A new technique using the pubic bone as a source of bone for grafting may avoid the complications of harvesting bone from the iliac crest, or "hip bone," according to a report in the November/December issue of The Journal of Craniofacial Surgery.
With further study, the pubic bone could become the new standard for harvesting bone grafts for certain types of reconstructive surgery, write Dr. John W. Polley and colleagues of Rush University Medical Center, Chicago.
Dr. Polley and colleagues developed their approach to harvesting pubic bone in a series of cadaver dissections. They found that the pubic bone, found at the front of the pelvis, could be easily reached through a small incision about 1 inch. Just as importantly, minimal dissection of the soft tissue was necessary to expose the pubic bone and collect the cancellous bone (sponge-like interior bone) needed for grafting.
The researchers report on their initial experience with the pubic bone graft technique in a 10-year-old boy who needed follow-up surgery for a cleft palate defect. The procedure to collect the bone needed for grafting was quick and simple. The day after surgery the patient had little or no pain in the pubic area, which healed without problems.
The iliac crest is the standard site for harvesting bone grafts for reconstructive surgery in the face and jaws, as well as other areas. However, several types of complications can occur after the iliac crest donor procedure, including nerve injuries, pain problems, and scarring.
The pubic bone graft technique is a promising approach to avoiding these problems, Dr. Polley and colleagues point out. Because it requires a small incision with minimal dissection, the pubic bone technique is less traumatic than harvesting bone from the iliac crest site. Since there are no nerves supplying sensation to the skin in the area of the incision, the risk of nerve injury is reduced. Even scarring is less of a concern, because the incision is made in an area normally covered by hair.
"The pubic bone graft compares favorably with more traditional techniques of cancellous bone harvesting," Dr. Polley and colleagues conclude. The procedure appears safe and reliable, allowing faster collection of bone grafts and fewer complications than with the iliac crest technique. With further experience and follow-up, the researchers believe the pubic bone graft could become the new standard for patients undergoing cleft palate reconstruction.
About The Journal of Craniofacial Surgery
The Journal of Craniofacial Surgery serves as a forum of communication for all those involved in craniofacial and maxillofacial surgery. Coverage ranges from practical aspects of craniofacial surgery to the basic science that underlies surgical practice. Founded and edited by Mutaz B. Habal, MD, of Tampa, FL, the Journal is affiliated with major specialty societies worldwide, including the American Association of Pediatric Plastic Surgeons, the American Academy of Pediatrics Section of Pediatric Plastic Surgery, the American Society of Craniofacial Surgeons, the European Society of Craniofacial Surgery, the International Society of Craniofacial Surgery, the Japanese Society of Craniofacial Surgery, the Korean Society of Craniofacial Surgery, the Argentine Society of Plastic Surgery Section of Pediatric Plastic Surgery, the American Society of Maxillofacial Surgeons, the World Craniofacial Foundation, and the Brazilian Society of Craniomaxillofacial Surgery. Visit the journal website at jcraniofacialsurgery.
About Lippincott Williams & Wilkins
Lippincott Williams & Wilkins (LWW) is a leading international publisher for physicians, nurses, specialized clinicians, and students. Nearly 275 periodicals and 1,500 books in more than 100 disciplines are published under the LWW brand, as well as content-based sites and online corporate and customer services. LWW is part of Wolters Kluwer Health, a leading provider of information for professionals and students in medicine, nursing, allied health, pharmacy, and the pharmaceutical industry. Wolters Kluwer Health is a division of Wolters Kluwer, a leading multinational publisher and information services company with annual sales of ?‚¬3.4 billion (2005) and approximately 18,400 employees worldwide.
Lippincott Williams & Wilkins
530 Walnut St.
Philadelphia, PA 19106
United States
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понедельник, 16 мая 2011 г.
Tibetan Plant Worm Can Regulate Cholesterol Metabolism, NOEVIR Confirms
Tokyo (JCN) - NOEVIR announced on August 18 that it has identified a unique property of cordyceps sinensis saccardo, a plant worm native to Tibet.
In its recent experiments using rats and human white adipocytes, the company confirmed that extracts of the plant worm can promote the production of adiponectin, a kind of protein that helps promote fat-burning activities and inhibit the development of lifestyle-related diseases.
