In Cancer Screening, Why Not Tell the Truth?

John M Mandrola, MD

|January 12, 2016

An unpleasant emotion caused by the belief that something is dangerous. This is fear. This is cancer.

The motivation to screen for cancer, therefore, is easy to understand.

The problem: cancer screening has not worked. Recent reviews of the evidence show that current-day screening techniques do not save lives. Worse, in many cases, these good-intentioned searches bring harm to previously healthy people.

I realize this sounds shocking. It did to me, too. Millions of women and men have had their breasts squished, veins poked, lungs irradiated, and bowels invaded in the name of “health” maintenance. I’ve been scolded for forgoing PSA tests and colonoscopy — “you should know better, John.”

I know what you may be thinking. We have all heard the anecdotes — cases that are often celebrated in local news reports and hospital marketing material. People saved by early detection, and the opposite: the unscreened felled by late-stage disease.

Anecdotes, however compelling, are not evidence. When you pull up a chair, open your computer, take a breath, suspend past beliefs, and look for the evidence that screening saves lives, it simply isn’t there.

One reason that this many people (doctors and patients alike) have been misled about screening has been our collective attachment to the belief that if screening lowers disease-specific death rates, that would translate to lower overall mortality. That is: breast, lung, and colon cancer are bad diseases, so it makes sense that lowering death from those three types of cancer would extend life.

It is not so.

Facts, Not Fear

In a comprehensive review of the literature^[1] published in the BMJ, Drs Vinay Prasad (Oregon Health Sciences University, Portland) and David Newman (School of Medicine at Mount Sinai, New York), along with journalist Jeanne Lenzer, find that disease-specific mortality is a lousy surrogate for overall mortality. They report that when a screening technique does lower disease-specific death rates, which is both uncommon and of modest degree, there are no differences in overall mortality.

The authors cite three reasons why cancer screening might not reduce overall mortality:

Screening trials were underpowered to detect differences. I’m no statistician, but doesn’t the fact that a trial requires millions of subjects to show a difference, mean there is little, if any, difference?
“Downstream effects of screening may negate any disease-specific gains.” My translation: harm. Dr Peter Gøtzsche (Nordic Cochrane Center, Copenhagen) wrote in a commentary^[2] that “screening always causes harm. Sometimes it also leads to benefits, and sometimes these benefits outweigh the harms.” To understand harm resulting from screening, one need only to consider that a prostate biopsy entails sticking a needle through the rectum, or that some drugs used to treat breast cancer damage the heart.
Screening might not reduce overall mortality because of “off-target deaths.” An illustration of this point is provided by a cohort study^[3]that found a possible increased risk of suicide and cardiovascular death in men in the year after being diagnosed with prostate cancer. People die — of all sorts of causes, not just cancer.

Let’s also be clear that this one paper is not an outlier. A group of Stanford researchers performed a systematic review and meta-analyses^[4] of randomized trials of screening tests for 19 diseases (39 tests) where mortality is a common outcome. They found reductions in disease-specific mortality were uncommon and reductions in overall mortality were rare or nonexistent.

Drs Archie Bleyer and H Gilbert Welch (St Charles Health System, Central Oregon, Portland) reviewed Surveillance, Epidemiology, and End Results (SEER) data from 1976 through 2008 and concluded that “screening mammography has only marginally reduced the rate at which women present with advanced cancer and that overdiagnosis may account for nearly a third of all new breast cancer cases.”^[5]Likewise, a Cochrane Database Systematic review^[6] of eight trials and 600,000 women did not find an effect of screening on either breast cancer mortality or all-cause mortality. This evidence caused the Swiss medical board to abolish screening mammography.^[7]

These are the data. It’s now clear to me that mass cancer screening does not save lives. But I’m still trying to understand how this practice became entrenched as public-health gospel. It has to be more than fear.

How We Say It Matters

Dr Gerd Gigerenzer (Max Planck Institute, Berlin, Germany) offered a clue in his editorial^[8] accompanying the recently published literature review and analysis by Prasad and colleagues. He pointed to language and the ability of words to persuade. Instead of saying “early detection,” advocates might use the term “prevention.” This, Dr Gigerenzer says, wrongly suggests screening reduces the odds of getting cancer. Doesn’t looking for cancer increase the odds of getting the diagnosis of cancer?

