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| Vascular Example 8: Pharmaceuticals: Fenofibrate |
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| fibrates | |||
| fenofibrate & fibrates | |||
| Abstract Title | Lead Author | Publication | Pub Date |
| The effects of fenofibrate treatment on cardiovascular disease risk in 9795 people with type 2 diabetes and various components of the metabolic syndrome: the FIELD study. | Scott R | Diabetes Care. | 2008-11-04 |
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| Abbott Labs & fenofibrate | |||
| TriCor Triglide / fenofibrate & Abbott | |||
| Oscient Pharmaceuticals & fenofibrate | |||
| Antara / fenofibrate & Oscient | |||
| Abstract Title | Lead Author | Publication | Pub Date |
| Oscient Pharmaceuticals Reports Third Quarter 2008 Financial Results | [none given] | Business Wire | 2008-11-04 |
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| ProEthic Pharmaceuticals & fenofibrate | |||
| Lipofen / fenofibrate & ProEthic | |||
| Solvay Pharmaceutical & fenofibrate | |||
| Abstract Title | Lead Author | Publication | Pub Date |
| Delaying diabetic retinopathy | [none given] | PR Newswire | 2008-10-30 |
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| Lipanthyl / fenofibrate & Solvay | |||
| Teva Pharmaceuticals & fenofibrate | |||
| Lofibra / fenofibrate & Teva | |||
| fenofibrate, AB-rated generic & Teva | |||
| ApoA-1 Milano | |||
| Pfizer / Esperion & ApoA-1 | |||
| ETC-216 & Pfizer | |||
| Limone sul Garda & ApoA-1 | |||
| Ezetimibe | |||
| Merck & Co./Schering-Plough Pharmaceuticals & Ezetimibe | |||
| Ezetrol & Merck & Co. | |||
| Zetia & Merck & Co. | |||
| Ezemibe & Merck & Co. | |||
| Ezetimibe/simvastatin | |||
| Merck & Co./Schering-Plough Pharmaceuticals & Ezet./simvastatin | |||
| Vytorin & Merck & Co. | |||
| Abstract Title | Lead Author | Publication | Pub Date |
| Feds, States Probe Vytorin Marketing | Sarah Rubenstein | Wall Street Journal | 2008-11-04 |
| Expert Panel Recommends Doctors Abandon Vytorin Cholesterol Drug | David Gutierrez | Natural News | 2008-11-04 |
| Return to ToC | |||
| Inegy & Merck & Co. | |||
| Orlistat / tetrahydrolipstatin | |||
| Hoffmann La Roche & Orlistat | |||
| Xenical & Hoffmann | |||
| Abstract Title | Lead Author | Publication | Pub Date |
| Risks outweigh the benefits | [none given] | Pharma Weekly | 2008-11-04 |
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| GlaxoSmithKline & Orlistat | |||
| alli & Glaxo | |||
| Cardiovascular disease | |||
| apolipoprotein A1 & Cardio disease | |||
| Abstract Title | Lead Author | Publication | Pub Date |
| Apolipoproteins, cardiovascular risk and statin response in type 2 diabetes: the Collaborative Atorvastatin Diabetes Study (CARDS). | Charlton-Menys V | Diabetologia. | 2008-10-30 |
| Low-density lipoprotein (LDL), which includes apolipoprotein A-I (apoAI-LDL) as a novel marker of coronary artery disease. | Ogasawara K | Clin Chim Acta. | 2008-11-01 |
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| Cholesterol & Cardio disease | |||
| above 150 & Cholesterol | |||
| below 150 & Cholesterol | |||
| combination therapy & Cardio disease | |||
| Abstract Title | Lead Author | Publication | Pub Date |
| LDL reduction: how low should we go and is it safe? | Robinson JG. | Curr Cardiol Rep. | 2008-11-01 |
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| ezetimibe & Cardio disease | |||
| Abstract Title | Lead Author | Publication | Pub Date |
| Ezetimibe and Other Statins Achieve Established Low-Density Lipoprotein Targets in Coronary Artery Disease: Presented at CCC | Marvin Ross | PR Newswire | 2008-10-29 |
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| fibrates & Cardio disease | |||
| Abstract Title | Lead Author | Publication | Pub Date |
| Ezetimibe and Other Statins Achieve Established Low-Density Lipoprotein Targets in Coronary Artery Disease: Presented at CCC | Marvin Ross | PR Newswire | 2008-10-29 |
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| Hypolipidemic or antihyperlipidemic agents & Cardio disease | |||
| HDL & Cardio disease | |||
| LDL & Cardio disease | |||
| Abstract Title | Lead Author | Publication | Pub Date |
| Low-density lipoprotein (LDL), which includes apolipoprotein A-I (apoAI-LDL) as a novel marker of coronary artery disease. | Ogasawara K | Clin Chim Acta. | 2008-11-01 |
| LDL reduction: how low should we go and is it safe? | Robinson JG. | Curr Cardiol Rep. | 2008-11-01 |
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| mevalonate & Cardio disease | |||
