Los kilos de más no sólo perjudican al corazón, las articulaciones o el control de la glucosa, entre otros factores. También suponen un escollo importante a la hora de luchar contra los virus y hacer frente a las infecciones, según una reciente investigación.
Los datos de este trabajo, que se publican en el último número de la revista 'International Journal of Obesity', muestran que las personas con obesidad son menos sensibles a la vacuna de la gripe, es decir, tienen más probabilidades de que la inmunización no surta efecto en sus organismos.
"Nuestros resultados sugieren que la obesidad podría frenar la capacidad de crear una respuesta inmune protectora frente a los virus de la gripe", señalan los investigadores, de la Universidad de North Carolina (EEUU), en la revista médica.
"De todas maneras, no estamos diciendo que la vacuna contra la gripe sea inefectiva para las personas con obesidad, sólo que su respuesta inmune no es tan robusta como la de las personas sanas", aclara a ELMUNDO.es Melinda Beck, principal firmante del trabajo. "A día de hoy aún no tenemos datos suficientes para saber si las personas obesas vacunadas tienen más riesgo de desarrollar gripe que las personas sanas", subraya.
-La investigación
Su equipo realizó un seguimiento a casi 500 pacientes que se habían vacunado frente a la gripe estacional en 2009 en una clínica de Chapel Hill (EEUU). En un primer análisis, un mes después de la inmunización, los investigadores comprobaron que todos los individuos vacunados –tanto los que estaban delgados, como los que presentaban un índice de masa corporal por encima de lo normal- habían desarrollado anticuerpos contra el virus de la gripe.
Sin embargo, un año después del 'pinchazo' las cosas eran bien diferentes. Casi un 50% de los individuos con sobrepeso habían experimentado una caída significativa en sus niveles de anticuerpo (hasta cuatro veces el valor inicial), mientras que este decrecimiento sólo era patente en un 25% de los participantes sin exceso de peso.
Es más, en ese momento, hasta el 75% de las personas delgadas era capaz de activar sus defensas y producir una proteína clave en la lucha contra el virus de la gripe. En cambio, sólo lograba hacerlo el 25% de los pacientes obesos, según pusieron de manifiesto varias pruebas en el laboratorio.
"Durante la reciente pandemia de gripe A/H1N1, la obesidad se reconoció por primera vez como un factor de riego independiente de morbilidad y mortalidad [...] Sin embargo, ningún estudio hasta ahora había examinado cómo afecta la obesidad a la respuesta de la vacunación", comentan los investigadores en el trabajo.
"Nuestros datos", continúan, "sugieren un mecanismo que explica ese elevado riesgo de enfermedad severa entre la población obesa", aunque, subrayan, "son necesarios más trabajos" que determinen a fondo esta relación.
Según la hipótesis de Beck, la clave podría estar en los cambios en las secreciones hormonales que se producen en las personas obesas –los altos niveles de leptina que se producen con el sobrepeso podrían afectar a las células inmunitarias- o en el impacto que produce la grasa en las membranas celulares.
Averiguar los mecanismos subyacentes de esta asociación y dilucidar si la "protección contra la gripe está comprometida en pacientes obesos que hayan recibido la vacuna" serán los siguientes pasos en la investigación, señala Beck, quien recuerda que otros estudios ya han señalado que las personas con sobrepeso tienen una peor respuesta a las vacunas contra la hepatitis o el tétanos.
"En mi opinión, los individuos obesos tienen una peor respuesta a las vacunas en general", concluye.
**Publicado en "EL MUNDO"
26 October 2011
Doctors happily cite alcohol as cause of death, but not smoking, for fear of stigmatization
UK doctors are willing to cite alcohol as a cause of death on death certificates, but not smoking, for fear of stigmatising the deceased, shows research published online in the Journal of Clinical Pathology. This has implications for the true extent of the impact of smoking on health, say the researchers, who point out that the current statistical estimates of the death toll from smoking are potentially flawed.
