Hypertension causes heart failure, and antihypertensive drugs help prevent it. Some work better than others, according to a network meta-analysis of 26 trials. Diuretics looked best at preventing heart failure, followed by angiotensin converting enzyme inhibitors and angiotensin receptor blockers. Firstline treatment with β blockers or α blockers looked no more effective than placebo in these analyses, whereas calcium channel blockers worked better than placebo, definitely worse than diuretics, and probably worse than inhibitors of the renin-angiotensin system.
The authors couldn’t tell whether the differential effects on heart failure were linked to differential effects on blood pressure, but they think it unlikely. Patients with hypertension and a high risk of heart failure should probably start with diuretics or an inhibitor of the renin-angiotensin system, they write. More than 200 000 patients took part in these trials. Almost 4% (8554/223 313; 3.8%) developed heart failure during follow-up. The results were broadly comparable in men and women.
Heart failure is a neglected consequence of hypertension, and these findings should help raise its profile, says a linked comment (doi:10.1001/archinternmed.2010.414). But doctors on the front line are also trying to prevent stroke, heart attack, and cardiovascular deaths while at the same time protecting quality of life. As usual, they must juggle with medical history, likely complications, other drug treatments, and patient preferences when deciding between first line agents for high blood pressure.
BMJ 2010; 341:c6530 doi: 10.1136/bmj.c6530 (Published 16 November 2010)
Cite this as: BMJ 2010; 341:c6530
Arch Intern Med2010; doi:10.1001/archinternmed.2010.427 [PubMed Abstract]
sábado, 26 de febrero de 2011
Consensus Document on Concomitant Use of Clopidogrel and PPIs
Proton-pump inhibitors are endorsed for clopidogrel patients at high risk for gastrointestinal bleeding.
To address the somewhat confusing literature on the interaction between proton-pump inhibitors (PPIs) and clopidogrel, a new "consensus document" has been published jointly by the American College of Cardiology, American College of Gastroenterology, and American Heart Association.
Clopidogrel is converted to its active form by the hepatic enzyme CYP2C19, which is competitively inhibited by PPIs. Although platelet function studies have shown that PPI use lessens clopidogrel-mediated inhibition of platelet aggregation, the clinical relevance of this observation has been debated.
The consensus writers make the following points:
Some, but not all, observational studies have shown small statistically significant higher risk for adverse cardiovascular events among patients who received PPIs and clopidogrel concomitantly (compared with clopidogrel alone). However, in the only large randomized trial (the recently published COGENT study; JW Cardiol Oct 6 2010), patients who received omeprazole plus clopidogrel had similar rates of adverse cardiovascular events and lower rates of adverse gastrointestinal (GI) events than recipients of clopidogrel alone.
In patients with histories of upper GI bleeding and those at high risk for this complication (e.g., advanced age; concomitant use of warfarin, steroids, or nonsteroidal anti-inflammatory drugs; Helicobacter pylori infection), the benefits of PPI therapy probably outweigh the very small risk that PPI therapy will interfere with clopidogrel's efficacy.
Patients at low risk for GI bleeding who require clopidogrel therapy should not receive concomitant PPIs.
Comment: This document will disappoint readers who expect an unambiguous algorithm that is easily applied to all patients. Nevertheless, by endorsing use of PPIs for clopidogrel-treated patients at high risk for upper GI bleeding, the authors provide validation for this widespread practice.
— Allan S. Brett, MD
Published in Journal Watch General Medicine December 9, 2010
Citation:
Abraham NS et al. ACCF/ACG/AHA 2010 expert consensus document on the concomitant use of proton pump inhibitors and thienopyridines: A focused update of the ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use. J Am Coll Cardiol 2010 Dec 7; 56:2051. [Medline® Abstract]
To address the somewhat confusing literature on the interaction between proton-pump inhibitors (PPIs) and clopidogrel, a new "consensus document" has been published jointly by the American College of Cardiology, American College of Gastroenterology, and American Heart Association.
Clopidogrel is converted to its active form by the hepatic enzyme CYP2C19, which is competitively inhibited by PPIs. Although platelet function studies have shown that PPI use lessens clopidogrel-mediated inhibition of platelet aggregation, the clinical relevance of this observation has been debated.