| micelles & Cardio disease | |||
| niacin & Cardio disease | |||
| Abstract Title | Lead Author | Publication | Pub Date |
| Ezetimibe and Other Statins Achieve Established Low-Density Lipoprotein Targets in Coronary Artery Disease: Presented at CCC | Marvin Ross | PR Newswire | 2008-10-29 |
| Return to ToC | |||
| phytosterols & Cardio disease | |||
| triglycerides & Cardio disease | |||
| fibrates | |
| fenofibrate & fibrates | |
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The effects of fenofibrate treatment on cardiovascular disease risk in 9795 people with type 2 diabetes and various components of the metabolic syndrome: the FIELD study. Lead Author: Scott R Additional Authors: O'Brien R, Fulcher G, Pardy C, d'Emden M, Tse D, Taskinen MR, Ehnholm C, Keech A; on behalf of the FIELD Study Investigators. Diabetes Care. , 2008-11-04, [Epub ahead of print] Lipid & Diabetes Research Group, Christchurch Hospital, Christchurch, New Zealand Objective: We explored whether cardiovascular disease (CVD) risk and the effects of fenofibrate differed in subjects with and without metabolic syndrome (MS) and according to various features of MS defined by ATP III in subjects with type 2 diabetes in the FIELD study. Research design and methods: The prevalence of MS and its features were calculated. Cox proportional models adjusted for age, gender, CVD status and baseline HbA1c levels were used to determine the independent contributions of MS features to total CVD event rates and the effects of fenofibrate. Results: Over 80% of FIELD participants met the ATPIII criteria for MS. Each ATPIII feature of MS, apart from increased waist circumference, increased the absolute risk of CVD events over 5 years by at least 3%. Those with marked dyslipidemia (elevated triglycerides >/=2.3 mmol/L and low HDLc) were at the highest risk of CVD (17.8% over 5 years). Fenofibrate significantly reduced CVD events in those with low HDLc or hypertension. The largest effect of fenofibrate to reduce CVD risk was observed in subjects with marked dyslipidaemia where a 27% relative risk reduction (95%CI 9-42, p=0.005; number needed to treat [NNT]=23) was observed. Subjects with no prior CVD had greater risk reductions than the entire group. Conclusions: MS components identify higher CVD risk in people with type 2 diabetes, so the absolute benefits of fenofibrate is likely to be greater when MS features are present. The highest risk and greatest benefits of fenofibrate are seen among those with marked hypertriglyceridemia. MIB Abstract ID Number: 16139 PreMedline Identifier: 18984774 *To access this PubMed use the PreMedline Identifier in the PubMed search field |
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| Abbott Labs & fenofibrate | |
| TriCor Triglide / fenofibrate & Abbott | |
| Oscient Pharmaceuticals & fenofibrate | |
| Antara / fenofibrate & Oscient | |
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Oscient Pharmaceuticals Reports Third Quarter 2008 Financial Results Lead Author: [none given] Business Wire, 2008-11-04 Oscient Pharmaceuticals Corporation (OSCI: 0.78, +0.11, +16.5%) today reported financial results for the third quarter ended September 30, 2008. Total revenues for the third quarter of 2008 were $21.8 million, compared to $15.6 million in the third quarter of 2007. Revenue from the cardiovascular drug ANTARA(R) (fenofibrate) capsules increased 41% to $18.1 million in the third quarter of 2008, from $12.8 million in the third quarter of 2007. Revenues from the antibiotic FACTIVE(R) (gemifloxacin mesylate) tablets totaled $3.7 million in the third quarter of 2008, compared to $2.8 million in the third quarter of 2007.
"Our sales effort on ANTARA continues to yield strong growth, particularly in light of the challenging economic climate," stated Steven M. Rauscher, President and CEO. "As we enter into the fourth quarter, our team remains focused on recalibrating our balance sheet through a convertible debt exchange transaction, securing additional products for our sales force and growing revenues for both ANTARA and FACTIVE."
For the third quarter ended September 30, 2008, the Company reported a net loss of ($15,027,000), or ($1.09) per basic and diluted share. For the third quarter ended September 30, 2007, the Company reported a net loss of ($19,497,000), or ($1.43) per basic and diluted share. During the quarter ended September 30, 2008, the Company's cash position decreased by approximately $2.8 million to approximately $29.0 million in total cash, cash equivalents and restricted cash.