They looked at just over 2,000 death certificates and 236 post mortem reports, issued at a large London teaching hospital between 2003 and 2009, to see what cause of death doctors had cited.
Doctors have been allowed to cite smoking and alcohol as a direct or underlying cause of death without the need to refer the case to a coroner since 1992.
Smoking was identified as the cause of death in only two certificates (0.1% of the total) and included in part II of the death certificate, which outlines other contributory conditions, in only 10 cases (0.5% of the total).
The two cases in which smoking was cited were lung cancer and chronic obstructive pulmonary disease (COPD). Yet 279 deaths included these diagnoses, and in most cases the deceased was a current (over 45%) or former (over 23%) smoker. It is well known that smoking is the primary cause of both lung cancer and COPD.
In all, 407 deaths were caused by conditions in which smoking is thought to have a substantial role. Yet smoking was cited as the cause of death in only two of these certificates and as a contributory factor in six.
The post mortem reports were no better: not a single case cited smoking as causing or contributing to death, which the authors describe as "surprising."
Yet doctors willingly cited alcohol as a direct or contributory cause of death. This was cited in over half (57.4%) of the 54 death certificates, which included diagnoses linked to alcohol use.
"Death certification is an important source of mortality data and directly captures 99.79% of all deaths in the UK," say the authors, who point out that the doctors in this study are not unique in their reluctance to cite smoking as a cause of death.
"There are many reasons why smoking is not cited as a [cause of death] by doctors in the UK," they write. "The first and frequently debated reason relates to doctors' desire not to cause relatives distress by stigmatising the deceased and their smoking habit."
They continue: "While the results of this study would support this assumption, it is interesting that the same clinicians frequently cited alcohol use as an underlying cause of death."
This may be because alcohol use is generally more accepted culturally, suggest the authors, adding that the stigma associated with smoking is well documented, and may be worsening as a result of the recent legislation, banning smoking in public places.
"Given the overwhelming evidence showing a causal link between smoking and certain terminal conditions, more effort should be made to record smoking on the death certificate. It is clear that the current arrangements fail to achieve this," they conclude.
**Source: BMJ-British Medical Journal
They looked at just over 2,000 death certificates and 236 post mortem reports, issued at a large London teaching hospital between 2003 and 2009, to see what cause of death doctors had cited.
Doctors have been allowed to cite smoking and alcohol as a direct or underlying cause of death without the need to refer the case to a coroner since 1992.
Smoking was identified as the cause of death in only two certificates (0.1% of the total) and included in part II of the death certificate, which outlines other contributory conditions, in only 10 cases (0.5% of the total).
The two cases in which smoking was cited were lung cancer and chronic obstructive pulmonary disease (COPD). Yet 279 deaths included these diagnoses, and in most cases the deceased was a current (over 45%) or former (over 23%) smoker. It is well known that smoking is the primary cause of both lung cancer and COPD.
In all, 407 deaths were caused by conditions in which smoking is thought to have a substantial role. Yet smoking was cited as the cause of death in only two of these certificates and as a contributory factor in six.
The post mortem reports were no better: not a single case cited smoking as causing or contributing to death, which the authors describe as "surprising."
Yet doctors willingly cited alcohol as a direct or contributory cause of death. This was cited in over half (57.4%) of the 54 death certificates, which included diagnoses linked to alcohol use.
"Death certification is an important source of mortality data and directly captures 99.79% of all deaths in the UK," say the authors, who point out that the doctors in this study are not unique in their reluctance to cite smoking as a cause of death.
"There are many reasons why smoking is not cited as a [cause of death] by doctors in the UK," they write. "The first and frequently debated reason relates to doctors' desire not to cause relatives distress by stigmatising the deceased and their smoking habit."
They continue: "While the results of this study would support this assumption, it is interesting that the same clinicians frequently cited alcohol use as an underlying cause of death."