Gigerenzer noted two other ways language is used to emphasize screening benefits over harms:

The reporting of benefits in relative, not absolute terms.
The equating of increases in 5-year survival rates with decreases in mortality.

I would add to this list of word misuse, the practice of referring to women sent to mammography screening as patients. They are not patients; they are well people.

Dr Gigerenzer agreed with the commonsense notion that overall mortality should be reported along with cancer-specific mortality. His editorial included a fact box on breast cancer early detection using mammography provided by the Harding Center for Risk Literacy. I challenge you to tell me why such text boxes should not be shown to people before they undergo screening,

Fixing a Public-Health Problem

Given these revelations, I conclude that we have a massive public-health problem. Any expert in problem solving will tell you the first step of getting out of hole is to stop digging. I see three obvious next steps:

The first action healthcare experts should take is to spread the word that there is nothing about the mass screening of healthy people for cancer that equates to health maintenance. Embrace clear language. Saying or implying that screening saves lives when there are no data to support it and lots to refute it undermines trust in the medical profession.

The second action healthcare experts should take is to stop wasting money on screening. If the evidence shows no difference in overall mortality, why pay for it? I’m not naive to the fact that use of clear language will decrease the number of billable procedures. I am not saying this will be easy. One first move that would be less painful would be to get rid of quality measures or incentives that promote screening.

I want to be clear; I’m not saying all cancer screening is worthless. People at higher baseline risk for cancer, such as those with a family history of cancer or environmental exposures, might derive more benefit than harm from screening. Prasad, Lenzer, and Newman say this group of patients would be a good place to spend future research dollars. That sounds reasonable. I also acknowledge that some people, even when presented with the evidence, will want to proceed with screening. We can argue about who should pay for non–evidence-based medical procedures.

The most important action that all of us (patients, nurses, doctors, and healthcare writers) should take is to learn from this revelation. There’s nothing bad about the fact that current-day screening tests don’t save lives. Cancer is a tough disease, and in some ways, it may be the natural order of cell biology. What’s bad about this medical reversal has been our blindness to the evidence.

We let what we believe become what we know. In clinical medicine, that should be a never event.

References

Prasad V, Lenzer J, Newman DH. Why cancer screening has never been shown to “save lives”—and what we can do about it. BMJ. 2016;352:h6080. Article
Gøtzsche PC. Commentary: Screening: a seductive paradigm that has generally failed us. Int J Epidemiol. 2015;44:278-280.Editorial
Fang F, Keating NL, Mucci LA, et al. Immediate risk of suicide and cardiovascular death after a prostate cancer diagnosis: cohort study in the United States. J Natl Cancer Inst. 2010;102:307-314. Article
Saquib N, Saquib J, Ioannidis JP. Does screening for disease save lives in asymptomatic adults? Systematic review of meta-analyses and randomized trials. Int J Epidemiol. 2015;44:264-277. Abstract
Bleyer A, Welch HG. Effect of three decades of screening mammography on breast-cancer incidence. N Engl J Med. 2012;367:1998-2005. Article
Gøtzsche PC, Jørgensen KJ. Screening for breast cancer with mammography. Cochrane Database Syst Rev. 2013;6:CD001877. Abstract
Biller-Andorno N, Jüni P. Abolishing mammography screening programs? A view from the Swiss Medical Board. N Engl J Med. 2014;370:1965-1967. Editorial
Gigerenzer G. Full disclosure about cancer screening. BMJ. 2016;352:h6967 Editorial

New Push Ties Cost of Drugs to How Well They Work

Source: Wall Street Journal

As drug costs rise, Express Scripts seeks new payment deals for some cancer medications

PETER LOFTUS

May 26, 2015 7:59 p.m. ET

Express Scripts Holding Co., a large manager of prescription-drug benefits for U.S. employers and insurers, is seeking deals with pharmaceutical companies that would set pricing for some cancer drugs based on how well they work.

The effort is part of a growing push for so-called pay-for-performance deals amid complaints about the rising price of medications, some of which cost more than $100,000 per patient a year.

Some insurers and prescription-benefit managers are pushing back by arguing that they should pay less when drugs don’t work well in certain patients. Drug companies are countering with pricing models of their own, such as offering free doses during a trial period.