Selling and marketing expenses were $18.3 million in the third quarter of 2008, compared to $17.6 million in the third quarter of 2007. General and administrative expenses for the third quarter of 2008 totaled $2.9 million, compared to $3.4 million in the third quarter of 2007. Third quarter 2008 results included $6.2 million in non-cash charges, compared to $6.6 million in the third quarter of 2007. Non-cash charges in the third quarter of 2008 included $3.6 million recorded as interest expense, $2.3 million related to the amortization of intangible assets and $0.3 million of stock-based compensation. Non-cash charges in the third quarter of 2007 included $3.6 million recorded as interest expense, $2.3 million related to the amortization of intangible assets and $0.7 million of stock-based compensation.
For the nine months ended September 30, 2008, the Company reported total revenues of $60.4 million, reflecting ANTARA revenues of $49.1 million and FACTIVE revenues of $11.3 million. This compares to total revenues of $54.7 million in the first nine months of 2007, including ANTARA revenues of $39.2 million and FACTIVE revenues of $15.5 million. The Company reported a net loss of ($53,229,000), or ($3.86) per basic and diluted share, for the first nine months of 2008. The Company reported a net loss of ($15,182,000), or ($1.12) per basic and diluted share, for the first nine months of 2007. Exclusive of the one-time, non-cash gain related to the convertible debt exchange completed during the first half of 2007, the Company's pro forma net loss for the first nine months of 2007 was ($46,006,000), or ($3.38) per basic and diluted share.
MIB Abstract ID Number: 16119 *To access this Lexis-Nexis article the user must create an account. |
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| ProEthic Pharmaceuticals & fenofibrate | |
| Lipofen / fenofibrate & ProEthic | |
| Solvay Pharmaceutical & fenofibrate | |
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Lead Author: [none given] PR Newswire, 2008-10-30 The results of the FIELD (Fenofibrate Intervention and Event Lowering in Diabetes) study confirmed fenofibrate’s protective effect on the eyes of patients with diabetes as unique compared to other lipid-modifying agents, including statins. This made fenofibrate as the first lipid-modifying agent to demonstrate protection against diabetic retinopathy and was independent from blood glucose and blood pressure control. The FIELD study offered hope to patients with diabetes as the sub-analysis and the sub-study concluded that fenofibrate, a lipid-modifying agent, slowed down the progression of diabetic retinopathy in patients with type 2 diabetes and diminished the need for laser coagulation therapy. FIELD, a multinational, randomized study, was conducted to evaluate whether the treatment with fenofibrate for a median of five years could reduce the macrovascular and microvascular complications. The detailed results of the study were published in the November 2007 issue of the Lancet journal. Diabetic retinopathy, a condition on which the retina (inner surface of the back of the eye) is progressively damaged, has affected approximately 50 million of 200 million people with diabetes worldwide. This grim situation has burdened patients with diabetes as it caused 80 percent of vision loss. Diabetic retinopathy is commonly treated using laser coagulation therapy or laser treatment. An outpatient procedure performed by using anesthetic eye drops, laser treatment aims to control the leakage of blood and fluid in the retina, as well as the growth of new blood vessels, in an attempt to delay the progression of diabetic retinopathy, as with vision loss. The FIELD study is one of the many breakthrough undertakings of Solvay Pharma. MIB Abstract ID Number: 16120 *To access this Lexis-Nexis article the user must create an account. |
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| Lipanthyl / fenofibrate & Solvay | |
| Teva Pharmaceuticals & fenofibrate | |
| Lofibra / fenofibrate & Teva | |
| fenofibrate, AB-rated generic & Teva | |
| ApoA-1 Milano | |
| Pfizer / Esperion & ApoA-1 | |
| ETC-216 & Pfizer | |
| Limone sul Garda & ApoA-1 | |
| Ezetimibe | |
| Merck & Co./Schering-Plough Pharmaceuticals & Ezetimibe | |
| Ezetrol & Merck & Co. | |
| Zetia & Merck & Co. | |
| Ezemibe & Merck & Co. | |
| Ezetimibe/simvastatin | |
| Merck & Co./Schering-Plough Pharmaceuticals & Ezet./simvastatin | |
| Vytorin & Merck & Co. | |
