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Ezetimibe: a Novel Selective Cholesterol Absorption Inhibitor by Michele Koder, Pharm.D
OREGON DUR BOARD NEWSLETTER A N E VIDENCE B ASED D RUG T HERAPY R ESOURCE COPYRIGHT 2003 OREGON STATE UNIVERSITY. ALL RIGHTS RESERVED Volume 5, Issue 2 Also available on the web and via e-mail list-serve at February 2003 http://pharmacy.orst.edu/drug_policy/newsletter_email.html Ezetimibe: A novel selective cholesterol absorption inhibitor By Michele Koder, Pharm.D. , OSU College of Pharmacy Ezetimibe (Zetia) is a novel selective cholesterol absorption inhibitor that was approved by the FDA in October 2002. Unlike statins (HMG-CoA reductase inhibitors) and bile acid sequestrants, ezetimibe does not inhibit hepatic cholesterol synthesis or increase bile acid secretion. In contrast, ezetimibe selectively inhibits the uptake of dietary cholesterol from enterocytes in the brush border of the intestinal lumen resulting in a decrease in the delivery of dietary cholesterol to the liver and a subsequent decrease in hepatic cholesterol stores and increased cholesterol clearance from the blood.1 Ezetimibe’s unique action has generated interest in its use in combination with other cholesterol-lowering agents. It is indicated for the treatment of primary hypercholesterolemia as monotherapy and in combination with a statin. Ezetimibe is also approved for homozygous familial hypercholesterolemia and homozygous sitosterolemia. TABLE 1: EZETIMIBE CLINICAL TRIAL SUMMARY Study / Design Population Treatment % Change LDL % Change HDL % Change TG Bays et al3 N=432 EZ 5 mg -15.7 +2.9 MC, R, DB, PC LDL 130-250mg/dl EZ 10 mg -18.5 +3.5 NS 12 wk; Phase II TG -
Dyslipidemia in Newfoundland: Findings from Canadian Primary Care Sentinel Surveillance Network in Newfoundland and Labrador
Dyslipidemia in Newfoundland: Findings from Canadian Primary Care Sentinel Surveillance Network in Newfoundland and Labrador By Justin D. Oake A thesis submitted to the School of Graduate Studies in partial fulfillment of the requirements for the degree of Master of Science in Medicine Clinical Epidemiology Program, Faculty of Medicine, Memorial University of Newfoundland St. John’s, NL May 2019 Abstract Newfoundland and Labrador (NL) has a higher level of cardiovascular disease (CVD) mortality than any other Canadian province. One factor which may explain this trend is the lipid profile pattern in this province. Given the limited lipid profile data which has been reported from NL, we organized three studies in this thesis to describe the lipid profile of Newfoundlanders. The first study was a secondary analysis of Canadian Primary Care Sentinel Surveillance Network (CPCSSN) data to document single and mixed dyslipidemia in NL. The second study compared lipid profiles and the prevalence of dyslipidemia between NL CPCSSN data and the Canadian Health Measures Survey (CHMS). The third study used electronic medical record (EMR) data in assessing the validity of ICD codes for identifying patients with dyslipidemia. This was a secondary analysis of EMR data in NL. Most recent lipid profile scores, co-morbidities, and demographic information were extracted from the CPCSSN database. We demonstrated that single and mixed dyslipidemia are quite prevalent in the NL population. Unhealthy levels of HDL were also more prevalent in NL men, compared to the Canadian sample. Of importance, the use of the ICD coding, either alone or in combination with laboratory data or lipid-lowering medication records, was an inaccurate indicator in identifying dyslipidemia. -
FIELD Study Revealed Fenofibrate Reduced Need for Laser Treatment for Diabetic Retinopathy by Anthony C