Consequently, NOEVIR has concluded that the extracts have potential to prevent and improve lifestyle-related diseases. The company plans to apply these findings to the development of dietary supplement products.
Details of the research is to be presented at the 22th Annual Meeting of the Medical and Pharmaceutical Society for WAKAN-YAKU to be held in Tokyo on August 20 and 21.
View NOEVIR company profile here
Copyright © 2005 JCN. All rights reserved. A division of Japan Corporate News Network KK.
japancorp
In its recent experiments using rats and human white adipocytes, the company confirmed that extracts of the plant worm can promote the production of adiponectin, a kind of protein that helps promote fat-burning activities and inhibit the development of lifestyle-related diseases.
Consequently, NOEVIR has concluded that the extracts have potential to prevent and improve lifestyle-related diseases. The company plans to apply these findings to the development of dietary supplement products.
Details of the research is to be presented at the 22th Annual Meeting of the Medical and Pharmaceutical Society for WAKAN-YAKU to be held in Tokyo on August 20 and 21.
View NOEVIR company profile here
Copyright © 2005 JCN. All rights reserved. A division of Japan Corporate News Network KK.
japancorp
Children May Have Cholesterol Problems, Too
High cholesterol levels
are not just found in adults. Children may have high cholesterol, too, even
without being overweight. Over years, cholesterol overload has similar
hazards as in adults -- clogged arteries and injury to the heart.
The Children's Hospital of Philadelphia recommends that children,
starting at age two years, should have a complete cholesterol profile
checked after an overnight fasting if they have a family history of high
cholesterol or of early heart disease, in line with similar recommendations
from the American Academy of Pediatrics and the American Heart Association.
Those who do not have a family history but have other risk factors for
early heart disease, such as being overweight, high blood pressure,
diabetes, smoking, poor diet, and sedentary lifestyle should also be
screened.
"Although the most common reasons for high cholesterol are poor diet,
being overweight, and not getting enough exercise, some apparently healthy
children inherit high cholesterol levels from their parents," said Julie
Brothers, M.D., medical director of the Lipid Heart Clinic at The
Children's Hospital of Philadelphia. "Overall, we've noticed an increase in
children's cholesterol levels the past several years and this is a
disturbing trend."
Children with a family history of high cholesterol or early heart
disease, even if they have normal weight, should be routinely screened, as
they may have a genetic predisposition for excess cholesterol levels --
familial hypercholesterolemia (FH). These children have high levels of
low-density lipoprotein (LDL), also called "bad cholesterol," beginning at
birth, which can lead to early thickening of the artery walls, premature
cardiovascular disease and an increased risk of early heart attack.
Familial hypercholesterolemia is underestimated in the community and in
pediatric primary care practices. Children with FH have no symptoms or
signs of their condition and often do not fit the profile of someone who is
at risk; they usually have a normal weight and a healthy lifestyle and
diet. However, in addition to a family history of high cholesterol, they
usually have a family history of early heart disease. Children with a
parent, grandparent, sibling, aunt, or uncle with high cholesterol or who
has suffered a cardiac event before the age of 55 should be routinely
monitored.
Children who are overweight or obese should also have their cholesterol
levels routinely screened by pediatric healthcare professionals, as this
also places them at increased risk of developing early heart disease.
It is important to differentiate between obese children with high
cholesterol and those with FH, which is not traditionally associated with
obesity; however, with the obesity epidemic, many children with FH now also
are overweight or obese.
"Cholesterol levels in children who are obese usually respond well to
diet and lifestyle modifications, whereas children with FH often need
medications in addition to diet and exercise," added Dr. Brothers.
Modifications to diet and increased physical activity are the
first-line treatments for children identified with raised cholesterol
levels. Another option is putting a child on statin therapy, which is a
lifetime commitment.
The Lipid Heart Clinic at The Children's Hospital of Philadelphia
evaluates and treats children and adolescents who have high levels of
lipids (fats) in their blood. Elevated lipids put young people at risk for
heart disease later in life.