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Feds, States Probe Vytorin Marketing Lead Author: Sarah Rubenstein Wall Street Journal, 2008-11-04 The latest in the never-ending Vytorin saga: The Department of Justice and attorneys general from 35 states are investigating whether Merck and Schering-Plough improperly promoted the cholesterol drug. Merck said the DOJ is investigating whether the companies’ Vytorin promotion caused false claims to be submitted to federal health care programs. What’s that mean? The False Claims Act (and state versions of it) has become a popular legal tool that public officials use against drug makers, saying for instance that their alleged improper marketing of drugs causes government programs such as Medicare or Medicaid to pay for the drugs under false pretenses. An example: Last year New York AG Andrew Cuomo brought a civil lawsuit against Merck for allegedly violating New York’s False Claims Act vis a vis past marketing of its withdrawn painkiller Vioxx. Merck’s filing also says the company has received five “civil investigative demands” from a multistate group of 35 state AGs who are jointly investigating whether Merck and Schering-Plough violated state consumer protection laws when marketing Vytorin. Merck said it’s cooperating with the latest investigations and is working with Schering-Plough to respond to the inquiries. Merck spokeswoman Amy Rose added that the company takes “the matter very seriously.” Schering-Plough spokeswoman Rosemarie Yancosek said the company is also “cooperating with these investigations and working with Merck to respond to the inquiries.” The companies’ to-do lists already include a bunch of other inquiries on the Vytorin front. And Merck said that it’s aware of about 140 civil class action lawsuits related to the companies’ promotion of Vytorin and its sister drug, Zetia. MIB Abstract ID Number: 16126 Factiva Identifier: WSJ000020081104uo556024fge * To access this Factiva article the user must create an account. |
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Expert Panel Recommends Doctors Abandon Vytorin Cholesterol Drug Lead Author: David Gutierrez Natural News, 2008-11-04 An expert panel from the American College of Cardiology has recommended that doctors stop prescribing the cholesterol-lowering drugs Zetia and Vytorin and stick with the older, proven class of cholesterol drugs known as statins. Vytorin is a combination of the statin Zocor (generic name simvastatin) and the newer cholesterol drug Zetia (generic name ezetimibe). Because Zetia reduces LDL ("bad") cholesterol by a different mechanism than statins do, doctors enthusiastically embraced the combination Vytorin drug as a way to bring LDL levels much lower than would be possible with Zocor alone. Together, Zetia and Vytorin have pulled in $5 billion per year for manufacturers Merck and Schering-Plough. Zetia lowers LDL levels by hampering the intestine's ability to absorb dietary cholesterol, while statins accelerate the filtering out of LDL cholesterol from the blood. Krumholz said that because the effects of statins are well-known, doctors should stick to those drugs instead of the unproven Zetia and Vytorin. "We know statins are good drugs and we know they reduce risks. We believe in general to get to a $5 billion-a-year drug, there was a lot of premature use of ezetimibe before the statin option had been exhausted," he said. In contrast to statins, the risks of Zetia and Vytorin are not well-studied or well-known, Krumholz emphasized. "We do not know. This is a new drug with a novel mechanism - first in class. We do not have outcomes studies," he said No large-scale studies have ever been conducted into the safety of Zetia and Vytorin, in particular whether they raise the risk of heart attacks and strokes. The first such study is due to be completed in 2012. The Enhance study and the panel's recommendations should have wider ramifications in the way that doctors approach heart health and new drugs, the panelists said. The panelists noted that many doctors assumed that just because Zetia and Vytorin lowered LDL cholesterol, they must be improving heart health. But this assumption appears to have been faulty, as the mechanism by which cholesterol is lowered may be just as significant as the size of the cholesterol decrease. "Drugs are complex compounds with an array of biological effects. Knowing how they affect lipids does not tell us how they affect people," Krumholz said. Enhance "reminds us to look at the trial endpoint and how (drugs) affect patients and not to just look at the numbers," panelist Rick Nishimura of the Mayo Clinic agreed. Following the panel's recommendations, shares of Merck fell 15 percent, while shares of Schering-Plough dropped 26 percent. The two companies had previously been accused of intentionally delaying the release of the Enhance results in order to preserve their profits, and of concealing evidence that Zetia may lead to liver damage. MIB Abstract ID Number: 16127 *To access this Lexis-Nexis article the user must create an account. |
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| Inegy & Merck & Co. | |
| Orlistat / tetrahydrolipstatin | |
| Hoffmann La Roche & Orlistat | |
| Xenical & Hoffmann | |
