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(2. Of all anti-lipidemic drugs. that is uniquely formulated in lidose technology. Specific Objective: (1.000) There was no significant change in the SGOT (p=0. and side effects Methodology: This was an open labeled study of Fenogal 160 mg once daily involving adult out-patients of cardiologists and internist in all over the Philippines who have hypertriglyceridemia.000 patients included in this open label study with a mean age of 52 ± 11. The improvement in blood pressure.05 was considered significant. and LDL.1. week 4. However. and HDL) were taken at baseline. LDL.37% after 12 weeks (p=0. Bloatedness was the most common complaint. and can be safely and effectively used among Filipino patients.000).12 mg/dl at 4 weeks of treatment (p=0.30 at 4 weeks and p=0. Blood pressure. paired t-test was applied to the data.72% after 4 weeks and by 33. hypercholesterolemia. triglycerides. Fenogal is one such fibrate.91% after 4 weeks of treatment and by 16. and biological markers (SGOT.) To determine the efficacy of Fenogal in decreasing triglycerides. fenofibrates exert the highest lowering of triglycerides by as much as 40% to 50%. there were 10 patients with gender not indicated. or both from August 2007 to May 2009. and almost equal number of males (50. Conclusion: The authors conclude that Fenogal (lidose technology) is effective in improving the lipid profile of dyslipidemic patients. and height were described using mean and SD. and heart rate may reflect the patient’s overall change in lifestyle brought about by the physician’s recommendation for such a change. alkaline phosphatase.) To determine the safety of the lidose technology using clinical parameters.64% after 4 weeks and by 23. General Objective: To determine the efficacy and safety of fenofibrates particularly Fenogal (lidose technology) in dyslipidemic patients. while increasing HDL. Demographic data of patients were based upon OPD charts.000). heart rate. increase by HDL 10-20% and decrease LDL by 5-25%. Increase in alkaline phosphatase needs further investigation.000). HDL significantly increased by 15. total cholesterol. weight. At 37oC in-vivo. The adverse event rate was 1.51% after 12 weeks (p=0.15% after 12 weeks (p=0.2%) of the patients had both hypercholesterolemia and hypertriglyceridemia. and week twelve. which combines the advantages of a capsule and a liquid.326 at 12 weeks) and SGPT (p=0. Results: There were 3. a very fine emulsion is formed coating the gastric mucosa thereby enhancing bioavalability of active ingredients and reducing risks of gastrointestinal side effects. FBS decreased significantly by 10. Fenogal significantly decreased total cholesterol by 9.817 at 4 weeks and p=0. The presence of atherosclerosis is associated with 50% of myocardial infarctions. Categorical data were presented in frequency and percent distribution.000) and by 13.000).ABSTRACT Background: Hypertriglyceridemia is a common form of dyslipidemia that is usually correlated with cardiovascular diseases including the occurrence of an acute coronary syndrome or the need for a coronary intervention.15% after 4 weeks of treatment and by 15. To determine the significance of change in the different outcome variables. and 70% of deaths due are to cardiovascular diseases.3-1. Assessment of lipid parameters (total cholesterol. More than half (50. Statistical Analysis: Continuous data such as age. There was a significant decrease in heart rate by a mean of 1.8 bpm (p=0. A p-value ≤ 0.945 at 12 weeks). LDL likewise significantly decreased by 8.1% and was mostly gastrointestinal related. Major epidemiological studies showed that the modification of the plasma lipoproteins profile has major beneficial effects on mortality and morbidity related to cardiovascular diseases.91% after 12 weeks (p=0. Likewise fibrates lower serum cholesterol as much as 20% to 25%. In addition a good mass and drug content uniformity is formed. Previous medications for dyslipidemia of patients were discontinued.000).0%). Lidose protects the active ingredient against oxidation. Trigylcerides decreased significantly by 20.34 mg/dl at 12 weeks of treatment (p=0. SGPT. biochemical profile. Included among the most important modifiable risk factors 1 .000).60 years. Introduction: Cardiovascular diseases are the main causes of mortality and morbidity in the industrialized countries.2 It is therefore imperative to focus on risk factors modification. and FBS) were also measured at same interval.6%) and females (49. The systolic blood pressure decreased significantly by a mean of 10-14 mmHg as well as the diastolic blood pressure by a mean of 6-8 mmHg (p=0. FBS.
