Atlheltes with marked ECG repolarizacion abnormalities


Pelliccia A, Di Paolo FM, Quattrini FM, Basso C, Culasso F, Popoli G et alOutcomes in Athletes with Marked ECG Repolarization Abnormalities. N Engl J Med 2008; 358: 152-161.   TC   PDF

Introducción

Los deportistas presentan alteraciones ECG parecidas a las de la HVI. Estas consisten habitualmente en ondas R o S pronunciadas, pero en ocasiones también presentan T invertidas y profundas. Se desconoce si estas alteraciones de la repolarización son indicativas de alguna cardiomiopatía subyacente.

Objetivo

Evaluar los resultados clínicos asociados a la presencia de trastornos de la repolarización en atletas jóvenes.

Perfil del estudio

Tipo de estudio: Estudio de cohortes
Área del estudio: Pronóstico
Ámbito del estudio: Comunitario

Métodos

En Italia es obligatorio desde hace 25 años que todos los participantes en competiciones oficiales pasen un examen médico y un ECG previo a las mismas. Los deportistas que forman parte de las selecciones nacionales y aquellos a los que se les detectan anomalías electrocardiográficas son atendidos en el Instituto de Ciencia y Medicina de los Deportes, donde se lleva a cabo un estudio que incluye un ECG convencional, una prueba de esfuerzo y un ecocardiograma.
Se revisó la base de datos de los deportistas atendidos en este Instituto entre 1979 y 2001 y se identificaron los que presentaban trastornos de la repolarización importantes (ondas T negativas ≥2 mm en ≥3 derivaciones excepto en DIII y predominantemente en las derivaciones V2-V6). Se excuyó a los que tenían evidencia de lesiones estructurales en el ecocardiograma inicial. Como controles se seleccionaron deportistas entre los 20 siguientes a cada uno de los casos con ECG normal apareados por edad, sexo y duración del seguimiento.

Resultados

Se incluyeron en el grupo de casos 81 deportistas (fig. 1). Para ellos se seleccionaron 229 controles que fueron seguidos durante el mismo periodo de tiempo. En el 67% de los casos se detectaron más alteraciones ECG, entre las que destacaban incrementos de los voltajes de las R o las S (52%) y Q profundas (10%). No se apreciaron diferencias entre los casos y los controles. La edad media de los participantes era de 22 años y el 71% eran varones. Los deportes en los que participaban más frecuentemente eran remo, fútbol y waterpolo. El seguimiento medio fue de 9 años. Al final del periodo de seguimiento, el 78% seguían haciendo deporte regularmente, un 21% habían abandonado la práctica deportiva y 1 de los individuos había muerto.
Durante el seguimiento, las alteraciones de la repolarización se mantuvieron inalteradas en el 67% de los individuos, mejoraron en el 18% (menos derivaciones o menor profundidad de las ondas T) y se normalizaron en el 15% restante. En ninguno de los deportistas se apreciaron cambios en el volumen ventricular.
En 11 deportistas con alteraciones de la repolarización se detectaron cardiopatías en el seguimiento (14%). Uno murió a los 24 años un año después de la valoración inicial por una cardiomiopatía ventricular derecha arritmogénica que no se había detectado. En 3 se detectó una cardiomiopatía hipertrófica y en uno una cardiomiopatía dilatada. Uno de los individuos con cardiomiopatía hipertrófica sufrió un paro cardiorrespiratorio del que se recuperó. Otros 6 pacientes del grupo con alteraciones de la repolarización desarrollaron enfermedades cardiovasculares (3 HTA , 1 cardiopatía isquémica que requirió revascularización, 1 miocarditis y 1 taquicardia supraventricular paroxística que requirió ablación). En todos los deportistas que presentaron cardiomiopatías las anomalías ECG se mantuvieron a lo largo de todo el seguimiento.
Ninguno de los controles desarrolló una cardiomiopatía y sólo 4 desarrollaron algún trastorno cardiovascular: 2 taquicardia supraventricular, 1 miocarditis y 1 pericarditis.

Conclusiones

Los autores concluyen que las alteraciones ECG en deportistas jóvenes y aparentemente sanos pueden ser un indicio de cardiomiopatías subyacentes que pueden no hacerse evidentes hasta años más tarde, por lo que deben ser objeto de vigilancia clínica.

Conflictos de interés

Ninguno declarado. Financiado por el Comité Olímpico Italiano.