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Lead Author: [none given] Pharma Weekly, 2008-11-04 OBESE PATIENTS in the Republic have lost a potentially useful weapon in the fight against the condition. That's the response of consultant endocrinologist Dr Donal O'Shea to the news that the anti-obesity drug Acomplia - used by about 3,000 people in Ireland - was being temporarily taken off the European market by manufacturer Sanofi-aventis because of a risk of psychiatric side effects. "I was disappointed when Acomplia was withdrawn because it was a new class of anti-obesity medication," says O'Shea, who directs the State's largest public weight management clinic at St Columcille's Hospital in Loughlinstown. Unlike other anti-obesity medications on the market, Acomplia targets "cannabinoid" (CB1) receptors in the brain that are involved in regulating food intake. By blocking the receptors, the drug can help patients lose weight, but possible side effects include depression, aggression and anxiety. It has been on the Irish market since 2006. "In the first few months that [Acomplia] was out we had certainly seen a lot of psychiatric issues, but people fairly rapidly stopped using it if there was any hint of a problem. And we avidly warned patients if they got moody to stop taking it," says O'Shea, who is an associate professor of medicine at University College Dublin. About 47 suspected adverse drug reactions to Acomplia have been recorded in Ireland since 2006. However, when combined with positive changes in diet and exercise levels, some obese patients did very well on the drug, notes O'Shea. "We have seen patients who have gone down 20-25 kilos on Acomplia when they had been struggling along with great difficulty before that. It's also particularly good in people with diabetes where weight is an issue, it's helpful. And it's a pity to lose that weapon, even it is for a select group." Patients on Acomplia will no longer have prescriptions filled in Ireland, but they should have no concerns about stopping the drug cold, says O'Shea. "For a weight-reducing tablet there won't be anything rapid or sudden if they stop it," he explains. "But if it has been particularly helpful for them, they will have to fight extra hard to keep the weight they have lost off." On a wider scale O'Shea believes the suspension of Acomplia sales will stop other drug companies from developing CB1-blockers for use in tackling obesity. "It has sunk a new class of drug," he says. "Up until last month we had three agents that had been properly trialled over prospective two-year studies and beyond, and it looked like obesity was getting a proper spectrum of therapies. This is a setback to that." And he reckons it could have been avoided. "One of the things that's disappointing about Acomplia is that if the company had been more limited in the initial licence and excluded people with a history of depression then I think we would still have it," he says. "The problem is that it takes so much money to develop a drug now that companies need to target the biggest possible market, and excluding depression for a drug for obesity would take out a lot of your potential patients." But while O'Shea believes that anti-obesity medication combined with lifestyle change can substantially help suitable patients who are overweight or early obese, not everyone is disappointed to see Acomplia go. "In general for me are a last ditch option and I would discourage them greatly in the practice when people come in looking for them," says Louth-based GP Dr Harry Barry, author of Flagging the problem: a new approach to mental health. He prefers instead to target the psychological issues that may lie at the root of overeating. "I ask all patients who are overweight - what they are eating, when they are eating and why they are eating. And I would spend most of my time on the third,'' he explains. "My big problem with using these drugs is that it's like the quick fix -'I am not prepared to really take on the big issues in my life like why am I eating so much to start with, what's the pattern in my house. And if I don't really deal with that then I am not going to move on.' And in my experience, most of the people who use these kinds of drugs a lot of the time will lose a certain amount of weight, eventually they will come off them and then within six months they will be back to where they were. Tonight in an Irish Times/RDS Ireland in 2030 lecture in association with the Institute of Biology of Ireland, Prof Niall Moyna of DCU and Prof Donal OShea of UCD will jointly present a talk at 7pm at the RDS Merrion Room entitled Obesity- Treating the Epidemic, Preventing the Pandemic. For free admission tel: 01-2407289 or e-mail science@rds.ie 'Patients taking Acomplia should stop treatment and visit their GP' Last month three anti-obesity medications were available on prescription in Ireland. Now there are two. The newest of the drugs, Acomplia, was introduced in 2006. It blocks a type of receptor in the brain involved in hunger signals and so helps to suppress appetite. However, the medication also has the potential for side effects including depression, anxiety and aggression. As new data came to light, the European Medicines Agency (EMEA) added extra warnings, but finally decided last month that the benefits of Acomplia in helping patients lose weight and improve blood sugar control no longer outweighed the potential risks. In international studies involving about 36,000 patients, five suicides were reported among patients