The Children's Hospital of Philadelphia was founded in 1855 as the
nation's first pediatric hospital. Through its long-standing commitment to
providing exceptional patient care, training new generations of pediatric
healthcare professionals and pioneering major research initiatives,
Children's Hospital has fostered many discoveries that have benefited
children worldwide. Its pediatric research program is among the largest in
the country, ranking third in National Institutes of Health funding. In
addition, its unique family-centered care and public service programs have
brought the 430-bed hospital recognition as a leading advocate for children
and adolescents. For more information, visit chop.
The Children's Hospital of Philadelphia
chop
are not just found in adults. Children may have high cholesterol, too, even
without being overweight. Over years, cholesterol overload has similar
hazards as in adults -- clogged arteries and injury to the heart.
The Children's Hospital of Philadelphia recommends that children,
starting at age two years, should have a complete cholesterol profile
checked after an overnight fasting if they have a family history of high
cholesterol or of early heart disease, in line with similar recommendations
from the American Academy of Pediatrics and the American Heart Association.
Those who do not have a family history but have other risk factors for
early heart disease, such as being overweight, high blood pressure,
diabetes, smoking, poor diet, and sedentary lifestyle should also be
screened.
"Although the most common reasons for high cholesterol are poor diet,
being overweight, and not getting enough exercise, some apparently healthy
children inherit high cholesterol levels from their parents," said Julie
Brothers, M.D., medical director of the Lipid Heart Clinic at The
Children's Hospital of Philadelphia. "Overall, we've noticed an increase in
children's cholesterol levels the past several years and this is a
disturbing trend."
Children with a family history of high cholesterol or early heart
disease, even if they have normal weight, should be routinely screened, as
they may have a genetic predisposition for excess cholesterol levels --
familial hypercholesterolemia (FH). These children have high levels of
low-density lipoprotein (LDL), also called "bad cholesterol," beginning at
birth, which can lead to early thickening of the artery walls, premature
cardiovascular disease and an increased risk of early heart attack.
Familial hypercholesterolemia is underestimated in the community and in
pediatric primary care practices. Children with FH have no symptoms or
signs of their condition and often do not fit the profile of someone who is
at risk; they usually have a normal weight and a healthy lifestyle and
diet. However, in addition to a family history of high cholesterol, they
usually have a family history of early heart disease. Children with a
parent, grandparent, sibling, aunt, or uncle with high cholesterol or who
has suffered a cardiac event before the age of 55 should be routinely
monitored.
Children who are overweight or obese should also have their cholesterol
levels routinely screened by pediatric healthcare professionals, as this
also places them at increased risk of developing early heart disease.
It is important to differentiate between obese children with high
cholesterol and those with FH, which is not traditionally associated with
obesity; however, with the obesity epidemic, many children with FH now also
are overweight or obese.
"Cholesterol levels in children who are obese usually respond well to
diet and lifestyle modifications, whereas children with FH often need
medications in addition to diet and exercise," added Dr. Brothers.
Modifications to diet and increased physical activity are the
first-line treatments for children identified with raised cholesterol
levels. Another option is putting a child on statin therapy, which is a
lifetime commitment.
The Lipid Heart Clinic at The Children's Hospital of Philadelphia
evaluates and treats children and adolescents who have high levels of
lipids (fats) in their blood. Elevated lipids put young people at risk for
heart disease later in life.
The Children's Hospital of Philadelphia was founded in 1855 as the
nation's first pediatric hospital. Through its long-standing commitment to
providing exceptional patient care, training new generations of pediatric
healthcare professionals and pioneering major research initiatives,
Children's Hospital has fostered many discoveries that have benefited
children worldwide. Its pediatric research program is among the largest in
the country, ranking third in National Institutes of Health funding. In
addition, its unique family-centered care and public service programs have
brought the 430-bed hospital recognition as a leading advocate for children
and adolescents. For more information, visit chop.
The Children's Hospital of Philadelphia
chop
New mechanism for controlling cholesterol and lipid metabolism discovered
A team of investigators from the Uppsala Branch of the Ludwig Institute for Cancer Research (LICR) and Harvard Medical
School has uncovered novel targets for the development of drugs that would potentially complement, or replace, statins in
treating heart disease.
