Wednesday, July 27, 2011

Cell Phones and Cancer: Is There a Connection?

From Medscape Neurology

Bret Stetka, MD; Nora D. Volkow, MD

Editor's Note:
 
On May 31, 2011 the World Health Organization (WHO) announced their classification of radiofrequency electromagnetic fields emitted from cell phones as "possibly carcinogenic," and more recently published the evidence and rationale supporting their conclusion. Medscape recently spoke with National Institute on Drug Abuse Director (and BlackBerry® user) Nora D. Volkow, MD, about the implications of both the WHO statement and her own research showing that cell phone usage directly affects brain glucose metabolism.

Cell Phones and Cancer: Introduction

Medscape: Hello Dr. Volkow. What was your reaction to the WHO report concluding that electromagnetic fields from cell phones are "possibly carcinogenic?" Do you believe that the available data support this conclusion?
Dr. Volkow: I think that the report was justified on the basis of results that are inconsistent but which cannot be ignored. It seems prudent in this situation -- in which there are some results [linking cell phone use with malignancy] -- to be cautionary. I think that is why they came up with this recommendation.
It wasn't strong evidence, which the authors of The Lancet paper discuss. However, they couldn't just dismiss and ignore the findings.
Medscape: I found it interesting that the INTERPHONE study showed that in all exposure groups except that with the highest cell phone exposure, there was actually a reduced or equal incidence of glioma compared with those who'd never used a cell phone. What do you make of this finding?
Dr. Volkow: One could interpret this as implying that cell phone exposure at lower levels is actually protecting against glioma, whereas others would say that it means that long-term exposure is required to induce cancer. So you have both sides of the coin. It highlights how important it is to properly address this question -- to do a study that will be able to answer it definitively.
As The Lancet paper discussed, the effects that the researchers are looking for here may not be observable for 20 or 30 years. It could be similar to what was seen with cigarettes and cancer in which several decades of smoking behavior in patients were often necessary to uncover the linkage.
To summarize, there are studies that show [no association between cell phones and cancers] and there are some studies that do show an association.

Time Will Tell

Medscape: Cell phones weren't widely used until the last 10 or 15 years, so you're saying that it might just be too early to tell whether there's an association?
Dr. Volkow: It is clear that even though cell phones have now been out for the past 25 years, the rate of use then was limited to a few people and the amount of use was also limited. It wasn't until much more recently that their use became massively widespread.
In my view, by coming up with a conservative statement, the WHO is saying that we need to be observant and not become too complacent.

Cell Phones as Therapy?

Medscape: Can you give our readers a summary of your recent study linking cell phone use with altered glucose metabolism in the brain?
Dr. Volkow: Yes. We showed a correlation between exposure to electromagnetic radiation from a cell phone (the sound was muted) and increased brain glucose metabolism, which is a marker of brain function, in the areas of the brain closest to the antenna of the cell phone. So there is definitely a physiologic response in the brain to cell phone exposure, which we're attributing to electromagnetic radiation.
Medscape: Your data have shown no specific connection, and you've made no claims about a connection between this increased activity and malignancy. Correct?
Dr. Volkow: No, nothing. I wish! I would love for our data to illuminate this issue, but they don't; no matter how much imagination I use, there is no way of relating our finding to the issue of carcinogenicity. Our data just show that the brain is sensitive to the electromagnetic radiation emitted from cell phones.
Medscape: Your participants did not actually speak or listen on cell phones in order to control for potentially confounding brain activity, but could some of the increased activity have been caused by the brain anticipating and preparing for speech?
Dr. Volkow: Actually, in order to avoid that confounder, each participant had 2 cell phones -- one on each side of the head. Therefore, participants could not know where the signal was coming from. This was because expectations can profoundly affect brain processes. Indeed, that is at the basis of the placebo effect. We are very sensitive to the influence of expectation.
So is cell phone use harmful? We cannot say on the basis of our initial study. We need to look into whether there are long-lasting effects on the brain due to cell phone use and whether these have deleterious consequences. That is a question that remains unresolved.
If there are no negative effects, this could then be a very interesting technology to evaluate as a potential therapy, for example, in cases in which you need to rehabilitate an area of the brain and want to stimulate it.
Medscape: That's a good point because psychiatric and neurologic therapies such as transcranial magnetic stimulation work by applying an electromagnetic field to the brain.
Dr. Volkow: Yes, and this is a very accessible, low-cost technology. For me, the most important thing is to determine whether this type of stimulation is linked with any long-lasting negative consequences, and if it is not, evaluate the potential of this type of electromagnetic stimulation for therapeutic applications.