Comentario

La práctica habitual de deporte (no deporte de élite) tiene consecuencias cardiovasculares beneficiosas. Sin embargo, no es excepcional que en el deporte de élite se den casos de muerte súbita en el transcurso de una prueba deportiva. Se ha demostrado que un programa de cribado preparticipación disminuye el riesgo de estos accidentes.
En el corazón de las personas entrenadas se desarrollan unos cambios que se conocen como el corazón del deportista. Entre ellos destacan el aumento del tamaño y del volumen de las cavidades cardíacas, en especial del ventrículo izquierdo. Fruto de estos cambios, un 40% de los deportistas presentan alteraciones en el ECG, entre las que las más frecuentes son repolarizaciones precoces, incremento del voltaje del QRS, inversiones más o menos difusas de las ondas T y Q profundas, así como alteraciones de la conducción cardíaca (bradicardias, bloqueos AV tipo Wenkeback y ritmos nodales), así como arritmias ventriculares (extrasístoles e incluso salvas de taquicardia ventricular). Estas alteraciones pueden simular y dificulatar el diagnóstico de determinadas enfermedades cardíacas como las cardiomiopatias hipertrófica, dilatada o la cardioimiopatía ventricular derecha arritmogénica, que es la principal causa de muerte súbita en personas jóvenes.
De los resultados de este estudio se desprende que los deportistas que presentan alteraciones de la repolarización importantes (aproximadamente un 1%) tienen un mayor riesgo de presentar una cardiomiopatía que los que tienen un ECG normal, incluso aunque en la valoración inicial el resto de las exploraciones sean normales (valor predictivo positivo 6%). Estas cardiomiopatías pueden incluso poner en riesgo la vida de la persona (2 sufrieron cuadros de paro cardiorrespiratorio), por lo que parece prudente la recomendación de los autores de hacer un seguimiento clínico.

Bibliografía

  1. Corrado D, Basso C, Pavei A, Michieli P, Schiavon M, Thiene GTrends in Sudden Cardiovascular Death in Young Competitive Athletes After Implementation of a Preparticipation Screening Program. JAMA 2006; 296: 1593-1601.    TC   PDF  RC
  2. Maron BJ, Pelliccia AThe Heart of Trained Athletes: Cardiac Remodeling and the Risks of Sports, Including Sudden Death. Circulation 2006; 114: 1633-1644.   TC (s)   PDF (s)
  3. Pelliccia A, Maron BJ, Culasso F, et alClinical significance of abnormal electrocardiographic patterns in trained athletes. Circulation 2000; 102: 278-284.    TC  PDF

Autor

Manuel Iglesias Rodal. Correo electrónico: mrodal@menta.net.

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Cribado de cancer de prostata – Screening of prostaste cancer