Statins are commonly taken drugs that reduce the levels of low density lipoprotein (LDL) and have been shown to reduce risks
associated with heart disease, the number one killer in the Western world. However, statins are not suitable for all
patients, and reduce cardiovascular events by only 20%- 40%. Additionally, some genetic causes of high cholesterol cannot be
treated with statins.
According to LICR's Dr. Johan Ericsson, the senior author of the study published today in Cell Metabolism, the team found
that a protein called Fbw7 degrades the SREBP proteins that drive lipid and cholesterol production. "We found that inhibiting
Fbw7 resulted in increased SREBP levels and an enhanced uptake of LDL, so a drug that blocks the interaction between Fbw7 and
SREBP proteins would probably enhance the removal of harmful LDL-cholesterol from the circulation. We can only speculate at
this stage, but a two-pronged attack on LDL removal, combining a statin with a treatment that prevents Fbw7/SREBP interaction
would likely be of more benefit to some patients than statins alone."
Dr. Ericsson said that the team also found that the Fbw7/SREBP interaction may also be connected to diabetes, as insulin
signaling inhibited Fbw7's ability to affect SREBP levels and thus increased lipid and cholesterol synthesis. Finally, the
Fbw7/SREBP interaction also provides a theoretical link between lipid synthesis and the aberrant growth of cancer cells. The
loss of Fbw7, which is inactivated in some breast, endometrial, ovarian and colon cancers, has been shown to make cells
multiply faster and synthesize more lipids; factors that are critical for tumor growth. Aspects of both links are under
investigation.
Contact: Sarah L. White, Ph.D.
swhitelicr
1-917-974-7952
Ludwig Institute for Cancer Research
School has uncovered novel targets for the development of drugs that would potentially complement, or replace, statins in
treating heart disease.
Statins are commonly taken drugs that reduce the levels of low density lipoprotein (LDL) and have been shown to reduce risks
associated with heart disease, the number one killer in the Western world. However, statins are not suitable for all
patients, and reduce cardiovascular events by only 20%- 40%. Additionally, some genetic causes of high cholesterol cannot be
treated with statins.
According to LICR's Dr. Johan Ericsson, the senior author of the study published today in Cell Metabolism, the team found
that a protein called Fbw7 degrades the SREBP proteins that drive lipid and cholesterol production. "We found that inhibiting
Fbw7 resulted in increased SREBP levels and an enhanced uptake of LDL, so a drug that blocks the interaction between Fbw7 and
SREBP proteins would probably enhance the removal of harmful LDL-cholesterol from the circulation. We can only speculate at
this stage, but a two-pronged attack on LDL removal, combining a statin with a treatment that prevents Fbw7/SREBP interaction
would likely be of more benefit to some patients than statins alone."
Dr. Ericsson said that the team also found that the Fbw7/SREBP interaction may also be connected to diabetes, as insulin
signaling inhibited Fbw7's ability to affect SREBP levels and thus increased lipid and cholesterol synthesis. Finally, the
Fbw7/SREBP interaction also provides a theoretical link between lipid synthesis and the aberrant growth of cancer cells. The
loss of Fbw7, which is inactivated in some breast, endometrial, ovarian and colon cancers, has been shown to make cells
multiply faster and synthesize more lipids; factors that are critical for tumor growth. Aspects of both links are under
investigation.
Contact: Sarah L. White, Ph.D.
swhitelicr
1-917-974-7952
Ludwig Institute for Cancer Research
Obesity As Protection Against Metabolic Syndrome, Not Its Cause
The collection of symptoms that is the metabolic syndrome - insulin resistance, high cholesterol, fatty liver, and a greater risk for diabetes, heart disease, and stroke - are all related to obesity, but, according to a review in the March 9th issue of the Cell Press publication Trends in Endocrinology and Metabolism, not in the way you probably think they are.
In fact, says Roger Unger of the University of Texas Southwestern at Dallas, obesity is the body's way of storing lipids where they belong, in fat tissue, in an effort to protect our other organs from lipids' toxic effects. It's when the surplus of calories coming in gets to be too much for our fat tissue to handle that those lipids wind up in other places they shouldn't be, and the cascade of symptoms known as metabolic syndrome sets in.