Express Scripts this month told clients it is seeking deals with drug makers for differentiated pricing for certain cancer drugs based on how well they work against different types of tumors, Express Scripts Chief Medical Officer Steve Miller said in an interview. Currently, Express Scripts and most insurers pay the same per-unit rate for a cancer drug regardless of the type of cancer it is being used to treat.

Dr. Miller pointed to Tarceva, a drug co-marketed by Roche Holding AG and Astellas Pharma Inc., which has shown a smaller benefit in pancreatic cancer than in lung cancer. In one clinical trial, Tarceva extended the median survival of pancreatic cancer patients by less than two weeks versus placebo. In a separate trial, it prolonged survival among lung cancer patients by about 3 ½ months versus chemotherapy.

In an “indication-specific pricing” model, the per-pill cost of Tarceva would be lower for pancreatic-cancer patients than for lung-cancer patients, given the reduced efficacy, Dr. Miller said. Tarceva currently costs about $6,850 a month per patient, according to GoodRx, a website that tracks drug prices.

“One of the big frustrations has always been people paying top dollar for drugs that aren’t always giving them the best response,” Dr. Miller said. “If pharma is truly sincere about wanting value-based reimbursement, we now have the sophistication to do that.”

ENLARGE

Although Dr. Miller used Tarceva as an example, he wouldn’t identify the drugs for which Express Scripts is seeking indication-specific pricing. The company has begun approaching drug makers about arranging such deals, which could go into effect for 2016, he said.

A spokeswoman for Roche’s Genentech unit said that when Tarceva was approved to treat pancreatic cancer in 2005, it was the first medicine approved for the disease in more than a decade. She said the drug is now rarely used to treat pancreatic cancer because other drugs have since been approved for the disease. She said Genentech would welcome a system of pricing a medicine based on how it performs in different indications—and has one in place in Italy—but there are challenges to doing so in the U.S., including fragmented patient-record systems.

Express Scripts has in recent years been a vocal critic of high drug prices, which the company has used to promote its services to potential customers as it competes against CVS Health Corp. and others to administer drug benefits for health insurers and large employers. Pharmacy-benefit managers also sometimes keep a portion of the rebates and discounts they negotiate from pharmaceutical companies.

Express Scripts’ approach would be similar to that proposed by Peter Bach, director of the Center for Health Policy and Outcomes at Memorial Sloan Kettering Cancer Center.

In an article published last year in the Journal of the American Medical Association, he suggested that in an indication-specific arrangement, the monthly price for Eli Lilly & Co.’s cancer drug Erbitux would plummet from $10,320 a patient to about $470 a patient for its least effective use, treating recurrent or metastatic head and neck cancer. The drug also is used to treat locally advanced head and neck cancer, as well as colorectal cancer.

A Lilly spokeswoman said Lilly supports efforts to make cancer drug reimbursement “better reflect treatment value for different patient populations,” and it is “exploring alternative options to accurately represent the value our medicines offer across multiple indications.”

Drug pricing has been “very hard for the payers to do anything about,” said Steven Pearson, president of the Institute for Clinical and Economic Review, a Boston nonprofit that evaluates cost-effectiveness in medicine. “Now they’re starting to think very hard about it, to look for practical ways to have more of an influence on pricing.”

It can be difficult for drug companies and payers to agree on terms of alternative payment deals—and to actually administer the deals.

Pay-for-performance contracts often involve tracking certain health measures and outcomes in specific patients, such as changes in blood-sugar levels for diabetes patients. The cost and complexity of such tracking can offset the benefits, and the number of such deals in the U.S. to date has been relatively small.

“They’re very data intensive to administer and track these,” says Larry Blandford, executive vice president and managing partner at Precision for Medicine, a consulting firm advising drug makers on dealing with payers.

U.S. insurers and pharmacy-benefit managers also push for simple price cuts, and sometimes win them in the form of rebates paid by manufacturers. But drug makers have been able to avoid big, across-the-board price cuts in the U.S. because the market is so fragmented, with multiple public and private payers, and because rebate contracts are typically confidential. That allows drug companies to minimize or avoid discounting certain drugs for some payers.

Some drug companies have explored their own variations of alternative pricing, such as annuity-style payments for very expensive drugs. This involves an upfront payment and then ongoing payments stretched out over several years based on how well the drug works in individual patients.