Prostate and bladder, sagittal section.Image via Wikipedia

Editorial del NEJM 26 de Marzo 2009


In the United States, most men over the age of 50 years have had a prostate-specific–antigen (PSA) test,1 despite the absence of evidence from large, randomized trials of a net benefit. Moreover, about 95% of male urologists and 78% of primary care physicians who are 50 years of age or older report that they have had a PSA test themselves,2 a finding that suggests they are practicing what they preach. And indeed, U.S. death rates from prostate cancer have fallen about 4% per year since 1992, five years after the introduction of PSA testing.3 Perhaps the answer to the PSA controversy is already staring us in the face. At the same time, practice guidelines cite the unproven benefit of PSA screening, as well as the known side effects,4,5 which largely reflect the high risks of overdiagnosis and overtreatment that PSA-based screening engenders.6
The first reports from two large, randomized trials that many observers hoped would settle the controversy appear in this issue of the Journal. In the U.S. Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial, Andriole et al.7 report no mortality benefit from combined screening with PSA testing and digital rectal examination during a median follow-up of 11 years.8 In the European Randomized Study of Screening for Prostate Cancer (ERSPC) trial, Schröder et al.8 report that PSA screening without digital rectal examination was associated with a 20% relative reduction in the death rate from prostate cancer at a median follow-up of 9 years, with an absolute reduction of about 7 prostate cancer deaths per 10,000 men screened.8 The designs of the two trials are different and provide complementary insights.
First, one must ask, “Why were these results published now?” Neither set of findings seems definitive; that is, there was neither a clear declaration of futility in the PLCO trial nor an unambiguous net benefit in the ERSPC trial. Both studies are ongoing, with future updates promised. The report on the ERSPC trial follows a third planned interim analysis, which found a marginally significant decrease in prostate-cancer mortality after adjustment of the P value for the two previous looks in an attempt to avoid a false positive conclusion (yet apparently preserving no alpha for the planned final analysis). On the other hand, the investigators in the PLCO trial made the decision to publish their results now because of concern about the emerging evidence of net harm compared with potential benefits associated with PSA screening. Both decisions to publish now can be criticized as premature, leaving clinicians and patients to deal with the ambiguity.
The ERSPC trial is actually a collection of trials in different countries with different eligibility criteria, randomization schemes, and strategies for screening and follow-up. The report by Schröder et al. is based on a predefined core group of men between 55 and 69 years of age at study entry. Subjects were generally screened every 4 years, and 82% were screened at least once. Contamination of the control group with screening as part of usual care is not described. Biopsies were generally recommended for subjects with PSA levels of more than 3.0 ng per milliliter. It is unclear whether the clinicians and hospitals treating patients with prostate cancer differed between the two study groups.
Adjudications of causes of death were made by committees whose members were unaware of study-group assignments, though not of treatments. This point is important, since previous research has suggested that the cause of death is less likely to be attributed to prostate cancer among men receiving attempted curative treatment.9 Misattribution might then create a bias toward screening, since the diagnosis of more early-stage cancers in the ERSPC trial led to substantially more attempted curative treatments.
The ERSPC interim analysis revealed a 20% reduction in prostate-cancer mortality; the adjusted P value was 0.04. The estimated absolute reduction in prostate-cancer mortality of about 7 deaths per 10,000 men after 9 years of follow-up, if real and not the result of chance or bias, must be weighed against the additional interventions and burdens. The 73,000 men in the screening group underwent more than 17,000 biopsies, undoubtedly many more than did men in the control group, though the latter is not reported. Men had a substantially higher cumulative risk of receiving the diagnosis of prostate cancer in the screening group than in the control group (820 vs. 480 per 10,000 men). Diagnosis led to more treatment, with 277 versus 100 per 10,000 men undergoing radical prostatectomy and 220 versus 123 per 10,000 undergoing radiation therapy with or without hormones, respectively (tentative estimates given the unknown treatments in both groups).
Although estimates of the benefit of screening were somewhat greater for men who actually underwent testing (taking into account noncompliance) than for those who were not tested, the side effects would be proportionately higher as well. Given these trade-offs, the promise of future ERSPC analyses addressing quality of life and cost-effectiveness is welcome indeed. The ERSPC results also reemphasize the need for caution in screening men over the age of 69 years, given an early trend toward higher prostate-cancer mortality with screening in this age subgroup, although this finding may well be due to chance alone.
A final point to make about the ERSPC trial is that to the extent that the diagnosis and treatment of prostate cancer in the screening group differed from those in the control group, it becomes difficult to dissect out the benefit attributable to screening versus improved treatment once prostate cancer was suspected or diagnosed. A similar distribution of treatments among seemingly similar patients with cancer is only partially reassuring in this regard.
Despite a longer median follow-up, the PLCO trial was smaller and therefore less mature than the ERSPC trial, with 174 prostate-cancer deaths driving the power of the study, as compared with 540 such deaths in the ERSPC trial. The screening protocol was homogeneous across sites with an enrollment age of 55 to 74 years and annual PSA tests for 6 years and digital rectal examinations for 4 years, with about 85% compliance. Subjects in the screening group who had a suspicious digital rectal examination or a PSA level of more than 4.0 ng per milliliter received a recommendation for further evaluation. This strategy helped to ensure that any difference in outcome was attributable to screening, rather than downstream management. The effectiveness of screening, of course, will be determined by the effectiveness of subsequent “usual care,” but this is the same usual care that many practitioners assume has been responsible for the falling U.S. death rate from prostate cancer. Adjudication of causes of death was similar to that in the ERSPC trial.
Though the PLCO trial has shown no significant effect on prostate-cancer mortality to date, the relatively low number of end points begets a wide confidence interval, which includes at its lower margin the point estimate of effect from the ERSPC trial. Other likely explanations for the negative findings are high levels of prescreening in the PLCO population and contamination of the control group. Contamination was assessed by periodic cross-sectional surveys, with about half the subjects in the control group undergoing PSA testing by year 5. It is unclear whether these estimates reflect testing that year or since trial inception; if the former, the cumulative incidence may be even higher. The smaller difference in screening intensity between the two study groups in the PLCO trial, as compared with the ERSPC trial, is reflected in a smaller risk of overdiagnosis (23% vs. more than 70%) and a less impressive shift in cancer stage and grade distributions. Given that study-group contamination from the use of digital rectal examination was less problematic (only about 25%), ongoing results from both of these trials may necessitate rethinking the role of digital rectal examination in cancer screening.
After digesting these reports, where do we stand regarding the PSA controversy? Serial PSA screening has at best a modest effect on prostate-cancer mortality during the first decade of follow-up. This benefit comes at the cost of substantial overdiagnosis and overtreatment. It is important to remember that the key question is not whether PSA screening is effective but whether it does more good than harm. For this reason, comparisons of the ERSPC estimates of the effectiveness of PSA screening with, for example, the similarly modest effectiveness of breast-cancer screening cannot be made without simultaneously appreciating the much higher risks of overdiagnosis and overtreatment associated with PSA screening.
The report on the ERSPC trial appropriately notes that 1410 men would need to be offered screening and an additional 48 would need to be treated to prevent one prostate-cancer death during a 10-year period, assuming the point estimate is correct. And although the PLCO trial may not have the power as yet to detect a similarly modest benefit of screening, its power is already more than adequate to detect important harm through overdiagnosis. However, the implications of the trade-offs reflected in these data, like beauty, will be in the eye of the beholder. Some well-informed clinicians and patients will still see these trade-offs as favorable; others will see them as unfavorable. As a result, a shared decision-making approach to PSA screening, as recommended by most guidelines, seems more appropriate than ever.
Finally, despite these critiques, both groups of investigators deserve high praise for their persistence and perseverance: to manage such monstrous trials is a herculean task, made no easier when so many observers think the results are self-evident. Further analyses will be needed from these trials, as well as from others — such as the Prostate Cancer Intervention Versus Observation Trial (PIVOT) in the United States (ClinicalTrials.gov number, NCT00007644 [ClinicalTrials.gov] )10 and the Prostate Testing for Cancer and Treatment (PROTECT) trial in the United Kingdom (Current Controlled Trials number, ISRCTN20141297 [controlled-trials.com] )11 — if the PSA controversy is finally to sleep the big sleep.
No potential conflict of interest relevant to this article was reported.

Source Information

From Massachusetts General Hospital and Harvard Medical School, Boston.

