ACC 2010 - ACCORD BP: Intensive BP lowering futile in diabetics
New data from the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study show that there is no benefit to be gained in diabetics from intensively lowering their systolic blood pressure to a goal of <120 mm Hg [1].
There was no difference in the primary end point—a composite of fatal and nonfatal major cardiovascular events—between this group and those who received standard antihypertensive therapy to get their pressure down to <140 mm Hg, said lead author Dr William C Cushman (Veterans Affairs Medical Center, Memphis, TN), who presented the results at a late-breaking clinical-trials session here at the American College of Cardiology (ACC) 2010 Scientific Sessions; they were simultaneously published online in the New England Journal of Medicine.
To heartwire, Cushman admitted he was surprised by the results: "We wouldn't have done the study if we didn't think there was a reason to think it might be beneficial." But he countered, "I've said all along, that whichever the answer is, it is extremely important. If it doesn't show benefit, we should not be aggressive, because it's hard enough to get diabetics to below 140 mm Hg, so this is a good answer."
Also presented today during the same late-breaking clinical-trials session was a retrospective analysis of the INVEST trial. This showed that diabetic patients with coronary artery disease whose systolic blood pressure was lowered to 130 to 140 mm Hg had a better outcome than those with systolic pressures over 140 mm Hg. But reduction below 130 mm Hg did not appear to offer any additional benefit and those patients had a higher mortality rate.
No justification for target below 120 mm Hg in diabetics?
I've said all along, that whichever the answer is, it is extremely important.
In an editorial accompanying the published ACCORD BP study [2], Dr Peter M Nilsson (University Hospital, Malmö, Sweden) agrees: "The main conclusion to draw from this study must be that a systolic BP target below 120 mm Hg in patients with type 2 diabetes is not justified by the evidence."
Nilsson added that with the conclusion of the ACCORD study—which as well as this ACCORD BP trial included the ACCORD lipid trial, also reported here at the ACC meeting—a period of three landmark studies (UKPDS, ADVANCE, and ACCORD) has now come to an end. "We learn from the completed ACCORD study that flexible goals should probably be applied to the control of hyperglycemia, blood pressure, and dyslipidemia in patients with type 2 diabetes, taking into account individual clinical factors of importance," he states.
Completo: theheart.org
Especializado en DIABETES, EDUCACIÓN DIABETOLÓGICA y MEDICINA INTERNA Aquí encontrarás temas relacionados a la medicina del adulto y otros temas interesantes
martes, 30 de marzo de 2010
Sibutramine Now Contraindicated in Patients With a History of Cardiovascular Disease
January 29, 2010 — Sibutramine, marketed as Meridia in the United States by Abbott, is now contraindicated in patients with a history of cardiovascular disease, the US Food and Drug Administration (FDA) announced On January 21.
According to an alert posted by MedWatch, the FDA's safety information and adverse event reporting program, the announcement is a follow-up to an ongoing safety review of preliminary results reported in November 2009, which first raised concerns about this issue.
According to the FDA, the drug label already warns against the use of sibutramine in patients with cardiovascular disease. "However, based on the serious nature of the review findings, FDA requested and the manufacturer agreed to add a new contraindication to the sibutramine drug label," stating that sibutramine should not be used in patients with a history of cardiovascular disease, including patients with a:
History of coronary artery disease (eg, myocardial infarction, angina)
History of stroke or transient ischemic attack
History of heart arrhythmias
History of congestive heart failure
History of peripheral arterial disease
Uncontrolled hypertension (eg, >145/90 mm Hg)
The safety review was based on data from the Sibutramine Cardiovascular Outcomes Trial (SCOUT), which enrolled more than 10,000 overweight or obese patients with diabetes or a history of coronary artery disease, peripheral vascular disease, or stroke, along with other cardiovascular risk factors.
An analysis of the trial's primary end point — a composite of myocardial infarction, stroke, resuscitated cardiac arrest, or death — found the rate to be 11.4% for patients receiving sibutramine and 10% for those receiving placebo. The current review found that the risk for cardiovascular events with sibutramine was significantly increased only in patients with a history of cardiovascular disease (P = .023).
Healthcare professionals should regularly monitor blood pressure and heart rate in patients taking sibutramine, the FDA notes.
"If sustained increases in blood pressure and/or heart rate are observed, sibutramine should be discontinued," according to the FDA. "Additionally, sibutramine should be discontinued in patients who do not lose at least 5% of their baseline body weight within the first 3 to 6 months of treatment, as continued treatment is unlikely to be effective and exposes the patient to unnecessary risk."
The full study report for SCOUT is expected in March 2010, at which time an open public advisory committee meeting will be convened to determine whether additional regulatory actions should be taken to ensure the safe use of sibutramine.
EMEA
Meanwhile, the European Medicines Agency (EMEA) also announced the results of its safety review of drugs containing sibutramine, citing the SCOUT data. According to a press release issued today, the EMEA concluded, "the risks of these medicines are greater than their benefits."
Sibutramine-containing brands in the United Kingdom and Europe include Reductil, Reduxade, and Zelium, among others. The agency now "recommend[s] the suspension of marketing authorizations for these medicines across the European Union."
The EMEA statement goes on to say that physicians should no longer prescribe sibutramine-containing agents, pharmacists should no longer dispense them, and patients taking them should make an appointment to see their physicians "at the next convenient time."
More information is available on the FDA's MedWatch Web site and on the EMEA Web site.
Adverse events related to sibutramine should be communicated to MedWatch by telephone at 1-800-FDA-1088, by fax at 1-800-FDA-0178, online at http://www.fda.gov/medwatch, or by mail to 5600 Fishers Lane, Rockville, Maryland 20852-9787.
Clinical Implications
Sibutramine is now contraindicated in patients with a history of cardiovascular disease, including coronary artery disease, stroke/transient ischemic attack, arrhythmias, congestive heart failure, or peripheral arterial disease; it also should not be used in those with uncontrolled hypertension.
Data from ongoing SCOUT of more than 10,000 overweight or obese patients have linked sibutramine to an increased risk for a composite endpoint of myocardial infarction, stroke, resuscitated cardiac arrest, or death relative to placebo; the increase was associated with a history of cardiovascular disease.
Blood pressure and heart rate should be regularly monitored during sibutramine therapy; treatment should be discontinued for sustained increases in these parameters. Sibutramine should also be stopped in patients who do not lose at least 5% of their baseline body weight within 3 to 6 months, as continued therapy is unlikely to be effective and is linked to unnecessary risk.
According to an alert posted by MedWatch, the FDA's safety information and adverse event reporting program, the announcement is a follow-up to an ongoing safety review of preliminary results reported in November 2009, which first raised concerns about this issue.
According to the FDA, the drug label already warns against the use of sibutramine in patients with cardiovascular disease. "However, based on the serious nature of the review findings, FDA requested and the manufacturer agreed to add a new contraindication to the sibutramine drug label," stating that sibutramine should not be used in patients with a history of cardiovascular disease, including patients with a:
History of coronary artery disease (eg, myocardial infarction, angina)
History of stroke or transient ischemic attack
History of heart arrhythmias
History of congestive heart failure
History of peripheral arterial disease
Uncontrolled hypertension (eg, >145/90 mm Hg)
The safety review was based on data from the Sibutramine Cardiovascular Outcomes Trial (SCOUT), which enrolled more than 10,000 overweight or obese patients with diabetes or a history of coronary artery disease, peripheral vascular disease, or stroke, along with other cardiovascular risk factors.
An analysis of the trial's primary end point — a composite of myocardial infarction, stroke, resuscitated cardiac arrest, or death — found the rate to be 11.4% for patients receiving sibutramine and 10% for those receiving placebo. The current review found that the risk for cardiovascular events with sibutramine was significantly increased only in patients with a history of cardiovascular disease (P = .023).
Healthcare professionals should regularly monitor blood pressure and heart rate in patients taking sibutramine, the FDA notes.
"If sustained increases in blood pressure and/or heart rate are observed, sibutramine should be discontinued," according to the FDA. "Additionally, sibutramine should be discontinued in patients who do not lose at least 5% of their baseline body weight within the first 3 to 6 months of treatment, as continued treatment is unlikely to be effective and exposes the patient to unnecessary risk."