Supplement to Supported by an unrestricted educational grant from Abbott Laboratories March/April 2008 FIELD Study Revealed Fenofibrate Reduced Need for Laser Treatment for Diabetic Retinopathy By Anthony C. Keech, MBBS, Msc Epid, FRANZCS, FRACP; and Paul Mitchell, MBBS(Hons), MD, PhD, FRANZCO, FRACS, FRCOphth, FAFPHM This agent’s mechanism of benefit in diabetic retinopathy appears to go beyond its effects on lipid concentration or blood pressure, and this potential mechanism of action operates even when glycemic control and blood pressure levels are within goal. ABSTRACT icant relative reduction was seen of almost one-third in PURPOSE the rate of first laser application for retinopathy after The FIELD (Fenofibrate Intervention and Event an average treatment duration of 5 years with fenofi- Lowering in Diabetes) study sought to investigate brate 200 mg/day. whether long-term lipid-lowering therapy with fenofi- In this report, we detail the effects of fenofibrate brate would reduce macro- and microvascular compli- administration on ophthalmic microvascular compli- cations among patients with type 2 diabetes. We previ- cations and attempt to clarify some of the underlying ously reported that in type 2 diabetes patients with pathologies being addressed among patients undergo- adequate glycemic and blood pressure control, a signif- ing laser treatment. Jointly sponsored by The Dulaney Foundation and Retina Today MARCH/APRIL 2008 I SUPPLEMENT TO RETINA TODAY I 1 FIELD Study Revealed Fenofibrate Reduced Need for Laser Treatment for Diabetic Retinopathy Jointly sponsored by The Dulaney Foundation and Retina Today. Release date: April 2008. Expiration date: April 2009. This continuing medical education activity is supported by an unrestricted educational grant from Abbott Laboratories. -
Effects of Generic Substitution on Refill Adherence to Statin Therapy: a Nationwide Population-Based Study Henrik Trusell1 and Karolina Andersson Sundell1,2*
Trusell and Andersson Sundell BMC Health Services Research 2014, 14:626 http://www.biomedcentral.com/1472-6963/14/626 RESEARCH ARTICLE Open Access Effects of generic substitution on refill adherence to statin therapy: a nationwide population-based study Henrik Trusell1 and Karolina Andersson Sundell1,2* Abstract Background: Several countries have introduced generic substitution, but few studies have assessed its effect on refill adherence. This study aimed to analyse whether generic substitution influences refill adherence to statin treatment. Methods: Between 1 July 2006 and 30 June 2007, new users of simvastatin (n = 108,806) and atorvastatin (n = 7,464) were identified in the Swedish Prescribed Drug Register . The present study included atorvastatin users as an unexposed control group because atorvastatin was patent-protected and thus not substitutable. We assessed refill adherence using continuous measure of medication acquisition (CMA). To control for potential confounders, we used analysis of covariance (ANCOVA). Differences in CMA associated with generic substitution and generic substitution at first-time statin purchase were analysed. Results: Nine of ten simvastatin users were exposed to generic substitution during the study period, and their adherence rate was higher than that of patients without substitution [84.6% (95% CI 83.5-85.6) versus 59.9% (95% CI 58.4-61.4), p < 0.001]. CMA was higher with increasing age (60–69 years 16.7%, p < 0.0001 and 70–79 years 17.8%, p < 0.0001, compared to 18–39 years) and secondary prevention (12.8%, p < 0.0001). CMA was lower among patients who were exposed to generic substitution upon initial purchase, compared to those who were exposed to a generic substitution subsequently [80.4% (95% CI 79.4-90.9) versus 89.8% (88.7-90.9), p < 0.001]. -
Clinofibrate Improved Canine Lipid Metabolism in Some but Not All Breeds