The consensus writers make the following points:
Some, but not all, observational studies have shown small statistically significant higher risk for adverse cardiovascular events among patients who received PPIs and clopidogrel concomitantly (compared with clopidogrel alone). However, in the only large randomized trial (the recently published COGENT study; JW Cardiol Oct 6 2010), patients who received omeprazole plus clopidogrel had similar rates of adverse cardiovascular events and lower rates of adverse gastrointestinal (GI) events than recipients of clopidogrel alone.
In patients with histories of upper GI bleeding and those at high risk for this complication (e.g., advanced age; concomitant use of warfarin, steroids, or nonsteroidal anti-inflammatory drugs; Helicobacter pylori infection), the benefits of PPI therapy probably outweigh the very small risk that PPI therapy will interfere with clopidogrel's efficacy.
Patients at low risk for GI bleeding who require clopidogrel therapy should not receive concomitant PPIs.
Comment: This document will disappoint readers who expect an unambiguous algorithm that is easily applied to all patients. Nevertheless, by endorsing use of PPIs for clopidogrel-treated patients at high risk for upper GI bleeding, the authors provide validation for this widespread practice.
— Allan S. Brett, MD
Published in Journal Watch General Medicine December 9, 2010
Citation:
Abraham NS et al. ACCF/ACG/AHA 2010 expert consensus document on the concomitant use of proton pump inhibitors and thienopyridines: A focused update of the ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use. J Am Coll Cardiol 2010 Dec 7; 56:2051. [Medline® Abstract]
miércoles, 23 de febrero de 2011
Que horror !!!
Que horror, que dolor, que inconsciencia, maldita gente... Darle muerte a un jaguar fué un paso más para nuestra propia muerte. Malditos, maldita miseria, maldita ignorancia, maldito sistema !!!
Y el maldito crimen, sigue impune !!!
http://gestionterritorialmuncipal.blogspot.com/2011/01/jaguar-asesinado-descuartizado-y.html
http://gestionterritorialmuncipal.blogspot.com/2011/01/jaguar-asesinado-descuartizado-y.html
Muy acertado pensamiento !
El brillante Sir George Bernard Shaw es la única persona que ha ganado un Premio Nobel de literatura 1925 y también un Oscar en la categoría de mejor guión, por "My Fair Lady", basada en su obra Pigmalion... Él escribió esta breve frase, plena de sabiduría:
"A los políticos y a los pañales hay que cambiarlos seguido... Y por las mismas razones."
viernes, 11 de febrero de 2011
miércoles, 9 de febrero de 2011
La Dra. House !!!
Lisa Sanders, la médica detrás de los casos de “Dr. House”
Su columna sobre enfermedades raras en una revista originó la serie de la que aún es asesora. Defiende la maldad de Gregory House.
Su historia aquí: http://www.intramed.net/contenidover.asp?contenidoID=69321
Su columna sobre enfermedades raras en una revista originó la serie de la que aún es asesora. Defiende la maldad de Gregory House.
Su historia aquí: http://www.intramed.net/contenidover.asp?contenidoID=69321
Seguridad de los inhibidores de la bomba de protones al comienzo del embarazo
La exposición a inhibidores de la bomba de protones en el primer trimestre del embarazo no se asocia con un aumento significativo del riesgo de defectos congénitos importantes.
Dres. Bjorn Pasternak, Anders Hviid.N Engl J Med 2010;363:2114-23.
Dres. Bjorn Pasternak, Anders Hviid.N Engl J Med 2010;363:2114-23.
martes, 8 de febrero de 2011
What are the cardiovascular risks from NSAIDs?
The cardiovascular risk with non-steroidal anti-inflammatory drugs (NSAIDs) is a concern, and has contributed to some drugs being removed from certain markets. This group of Swiss researchers sought to analyze the evidence on cardiovascular risk of NSAIDs via a metanalysis of large scale randomized placebo-controlled trials.
They searched bibliographic databases, conference proceedings, study registers, the Food and Drug Administration website, reference lists, and the Science Citation Index, and also received additional data provided by the makers of celecoxib and lumiracoxib.
The primary outcome was myocardial infarction. Secondary outcomes included stroke, death from cardiovascular disease, and death from any cause.
The researchers report: "31 trials in 116,429 patients with more than 115,000 patient years of follow-up were included. Patients were allocated to naproxen, ibuprofen, diclofenac, celecoxib, etoricoxib, rofecoxib, lumiracoxib, or placebo.
Compared with placebo, rofecoxib was associated with the highest risk of myocardial infarction (rate ratio 2.12), followed by lumiracoxib (2.00). Ibuprofen was associated with the highest risk of stroke (3.36), followed by diclofenac (2.86). Etoricoxib (4.07) and diclofenac (3.98) were associated with the highest risk of cardiovascular death.