So What's Next?

Medscape: Do you and your colleagues have any follow-up studies planned?
Dr. Volkow: First, we want to replicate our finding and extend it to determine whether there is any evidence that there may be long-lasting effects. Although the ideal study would be to evaluate participants prospectively, that is very costly and we don't have the resources to do such a study; we will need to address it retrospectively on the basis of previous cell phone exposure.
We will control for exposure on the basis of cell phone records and behavioral questionnaires, but we also want to use different markers in brain imaging beyond just brain glucose metabolism. Among others we want to assess the effects of cell phone exposure on brain functional connectivity.
To do this we will obtain a functional MR map of functional connections before and after cell phone exposure to see whether the areas in which we are observing increases in metabolism are linked to changes in the way that the brain is transmitting information.

Should We Throw Out Our Cell Phones?

Medscape: On the basis of your findings and the WHO report, how do you think clinicians should approach this subject with patients? Should they cut back on cell phone usage -- or better yet, just throw them out?
Dr. Volkow: No, no! I haven't thrown mine out. That would be too deleterious to my life.
An important point that some people have made is that the most dangerous aspect of cell phones is using them while driving or in other inappropriate situations. The other day I found myself texting while walking across the street. I said to myself, "No, I should not be doing this." Regardless of what the data end up showing, this type of behavior is likely the greatest cause of mortality and morbidity related to cell phones.
Therefore, I would explain that although some studies reported an increased risk for malignancy associated with cell phones others did not, so we just don't know. I think it's important to bring knowledge to people in a way that is comprehensive and accurate and let them make the decisions about how they are going to use technology. Even if there is an association, it's not the end of the world because you can still use your cell phone -- just change the behavior by which you use them. Don't bring them close to your head, and use a headset or the speakerphone option -- anything that keeps the phone way from your head.
However, I would feel confident saying to parents in particular that they should educate their children to avoid using cell phones close to their ears. Due to children's size, the amount of deposition of energy is higher than that in an adult. The Lancet paper discusses this.
It also has greater effects on the bone marrow of children. Another aspect that they don't discuss but which is relevant is that the brains of children and adolescents are undergoing very fast developmental changes. Their brains are much more neuroplastic and susceptible to changes triggered by environmental stimuli.
Basically we don't have sufficient knowledge to know how cell phone signals affect brain processes. Why not play it safe? How you modify your behavior depends in part how you handle uncertainty: I am very bad at dealing with uncertainty in regard to potential effects to my brain so I chose to be conservative
Medscape: Has your cell phone usage changed in light of the current evidence?
Dr. Volkow: I haven't decreased the amount of time that I use my cell phone. However, I do try to avoid placing the cell phone to my ear whenever possible. I can't always put it on speakerphone, then everyone would hear my conversations!
 

