JAMA

doi: 10.1001/jama.2010.845pmid: N/A

Process-of-Care Measures and Postoperative Infection The Surgical Care Improvement Project (SCIP)—a national quality partnership dedicated to reducing the rate of surgical complications—identified 6 infection prevention process-of-care measures for assessment and reporting. To examine the relationship between self-reported adherence to these measures and postoperative infection rates, Stulberg and colleagues Article analyzed data from 405 720 patients discharged from 398 regionally representative hospitals and found that SCIP adherence—measured as a global all-or-none composite score—was associated with a lower probability of postoperative infection. However, adherence to individual SCIP measures—the format of publicly reported SCIP performance data—was not associated with a lower probability of infection. In an editorial, Hawn Article discusses evidence that suggests SCIP has not improved surgical outcomes. Homocysteine-Lowering and Vascular Outcomes In the randomized placebo-controlled Study of the Effectiveness of Additional Reductions in Cholesterol and Homocysteine trial that enrolled patients with a history of myocardial infarction, the investigators assessed the effects of reducing homocysteine levels with folic acid plus vitamin B12 on vascular and nonvascular outcomes. The investigators report that compared with placebo, patients randomly assigned to receive the study vitamins experienced a mean 3.8 μmol/L (28%) reduction in homocysteine levels; however, this reduction was not associated with beneficial effects on vascular outcomes, including major coronary events, fatal or nonfatal stroke, and noncoronary revascularization during 6.7 years of follow-up. Article Racial Differences in Severe Sepsis Severe sepsis—infection complicated by acute organ dysfunction—occurs more frequently in black than white individuals. Whether this is due to higher rates of infection or higher risks of acute organ dysfunction among black patients is not clear. In an analysis of data from the 2003-2007 National Ambulatory Care Survey, Mayr and colleagues found that higher rates of severe sepsis among black patients are a consequence of both higher rates of infection and higher risks of acute organ dysfunction than what white patients experience. Article Adiposity and Risk of Diabetes in Older Adults Biggs and colleagues analyzed data from the Cardiovascular Health Study, a prospective cohort study of individuals aged 65 years and older, to examine the relationship between adiposity, changes in adiposity, and risk of type 2 diabetes. During a median follow-up of 12.4 years (range, 0.9-17.8 years) the authors found that overall and central adiposity and weight gain during midlife (after age 50 years) and after age 65 years were associated with the risk of incident diabetes. Article CLINICIAN'S CORNER Primary Myelofibrosis Grand Rounds Primary myelofibrosis, the rarest of the myeloproliferative neoplasms, has a highly variable natural history. Stein and Moliterno discuss the case of Mrs W, a 79-year-old woman who was diagnosed with myelofibrosis with myeloid metaplasia (now called primary myelofibrosis) in 1982. The authors review the epidemiology and natural history, molecular pathogenesis, diagnosis, and management of primary myelofibrosis. Article A Piece of My Mind “There are abrasions on her knees and legs. There is a pressure ulcer on her heel. I roll her over and find the lesions on her buttocks that the home health nurse was concerned about.” From “Rubbing Against the Late Day.” Article Medical News & Perspectives Pediatric hepatitis C infection is underestimated, leaving many children with potentially severe health consequences later in life. Article Diet and Prevention of Alzheimer Disease From the Archives Journals An article in the June issue of the Archives of Neurology reports the association of different dietary patterns with the risk of Alzheimer disease. Morris and Tangney discuss the advantages of dietary pattern analysis to inform health-promoting dietary recommendations. Article Commentaries Health care reform and social policy Article Genomic analysis of mental illness Article Down syndrome: new prospects Article Author in the Room Teleconference Join Kenneth J. Mukamal, MD, MPH, MA, Wednesday, July 21, from 2 to 3 PM eastern time to discuss advising a 42-year-old patient about whether he should drink alcohol for his health. To register, go to http://www.ihi.org/AuthorintheRoom. JAMA Patient Page For your patients: Information about postoperative infections. Article

doi: 10.1001/jama.303.24.2445pmid: N/A

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Torpy, Janet M.