This article (10.1056/NEJMe0901166) was published at NEJM.org on March 18, 2009.
References

  1. Ross LE, Berkowitz Z, Ekwueme DU. Use of the prostate-specific antigen test among U.S. men: findings from the 2005 National Health Interview Survey. Cancer Epidemiol Biomarkers Prev 2008;17:636-644. [Free Full Text]
  2. Chan EC, Barry MJ, Vernon SW, Ahn C. Brief report: physicians and their personal prostate cancer-screening practices with prostate-specific antigen: a national survey. J Gen Intern Med 2006;21:257-259. [CrossRef][ISI][Medline]
  3. Ries LAG, Melbert D, Krapcho M, et al. SEER cancer statistics review, 1975–2005. Bethesda, MD: National Cancer Institute, 2008. (Accessed March 6, 2009 at http://seer.cancer.gov/csr/1975_2005/.)
  4. Smith RA, Cokkinides V, Brawley OW. Cancer screening in the United States, 2008: a review of current American Cancer Society guidelines and cancer screening issues. CA Cancer J Clin 2008;58:161-179. [Free Full Text]
  5. U. S. Preventive Services Task Force. Screening for prostate cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med 2008;149:185-191. [Free Full Text]
  6. Barry MJ. Why are a high overdiagnosis probability and a long lead time for prostate cancer screening so important? J Natl Cancer Inst (in press).
  7. Andriole GL, Grubb RL III, Buys SS, et al. Mortality results from a randomized prostate-cancer screening trial. N Engl J Med 2009;360:1310-1319. [Free Full Text]
  8. Schröder FH, Hugosson J, Roobol MJ, et al. Screening and prostate-cancer mortality in a randomized European study. N Engl J Med 2009;360:1320-1328. [Free Full Text]
  9. Newschaffer CJ, Otani K, McDonald MK, Penberthy LT. Causes of death in elderly prostate cancer patients and in a comparison nonprostate cancer cohort. J Natl Cancer Inst 2000;92:613-621. [Free Full Text]
  10. Wilt TJ, Brawer MK, Barry MJ, et al. The Prostate cancer Intervention Versus Observation Trial: VA/NCI/AHRQ Cooperative Studies Program #407 (PIVOT): design and baseline results of a randomized controlled trial comparing radical prostatectomy to watchful waiting for men with clinically localized prostate cancer. Contemp Clin Trials 2009;30:81-87. [CrossRef][ISI][Medline]
  11. Donovan J, Hamdy F, Neal D, et al. Prostate Testing for Cancer and Treatment (ProtecT) feasibility study. Health Technol Assess 2003;7:1-88. [Medline]

Routine HIV Screening – HIV: CDC x USPSTF


Após acabar de publicar as recomendações do US Preventive Services Task Force sobre ECG (não triar), acabo de ler o ahead of print do New England Journal of Medicine que discute justamente as recomendações da Task Force (não triar universalmente HIV) contra as recomendações do Centers for Disease Control (triagem universal).

O artigo faz um apanhado interessante da discussão entre as duas entidades acerca da análise das mesmas evidências científicas, destacando que, a despeito das evidências não serem as mesmas, a análise de diferentes pesquisadores (cochranistas x especialistas).

Os dois grupos debatem sob diversas óticas, incluindo a da economia da saúde (de custo-benefício e custo-efetividade), a do risco relacionado a triagem e da responsabilidade das próprias entidades em se obrigarem a fazer ou não recomendações.

As referências são bastante interessantes, e a ótica do autor deste artigo traduz a panacéia que existe em torno da Medicina Baseada em Evidências.

Lembrando que só recentemente o atual presidente Barack Obama suspendeu a obrigatoriedade do exame de HIV para imigrantes, uma exigência da administração anterior, é importante entender o contexto em que se desenvolvem estas recomendações.

Leia o artigo do NEJM:




Publicado originalmente por Leonardo C M Savassi

Statins, Diabetes, and Attacking a Meta-Analysis


P-values from Fisher's meta analysis applied t...Image via Wikipedia

Source: Evidence Based Medicine

I’m a little late reading the June 19th 2010 Lancet, but was intrigued to find letters in response to the meta-analysis by Sattar et al. looking at whether statin therapy increases the risk of diabetes.