Antibiotic Better Than Cranberries for UTI Prevention

From Medscape Medical News

Laurie Barclay, MD

July 26, 2011 — Trimethoprim-sulfamethoxazole (TMP-SMX) is more effective than cranberry capsules for prevention of recurrent urinary tract infection (UTI) in premenopausal women, according to the results of a double-blind, double-dummy noninferiority trial reported in the July 25 issue of the Archives of Internal Medicine.
"The increasing prevalence of uropathogens resistant to antimicrobial agents has stimulated interest in cranberries to prevent recurrent ...UTIs," write Mariëlle A. J. Beerepoot, MD, from the Academic Medical Center in Amsterdam, the Netherlands, and colleagues.
"For premenopausal women with more than 2 UTIs per year, low-dose antibiotic prophylaxis is commonly recommended. However, this may lead to drug resistance not only of the causative microorganisms but also of the indigenous flora."
In this study, 221 premenopausal women with recurrent UTIs were randomly assigned to receive prophylaxis with TMP-SMX, 480 mg once daily, or cranberry capsules, 500 mg twice daily, for 12 months.
The main study outcomes were the mean number of symptomatic UTIs during the 12-month period of prophylaxis, the proportion of women who had 1 or more symptomatic UTIs, the median time to first UTI, and development of antibiotic resistance in indigenous Escherichia coli.
Compared with the TMP-SMX group, the cranberry group had a higher mean number of patients with at least 1 symptomatic UTI after 12 months (4.0 vs 1.8; P = .02) and a higher proportion of patients with at least 1 symptomatic UTI (78.2% vs 71.1%). In the cranberry group, median time to the first symptomatic UTI was 4 months, compared with 8 months in the TMP-SMX group.
TMP-SMX resistance after 1 month was present in 23.7% of fecal and 28.1% of asymptomatic bacteriuria E coli isolates in the cranberry group, compared with 86.3% and 90.5%, respectively, in the TMP-SMX group. Resistance rates for trimethoprim, amoxicillin, and ciprofloxacin in these E coli isolates after 1 month were also increased in the TMP-SMX group. When TMP-SMX was discontinued, resistance returned to baseline levels after 3 months.
In the cranberry group, antibiotic resistance did not increase. Participants tolerated cranberries and TMP-SMX equally well.
"In premenopausal women, TMP-SMX, 480 mg once daily, is more effective than cranberry capsules, 500 mg twice daily, to prevent recurrent UTIs, at the expense of emerging antibiotic resistance," the study authors write.
Limitations of this study include high withdrawal rates, lack of microbiological confirmation of all recurrent UTIs, inability to confirm that all women took the cranberry prophylaxis, and unclear optimal dosage of cranberries.
"From clinical practice and during the recruitment phase of this study, we learned that many women are afraid of contracting drug-resistant bacteria using long-term antibiotic prophylaxis and preferred either no or nonantibiotic prophylaxis," the study authors concluded.
"In those women, cranberry prophylaxis may be a useful alternative despite its lower effectiveness."
An invited commentary by Bill J. Gurley, PhD, from the University of Arkansas for Medical Sciences, Little Rock, notes that the comparison may not have been fair regarding dose and bioavailability of active ingredients.
"To date, few botanical dietary supplements have lived up to their claims as effective 'alternative' medicines, and until more is known about phytochemical disposition in humans, efficacy concerns will continue to plague these products," Dr. Gurley writes.
"Uncertainty regarding mechanisms of action and adequate dosing regimens underscore many of these concerns. It would appear, however, that cranberry has the potential to dispel some of this uncertainty."


Arch Intern Med. 2011;171:1270-1278, 1279-1280.

Monday, July 25, 2011

Unsafe Injection Practices: Outbreaks, Incidents, and Root Causes

From Medscape Education Infectious Diseases

David Pegues, MD; Karen Hoffman, RN, MS; Joseph Perz, DrPH, MA; Robin Stackhouse, MD
Another example of an outbreak resulting from direct syringe reuse occurred in a hospital-based pain clinic in Oklahoma in 2002. The staff prefilled syringes with fentanyl and propofol to treat multiple patients. It seemed like a good idea, but they reused the syringes through heparin locks, which they thought was the safety factor, into the intravenous lines. This breach resulted in a large number of infections: 71 cases of HCV infection and 31 cases of HBV infection.

It's not just the number of patients infected, but the hundreds, sometimes tens of thousands, of patients who require notification and who must live with uncertainty while awaiting their test results.
Imagine as a parent being notified that your child was potentially exposed to blood-borne viruses while receiving routine medical care.
It's the nature of hepatitis as well as HIV infections. There is an incubation period with the hepatitis viruses and HIV. If someone was exposed last week, it will take many months to rule out an infection. Healthcare workers go through this when they suffer a needle stick. This weighs heavily on patients who receive letters of notification about potential exposures.

Let's talk about contamination of a shared medication vial that occurs as a result of indirect syringe reuse. Indirect syringe reuse occurs when the same syringe used to administer medication to a patient is used to withdraw additional medications from vials for the same patient.
Those medication vials can become contaminated and serve as a source of infection to any patients who are administered medications from those vials. We also refer to this as "double dipping."