One example is Bluebird Bio Inc., which is developing an experimental gene therapy for rare diseases. At a health-care conference in February, Chief Executive Nick Leschly said that if the therapy makes it to market, he would consider asking insurers to make an upfront payment to cover costs and risk of development, plus additional ongoing payments if it works for a patient.

Other drug makers are trying different models. Since 2011, Acorda Therapeutics Inc. has provided its drug Ampyra, which can help multiple-sclerosis patients improve their walking, free for the first two months.

The reason: Studies have shown it only works in about 40% of patients, but there is no way to predict before starting therapy who will benefit. The two-months free program gives patients time to figure out if the drug is working—they usually know within several weeks, says Acorda Chief Executive Ron Cohen. If the drug works, the company begins charging the regular price, or about $21,000 a year per patient.

Acorda implemented the two-months free policy partly because some insurers were restricting its use. The two-months free program isn’t part of any contracts with insurers, but Dr. Cohen believes it sows goodwill among doctors and insurers.

“We saw that as a risk-sharing arrangement,” said Dr. Cohen.

He says “a significantly wider swath” of the drug industry is exploring alternative-pricing models than in the past. “A lot of the pressure emerges simply from the ongoing issues around the increasing cost of medicine,” he says.

Alnylam Pharmaceuticals Inc. would consider performance-based pricing if its experimental rare-disease drugs reach the market, CEO John Maraganore said in an interview. The company’s lead drug in development is a treatment for a rare disease called TTR-mediated amyloidosis. Regulators haven’t yet approved the drug for sale and Alnylam hasn’t set a price.

Mr. Maraganore said blood tests can measure the effectiveness of its experimental drug. “I think there are many opportunities for our medicines to be evaluated and potentially reimbursed on a performance basis,” he said. “We certainly would be open to that type of approach.”

The drug industry has made various stabs at alternative-pricing before. Several European state-run health systems have implemented pay-for-performance and indication-specific pricing arrangements with drug makers over the past decade. In the U.S., health insurer Cigna Corp. has signed deals that tie reimbursement for EMD Serono’s MS drug Rebif and Merck & Co.’s diabetes drug Januvia to certain patient outcomes.

—Joseph Walker contributed to this article.

Write to Peter Loftus at peter.loftus@wsj.com

El cáncer- los gorriones, los osos y las tortugas

By: Alberto Velazquez. TEDxUBA

Published on Dec 22, 2013

In the spirit of ideas worth spreading, TEDx is a program of local, self-organized events that bring people together to share a TED-like experience. At a TEDx event, TEDTalks video and live speakers combine to spark deep discussion and connection in a small group. These local, self-organized events are branded TEDx, where x = independently organized TED event. The TED Conference provides general guidance for the TEDx program, but individual TEDx events are self-organized.* (*Subject to certain rules and regulations).

Antigeno Prostatico Especifico: inutil para el cribado de cancer de prostata

Todavia desconozco en que idioma hay que escribir esto, pero por enesima vez sale otro articulo que dice que la PSA, no tiene ninguna utilidad en el cribado de cáncer de próstata y que sólo sirve para el seguimiento de pacientes con Cáncer de prostata. El tema es simple. Se trata de una prueba inespecifica, y el famoso antigeno es volumen-dependiente del tamaño de la prostata. Por ende, en la natural evolucion que tenemos los hombres la prostata se agranda con la edad. Por tanto, ningun valor sirve para diferenciar si ese agrandamiento se debió a la hipertrofia prostática benigna, que también es muy común luego de los 65 años. Por otro lado, un viejo anatomista, Testut, ya escribia en su tratado que data del año 1900, que en sus autopsias encontraba un 100% de cáncer de prostata en hombres mayores de 80 años. En otras palabras, y aunque los urólogos se empeñen en poner al cancer de próstata como un grave problema de salud, colocandolo entre las primeras causas de muerte, la realidad indica, que nos morimos más con cáncer de próstata que por el cáncer mismo. Por ende es un buen marcador de la evolución del cáncer pero no tiene ninguna utilidad, escrito en Inglés (también ha sido escrito en castellano, catalán, portugues, francés, ruso, y seguramente en esperanto) por el British Medical Journal.
Por ende tendremos que seguir lidiando con los expertos que aparecen en la prensa de todo el mundo, e intentan convencer a la gente de hacerse estos estudios desde los 50 años.