This may be because alcohol use is generally more accepted culturally, suggest the authors, adding that the stigma associated with smoking is well documented, and may be worsening as a result of the recent legislation, banning smoking in public places.
"Given the overwhelming evidence showing a causal link between smoking and certain terminal conditions, more effort should be made to record smoking on the death certificate. It is clear that the current arrangements fail to achieve this," they conclude.
**Source: BMJ-British Medical Journal
Los científicos quieren ser más rigurosos con sus estudios
"Cuesta un poco reconocer que las cosas no siempre se hacen con todo el rigor necesario". Miquel Porta, coordinador del grupo de investigación en epidemiología clínica y molecular del cáncer del Instituto de Investigación Hospital del Mar (IMIM) de Barcelona, admite que muchos estudios contienen deficiencias importantes que restan validez a los hallazgos. "Pero, por otra parte, los investigadores siempre hemos contado con directrices y la comunicación científica dispone de mecanismos para regularse", añade. Porta forma parte de un grupo internacional de científicos que ha elaborado unas normas para comunicar los estudios de factores de riesgo genético y molecular de forma más precisa y ética.
Las nuevas pautas, publicadas simultáneamente en siete revistas científicas, instan a contar con más detalle cómo se llevan a cabo los ensayos sobre los factores de riesgo que ayudan, entre otras cosas, a predecir el riesgo de sufrir una determinada enfermedad, o bien a diagnosticarla. Por ejemplo, la mutación de un gen o la presencia de cantidades elevadas de una proteína en sangre. Se trata de los denominados biomarcadores, cuyo uso se ha extendido rápidamente en los últimos tiempos y que han propiciado grandes avances, pero no han estado exentos de polémica.
"Efectivamente, se han generado falsas expectativas porque tendemos a exagerar las implicaciones de nuestros hallazgos", asevera Porta. La revista 'The Journal of the American Medical Association' ('JAMA') publicó este verano un artículo que constató que buena parte de los estudios con resultados muy positivos han sido posteriormente rebatidos por trabajos más amplios o revisiones sistemáticas. Es lo que sucedió con la vinculación entre la proteína C reactiva en sangre y las enfermedades cardiovasculares, así como con el gen BRCA1 y el riesgo de cáncer de colon.
Los investigadores publican preferentemente los estudios con resultados positivos, guardando en el cajón los que no les han llevado a las conclusiones deseadas. Pero es que los propios directores de revistas científicas desechan los ensayos cuyos descubrimientos no son 'redondos'.
Porta cita como ejemplo de lo que no se debe hacer las investigaciones realizadas hace algunos años que observaron una asociación entre un alto nivel de pesticidas en el cuerpo y un mayor riesgo de cáncer de mama. "Esos resultados iniciales no se confirmaron, pero tampoco es que se hayan descartado", comenta. "Los trabajos que se realizaron posteriormente no se hicieron bien y, finalmente, se abandonó esa línea de investigación", resume.
En el ámbito de la genética, el panorama es, según el epidemiólogo barcelonés, "desolador", ya que "sólo se confirma el 0,2% de los hallazgos que relacionan un gen con una enfermedad". Ante esta situación, las nuevas directrices se perfilan como un paso obligado. Lógicamente, no se puede forzar a ningún científico a que las cumpla, pero las revistas que las suscriben ('PLoS Medicine, 'European Journal of Clinical Investigation', 'European Journal of Epidemiology, 'Journal of Epidemiology and Community Health, 'Journal of Clinical Epidemiology', 'Preventive Medicine y 'Mutagenesis') se han comprometido a publicar sólo aquellos estudios que se ajusten a ellas.