The full study report for SCOUT is expected in March 2010, at which time an open public advisory committee meeting will be convened to determine whether additional regulatory actions should be taken to ensure the safe use of sibutramine.
EMEA
Meanwhile, the European Medicines Agency (EMEA) also announced the results of its safety review of drugs containing sibutramine, citing the SCOUT data. According to a press release issued today, the EMEA concluded, "the risks of these medicines are greater than their benefits."
Sibutramine-containing brands in the United Kingdom and Europe include Reductil, Reduxade, and Zelium, among others. The agency now "recommend[s] the suspension of marketing authorizations for these medicines across the European Union."
The EMEA statement goes on to say that physicians should no longer prescribe sibutramine-containing agents, pharmacists should no longer dispense them, and patients taking them should make an appointment to see their physicians "at the next convenient time."
More information is available on the FDA's MedWatch Web site and on the EMEA Web site.
Adverse events related to sibutramine should be communicated to MedWatch by telephone at 1-800-FDA-1088, by fax at 1-800-FDA-0178, online at http://www.fda.gov/medwatch, or by mail to 5600 Fishers Lane, Rockville, Maryland 20852-9787.
Clinical Implications
Sibutramine is now contraindicated in patients with a history of cardiovascular disease, including coronary artery disease, stroke/transient ischemic attack, arrhythmias, congestive heart failure, or peripheral arterial disease; it also should not be used in those with uncontrolled hypertension.
Data from ongoing SCOUT of more than 10,000 overweight or obese patients have linked sibutramine to an increased risk for a composite endpoint of myocardial infarction, stroke, resuscitated cardiac arrest, or death relative to placebo; the increase was associated with a history of cardiovascular disease.
Blood pressure and heart rate should be regularly monitored during sibutramine therapy; treatment should be discontinued for sustained increases in these parameters. Sibutramine should also be stopped in patients who do not lose at least 5% of their baseline body weight within 3 to 6 months, as continued therapy is unlikely to be effective and is linked to unnecessary risk.
Fuente: http://cme.medscape.com/viewarticle/716102?src=emailthis
lunes, 29 de marzo de 2010
Se aplica de maravilla a mi país o a la gran mayoría
Aunque no comparto los lineamientos del Dr. Rogers, si me parece muy atinado éste análisis x parte suya:
Todo lo que una persona recibe sin haber trabajado para obtenerlo, otra persona deberá haber trabajado para ello, pero sin recibirlo. El gobierno no puede entregar nada a alguien, si antes no se lo ha quitado a alguna otra persona. Cuando la mitad de las personas llegan a la conclusión de que ellas no tienen que trabajar porque la otra mitad está obligada a hacerse cargo de ellas, y cuando esta otra mitad se convence de que no vale la pena trabajar porque alguien les quitará lo que han logrado con su esfuerzo, y eso... mi querido amigo......es el fin de cualquier nación.
“No se puede multiplicar la riqueza dividiéndola”.
Dr. Adrian Rogers, 1985
Significant Visceral Fat Loss Seen Within 12 Weeks With Orlistat
Solo muchísimo cuidado con la "pruebas de función hepática"
Fuente: http://www.medscape.com/viewarticle/716415?src=emailthis
February 3, 2010 — A randomized placebo controlled trial of orlistat (Alli, GlaxoSmithKline) 60 mg daily for overweight to obese but otherwise healthy subjects showed that the weight-loss agent was not only associated with greater overall weight loss than placebo, but that there was a greater loss of visceral fat with active treatment.
Furthermore, effects were seen within 3 months, investigator Rex Newbould, PhD, head of the Clinical Imaging Center at Hammersmith Hospital in London, United Kingdom, reported at the first International Congress on Abdominal Obesity (ICAO) underway in Hong Kong.
Of the 26 overweight and obese subjects (body mass index [BMI], 25.0 to 35.0 kg/m2; waist circumference >88 cm for women and >102 cm for men) enrolled, 24 completed the 12-week study.
Subjects took orlistat 60 mg 3 times a day and ate a hypocaloric (reduced by 500 kcal) low-fat diet. Subjects received a single dietary counseling session, and an abdominal magnetic resonance imaging (MRI) scan was performed to measure visceral adipose tissue (VAT) at baseline. Body weight and waist circumference were measured at weeks 4, 8, and 12, and a repeat abdominal MRI scan was performed at week 12.
After 12 weeks, orlistat was associated with a significant reduction in body weight, waist circumference, and VAT, according to MRI.
"MRI measures fat more accurately than weight or waist measurement," Dr. Newbould told Medscape Medical News. "It measures the fat inside the fat, and has less 'noise' than other measurements. It measures only fat, whereas weight is a measure of fat, fluid, and other factors."
The change in VAT was correlated with the change in weight (P < .0001) but not waist circumference (P = .35). The mean change in weight was –5.24 kg (–5.6%), in waist circumference was –4.54 cm (–4.3%), and in VAT was –0.60 L (–10.6%).
"Visceral fat is the metabolically active type of fat that is associated with adverse outcomes," Dr. Newbould explained. "We would expect [a loss of VAT] to be associated with improved outcomes."
A similar study was presented by Kaj Stenlöf, MD, executive director of the Clinical Trial Center at Sahlgrenska Academy in Göteborg, Sweden.
He and his colleagues randomized 131 overweight and obese subjects (BMI, 25 to 35 kg/m2; waist circumference >88 cm for women and >102 cm for men) to orlistat 60 mg or placebo 3 times a day plus a hypocaloric low-fat diet for 24 weeks. Subjects were "encouraged to exercise," but were not on a prescribed exercise regimen.
Treatment was well tolerated, Dr. Stenlöf said, and 107 subjects completed the study. The primary adverse effects were gastrointestinal.
Mean change in VAT after 24 weeks of orlistat treatment was –9.39% in the placebo group (P < .0001) and –15.66% in the orlistat group (P < .0001). The percent change difference from baseline to week 24 between the placebo and orlistat groups was 0.227 (P < .0244).
In addition, there was a significant reduction in mean body weight from baseline to week 24 in both groups, with a loss of 5.96 kg in the orlistat group and 3.91 kg in the placebo group (P < .05).
Although only data on VAT were presented at the meeting, Dr. Stenlöf told Medscape Medical News that they are calculating cardiac muscle fat and fat in other muscles, and are computing other parameters, such as blood pressure and blood glucose. These data will be presented this summer at the International Conference on Obesity in Stockholm, Sweden.
"With the over-the-counter formulation of orlistat, there has been a conceptual shift in the treatment of obesity," Jean-Pierre Després, PhD, director of research in cardiology at the Quebec Heart and Lung Institute at Laval University in Quebec City, told Medscape Medical News.
"Instead of overall weight loss, we are now focusing on this high-risk form of obesity, with loss of the more metabolically active visceral fat — the fat that carries a high risk of heart disease."
"We don't know if orlistat induces a preferential loss of visceral fat. Those data are just now coming in, and we heard some new data here," said Dr. Després, who is chair of the ICAO. "We don't know if the loss of visceral fat is part of overall weight loss. The key point is that there has been a paradigm shift to focus on the reduction of this most dangerous form of obesity."
"Orlistat is very safe and is an effective therapy in motivated patients," said Christie M. Ballantyne, MD, professor of medicine at Baylor College of Medicine and director of the Center for Cardiovascular Disease Prevention at Methodist DeBakey Heart Center in Houston, Texas, in an interview with Medscape Medical News. He was not involved in either study.
"I think it has been underutilized because of [gastrointestinal] side effects, but the data are very clear that this provides additional weight loss to a program of lifestyle modification. It has clearly been shown to have favorable effects on metabolism, and the newer data on visceral fat are also encouraging."
"This therapy should be discussed as an option, particularly in patients with comorbidities, because both the efficacy and safety are proven," Dr. Ballantyne asserted.
Both studies were supported by grants from GlaxoSmithKline. Dr. Després has disclosed no relevant financial relationships. Dr. Ballantyne reports being a consultant to GlaxoSmithKline for lipid reduction (Lovaza) and to other companies in field of lipid research, including Merck, AstraZeneca, and Abbott.