Utilizando una cohorte grande Seuca relacionada con un registro nacional de cáncer, los investigadores compararon los valores iniciales de PSA de aquellos que desarrollaron cáncer de próstata en el curso de 7 años post escrutinio, con otros hombres de similares características que no desarrollaron cáncer de próstata. La sobreposición de los valores de PSA frustraron los esfuerzos de los investigadores de encontrar un valor que tenga alta especificidad así como una sensibilidad del 50%. Sin embargo, notaron que un valor de PSA menor de 1 ng/mL virtualmente descarta el diagnóstico durante el período de seguimiento.

Debido a los resultados de este estudio, se podría decir que los datos sobre los costos y beneficios de las pruebas de PSA permanecen insuficientes para apoyar el escrutinio masivo.

Referencia: Benny Holmström, et al. Prostate specific antigen for early detection of prostate cancer: longitudinal study. BMJ. Septiembre 2009;339:b3537.

Using Evidence to Combat Overdiagnosis and Overtreatment: Evaluating Treatments, Tests, and Disease Definitions in the Time of Too Much

Source

PLOS Medicine.

Ray Moynihan

As a matter of urgency, the potential for overdiagnosis and related overtreatment should be routinely considered for inclusion in the introduction and discussion sections of reports of studies of therapies, studies of diagnostic test accuracy, systematic reviews of those studies, clinical guidelines, and changes to disease definitions (Box 1). Second, there is a clear need for more research—both original studies and reviews of studies—into the nature and extent of overdiagnosis and related overtreatment within specific conditions—as, for example, has occurred with studies on the risks associated with mammography [5]. Third, the potential harms associated with new treatments and tests, or expanded disease definitions, demand much greater attention in primary studies and reviews.

Box 1. Summary of Suggestions for Improving the Evidence Base to Combat Overdiagnosis and Related Overtreatment

Routine consideration of overdiagnosis and related overtreatment in the introduction and discussion sections of primary studies and systematic review articles about tests and treatments
More condition-specific studies and reviews on the risk of overdiagnosis and related overtreatment—e.g., diagnosis of pulmonary embolism
More rigorous routine evaluation of potential harms of treatments, tests, and changes to disease definitions
In studies and reviews of studies of therapies, clearer stratification by baseline risk, to better identify treatment thresholds where benefits are likely to outweigh harms
In studies and reviews of studies of test accuracy, more clarity about which target condition or spectrum of a disease is being considered, with a shift from a dichotomous “disease/no disease” frame to a “spectrum of disease severity” frame, and a linking of test accuracy to consequences for treatment and patient outcomes
Panels that review and change disease definitions that are free of conflicts, and routinely consider evidence for potential harms as well as potential benefits of the changes they propose

For evaluation of treatments, more clarity is required about the specific definitions of diseases being treated in primary treatment studies and subsequent systematic reviews. As per the recommendations of Kent and colleagues [11], clearer stratification of groups at varying degrees of baseline risk or disease stage is needed, to better identify treatment thresholds at which the harms of treatment start to outweigh benefits. Sometimes this will require re-analysis of large (e.g., pooled individual participant) datasets, underscoring the need for access to raw data from trials.

For primary studies and reviews of studies of diagnostic test accuracy, there is a need to make explicit exactly which stages or spectrum of a target disease is being considered—also referred to as the “target condition” [14]. Where possible, it may be desirable to shift the paradigm from a dichotomous frame—disease presence versus absence—to thinking about a spectrum of disease severity. Moreover, when diagnostic studies show improved detection (or exclusion) of specific disease stages, researchers should try to link the consequences of such improved diagnostic accuracy to subsequent treatment decisions. Ideally, the consequences of such changed treatment decisions for patient outcomes might also be addressed [16]. Such elaborations to conventional diagnostic test accuracy studies would help identify at what diagnostic disease spectrum thresholds subsequent treatments will do more good than harm.

And, finally, the need to improve the process of disease definition—with awareness of the dangers of overdiagnosis and overtreatment—is being increasingly accepted, with international organisations, including the Guidelines International Network, currently looking to develop new guidance. While a detailed debate will ensue in coming years, we believe several key principles might underpin the reform of how disease definitions are changed: panel members should be free of financial and reputational conflicts of interest; strong evidence, ideally from randomised trial data, should demonstrate that the use of new criteria will meaningfully reduce mortality and/or morbidity; and potential benefits and potential harms of labelling and treatment using the new criteria should be explicitly investigated and reported.