Por otro lado, la experiencia muestra que las anteriores directrices, referidas a otros aspectos de la investigación, han servido como revulsivo para reducir las malas prácticas. Bajo el nombre de STROBE-ME (acrónimo en inglés de Fortaleciendo la Conmunicación de los Estudios Observacionales en Epidemiología-Epidemiología Molecular), se recoge el conjunto de recomendaciones que ayudarán a los investigadores a contar de forma más completa y precisa los resultados de sus trabajos, de tal manera que la comunidad científica pueda evaluar sus puntos fuertes y débiles e interpretar claramente los resultados. Los promotores de STROBE-ME harán un seguimiento para comprobar el grado de cumplimiento de la iniciativa.
**Publicado en "EL MUNDO"
Las nuevas pautas, publicadas simultáneamente en siete revistas científicas, instan a contar con más detalle cómo se llevan a cabo los ensayos sobre los factores de riesgo que ayudan, entre otras cosas, a predecir el riesgo de sufrir una determinada enfermedad, o bien a diagnosticarla. Por ejemplo, la mutación de un gen o la presencia de cantidades elevadas de una proteína en sangre. Se trata de los denominados biomarcadores, cuyo uso se ha extendido rápidamente en los últimos tiempos y que han propiciado grandes avances, pero no han estado exentos de polémica.
"Efectivamente, se han generado falsas expectativas porque tendemos a exagerar las implicaciones de nuestros hallazgos", asevera Porta. La revista 'The Journal of the American Medical Association' ('JAMA') publicó este verano un artículo que constató que buena parte de los estudios con resultados muy positivos han sido posteriormente rebatidos por trabajos más amplios o revisiones sistemáticas. Es lo que sucedió con la vinculación entre la proteína C reactiva en sangre y las enfermedades cardiovasculares, así como con el gen BRCA1 y el riesgo de cáncer de colon.
Los investigadores publican preferentemente los estudios con resultados positivos, guardando en el cajón los que no les han llevado a las conclusiones deseadas. Pero es que los propios directores de revistas científicas desechan los ensayos cuyos descubrimientos no son 'redondos'.
Porta cita como ejemplo de lo que no se debe hacer las investigaciones realizadas hace algunos años que observaron una asociación entre un alto nivel de pesticidas en el cuerpo y un mayor riesgo de cáncer de mama. "Esos resultados iniciales no se confirmaron, pero tampoco es que se hayan descartado", comenta. "Los trabajos que se realizaron posteriormente no se hicieron bien y, finalmente, se abandonó esa línea de investigación", resume.
En el ámbito de la genética, el panorama es, según el epidemiólogo barcelonés, "desolador", ya que "sólo se confirma el 0,2% de los hallazgos que relacionan un gen con una enfermedad". Ante esta situación, las nuevas directrices se perfilan como un paso obligado. Lógicamente, no se puede forzar a ningún científico a que las cumpla, pero las revistas que las suscriben ('PLoS Medicine, 'European Journal of Clinical Investigation', 'European Journal of Epidemiology, 'Journal of Epidemiology and Community Health, 'Journal of Clinical Epidemiology', 'Preventive Medicine y 'Mutagenesis') se han comprometido a publicar sólo aquellos estudios que se ajusten a ellas.
Por otro lado, la experiencia muestra que las anteriores directrices, referidas a otros aspectos de la investigación, han servido como revulsivo para reducir las malas prácticas. Bajo el nombre de STROBE-ME (acrónimo en inglés de Fortaleciendo la Conmunicación de los Estudios Observacionales en Epidemiología-Epidemiología Molecular), se recoge el conjunto de recomendaciones que ayudarán a los investigadores a contar de forma más completa y precisa los resultados de sus trabajos, de tal manera que la comunidad científica pueda evaluar sus puntos fuertes y débiles e interpretar claramente los resultados. Los promotores de STROBE-ME harán un seguimiento para comprobar el grado de cumplimiento de la iniciativa.
