martes, 24 de mayo de 2011

Riesgo de hemorragia en el infarto agudo de miocardio

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Artículo nº 1639. Vol 11 nº 5, mayo 2011.
Autor: Domingo Díaz Díaz

Riesgo de hemorragia en el infarto agudo de miocardio

Artículo original: In-hospital major bleeding during ST-elevation and non-ST-elevation myocardial infarction care: derivation and validation of a model from the ACTION Registry(R)-GWTG. Mathews R, Peterson ED, Chen AY, Wang TY, Chin CT, Fonarow GC, Cannon CP, Rumsfeld JS, Roe MT, Alexander KP. Am J Cardiol 2011; 107(8): 1136-1143. [Resumen] [Artículos relacionados]

Introducción: El sangrado es una complicación habitual del tratamiento del infarto agudo de miocardio (IAM) con y sin elevación del segmento ST, asociándose con peores resultados. La obtención de un modelo de riesgo de hemorragias graves permitiría estratificar a los pacientes y ajustar el tratamiento antitrombótico óptimo del IAM.

Resumen: Utilizando la base de datos del "Acute Coronay Treatment and Intervention Outcomes Network Registry- Get With the Guidelines" (ACTION Registry-GWTG), que recoge pacientes con IAM (con y sin elevación del ST), se desarrolla y valida un modelo de riesgo de sangrado grave en el hospital. El modelo utiliza variables de referencia al ingreso. Se desarrolla en 72.313 pacientes y es validado en 17.960, durante 2 años en 251 hospitales de Estados Unidos. Se seleccionaron 12 variables, en base a la importancia clínica y significación estadística. Se produjo hemorragia grave en el 10,8%. Los 12 factores asociados con hemorragia grave fueron: frecuencia cardiaca, hemoglobina al ingreso inferior a 12 g/dl, sexo femenino, creatinina serica basal, edad, cambios en el electrocardiograma, insuficiencia cardiaca o shock, diabetes, enfermedad arterial periférica, peso corporal, presión arterial sistólica y tratamiento con warfarina. La puntuación del riesgo se calculó sumando los valores ponderados de cada variable, y la estimación final del riesgo de sangrado grave se dividió en percentiles: muy bajo riesgo (< 20), bajo riesgo (21-30), riesgo moderado (31-40), alto riesgo (41-50) y muy alto riesgo (> 50). El modelo mostró una buena correlación entre los valores observados y predichos de hemorragia grave, así como una buena discriminación entre los pacientes que recibieron tratamiento y no desarrollaron grandes eventos de sangrado grave en la cohorte de derivación (estadístico C 0,73), y de validación (estadístico C 0,71). Los porcentajes de sangrado grave aumentaron a medida que aumentaba la puntuación de las categorías de riesgo en la cohorte de derivación y validación: muy bajo riesgo (3,9%), bajo riesgo (7,3%), riesgo moderado (16,1%), alto riesgo (29,0%) y muy alto riesgo (39,8%).

Comentario: El tratamiento del IAM debe barajar riesgo de isquemia y complicaciones hemorrágicas. Este modelo permite estratificar el riesgo hemorrágico de forma rápida y en un amplísimo espectro de pacientes con IAM, con variables no incluidas en otros modelos. Sin embargo presenta algunas limitaciones, dado que la definición de sangrado grave esta basada en la disposición de variables y procedimientos de recopilación de datos; además, no contempla la historia de sangrado previo, siendo un factor de predicción utilizado en otros modelos.

Domingo Díaz Díaz
Hospital Universitario Infanta Leonor, Madrid.
© REMI, http://medicina-intensiva.com. Mayo 2011.

Enlaces:

Peterson ED, Roe MT, Rumsfeld JS, Shaw RE, Brindis RG, FonarowGC, Cannon CP. A call to ACTION (Acute Coronary Treatment and Intervention Outcomes Network): a national effort to promote timely clinical feedback and support continuous quality improvement for acute myocardial infarction. Circ Cardiovasc Qual Outcomes 2009; 2: 491- 499. [PubMed]
Moscucci M, Fox KAA, Cannon CP, Klein W, Lopez-Sendon J,Montalescot G, White K, Goldberg RJ, for the GRACE Investigators. Predictors of major bleeding in acute coronary syndromes: the Global Registry of Acute Coronary Events (GRACE). Eur Heart J 2003; 24: 1815-1823. [PubMed]
Manoukian SV, Feit F, Mehran R, Voeltz MD, Ebrahimi R, Hamon M,Dangas GD, Lincoff AM, White HD, Moses JW, King SB III, OhmanEM, Stone GW. Impact of major bleeding on 30-day mortality and clinical outcomes in patients with acute coronary syndromes: an analysis from the ACUITY trial. J Am Coll Cardiol 2007; 49: 1362-1368. [PubMed]
Subherwal S, Bach RG, Chen AY, Gage BF, Rao SV, Newby LK,Wang TY, Gibler WB, Ohman EM, Roe MT, Pollack CV Jr, Peterson ED, Alexander KP. Baseline risk of major bleeding in non-ST-segment-elevation myocardial infarction: the CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes With Early Implementation of the ACC/AHA Guidelines) bleeding score. Circulation 2009; 119: 1873-1882. [PubMed]