"The researchers concluded: "Although uncertainty remains, little evidence exists to suggest that any of the investigated drugs are safe in cardiovascular terms. Naproxen seemed least harmful. Cardiovascular risk needs to be taken into account when prescribing any non-steroidal anti-inflammatory drug."
Fuente: BMJ 342:c7086, 11 January 2011 © 2011 BMJ Publishing Group Ltd.Cardiovascular safety of non-steroidal anti-inflammatory drugs: network meta-analysis. Sven Trelle, Stephan Reichenbach, Simon Wandel, et al. Correspondence to P Jüni: juni@ispm.unibe.ch
ALT is not a reliable guide to underlying Chronic Hepatitis B
Chronic Hepatitis B (CHB) has an estimated prevalence of 90,000 to 160,000 in Australia. Cirrhosis and hepatocellular carcinoma are important complications of CHB and appropriate evaluation of HBsAg positive individuals is vital to identify treatment candidates. This study by researchers from Australia consisted of a review of the database of a tertiary hospital was performed and 348 HBsAg positive individuals with baseline demographic, virological, serological and biochemical variables were identified and evaluated cross sectionally. A small subgroup of HBeAg negative patients with normal ALT at baseline were identified and followed longitudinally.
175/348 (50%) of patients were in the HBeAg negative, chronic hepatitis phase of disease, 22% in the HBeAg positive immune clearance and 6% in the immune tolerant phases. HBeAg negative patients were older and more likely to be male than HBeAg positive patients. The correlation between HBV DNA and ALT levels was examined. ALT and HBV DNA levels showed no correlation in HBeAg positive CHB and only a weak correlation in HBeAg negative patients. Furthermore, 35% of HBeAg negative patients with detectable HBV DNA had a normal ALT. Conversely 38% of HBeAg negative patients with no detectable HBV DNA had an elevated ALT. A persistently normal ALT over 24 months was seen in 5 of 9 HBeAg negative patients with normal initial ALT and detectable HBV DNA.
The researchers concluded: "Appropriate evaluation of HBeAg negative CHB must include HBV DNA since the ALT is not a reliable guide to underlying viral replication."
Fuente: Internal Medicine Journal published online 17 January 2011 © 2011 Royal Australasian College of PhysiciansAssessment of Chronic Hepatitis B - the importance of HBV DNA testing. Catherine M.N. Croagh, Sally J. Bell, Stephen Locarnini, Paul V Desmond. Correspondence to Catherine Croagh: Catherine.Croagh@svhm.org.au
Effects of vitamin E on stroke subtypes: meta-analysis of randomised controlled trials
Markus Schurks, instructor of medicine, Robert J Glynn, associate professor of medicine and biostatistics, Pamela M Rist, doctoral student in epidemiology, Christophe Tzourio, senior director of research, Tobias Kurth, director of researchCorrespondence to: M Schurks mschuerks@rics.bwh.harvard.edu, T Kurth tobias.kurth@upmc.fr
Fig 3 Relative risks of the effect of vitamin E on haemorrhagic stroke for individual trials and for the pooled population
Abstract
Objective
To evaluate the effect of vitamin E supplementation on incident total, ischaemic, and haemorrhagic stroke.
Design
Systematic review and meta-analysis of randomised, placebo controlled trials published until January 2010.
Data sources
Electronic databases (Medline, Embase, Cochrane Central Register of Controlled Trials) and reference lists of trial reports.Selection criteria Randomised, placebo controlled trials with ≥1 year of follow-up investigating the effect of vitamin E on stroke.
Review methods and data extraction
Two investigators independently assessed eligibility of identified trials. Disagreements were resolved by consensus. Two different investigators independently extracted data. Risk ratios (and 95% confidence intervals) were calculated for each trial based on the number of cases and non-cases randomised to vitamin E or placebo. Pooled effect estimates were then calculated.