1 The addition of fenofibrate to statins seems to be beneficial in patients with acute coronary syndrome. biochemical profile and side effects Significance of the Study: Fenofibrates are mainly indicated in the treatment of hypertriglyceridemia when diet and lifestyle changes are not sufficient. statins are considered the first line of treatment for cholesterol control. increased triglyceride level is also associated with increased vascular risk. while increasing HDL when statins are not tolerated. diabetes mellitus. an important characteristic abnormal level of plasma lipids is seen. and serum cholesterol as much as 20% to 25%. A hydroxypropylcellulose type of polymer is present to prevent any formation of fenofibrate crystal when exposed to dition of fenofibrate further enhanced this reduction of the novel risk factor fibrinogen. Fibrates are known to lower total cholesterol. In all of these risk factors. This technology has enhanced bioavailability as compared to the standard formulation. When in contact with a physiological medium at a temperature of 37oC. Other advantages of lidose technology are: (1) a good mass and drug content uniformity.. which is generally defined by the occurrence of an acute coronary syndrome or the need for a coronary intervention. To determine the safety of the lidose technology using clinical parameters.6 Fenogal in lidose technology combines the advantages of a capsule and a liquid. It is a known fact that the directly proportional relationship between hypercholesterolemia and atherosclerosis existed and has been well established. the volumetric filling of a liquid is not influenced by density of the product. To determine the efficacy of Fenogal in decreasing triglycerides. It exerts favorable effects on the atherogenic lipid profile of mixed dyslipidemia and can effectively reduce cardiovascular disease in patients with mixed dyslipidemia. Cholesterol reduction is obtained by lowering low density atherogenic factors such as VLDL and LDL. al. total cholesterol. low dosing substances so as to obtain a uniform blend of sensitive substances.5. and increasing HDL 2. and LDL.3 2 . Fenofibrates can lower both triglycerides by 40% to 50%. With its IUPAC name of: propan-2-yl 2-[4-(4-chlorobenzoyl) phenoxy]-2-methylpropanoate. and slightly soluble drugs to obtain dispersion. Lidose enhances bioavailability of active ingredients and it reduces risks of gastrointestinal side effects.are dyslipidemia. and hypertension. (2) lidose protects the active ingredient against oxidation. low level of HDL is also associated with an increased coronary risk. and (3) capability to use hard gelatin capsules for: liquid substances.1 Mixed dyslipidemia is a common lipid disorder described by the presence of an atherogenic lipoprotein phenotype due to abnormalities in various atherogenic and anti-atherogenic lipoproteins. LDL. Side effects of statins are very well known. statins decreased plasma fibrinogen significantly and the ad- It is a hard capsule with a semi-solid content in which fenofibrate 160mg is homogeneously dispersed within a mixture of lipid excipients. However. it forms a very fine emulsion that coats the gastric mucosa (one dose produces approximately 50 micro micelles droplets). gastrointestinal fluids. Various anti-lipidemic drugs are available. Considering all other factors. OBJECTIVES: General Objective: To determine the efficacy and safety of fenofibrates particularly Fenogal (lidose technology) in dyslipidemic patients Specific Objective: 1. According to Shah et. and it is continuously released by a diffusion-erosion process. Fenofibrates are particularly useful in high residual risk seen in statin trials which may be due to lipoprotein abnormalities other than LDL. Among these.3 Hypertriglyceridemia is a common form of dyslipidemia that is usually correlated with cardiovascular diseases.4. obesity.