First International Congress on Abdominal Obesity (ICAO). Presented January 28, 2010.
Furthermore, effects were seen within 3 months, investigator Rex Newbould, PhD, head of the Clinical Imaging Center at Hammersmith Hospital in London, United Kingdom, reported at the first International Congress on Abdominal Obesity (ICAO) underway in Hong Kong.
Of the 26 overweight and obese subjects (body mass index [BMI], 25.0 to 35.0 kg/m2; waist circumference >88 cm for women and >102 cm for men) enrolled, 24 completed the 12-week study.
Subjects took orlistat 60 mg 3 times a day and ate a hypocaloric (reduced by 500 kcal) low-fat diet. Subjects received a single dietary counseling session, and an abdominal magnetic resonance imaging (MRI) scan was performed to measure visceral adipose tissue (VAT) at baseline. Body weight and waist circumference were measured at weeks 4, 8, and 12, and a repeat abdominal MRI scan was performed at week 12.
After 12 weeks, orlistat was associated with a significant reduction in body weight, waist circumference, and VAT, according to MRI.
"MRI measures fat more accurately than weight or waist measurement," Dr. Newbould told Medscape Medical News. "It measures the fat inside the fat, and has less 'noise' than other measurements. It measures only fat, whereas weight is a measure of fat, fluid, and other factors."
The change in VAT was correlated with the change in weight (P < .0001) but not waist circumference (P = .35). The mean change in weight was –5.24 kg (–5.6%), in waist circumference was –4.54 cm (–4.3%), and in VAT was –0.60 L (–10.6%).
"Visceral fat is the metabolically active type of fat that is associated with adverse outcomes," Dr. Newbould explained. "We would expect [a loss of VAT] to be associated with improved outcomes."
A similar study was presented by Kaj Stenlöf, MD, executive director of the Clinical Trial Center at Sahlgrenska Academy in Göteborg, Sweden.
He and his colleagues randomized 131 overweight and obese subjects (BMI, 25 to 35 kg/m2; waist circumference >88 cm for women and >102 cm for men) to orlistat 60 mg or placebo 3 times a day plus a hypocaloric low-fat diet for 24 weeks. Subjects were "encouraged to exercise," but were not on a prescribed exercise regimen.
Treatment was well tolerated, Dr. Stenlöf said, and 107 subjects completed the study. The primary adverse effects were gastrointestinal.
Mean change in VAT after 24 weeks of orlistat treatment was –9.39% in the placebo group (P < .0001) and –15.66% in the orlistat group (P < .0001). The percent change difference from baseline to week 24 between the placebo and orlistat groups was 0.227 (P < .0244).
In addition, there was a significant reduction in mean body weight from baseline to week 24 in both groups, with a loss of 5.96 kg in the orlistat group and 3.91 kg in the placebo group (P < .05).
Although only data on VAT were presented at the meeting, Dr. Stenlöf told Medscape Medical News that they are calculating cardiac muscle fat and fat in other muscles, and are computing other parameters, such as blood pressure and blood glucose. These data will be presented this summer at the International Conference on Obesity in Stockholm, Sweden.
"With the over-the-counter formulation of orlistat, there has been a conceptual shift in the treatment of obesity," Jean-Pierre Després, PhD, director of research in cardiology at the Quebec Heart and Lung Institute at Laval University in Quebec City, told Medscape Medical News.
"Instead of overall weight loss, we are now focusing on this high-risk form of obesity, with loss of the more metabolically active visceral fat — the fat that carries a high risk of heart disease."
"We don't know if orlistat induces a preferential loss of visceral fat. Those data are just now coming in, and we heard some new data here," said Dr. Després, who is chair of the ICAO. "We don't know if the loss of visceral fat is part of overall weight loss. The key point is that there has been a paradigm shift to focus on the reduction of this most dangerous form of obesity."
"Orlistat is very safe and is an effective therapy in motivated patients," said Christie M. Ballantyne, MD, professor of medicine at Baylor College of Medicine and director of the Center for Cardiovascular Disease Prevention at Methodist DeBakey Heart Center in Houston, Texas, in an interview with Medscape Medical News. He was not involved in either study.
"I think it has been underutilized because of [gastrointestinal] side effects, but the data are very clear that this provides additional weight loss to a program of lifestyle modification. It has clearly been shown to have favorable effects on metabolism, and the newer data on visceral fat are also encouraging."
"This therapy should be discussed as an option, particularly in patients with comorbidities, because both the efficacy and safety are proven," Dr. Ballantyne asserted.
Both studies were supported by grants from GlaxoSmithKline. Dr. Després has disclosed no relevant financial relationships. Dr. Ballantyne reports being a consultant to GlaxoSmithKline for lipid reduction (Lovaza) and to other companies in field of lipid research, including Merck, AstraZeneca, and Abbott.
First International Congress on Abdominal Obesity (ICAO). Presented January 28, 2010.
Fuente: http://www.medscape.com/viewarticle/716415?src=emailthis
Bees in more trouble than ever
MERCED, Calif. – The mysterious 4-year-old crisis of disappearing honeybees is deepening. A quick federal survey indicates a heavy bee die-off this winter, while a new study shows honeybees' pollen and hives laden with pesticides.
Two federal agencies along with regulators in California and Canada are scrambling to figure out what is behind this relatively recent threat, ordering new research on pesticides used in fields and orchards. Federal courts are even weighing in this month, ruling that the U.S. Environmental Protection Agency overlooked a requirement when allowing a pesticide on the market.
And on Thursday, chemists at a scientific conference in San Francisco will tackle the issue of chemicals and dwindling bees in response to the new study.
Scientists are concerned because of the vital role bees play in our food supply. About one-third of the human diet is from plants that require pollination from honeybees, which means everything from apples to zucchini.
Bees have been declining over decades from various causes. But in 2006 a new concern, "colony collapse disorder," was blamed for large, inexplicable die-offs. The disorder, which causes adult bees to abandon their hives and fly off to die, is likely a combination of many causes, including parasites, viruses, bacteria, poor nutrition and pesticides, experts say.
"It's just gotten so much worse in the past four years," said Jeff Pettis, research leader of the Department of Agriculture's Bee Research Laboratory in Beltsville, Md. "We're just not keeping bees alive that long."
This year bees seem to be in bigger trouble than normal after a bad winter, according to an informal survey of commercial bee brokers cited in an internal USDA document. One-third of those surveyed had trouble finding enough hives to pollinate California's blossoming nut trees, which grow the bulk of the world's almonds. A more formal survey will be done in April.
"There were a lot of beekeepers scrambling to fill their orders and that implies that mortality was high," said Penn State University bee researcher Dennis vanEngelsdorp, who worked on the USDA snapshot survey.
Beekeeper Zac Browning shipped his hives from Idaho to California to pollinate the blossoming almond groves. He got a shock when he checked on them, finding hundreds of the hives empty, abandoned by the worker bees.
The losses were extreme, three times higher than the previous year.
"It wasn't one load or two loads, but every load we were pulling out that was dead. It got extremely depressing to see a third of my livestock gone," Browning said, standing next to stacks of dead bee colonies in a clearing near Merced, at the center of California's fertile San Joaquin Valley.
Among all the stresses to bee health, it's the pesticides that are attracting scrutiny now. A study published Friday in the scientific journal PLOS (Public Library of Science) One found about three out of five pollen and wax samples from 23 states had at least one systemic pesticide — a chemical designed to spread throughout all parts of a plant.
EPA officials said they are aware of problems involving pesticides and bees and the agency is "very seriously concerned."
The pesticides are not a risk to honey sold to consumers, federal officials say. And the pollen that people eat is probably safe because it is usually from remote areas where pesticides are not used, Pettis said. But the PLOS study found 121 different types of pesticides within 887 wax, pollen, bee and hive samples.
"The pollen is not in good shape," said Chris Mullin of Penn State University, lead author.
None of the chemicals themselves were at high enough levels to kill bees, he said, but it was the combination and variety of them that is worrisome.
University of Illinois entomologist May Berenbaum called the results "kind of alarming."
Despite EPA assurances, environmental groups don't think the EPA is doing enough on pesticides.