Búsqueda en PubMed:

Enunciado: Riesgo hemorrágico en el síndrome coronario agudo
Sintaxis: hemorrhagic risk AND acute coronary syndrome[mh]
[Resultados]

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X Congreso Chileno de Mastología


	Preinscripciones abiertas Estimado/a Victor Manuel Valdes: Nos complace anunciar que las preinscripciones para el X Congreso Chileno de Mastología a realizarse del 19 al 21 de octubre de 2011 en el Hotel Patagónico de Puerto Varas ya se encuentran abiertas. Para preinscribirse en el congreso y reservar su cupo ingrese a la página deInscripciones. La preinscripción no tiene costo. La inscripción tiene los valores siguientes: Valores de inscripción hasta el 15 de julio: Socios con cuotas al día: $80.000 No socios: $90.000 Profesionales no médicos y becados: $70.000 Estos valores incluyen el acceso libre a todas las actividades paralelas de la industria, las que contarán con desayunos, almuerzos y recepciones. Para más información, visite el sitio web del evento. Secretaría de Inscripciones María José Prado Contacto: congresomastologia@mednet.cl. Fonos: (56-2) 2743013/(56-2) 3731570

Use of chloroquine in viral diseases

Use of chloroquine in viral diseases

The Lancet Infectious Diseases

online 5 May 2011

Article Outline In The Lancet Infectious Diseases, Paton and colleagues¹ report results of a clinical trial investigating chloroquine for prevention of influenza, which show that this antimalarial drug had no effect on disease acquisition and clinical course. Chloroquine, and its hydroxyl analogue hydroxychloroquine, became plausible candidates for treatment of several viral diseases after many reports of their in-vitro inhibitory effects on different viruses.² Although these effects proved highly reproducible,² the antiviral effects of chloroquine in vivo have been shown only in a mouse model for coronavirus infection.³ The antiviral effect of hydroxychloroquine was shown in two clinical trials of individuals infected with HIV-1;^[4]^and^[5] the results, however, could not be reproduced with an equivalent dose of chloroquine.⁶

Several possible reasons exist for the failure of translation of the in-vitro effects to in-vivo settings: narrow therapeutic indexes (ie, the ratio between the 50% cytotoxic concentration [CC₅₀] and the 50% antivirally effective concentration [EC₅₀]); EC₅₀ in the micromolar range (about three orders of magnitude greater than that necessary to inhibit chloroquine-sensitive malaria parasites—the microorganisms against which the drug was originally prescribed); poor penetration in specific tissues; and high interstrain variability of the effects of chloroquine on influenza A viruses.⁷ Maybe, in the future, chloroquine derivatives with improved pharmacokinetics will be able to bridge the gap between the in-vitro and in-vivo effects.

For treatment of RNA-virus infections, I think that monotherapy should be avoided because of the potential for rapid development of drug resistance. Therefore, chloroquine and hydroxychloroquine could still be considered for treatment in combination with other antiviral drugs. An effect that merits consideration is inhibition, by chloroquine, of some cellular proteins, including the P-glycoprotein and multidrug-resistance-associated proteins, which extrude drugs from the cells and other anatomic compartments.⁸ Although current anti-influenza drugs act on extracellular or transmembrane targets, new intracytosolic drug targets in the viral life cycle are being explored.⁹

My colleagues and I proposed the use of chloroquine as a therapeutic agent for some viral infections (eg, SARS and AIDS; the pathogenesis of which is characterised by deleteriously strong or persistent immune activation).² Chloroquine is a well known immunomodulatory agent, as shown by its continued use for treatment of rheumatoid arthritis and other immune-mediated diseases.² In this context, poor efficacy of this drug against pandemic influenza disease severity shown by Paton and colleagues¹ can be explained not only by absence of an antiviral effect in vivo, but also by the fact that pandemic influenza shows, in most patients, a benign clinical course and is generally uncomplicated by immune-mediated damage.