**Publicado en "EL MUNDO"
Increased tanning bed use increases risk for deadly skin cancers
Researchers confirmed an association between tanning bed use and an increased risk for three common skin cancers -- basal cell carcinoma, squamous cell carcinoma and melanoma, according to results presented at the 10th AACR International Conference on Frontiers in Cancer Prevention Research, held Oct. 22-25, 2011. The popularity of indoor tanning is widespread, with roughly 10 percent of Americans using a tanning facility each year. However, use of tanning beds has been shown to be associated with an increased risk for skin cancer, according to lead researcher Mingfeng Zhang, M.D., research fellow in the department of dermatology at Brigham and Women's Hospital and Harvard Medical School in Boston.
For this cohort study, Zhang and colleagues followed 73,494 nurses who participated in the Nurses' Health Study II from 1989 to 2009. They tracked tanning bed use during high school and college and when women were aged between 25 and 35 years old. They also tracked the overall average usage during both periods in relation to basal cell carcinoma, squamous cell carcinoma and melanoma.
Results showed that tanning bed use increased skin cancer risk with a dose-response effect. More tanning bed exposure led to higher risks. Compared with nonusers, the risk for basal cell carcinoma and squamous cell carcinoma increased by 15 percent for every four visits made to a tanning booth per year; the risk for melanoma increased by 11 percent.
"The use during high school/college had a stronger effect on the increased risk for basal cell carcinoma compared with use during ages 25 to 35," Zhang said.
"These results have a public health impact on skin cancer prevention for all three types of skin cancer," she said. "[They] can be used to warn the public against future use of tanning beds and to promote restrictions on the indoor tanning industry by policymakers."
In follow-up studies, the researchers plan to monitor skin cancer incidence and to assess the association with tanning bed usage in this cohort during a longer term.
*Source: American Association for Cancer Research
For this cohort study, Zhang and colleagues followed 73,494 nurses who participated in the Nurses' Health Study II from 1989 to 2009. They tracked tanning bed use during high school and college and when women were aged between 25 and 35 years old. They also tracked the overall average usage during both periods in relation to basal cell carcinoma, squamous cell carcinoma and melanoma.
Results showed that tanning bed use increased skin cancer risk with a dose-response effect. More tanning bed exposure led to higher risks. Compared with nonusers, the risk for basal cell carcinoma and squamous cell carcinoma increased by 15 percent for every four visits made to a tanning booth per year; the risk for melanoma increased by 11 percent.
"The use during high school/college had a stronger effect on the increased risk for basal cell carcinoma compared with use during ages 25 to 35," Zhang said.
"These results have a public health impact on skin cancer prevention for all three types of skin cancer," she said. "[They] can be used to warn the public against future use of tanning beds and to promote restrictions on the indoor tanning industry by policymakers."
In follow-up studies, the researchers plan to monitor skin cancer incidence and to assess the association with tanning bed usage in this cohort during a longer term.
*Source: American Association for Cancer Research
CT scans for lung cancer screening may be beneficial in detecting COPD
Among men who were current or former heavy smokers, undergoing lung cancer screening with computed tomography (CT) scanning identified a substantial proportion who had chronic obstructive pulmonary disease (COPD), suggesting that this method may be helpful as an additional tool in detecting COPD, according to a study in the Oct. 26 issue of JAMA. "Smoking is annually projected to cause more than 8 million deaths worldwide in the coming decades. Besides cardiovascular disease and cancer, chronic obstructive pulmonary disease is a major cause of death in heavy smokers. Nevertheless, COPD is substantially underdiagnosed. Despite a decrease in cardiovascular mortality and stabilization of cancer mortality worldwide, mortality from COPD is increasing," according to background information in the article. Early cessation of smoking can prevent COPD progression, underscoring the importance of early detection. Computed tomography-based lung cancer screening may provide an opportunity to detect individuals with COPD at an early stage.