Conclusions

We offer these suggestions as part of the wider scientific debate underway on how to safely and fairly wind back the harms of too much medicine [17]. We are hopeful that a heightened attention to the dangers of overdiagnosis and related overtreatment may lead to an enhanced evidence base on these topics. This, in turn, will help produce fairer, more rational, and less wasteful health care systems, built on a reformed process of disease definition that offers diagnostic labels and medical interventions only to those likely to benefit from them.

Comparative evaluation of radiation treatments for clinically localized prostate cancer: an update

Source: Centers of Medicare

With the advent of the prostate-specific antigen (PSA) test in the 1990s, the lifetime risk of being diagnosed with prostate cancer in the United States has nearly doubled to twenty percent. However, the risk of dying of prostate cancer remains at approximately three percent. Once prostate cancer has been diagnosed, the decision on the best course of treatment can be complex. Numerous factors can influence the decision on how to proceed, including that some prostate cancers grow so slowly they would likely never cause significant problems during a patient’s lifetime. The adverse effects of the available interventions and how they affect quality of life must also be considered.

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Prevencion del cancer colorrectal

Pruebas de detección habituales previenen el cáncer colorrectal

MMWR, Apr 14, 2008 18:15:00 GMT

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El cáncer colorrectal es el segundo tipo de cáncer que causa más muertes en Estados Unidos. Este cáncer afecta a hombres y mujeres de todos los grupos étnicos y raciales, pero es más común en las personas mayores de 50 años. El cáncer colorrectal se puede prevenir. Las pruebas periódicas pueden detectar pólipos en el colon que pueden ser retirados antes de convertirse en cáncer. Las personas de 50 años o más, con antecedentes familiares de este cáncer, deben ver al doctor para hacerse prueabas periódicas.

Relacion entre IMC y cancer

Relación entre el IMC y el riesgo de cáncer

Renehan AW, Tyson M, Egger M, Heller RF, Zwahlen M. Body-mass index and incidence of cancer: a systematic review and meta-analysis of prospective observational studies. Lancet 2008; 336: 569-578. R TC (s) PDF (s)

Introducción

En numerosos estudios, el exceso de peso se ha relacionado con un incremento del riesgo de desarrollar determinados tumores. Sin embargo, la diversidad de localizaciones, tipos de estudios y medidas de resultado utilizadas dificultan la comparación de los datos.

Objetivo

Rervisar la relación entre el IMC y la fuerza de la asociación con determinados tumores e investigar las diferencias respecto al sexo y distintos grupos étnicos.

Perfil del estudio

Tipo de estudio: Metaanálisis

Área del estudio: Causa

Ámbito del estudio: Comunitario

Métodos

Se llevó a cabo una búsqueda en Medline, Embase, las listas de referencias de los trabajos localizados y otras fuentes bibliográficas relevantes para localizar los estudios de cohortes (y los de casos y controles anidados dentro de éstos), publicados en cualquier idioma, en los que se investigaba la relación entre el IMC y la incidencia de 20 tipos diferentes de tumores en 15 localizaciones diferentes (colorrectal, gastroesofágico, hepatobiliar, leucemia, pulmonar, melanoma, mieloma, linfoma no hodgkiniano, leucemia, pancreático, renal, tiroideo, prostático, mamario, endometrial y ovárico.

Los criterios de inclusión fueron que se midiese el IMC al inicio del estudio, se registrase la incidencia de nuevos tumores en el seguimiento, que proporcionasen medidas de estimación del riesgo para al menos 3 categorías de IMC. Se excluyeron las publicaciones que no eran informes completos, los que sólo proporcionaban datos de mortalidad (en vez de incidencia) y los estudios sobre lesiones preneoplásicas. En función de su origen étnico, se clasificaron a los participantes como norteamericanos (>80% blancos), europeos-australianos, afroamericanos, asiáticos y multiétnicos.

Resultados

Cumplieron los criterios de inclusión 141 artículos que aportaron datos de 76 estudios con 221 conjuntos de datos que supusieron más de 133 millones de personas-año de observación y 282.173 casos incidentes de cáncer. Más de la mitad de los trabajos y los de mayor tamaño se habían publicado a partir de 2004.