It comes down to simple facts that all of us know on some level or another: Americans since the 1950s eat too much high-calorie food loaded with carbs and fat (what Unger calls "potent adipogenic nutrient mixtures") and, thanks to modern technology, we move far too little. Until that changes, Unger doesn't see any end to the growing epidemic of metabolic syndrome. Still, our metabolisms aren't broken; the pathways that squirrel fat away as an energy source for use in lean times are just completely overwhelmed. "We are pushing our homeostatic capability to the maximum," says Unger, who coined the term "lipotoxicity" in 1994. "Overnutrition used to be rare - reserved for those in the castle. Today, it's just the opposite. Bad calories are so cheap that anyone can afford to get overweight."
Unger cites plenty of evidence in support of a protective role for obesity. Genetic manipulations in mice that increase or decrease fat formation have provided evidence that adipogenesis, meaning the generation of fat cells, delays other metabolic consequences of overeating. The reverse is also true, he writes. Obesity-resistant mice have in some cases been found to develop severe diabetes upon eating too much, as a result of lipid accumulation in tissues other than fat.
There is some disagreement in the field about whether insulin resistance is a primary cause of metabolic syndrome or just one of its features, Unger notes. But on this, too, he has a clear view. Insulin resistance is not the cause of metabolic syndrome, he says, it is a "passive byproduct" of fat deposition in the liver and muscle once storage in fat cells begins to fail.
It also makes sense in Unger's estimation that cells that have already taken on too much fat would begin to exclude glucose, causing its levels in blood and urine to rise. Once in cells, glucose becomes a substrate for the production of more fat. "The body is doing what we should have done - keep excess calories out - and it may be protective," Unger says.
At the center of the transition from protective obesity to metabolic syndrome is resistance to the fat hormone leptin, well known for its appetite-suppressing effects, Unger says. The hormone is also responsible for partitioning fat in the body. The rise of leptin as fat stores grow is therefore an adaptive response, but that can only go so far before resistance sets in.
Based on the genes they carry, some people will be better able to sustain lipid storage in fat and can get away with being overweight, even obese, without the other symptoms. Eventually, though, the need to cut calories is something all of us will face.
"Once you reach a certain age, almost everybody is leptin resistant," he says. "Nature stops protecting you once you pass the reproductive years," requiring all of us to watch our diets and do exercise.
Unger's perspective comes from the research he does at UT Southwestern's Touchstone Center for Diabetes Research and a thorough understanding of the scientific literature, but it also stems from his own memories in childhood when one only saw fat ladies at the circus. "That's how unusual it was," he says. "The younger you are, the more skewed your perception is of an epidemic that surrounds you."
Unger concludes his review article this way: "Based on evidence reviewed here, it seems that prevalent forms of metabolic syndrome and T2DM [type 2 diabetes mellitus] result from unremitting caloric surplus complicated by failure of adipocytes to maintain protection against lipotoxicity. If one imagines the USA population to be unwitting volunteers in the largest (300 million subjects) and longest (50 years) clinical research project in history, the specific aim of which was to determine if the deleterious effects of sustained caloric surplus in rodents also can occur in humans, the outcome of the project becomes clear - after 50 years of exposure to an inexpensive calorie-dense diet high in fat and carbohydrates, 200 million subjects are overweight and >50 million have metabolic syndrome. The failure of healthcare providers and pharmaceutical industries to contain the pandemic suggests that elimination of 'bargain basement' calories will be required to 'price obesity out of the market.' Unfortunately, this would have profound socioeconomic implications: How do we tax excessive calories while at the same time guaranteeing sufficient access to high-quality foods for the underprivileged?"
Scherer et al.: "Gluttony, sloth and the metabolic syndrome: a roadmap to lipotoxicity."
In fact, says Roger Unger of the University of Texas Southwestern at Dallas, obesity is the body's way of storing lipids where they belong, in fat tissue, in an effort to protect our other organs from lipids' toxic effects. It's when the surplus of calories coming in gets to be too much for our fat tissue to handle that those lipids wind up in other places they shouldn't be, and the cascade of symptoms known as metabolic syndrome sets in.