Onno M. Mets, M.D., of the University Medical Center Utrecht, the Netherlands, and colleagues conducted a study to examine whether low-dose lung cancer screening CT scans could be used to identify participants with COPD. The study, conducted within an ongoing lung cancer screening trial, included prebronchodilator pulmonary function testing with inspiratory (inhalation of air into the lungs) and expiratory (exhalation of air from the lungs) CT scans performed on the same day from 1,140 male participants between July 2007 and September 2008. The pulmonary function tests were used as the reference standard in determining the COPD diagnostic accuracy of the CT scans.
The average age of participants was 62.5 years. Data for self-reported respiratory symptoms were available from 1,085 participants; a total of 566 participants were symptomatic, and 519 participants were asymptomatic. Forty-one participants (3.6 percent) reported physician-diagnosed emphysema and 93 (8.2 percent), bronchitis. Based on the results of pulmonary function testing, 437 participants (38 percent) were classified as having COPD.
The final diagnostic model for the study included 5 factors independently associated with obstructive pulmonary disease: CT emphysema, CT air trapping (an abnormal retention of air in the lungs), body mass index, pack-years (the number of packs of cigarettes smoked per day multiplied by the number of years the person has smoked), and smoking status. Using the point of optimal accuracy, the model identified 274 participants with COPD with 85 false-positives, a sensitivity of 63 percent, a specificity of 88 percent, and a positive predictive value of 76 percent, which corresponds to 63 percent (274 of 437) of all participants with COPD. These 274 participants comprised 54 percent (150 of 277) of all participants with mild obstruction, 73 percent (99 of 135) of all participants with moderate obstruction, and 100 percent (25 of 25) of all participants with severe obstruction.
"Our study findings suggest several practical considerations. If the results of this study are validated and confirmed and are found to be generalizable, it may be reasonable to consider adding an expiratory CT scan to the (baseline) inspiratory CT scan for additional evaluation of COPD because this would improve diagnostic accuracy. Although an additional ultralow-dose expiration CT scan increases the radiation dose, this exposure is limited. The additional scan can be obtained within the 5 minutes needed for lung cancer screening, so a substantial amount of extra scan time is not required," the authors write.
The researchers add that this possible strategy of using quantitative CT for detection of airflow limitation is not proposed as a primary screening method for COPD, for which pulmonary function testing is the preferred method. "A screening test should have a high sensitivity to identify most of the participants with unsuspected disease, and the performance of our strategy at optimal accuracy is not sufficient for CT to serve as a COPD screening test."
**Source: JAMA and Archives Journals
Onno M. Mets, M.D., of the University Medical Center Utrecht, the Netherlands, and colleagues conducted a study to examine whether low-dose lung cancer screening CT scans could be used to identify participants with COPD. The study, conducted within an ongoing lung cancer screening trial, included prebronchodilator pulmonary function testing with inspiratory (inhalation of air into the lungs) and expiratory (exhalation of air from the lungs) CT scans performed on the same day from 1,140 male participants between July 2007 and September 2008. The pulmonary function tests were used as the reference standard in determining the COPD diagnostic accuracy of the CT scans.
The average age of participants was 62.5 years. Data for self-reported respiratory symptoms were available from 1,085 participants; a total of 566 participants were symptomatic, and 519 participants were asymptomatic. Forty-one participants (3.6 percent) reported physician-diagnosed emphysema and 93 (8.2 percent), bronchitis. Based on the results of pulmonary function testing, 437 participants (38 percent) were classified as having COPD.
The final diagnostic model for the study included 5 factors independently associated with obstructive pulmonary disease: CT emphysema, CT air trapping (an abnormal retention of air in the lungs), body mass index, pack-years (the number of packs of cigarettes smoked per day multiplied by the number of years the person has smoked), and smoking status. Using the point of optimal accuracy, the model identified 274 participants with COPD with 85 false-positives, a sensitivity of 63 percent, a specificity of 88 percent, and a positive predictive value of 76 percent, which corresponds to 63 percent (274 of 437) of all participants with COPD. These 274 participants comprised 54 percent (150 of 277) of all participants with mild obstruction, 73 percent (99 of 135) of all participants with moderate obstruction, and 100 percent (25 of 25) of all participants with severe obstruction.