The outbreak in an outpatient endoscopy center in Nevada is a good example. This involved administration of a sedative in an outpatient setting. Anesthesia providers reused syringes to reenter vials of propofol. It's interesting that there was some perception of risk because these providers changed the needles on the syringes. A common misperception is that contamination is limited to the needle, representing a failure to appreciate that the needle and syringe are a contiguous unit and that the syringe can be contaminated in the process of injecting a patient with medication.
It's also important to note that contamination of the needle, and subsequently the syringe, can occur in the absence of obvious blood contamination. Another misperception is that if you can't see blood in the syringe, it doesn't contain a blood-borne pathogen.
Single-dose vials do not routinely contain a preservative or antiseptic, and although they're not intended for use in multiple patients, contamination does occur and contributes to the transmission of bacterial pathogens.

The fundamental take-home points about safe injection practices:-

  • First, it's important for providers to remember that needles and syringes are single-use devices. This isn't new, but it's something that we all need to understand and practice. Needles and syringes should not be used for more than 1 patient or be reused to draw up additional medication. Changing needles does not offer additional protection. If anything, it puts providers at risk.
  • Second, if we limit the sharing of medications, we can better achieve the double layer of protection. To that end, it's important to remind providers that we must not administer medications from a single-dose vial or bag of intravenous solution to multiple patients.
  • Third, we should attempt to limit the use of all shared medications, including vials that are approved and labeled by the US Food and Drug Administration as multidose vials. Ideally, we should use vials in the smallest quantity appropriate for a given clinical application.

CDC Issues Revised Guidelines for Postpartum Contraceptive Use

From Medscape Education Clinical Briefs

News Author: Laurie Barclay, MD
CME Author: Charles P. Vega, MD
07/12/2011;

Study Highlights


  • The CDC convened a group of 13 ad hoc reviewers to evaluate current recommendations for postpartum contraception from the WHO.
  • Ovulation can occur as early as 25 days postpartum among non–breast-feeding women, although fertile ovulation will not usually occur until at least 42 days after delivery.
  • Short interpregnancy interval is associated with a higher risk for low birth weight and preterm birth.
  • Competing with these issues is that the risk for VTE is elevated by 22-fold to 84-fold in women during the first 42 days of the postpartum period vs control participants. This risk is particularly high in the 3 weeks after delivery.
  • Women with other risk factors for VTE, such as advanced maternal age, smoking, or cesarean delivery, carry an even higher risk for postpartum VTE.
  • Nonetheless, there is no direct evidence examining the risk for VTE among postpartum women using combined hormonal contraceptives.
  • The current recommendations strongly discourage the use of combined oral contraceptives during the first 21 days after delivery. The risk for pregnancy is low during this period, but the risk for VTE is significantly elevated.
  • Combined hormonal contraceptives may be initiated between 21 and 42 days postpartum among women without other risk factors for VTE. However, among women with a risk factor, including age 35 years or older, previous VTE, immobility, transfusion after delivery, obesity, smoking, or postpartum hemorrhage, the use of combined hormonal contraceptives should be avoided until at least 42 days postpartum.
  • After 42 days postpartum, there are no restrictions on the use of combined hormonal contraceptives based on postpartum status.
  • Clinicians should also bear in mind that combined hormone contraceptives can interfere with successful breast-feeding.

Clinical Implications


  • Progestin-only hormonal contraceptives and the IUD may be initiated immediately after delivery, whereas women should not initiate contraception with a diaphragm or cervical cap until 6 weeks postpartum.
  • The current recommendations strongly discourage the initiation of combined hormonal contraceptives in the first 21 days postpartum among all women. Women without any risk factor for VTE may initiate combined hormonal contraceptives between 21 and 42 days postpartum, but women with a risk factor for VTE should wait until more than 42 days postpartum.

Friday, July 22, 2011

Vitamin E and Dementia: An Update

From Medscape Neurology > Viewpoints

Laurie Barclay, MD
Posted: 07/28/2010
Dietary Antioxidants and Long-term Risk of Dementia

Devore EE, Grodstein F, van Rooij FJ, et al
Arch Neurol. 2010;67:819-825

Summary

Higher dietary consumption of vitamins E and C was previously associated with lower risk for dementia and Alzheimer disease (AD), according to 6-year findings from the Rotterdam Study.
The goal of the present population-based, prospective study was to further examine the relationship between intake of major dietary antioxidants and long-term risk of dementia in the same Dutch cohort.
The study sample consisted of 5395 participants at least 55 years old who had no dementia and who provided dietary information at study baseline.
Mean duration of follow-up was 9.6 years.