NOTE Internal Medicine Clinofibrate improved canine lipid metabolism in some but not all breeds Yohtaro SATO1), Nobuaki ARAI2), Hidemi YASUDA3) and Yasushi MIZOGUCHI4)* 1)Graduate School of Agriculture, Meiji University, 1-1-1 Higashimita, Tama-ku, Kawasaki, Kanagawa 214-8571, Japan 2)Spectrum Lab Japan, 1-5-22-201 Midorigaoka, Meguro-ku, Tokyo 152-0034, Japan 3)Yasuda Veterinary Clinic, 1-5-22 Midorigaoka, Meguro-ku, Tokyo 152-0034, Japan 4)School of Agriculture, Meiji University, 1-1-1 Higashimita, Tama-ku, Kawasaki, Kanagawa 214-8571, Japan ABSTRACT. The objectives of this study were to assess if Clinofibrate (CF) treatment improved J. Vet. Med. Sci. lipid metabolism in dogs, and to clarify whether its efficacy is influenced by canine characteristics. 80(6): 945–949, 2018 We collected medical records of 306 dogs and performed epidemiological analyses. Lipid values of all lipoproteins were significantly decreased by CF medication, especially VLDL triglyceride doi: 10.1292/jvms.17-0703 (TG) concentration (mean reduction rate=54.82%). However, 17.65% of dogs showed drug refractoriness in relation to TG level, and Toy Poodles had a lower CF response than other breeds (OR=5.36, 95% CI=2.07–13.90). Therefore, our study suggests that genetic factors may have an Received: 22 December 2017 effect on CF response, so genetic studies on lipid metabolism-related genes might be conducted Accepted: 9 March 2018 to identify variations in CF efficacy. Published online in J-STAGE: KEY WORDS: clinofibrate, descriptive epidemiology, drug response, dyslipidemia, Toy Poodle 26 March 2018 High serum cholesterol (Cho) and triglyceride (TG) concentrations in dogs are caused by various factors such as lack of exercise, high fat diets, obesity, neutralization, age, diseases and breed [6, 21, 24]. -
Effects of Clofibrate Derivatives on Hyperlipidemia Induced by a Cholesterol-Free, High-Fructose Diet in Rats
Showa Univ. J. Med. Sci. 7(2), 173•`182, December 1995 Original Effects of Clofibrate Derivatives on Hyperlipidemia Induced by a Cholesterol-Free, High-Fructose Diet in Rats Hideyukl KURISHIMA,Sadao NAKAYAMA,Minoru FURUYA and Katsuji OGUCHI Abstract: The effects of the clofibrate derivatives fenofibrate (FF), bezafibrate (BF), and clinofibrate (CF), on hyperlipidemia induced by a cholesterol-free, high-fructose diet (HFD) in rats were investigated. Feeding of HFD for 2 weeks increased the high-density lipoprotein subfraction (HDL1) and decreased the low-density lipoprotein (LDL) fraction. The levels of total cholesterol (TC), free cholesterol, triglyceride (TG), and phospholipid in serum were increased by HFD feeding. Administration of CF inhibited the increase in HDL1 content. All three agents inhibited the decrease in LDL level. Both BF and CF decreased VLDL level. Administration of FF, BF, or CF inhibited the increases of serum lipids, especially that of TC and TG. The inhibitory effects of CF on HFD- induced increases in HDL1, TC, and TG were greater than those of FF and BF. These results demonstrate that FF, BF, and CF improve the intrinsic hyper- lipidemia induced by HFD feeding in rats. Key words: fenofibrate, bezafibrate, clinofibrate, fructose-induced hyperlipide- mia, lipoprotein. Introduction Clofibrate is one of the most effective antihypertriglycedemic agents currently available. However, because of its adverse effects, such as hepatomegaly1, several derivatives, such as clinofibrate (CF) and bezafibrate (BF) have been developed which are more effective and have fewer adverse effects. For example, it has been shown that the hypolipidemic effect of CF is greater than that of clofibrate while its tendency to produce hepatomegaly is less1. -
Regulation of Pharmaceutical Prices: Evidence from a Reference Price Reform in Denmark