It comes down to simple facts that all of us know on some level or another: Americans since the 1950s eat too much high-calorie food loaded with carbs and fat (what Unger calls "potent adipogenic nutrient mixtures") and, thanks to modern technology, we move far too little. Until that changes, Unger doesn't see any end to the growing epidemic of metabolic syndrome. Still, our metabolisms aren't broken; the pathways that squirrel fat away as an energy source for use in lean times are just completely overwhelmed. "We are pushing our homeostatic capability to the maximum," says Unger, who coined the term "lipotoxicity" in 1994. "Overnutrition used to be rare - reserved for those in the castle. Today, it's just the opposite. Bad calories are so cheap that anyone can afford to get overweight."
Unger cites plenty of evidence in support of a protective role for obesity. Genetic manipulations in mice that increase or decrease fat formation have provided evidence that adipogenesis, meaning the generation of fat cells, delays other metabolic consequences of overeating. The reverse is also true, he writes. Obesity-resistant mice have in some cases been found to develop severe diabetes upon eating too much, as a result of lipid accumulation in tissues other than fat.
There is some disagreement in the field about whether insulin resistance is a primary cause of metabolic syndrome or just one of its features, Unger notes. But on this, too, he has a clear view. Insulin resistance is not the cause of metabolic syndrome, he says, it is a "passive byproduct" of fat deposition in the liver and muscle once storage in fat cells begins to fail.
It also makes sense in Unger's estimation that cells that have already taken on too much fat would begin to exclude glucose, causing its levels in blood and urine to rise. Once in cells, glucose becomes a substrate for the production of more fat. "The body is doing what we should have done - keep excess calories out - and it may be protective," Unger says.
At the center of the transition from protective obesity to metabolic syndrome is resistance to the fat hormone leptin, well known for its appetite-suppressing effects, Unger says. The hormone is also responsible for partitioning fat in the body. The rise of leptin as fat stores grow is therefore an adaptive response, but that can only go so far before resistance sets in.
Based on the genes they carry, some people will be better able to sustain lipid storage in fat and can get away with being overweight, even obese, without the other symptoms. Eventually, though, the need to cut calories is something all of us will face.
"Once you reach a certain age, almost everybody is leptin resistant," he says. "Nature stops protecting you once you pass the reproductive years," requiring all of us to watch our diets and do exercise.
Unger's perspective comes from the research he does at UT Southwestern's Touchstone Center for Diabetes Research and a thorough understanding of the scientific literature, but it also stems from his own memories in childhood when one only saw fat ladies at the circus. "That's how unusual it was," he says. "The younger you are, the more skewed your perception is of an epidemic that surrounds you."
Unger concludes his review article this way: "Based on evidence reviewed here, it seems that prevalent forms of metabolic syndrome and T2DM [type 2 diabetes mellitus] result from unremitting caloric surplus complicated by failure of adipocytes to maintain protection against lipotoxicity. If one imagines the USA population to be unwitting volunteers in the largest (300 million subjects) and longest (50 years) clinical research project in history, the specific aim of which was to determine if the deleterious effects of sustained caloric surplus in rodents also can occur in humans, the outcome of the project becomes clear - after 50 years of exposure to an inexpensive calorie-dense diet high in fat and carbohydrates, 200 million subjects are overweight and >50 million have metabolic syndrome. The failure of healthcare providers and pharmaceutical industries to contain the pandemic suggests that elimination of 'bargain basement' calories will be required to 'price obesity out of the market.' Unfortunately, this would have profound socioeconomic implications: How do we tax excessive calories while at the same time guaranteeing sufficient access to high-quality foods for the underprivileged?"
Scherer et al.: "Gluttony, sloth and the metabolic syndrome: a roadmap to lipotoxicity."
Chronic Care Model Associated With Improved Diabetes Care
Incorporating elements of the Chronic Care Model (CCM) in small independent primary care practices can be done with ease and is associated with better intermediate outcomes of diabetes care. This study of 90 clinicians and 886 patients found that clinician-reported use of CCM elements was significantly associated with lower glycosylated hemoglobin levels (the standard measure of the degree of control of diabetes) and ratios of cholesterol to high-density lipoprotein cholesterol. Specifically, for every unit increase in clinician-reported CCM use (e.g., from "rarely" to "occasionally"), there was an associated 0.30% reduction in glycosylated hemoglobin values and a 0.17 reduction in the lipid ratio.