I had previously written about this well-performed meta-analysis, and also written about some unfair ways that people use to try to attack randomized trials, and these letters provide an interesting (at least to me) intersection between these posts.
Letters in academic scientific journals are sociologically revealing. There’s typically a polite veneer on even the most vicious attacks. Letters written to European medical journals have a somewhat different feel from those to American medical journals, and letters to the Lancet often seem to have a sneering tone that would be unusual to find in the NEJM or JAMA.
One letter about the meta-analysis objects that the results cease to be statistically significant when diabetes diagnosed only by physician report are excluded, and secondly that the results involved a post-hoc analysis of the data, with the warning that we might fall victim to the logical fallacy, “Post hoc ergo propter hoc“.
Are these fair objections?
Diagnosing diabetes by physician report rather than blood glucose measurement is likely to lead to misclassification: some patients will be classified as having diabetes who don’t, and some who have diabetes will be missed. In an RCT, though, misclassification like this will almost certainly be random as well, leading to random misclassification bias. Bias of this sort is toward the null hypothesis (no difference between the groups), as you can convince yourself of if you imagine that the classification is perfectly random such that there is no relation between the classification and diabetes. Under such perfect misclassification, the two groups would have equal numbers of patients classified as having diabetes and there would be no difference between treatment and control. In a meta-analysis that found higher rates of diabetes in patients receiving statins, misclassification bias can be expected to have somewhat reduced the true effect, not to have created an effect out of thin air.
The second objection might be called the “post-hoc-ergo-propter-hoc-fallacy fallacy”. The actual fallacy is, of course, a way of saying that just because B follows A, you should not conclude that A caused B. This question of causality is central to epidemiologic research and one of the primary reasons for performing randomized trials, which have particular strengths when arguing for causality. The fallacy has nothing to do with performing post hoc analyses of trials. (To be fair, it’s possible the letter writer understood this and was being humorous when writing of this fallacy.) The main problem with a post hoc analysis of a randomized trial is that it often involves multiple comparisons/data dredging, where statistical blips are likely to confuse the issue of what is a true effect. As discussed in my earlier post, a prime issue preceding this meta-analysis was whether JUPITER had found just such a random blip or detected a real problem. The meta-analysis’ reason for being performed was primarily to answer this question, and in such a setting there is nothing at all concerning about going back to previously conducted RCTs and performing post hoc analyses looking for diabetes effects. No data dredging was involved, and the analysis should not be looked at askance simply for being post hoc. Revealingly, the meta-analysis found an increased risk of diabetes even when data from JUPITER were excluded.
A second letter complained that the analysis would have been better had it been carried out using hazard ratios rather than odds ratios. While this would likely be true, such an analysis was not possible given the information available to the authors, and it is hard to imagine why an OR analysis would have shown statins to be causing diabetes if it were not true. The same letter also re-raised the possibility that statins appeared to be causing people to have more diabetes by keeping them alive longer to develop diabetes. However, the authors had already addressed this in their meta-analysis and reiterated in their response to the letters that differences in survival were much too small to produce such an effect.
A third letter mis-states the definition of a type I error on its way to arguing that the meta-analysis should have used 99% confidence intervals (p-value cutoff of 0.01) for some reason that was not made terribly clear, but seemed related to concerns that a very large meta-analysis would be more likely to detect a spurious result. It is true that given the enormous N in the analysis, it was possible to find a statistically significant difference in diabetes rates that is likely of little clinical significance, but this has nothing to do with the truth or falsehood of the result itself. The letter also argues that the result is biologically implausible, though it does not seem implausible that a medication could increase diabetes rates during the time of a randomized trial, if only by raising blood sugars in patients near the margin between insulin resistance and diabetes.
A fourth letter suggests that the “diabetes” found in the study might be different in terms of patient-important outcomes than the clinical condition we think of as diabetes. That is, statins might be raising blood sugars in a way that is harmless. While this is possible, it’s interesting that when a drug class raises blood sugar people are willing to argue it might be harmless, but when a drug class lowers  blood sugar there’s a tendency (at least for the manufacturer) to argue that blood sugar control is an excellent surrogate for clinical outcomes. The author of the letter suggests an analysis that might have been done to sort out this issue, which the authors of the meta-analysis correctly point out would not have answered the question.
There were a few other replies to the article, which I have not detailed. Overall, though, this is a fairly typical picture of what happens when someone publishes a trial that conflicts with conventional beliefs, such as “statins are good”. This occurs even when the conflict is quite minor — the meta-analysis merely shows a small increase in diabetes that would be heavily outweighed by cardiovascular benefit in anyone who would be appropriately treated with a statin.
There is no guarantee that the meta-analysis by Sattar et al. is correct about statins and diabetes, but none of the letters published by Lancet raise a sensible reason to think that the post-analysis state of knowledge should change: it is now far more likely than not that statins cause a small increase in diabetes risk. Our response to a meta-analysis like this should be to congratulate the authors on a job well done, while recognizing the possibilities for errors and chance to disrupt the conclusions. It should not be to search high and low for far-fetched flaws that would allow us to discard the inconvenient likelihood that a new statin side-effect has been detected.

El cribado del cancer de prostata no se asocia a una disminucion de la mortalidad


Age-standardised death rates from Prostate can...                              Image via WikipediaConcato J, Wells CK, Horwitz RI, Penson D, Fincke G, Berlowitz DR, et al. The Effectiveness of Screening for Prostate Cancer: A Nested Case-Control Study. Arch Intern Med 2006; 166: 38-43. R TC (s) PDF (s)

Introducción

Diferentes grupos de trabajo han hecho distintas recomendaciones sobre el cribado del cáncer de próstata. A pesar de que el cribado con PSA se ha mostrado eficaz para detectar tumores de próstata asintomáticos, no se ha demostrado claramente que esta detección redunde en una reducción de la mortalidad.

Objetivo

Estudiar si el cribado del cáncer de próstata mediante determinación del PSA con o sin tacto rectal mejora la supervivencia.