A Service of Leibniz-Informationszentrum econstor Wirtschaft Leibniz Information Centre Make Your Publications Visible. zbw for Economics Kaiser, Ulrich; Mendez, Susan J.; Rønde, Thomas Working Paper Regulation of pharmaceutical prices: Evidence from a reference price reform in Denmark ZEW Discussion Papers, No. 10-062 Provided in Cooperation with: ZEW - Leibniz Centre for European Economic Research Suggested Citation: Kaiser, Ulrich; Mendez, Susan J.; Rønde, Thomas (2010) : Regulation of pharmaceutical prices: Evidence from a reference price reform in Denmark, ZEW Discussion Papers, No. 10-062, Zentrum für Europäische Wirtschaftsforschung (ZEW), Mannheim This Version is available at: http://hdl.handle.net/10419/41440 Standard-Nutzungsbedingungen: Terms of use: Die Dokumente auf EconStor dürfen zu eigenen wissenschaftlichen Documents in EconStor may be saved and copied for your Zwecken und zum Privatgebrauch gespeichert und kopiert werden. personal and scholarly purposes. Sie dürfen die Dokumente nicht für öffentliche oder kommerzielle You are not to copy documents for public or commercial Zwecke vervielfältigen, öffentlich ausstellen, öffentlich zugänglich purposes, to exhibit the documents publicly, to make them machen, vertreiben oder anderweitig nutzen. publicly available on the internet, or to distribute or otherwise use the documents in public. Sofern die Verfasser die Dokumente unter Open-Content-Lizenzen (insbesondere CC-Lizenzen) zur Verfügung gestellt haben sollten, If the documents have been made available under an Open gelten abweichend von diesen Nutzungsbedingungen die in der dort Content Licence (especially Creative Commons Licences), you genannten Lizenz gewährten Nutzungsrechte. may exercise further usage rights as specified in the indicated licence. www.econstor.eu Dis cus si on Paper No. 10-062 Regulation of Pharmaceutical Prices: Evidence from a Reference Price Reform in Denmark Ulrich Kaiser, Susan J. -
Protective Lipid-Lowering Genetic Variants in Healthy Older Individuals Without Coronary
medRxiv preprint doi: https://doi.org/10.1101/2021.02.16.21251811; this version posted February 19, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license . TITLE PAGE Title: Protective lipid-lowering genetic variants in healthy older individuals without coronary heart disease Running title: Lacaze - Protective lipid-lowering variants Authors: Paul Lacaze, PhD1*, Moeen Riaz, PhD1, Robert Sebra, PhD2, Amanda J Hooper, PhD3,4, Jing Pang, PhD3, Jane Tiller, LLB, MSc GenCoun1, Galina Polekhina, PhD1, Andrew M Tonkin, PhD1, Christopher M Reid, PhD1,5, Sophia Zoungas, MD, PhD1, Anne M Murray, MD, MSc6, Stephen J Nicholls MD, PhD7, Gerald F Watts, MD, PhD4,8, Eric Schadt, PhD2 & John J McNeil, MD, PhD1 Departments and institutions: 1 Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia. 2 Department of Genetics and Genomic Sciences, Icahn Institute for Data Science and Genomic Technology, Icahn School of Medicine at Mount Sinai, New York, USA. 3 School of Medicine, Faculty of Medicine and Health Sciences, The University of Western Australia, Perth, Australia 4 Department of Clinical Biochemistry, PathWest Laboratory Medicine WA, Royal Perth Hospital and Fiona Stanley Hospital Network, Perth, Western Australia, Australia. 5 School of Public Health, Curtin University, Perth, WA, Australia 6 Berman Center for Outcomes and Clinical Research, Hennepin Healthcare Research Institute, Hennepin Healthcare, Minneapolis, MN, USA 7 Monash Cardiovascular Research Centre, Monash University and MonashHeart, Monash Health, Clayton, Victoria, Australia; 1 NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. -
Product Monograph