In individuals with HIV/AIDS, chloroquine was repeatedly reported to be effective in counteracting the deleterious immune activation associated with the disease.^[2]^,^[4]^and^[6] A recent study by Murray and colleagues⁶ showed that chloroquine significantly decreased expression of CD38 (a marker of treatment failure and progression to AIDS, which is associated with immune activation induced by viral replication) on CD8 T cells¹⁰ and induced downmodulation of Ki67 (a marker associated with immune-activation-induced lymphocyte mitosis) on memory T cells;¹¹ in-vitro and in-vivo anti-inflammatory effects were in good agreement. One reason behind this agreement is suggested by a recent study of hydroxychloroquine,¹² which showed that the drug accumulates at high concentrations in lymphoid tissues of patients infected with HIV. These reproducible in-vivo effects of quionoline antimalarials could be used as, or added to, new strategies for restricting the HIV reservoir, which are aimed at counteracting the residual immune activation during antiretroviral therapy (favouring sustained viral replication in anatomic sanctuaries), and targeting activation or proliferation of central and transitional memory T cells harbouring silent copies of the HIV proviral DNA (contributing to maintenance of the virus's genome during treatment).¹¹ Notwithstanding the poor efficacy of chloroquine for influenza prevention, the results reported by Paton and colleagues¹ will help to address the process of drug repositioning for treatment of infectious diseases.

I declare that I have no conflicts of interest.

References

1 NI Paton, L Lee and Y Xu et al., Chloroquine for influenza prevention: a randomised, double-blind, placebo controlled trial, Lancet Infect Dis (2011) 10.1016/S1473-3099(11)70065-2 published online May 6..

2 A Savarino, JR Boelaert, A Cassone, G Majori and R Cauda, Effects of chloroquine on viral infections: an old drug against today's diseases?, Lancet Infect Dis 3 (2003), pp. 722–727. Article |

PDF (291 K) | View Record in Scopus | Cited By in Scopus (79)

3 E Keyaerts, S Li and L Vijgen et al., Antiviral activity of chloroquine against human coronavirus OC43 infection in newborn mice, Antimicrob Agents Chemother 53 (2009), pp. 3416–3421. Full Text via CrossRef| View Record in Scopus | Cited By in Scopus (0)

4 K Sperber, M Louie and T Kraus et al., Hydroxychloroquine treatment of patients with human immunodeficiency virus type 1, Clin Ther 17 (1995), pp. 622–636. Abstract |

PDF (1030 K) | View Record in Scopus | Cited By in Scopus (51)

5 K Sperber, G Chiang and H Chen et al., Comparison of hydroxychloroquine with zidovudine in asymptomatic patients infected with human immunodeficiency virus type 1, Clin Ther 19 (1997), pp. 913–923. Abstract |

PDF (732 K) | View Record in Scopus | Cited By in Scopus (40)

6 SM Murray, CM Down and DR Boulware et al., Reduction of immune activation with chloroquine therapy during chronic HIV infection, J Virol 84 (2010), pp. 12082–12086. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (3)

7 L Di Trani, A Savarino and L Campitelli et al., Different pH requirements are associated with divergent inhibitory effects of chloroquine on human and avian influenza A viruses, Virol J 4 (2007), p. 39. Full Textvia CrossRef | View Record in Scopus | Cited By in Scopus (6)

8 M Vezmar and E Georges, Reversal of MRP-mediated doxorubicin resistance with quinoline-based drugs,Biochem Pharmacol 59 (2000), pp. 1245–1252. Article |

PDF (482 K) | View Record in Scopus | Cited By in Scopus (35)

Celis Salinas Juan Carlos

Médico Infectólogo/Tropicalista

Medicina del Viajero

CMP 40900 RNE 18872

Hospital Regional de Loreto, Iquitos, Perú

lunes, 23 de mayo de 2011

artículos sobre neumología pediátrica

@evidpediatriaEvid Pediatría

Todos los artículos sobre neumología pediátrica, a un clic http://goo.gl/Zl1x2

Web 2.0 Guru - Tools By Subject

Clasificación Internacional de la Atención Primaria, CIAP-2, traducida al castellano

Clasificación (CIAP-2)

La Clasificación Internacional de la Atención Primaria, CIAP-2, traducida al castellano

Existen clasificaciones para registrar la actividad realizada en Atención Primaria, pero solamente una se ha diseñado para describirla de forma global. Es la Clasificación Internacional de la Atención Primaria (CIAP) que permite la recogida y análisis de tres importantes componentes de la consulta médico-paciente: la razón de consulta, el problema atendido, y el proceso de atención.

Presentamos y ofrecemos la versión electrónica de la Clasificación Internacional de la Atención Primaria-2-E (CIAP-2-E) traducida al español, una herramienta diseñada para ordenar, investigar y entender mejor el contenido de la Medicina de Familia y de la Atención Primaria.

En esta introducción se repasa brevemente la historia de la CIAP hasta llegar a la última versión de la CIAP-2-E, que se puede descargar en español (sin que esta descarga implique pérdida de los derechos de copia y utilización por sus titulares).

Podéis dirigir vuestras dudas y sugerencias sobre esta traducción o la CIAP en general a ciap2E@semfyc.es.

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Recomendaciones Transtorno Depresivo
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Ayuda en consulta

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domingo, 22 de mayo de 2011

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