Of 465 participants in whom dementia developed during follow-up, 365 were diagnosed with AD.
Higher baseline intake of vitamin E was associated with lower long-term risk of dementia (P=.02 for trend), after adjustment for age, education, apolipoprotein E4 genotype, total energy intake, alcohol intake, smoking, body mass index, and use of supplements.
Dementia was 25% less likely to develop in participants in the lowest tertile vs the highest tertile of vitamin E intake (adjusted hazard ratio, 0.75; 95% confidence interval [CI], 0.59-0.95).
After multivariate adjustment, dietary intake of vitamin C, beta carotene, and flavonoids were not linked to dementia risk. Findings were similar for AD risk.

Viewpoint

Compared with previous research, important contributions of this study are population-based estimates of incident dementia risk over a decade, evaluation of food-based antioxidants typically found in a Western-type diet, and assessment of various antioxidants and total vitamin E, including all 8 forms.

Despite study limitations of observational design with possible residual confounding, the findings suggest a modest reduction in long-term risk for dementia and AD associated with increased consumption of vitamin E-rich foods. Although an earlier study suggested a possible inverse association between vitamin C intake and dementia risk, this was not observed in this study.
A possible explanation is that intake of different antioxidants may affect risk at different time points in the course of dementia, supporting the need for additional research to address this question.

Abstract

Thursday, July 21, 2011

Early ART Reduces the Risk of Acquiring HIV Infection

July 19, 2011 (Rome, Italy) — Early initiation of antiretroviral therapy (ART) reduced rates of sexual transmission of HIV-1 and clinical events in couples in which one partner was HIV-1-positive and the other was HIV-1-negative, according to new findings from the HIV Prevention Trials Network (HPTN) 052 Study Team.
The findings coincide with reports from the TDF2 and Partners PrEP studies suggesting that ART can dramatically reduce transmission of HIV-1 from infected to uninfected partners.
Myron Cohen, MD, from the University of North Carolina at Chapel Hill, presented the findings for the HPTN 052 study here at the 6th International AIDS Society (IAS) Conference on HIV Pathogenesis, Treatment and Prevention.
Dr. Cohen's presentation was met with a rare standing ovation from audience members. The findings were also published online July 18 in The New England Journal of Medicine.

HPTN 052 researchers sought to compare early vs delayed antiretroviral therapy in patients with HIV-1 infection who had CD4 counts between 350 and 550 cells/mm3 and who were in a stable sexual relationship with a partner who was not infected.
A total of 1763 HIV-1 serodiscordant couples at 13 sites in 9 countries were included in the analysis. Just more than half of the participants were from Africa, and 50% of infected partners were men. Patients were randomly assigned to receive therapy either immediately or after CD4 cell counts had dropped to 250 cells/mm3 or less or HIV-1-related symptoms had occurred. Study drugs included lamivudine/zidovudine, efavirenz, atazanavir, nevirapine, tenofovir, lamivudine, zidovudine, didanosine, stavudine, lopinavir/ritonavir, ritonavir, and emtricitabine/tenofovir.

A total of 39 HIV-1 transmissions were observed during the study, indicating an incidence rate of 1.2/100 person-years (95% confidence interval [CI], 0.9 - 1.7). Of the 39 HIV-1 transmissions, 28 were virologically linked to the infected partner, indicating an incidence rate of 0.9/100 person-years (95% CI, 0.6 - 1.3). The remaining 11 infections were not linked to the study partner.
Of the linked transmissions, only 1 occurred in the early-therapy group compared with 27 in the late-therapy group (hazard ratio, 0.04; 95% CI, 0.01 - 0.27; P < .001), suggesting a strong benefit for the early initiation of antiretroviral therapy. In addition, participants receiving early therapy had fewer treatment endpoints (hazard ratio, 0.59; 95% CI, 0.40 - 0.88; P = .01).