taking the drug, compared with one reported suicide on a placebo regime, according to the EMEA. "As a precautionary measure to protect patient health, this product will no longer be available," said Dr Joan Gilvarry, director of human medicines at the Irish Medicines Board, in a statement. "Patients currently taking Acomplia should stop their treatment and visit their GP at their convenience for further advice." Two other anti-obesity medications- Reductil and Xenical - remain on prescription in Ireland and have different modes of action in the body than Acomplia. However, just as news of Acomplia's demise was filtering through, two other anti-obesity medications appeared on the European horizon. A positive opinion from the EMEA on GlaxoSmithKline's weight-loss boosting drug orlistat (currently sold over the counter as Alli in the United States) has prompted estimates that it could be on sale in Europe by 2009. And a report in The Lancet highlights the success in human trials of the drug tesofensine, manufactured by Danish company NeuroSearch, which acts on the brain to make patients feel full early in a meal. MIB Abstract ID Number: 16129 *To access this Lexis-Nexis article the user must create an account. |
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| GlaxoSmithKline & Orlistat | |
| alli & Glaxo | |
| Cardiovascular disease | |
| apolipoprotein A1 & Cardio disease | |
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Apolipoproteins, cardiovascular risk and statin response in type 2 diabetes: the Collaborative Atorvastatin Diabetes Study (CARDS). Lead Author: Charlton-Menys V Additional Authors: Betteridge DJ, Colhoun H, Fuller J, France M, Hitman GA, Livingstone SJ, Neil HA, Newman CB, Szarek M, Demicco DA, Durrington PN. Diabetologia., 2008-10-30, [Epub ahead of print] Cardiovascular Research Group, School of Clinical & Laboratory Sciences, Core Technology Facility (3rd Floor), University of Manchester, 46 Grafton Street, Manchester, M13 9NT, UK. AIMS/HYPOTHESIS: Controversy surrounds whether the ratio of apolipoprotein B (ApoB) to apolipoprotein A-I (ApoA-I) is the best lipoprotein discriminator of CHD risk in non-diabetic populations, but the issue has never been investigated in type 2 diabetes. METHODS: In 2,627 participants without known vascular disease in the Collaborative Atorvastatin Diabetes Study, ApoB, ApoA-I, LDL-cholesterol (LDLC) and HDL-cholesterol (HDLC) were assayed at baseline. RESULTS: There were 108 CHD and 59 stroke endpoints over 3.9 years. The ApoB:A-I ratio at baseline was the lipoprotein variable most closely predicting CHD risk both by comparison of the hazard ratio for a 1 SD change or tertiles of frequency distribution. The areas under the receiver-operator curve for the ApoB:ApoA-I and the LDLC to HDL-HDLC ratios, although not significantly different from each other, were greater (p = 0.0005 and p = 0.0125 respectively) than that of non-HDLC:HDLC. The 27% decrease in the ApoB:ApoA-I ratio on atorvastatin predicted a 32% (95% CI 5.4-51.2%) risk reduction in CHD, close to the 36% decrease observed. Neither the ApoB:ApoA-I nor any other lipoprotein concentration or ratio predicted the stroke outcome. CONCLUSIONS/INTERPRETATION: Overall, the ApoB:ApoA-I ratio improved on the non-HDLC:HDLC ratio in predicting CHD, but, depending on the assessment chosen, its superiority over LDLC:HDLC may be marginal. The statin-induced decrease in stroke risk may not be lipoprotein mediated. Trial registration: ClinicalTrials.gov NCT00327418 Funding: The study was supported by unrestricted grants from Diabetes UK, the Department of Health and Pfizer to the University of Manchester and to University College, London. MIB Abstract ID Number: 16106 PreMedline Identifier: 18972097 *To access this PubMed use the PreMedline Identifier in the PubMed search field |
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Low-density lipoprotein (LDL), which includes apolipoprotein A-I (apoAI-LDL) as a novel marker of coronary artery disease. Lead Author: Ogasawara K Additional Authors: Mashiba S, Hashimoto H, Kojima S, Matsuno S, Takeya M, Uchida K, Yajima J. Clin Chim Acta. , 2008-11-01, 397(1-2):42-7. Epub 2008 Jul 18. The Cardiovascular Institute, Tokyo, Japan. BACKGROUND: Serum low-density lipoprotein (LDL), which includes apolipoprotein A-I (apoAI-LDL) may be generated by oxidization in the serum of patients with coronary artery disease (CAD). We determine the utility of the serum apoAI-LDL level as a novel coronary risk factor. METHODS: We measured serum apoAI-LDL in 473 consecutive patients who underwent diagnostic coronary angiography. Serum levels of apoAI-LDL were assayed by a newly developed ELISA. RESULTS: The patients consisted of 84 with unstable angina (UA), 259 with stable CAD, and 130 without CAD (control). The serum level of apoAI-LDL was higher in CAD patients than in the control group (31.4 (22.1-41.4) microg/ml vs. 24.6 (18.4-29.2) microg/ml, respectively, p<0.001), as well as in patients with UA compared to those with stable CAD 44.5 (35.8-51.9) microg/ml vs. 27.1 (19.5-35.6) microg/ml, respectively, p<0.0001) (data are expressed as the median (25th-75th percentiles)). By logistic regression analysis, only apoAI-LDL was independent, being significantly able to predict CAD (odds ratio: 1.50, 95% CI: 1.23-1.82, p<0.001), and differentiate unstable angina (odds ratio: 1.80, 95% CI: 1.48-2.17, p<0.001) after controlling for classical risk factors. CONCLUSION: The serum level of apoAI-LDL, a newly identified component of oxidized LDL, may be a more sensitive marker of CAD and acute coronary syndrome than CRP. MIB Abstract ID Number: 16111 PreMedline Identifier: 18691566 *To access this PubMed use the PreMedline Identifier in the PubMed search field |