Use of Chronic Care Model Elements Is Associated with Higher-Quality Care for Diabetes
By Paul A. Nutting, M.D., M.S.P.H., et al
Annals of Family Medicine tip sheet
Annals of Family Medicine is a peer-reviewed, indexed research journal that provides a cross-disciplinary forum for new, evidence-based information affecting the primary care disciplines. Annals of Family Medicine is sponsored by six family medical organizations, including the American Academy of Family Physicians, the American Board of Family Medicine, the Society of Teachers of Family Medicine, the Association of Departments of Family Medicine, the Association of Family Medicine Residency Directors and the North American Primary Care Research Group. Annals of Family Medicine is published six times each year and contains original research from the clinical, biomedical, social and health services areas, as well as contributions on methodology and theory, selected reviews, essays and editorials. Complete editorial content and interactive discussion groups for each published article can be accessed free of charge on the journal's Web site, annfammed/.
Contact: Kristin Robinson
American Academy of Family Physicians
Use of Chronic Care Model Elements Is Associated with Higher-Quality Care for Diabetes
By Paul A. Nutting, M.D., M.S.P.H., et al
Annals of Family Medicine tip sheet
Annals of Family Medicine is a peer-reviewed, indexed research journal that provides a cross-disciplinary forum for new, evidence-based information affecting the primary care disciplines. Annals of Family Medicine is sponsored by six family medical organizations, including the American Academy of Family Physicians, the American Board of Family Medicine, the Society of Teachers of Family Medicine, the Association of Departments of Family Medicine, the Association of Family Medicine Residency Directors and the North American Primary Care Research Group. Annals of Family Medicine is published six times each year and contains original research from the clinical, biomedical, social and health services areas, as well as contributions on methodology and theory, selected reviews, essays and editorials. Complete editorial content and interactive discussion groups for each published article can be accessed free of charge on the journal's Web site, annfammed/.
Contact: Kristin Robinson
American Academy of Family Physicians
Merck, Schering-Plough Offer Explanation For Delay In Release Of Vytorin Study Results
Merck and Schering-Plough recently offered a detailed explanation of their decision to delay the release of the results of a study of the cholesterol medication Vytorin, the Wall Street Journal reports. The study, called Enhance, ended in April 2006, but the companies did not release the results until Jan. 14 (Winslow/Wilde Mathews, Wall Street Journal, 1/26).
The study found that Vytorin is no more effective than a medication available in generic form in the prevention of accumulation of plaque on artery walls. For the study, 720 participants took either Vytorin -- a combination of Zetia, which blocks absorption of cholesterol in the intestines, and Zocor, a statin available in generic form -- or Zocor alone. The two-year study found that participants who took Vytorin experienced a 58% decrease in their LDL cholesterol levels, compared with 41% for those who took Zocor. However, the study found no statistically significant difference in the accumulation of plaque on artery walls among participants who took Vytorin and those who took Zocor (Kaiser Daily Health Policy Report, 1/17).
The companies attributed the delay in the release of the results to efforts to ensure accuracy of imaging data collected during the study. The companies in late 2005 raised concerns about the quality of the imaging data. In subsequent months, the companies established a plan to reanalyze the images that included the establishment of two panels of outside experts to discuss the issue. In January 2007, one expert said the concerns about the quality of the imaging data were similar to those in other studies, but the companies decided to continue with the plan. The companies also said that the results of the study were "blinded" throughout the process and that they remained unaware of whether the results were positive or negative until Dec. 31, 2007.
According to the Journal, "Critics said that, despite the recounting, they didn't fully understand why the companies spent so long working on the data," and the "affair shows the problems that can arise when corporate sponsors, rather than independent academic investigators, control how a study is run" (Wall Street Journal, 1/26).