Bayer Crop Science started petitioning the agency to approve a new pesticide for sale in 2006. After reviewing the company's studies of its effects on bees, the EPA gave Bayer conditional approval to sell the product two years later, but said it had to carry a label warning that it was "potentially toxic to honey bee larvae through residues in pollen and nectar."
The Natural Resources Defense Council sued, saying the agency failed to give the public timely notice for the new pesticide application. In December, a federal judge in New York agreed, banning the pesticide's sale and earlier this month, two more judges upheld the ruling.
"This court decision is obviously very painful for us right now, and for growers who don't have access to that product," said Jack Boyne, an entomologist and spokesman for Bayer Crop Science. "This product quite frankly is not harmful to honeybees."
Boyne said the pesticide was sold for only about a year and most sales were in California, Arizona and Florida. The product is intended to disrupt the mating patterns of insects that threaten citrus, lettuce and grapes, he said.
Berenbaum's research shows pesticides are not the only problem. She said multiple viruses also are attacking the bees, making it tough to propose a single solution.
"Things are still heading downhill," she said.
For Browning, one of the country's largest commercial beekeepers, the latest woes have led to a $1 million loss this year.
"It's just hard to get past this," he said, watching as workers cleaned honey from empty wooden hives Monday. "I'm going to rebuild, but I have plenty of friends who aren't going to make it."
___
AP Science Writer Seth Borenstein reported from Washington, D.C.
Two federal agencies along with regulators in California and Canada are scrambling to figure out what is behind this relatively recent threat, ordering new research on pesticides used in fields and orchards. Federal courts are even weighing in this month, ruling that the U.S. Environmental Protection Agency overlooked a requirement when allowing a pesticide on the market.
And on Thursday, chemists at a scientific conference in San Francisco will tackle the issue of chemicals and dwindling bees in response to the new study.
Scientists are concerned because of the vital role bees play in our food supply. About one-third of the human diet is from plants that require pollination from honeybees, which means everything from apples to zucchini.
Bees have been declining over decades from various causes. But in 2006 a new concern, "colony collapse disorder," was blamed for large, inexplicable die-offs. The disorder, which causes adult bees to abandon their hives and fly off to die, is likely a combination of many causes, including parasites, viruses, bacteria, poor nutrition and pesticides, experts say.
"It's just gotten so much worse in the past four years," said Jeff Pettis, research leader of the Department of Agriculture's Bee Research Laboratory in Beltsville, Md. "We're just not keeping bees alive that long."
This year bees seem to be in bigger trouble than normal after a bad winter, according to an informal survey of commercial bee brokers cited in an internal USDA document. One-third of those surveyed had trouble finding enough hives to pollinate California's blossoming nut trees, which grow the bulk of the world's almonds. A more formal survey will be done in April.
"There were a lot of beekeepers scrambling to fill their orders and that implies that mortality was high," said Penn State University bee researcher Dennis vanEngelsdorp, who worked on the USDA snapshot survey.
Beekeeper Zac Browning shipped his hives from Idaho to California to pollinate the blossoming almond groves. He got a shock when he checked on them, finding hundreds of the hives empty, abandoned by the worker bees.
The losses were extreme, three times higher than the previous year.
"It wasn't one load or two loads, but every load we were pulling out that was dead. It got extremely depressing to see a third of my livestock gone," Browning said, standing next to stacks of dead bee colonies in a clearing near Merced, at the center of California's fertile San Joaquin Valley.
Among all the stresses to bee health, it's the pesticides that are attracting scrutiny now. A study published Friday in the scientific journal PLOS (Public Library of Science) One found about three out of five pollen and wax samples from 23 states had at least one systemic pesticide — a chemical designed to spread throughout all parts of a plant.
EPA officials said they are aware of problems involving pesticides and bees and the agency is "very seriously concerned."
The pesticides are not a risk to honey sold to consumers, federal officials say. And the pollen that people eat is probably safe because it is usually from remote areas where pesticides are not used, Pettis said. But the PLOS study found 121 different types of pesticides within 887 wax, pollen, bee and hive samples.
"The pollen is not in good shape," said Chris Mullin of Penn State University, lead author.
None of the chemicals themselves were at high enough levels to kill bees, he said, but it was the combination and variety of them that is worrisome.
University of Illinois entomologist May Berenbaum called the results "kind of alarming."
Despite EPA assurances, environmental groups don't think the EPA is doing enough on pesticides.
Bayer Crop Science started petitioning the agency to approve a new pesticide for sale in 2006. After reviewing the company's studies of its effects on bees, the EPA gave Bayer conditional approval to sell the product two years later, but said it had to carry a label warning that it was "potentially toxic to honey bee larvae through residues in pollen and nectar."
The Natural Resources Defense Council sued, saying the agency failed to give the public timely notice for the new pesticide application. In December, a federal judge in New York agreed, banning the pesticide's sale and earlier this month, two more judges upheld the ruling.
"This court decision is obviously very painful for us right now, and for growers who don't have access to that product," said Jack Boyne, an entomologist and spokesman for Bayer Crop Science. "This product quite frankly is not harmful to honeybees."
Boyne said the pesticide was sold for only about a year and most sales were in California, Arizona and Florida. The product is intended to disrupt the mating patterns of insects that threaten citrus, lettuce and grapes, he said.
Berenbaum's research shows pesticides are not the only problem. She said multiple viruses also are attacking the bees, making it tough to propose a single solution.
"Things are still heading downhill," she said.
For Browning, one of the country's largest commercial beekeepers, the latest woes have led to a $1 million loss this year.
"It's just hard to get past this," he said, watching as workers cleaned honey from empty wooden hives Monday. "I'm going to rebuild, but I have plenty of friends who aren't going to make it."
___
AP Science Writer Seth Borenstein reported from Washington, D.C.
Fuente: http://news.yahoo.com/s/ap/20100324/ap_on_sc/us_food_and_farm_disappearing_bees
Approach to Leg Edema of Unclear Etiology
Excelente revisión del Journal of the American Board of Family Medicine , 2006-03-01
http://www.medscape.com/viewarticle/524606?src=emailthis
http://www.medscape.com/viewarticle/524606?src=emailthis
sábado, 27 de marzo de 2010
URGENTE - LA HORA DEL PLANETA
Apaga todas tus luces el 27 de marzo del 2010 a las 20:30 hrs evita consumir energìa elèctrica por una hora, reflexiona y exige consciencia por el planeta !!!
domingo, 21 de marzo de 2010
miércoles, 17 de marzo de 2010
COX-2 inhibitors blunt "preconditioning" effect of statin
Mar 1, 2010Lisa Nainggolan
Toronto, ON - The COX-2 inhibitor celecoxib completely abolished the beneficial preconditioning effect of rosuvastatin in a small mechanistic study in human volunteers [1]. Dr Andrew Liuni (University of Toronto, ON) and colleagues report their findings in the March 9, 2010 issue of the Journal of the American College of Cardiology.Senior author Dr John D Parker (University of Toronto) explained to heartwire that it has been known for some time that exposure to brief periods of ischemia prior to a prolonged period of ischemia can reduce the amount of damage that occurs. This is known as "preconditioning," and some pharmacologic agents, including statins, are thought to have the same effect, a phenomenon termed pharmacological preconditioning. "We decided we would like to pursue the mechanisms of how that occurs, how a statin could favorably precondition," he noted, adding that research in animal models of preconditioning has shown upregulation of the COX-2 enzyme.