"We now know that early initiation of antiretroviral therapy prevents the linked transmission of HIV," Dr. Cohen said in a summary session after his talk. "We know also that early antiretroviral therapy reduced the number of clinical events observed, and this further strengthens the argument for when discussion of therapy should be initiated."
According to Dr. Cohen, this study is definitive proof of the concept that early therapy can help prevent transmission. "We proved that, and we're pleased with that," he said.
Beatrice Grinsztejn, MD, from the Oswaldo Cruz Foundation, Instituto de Pesquisa Clínica Evandro Chagas, in Rio de Janeiro, Brazil, presented data on the trial's clinical outcomes at the same session, reporting a 41% reduction in HIV-1-related clinical events.
"ART not only prevented transmissions but also benefited the person taking the drugs," Dr. Grinsztejn told Medscape Medical News. According to Dr. Grinsztejn, the incidence rates of tuberculosis were almost double in the delayed-therapy group compared with in the immediate-treatment group (1.9/100 person-years vs 1.0/100 person-years).
She added that ART therapy was well-tolerated in this wide range of high-CD4 population, with low rates of serious lab abnormalities and adverse events. "No apparent difference was observed in the time to death in the delayed arm compared to the immediate arm," she said.
In a related editorial, also published online July 18 in The New England Journal of Medicine, Scott M. Hammer, MD, from the Division of Infectious Diseases, Columbia University Medical Center, New York–Presbyterian Hospital, New York City, notes that drugs to prevent HIV-1 transmission are being investigated in both infected and uninfected persons.
"In HIV-1–negative persons, drugs can be used before or after high-risk exposure (or both). The use of 1% tenofovir topical gel as a microbicide in women and of oral combination therapy with tenofovir and emtricitabine in men who have sex with men has reduced rates of HIV-1 acquisition by 39% and 44%, respectively, findings that have provided strong encouragement for these approaches," he writes.
Last week, results from 2 additional clinical trials of preexposure prophylaxis for HIV prevention among heterosexuals were presented at a press conference held by the US Centers for Disease Control and Prevention (CDC).

The CDC's Michael Thigpen, MD, principal investigator of the TDF2 study, conducted in partnership with the Botswana Ministry of Health, found that a once-daily tablet containing tenofovir/emtricitabine reduced the risk of acquiring HIV infection by 63% overall among heterosexual men and women. Results from the study were also presented in today's session at IAS.
Also at the CDC press conference, the University of Washington's Partners PrEP study found that 2 separate regimens, tenofovir and tenofovir/emtricitabine, significantly reduced HIV transmission (by 62% and 73%, respectively) among heterosexual couples in which one partner is infected with HIV and the other is not.


6th International AIDS Society (IAS) Conference on HIV Pathogenesis, Treatment and Prevention: Abstracts MOAX0102, MOAX0105. Presented July 18, 2011.
N Engl J Med. Published online July 18, 2011. Article full text, Editorial full text

Family History of Cancer Important in Screening Assessment

From Medscape Medical News

Pauline Anderson

July 19, 2011 — A family history of cancer, particularly breast and colorectal cancer, that may affect the need for prevention interventions increases with age and is particularly important in early adulthood, a new study suggests.
Cancer-related family history changes up to 3-fold between the ages of 30 and 50 years, according to the authors of the study. They recommend that, for purposes of determining cancer screening, clinicians update a patient's family history every 5 to 10 years.
"If a patient's family history is not updated during early and middle adulthood, the opportunity may be missed to intervene with earlier or more intensive screening that maximizes the likelihood of detecting cancer at an early, treatable stage," write the study authors, led by Argyrios Ziogas, PhD, from the University of California at Irvine.
The study was published in the July 13 issue of the Journal of the American Medical Association.
The aim of the study was to determine how often clinically important changes in cancer family history occur with time that would render a patient at increased risk and therefore a candidate for earlier or intensive screening.
To quantify how often significant changes in family history of breast, colorectal, or prostate cancer occur in adulthood, researchers used data from the Cancer Genetics Network (CGN), a US national registry of people with a personal or family history of cancer. They assessed changes in self-reported family history retrospectively (from birth to enrollment in the CGN) and prospectively (from enrollment to time of last follow-up.)
The analysis included 11,129 participants who were included in 1 or more of the retrospective cancer screening specific analyses; those included in the prospective analyses were a subset of this population.
 