Results
Nine trials investigating the effect of vitamin E on incident stroke were included, totalling 118 765 participants (59 357 randomised to vitamin E and 59 408 to placebo). Among those, seven trials reported data for total stroke and five trials each for haemorrhagic and ischaemic stroke. Vitamin E had no effect on the risk for total stroke (pooled relative risk 0.98 (95% confidence interval 0.91 to 1.05), P=0.53). In contrast, the risk for haemorrhagic stroke was increased (pooled relative risk 1.22 (1.00 to 1.48), P=0.045), while the risk of ischaemic stroke was reduced (pooled relative risk 0.90 (0.82 to 0.99), P=0.02). There was little evidence for heterogeneity among studies. Meta-regression did not identify blinding strategy, vitamin E dose, or morbidity status of participants as sources of heterogeneity. In terms of absolute risk, this translates into one additional haemorrhagic stroke for every 1250 individuals taking vitamin E, in contrast to one ischaemic stroke prevented per 476 individuals taking vitamin E.
Conclusion In this meta-analysis, vitamin E increased the risk for haemorrhagic stroke by 22% and reduced the risk of ischaemic stroke by 10%. This differential risk pattern is obscured when looking at total stroke. Given the relatively small risk reduction of ischaemic stroke and the generally more severe outcome of haemorrhagic stroke, indiscriminate widespread use of vitamin E should be cautioned against.
Fuente: BMJ 2010; 341:c5702 doi: 10.1136/bmj.c5702 (Published 4 November 2010)
Resultados del uso de Sibutramina y Orlistat en adolescentes
Los médicos han respondido a la epidemia global de obesidad entre niños y adolescentes con un incremento en las prescripciones de Orlistat y Sibutramina, pero no hay muchos estudios independientes que analicen la seguridad y eficacia de las drogas disponibles en el mercado. Es por esta razón que el Dr. Vinner y su equipo del Instituto de Salud Infantil de Londres decidieron realizar un análisis de los efectos de ambos medicamentos para evaluar el nivel de eficacia y seguridad de las drogas antiobesidad utilizadas actualmente.
El Orlistat es un inhibidor de las lipasas gástrica y pancreática, y la sibutramina es un inhibidor de la recaptación de serotonina y noradrenalina. Hasta hace algunos años también se utilizaba el Rimonabant, pero este medicamento ya ha sido retirado del mercado.
El Dr Vinner y su equipo realizaron un análisis de los resultados de estudios realizados entre 1996 y julio del 2008. Se buscaron estudios en las bases de datos MEDLINE, EMBASE, y el Cochrane Central Register of Controlled Trials (CENTRAL). Se recuperaron datos de seis ensayos, 4 de sibutramina con 686 pacientes y dos de Orlistat con 573 pacientes en total, luego se analizaron los datos con un modelo de efectos aleatorios.
En comparación con Placebo, la sibutramina sumada al apoyo conductual logró una reducción del IMC en 2,20 Kg/m2, mientras que el Orlistat en combinación con apoyo conductual logró una reducción del IMC en 0,83 kg/m2.
Con la Sibutramina se consiguió una mejora en la circunferencia de la cintura, así como de los niveles de triglicéridos y colesterol (lipoproteína de alta densidad (HDL) y colesterol total), pero su uso incrementó los niveles de presión arterial sistólica y diastólica, y la frecuencia cardíaca. El Orlistat por otro lado, incrementó el riesgo de efectos adversos gastrointestinales.
El Orlistat es un inhibidor de las lipasas gástrica y pancreática, y la sibutramina es un inhibidor de la recaptación de serotonina y noradrenalina. Hasta hace algunos años también se utilizaba el Rimonabant, pero este medicamento ya ha sido retirado del mercado.
El Dr Vinner y su equipo realizaron un análisis de los resultados de estudios realizados entre 1996 y julio del 2008. Se buscaron estudios en las bases de datos MEDLINE, EMBASE, y el Cochrane Central Register of Controlled Trials (CENTRAL). Se recuperaron datos de seis ensayos, 4 de sibutramina con 686 pacientes y dos de Orlistat con 573 pacientes en total, luego se analizaron los datos con un modelo de efectos aleatorios.
En comparación con Placebo, la sibutramina sumada al apoyo conductual logró una reducción del IMC en 2,20 Kg/m2, mientras que el Orlistat en combinación con apoyo conductual logró una reducción del IMC en 0,83 kg/m2.
Con la Sibutramina se consiguió una mejora en la circunferencia de la cintura, así como de los niveles de triglicéridos y colesterol (lipoproteína de alta densidad (HDL) y colesterol total), pero su uso incrementó los niveles de presión arterial sistólica y diastólica, y la frecuencia cardíaca. El Orlistat por otro lado, incrementó el riesgo de efectos adversos gastrointestinales.