Statin did protect from reperfusion injury; COX-2 inhibitor overrides this
They randomized 20 volunteers to a single 40-mg dose of rosuvastatin or placebo and 24 hours later measured endothelium-dependent, flow-mediated dilation (FMD) of the radial artery before and after 15 minutes of upper-arm ischemia followed by 15 minutes of reperfusion. In a separate experiment, 18 volunteers received 200 mg of celecoxib twice daily for five days; on day four, they were randomized to single-dose rosuvastatin (40 mg) or placebo and 24 hours later underwent the same above protocol (ie, 15 minutes of upper-arm ischemia followed by 15 minutes of reperfusion).Rosuvastatin prevented the development of ischemia and reperfusion-induced endothelial dysfunction, but pretreatment with celecoxib completely abolished this protective effect. "This study provides the first evidence in humans of a direct endothelial preconditioning effect by rosuvastatin and may provide a mechanistic explanation of previous observations from clinical settings," says Parker. In addition, it is the first look at the interaction between a statin and a selective COX-2 inhibitor. "The results show that celecoxib completely prevents the preconditioning effect of the statin. So, theoretically, there could be a net negative effect on a patient taking a COX-2 inhibitor who has an acute cardiac event who also happens to be on a statin or is given a statin acutely," he observes. The findings suggest a possible mechanistic explanation for the negative cardiovascular side effects of COX-2 inhibitors observed in clinical trials, say Parker and colleagues.We are a long way from clinical relevance here, because we've made just a mechanistic observation. Parker cautioned, however, that "we are a long way from clinical relevance here, because we've made just a mechanistic observation, but it is interesting. The next step will be to do this in patients." And there are many other unanswered questions, he says, "such as whether the pharmacologic 'preconditioning' effect of statins is maintained when they are given long-term, whether this effect is seen in those who already have overt coronary disease, and how celecoxib or other COX-2 inhibitors might affect these observations." The study was funded by a grant from the Heart and Stroke Foundation of Canada.
Source
Liuni A, Luca MC, Tommaso G, et al. Rosuvastatin prevents conduit artery endothelial dysfunction induced by ischemia and reperfusion by a cyclooxygenase-2-dependent mechanism. J Am Coll Cardiol 2010; 55:1002-1006.
Related links
Remote ischemic conditioning increases myocardial salvage during acute MI [Acute Coronary Syndromes > Acute coronary syndromes; Feb 26, 2010]
Discovery of new pathway reveals small molecule that may prevent ischemic damage [Acute Coronary Syndromes > Acute coronary syndromes; Sep 11, 2008]
Revisión sobre el empleo de la metformina para el control de peso
International Journal of Obesity 32(1):61-72
Introducción
El tratamiento del sobrepeso y de la obesidad forma parte del tratamiento general de la diabetes (DBT). Varias clases de agentes antidiabéticos orales se asocian con el aumento de peso, como los secretagogos de la insulina (sulfonilureas y meglitinidas), las tiazolidinedionas (TZD) y la propia insulina. Los nuevos agentes que actúan sobre el sistema de incretinas son neutros respecto del peso o promueven la pérdida de peso. Sin embargo, estos agentes no han sido aprobados como terapia de primera línea en algunas regiones, como por ejemplo Europa. La metformina (MET) y los inhibidores de la alfa glucosidasa no se asocian con aumento de peso. Las normas mundiales actuales para el tratamiento de la DBT tipo 2 (DBT2) recomiendan la MET como farmacoterapia inicial para todos los pacientes con esta afección, incluidos aquellos sin sobrepeso, en forma concomitante con la modificación del estilo de vida a partir del diagnóstico. En este artículo se analizaron el papel del sobrepeso y la obesidad en la patogénesis de las alteraciones en el metabolismo de la glucosa y los efectos de la MET sobre el peso y la adiposidad.
Papel de la obesidad en la patogenia y en el tratamiento de la DBT2
La alteración de la glucemia se asocia con una tendencia al sobrepeso o a la obesidad. La mayoría de los pacientes con DBT2 son obesos o tienen sobrepeso, por lo que la fisiopatología de la obesidad y de la DBT se encuentran relacionadas estrechamente. Los análisis del Nurses’ Health Study y del Health Professionals Follow-up Study mostraron que el riesgo de DBT aumentó en relación con el índice de masa corporal (IMC) y que la obesidad –especialmente la abdominal– incrementó el riesgo de DBT de 10 a 11 veces. La obesidad abdominal es reconocida actualmente como el componente central del síndrome metabólico (SM) de acuerdo con la clasificación de la International Diabetes Federation.La disminución de la adiposidad reduce el riesgo de DBT2 y de factores de riesgo cardiometabólicos (CM). Las intervenciones intensivas sobre el estilo de vida en los análisis del Diabetes Prevention Program (DPP) y del Finnish Diabetes Prevention Study (FDPS) redujeron el riesgo de DBT un 58% en comparación con los consejos estándar sobre el estilo de vida. La modificación del peso corporal en los pacientes con intervención intensiva sobre el estilo de vida en el DPP fue paralela a los efectos sobre la incidencia de DBT2 y sobre los factores de riesgo CM asociados. En el FDPS, el riesgo de presentar DBT2 en sujetos que adoptaron estilos de vida más saludables (dietas bajas en grasas y altas en fibras), fue la mitad del riesgo observado en el subgrupo de sujetos que no lo hicieron. La pérdida de peso mediante el empleo de fármacos también reduce el riesgo de DBT2 y mejora el perfil de riesgo cardiovascular (CV) de pacientes obesos.Por tanto, los pacientes con sobrepeso o con obesidad presentan un riesgo de DBT2 sustancialmente superior, mientras que los que pierden peso presentan mayor probabilidad de evitar el impacto de la morbimortalidad temprana asociada con el diagnóstico de DBT y de SM. El término “diabesidad” se acuñó en la década del 80 para describir los estrechos lazos patogénicos entre obesidad y DBT2.
Fuentes de datos
Muchos estudios clínicos han evaluado los efectos de la MET sobre el peso, la glucemia y otros parámetros CM. La revisión que se comenta a continuación incluye diversos estudios de la MET obtenidos de la bibliografía con preferencia de metanálisis (MA) y estudios de larga duración. Este último tipo de estudios, como el DPP o el FDPS, demuestran una reducción inicial del peso seguido por una tendencia a la inversión del efecto durante la continuación del tratamiento.
Efectos de la MET sobre el peso corporal en pacientes con DBT2
Pacientes con control subóptimo con dieta
El efecto de la MET sobre el peso corporal en estudios aleatorizados y controlados en pacientes con control subóptimo con dieta fue variable. La mitad de estos estudios demostró una reducción significativa del peso corporal con MET en relación con el peso al inicio del tratamiento o en relación con otros agentes. La mayor duración correspondió al UK Prospective Diabetes Study. Los pacientes tratados con dieta aumentaron unos 2 kg, mientras que aquellos tratados con MET tuvieron un aumento de peso menor, de 1.5 kg y los tratados con glibenclamida (GLI) aumentaron 4 kg. El Diabetes Progression Outcomes Trial aleatorizó 4 360 pacientes no controlados mediante intervención sobre el estilo de vida, a MET, a GLI o a rosiglitazona (RSG), durante un período de 4 años. Los pacientes del grupo de MET perdieron peso respecto de los demás grupos, que aumentaron. El incremento de este parámetro con RSG fue significativo en comparación con los otros tratamientos. Otros estudios de 1 año de duración no demostraron pérdida de peso sustancial en los grupos tratados con MET frente a placebo, aunque se observaron diferencias significativas en comparación con TZD o con sulfonilureas (SFU). El estudio aleatorizado PRESERVE-Beta, de 2 años de duración, evaluó la terapia inicial de pacientes sin tratamiento previo con drogas, con una combinación de GLI o de nateglinida (NAT) con MET. Las modificaciones del peso fueron relativamente pequeñas (-0.4 kg para MET-NAT y +0.8 kg para MET-GLI). La reducción de la hemoglobina glicosilada luego de 2 años fue de 1.2% para MET-NAT y de 1.5% para MET-GLI. El empleo de MET en forma combinada permite lograr eficacia antihiperglucémica notoria, mientras limita el aumento de peso. La MET puede influenciar la distribución de la grasa corporal en pacientes con DBT2 no controlados con dieta. Un análisis post hoc de un estudio aleatorizado de 26 semanas de duración (nivel de evidencia A), mostró que la MET redujo significativamente la grasa visceral frente a placebo, mientras que esto no ocurrió con la RSG.
Pacientes con control subóptimo con monoterapia antidiabética oral
Dos estudios aleatorizados de 12 y de 7 meses de duración aportaron datos sobre el peso corporal en pacientes previamente tratados con GLI y asignados al azar a recibir MET, GLI o ambas. El peso fue significativamente menor en el grupo de MET, frente a los grupos de SFU, al final del estudio. En pacientes no controlados, con dosis submáximas de MET, el aumento de la dosis de esta droga o el agregado de un segundo agente son alternativas para restaurar el control glucémico. Dos estudios aleatorizados de 6 meses de duración evaluaron estas opciones en una amplia población de pacientes, con TZD como segundo agente. Se observaron modificaciones similares del peso en los grupos de MET-TZD (1.3 y 1.8 kg) y se verificó pérdida de peso similar en los grupos de terapia intensificada con MET (-0.9 y -1.8 kg). La presencia de MET en el esquema combinado puede haber mitigado el aumento de peso con TZD.