doi: 10.1001/jama.2010.713pmid: 20571000

A galloping horse, a determined family fleeing a life of slavery, and the setting of the Civil War: these elements comprise A Ride for Liberty—The Fugitive Slaves (cover ). Now probably Eastman Johnson's (1824-1906) most discussed painting, A Ride for Liberty was not exhibited or sold during Johnson's lifetime; it represents a period when the plight of African Americans, specifically slaves, was briefly popular in American art. Other artists produced similar work, yet the emotional power and historical impact of Johnson's painting have led to its lasting interest. During the Civil War era, in the midst of battles too numerous to mention—and too horrible to forget—Americans seemed to desire, and to purchase, for the first time, art depicting slaves. Johnson, a native New Englander, had little first-hand knowledge of Southern plantation culture; his abolitionist sympathies reflected his upbringing in the privileged atmosphere of a politically active and influential Northern family. Johnson followed the Union army but did not participate in active duty; he joined the soldiers as a chronicler of events, a scribe whose pen was a brush and whose paper was canvas. Near Manassas, Virginia—also known as Bull Run—on March 2, 1862, 6 months before President Abraham Lincoln issued the Emancipation Proclamation, Johnson espied a family attempting to escape the bonds of slavery. Clearly moved by the situation, Johnson later produced at least 3 paintings based on this subject. He inscribed one painting, now at the Virginia Museum of Fine Arts, on its reverse: “A veritible [sic] incident in the civil war seen by myself at Centerville on this morning of McClellan's advance towards Manassas.” The nearly identical painting featured here bears no inscription, only Johnson's initials. Eastman Johnson (1824-1906), A Ride for Liberty—The Fugitive Slaves, circa 1862, American. Oil on paper board. 55.7 × 66.3 cm. Courtesy of the Brooklyn Museum (http://www.brooklynmuseum.org), Brooklyn, New York; gift of Gwendolyn O. L. Conkling, 40.59a.b. The symbolism of Johnson's work is not subtle. The father drives the horse, urging it toward freedom. He holds his older child, encompassing the boy in strong paternal arms that manage the reins just like the father steers his family. The woman, an almost imperceptible infant in her grasp, looks backward: she fears detection and pursuit by those who would drag the family back to virtual imprisonment. She knows that separation, beatings, even murder, may await them as punishment for their escape. The horse, working to the extent of its capability, is captured mid-stride, in full gallop; its hooves do not touch the ground. Johnson's deliberate brushwork has depicted the horse's tail so that there is no question of its speed and its power: the horse is the vehicle to this family's freedom. Sources suggest that the indistinct background represents the Manassas battlefield, with the glint of soldiers' bayonets in the distance, a mirror of the liberty that waits behind the Union lines. Johnson began his career in the limner tradition, making simple portraits in crayon and pastel. He traveled to Europe for study, primarily in Germany, but also in the Netherlands and in Paris. After returning to New York, he specialized in genre painting. He used his wife Elizabeth—and later his daughter Ethel ( JAMA cover, December 16, 2009)—as a model for kitchen scenes, indoor and outdoor venues, and works featuring realistic—often sentimental—glimpses into the lives of ordinary persons ( JAMA covers, March 6, 2002, and November 25, 2009). Johnson's talent led him into critical and financial success, and he received associate Academician status from the National Academy of Design in 1859 when he exhibited the large canvas Negro Life at the South; the painting presented vignettes of plantation life in the slave quarters. In 1862, the year he witnessed the scene depicted in A Ride for Liberty, Johnson submitted a self-portrait and a painting of an African American child as presentation pieces; on the strength of these works, he became a full Academician. Later Johnson transitioned away from genre painting and returned to highly remunerated portraiture of affluent and powerful individuals. Johnson remained a New Yorker but spent his summers in Nantucket. He maintained active membership in the Union League Club, which was originally established during the Civil War to support the aims of the Unionists. Johnson died when he was 82 years old and was buried in Brooklyn's Green-Wood cemetery, along with other prominent individuals, including several Roosevelts, Henry Ward Beecher, and Samuel F. B. Morse. Many of Johnson's works are housed in the Brooklyn Museum and at the Union League Club, befitting a man and a great artist—a cofounder of the Metropolitan Museum of Art—who adopted New York as his home and his studio. One of the most important artworks to arise from the Civil War era, A Ride for Liberty possesses artistic merit and historical significance; the painting makes unequivocal comment on social justice, years ahead of its time. However, viewed in the context of Johnson's oeuvre, this painting is a portrait: a portrait of freedom.