The study found that Vytorin is no more effective than a medication available in generic form in the prevention of accumulation of plaque on artery walls. For the study, 720 participants took either Vytorin -- a combination of Zetia, which blocks absorption of cholesterol in the intestines, and Zocor, a statin available in generic form -- or Zocor alone. The two-year study found that participants who took Vytorin experienced a 58% decrease in their LDL cholesterol levels, compared with 41% for those who took Zocor. However, the study found no statistically significant difference in the accumulation of plaque on artery walls among participants who took Vytorin and those who took Zocor (Kaiser Daily Health Policy Report, 1/17).
The companies attributed the delay in the release of the results to efforts to ensure accuracy of imaging data collected during the study. The companies in late 2005 raised concerns about the quality of the imaging data. In subsequent months, the companies established a plan to reanalyze the images that included the establishment of two panels of outside experts to discuss the issue. In January 2007, one expert said the concerns about the quality of the imaging data were similar to those in other studies, but the companies decided to continue with the plan. The companies also said that the results of the study were "blinded" throughout the process and that they remained unaware of whether the results were positive or negative until Dec. 31, 2007.
According to the Journal, "Critics said that, despite the recounting, they didn't fully understand why the companies spent so long working on the data," and the "affair shows the problems that can arise when corporate sponsors, rather than independent academic investigators, control how a study is run" (Wall Street Journal, 1/26).
Additional Developments
Summaries of several developments related to the results of the Vytorin study appear below.
FDA recommendations: FDA on Friday said that patients should not end treatment with Vytorin immediately based on the results of the study, CQ HealthBeat reports. According to FDA officials, the study does not indicate that Vytorin is ineffective. They added that patients who take Vytorin should discuss whether they should switch medication with their physicians. FDA officials also said that the agency will review the results of the study, with results expected in six months (Lubbes, CQ HealthBeat, 1/25).
New York investigation: The office of New York Attorney General Andrew Cuomo (D) on Saturday announced that he has sent subpoenas to Merck and Schering-Plough as part of an investigation into the delay in the release of the results of the study, the Journal reports. The investigation seeks to determine whether the company "deliberately concealed" results of the study. Both companies said that they have received the subpoenas and will cooperate with the investigation (Rubenstein, Wall Street Journal, 1/28).
Lawsuits: Merck and Schering-Plough face at least 10 federal lawsuits over allegations that the companies "reaped billions of dollars in profits" through their delay in the release of the results of the study, the Philadelphia Inquirer reports. The lawsuits -- filed in California, Colorado, New Jersey, New York and Ohio -- allege that the delay prompted patients to purchase Vytorin, rather than a lower-cost, generic version. Skip Irvine, a spokesperson for the companies, said that they plan to fight the lawsuits (Stark, Philadelphia Inquirer, 1/26).
Patient response: Many patients who are "dismayed by recently released research" on Vytorin "have been asking their doctors what to do," the Arkansas Democrat-Gazette reports. According to the Democrat-Gazette, many physicians are "keeping their patients on Vytorin, while others have made changes." The American College of Cardiology has recommended that physicians not make "major clinical decisions" based on the results of the study, and the American Heart Association has recommended that patients consult with their physician before they end treatment with Vytorin (Tubbs, Arkansas Democrat-Gazette, 1/28).
Opinion Piece
"The idea that cholesterol plays a key role in heart disease is so tightly woven into modern medical thinking that it is no longer considered open to question," but based on the results of the Vytorin study, scientists should "question the role of LDL cholesterol in heart disease," Gary Taubes -- author of "Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control and Disease" -- writes in a New York Times opinion piece.
Taubes writes, "If the evidence continues to challenge the role of cholesterol, then rethink it, without preconceptions, and consider what these other pathways in cardiovascular disease are implying about cause and prevention." He concludes, "A different hypothesis may turn out to fit the facts better and one day help prevent considerably more deaths" (Taubes, New York Times, 1/27).
Reprinted with kind permission from kaisernetwork. You can view the entire Kaiser Daily Health Policy Report, search the archives, or sign up for email delivery at kaisernetwork/dailyreports/healthpolicy. The Kaiser Daily Health Policy Report is published for kaisernetwork, a free service of The Henry J. Kaiser Family Foundation© 2005 Advisory Board Company and Kaiser Family Foundation. All rights reserved.
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