Retrospective Analyses
For colorectal cancer, the analysis found that at age 30 years, 2.1% of participants would have met criteria for early colonoscopy screening. By age 50 years, this trend increased to 7.1% and peaked at approximately 11% at age 70 years. The 10-year rates for newly meeting high-risk screening criteria peaked at a rate of 3 additional people per 100 during ages 40 to 49 years.

For breast cancer, the study found a similar pattern with steady increases in the percentage of participants who would have met criteria for magnetic resonance imaging screening through early and middle age, from 7.2% of women at age 30 years to 11.4% at age 50 years. After age 60 years, the percentage leveled off at approximately 13%. The 10-year rates for meeting high-risk criteria for screening were fairly even from ages 20 to 50 years at 3, 2, and 3 additional persons per 100, respectively, during each respective decade.
Although prostate cancer analysis had similar findings of increasing family history until age 60 years, the overall percentage of men who would have met criteria for early prostate-specific antigen screening was much lower, at 0.9% of men at age 30 years, a rate that increased to only 2.0% by age 50 years. The 10-year rates for newly meeting high-risk screening criteria were also relatively low, remaining constant at 1 additional person who met high-risk screening criteria per 100 followed up for 10 years for men aged 20 to 70 years.
 
Prospective Analyses
The analysis for colorectal cancer found a rate of 1 additional person becoming eligible for enhanced screening per 100 participants followed up for 10 years. The age-specific results suggest that more family history changes occur during their 30s (10-year rate, 2 per 100) than their 40s (10-year rate, 1 per 100).
Analysis of breast magnetic resonance imaging showed that the overall rate of newly meeting criteria for more intensive screening was 3 additional women per 100 followed up for 10 years, with 10-year rates of 0 per 100 among women aged 35 to 39 years, 4 per 100 for women aged 40 to 49 years, and 3 per 100 for women aged 50 to 59 years.
For prostate cancer, the 10-year rate of newly meeting criteria for more intensive prostate-specific antigen screening was 7 per 100 for men younger than 30 years, 5 per 100 for men aged 30 to 39 years, and 3 per 100 for men aged 40 to 49 years. These results may not be in complete agreement with those of the retrospective analysis because of the limited data available, the study authors note.
 
Study Limitations
A limitation of the study was that it relied on reported changes in family history of cancer with time and did not consider an individual's personal medical history or prior cancer screening results, which may change during adulthood and need to be assessed by clinicians, the study authors state. The study also did not evaluate indications for genetic risk assessment and did not assess whether participants who met criteria for high-risk screening actually had this screening.
In an accompanying editorial, Louise S. Acheson, MD, MS, from Case Western Reserve University School of Medicine, Cleveland, Ohio, said that although a family history of cancer is an integral part of medical history and decision making, this information has not, until recently, been standardized or widely recorded in a structured fashion.
"To optimize the use of clinical time and resources, it is important to know when (at what ages and how often) to update the family history of common cancers," she wrote. "Knowing this, health information systems can be designed to accomplish this task. Furthermore, estimating the age-specific prevalence of increased familial risk is important for planning risk-appropriate cancer prevention services."
Having clinicians and patients participate in reviewing and recording family history will become more feasible as electronic health records compile information from all patient caregivers, writes Dr. Acheson.
 
Cost Considerations
However, Dr. Acheson said, increased levels of screening come with some risks and increased costs from, for example, more false-positive test results and test-associated complications. She pointed out that, based on American Cancer Society guidelines and estimates of the current study, approximately 7.2% of women 30 to 40 years old and 8.9% of those 40 to 50 years old would be candidates for both annual breast magnetic resonance imaging and screening mammograms, which cost roughly 10 times more than a mammogram alone.
"It's possible that if family cancer risk status was updated from ages 40-50 years, many lower risk women in that age group may forgo mammography screening," added Dr. Acheson. "The benefits, harms, and empirical results of such an approach are ripe for investigation."
 
The CGN is supported by the National Cancer Institute. The study authors and Dr. Acheson have disclosed no relevant financial relationships.
JAMA. 2011;306:172-178, 208-210.