Metformina en combinación con insulina
La MET mejora la acción de la insulina, sobre todo a nivel hepático. La mayoría de los estudios que evaluaron la combinación de insulina más MET fueron de menos de 6 meses de duración. Sin embargo, como el aumento de peso es un evento inmediato luego del inicio de la insulina, los efectos a corto plazo de la MET sobre el peso pueden ser relevantes en el contexto del empleo concomitante de insulina. Varios de estos estudios demostraron reducciones significativas del peso en pacientes tratados con insulina y MET en comparación con insulina y placebo. El aumento de peso con insulina o con secretagogos deriva, en parte, de la mayor ganancia calórica por disminución de la glucosuria junto con retención hídrica y una respuesta anabólica a la insulina. Un estudio sugirió que la combinación insulina más MET se asoció con menor aumento de peso corregido por las modificaciones de la glucemia, que los esquemas con SFU o con TZD. El mecanismo por el cual la MET puede limitar el aumento de peso durante la terapia con insulina no es claro. La menor ingesta calórica puede ser más importante en este aspecto que las modificaciones del gasto energético; además, se ha observado que tanto la MET como la insulina modulan la secreción de leptina. Debe destacarse, sin embargo, que los principales beneficios del agregado de MET a la insulina probablemente deriven de la mejoría de la glucemia, del menor requerimiento de insulina secundario a la mejoría de la acción de la insulina y, en consecuencia, del menor riesgo de hipoglucemia. En pacientes tratados con insulina más MET se han observado reducciones ≥ 25% del requerimiento de la primera.
Metanálisis
De un MA de 11 estudios, publicado en 1995, con aleatorización de pacientes a MET o a SFU durante 6 a 52 semanas, 9 de estos estudios publicaron datos sobre modificación del peso. El tratamiento con SFU se asoció con aumento de peso en cada uno de estos análisis. En 7 de ellos se observó reducción del peso en el grupo de MET, mientras que en los 2 estudios restantes hubo aumento de peso. Todos los análisis, excepto uno, demostraron una reducción significativa del peso con MET frente a un incremento con SFU. En general, se observó una diferencia de tratamiento promedio de -4 kg para MET frente a SFU.Un MA más reciente confirmó estos resultados en términos de la reducción significativa del peso con MET frente a SFU.
Efectos de la MET sobre el peso corporal en pacientes no diabéticos
Sujetos obesos o con obesidad abdominal
Un estudio aleatorizado en 150 mujeres con IMC > 30 kg/m2 evaluó el efecto de la sibutramina, de la MET o del orlistat durante 6 meses. En todos los grupos disminuyó el peso, la circunferencia de la cintura y el IMC en forma significativa.Una revisión sistemática de estudios aleatorizados y controlados de MET (de hasta 1 año de duración) en poblaciones sin DBT o sin síndrome de ovarios poliquísticos (SOP) mostró pruebas insuficientes para considerar a la MET como terapia potencial para la pérdida de peso en pacientes con sobrepeso u obesidad.
Pacientes con intolerancia a la glucosa
El DPP incluyó pacientes con intolerancia a la glucosa y con glucemia en ayunas normal a elevada, y con IMC promedio de 34 kg/m2, y los aleatorizó a consejos estándar sobre el estilo de vida + MET o a placebo o a un programa intensivo de intervención sobre el estilo de vida. En todos los grupos disminuyó el peso, con un promedio de 0.1 kg con placebo, de 2.1 kg con MET y de 5.6 kg con intervención intensiva sobre el estilo de vida.
SOP
Una revisión sistemática y un MA de 13 estudios aleatorizados y controlados no encontraron un efecto global de la MET sobre el peso corporal.
Obesidad pediátrica
Un estudio reciente aleatorizado y cruzado, sobre 28 pacientes, mostró que el tratamiento con MET se asoció con mejoría significativa del peso, del IMC y de la circunferencia de la cintura frente a placebo.
MET y factores de riesgo CM asociados con la obesidad
La MET mejora la resistencia a la insulina, considerada por algunos investigadores un factor de riesgo CV independiente. El tratamiento con MET suele asociarse con la mejoría leve de los parámetros lipídicos, especialmente los triglicéridos y el colesterol asociado a lipoproteínas de baja densidad. En pacientes con DBT2 se ha asociado con mejoría de la función endotelial, así como en poblaciones no diabéticas con SM o con SOP.Varios mecanismos han sido propuestos para explicar los efectos cardioprotectores de la MET, incluidas las acciones vasculares, las acciones sobre las mitocondrias, sobre la homeostasis y sobre la formación de los productos finales de la glucosilación avanzada, entre otras.
Discusión
El tratamiento con MET se asoció con reducción del peso corporal en aproximadamente la mitad de los estudios en pacientes con DBT2 no tratados previamente con drogas. Los MA no apoyan un efecto reductor de peso sustancial de la MET en relación con placebo, tanto en pacientes diabéticos como no diabéticos. Sin embargo, destaca el autor, el efecto sobre la reducción del peso corporal que ejerce la MET parece mayor cuando se administra en forma concomitante con insulina o con SFU.
Conclusiones
Los efectos de la MET sobre el peso corporal varían entre las diferentes poblaciones de pacientes. Resulta claro, no obstante, que la MET no induce aumento de peso a diferencia de otros antidiabéticos orales, y puede ayudar a limitar el aumento de este parámetro asociado con terapias basadas en insulina o en SFU. La mejoría de la glucemia y los resultados CV observados con MET son independientes de las modificaciones del peso o de la adiposidad. Esto apoya las recomendaciones actuales sobre el empleo de MET como terapia farmacológica oral inicial en pacientes con DBT2, independientemente del peso. No hay pruebas convincentes sobre el empleo de MET para el control del peso corporal en poblaciones de pacientes no diabéticos, si bien pueden observarse beneficios en términos de reducción del riesgo de DBT en sujetos con intolerancia a la glucosa, o beneficios en cuanto a la reducción de síntomas asociados con la resistencia a la insulina en mujeres con SOP.
Fuente: Intramed
All-black penguin discovered
Lindo !!!
King Penguins are notorious for their prim, tuxedoed appearance -- but a recently discovered all-black penguin seems unafraid to defy convention. In what has been described as a "one in a zillion kind of mutation," biologists say that the animal has lost control of its pigmentation, an occurrence that is extremely rare. Other than the penguin's monochromatic outfit, the animal appears to be perfectly healthy -- and then some. "Look at the size of those legs," said one scientist, "It's an absolute monster."
The under-dressed penguin was photographed by Andrew Evans of National Geographic on the island of South Georgia near Antarctica. As the picture circulated, some biologists were taken aback -- including Dr. Allan Baker of the University of Toronto. His first response was disbelief:
Wow. That looks so bizarre I can't even believe it. Wow.
While multicolored birds will often show some variation, Dr. Baker explains that what makes this all-black King Penguin so rare is that the bird's melanin deposits have occurred where they are typically not present -- enough so that no light feathers even checker the bird's normally white chest.
Andrew Evans:
Melanism is merely the dark pigmentation of skin, fur -- or in this case, feathers. The unique trait derives from increased melanin in the body. Genes may play a role, but so might other factors. While melanism is common in many different animal species (e.g., Washington D.C. is famous for its melanistic squirrels), the trait is extremely rare in penguins. All-black penguins are so rare there is practically no research on the subject -- biologists guess that perhaps one in every quarter million of penguins shows evidence of at least partial melanism, whereas the penguin we saw appears to be almost entirely (if not entirely) melanistic.
Whether or not the all-black look catches on in the penguin fashion world, it's nice to see someone dressing-down for once.