Manejo de intolerancia a la lactosa
La intolerancia a la lactosa en centros de salud ha sido un problema frecuente, el diagnóstico y manejo de este mal ha sido siempre un tema complicado, por ello un equipo de investigadores del Minnesota Evidence-based Practice Center, en Maryland, USA, realizó un estudio para determinar cuál es la máxima dosis tolerable de la lactosa entre los sujetos afectados e identificar prácticas exitosas en el manejo de la intolerancia a la lactosa. En líneas generales, el estudio identificó que una tasa de leche es una dosis que es bien tolerada por la mayoría de adultos.
Los investigadores recurrieron a ensayos con registro en MEDLINE, la base de datos del Commonwealth Agricultural Bureau International, el Cochrane Central Register of Controlled Trials, BIOSIS Previews, Biological Abstracts, Global Health y el Food Science and Technology Abstracts entre 1967 y noviembre del 2009.
Se identificaron 36 ensayos con datos relevantes, con registros de 975 pacientes. Entre los ensayos seleccionados se identificaron 26 sobre suplementos con leche hidrolizada, leche reducida en lactosa o con la dosis tolerable de disacárido; siete ensayos de trabajos con probióticos, dos con dosis incrementales de lactosa para adaptación colónica y un estudio utilizando otro agente.
El estudio identificó que la mayoría de adultos afectados por intolerancia, soportan de 12 a 15 gramos de lactosa (el equivalente a una tasa de leche), sin embargo no se recopiló evidencia suficiente que pudiera sostener si las soluciones bajas en lactosa o leche con un contenido de disacárido menor a dos gramos, resulta efectiva para reducir los síntomas de la intolerancia, en comparación con la ingestión de 12 gramos.
La evidencia acerca del uso de probióticos, la adaptación colónica y otros agentes también fue insuficiente. Fue una limitante identificar estudios que evaluaron pacientes con malabsorción por lactosa en vez de intolerancia. Los estudios tenían criterios de inclusión, medidas de evolución y otros factores dispares que no permitieron realizar una síntesis de resultados y limitaron una interpretación óptima.
Cabe resaltar que el la revisión sistemática de Shaukat y colegas, se determinó también que las personas con intolerancia a la lactosa podían ingerir 12 gramos de lactosa sin experimentar síntomas relevantes, además se podía incrementar la dosis hasta 20 gramos cuando se administra con otros nutrientes, y se determinó que una ingestión de 50 gramos de lactosa provoca síntomas en la mayoría de pacientes con intolerancia a la latosa.
Los investigadores recurrieron a ensayos con registro en MEDLINE, la base de datos del Commonwealth Agricultural Bureau International, el Cochrane Central Register of Controlled Trials, BIOSIS Previews, Biological Abstracts, Global Health y el Food Science and Technology Abstracts entre 1967 y noviembre del 2009.
Se identificaron 36 ensayos con datos relevantes, con registros de 975 pacientes. Entre los ensayos seleccionados se identificaron 26 sobre suplementos con leche hidrolizada, leche reducida en lactosa o con la dosis tolerable de disacárido; siete ensayos de trabajos con probióticos, dos con dosis incrementales de lactosa para adaptación colónica y un estudio utilizando otro agente.
El estudio identificó que la mayoría de adultos afectados por intolerancia, soportan de 12 a 15 gramos de lactosa (el equivalente a una tasa de leche), sin embargo no se recopiló evidencia suficiente que pudiera sostener si las soluciones bajas en lactosa o leche con un contenido de disacárido menor a dos gramos, resulta efectiva para reducir los síntomas de la intolerancia, en comparación con la ingestión de 12 gramos.
La evidencia acerca del uso de probióticos, la adaptación colónica y otros agentes también fue insuficiente. Fue una limitante identificar estudios que evaluaron pacientes con malabsorción por lactosa en vez de intolerancia. Los estudios tenían criterios de inclusión, medidas de evolución y otros factores dispares que no permitieron realizar una síntesis de resultados y limitaron una interpretación óptima.
Cabe resaltar que el la revisión sistemática de Shaukat y colegas, se determinó también que las personas con intolerancia a la lactosa podían ingerir 12 gramos de lactosa sin experimentar síntomas relevantes, además se podía incrementar la dosis hasta 20 gramos cuando se administra con otros nutrientes, y se determinó que una ingestión de 50 gramos de lactosa provoca síntomas en la mayoría de pacientes con intolerancia a la latosa.
lunes, 7 de febrero de 2011
domingo, 6 de febrero de 2011
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