"Our study findings suggest several practical considerations. If the results of this study are validated and confirmed and are found to be generalizable, it may be reasonable to consider adding an expiratory CT scan to the (baseline) inspiratory CT scan for additional evaluation of COPD because this would improve diagnostic accuracy. Although an additional ultralow-dose expiration CT scan increases the radiation dose, this exposure is limited. The additional scan can be obtained within the 5 minutes needed for lung cancer screening, so a substantial amount of extra scan time is not required," the authors write.
The researchers add that this possible strategy of using quantitative CT for detection of airflow limitation is not proposed as a primary screening method for COPD, for which pulmonary function testing is the preferred method. "A screening test should have a high sensitivity to identify most of the participants with unsuspected disease, and the performance of our strategy at optimal accuracy is not sufficient for CT to serve as a COPD screening test."
**Source: JAMA and Archives Journals
Un estudio revela que el yoga mejora los síntomas en el dolor de espalda
El yoga es una disciplina de origen indio que tiene fama de equilibrar cuerpo y mente, pero además se ha revelado, junto con los estiramientos, como analgésico eficaz contra el dolor de espalda crónico. Así se desprende del mayor estudio sobre las propiedades de esta actividad realizado en EE.UU. hasta la fecha, y que ha sido publicado en la revista «Archives of Internal Medicine».
En el estudio participaron 228 adultos con dolores de espalda moderados, que fueron divididos en tres grupos: unos practicaron yoga, otros estiramientos y a otros se les dio un libro de autocuidado que explicaba como evitar las molestias.
«Las clases de yoga fueron más efectivas que el manual, pero igual de buenas que los estiramientos», asegura el doctor Karen J. Sherman, autor principal del estudio.
Los dolores disminuyeron y las funciones de la espalda mejoraron tras 12 semanas practicando yoga, además de obtener importantes beneficios clínicos, incluido un menor consumo de medicamentos para las molestias.
El tipo de yoga utilizado para este estudio fue el «viniyoga», que adapta los principios de esta disciplina a la condición física de cada individuo. Además incluía ejercicios de respiración y una gran relajación al final de la clase.
«Nuestros resultados sugieren que tanto el yoga como los estiramientos son opciones buenas y seguras para aquellos que quieran probar la actividad física para aliviar sus dolores de espalda», concluye el doctor Sherman, que matiza: «Es importante que las clases estén orientadas por un terapeuta que sepa adaptar las posturas a las limitaciones de los participantes».
En el estudio participaron 228 adultos con dolores de espalda moderados, que fueron divididos en tres grupos: unos practicaron yoga, otros estiramientos y a otros se les dio un libro de autocuidado que explicaba como evitar las molestias.
«Las clases de yoga fueron más efectivas que el manual, pero igual de buenas que los estiramientos», asegura el doctor Karen J. Sherman, autor principal del estudio.
Los dolores disminuyeron y las funciones de la espalda mejoraron tras 12 semanas practicando yoga, además de obtener importantes beneficios clínicos, incluido un menor consumo de medicamentos para las molestias.
El tipo de yoga utilizado para este estudio fue el «viniyoga», que adapta los principios de esta disciplina a la condición física de cada individuo. Además incluía ejercicios de respiración y una gran relajación al final de la clase.
«Nuestros resultados sugieren que tanto el yoga como los estiramientos son opciones buenas y seguras para aquellos que quieran probar la actividad física para aliviar sus dolores de espalda», concluye el doctor Sherman, que matiza: «Es importante que las clases estén orientadas por un terapeuta que sepa adaptar las posturas a las limitaciones de los participantes».