The under-dressed penguin was photographed by Andrew Evans of National Geographic on the island of South Georgia near Antarctica. As the picture circulated, some biologists were taken aback -- including Dr. Allan Baker of the University of Toronto. His first response was disbelief:
Wow. That looks so bizarre I can't even believe it. Wow.
While multicolored birds will often show some variation, Dr. Baker explains that what makes this all-black King Penguin so rare is that the bird's melanin deposits have occurred where they are typically not present -- enough so that no light feathers even checker the bird's normally white chest.
Andrew Evans:
Melanism is merely the dark pigmentation of skin, fur -- or in this case, feathers. The unique trait derives from increased melanin in the body. Genes may play a role, but so might other factors. While melanism is common in many different animal species (e.g., Washington D.C. is famous for its melanistic squirrels), the trait is extremely rare in penguins. All-black penguins are so rare there is practically no research on the subject -- biologists guess that perhaps one in every quarter million of penguins shows evidence of at least partial melanism, whereas the penguin we saw appears to be almost entirely (if not entirely) melanistic.
Whether or not the all-black look catches on in the penguin fashion world, it's nice to see someone dressing-down for once.
La leptina podría sustituir el tratamiento con insulina en diabéticos
Una hormona de la grasa, la leptina, podría proporcionar un tratamiento equivalente a las inyecciones de insulina para los pacientes de diabetes tipo 1 pero sin sus efectos secundarios sobre el metabolismo de las grasas, según un estudio del Centro de Investigación de la Diabetes Touchstone en Dallas (Estados Unidos) que se publica en la revista Procedings of the National Academy of Sciences (PNAS).
Los científicos, dirigidos por Roger Unger, trataron a ratones diabéticos con leptina y consiguieron un control de la enfermedad mejor o equivalente en comparación con la insulina, además de reducir en los animales la grasa corporal, el colesterol y los factores de riesgo de enfermedad arterial coronaria.
Los investigadores descubrieron que los ratones diabéticos no obesos tratados con leptina o insulina demostraron niveles similares de azúcar en sangre y de recuperación de la enfermedad. Sin embargo, los ratones tratados sólo con leptina, o en combinación con la insulina, mostraban una menor fluctuación del azúcar en sangre, la formación de grasa corporal y los niveles de colesterol en comparación con los animales tratados sólo con insulina.Desde su descubrimiento en 1922, la inyección de insulina ha sido el principal tratamiento para los pacientes diabéticos. Sin embargo, demasiada insulina podría aumentar el riesgo de una persona de niveles elevados de colesterol y grasas y, potencialmente, enfermedad arterial.
Los autores sugieren que la leptina podría proporcionar un tratamiento alternativo para la diabetes que podría ayudar a superar algunos de los efectos secundarios negativos de la insulina causados por la inherente complejidad de la regulación de la dosis de insulina en todos los tejidos del organismo.
Fuente: intramed
sábado, 6 de marzo de 2010
EVIDENCE BASED RECOMMENDATIONS FOR THE DIAGNOSIS OF KNEE OSTEOARTHRITIS
Objectives: To develop evidence based recommendations for the diagnosis of knee osteoarthritis (OA).
Methods: The multidisciplinary guideline development group, representing 12 European countries, generated 10 key propositions regarding diagnosis using a Delphi consensus approach. For each recommendation research evidence was searched systematically. Whenever possible, the sensitivity, specificity and likelihood ratio were calculated for individual diagnostic indicators and a diagnostic ladder was developed using Bayes' method. Secondary analyses were undertaken to directly test the recommendations using multiple predictive models in two populations from the UK and the Netherlands. Strength of recommendation was assessed by the EULAR visual analogue scale.
Results: Recommendations covered the definition of knee OA and its risk factors, subsets, typical symptoms and signs, the use of imaging and laboratory tests, and differential diagnosis. Three symptoms (persistent knee pain, limited morning stiffness and reduced function) and three signs (crepitus, restricted movement and bony enlargement) appeared to be the most useful. Assuming a 12.5% background prevalence of knee OA in adults aged 45 years and older, the estimated probability of having radiographic knee OA increased with increasing number of positive features, to 99% when all 6 symptoms and signs were present. The performance of the recommendations in the study populations varied according to the definition of knee OA, background risk and number of tests applied.
Conclusion: 10 key recommendations for diagnosis of knee OA were developed using both research evidence and expert consensus. Although there is no agreed reference standard, thorough clinical assessment alone can provide a confident rule-in diagnosis.
2009 BMJ Publishing Group Ltd & European League Against Rheumatism. All rights reserved.
ACE Inhibitors, ARBs, and Beta Blockers Reduce Risk of AF
January 25, 2010 — Hypertensive patients receiving long-term monotherapy with ACE inhibitors, angiotensin-receptor blockers (ARBs), or beta blockers were less likely to develop atrial fibrillation (AF) than those who received only calcium-channel blockers (CCBs), a new study has found [1]. Dr Beat A Schaer (University Hospital, Basel, Switzerland) and colleagues report their study in the January 18, 2010 issue of the Annals of Internal Medicine.
"The most likely explanation for this finding is that ACE inhibitors, ARBs, and beta blockers reduce the risk of AF rather than that CCBs increase the risk," senior author of the paper, Dr Christoph R Meier (University Hospital, Basel, Switzerland), told heartwire .
But Meier says the "practical implications" of these findings are few, because "we studied a sample, a subset of patients on monotherapy, and therefore one cannot generalize to a more complicated hypertensive population." Nevertheless, he says, "If a patient is believed to be at risk for AF, this may be good to know for the doctor, that certain drugs might have a beneficial effect [on AF]. It could be yet another criterion to look at when selecting an antihypertensive drug, just one more piece of the puzzle."
"The most likely explanation for this finding is that ACE inhibitors, ARBs, and beta blockers reduce the risk of AF rather than that CCBs increase the risk," senior author of the paper, Dr Christoph R Meier (University Hospital, Basel, Switzerland), told heartwire .
But Meier says the "practical implications" of these findings are few, because "we studied a sample, a subset of patients on monotherapy, and therefore one cannot generalize to a more complicated hypertensive population." Nevertheless, he says, "If a patient is believed to be at risk for AF, this may be good to know for the doctor, that certain drugs might have a beneficial effect [on AF]. It could be yet another criterion to look at when selecting an antihypertensive drug, just one more piece of the puzzle."
Clinical Implications
All-cause congestive heart failure, mitral regurgitation, and hypertension have been identified as major predisposing factors for AF.
In patients with hypertension, long-term receipt of ACE inhibitors, ARBs, or beta-blockers reduces the risk for AF vs receipt of CCBs.
All-cause congestive heart failure, mitral regurgitation, and hypertension have been identified as major predisposing factors for AF.
In patients with hypertension, long-term receipt of ACE inhibitors, ARBs, or beta-blockers reduces the risk for AF vs receipt of CCBs.
Para el artìculo completo: http://cme.medscape.com/viewarticle/715742
Chlorhexidine-alcohol superior to povidone-iodine for surgical prep
Clorhexidina de alcohol superior a la povidona yodada para cirugía prepThese investigadores de EE.UU. asignados aleatoriamente adultos sometidos a cirugía limpia-contaminada, en seis hospitales de la preparación preoperatoria de la piel con clorhexidina o alcohol o matorrales matorrales povidona yodada y la pintura. El resultado primario fue cualquier infección del sitio quirúrgico en los 30 días después de la cirugía. Los resultados secundarios incluyeron los distintos tipos de infections.They quirúrgica sitio encontrado: "Un total de 849 sujetos (409 en el grupo de clorhexidina alcohol y 440 en el grupo de povidona yodada) calificado para el propósito de tratar de análisis. La tasa global de infección de sitio quirúrgico fue significativamente menor en el grupo de clorhexidina alcohol que en el grupo de la povidona yodada (9,5% frente a 16,1, el riesgo relativo, 0,59). De clorhexidina alcohol fue significativamente mayor protección que la povidona yodada contra ambas infecciones superficiales en la incisión (4,2% vs 8,6) y de infecciones profundas de la incisión (1% frente al 3%), pero no contra infecciones de órganos espacio (4,4% vs 4,5%), . Resultados similares fueron observados en el análisis por protocolo de los 813 pacientes que permanecieron en el estudio durante los 30 días de periodo de seguimiento. Los eventos adversos fueron similares en ambos grupos de estudio. "Los autores concluyeron:" limpieza preoperatoria de la piel del paciente con clorhexidina alcohol es superior a la limpieza con povidona yodada para la prevención de la infección del sitio quirúrgico después de la cirugía limpia-contaminada.