Perfil del estudio

Tipo de estudio: Estudio de casos y controles
Área del estudio: Prevención
Ámbito del estudio: Comunitario
Métodos
La población de estudio estuvo formada por los pacientes varones >50 años que se visitaron entre 1989 y 1990 en cualquiera de los 10 centros del departamento de Veterans Affairs del estado de Nueva Inglaterra y que no tenían un diagnóstico de cáncer antes de 1991. Se incluyeron como casos los pacientes a los que se les diagnosticó un cáncer de próstata entre esa fecha y 1995 y que murieron antes de 2000. Para cada uno de los casos se seleccionó un control entre los pacientes que estaban vivos en la fecha de la muerte del caso hubiese sido o no diagnosticado de cáncer de próstata en ese momento ajustado por fecha de nacimiento y centro en el que se había visitado.
Un investigador que desconocía la asignación del paciente a los grupos revisaba las historias clínicas para saber si se le había hecho cribado del cáncer de próstata mediante una determinación del o tacto rectal desde 1991 hasta la fecha del diagnóstico del cáncer de próstata del caso.
La variable principal de resultado fue la muerte por cualquier causa. Como variables secundarias se utilizaron la muerte por cáncer de próstata y el cáncer de próstata progresivo.

Resultados

La figura 1 muestra el flujo de los participantes en el estudio. La edad media fue de 72 años. Entre los casos se detectó un exceso de pacientes de raza negra (10,0% frente a 4,2%; P<0,001)>

Se había llevado a cabo un cribado previo en el 14% de los casos y en el 13% de los controles. No se apreciaron diferencias estadísticamente significativas ni en la mortalidad total, ni en la mortalidad específica por cáncer de próstata ni en los análisis por subgrupos de los pacientes por edad ni en los pacientes con hipertrofia benigna de próstata (tabla 1).

OR (IC95%) P
Mortalidad total 1,08 (0,71 a 1,64) 0,72
Muerte por cáncer de próstata 1,13 (0,63 a 2,08) 0,68

Conclusiones

Los autores concluyen que los resultados de este estudio no sugieren que el cribado mediante PSA ni mediante tacto rectal reduzcan la mortalidad total ni por cáncer de próstata.

Conflictos de interés

Ninguno declarado. Financiado por una beca del Department of Veterans Affairs.

Comentario

El cribado del cáncer de próstata sigue siendo objeto de polémica. A pesar de que el PSA se ha mostrado eficaz para detectarlo, siguen existiendo dudas importantes sobre si este adelanto diagnóstico aporta más beneficios que riesgos. Desde que se ha extendido el cribado mediante PSA (sin que se haya llegado a la universalización del mismo), la probabilidad de que a un adulto se le diagnostique un cáncer de próstata casi se ha doblado. Por otro lado, la cirugía de próstata se acompaña de un elevado riesgo de disfunciones sexuales y de incontinencia. Valdría la pena pagar este precio si los beneficios en términos de mejoría del pronóstico estuviesen claros, pero los resultados de este trabajo arrojan más dudas sobre el tema.
En ausencia de datos inequívocos sobre la eficacia de una técnica de cribado provinientes de estudios de intervención, los estudios de casos y controles se han mostrado útiles para esclarecer la eficacia de algunas técnicas (como en el caso del Papanicolaou). Los autores de este trabajo han elegido como variable de respuesta principal la mortalidad total que parece una variable importante, que evita algunos de los sesgos inherentes a los estudios de prevención (sesgo del adelanto diagnóstico) y permite salvar el problema del posible error en la causa de muerte en el certificado de defunción. Un estudio de casos y controles publicado recientemente y que utilizaba como variable principal la presencia de metástasis por cáncer de próstata sí que encontró una asociación entre el cribado y un menor riesgo.
En 2009 está prevista la publicación de dos estudios de intervención, uno americano y otro europeo, que es probable que despejen las dudas actuales sobre la conveniencia de llevar a cabo o no el cribado.

Bibliografía

  1. Nelson WG, De Marzo AM, Isaacs WB. Prostate cancer. N Engl J Med 2003; 349: 366-381. TC (s) PDF (s)
  2. Barry MJ. The PSA Conundrum. Arch Intern Med 2006; 166: 7-8. TC (s) PDF (s)

Autor

Manuel Iglesias Rodal. Correo electrónico: mrodal@menta.net.

Catherization Urethra in male children


Catheterizacion Urethra http://d1.scribdassets.com/ScribdViewer.swf?document_id=41085743&access_key=key-xv3mdvig09uz23dxy19&page=1&viewMode=list

Crisis en atencion primaria


The editors asked several experts to share their perspectives on the crisis in U.S. primary care. Their articles, which address this crisis from six different angles, follow. We also brought the five U.S. contributors together for a roundtable discussion of the problems and potential solutions for training, practice, compensation, and systemic change. A video of the discussion and reader comments can be seen at http://www.nejm.org.

Primary care has been one of the best jobs in medicine, and it can be again. In fact, primary care must recapture its attraction for the next generation’s best trainees — or the chaos and inefficiency of U.S. health care will only worsen.

The challenges are formidable, for there are so many reasons for young physicians to go into other fields. Many physicians graduate from medical school with staggering debts, and procedure-oriented specialties offer higher potential incomes. The work of primary care is itself overwhelming. Primary care physicians often go home worried that they may have made mistakes, or dispirited because they did not complete their work.

But as Treadway’s story reminds us, failure is not an option. Throughout their lives, but particularly at the end, patients want and need physicians who focus on the people who have diseases, not just the diseases that they have.

Redesigning Primary Care
In a video roundtable discussion moderated by Dr. Thomas Lee, four experts in primary care and related policy explore the crisis, as well as possible solutions for training, practice, compensation, and systemic change.