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| Cholesterol & Cardio disease | |
| above 150 & Cholesterol | |
| below 150 & Cholesterol | |
| combination therapy & Cardio disease | |
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LDL reduction: how low should we go and is it safe? Lead Author: Robinson JG. Curr Cardiol Rep., 2008-11-01, 10(6):481-7 Lipid Research Clinic, 200 Hawkins Drive SE 226 GH, Iowa City, IA 52242, USA. jennifer-g-robinson@uiowa.edu High-dose statin therapy or combination statin treatment is necessary for most patients to achieve aggressive low-density lipoprotein cholesterol goals. Adding ezetimibe or bile acid sequestrants appears unlikely to increase the risk of myopathy. Although the combination of niacin or fenofibrate with moderate-dose statins appears to be reasonably safe, the safety of combination with high-dose statins has yet to be determined. To enhance patient outcomes, attention must be paid to characteristics that predict muscle and hepatic statin toxicity when considering using high-dose statin or combination statin therapy. MIB Abstract ID Number: 16140 PreMedline Identifier: 18950559 *To access this PubMed use the PreMedline Identifier in the PubMed search field |
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| ezetimibe & Cardio disease | |
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Ezetimibe and Other Statins Achieve Established Low-Density Lipoprotein Targets in Coronary Artery Disease: Presented at CCC Lead Author: Marvin Ross PR Newswire, 2008-10-29 Statin use and, in particular, the use of ezetimibe is vital in reaching a low-density lipoprotein (LDL) goal of 2 mmol/L or less in the majority of patients with coronary artery disease, researchers stated here at the Canadian Cardiovascular Congress (CCC). Combination therapy was required in 101 patients (28.1%). The agents used were ezetimibe (22.2%), fibrates (4.4%), and niacin (1.4%). Of the 360 patients, 307 (85.3%) were able to achieve an LDL of 2 mmol/L or less. Baseline total cholesterol, LDL, high-density lipoprotein, and triglycerides were 5.73 +- 0.06; 3.71 +- 0.06; 1.11 +- 0.01; and 2.22 +- 0.09, respectively. At the end of the rehabilitation program, the measures were 3.25 +- 0.03; 1.65 +- 0.02; 0.99 +- 0.01; and 1.36 +- 0.04, respectively. A univariate regression analysis found the following to be significant in achieving these levels: statin use, attending nutrition classes, and employment status (all with P < .001), as well as baseline cholesterol (P = .006); baseline LDL (P = .02); and time in rehabilitation (P = .04). In a multivariate regression analysis, variables having significant independent influence were statin use (P < .001), employment status (P < .001), and attending nutrition classes (P = .009). MIB Abstract ID Number: 16124 *To access this Lexis-Nexis article the user must create an account. |
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| fibrates & Cardio disease | |
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Ezetimibe and Other Statins Achieve Established Low-Density Lipoprotein Targets in Coronary Artery Disease: Presented at CCC Lead Author: Marvin Ross PR Newswire, 2008-10-29 Statin use and, in particular, the use of ezetimibe is vital in reaching a low-density lipoprotein (LDL) goal of 2 mmol/L or less in the majority of patients with coronary artery disease, researchers stated here at the Canadian Cardiovascular Congress (CCC). Combination therapy was required in 101 patients (28.1%). The agents used were ezetimibe (22.2%), fibrates (4.4%), and niacin (1.4%). Of the 360 patients, 307 (85.3%) were able to achieve an LDL of 2 mmol/L or less. Baseline total cholesterol, LDL, high-density lipoprotein, and triglycerides were 5.73 +- 0.06; 3.71 +- 0.06; 1.11 +- 0.01; and 2.22 +- 0.09, respectively. At the end of the rehabilitation program, the measures were 3.25 +- 0.03; 1.65 +- 0.02; 0.99 +- 0.01; and 1.36 +- 0.04, respectively. A univariate regression analysis found the following to be significant in achieving these levels: statin use, attending nutrition classes, and employment status (all with P < .001), as well as baseline cholesterol (P = .006); baseline LDL (P = .02); and time in rehabilitation (P = .04). In a multivariate regression analysis, variables having significant independent influence were statin use (P < .001), employment status (P < .001), and attending nutrition classes (P = .009). MIB Abstract ID Number: 16124 *To access this Lexis-Nexis article the user must create an account. |