PRODUCT MONOGRAPH Pr AA-FENO-MICRO Fenofibrate Capsules 67 mg and 200 mg fenofibrate, micronized formulation House Standard Pr FENOFIBRATE Fenofibrate Capsules 100 mg fenofibrate, non-micronized formulation House Standard Lipid Metabolism Regulator AA PHARMA INC. Date of Preparation: 1165 Creditstone Road Unit #1 October 08, 2019 Vaughan, Ontario L4K 4N7 Control No.: 230394 PRODUCT MONOGRAPH Pr AA-FENO-MICRO Fenofibrate Capsules 67 mg and 200 mg fenofibrate, micronized formulation House Standard Pr FENOFIBRATE Fenofibrate Capsules 100 mg fenofibrate, non-micronized formulation House Standard THERAPEUTIC CLASSIFICATION Lipid Metabolism Regulator ACTIONS AND CLINICAL PHARMACOLOGY Fenofibrate lowers elevated serum lipids by decreasing the low-density lipoprotein (LDL) fraction rich in cholesterol and the very low density lipoprotein (VLDL) fraction rich in triglycerides. In addition, fenofibrate increases the high density lipoprotein (HDL) cholesterol fraction. Fenofibrate appears to have a greater depressant effect on the VLDL than on the low density lipoproteins (LDL). Therapeutic doses of fenofibrate produce elevations of HDL cholesterol, a reduction in the content of the low density lipoproteins cholesterol, and a substantial reduction in the triglyceride content of VLDL. The mechanism of action of fenofibrate has not been definitively established. Work carried out to date suggests that fenofibrate: · enhances the liver elimination of cholesterol as bile salts; · inhibits the biosynthesis of triglycerides and enhances the catabolism of VLDL by increasing the activity of lipoprotein lipase; · has an inhibitory effect on the biosynthesis of cholesterol by modulating the activity of HMG- CoA reductase. Metabolism and Excretion After oral administration with food, fenofibrate is rapidly hydrolysed to fenofibric acid, the active metabolite. -
Fenofibrate Capsules Apotex Standard 67 Mg and 200 Mg
PRODUCT MONOGRAPH PrAPO-FENO-MICRO Fenofibrate Capsules Apotex Standard 67 mg and 200 mg PrAPO-FENOFIBRATE Fenofibrate Capsules Apotex Standard 100 mg Lipid Metabolism Regulator APOTEX INC. 150 Signet Drive Toronto, Ontario DATE OF REVISION: M9L 1T9 October 7, 2014 Control No.: 169773 - 1 - PRODUCT MONOGRAPH PrAPO-FENO-MICRO Fenofibrate Capsules Apotex Standard 67 mg and 200 mg PrAPO-FENOFIBRATE Fenofibrate Capsules Apotex Standard 100 mg THERAPEUTIC CLASSIFICATION Lipid Metabolism Regulator ACTIONS AND CLINICAL PHARMACOLOGY Fenofibrate lowers elevated serum lipids by decreasing the low-density lipoprotein (LDL) fraction rich in cholesterol and the very low density lipoprotein (VLDL) fraction rich in triglycerides. In addition, fenofibrate increases the high density lipoprotein (HDL) cholesterol fraction. Fenofibrate appears to have a greater depressant effect on the VLDL than on the low density lipoproteins (LDL). Therapeutic doses of fenofibrate produce elevations of HDL cholesterol, a reduction in the content of the low density lipoproteins cholesterol, and a substantial reduction in the triglyceride content of VLDL. The mechanism of action of fenofibrate has not been definitively established. Work carried out to date suggests that fenofibrate: · enhances the liver elimination of cholesterol as bile salts; · inhibits the biosynthesis of triglycerides and enhances the catabolism of VLDL by increasing the activity of lipoprotein lipase; · has an inhibitory effect on the biosynthesis of cholesterol by modulating the activity of HMG- CoA reductase. Metabolism and Excretion After oral administration with food, fenofibrate is rapidly hydrolyzed to fenofibric acid, the active metabolite. In man it is mainly excreted through the kidney. Half-life is about 20 hours. In patients with severe renal failure, significant accumulation was observed with a large increase in half-life. -
DESCRIPTION TRIGLIDE® (Fenofibrate) Tablets Is a Lipid