Stein, Gary

doi: 10.1001/jama.2010.614pmid: N/A

If I had a dog his soft fur would not foliate the sofa or trigger asthma attacks in my dear wife, ending with a hospital trip, an adrenaline shot and those inhaler tubes littering the house. His rich brown eyes will convey profound intelligence and sensitivity to the subtlest shifts in my mood. Those eyes will never get infected and fill with viscous yellow pus we must wipe with Q-Tips and cure with sticky ointment, awkward for us both. My dog will lie by my feet while I read the Sunday Times he fetched from the lawn and delivered dry from his slobber-free mouth, and he’ll wait for his walk until I complete the crossword. And when we walk he’ll heel until I hurl a tennis ball. Watch him streak across the grassy field, catch it on first bounce and, with gleeful tail, surrender the prize to me for another go. He will never drop dead birds or vermin on the front stoop like the neighbor's dog they had to put to sleep. At poop time he will drag his leash from the closet, jangling across the tile to my chair. He will never get diarrhea and soil the Oriental, then whimper or cower in the corner. And when I have my heart attack, I don't know if he will punch 9-1-1 with his nose like the schnauzer in the news, but surely he’ll cover my body with his, so the EMTs won't find me jittery with shock. While waiting for the ambulance, I’ll thank my wife for this beast, warming the pain, a gift as perfect as our children who, when we play tennis, won't serve as hard as they can and will blow some shots to let me think that by some necessary miracle I’ve survived and will win in the end.

Burns, Robert

doi: 10.1001/jama.2010.802pmid: 20571001

I knock on the door. They are at home, I just called them, but they are slow to respond. I knock again, harder this time, the tempo faster, more urgent. The door opens slowly, tentative at first, then a little broader. I am not a surprise visitor, but I am unexpected and therefore a puzzle. “I’m the doctor. I called a few minutes ago.” I raise my identification badge higher so she can see it; her eyes flicker back and forth between the picture and my face. “It's an old picture. I had more hair then,” I say, trying to take the edge off the situation. “Why are you here?” Her eyes are tired. Her affect is flat, but fear provides a spark. “Carol, the nurse from home health, asked me to stop by and check on your mother.” “She was just here, said that Mama was fine.” “She just had some questions and wanted me to take a look at your mother.” “She's sleeping.” She steps back from the door. Her hand is on the knob, ready to push it closed. “I won't be long,” I say firmly. “I’ll only wake her for a few minutes and then she can go back to sleep.” “She sleeps a lot.” “Well, then she’ll be able to fall back asleep. I’ll only be a few minutes.” We go back and forth. A dance, both of us tentative at first; I get more assertive, but careful that I don't get the door permanently closed. “Just for a minute, then,” she finally says. She looks defeated. We walk through the house, the kitchen, hall, toward the back. It is dark, emotionally cold, jumbled. Even chaos often has an organization, a pattern, if you look hard enough, but I cannot find any here. It is a room and a house and a life out of control, cluttered and unstructured as I walk through the building. “She's in there.” Her voice has a tone of resignation. Or resentment. There is a difference between being directed and led, and the journey down the hall is the former. I knock on the door, wait a brief moment, and knock again. Her daughter looks away, and I assume the lead and push the door open and enter the room. The windows are covered with heavy curtains, and despite the bright spring day, the room is dark. I feel along the wall, find a switch, and turn on the light. She is in a child's bed, small and quiet and unaware of my presence. I kneel beside her and call her name as I gently touch her hand, trying to wake her. She stretches in her sleep like a puppy on its bed and moves her arms. “Kathryn, it's the doctor. I’m here to see you.” I stroke her arm, trying to wake her from her slumber. Her eyes open, slowly at first, getting used to the sudden light in the room, and she smiles. A sweet smile, lit with joy, which takes over her face. She reaches out and touches my face, her delicate fingers brushing my cheek, the soft skin of her fingertips rubbing against the late-day stubble of my beard. “I knew you were coming,” she said. “You did? Who told you?” “You said you’d come back.” “See, told you, she doesn't know what she's talking about. She's never seen you. She thinks she knows