And when people want and need something, the market usually gives it to them. Right now, patients throughout the UnitedStates are having difficulty finding primary care physicians, so incomes for such practitioners will probably rise as health care organizations struggle to meet the demand for primary care. At the delivery system where I work, we are actively discussingquestions such as how high primary care salaries need to be, where the money to pay them will come from, and how quicklyhigher incomes might work to expand the primary care pipeline.

These questions are difficult to answer, because money is only part of the problem and therefore can be only part of the solution. We have to figure out how to make the job of primary care doable once again. We have to learn how to surround primary care physicians with teams that help them care for their populations of patients, as Bodenheimer argues in his article, and we have to equip them with systems such as electronic medical records to help them manage the flood of information that moves through their offices every day. And, as Goroll suggests in his article, we have to develop payment policies that make these innovations sustainable.

Many organizations have found that when they increase payments to primary care physicians, the physicians respond by reducing the number of patients they see. These physicians, it turns out, place a higher priority on trying to do a good job andhaving a sane life than on making a higher income. The message they’re sending is that more money will not be enough to revitalize primary care.

Revitalization will take something more like reinvention, and it will demand creativity and flexibility from all parties — including primary care physicians themselves. These physicians need to learn to work in teams and adjust to the notion that much of primary care can be delivered by nonphysician team members, some of whom are located in nontraditional settings, such aslimited-service clinics in retail stores.

In this collection of articles, Starfield describes some of the major policy issues that must be addressed as the U.S. health care system develops a stronger primary care focus, and Roland suggests that there are some features of primary care in the United Kingdom that might warrant adaptation. As we test new concepts in the years ahead, primary care will undoubtedly changedramatically. But if we are successful and wise, these changes should allow key aspects of being a primary care physician toremain the same.

Primary care doctors should once again feel a deep sense of satisfaction when they leave their offices or patients’ homes after helping people through difficult times. They should be able to leave work thinking not of their income, or of unanswered phone calls, or of test results that they might have overlooked. They should go home thinking, “This is what I was meant to do.”

No potential conflict of interest relevant to this article was reported.


Source Information

Dr. Lee is network president at Partners HealthCare System, Boston, and an associate editor of the Journal.

Crisis en atencion primaria


The editors asked several experts to share their perspectives on the crisis in U.S. primary care. Their articles, which address this crisis from six different angles, follow. We also brought the five U.S. contributors together for a roundtable discussion of the problems and potential solutions for training, practice, compensation, and systemic change. A video of the discussion and reader comments can be seen at http://www.nejm.org.

Primary care has been one of the best jobs in medicine, and it can be again. In fact, primary care must recapture its attraction for the next generation’s best trainees — or the chaos and inefficiency of U.S. health care will only worsen.
The challenges are formidable, for there are so many reasons for young physicians to go into other fields. Many physicians graduate from medical school with staggering debts, and procedure-oriented specialties offer higher potential incomes. The work of primary care is itself overwhelming. Primary care physicians often go home worried that they may have made mistakes, or dispirited because they did not complete their work.
But as Treadway’s story reminds us, failure is not an option. Throughout their lives, but particularly at the end, patients want and need physicians who focus on the people who have diseases, not just the diseases that they have.

Redesigning Primary Care
In a video roundtable discussion moderated by Dr. Thomas Lee, four experts in primary care and related policy explore the crisis, as well as possible solutions for training, practice, compensation, and systemic change.

And when people want and need something, the market usually gives it to them. Right now, patients throughout the UnitedStates are having difficulty finding primary care physicians, so incomes for such practitioners will probably rise as health care organizations struggle to meet the demand for primary care. At the delivery system where I work, we are actively discussingquestions such as how high primary care salaries need to be, where the money to pay them will come from, and how quicklyhigher incomes might work to expand the primary care pipeline.
These questions are difficult to answer, because money is only part of the problem and therefore can be only part of the solution. We have to figure out how to make the job of primary care doable once again. We have to learn how to surround primary care physicians with teams that help them care for their populations of patients, as Bodenheimer argues in his article, and we have to equip them with systems such as electronic medical records to help them manage the flood of information that moves through their offices every day. And, as Goroll suggests in his article, we have to develop payment policies that make these innovations sustainable.
Many organizations have found that when they increase payments to primary care physicians, the physicians respond by reducing the number of patients they see. These physicians, it turns out, place a higher priority on trying to do a good job andhaving a sane life than on making a higher income. The message they’re sending is that more money will not be enough to revitalize primary care.
Revitalization will take something more like reinvention, and it will demand creativity and flexibility from all parties — including primary care physicians themselves. These physicians need to learn to work in teams and adjust to the notion that much of primary care can be delivered by nonphysician team members, some of whom are located in nontraditional settings, such aslimited-service clinics in retail stores.
In this collection of articles, Starfield describes some of the major policy issues that must be addressed as the U.S. health care system develops a stronger primary care focus, and Roland suggests that there are some features of primary care in the United Kingdom that might warrant adaptation. As we test new concepts in the years ahead, primary care will undoubtedly changedramatically. But if we are successful and wise, these changes should allow key aspects of being a primary care physician toremain the same.
Primary care doctors should once again feel a deep sense of satisfaction when they leave their offices or patients’ homes after helping people through difficult times. They should be able to leave work thinking not of their income, or of unanswered phone calls, or of test results that they might have overlooked. They should go home thinking, “This is what I was meant to do.”
No potential conflict of interest relevant to this article was reported.

