular risk
El Texto completo está disponible en PDF
Bibliografía
[1.]
F.J.J. Palella, K.M. Delaney, A.C. Moorman, et al.
Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection.
N Engl J Med, 338 (1998), pp. 853-860
[2.]
D.D. Richman.
HIV chemotherapy.
Nature, 410 (2001), pp. 995-1001
[3.]
J.Q. Purnell, A. Zambon, R.H. Knopp, et al.
Effect of ritonavir on lipids and post-heparin lipase activities in normal subjects.
AIDS, 14 (2000), pp. 51-57
[4.]
D. Periard, A. Telenti, P. Sudre, For the Swiss HIV Cohort Study, et al.
Atherogenic dyslipidemia in HIV-infected individuals treated with protease inhibitors.
Circulation, 100 (1999), pp. 700-705
[5.]
H. Pernerstorfer-Schoen, B. Jilma, A. Perschler, et al.
Sex differences in HAART-associated dyslipidaemia.
AIDS, 15 (2001), pp. 725-734
[6.]
A.D. Roberts, R.A. Muesing, D.M. Parenti, J. Hsia, A.G. Wasserman, G.L. Simon.
Alterations in serum levels of lipids and lipoproteins with indinavir therapy for human immunodeficiency virus-infected patients.
Clin Infect Dis, 29 (1999), pp. 441-443
[7.]
K. Mulligan, C. Grunfeld, V.W. Tai, et al.
Hyperlipidemia and insulin resistance are induced by protease inhibitors independent of changes in body composition in patients with HIV infection.
J Acquir Immune Defic Syndr, 23 (2000), pp. 35-43
[8.]
M.A. Noor, J.C. Lo, K. Mulligan, et al.
Metabolic effects of indinavir in healthy HIV-seronegative men.
AIDS, 15 (2001), pp. F11-F18
[9.]
A. Hsu, G.R. Granneman, G. Witt, C. Locke, J. Denissen, A. Molla, et al.
Multiple-dose pharmacokinetics of ritonavir in human immunodeficiency virus-infected subjects.
Antimicrob Agents Chemother, 41 (1997), pp. 898-905
[10.]
S.D. Shafran, L.D. Mashinter, S.E. Roberts.
The effect of low-dose ritonavir monotherapy on fasting serum lipid concentrations.
[11.]
The Data Collection on Adverse Events of Anti-HIV Drugs (DAD) Study Group.
Combination antiretroviral therapy and the risk of myocardial infarction.
N Engl J Med, 349 (2003), pp. 1993-2003
[12.]
The DAD Study Group.
Class of antiretroviral drugs and the risk of myocardial infarction.
N Engl J Med, 356 (2007), pp. 1723-1735
[13.]
DAD Study Group.
Use of nucleoside reverse transcriptase inhibitors and risk of myocardial infarction in HIV-infected patients enrolled in the D:A:D study: a multi-cohort collaboration.
Lancet, 371 (2008), pp. 1417-1426
[14.]
Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults.
Executive summary of the third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III).
JAMA, 285 (2001), pp. 2486-2497
[15.]
M.P. Dubé, J.H. Stein, J. Aberg, C.J. Fichtenbaum, J.G. Gerber, K.T. Tashima, Guidelines for the evaluation and management of dyslipidemia in human immunodeficiency virus (HIV)-infected adults receiving antiretroviral therapy: recommendations of the HIV Medical Association of the Infectious Disease Society of America and the Adult AIDS Clinical Trials Group, et al.
Clin Infect Dis, 37 (2003), pp. 613-627
[16.]
J.D. Lundgren, M. Battegay, G. Behrens, S. De Wit, G. Guaraldi, C. Katlama, The EACS Executive Committee.
European AIDS Clinical Society (EACS) guidelines on the prevention and management of metabolic diseases in HIV.
[17.]
C. Grunfeld, M. Pang, W. Doerrler, J.K. Shigenaga, P. Jensen, K.R. Feingold.
Lipids, lipoproteins, triglyceride clearance, and cytokines in human immunodeficiency virus infection and the acquired immunodeficiency syndrome.
J Clin Endocrinol Metab, 74 (1992), pp. 1045-1052
[18.]
M. Van der Valk, J.J.P. Kastelein, R. Murphy, F. Van Leth, C. Katlama, A. Horban, et al.
Nevirapine-containing antiretroviral therapy in HIV-1 infected patients results in an anti-atherogenic lipid profile.
AIDS, 15 (2001), pp. 2407-2414
[19.]
The Strategies for Management of Antiretroviral Therapy (SMART) Study Group.
CD4+ Count-Guided Interruption of Antiretroviral Treatment.
N Engl J Med, 355 (2006), pp. 2283-2296
[20.]