you.” The voice startles me. Her daughter has stayed out of the room until now. “I just look familiar.” “It's that dementia, that Alzheimer's makes her make things up.” “Well, as long as it doesn't bother her, it's . . .” “It bothers me.” She walks away from the door again, down the hall, or just out of sight, I can't tell. I examine her quickly, engaging her in conversation while I check her head and mouth, heart, lungs, and skin. She tries to answer my questions. I ask her age, and she is close and then stumbles with an answer for her birthday. The frustration at not knowing washes over her face. “You stopped counting them, haven't you,” I say. “A long time ago.” The smile brightens the room again. “A long time ago I went to Brisbane, the city of whales. I stayed there for 12 years, and then I came home again.” “Where are we now?” “Home. Home.” “Where's that?” “Brisbane.” She mentions the whales and water, blurring the past and the present, perhaps reality and delusion. There are abrasions on her knees and legs. There is a pressure ulcer on her heel. I roll her over and find the lesions on her buttocks that the home health nurse was concerned about. “There's a funny one on her bottom,” she had said on the telephone. “Define funny,” I had asked. “Round. Red.” We went back and forth, trying to decide what the lesion could be. We eliminated the obvious causes such as infections and dermatitis. “I never saw anything like it in nursing school.” She had graduated three months ago. I understand, because there was a lot I never saw in medical school, and it took a life to experience some things. There is a circular welt on her buttocks, almost the shape of a horseshoe, except bigger, nearly eight inches in diameter, mostly healing, with some area of bruising at the margins. It is not an infection, it is traumatic. I look over at the potty seat near the bed. Her skin is thin and fragile. But it would still require her sitting for a very long time on the chair to permanently disrupt the skin, to leave a brand from the toilet seat in her buttocks. She says it does not hurt. There is a pressure ulcer where her kyphotic spine has pushed through the thin skin of her back. I have seen enough. I call the police. I have broken bad news to more people than I can count. It is one thing to tell someone that their body has failed, that treatment has failed, that I have failed, and that their independence or health or life is on the decline. They can blame age or time or nature for their problems. This is not one of those times. Her daughter has failed her, neglected her, and led to this harm. I call her daughter into the room, and she reluctantly enters. Her eyes avoid mine. It is hard for me to tell her what I see. But I tell her, pointing to the evidence on the frail body on the child's bed on the floor in the dark room in the messy house in the chaotic life. Why is it hard? Am I uncertain of my conclusion? There is no test for neglect—it is a history, an examination, and an interview. And of course it is the vulnerable and frail and demented who are frequently abused. Kathryn cannot remember her birth date, something repeated throughout her life countless times. Would she remember being left sitting too long, probably more than once? I show her daughter the wounds, trying to get her to tell me when and how they occurred. Just as for her mother, the days and care have blended together, and there is no clear start or ending of the days. “They just happened,” she says. “Today, yesterday, longer?” I ask. “Maybe yesterday. Or the day before, I’m not . . .” I stop beating around the issue and tell her the truth. I am not gentle, I do not put the bad news into six steps like I have been taught or teach others. I am blunt and to the point. Kathryn has been neglected for days and will get worse unless she is moved out of the house. Her daughter explodes into a rage and yells at me, at her mother, at herself. “You aren't here by yourself every day, doing everything, for someone who doesn't even know who you are! I’ll fix it. Get out!” She forces me out of the house. Past the dirt and collected detritus of life to the yard. I shield my eyes from the spring sun for a moment until my eyes adjust. She slams the door behind me. I walk to the end of the driveway and, waiting for the police, I punch a number on my cell phone and hit Send. I speak to the voice that answers: “Hi, Mom. Just making sure you're okay.” Back to top Article Information Acknowledgment: I wish to thank Natalie Parker Lawrence, Stephen Malin, PhD, and Linda O. Nichols, PhD, for comments on earlier drafts of this essay. Editor’s Note: Kathryn is a fictitious name.