Los IMC elevados se asociaron a un mayor riesgo de presentar cáncer en numerosas localizaciones en ambos sexos (adenocarcinoma de esófago, tiroides, colon, riñón, mieloma y leucemia), así como en algunos tumores propios de la mujer (endometrio y mama en la postmenopausia). En cambio, el exceso de peso se asoció a un menor riesgo de cáncer de pulmón y de carcinoma escamoso de esófago. En estos casos, es posible que esta asociación se deba en gran parte al efecto de confusión del tabaco, que se asocia a un menor peso y a un mayor riesgo de estos tipos de tumores.

Tabla 1. Riesgo relativo para diferentes tipos de tumores por cada 5 kg/m² de IMC.
	Varones	Mujeres
Adenocarcinoma de esófago	1,52 (1,33 a 1,74)	1,51 (1,31 a 1,74)
Tiroides	1,33 (1,04 a 1,70)	1,14 (1,06 a 1,23)
Colon	1,24 (1,20 a 1,28)	1,09 (1,05 a 1,13)
Renal	1,24 (1,15 a 1,34)	1,34 (1,25 a 1,43)
Hígado	1,24 (0,95 a 1,62)	1,07 (0,55 a 2,08)
Melanoma	1,17 (1,05 a 1,30)	0,96 (0,92 a 1,01)
Mieloma	1,11 (1,05 a 1,18)	1,11 (1,07 a 1,15)
Recto	1,09 (1,06 a 1,12)	1,02 (1,00 a 1,05)
Vesícula	1,09 (0,99 a 1,21)	1,59 (1,02 a 2,47)
Leucemia	1,08 (1,02 a 1,14)	1,17 (1,04 a 1,32)
Páncreas	1,07 (0,93 a 1,23)	1,12 (1,02 a 1,22)
Linfoma no hodgkiniano	1,06 (1,03 a 1,09)	1,07 (1,00 a 1,14)
Próstata	1,03 (1,00 a 1,07)	–
Gástrico	0,97 (0,88 a 1,06)	1,04 (0,90 a 1,20)
Pulmón	0,76 (0,70 a 0,83)	0,80 (0,66 a 0,97)
Escamoso de esófago	0,71 (0,60 a 0,85)	0,57 (0,47 a 0,69)
Endometrio	–	1,59 (1,50 a 1,68)
Mama (postmenopausia)	–	1,12 (1,08 a 1,16)
Ovario	–	1,03 (0,99 a 1,08)
Mama (premenopausia)	–	0,92 (0,88 a 0,97)

En los análisis de subgrupos, las asociaciones ente el IMC y el riesgo de cáncer fueron más fuertes para los varones que para las mujeres para el cáncer colorrectal y a la inversa para el cáncer renal. La mayor parte de las asociaciones fueron pareceidas para las diferentes áreas geográficas, pero para el cáncer de mama en la premenopausia se encontró una relación directa con el IMC para los estudios llevados a cabo en países asiáticos e inversa para el resto de las regiones geográficas. En los países asiáticos la relación entre el IMC y el cáncer de mama en la postmenopausia también fue mas fuerte que en las otras regiones.

Conclusiones

Los autores concluyen que el IMC elevado se asocia a un mayor riesgo de sufrir determinados tumores y que esta asociación puede variar entre los dos sexos y para personas de diferentes orígenes étnicos.

Conflictos de interés

Uno de los autores ha recibido honorarios de varios laboratorios farmacéuticos. Financiado parcialmente por una beca de la British Medical Association.

Comentario

En este estudio se confirma el hallazgo de estudios previos de que la presencia de obesidad se asocia a un mayor riesgo de desarrollar determinado tipo de tumores. El hecho de que para el mismo sólo se hayan utilizado los datos de estudios prospectivos limita la posibilidad de determinados sesgos como el del recuerdo selectivo. Por otro lado, el que sólo se hayan utilizado datos de incidencia permite limitar el efecto de otros factores como el peor pronóstico que presentan los obesos para determinados tipos de tumores, que pueden afectar a los estudios que se llevan a cabo con datos de mortalidad.

Una limitación de este estudio es que el análisis estadístico da como resultado un incremento de riesgo por cada unidad de IMC, pero es posible que el incremento de riesgo no sea lineal, puesto que en algunos estudios previos el exceso de riesgo de tumores se concentró en los pacientes con obesidades mórbidas. Por otro lado, tampoco permite analizar si, como en el caso de las enfermedades cardiovasculares, determinados tipos de obesidad, como la abdominal, se asocian a un mayor riesgo.