6 49.67 161.07%.3 100 12.000 patients included in this open labeled study with a mean age of 52 ± 11. Table 1 Baseline Characteristics of Patients Included in the Study CHARACTERISTICS Age (Years) Weight (lbs.60% followed by atorvastatin.27 mg/dl and percent increase from baseline of 15. weight. hypercholesterolemia.) Gender: Male Female Not Indicated Total Type of Dyslipidemia: Hypercholesterolemia Hypertriglyceridemia Both Not Indicated Total The most common medicines taken by patients before entering the study were simvastatin.4% with hypertriglyceridemia.08 8. Assessment of lipid parameters (total cholesterol.0%).86 mg/dl with percent change of 15.10%) who were already on Fenogal before the study started. LDL. To determine the significance of change in the different outcome variables.91%. 2. The total cholesterol decreased significantly as early as week 4 of therapy with actual change of 28.64%.37%. Statistical Analysis: Continuous data such as age. see Appendix A.15% while at week 12 the mean decrease was 29. heart rate. and height were described using mean and standard deviation. Mean 52 150.Methodology: This was an open labeled study of Fenogal 160mg once daily involving adult out-patients of cardiologists and internist all over the Philippines who have hypertriglyceridemia.12 mg/dl and percent change from baseline of 9. triglycerides. from August 2007 to May 2009. the actual increase was 6. 19. 3 .05 was considered significant.60 25.47% and Lipanthyl.6%) and females (49. 3. as shown in Table 1. fenofibrates. A p-value ≤ 0. and biological markers (SGOT. More than half (50. and HDL) and were taken at baseline.60 years.80 mg/dl with percent change from baseline of 23. paired t-test was applied to the data. and majority at 50. Previous medications for dyslipidemia (statins. There were 3 patients (0. Blood pressure. Demographic data of patients were based upon OPD charts.4 50.) Height (cms. there were 10 patients with gender not indicated.1 100 LDL likewise significantly decreased from baseline to week 4 and week 12. alkaline phosphatase.3% were with hypercholesterolemia. 1519 1471 10 3000 370 1002 1506 122 3000 SD 11. However.0 0. At week 12. Results: There were 3. and FBS) were also measured at same interval. gemfibrozil. SGPT.51%.41 mg/dl with percent change of 8. ezetemibe) were discontinued prior to administration of Fenogal. Categorical data were presented in frequency and percent distribution.42 % 50. At week 12.2%) of the patients were with both hypercholesterolemia and hypertriglyceridemia. 33. HDL on the other hand increased significantly after 4 weeks and 12 weeks of treatment. Only 12. There were almost equal number of males (50. The actual mean decrease at week 4 was 17. or both. the actual mean decrease was 44.2% were with both.91%. The actual mean increase was 4.2 4. and week twelve. week 4.3 33.01 mg/dl with percent change from baseline of 16.43 No.
33 28.15 139.39 51.000* 0.00 41.30 mg/dl from baseline up to week 4 of therapy.33 20.91 229.01 16.18 51. there was 90.12 48.84 185.41 8.32 22.38 232.19 19.47 123. Table 2 shows the details of the effect of the treatment on lipid profile of the patients.19 31.64 49.18 48.97 26.16 4.61 mg/dl actual decrease and 33. Table 2 Assessment of Lipid Profile of Patients by Observation Periods Observation Period Total Cholesterol Baseline (n=2489) Week 4 Difference: Actual Percent from baseline p-value Baseline (n=2909 Week 12 Difference: Actual Percent from baseline p-value LDL Baseline (n=2239) Week 4 Difference: Actual Percent from baseline p-value Baseline (n=2599) Week 12 Difference: Actual Percent from baseline p-value HDL Baseline (n=2217) Week 4 Difference: Actual Percent from baseline p-value Baseline (n=2580) Week 12 Difference: Actual Percent from baseline p-value Mean Lipid Profile SD 64. The percent decrease was 20.80 23.26 6.15% change from baseline.72%.51 0.67 62.06 17.46 56.Triglycerides decreased significantly with actual mean of 60.27 15.15 29.88 54.000* 0.88 51.76 27.000* 4 .11 39.31 140.82 45.60 26.13 25. At week 12.82 34.75 56.91 49.000* 0.12 9.26 42.000* 0.01 109.000* 0.45 204.91 36.83 44.86 15.81 19.32 26.