Voelker, Rebecca

doi: 10.1001/jama.2010.830pmid: 20571002

The great unknown in pediatric hepatitis C infection is what course the disease will take as patients mature from childhood to adolescence and into adulthood. Some will spontaneously clear the infection, while others eventually may develop liver cancer. But researchers find it difficult, if not impossible, to arrive at any conclusions about disease progression because so few children infected with hepatitis C virus (HCV) are identified early in their lives. Hepatitis C virus infection in children and teens is greatly underestimated, according to a new study. Experts say better surveillance is needed to track disease progression in children. The Institute of Medicine made the case in a January report for stepped-up surveillance of hepatitis B and C infection, but a recent study highlights the particular inadequacies in diagnosing and treating children and teens infected with hepatitis C. “There's a frightening lack of awareness among both the public and clinicians about hepatitis C virus infection in pediatric patients,” said lead author Aymin Delgado-Borrego, MD, MPH, a pediatric gastroenterologist at the University of Miami Miller School of Medicine. She presented the findings in early May during the Digestive Disease Week conference. Delgado-Borrego and her colleagues focused on undiagnosed pediatric hepatitis C infection in Florida because the state is among only a few that require reporting of acute and chronic cases. They used data from the 3rd National Health and Nutrition Examination Survey and the US Census Bureau to estimate that about 0.3% of US children and teens aged 6 to 19 years are infected with HCV. About 75% have chronic infections. Applying the national 0.3% prevalence rate, the researchers calculated that Florida would have 12 155 cases of pediatric hepatitis C infection. But a state database contained 1755 unique cases, reflecting only 14.4% of the number of cases that should be expected. In contrast, 46.3% of the expected adult cases were reported in the database. Among pediatric cases, 51% were aged 12 years or younger and 49% were aged 13 to 18 years; 40% were aged 16 to 18 years. Only 8.5% of pediatric cases had been evaluated by a hepatologist, Delgado-Borrego added. “This is highly concerning,” she said. “Preliminary data that we have indicate that this is likely not isolated to Florida and, in fact, may be even worse in most of the states,” because of less stringent surveillance. Some experts agree. “This is reflecting what's going on in the whole United States; it's not just specific to Florida,” said Philip Rosenthal, MD, director of pediatric hepatology at the University of California, San Francisco, School of Medicine. “This is underappreciated within the pediatric community.” Usually, adults are infected through contact with contaminated blood. Transfusions prior to 1992 (when screening of the blood supply began), injection drug use, and needlesticks in health care settings are common transmission routes. But Rosenthal, who was not involved with the study, said most children acquire the infection through maternal neonatal transmission. “The majority of the time, the child looks well,” he said. “If you don't ask about risk factors, then [HCV] is not even going to be on the radar screen.” Of approximately 3.2 million individuals living with HCV in the United States, an estimated 240 000 are children, said John Ward, MD, director of the division of viral hepatitis at the Centers for Disease Control and Prevention (CDC) in Atlanta, Ga. More precise figures are not available. “Because of the limitations of our surveillance system in the United States, we don't have good data for viral hepatitis,” he said “Some evidence suggests that disease may not progress as rapidly [in children] as for those who are infected in later life,” Ward noted. “More long-term follow-up is needed to really see how that natural history will change as that [child] ages and maybe begins to have other insults to the liver, like alcohol use.” No vaccine is available to protect against hepatitis C infection, and screening is more complicated than for hepatitis B infection. The infection can be present without elevated serum transaminases, and tests for anti-HCV antibodies must be confirmed with polymerase chain reaction. The CDC and the American Medical Association have developed a physician toolkit for HCV, which is available at http://www.cdc.gov/hepatitis. Rosenthal offered a list of shortcomings in current HCV treatment. First, 6 genotypes of HCV exist. The treatment response rate is about 90% in genotypes 2 and 3 compared with 30% to 40% in genotype 1. But genotypes 1a and 1b are the most prevalent in the United States. Next, adherence to treatment is difficult. Some patients will need the regimen of weekly injections of pegylated interferon and daily oral ribavirin for up to 1 year. Adverse effects include flu-like symptoms, fatigue, and cognitive changes. But Delgado-Borrego said many children tolerate treatment better than adults. She also noted that children who are treated earlier may have better outcomes because of the shorter duration of infection. “Many children could be cured if we did nothing else but identify their infection and refer them for proper medical management,” she said.