Uso de la clorhexidina alcohol de preparación del sitio quirúrgico debe ser la norma procedimiento.
Uso de la clorhexidina alcohol de preparación del sitio quirúrgico debe ser la norma procedimiento.
miércoles, 3 de marzo de 2010
Cuánto debiera exponerse a la luz solar para evitar el déficit de VITAMINA D ?
Lo recomendado para prevenir déficit de Vit D una exposición a nivel de brazos y piernas por unos 5 a 30 min suficiente dos veces x semana , de preferencia entre las 10 AM a 3 PM. Esto podría variar según el tipo de piel y altitud a la que se vive.
Fuente:
http://www.jabfm.org/cgi/content/full/22/6/698?maxtoshow=&hits=10&RESULTFORMAT=&author1=Kulie&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT
Fuente:
http://www.jabfm.org/cgi/content/full/22/6/698?maxtoshow=&hits=10&RESULTFORMAT=&author1=Kulie&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT
Contaminación pro-cancerígena en las cápsulas de omega 3 !!!!
Verdaderamente me hace preocuparme muchísimo!!! Se los comparto ... (Pueden ver el vídeo en ABC news)
Un grupo ambientalista presentó una demanda en San Francisco el martes
alegando que 10 tipos de aceite de pescado o suplementos de aceite de tiburón contiene una
compuestos industriales tóxicos, y que los fabricantes y los vendedores necesitan para advertir a
los consumidores.
La demanda, presentada en San Francisco, el Tribunal Superior por el grupo de Oregon
Mateel Environmental Justice Foundation y dos personas, afirma que
bajo la Proposición 65 de California, los fabricantes y vendedores de aceite de pescado,
los suplementos están obligados a decir a los consumidores que las píldoras que contienen las
bifenilos policlorados, compuestos, o PCB.
El aceite de pescado se ha convertido en un complemento cada vez más popular porque tiene un alto
los niveles de ácidos grasos omega-3 saludables ácidos grasos y vitamina D.
Más de 100 marcas de aceite de pescado están disponibles. Los demandantes en el
juicio a prueba 10 productos, todos los cuales tenían una cierta cantidad de PCB, dicen.
Ellos encontraron amplios rangos en los niveles de PCB, sino porque los científicos no han
de acuerdo en un nivel seguro de consumo, los consumidores deben ser conscientes de
compuestos potencialmente tóxicos en sus suplementos, no importa lo que la
cantidad, dijo David Roe, abogado de los demandantes.
"La gente compra el aceite de pescado para mejorar su salud", dijo Roe el martes en un
teleconferencia con los reporteros. "No tenemos forma de saber si todos los
otros productos de aceite de pescado han PCB, también. "
La demanda nombra a CVS / Pharmacy, General Nutrition Corporation (tiendas GNC), ya!
Health Group, Omega Protein, Rite Aid, Solgar, Twinlab y Pharmavite,
que produce la naturaleza suplementos hechos, como los acusados.
Representante de las empresas dijeron que no haría comentarios, ya que
no había visto la demanda.
Los PCB, una vez se usa para aislar los transformadores y condensadores, pero se
prohibido más de 30 años. Todavía se encuentran en Bahía de San Francisco
y otras vías navegables, donde son consumidos por peces.
La mayoría de la gente no come pescado suficiente para la exposición de riesgo grave para los PCB, Roe
, dijo, sino porque la gente en general, tomar suplementos de aceite de pescado todos los días,
que potencialmente puede consumir niveles nocivos de la sustancia química.
Los PCB pueden causar cáncer, problemas reproductivos y daños al sistema nervioso
del sistema, los científicos del medio ambiente han dicho.
Una lista de los productos mencionados en la demanda de PCB. C4
El aceite de pescado
Los productos mencionados en la demanda PCB son:
- GNC líquido de aceite de hígado de bacalao de Noruega
- Nature Made aceite de hígado de bacalao
- Nature Made aceite de pescado sin olor
- Alimentos Ahora Doble Fuerza aceite de hígado de bacalao
- Ahora los alimentos el aceite de salmón
- Ahora Alimentos Aceite de hígado de tiburón
- Solgar 100 por ciento puro de Noruega Aceite de hígado de tiburón Complejo
- Solgar Aceite de hígado de bacalao de Noruega
- Twinlab emulsionadas de aceite de hígado de bacalao de Noruega
- Twinlab Aceite de hígado de bacalao de Noruega
Original:
http://www.sfgate.com/cgi-bin/article.cgi?file=/c/a/2010/03/03/BARO1C9RD3.DTL
Un grupo ambientalista presentó una demanda en San Francisco el martes
alegando que 10 tipos de aceite de pescado o suplementos de aceite de tiburón contiene una
compuestos industriales tóxicos, y que los fabricantes y los vendedores necesitan para advertir a
los consumidores.
La demanda, presentada en San Francisco, el Tribunal Superior por el grupo de Oregon
Mateel Environmental Justice Foundation y dos personas, afirma que
bajo la Proposición 65 de California, los fabricantes y vendedores de aceite de pescado,
los suplementos están obligados a decir a los consumidores que las píldoras que contienen las
bifenilos policlorados, compuestos, o PCB.
El aceite de pescado se ha convertido en un complemento cada vez más popular porque tiene un alto
los niveles de ácidos grasos omega-3 saludables ácidos grasos y vitamina D.
Más de 100 marcas de aceite de pescado están disponibles. Los demandantes en el
juicio a prueba 10 productos, todos los cuales tenían una cierta cantidad de PCB, dicen.
Ellos encontraron amplios rangos en los niveles de PCB, sino porque los científicos no han
de acuerdo en un nivel seguro de consumo, los consumidores deben ser conscientes de
compuestos potencialmente tóxicos en sus suplementos, no importa lo que la
cantidad, dijo David Roe, abogado de los demandantes.
"La gente compra el aceite de pescado para mejorar su salud", dijo Roe el martes en un
teleconferencia con los reporteros. "No tenemos forma de saber si todos los
otros productos de aceite de pescado han PCB, también. "
La demanda nombra a CVS / Pharmacy, General Nutrition Corporation (tiendas GNC), ya!
Health Group, Omega Protein, Rite Aid, Solgar, Twinlab y Pharmavite,
que produce la naturaleza suplementos hechos, como los acusados.
Representante de las empresas dijeron que no haría comentarios, ya que
no había visto la demanda.
Los PCB, una vez se usa para aislar los transformadores y condensadores, pero se
prohibido más de 30 años. Todavía se encuentran en Bahía de San Francisco
y otras vías navegables, donde son consumidos por peces.
La mayoría de la gente no come pescado suficiente para la exposición de riesgo grave para los PCB, Roe
, dijo, sino porque la gente en general, tomar suplementos de aceite de pescado todos los días,
que potencialmente puede consumir niveles nocivos de la sustancia química.
Los PCB pueden causar cáncer, problemas reproductivos y daños al sistema nervioso
del sistema, los científicos del medio ambiente han dicho.
Una lista de los productos mencionados en la demanda de PCB. C4
El aceite de pescado
Los productos mencionados en la demanda PCB son:
- GNC líquido de aceite de hígado de bacalao de Noruega
- Nature Made aceite de hígado de bacalao
- Nature Made aceite de pescado sin olor
- Alimentos Ahora Doble Fuerza aceite de hígado de bacalao
- Ahora los alimentos el aceite de salmón
- Ahora Alimentos Aceite de hígado de tiburón
- Solgar 100 por ciento puro de Noruega Aceite de hígado de tiburón Complejo
- Solgar Aceite de hígado de bacalao de Noruega
- Twinlab emulsionadas de aceite de hígado de bacalao de Noruega
- Twinlab Aceite de hígado de bacalao de Noruega
Original:
http://www.sfgate.com/cgi-bin/article.cgi?file=/c/a/2010/03/03/BARO1C9RD3.DTL
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