000* A statistically significant favorable lipid lowering response based on NCEP-ATP III goals was achieved as early as 4 weeks of treatment and was sustained up to 12 weeks of treatment.1 34. Follow-up % p-value Week 12 1806 683 2489 2061 848 2909 1281 1208 2489 944 1965 2909 51.66 74.5 67.84 54.9 100 0.4 100 70.3 21.000* 0.6 100 37.8 29.5 100 0.Triglyceride Baseline (n=2532) Week 4 Difference: Actual Percent from baseline p-value Baseline (n=2944) Week 12 Difference: Actual Percent from baseline p-value 234.30 9.98 174.9 100 48.11 64.7 100 1458 781 2239 1264 1335 2599 65.2 10.000* LDL Week 4 ≥ 100mg/dl < 100mg/dl Total ≥ 100mg/dl or ↓ < 30% < 100mg/dl or ↓ ≥ 30% Total 1758 481 2239 2035 564 2599 78. see table 3.4 100 0.0 76.000* HDL Week 4 Week 12 < 40mg/dl ≥ 40mg/dl Total < 40mg/dl ≥ 40mg/dl Total 852 1365 2217 974 848 2580 38.5 21.66 90.000* 0.8 29.000* 0.6 100 44.15 98.8 100 1706 826 2532 1298 1646 2944 67.86 0.9 11.99 86.000* Week 12 0.5 100 32.5 48.000* 0.000* Triglyceride Week 4 Week 12 ≥ 150mg/dl < 150mg/dl Total ≥ 150mg/dl < 150mg/dl Total 2250 282 2532 2625 319 2944 88.2 100 No.5 100 78.34 31.0 100 18.68 60.2 100 531 1686 2217 487 1965 2580 24.1 100 0.9 81.68 28.91 235.16 97.1 100 89.61 33.000* 5 .27 144. Table 3 Assesment of LIPID Response by NCEP-ATPIII Guideline by Observation Period Lipid Total Cholesterol Week 4 ≥ 200mg/dl < 200mg/dl Total ≥ 200mg/dl < 200mg/dl Total No.6 51.1 55.4 61. Baseline % 72.4 32.6 27.
000* 20.59 138 124 14.78 9.99 87 79 7.22 11.000* 84 82 5.51 13.57 8.67 0.000* 79 78 1.65 0.18 6.87 8.95 0.76 0.66 Lipid Profile Mean SD 6 .71 7.90 17.80 0.05 11.89 10. as shown in Table 4. Table 4 Assessment of Vital Signs of Patients by Observation Period Observation Period Systole Baseline (n=2624) Week 4 Difference p-value Baseline (n=2949) Week 12 Difference p-value Diastole Baseline (n=2624) Week 4 Difference p-value Baseline (n=2949) Week 12 Difference p-value Heart Rate Baseline (n=2498) Week 4 Difference p-value Baseline (n=2750) Week 12 Difference p-value 79 77 1.The systolic and diastolic blood pressures of patients decreased significantly from baseline to week 4 and week 12 of therapy.000* 11.000* 140 129 10.66 8. Heart rate likewise decreased significantly.88 13.09 9.80 8.53 0.000* 9.65 20.
33 19.54 0.34 0. Table 5 Assessment of Laboratory Results by Observation Periods Observation Period SGOT Baseline (n=1604) Week 4 Difference p-value Baseline (n=2949) Week 12 Difference p-value SGPT Baseline (n=1902) Week 4 Difference p-value Baseline (n=2239) Week 12 Difference p-value Alkaline phosphatase Baseline (n=943) Week 4 Difference p-value Baseline (n=1061) Week 12 Difference p-value Fasting Blood Sugar Baseline (n=2076) Week 4 Difference p-value Baseline (n=2398) Week 12 Difference p-value 35.81 35.93 34.18 24.000* 41.78 14.94 10.15 26.68 71.27 13.85 2.85 0.54 19.945 ns 69.62 100.82 43.000* 69.326 ns 18.47 3.33 17.23 39.817 ns 35.22 27. Table 5 shows the results.89 36.22 15.92 27.59 22.66 25.64 0.05 104.300 ns 33.47 15.There were no significant changes in SGOT and SGPT of patients.44 0.12 32.009 115.13 32. Alkaline phosphatase however showed significant increase in both 4th and 12th week observation periods.63 19.93 73.18 0.04 0.05 31.74 Lipid Profile Mean SD 7 .41 0.03 38.74 21.13 35.69 0.93 0.10 0.37 19. FBS decreased significantly at week 4 and week 12 follow-up.12 0.26 19.03 34.000* 113.