Mitka, Mike

doi: 10.1001/jama.2010.831pmid: 20571003

The true burden of environmentally induced cancer has been grossly underestimated, warns the President's Cancer Panel in its latest annual report. But others say the report is too sensationalistic and could cause researchers and the public to downplay the factors that cause the majority of cancers. Environmental factors, such as pesticide use on crops, are greatly underappreciated as sources of increased risk for cancer, said a Presidential advisory panel in a report released in May. Issued May 6, the 240-page report, Reducing Environmental Cancer Risk: What We Can Do Now, lays out the sources and types of environmental contaminants linked to cancer risk and offers suggestions to researchers, government agencies, and individuals about how to reduce the risk (http://deainfo.nci.nih.gov/advisory/pcp/pcp08-09rpt/PCP_Report_08-09_508.pdf). The Cancer Panel (http://deainfo.nci.nih.gov/advisory/pcp/pcp.htm) has been issuing annual reports since its creation in 1971 by President Richard M. Nixon when he launched the so-called war on cancer. Previous recent reports by the panel focused on maximizing the nation's investment in fighting cancer and promoting healthy lifestyles. The report is the result of 4 meetings conducted by the panel between September 2008 and January 2009 involving testimony from 45 invited experts from academia, government, industry, the environmental and cancer-related advocacy communities, and the public. The panel assessed the state of environmental cancer research, policy, and programs addressing known and potential effects of environmental exposures on cancer risk. Panel members were LaSalle D. Leffall Jr, MD, professor of surgery at Howard University College of Medicine in Washington, DC, and Margaret L. Kripke, PhD, professor of immunology at the University of Texas M. D. Anderson Cancer Center in Houston. The panel's introductory letter to President Barack Obama said, “The Panel urges you most strongly to use the power of your office to remove the carcinogens and other toxins from our food, water, and air that needlessly increase health care costs, cripple our nation's productivity, and devastate American lives.” The panel added that it “was particularly concerned to find that the true burden of environmentally-induced cancer has been grossly underestimated.” Differing opinions Some criticized the tone of the report as alarmist, while others applauded its message. Although Michael J. Thun, MD, MS, vice president emeritus of epidemiology for the American Cancer Society, said many of the elements of the report are in line with the society's findings and positions (Fontham ETH et al. CA Cancer J Clin. 2009;59[6]:343-351), he dismissed other elements. “The statement that got all the press attention was that the panel said it was particularly concerned that the burden of environmental cancer is grossly underestimated, but it provided no evidence to support that concern,” Thun said. “Their argument reflects a 30-year dispute in the scientific debate regarding the degree of cancer risk that should be linked to various environmental exposures.” Thun added that he was also bothered by the panel's framing of current cancer prevention efforts as being “focused narrowly” on smoking, other lifestyle behaviors, and chemopreventive interventions. “You do not like to see the major causes of cancer and attempts to prevent them being dismissed as ‘narrowly focused’—the obesity epidemic and tobacco use are not narrow problems.” But Samuel S. Epstein, MD, professor emeritus of Environmental and Occupational Medicine at the University of Illinois School of Public Health in Chicago and chairman of the Cancer Prevention Coalition, applauded the panel's report. “The report is scholarly and goes into scientific issues in great depth,” Epstein said. “Its position on the need for the phasing out of avoidable causes of cancer is commendable.” The report The panel's report said the problem of reducing environmental cancer risk is due to limited research; conflicting or inadequate exposure measurement, assessment and classification; and ineffective regulation of exposures to hazardous chemicals and other environmental factors. It focuses on 6 sources of exposure related to environmental cancer risk: industrial and manufacturing, agriculture, medical, military, natural, and modern lifestyles. The report also provides policy, research, and program recommendations to reduce environmental cancer risk and suggestions for individuals to minimize exposure. As one of its key recommendations, the panel called for a precautionary, prevention-oriented approach to chemical exposures as the cornerstone of a new national cancer prevention strategy. Under such an approach, the burden of proving the safety of a chemical would shift to manufacturers before approval of a new chemical, in mandatory postmarket studies for new and existing agents, and in renewal applications for chemical approval. This tactic would replace what the panel described as the current “reactionary” approach in which human harm must be proven first before action is taken to reduce or eliminate exposure. Although Thun said he does not dismiss the precautionary principle, he questions how it could be practically implemented. “Public health is basically built on the precautionary principle, but it really does not get around the problem of making a judgment of what the risk is and what the risk-benefit ratio will be,” he said. “The problem is in our regulatory structure in that we do not have a basis for warnings in the absence of evidence. So the first thing that would happen if the government would require people to adopt it is that lawsuits would be filed by companies asking what evidence is being used to show that a chemical should be banned.” Whatever the arguments for or against implementing the precautionary principle to environmental exposures, legislation proposed by Sen Frank R. Lautenberg (D, NJ) would incorporate elements of this approach. Lautenberg's bill, the Safe Chemical Act of 2010, would overhaul the current law regulating new and existing chemicals, the Toxic Substances Control Act of 1976, by requiring manufacturers to submit to the US Environmental Protection Agency evidence of the safety of every chemical currently being produced and any new chemical they seek to put on the market. Research priorities Whether the report's call for adding a focus on cancer-related environmental exposures to research priorities is answered remains to be seen. If it helps direct President Obama to make such research a priority, that message might filter down to the Department of Health and Human Services and ultimately to the National Institutes of Health (NIH), which controls the federal grants for health research, said Deborah M. Winn, PhD, deputy director of the National Cancer Institute's (NCI’s) division of cancer control and population sciences. It also might signal opportunities for study to researchers, she added. For example, when NIH Director Francis S. Collins, MD, PhD, began his tenure, Winn noted, “he said he had 5 scientific areas he thought were very important and said he wanted to use funding to work in those areas,” Winn said. “But ideas for research can also come from the scientific community, and it is the role of the staff at NCI to identify important scientific areas that should have a high priority.” Shelia Hoar Zahm, ScD, NCI's deputy director of the division of cancer epidemiology and genetics, said that while one may know there are environmental factors associated with cancer risk, proving that link through rigorous research remains difficult. “Cancer risk is not all about genetics—look at migrant studies [showing that] colon cancer risks change when people move from one place to another,” Zahm said. “But teasing out exposures is difficult because of confounders. How are you sure, what steps can you take, to know that an effect you are looking at is due to what you think it is?” While Epstein praised the panel's report in general, its focus on more research on cancer-related environmental factors troubles him. “The research has been done over the last 30 years showing the link between environmental factors and avoidable cancers, but this research has been ignored or trivialized by the National Cancer Institute and the American Cancer Society, except for lifestyle, tobacco, and sun exposure,” Epstein said. “We are not dealing with scientific issues, we are dealing with public policy issues.” Thun argues that the American Cancer Society does not ignore or trivialize possible cancer risks, but rather takes into consideration the need to place those risks in context. “Our investment in prevention has been substantially smaller than our investment in treatments; maybe we are not taking prevention seriously enough,” he said. “But you want to invest in the things that will make the biggest difference, and what is missing is the evidence that levels of pollutants that Americans are exposed to in daily life are carcinogenic.”