El hecho de que se dé esta asociación estadística no prueba por sí solo que esta relación sea causal. Irían a favor de una relación de este tipo la especificidad del efecto y el hecho de que en los estudios de intervención sobre la obesidad se detectase en las personas asignadas al grupo intervención una reducción de la incidencia de tumores malignos. Sin embargo, los estudios publicados de este tipo suelen tener unos efectos modestos y acostumbran a tener unos seguimientos no demasiado largos. No obstante, en un ensayo clínico llevado a cabo en pacientes con obesidad mórbida tratados mediante cirugía bariátrica en los pacientes asignados al grupo intervención la mortalidad fue inferior que en los asignados al grupo control y entre las enfermedades que presentaron una reducción importante de la mortalidad (próxima a la mitad) se encontraban los tumores.

Bibliografía

Hu FB, Stampfer MJ, Manson JE, Grodstein F, Colditz GA, Speizer FE, Willett WC. Trends in the incidence of coronary heart disease and changes in diet and lifestyle in women. N Engl J Med 2000; 343: 530-537. R TC PDF

Autor

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

Shared care by paediatric oncologists and family doctors for long-term follow-up of adult childhood cancer survivors: a pilot study

Lancet Oncology 2008; 9:232-238

DOI:10.1016/S1470-2045(08)70034-2

Articles

Dr Ria Blaauwbroek MD a , Wemke Tuinier RN a, Prof Betty Meyboom-de Jong PhD b, Prof Willem A Kamps PhD a and Aleida Postma PhD a

Summary

Background

Since 75% of children with cancer will become long-term survivors, late effects of treatment are an ever increasing issue for patients. Paediatric oncologists generally agree that cancer survivors should be followed up for the remainder of their lives, but they might not be the most suitable health-care providers to follow up survivors into late adulthood. We designed a 3-year study to assess whether shared-care by paediatric oncologists and family doctors in the long-term follow-up of survivors of childhood cancers is feasible, whether a shared-care model is compatible with collection of data needed for registration of late effects, and how a shared-care model is assessed by survivors and family doctors.

Methods

In 2004 and 2005, adult survivors of childhood cancers were randomly chosen from eligible patients diagnosed with childhood cancer (excluding CNS tumours) or Langerhans-cell histiocytosis between January, 1968, and December, 1997, and recalled to the long-term follow-up (LTFU) clinic at the University Medical Centre Groningen, Groningen, Netherlands, where they underwent physical and clinical assessments by an on-site family doctor (visit 1). At this visit, assessments were done according to guidelines of the UK Children’s Cancer Study Group Late Effects Group, and late effects were graded by use of Common Terminology Criteria for Adverse Events (version 3). Follow-up assessments were done 1 year later in 2005 and 2006 by local family doctors (visit 2), who were asked to return data to the LTFU clinic. At this visit, the local family doctors were asked to complete a three-item questionnaire and patients were asked to complete a seven-item questionnaire about their satisfaction with the shared-care model. At the next consultation, which was planned for the end of the study (visit 3), the on-site family doctor advised patients about future follow-up on the basis of their individual risk of late effects. Main endpoints were numbers of participants, satisfaction ratings, and proportions of local family doctors who returned data that they obtained at visit 2 to the LTFU clinic.

Findings

133 individuals were chosen at random from 210 enrolled adult survivors. 123 of 133 (92%) randomly selected survivors and 115 of 117 (98%) of their family doctors agreed to participate in the share-care programme. 103 of 115 (90%) family doctors returned data to the LTFU clinic at visit 2. 89 of 101 (88%) of survivors were satisfied with this shared-care model, as were 94 of 115 (82%) family doctors; 18 of 115 (16%) family doctors had no views either way; and three of 115 (3%) family doctors were dissatisfied.

Interpretation

Shared-care by paediatric oncologists and family doctors is feasible for long-term follow-up of adult survivors of childhood cancers.

Affiliations

a. Department of Paediatrics, Division of Paediatric Oncology, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands
b. Department of General Practice, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands

Correspondence to: Dr Ria Blaauwbroek, Department of Paediatrics, Division of Paediatric Oncology, University Medical Centre Groningen, University of Groningen, 9700 RB Groningen, Netherlands

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