3 3.03 0.03 0.3% as shown in Table 7 Table 7 Adverse Events Experienced by Patients Compliance Yes No Not Indicated Total No.07 0.03 0.2 1. 95.03 Bloatedness Chest constriction Constipation Dyspepsia Elevated transaminase Elevated SGOT Elevated SGPT Elevated LDL Epigastric pain Epigastric discomfort Flatulence Abdominal fullness Nausea Gas pains Muscle pain Ringing of both ears The compliance of patients was high.07 0.1% event rate. Table 6 Adverse Events Experienced by Patients Adverse Events Present Absent Total Specific Events No.03 0.37 0. 2860 97 43 3000 % 95.03 0.07 0. Bloatedness was the most common.07 0.1 98.17 0.03 0.10 0.There were 34 patients who experience adverse events with 1.9 100 0.07 0. There were also elevated laboratory results noted as shown in Table 6. 34 2966 3000 11 1 2 1 2 2 3 1 2 1 5 1 1 1 2 1 % 1.4 100 8 . Most of the events were gastrointestinal related.03 0.
namely a decrease in TG by 90. increase HDL by 10-20%. HDL ≥40mg/dl. It was generally well tolerated in clinical trials.0mg/dL (20/6%). Average LDL of 109.45mg/dL).7.1mg/dL (54..91%). This may mean that the population in this study represents a high risk population while the NNHes study included the normal average adult Filipino.4mg/dL (3.15mg/dL corresponding to a 15. and triglycerides <150mg/dL.al.86 mg/dL (15.4mg/dL (8.15. LDL 119. and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report state that the recommended levels of plasma lipids are as follows: total cholesterol <200mg/ dL. Elevations in serum transaminase and creatine phosphokinase levels have been reported rarely with micronised fenofibrate.80 mg/dL (23. HDL 41.61 mg/dL (33. LDL (140.8 According to the National Nutrition and Health Survey (NNHeS) study10 in 2003-2004. ment of dyslipidemic patients as evidenced by no significant changes in the SGOT and SGPT levels. it was noted a higher mean baseline total cholesterol (232.51%).1% and was mostly gastrointestinal related. results have indicated a general trend that fibrates can reduce cardiovascular events. and total cholesterol.15%).37%). an increase in HDL by 6.66mg/dL. Similarly.8 In this study.88mg/dL). Total cholesterol decreased to a mean of 185.2%).Discussion: Results of this study revealed that Fenogal (lidose technology) can significantly decrease triglycerides.15mg/dL at 12 weeks was close to the recommended value of <100mg/dL as well as mean HDL of 56.26mg/dL at 12 weeks was greater than the prescribed value of ≥40mg/dL. In addition.8 prevalence of dyslipidemia among adult Filipinos >20 years old are as follows: total cholesterol 184. 12 The improvement in the blood pressure. Evaluation.16 have been done worldwide to determine the effectiveness of fibrates in the prevention of cardiovascular disease.14.10 In the present study. Likewise such improvements may represent an overall progress in the cardiovascular status of the patients as a consequence of the correction of the lipid levels. Based on the ATP III study. in a study done by Keating et. FBS and heart rate may reflect the patients’ overall change in lifestyle brought about by the physicians’ recommendation for such a change. Grundy et.01 mg/dL (16. However. al. and indicated that gastrointestinal disorders are the most frequent adverse events. reported that when LDL lowering drug therapy is employed in high-risk or moderately high-risk persons. triglycerides (235. 9 .83mg/dL and mean triglyceride level was 144. The results may not have reached the target of the NCEP guidelines however the mean LDL was close to the target level of 100mg/dL. These include: Helsinki Heart Study.11. Bezafibrate Infarct Prevention (BIP) trial.9 In our study. multiple (>2) risk factors with a target of <130mg/dL and with 0-1 risk factor with a target of <160mg/dL. Veterans Affairs High Density Lipoprotein Cholesterol Intervention Trial (VA-HIT). a mean LDL level of 109. these targets were achieved as early as 4 weeks of treatment and was sustained up to 12 weeks of treatment with Fenogal. HDL-C and TG levels than placebo in patients with type 2 diabetes mellitus and metabolic syndrome as well as with significantly less progression of coronary atherosclerosis than placebo.91% reduction was achieved from baseline up to the 12 weeks of study. similar changes in the lipid profile was achieved. and Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial which focused on patients with diabetes