Voelker, Rebecca

doi: 10.1001/jama.2010.832pmid: 20571004

As a clinician, Carl Bell, MD, wants physicians to be able to give their patients the most accurate information on cognitive decline and Alzheimer disease. But as a leading-edge baby boomer, Bell, a professor of psychiatry at the University of Illinois at Chicago, also has a personal stake in compiling state-of-the-science data on ways to prevent both conditions. Vitamins and dietary supplements cannot help prevent cognitive decline and dementia, according to a recent National Institutes of Health consensus panel statement. “I’m 63 and I’m scared to death of these disorders,” Bell said during a press briefing following the release of a National Institutes of Health consensus panel statement on whether existing interventions can effectively prevent cognitive decline and Alzheimer disease (http://consensus.nih.gov/2010/alzstatement.htm). As a member of the consensus panel, he offered little optimism that preventive measures described in the current medical literature can stave off either condition. “We don't have any solid evidence that there is anything that will prevent either kind of decline or dementia,” he said. The panel concluded that current evidence does not support the use of any prescription medications, vitamins, nutrients, or dietary supplements to prevent either cognitive decline or Alzheimer disease. Panel members said rigorous randomized controlled trials of some of these interventions simply showed no efficacy in preventing either condition. Other studies could not produce evidence of clinical benefits because they used inconsistent definitions of cognitive decline or had too few participants, insufficient duration, high drop-out rates, or low adherence. Panel chair Martha Daviglus, MD, PhD, MPH, professor of preventive medicine and medicine at Northwestern University's Feinberg School of Medicine in Chicago, also noted that diagnostic criteria for cognitive decline, mild cognitive impairment, and Alzheimer disease have not been used uniformly across the numerous studies that have evaluated potential preventive approaches. Even though the panel's conclusions are based on scientific data, the Alzheimer's Association's chief medical and scientific officer criticized their work. “They were excessively negative,” said Bill Thies, PhD. “It's possible to read this document and decide there's really no point . . . people get the disease and there's nothing you can do about it.” Thies said the panel did not distinguish clearly enough between interventions that plainly are not effective and those that show promise, despite inconclusive evidence. “There are significant data around physical activity,” he said. But Daviglus mentioned physical activity as well as antihypertensive medication, consumption of omega-3 fatty acids, and cognitive engagement as promising preventive interventions that currently are being studied. The report also noted the need for research that follows individuals from midlife into old age to determine how biological, lifestyle, dietary, clinical, and socioeconomic factors may influence cognitive decline or Alzheimer disease. “Large-scale population-based studies and randomized controlled clinical trials are critically needed to investigate strategies to maintain cognitive function in individuals at risk for decline,” she said. The panel's report noted the high toll of Alzheimer disease. Up to 5.3 million individuals in the United States have the condition, and the number of those affected is increasing. Conclusions in the report also highlight the frustrations of physicians who care for patients with dementia. “There isn't a whole lot to be done treatment-wise . . . and there isn't a whole lot in the way of prevention,” said Alan Adelman, MD, MS, of Penn State University College of Medicine in Hershey, Pa. But Adelman, who was not involved in the report, said the panel's work serves as a warning for patients and their families. “There are a lot of things that have been tried that are not effective,” he said. “People should be aware of that so they don't get false hope thinking that if they take this or that, it will be a miraculous cure.” Even though the report does not offer any new clinical recommendations, panel member Arnold Potosky, PhD, of Georgetown University Medical Center in Washington, DC, said the information should prompt physicians and their patients to get involved in clinical trials. “There is a vital need for more research and our conclusions were very heavy on recommendations to track these diseases over the long term to learn more about their causes and progression, especially from cognitive impairment to full dementia.” A list of clinical trials is available at http://clinicaltrials.gov.