DESCRIPTION TRIGLIDE® (fenofibrate) tablets is a lipid-regulating agent available as tablets for oral administration. Each tablet contains 50 mg or 160 mg of fenofibrate. The chemical name for fenofibrate is 2-[4-(4-chlorobenzoyl) phenoxy] 2-methyl-propanoic acid, 1 methylethyl ester with the following structural formula: The empirical formula is C20H21O4Cl and the molecular weight is 360.83; fenofibrate is insoluble in water. The melting point is 79°C to 82°C. Fenofibrate is a white solid that is stable under ordinary conditions. Inactive Ingredients: Each tablet also contains crospovidone, lactose monohydrate, mannitol, maltodextrin, carboxymethylcellulose sodium, egg lecithin, croscarmellose sodium, sodium lauryl sulfate, colloidal silicon dioxide, magnesium stearate, and monobasic sodium phosphate. Clinical Pharmacology A variety of clinical studies have demonstrated that elevated levels of total cholesterol (TC), low- density lipoprotein cholesterol (LDL-C), and apolipoprotein B (apo B), an LDL membrane complex, are associated with human atherosclerosis. Similarly, decreased levels of high-density lipoprotein cholesterol (HDL-C) and its transport complex, apolipoprotein A (apo A-I and apo A-II) are associated with the development of atherosclerosis. Epidemiologic investigations have established that cardiovascular morbidity and mortality vary directly with the level of TC, LDL-C, and triglycerides (TG), and inversely with the level of HDL-C. The independent effect of raising HDL-C or lowering TG on the risk of cardiovascular morbidity and mortality has not been determined. Fenofibric acid, the active metabolite of fenofibrate, produces reductions in total cholesterol, LDL cholesterol, apolipoprotein B, total triglycerides and triglyceride rich lipoprotein (VLDL) in treated patients. In addition, treatment with fenofibrate results in increases in high density lipoprotein (HDL) and apoproteins apo AI and apo AII. -
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Sex Differences in Health Status, Health Care Use, and Quality of Care: A Population-Based Analysis for Manitoba’s Regional Health Authorities November 2005 Manitoba Centre for Health Policy Department of Community Health Sciences Faculty of Medicine, University of Manitoba Randy Fransoo, MSc Patricia Martens, PhD The Need to KnowTeam (funded through CIHR) Elaine Burland, MSc Heather Prior, MSc Charles Burchill, MSc Dan Chateau, PhD Randy Walld, BSc, BComm (Hons) This report is produced and published by the Manitoba Centre for Health Policy (MCHP). It is also available in PDF format on our website at http://www.umanitoba.ca/centres/mchp/reports.htm Information concerning this report or any other report produced by MCHP can be obtained by contacting: Manitoba Centre for Health Policy Dept. of Community Health Sciences Faculty of Medicine, University of Manitoba 4th Floor, Room 408 727 McDermot Avenue Winnipeg, Manitoba, Canada R3E 3P5 Email: [email protected] Order line: (204) 789 3805 Reception: (204) 789 3819 Fax: (204) 789 3910 How to cite this report: Fransoo R, Martens P, The Need To Know Team (funded through CIHR), Burland E, Prior H, Burchill C, Chateau D, Walld R. Sex Differences in Health Status, Health Care Use and Quality of Care: A Population-Based Analysis for Manitoba’s Regional Health Authorities. Winnipeg, Manitoba Centre for Health Policy, November 2005. Legal Deposit: Manitoba Legislative Library National Library of Canada ISBN 1-896489-20-6 ©Manitoba Health This report may be reproduced, in whole or in part, provided the source is cited. 1st Printing 10/27/2005 THE MANITOBA CENTRE FOR HEALTH POLICY The Manitoba Centre for Health Policy (MCHP) is located within the Department of Community Health Sciences, Faculty of Medicine, University of Manitoba.