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| Hypolipidemic or antihyperlipidemic agents & Cardio disease | |
| HDL & Cardio disease | |
| LDL & Cardio disease | |
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Low-density lipoprotein (LDL), which includes apolipoprotein A-I (apoAI-LDL) as a novel marker of coronary artery disease. Lead Author: Ogasawara K Additional Authors: Mashiba S, Hashimoto H, Kojima S, Matsuno S, Takeya M, Uchida K, Yajima J. Clin Chim Acta. , 2008-11-01, 397(1-2):42-7. Epub 2008 Jul 18. The Cardiovascular Institute, Tokyo, Japan. BACKGROUND: Serum low-density lipoprotein (LDL), which includes apolipoprotein A-I (apoAI-LDL) may be generated by oxidization in the serum of patients with coronary artery disease (CAD). We determine the utility of the serum apoAI-LDL level as a novel coronary risk factor. METHODS: We measured serum apoAI-LDL in 473 consecutive patients who underwent diagnostic coronary angiography. Serum levels of apoAI-LDL were assayed by a newly developed ELISA. RESULTS: The patients consisted of 84 with unstable angina (UA), 259 with stable CAD, and 130 without CAD (control). The serum level of apoAI-LDL was higher in CAD patients than in the control group (31.4 (22.1-41.4) microg/ml vs. 24.6 (18.4-29.2) microg/ml, respectively, p<0.001), as well as in patients with UA compared to those with stable CAD 44.5 (35.8-51.9) microg/ml vs. 27.1 (19.5-35.6) microg/ml, respectively, p<0.0001) (data are expressed as the median (25th-75th percentiles)). By logistic regression analysis, only apoAI-LDL was independent, being significantly able to predict CAD (odds ratio: 1.50, 95% CI: 1.23-1.82, p<0.001), and differentiate unstable angina (odds ratio: 1.80, 95% CI: 1.48-2.17, p<0.001) after controlling for classical risk factors. CONCLUSION: The serum level of apoAI-LDL, a newly identified component of oxidized LDL, may be a more sensitive marker of CAD and acute coronary syndrome than CRP. MIB Abstract ID Number: 16111 PreMedline Identifier: 18691566 *To access this PubMed use the PreMedline Identifier in the PubMed search field |
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LDL reduction: how low should we go and is it safe? Lead Author: Robinson JG. Curr Cardiol Rep., 2008-11-01, 10(6):481-7 Lipid Research Clinic, 200 Hawkins Drive SE 226 GH, Iowa City, IA 52242, USA. jennifer-g-robinson@uiowa.edu High-dose statin therapy or combination statin treatment is necessary for most patients to achieve aggressive low-density lipoprotein cholesterol goals. Adding ezetimibe or bile acid sequestrants appears unlikely to increase the risk of myopathy. Although the combination of niacin or fenofibrate with moderate-dose statins appears to be reasonably safe, the safety of combination with high-dose statins has yet to be determined. To enhance patient outcomes, attention must be paid to characteristics that predict muscle and hepatic statin toxicity when considering using high-dose statin or combination statin therapy. MIB Abstract ID Number: 16140 PreMedline Identifier: 18950559 *To access this PubMed use the PreMedline Identifier in the PubMed search field |
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| mevalonate & Cardio disease | |
| micelles & Cardio disease | |
| niacin & Cardio disease | |
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Ezetimibe and Other Statins Achieve Established Low-Density Lipoprotein Targets in Coronary Artery Disease: Presented at CCC Lead Author: Marvin Ross PR Newswire, 2008-10-29 Statin use and, in particular, the use of ezetimibe is vital in reaching a low-density lipoprotein (LDL) goal of 2 mmol/L or less in the majority of patients with coronary artery disease, researchers stated here at the Canadian Cardiovascular Congress (CCC). Combination therapy was required in 101 patients (28.1%). The agents used were ezetimibe (22.2%), fibrates (4.4%), and niacin (1.4%). Of the 360 patients, 307 (85.3%) were able to achieve an LDL of 2 mmol/L or less. Baseline total cholesterol, LDL, high-density lipoprotein, and triglycerides were 5.73 +- 0.06; 3.71 +- 0.06; 1.11 +- 0.01; and 2.22 +- 0.09, respectively. At the end of the rehabilitation program, the measures were 3.25 +- 0.03; 1.65 +- 0.02; 0.99 +- 0.01; and 1.36 +- 0.04, respectively. A univariate regression analysis found the following to be significant in achieving these levels: statin use, attending nutrition classes, and employment status (all with P < .001), as well as baseline cholesterol (P = .006); baseline LDL (P = .02); and time in rehabilitation (P = .04). In a multivariate regression analysis, variables having significant independent influence were statin use (P < .001), employment status (P < .001), and attending nutrition classes (P = .009). MIB Abstract ID Number: 16124 *To access this Lexis-Nexis article the user must create an account. |
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| phytosterols & Cardio disease | |
| triglycerides & Cardio disease | |