Source Information
Dr. Lee is network president at Partners HealthCare System, Boston, and an associate editor of the Journal.

El cribado del cancer de prostata no se asocia a una disminucion de la mortalidad


Concato J, Wells CK, Horwitz RI, Penson D, Fincke G, Berlowitz DR, et al. The Effectiveness of Screening for Prostate Cancer: A Nested Case-Control Study. Arch Intern Med 2006; 166: 38-43. R TC (s) PDF (s)

Introducción

Diferentes grupos de trabajo han hecho distintas recomendaciones sobre el cribado del cáncer de próstata. A pesar de que el cribado con PSA se ha mostrado eficaz para detectar tumores de próstata asintomáticos, no se ha demostrado claramente que esta detección redunde en una reducción de la mortalidad.

Objetivo

Estudiar si el cribado del cáncer de próstata mediante determinación del PSA con o sin tacto rectal mejora la supervivencia.

Perfil del estudio

Tipo de estudio: Estudio de casos y controles

Área del estudio: Prevención

Ámbito del estudio: Comunitario

Métodos

La población de estudio estuvo formada por los pacientes varones >50 años que se visitaron entre 1989 y 1990 en cualquiera de los 10 centros del departamento de Veterans Affairs del estado de Nueva Inglaterra y que no tenían un diagnóstico de cáncer antes de 1991. Se incluyeron como casos los pacientes a los que se les diagnosticó un cáncer de próstata entre esa fecha y 1995 y que murieron antes de 2000. Para cada uno de los casos se seleccionó un control entre los pacientes que estaban vivos en la fecha de la muerte del caso hubiese sido o no diagnosticado de cáncer de próstata en ese momento ajustado por fecha de nacimiento y centro en el que se había visitado.

Un investigador que desconocía la asignación del paciente a los grupos revisaba las historias clínicas para saber si se le había hecho cribado del cáncer de próstata mediante una determinación del o tacto rectal desde 1991 hasta la fecha del diagnóstico del cáncer de próstata del caso.

La variable principal de resultado fue la muerte por cualquier causa. Como variables secundarias se utilizaron la muerte por cáncer de próstata y el cáncer de próstata progresivo.

Resultados

La figura 1 muestra el flujo de los participantes en el estudio. La edad media fue de 72 años. Entre los casos se detectó un exceso de pacientes de raza negra (10,0% frente a 4,2%; P

Se había llevado a cabo un cribado previo en el 14% de los casos y en el 13% de los controles. No se apreciaron diferencias estadísticamente significativas ni en la mortalidad total, ni en la mortalidad específica por cáncer de próstata ni en los análisis por subgrupos de los pacientes por edad ni en los pacientes con hipertrofia benigna de próstata (tabla 1).

OR (IC95%) P
Mortalidad total 1,08 (0,71 a 1,64) 0,72
Muerte por cáncer de próstata 1,13 (0,63 a 2,08) 0,68

Conclusiones

Los autores concluyen que los resultados de este estudio no sugieren que el cribado mediante PSA ni mediante tacto rectal reduzcan la mortalidad total ni por cáncer de próstata.

Conflictos de interés

Ninguno declarado. Financiado por una beca del Department of Veterans Affairs.

Comentario

El cribado del cáncer de próstata sigue siendo objeto de polémica. A pesar de que el PSA se ha mostrado eficaz para detectarlo, siguen existiendo dudas importantes sobre si este adelanto diagnóstico aporta más beneficios que riesgos. Desde que se ha extendido el cribado mediante PSA (sin que se haya llegado a la universalización del mismo), la probabilidad de que a un adulto se le diagnostique un cáncer de próstata casi se ha doblado. Por otro lado, la cirugía de próstata se acompaña de un elevado riesgo de disfunciones sexuales y de incontinencia. Valdría la pena pagar este precio si los beneficios en términos de mejoría del pronóstico estuviesen claros, pero los resultados de este trabajo arrojan más dudas sobre el tema.

En ausencia de datos inequívocos sobre la eficacia de una técnica de cribado provinientes de estudios de intervención, los estudios de casos y controles se han mostrado útiles para esclarecer la eficacia de algunas técnicas (como en el caso del Papanicolaou). Los autores de este trabajo han elegido como variable de respuesta principal la mortalidad total que parece una variable importante, que evita algunos de los sesgos inherentes a los estudios de prevención (sesgo del adelanto diagnóstico) y permite salvar el problema del posible error en la causa de muerte en el certificado de defunción. Un estudio de casos y controles publicado recientemente y que utilizaba como variable principal la presencia de metástasis por cáncer de próstata sí que encontró una asociación entre el cribado y un menor riesgo.

En 2009 está prevista la publicación de dos estudios de intervención, uno americano y otro europeo, que es probable que despejen las dudas actuales sobre la conveniencia de llevar a cabo o no el cribado.

Bibliografía

  1. Nelson WG, De Marzo AM, Isaacs WB. Prostate cancer. N Engl J Med 2003; 349: 366-381. TC (s) PDF (s)
  2. Barry MJ. The PSA Conundrum. Arch Intern Med 2006; 166: 7-8. TC (s) PDF (s)

Autor

Manuel Iglesias Rodal. Correo electrónico: mrodal@menta.net.