A. Phillips, A. Carr, J. Neuhaus, F. Visnegarwala, R. Prineas, W.J. Burman, et al.
Interruption of antiretroviral therapy and risk of cardiovascular disease in persons with HIV-1 infection: exploratory analyses from the SMART trial.
Antivir Ther, 13 (2008), pp. 177-187
[21.]
W.B. Kannel.
Lipids, diabetes, and coronary heart disease: insights from the Framingham Study.
Am Heart J, 110 (1985), pp. 1100-1107
[22.]
F. Bonnet, M. Savès, C. Droz, E. Peuchant, G. Chene, J. Beylot, et al.
Increase of atherogenic plasma profile in HIV-infected patients treated with protease inhibitor-containing regimens.
J Acquir Immune Defic Syndr, 25 (2000), pp. 199-200
[23.]
J. Constans, J.L. Pellegrin, E. Peuchant, M.F. Dumon, I. Pellegrin, C. Sergeant, et al.
Plasma lipids in HIV-infected patients: a prospective study in 95 patients.
Eur J Clin Invest, 24 (1994), pp. 416-420
[24.]
A. Carr.
HIV protease inhibitor-related lipodystrophy syndrome.
Clin Infect Dis, 30 (2000), pp. S135-S142
[25.]
A.R. Miserez, P.Y. Muller, V. Spaniol.
Indinavir inhibits sterol-regulatory element- binding protein-1c- dependent lipoprotein lipase and fatty acid synthase gene activations.
AIDS, 16 (2002), pp. 1587-1594
[26.]
J.S. Liang, O. Distler, D.A. Cooper, H. Jamil, R.J. Deckelbaum, H. Ginsberg, et al.
HIV protease inhibitors protect apolipoprotein B from degradation by the proteasome: a potential mechanism for protease inhibitor-induced hyperlipidemia.
Nat Med, 7 (2001), pp. 1327-1331
[27.]
S. Wang, R. Mulvey, N. Laing, O. Flint, R.A. Parker.
Differentiation of atazanivir from other HIV-protease inhibitors in preclinical models of glucose uptake, lipogenesis, and proteasome function [abstract 10].
4th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV,
[28.]
D.W. Haas, C. Zala, S. Schrader, A. Thiry, R. McGovern, S. Schnittman.
Atazanavir plus saquinavir once daily favorably affects total cholesterol (TC), fasting triglyceride (TG), and fasting LDL cholesterol (LDL) profiles in patients failing prior therapy (trial AI424-009, week 48) [abstract 42].
9th Conference for Retroviruses and Opportunistic Infections,
[29.]
I. Sanne, P. Cahn, L. Percival, P. Phanuphak, T.GM. Kelleher, G. Pantaleo.
Comparative results (phase II 48-week): BMS-232632, stavudine, lamivudine as HAART for treatment-naïve HIV(+) patients (AI424-008) [abstract I- 667].
41st Interscience Conference on Antimicrobial Agents and Chemotherapy,
[30.]
H. Murata, P.W. Hruz, M. Mueckler.
The mechanism of insulin resistance caused by HIV protease inhibitor therapy.
J Biol Chem, 275 (2000), pp. 20251-20254
[31.]
M. Caron, M. Auclair, C. Vigouroux, M. Glorian, C. Forest, J. Capeau.
The HIV protease inhibitor indinavir impairs sterol regulatory element-binding protein- 1 intranuclear localization, inhibits preadipocyte differentiation, and induces insulin resistance.
Diabetes, 50 (2001), pp. 1378-1388
[32.]
R.A. Parker, S. Wang, R. Mulvey, C. Elosua, W. Fenderson, F. Wang, et al.
Differential effects of HIV protease inhibitors on proteasome, gene expresión, and lipogenesis provide a mechanism for PI-associated dyslipidemia and atazanavir's favourable lipid profile.
11th Conference on Retroviruses and opportunistic Infections,
[33.]
J.G. Jemsek, E. Arathoon, M. Arlotti, C. Perez, N. Sosa, Pokrovskiy., et al.
Body fat and other metabolic effects of atazanavir and efavirenz, each administered in combination with zidovudine plus lamivudine, in antiretroviral-naive HIV-infected patients.
Clin Infect Dis, 42 (2006), pp. 273-280
[34.]
D.RN. Malan, E. Krantz, N. David, V. Wirtz, J. Hammond, D. McGrath, et al.
Efficacy and safety of atazanavir, with or without ritonavir, as part of oncedaily highly active antiretroviral therapy regimens in antiretroviral-naive patients.
J Acquir immune Defic Syndr, 47 (2008), pp. 161-167
[35.]
K.Y. Smith, W.G. Weinberg, E. DeJesus, M.A. Fischl, Q. Liao, L.L. Ross, et al.
AIDS Res Ther, 5 (2008), pp. 5
[36.]