**Publicado en "Vocento"
Researchers identify factors associated with increased risk of blood clot within coronary stent
Patients with certain genes or specific factors related to use of the anti-clotting drug clopidogrel are more likely to experience a blood clot within a coronary stent shortly after placement, according to a study in the October 26 issue of JAMA. "Percutaneous coronary intervention [PCI; procedures such as balloon angioplasty or stent placement used to open narrowed coronary arteries] with stent implantation has become the standard of care for myocardial revascularization, especially in the setting of unstable coronary artery disease. Despite the use of dual antiplatelet therapy (DAPT; aspirin and clopidogrel), which reduces cardiovascular events after PCI by more than 80 percent, definite stent thrombosis [blood clot] remains a concern," according to background information in the article. Stent thrombosis can be a devastating (mortality rate up to 40 percent) and unpredictable complication of PCI. The majority of stent thromboses occur in the first month after placement and are defined as early stent thrombosis.
Guillaume Cayla, M.D., Ph.D., of the Pitie-Salpetriere Hospital, Paris, and colleagues conducted an analysis of clinical and genetic factors associated with definite early stent thrombosis. The study, conducted in 10 centers in France between January 2007 and May 2010, included 123 patients undergoing PCI who had definite early stent thrombosis (within 30 days of stent implantation) and DNA samples available, matched on age and sex with 246 stent thrombosis-free controls. The primary outcome measured was the accuracy of prediction of early stent thrombosis with 23 genetic variants.
Multivariable analyses were performed to identify which clinical, angiographic, and genetic variables were independently associated with the occurrence of early stent thrombosis. Among the 23 genetic variants investigated in 15 different genes, the researchers found that 3 genotypes related to clopidogrel metabolism and platelet function (CYP2C19, ABCB1, and ITGB3) were an independent risk factor for early stent thrombosis. The authors also identified 2 potentially modifiable factors of early stent thrombosis: clopidogrel loading dose and clopidogrel interaction with proton pump inhibitors. Patients in the highest tertile (one of three groups) of risk using a combined clinical and genetic model had a 7-fold increased risk of early stent thrombosis vs. patients in the lowest tertile.
"Our study adds to the understanding of the genetic profile of patients treated with clopidogrel who are at risk of early stent thrombosis," the researchers write.
"Combining genetic factors with clinical factors improved risk stratification for stent thrombosis. Whether treatment adjustment on the basis of such global risk stratification can improve the prognosis of patients undergoing PCI will require future validation in independent cohorts."
**Source: JAMA and Archives Journals
Guillaume Cayla, M.D., Ph.D., of the Pitie-Salpetriere Hospital, Paris, and colleagues conducted an analysis of clinical and genetic factors associated with definite early stent thrombosis. The study, conducted in 10 centers in France between January 2007 and May 2010, included 123 patients undergoing PCI who had definite early stent thrombosis (within 30 days of stent implantation) and DNA samples available, matched on age and sex with 246 stent thrombosis-free controls. The primary outcome measured was the accuracy of prediction of early stent thrombosis with 23 genetic variants.
Multivariable analyses were performed to identify which clinical, angiographic, and genetic variables were independently associated with the occurrence of early stent thrombosis. Among the 23 genetic variants investigated in 15 different genes, the researchers found that 3 genotypes related to clopidogrel metabolism and platelet function (CYP2C19, ABCB1, and ITGB3) were an independent risk factor for early stent thrombosis. The authors also identified 2 potentially modifiable factors of early stent thrombosis: clopidogrel loading dose and clopidogrel interaction with proton pump inhibitors. Patients in the highest tertile (one of three groups) of risk using a combined clinical and genetic model had a 7-fold increased risk of early stent thrombosis vs. patients in the lowest tertile.
"Our study adds to the understanding of the genetic profile of patients treated with clopidogrel who are at risk of early stent thrombosis," the researchers write.
"Combining genetic factors with clinical factors improved risk stratification for stent thrombosis. Whether treatment adjustment on the basis of such global risk stratification can improve the prognosis of patients undergoing PCI will require future validation in independent cohorts."
**Source: JAMA and Archives Journals
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