Kuehn, Bridget M.

doi: 10.1001/jama.2010.833pmid: N/A

For decades, the genetic cause of a rare and fatal X chromosome–linked syndrome characterized by talipes equinovarus, atrial septal defect, Robin sequence, and persistent left superior vena cava (TARP) eluded clinicians and scientists. But a new gene-finding strategy enabled scientists from the National Human Genome Research Institute (NHGRI) to discover the gene for TARP and to offer carrier testing to affected families (Johnston JJ et al. Am J Hum Genet. 2010;86[5]:743-748). The discovery was the latest in a string of successes for scientists using next-generation sequencing or massively parallel sequencing of the genome's protein-encoding regions and old-fashioned clinical investigation to zero in on the genetic causes of rare disorders that had evaded detection by more traditional methods. “It's a really rapid path to diagnosis and understanding that was either impossible or extremely difficult and expensive to do previously,” said Leslie G. Biesecker, chief of NHGRI's Genetic Disease Research Branch. The technique is likely to accelerate the identification of the genetic basis of a multitude of rare disorders. “There are thousands and thousands of cases where families are struggling with these very serious disorders and they don't have answers to their most basic questions,” Biesecker said. The new technology allows sequencing of billions of base pairs of DNA fragments in the time it took the old technology to sequence millions. To further expedite the process, Biesecker and colleagues sequenced DNA samples from 2 large families that have multiple affected members. They sequenced only the protein-encoding regions of the X chromosome, which they believed were most likely to house the variant, and used their clinical understanding of TARP to filter through the results. For example, based on the severity of the syndrome's effects, they hypothesized that the causative mutation resulted in a gene product with a reduced or complete loss of function. Within several weeks, a few NHGRI scientists were able to determine that in both families, the syndrome was caused by mutations in RBM10, the gene encoding RNA binding motif protein 10, findings that they validated in a mouse embryo model. The discovery means that females in affected families can now learn if they are carriers of the causative mutation. It may also help identify families with other mutations in this gene that result in severe or milder manifestations of the disorder. Other scientists have found that the strategy can also be used to identify mutations responsible for rare autosomal disorders. As a proof of principle, Michael J. Bamshad and colleagues at the University of Washington in Seattle used this technique and arrived at the same gene that traditional methods linked to Freeman-Sheldon syndrome, which features multiple joint contractures and other problems (Ng SB et al. Nature. 2009;461[7261]:272-276). Next, the team used the strategy to identify the cause of Miller syndrome, which features distinctive craniofacial malformations and limb abnormalities (Ng SB et al. Nat Genet. 2010;42[1]:30-35). They sequenced the protein-encoding regions of the genomes of 4 persons with the syndrome from 3 families and then filtered their results based on clinical factors; given previous evidence that the disorder is recessive, they predicted that those affected would have 2 defective copies of the same gene. They identified mutations in the gene that encodes the enzyme dihydroorotate dehydrogenase, confirming the finding in another 3 affected families. Bamshad predicted that the strategy will allow, with the exception of disorders caused by variation in noncoding genes, the identification of genes responsible for most of the remaining Mendelian disorders without a known cause. Already a few other genetic causes of rare diseases have been identified via this technique and are awaiting publication, he said. Understanding these disorders may also facilitate a greater understanding of normal human biology and development. Bamshad and Biesecker agreed that clinical tests based on this strategy are likely to be available for individuals who present with rare diseases in the future. “This technology potentially opens a pathway to clinical application of gene findings,” Biesecker said.

Kuehn, Bridget M.

doi: 10.1001/jama.2010.834pmid: N/A

Implementing an electronic medication-administration system that uses bar code verification technology cut drug-related errors at a large medical center by nearly half, according to a study funded by the Agency for Healthcare Research and Quality. Scientists affiliated with Brigham and Women's Hospital in Boston observed more than 14 000 medication administrations and reviewed 3082 order transcriptions before and after implementation of the system (Poon EG et al. N Engl J Med. 2010;362[18]:1698-1707). Errors that were not related to the timing of administration decreased by 41.4%, from 776 incidents (an 11% error rate) before the system was implemented to 495 (a 6.8% error rate) after implementation. Potential adverse drug events associated with nontiming errors decreased by half, from 3.1% before implementation to 1.6% after. Errors in which medication was given too early or too late decreased by 27.3%, from 16.7% before the system was in place to 12.2% after, but the rate of adverse events associated with such errors stayed constant.