R. Elion, E. De Jesus, M. Sension, D. Berger, W. Towner, G. Richmond, et al.
Once-daily abacavir/lamivudine and ritonavir-boosted atazanavir for the treatment of HIV-1 infection in antiretroviral-naive patients: a 48-week pilot study.
HIV Clin Trials, 9 (2008), pp. 152-163
[37.]
J.M. Molina, J. Andrade-Villanueva, J. Echevarria, P. Chetchotisakd, J. Corral, N. David, et al.
Efficacy and safety of once-daily atazanavir/ritonavir compared with twice-daily loipinavir/ritonavir, each in combination with tenofovir and emtricitabine in ARV-naive HIV-1-infected subjects: the CASTLE study, 48-week results.
Program and abstracts of the 15th Conference on Retroviruses and Opportunistic Infections,
[38.]
P.J. Piliero, P. Cahn, G. Pantaleo, J. Gatell, K. Squires, L. Percival, et al.
Atazanavir: a once-daily protease inhibitor with a superior lipid profile: results of clinical trials at week 48.
9th Conference on Retroviruses and Opportunistic Infections,
[39.]
D. Haas, C. Zala, S. Schrader, P. Piliero, H. Jaeger, D. Nunes, et al.
Therapy with atazanavir plus saquinavir in patients failing highly active antiretroviral therapy: a randomized comparative pilot trial.
[40.]
L. Nieto-Cisneros, C. Zala, W.J. Fessel, J. Gonzalez-Garcia, C. Cohen, R. McGovern.
Antiviral efficacy, metabolic changes and safety of atazanavir (ATV) versus lopinavir/ritonavir (LPV/RTV) in combination with two NRTIs in patients who have experienced virological failure with prior PI-containing regimen(s): 24-week results from BMS AI424-043.
Program and abstracts of the 2nd International AIDS Society Conference on HIV Pathogenesis and Treatment,
[41.]
R. Badaro, E. De Jesus, A. Lazzarin, J. Jemsek, B. Clotet, A. Rightmire, et al.
Efficacy and safety of atazanavir (ATV) with ritonavir (RTV) or saquinavir (SQV) versus lopinavir/ritonavir (LPV/RTV) in combination with tenofovir (TFV) and one NRTI in patients who have experienced virologic failure to multiple HAART regimens: 16 week results from BMS AI424-045.
Program and abstracts of the 2nd International AIDS Society Conference on HIV Pathogenesis and Treatment,
[42.]
Panel de expertos de GESIDA y Plan Nacional sobre el Sida.
Recomendaciones de GESIDA/Plan Nacional sobre el Sida respecto al tratamiento antirretroviral en adultos infectados por el virus de la inmunodeficiencia humana (actualización enero de 2007).
Enferm Infecc Microbiol Clin, 25 (2007), pp. 32-53
[43.]
J. Gatell, D. Salmon-Ceron, A. Lazzarin, Van. Wijngaerden, F. Antunes, C. Leen, et al.
Efficacy and safety of atazanavir-based highly active antiretroviral therapy in patients with virologic supresión switched from a stable, boosted or unboosted portease inhibitor treatment regimen: the SWAN study (AI424-097) 48-week results.
Clin Infect Dis, 44 (2007), pp. 1484-1492
[44.]
J. Mallolas, D. Podzamczer, P. Domingo, B. Clotet, E. Ribera, et al.
Efficacy and safety of switching from boosted lopinavir to boosted atazanavir in patients with virologic suppression receiving a lopinavir/ritonavir-containing HAART: the ATAZIP study.
4th IAS Conference on HIV Pathogenesis, Treatment and Prevention, Sydney, Australia,
[45.]
V. Soriano, P. García-Gascó, E. Vispo, A. Ruiz-Sancho, F. Blanco, L. Martín-Carbonero, et al.
Efficacy and safety of replacing lopinavir with atazanavir in HIV-infected patients with undetectable plasma viraemia: final results of the SLOAT trial.
J Antimcrob Chemother, 61 (2008), pp. 200-205
[46.]
G. Moyle, J. Andrade, P.M. Girard, A. Antinori, P. Salvato, J.R. Bogner, et al.
Continuation of BID boosted PI vs switch to once-daily boosted atazanavir in subjects with truncal adipositiy: 24-week interim analysis of the 96-week multicentre, open-label, randomised, prospective REAL study.
11th European AIDS Conference,
[47.]
M. Colafigli, S. Di Giambenedetto, L. Bracciale, E. Tamburrini, R. Cauda, A. De Luca.
Cardiovascular risk score change in HIV-1-infected patients switched to an atazanavir-based combination antiretroviral regimen.
HIV Medicine, 9 (2008), pp. 172-179
Copyright © 2008. Elsevier España S.L.. Todos los derechos reservados
Descargar PDF
Opciones de artículo
es en pt

¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?

Você é um profissional de saúde habilitado a prescrever ou dispensar medicamentos