and dyslipidemia.8 Comparing with the present study. LDL-C. The adverse event rate was 1. one reason for not achieving the goal may be that the subjects may represent a mixed dyslipidemic population such as in patients with combined hyperlipidemia wherein only slight changes in LDL cholesterol are observed with fibrates. it is advised that intensity of therapy be sufficient to achieve at least a 30-40% reduction in LDL-C levels. while significantly increasing the HDL. TG by 20-50%. The study affirmed the safety of Fenogal in the treatThe 3rd Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection. and triglycerides 118.7. micronised fenofibrate was associated with significantly greater improvements from baseline in TC. This was consistent with the NCEP ATP III guidelines which reported that fibrates are generally well tolerated and the most common adverse effects were gastrointestinal. the average lipid levels and A number of trials 13. Bloatedness was the most common complaint..47mg/dL).7%). In addition we report a total cholesterol decrease by 44. and a decrease in LDL by 29. For LDL the goal is based on the risk level: CHD and CHD risk equivalent with a target of <100mg/dL. fibric acids were able to lower LDL by 5-20%. LDL.7.98mg/dL) and a somewhat similar HDL level (49. Furthermore LDL levels may rise with fibrate therapy in patients with hypertriglyceridemia.5%).
Nevertheless.14.7. Combination therapy with a statin and fibrates offers significant therapeutic advantage for the treatment of severe or refractory mixed hyperlipidemia. 10 . Niacin may be added before a fibrate is considered. Based on the study done by Fiévet et.8 Conclusion: The authors conclude that Fenogal (lidose technology) can be safely and effectively included in the armamentarium of cardiovascular medications. statin treatment substantially reduces cardiovascular morbidity and mortality. combination therapy may be considered. The trials confirm the benefit of cholesterol-lowering therapy in highrisk patients and support the ATP III treatment goal of LDL-C <100mg/dL. with or without high LDL-C levels. It supported the inclusion of patients with diabetes in the high-risk category and confirms the benefits of LDLlowering therapy in these patients. fasting blood sugar.20. future therapeutic interventions based on combination therapy. Profiles of patients who had experienced rise in alkaline phosphatase needs further investigation. when a high-risk patient has high triglycerides or low HDL-C.al. this small risk of myopathy rarely outweighs the established morbidity and mortality benefits of achieving lipid goals. practical recommendations for clinicians who care for patients with refractory mixed hyperlipidemia are needed. In this context. with limited effects on other lipid parameters. When monotherapy with a statin fails to control mixed hyperlipidemia.al. as it appears to have less risk of myopathy. but when risk is very high. Statins lower LDL cholesterol (LDL-C). One of the major recommendations for modifications is that: in high-risk persons.21.22 The Adult Treatment Panel III of the National Cholesterol Education Program issued an evidence-based set of guidelines on cholesterol management. According to Shek et. such as statins and fibrates.Some studies have also suggested that fibrates may have some significant non-cardiac side effects that other drugs do not share. Although such a combination does increase the risk of myopathy. appears particularly promising. Disclosure: The study was performed as part of the PMS (Post Marketing Surveillance) required by the BFAD (Bureau of Food and Drug) for Fenogal brand of Fenofibrate. with an incidence of approximately 0. Since its release. The purpose of this review is to provide a rationale for the combined use of statins and fibrates in the management of patients with high residual cardiovascular risk related to atherogenic dyslipidemia and persisting after single therapy. This therapeutic option extends also to patients at very high risk who have a baseline LDL-C <100mg/ dL. the recommended LDL-C goal is <100mg/ dL. Fibrates decrease cardiovascular morbidity. Fibrates may also be appropriate for use in patients at risk of acute pancreatitis due to high triglyceride levels. and heart rate were significantly lowered. It further confirms that older persons benefit from therapeutic lowering of LDL-C. Statinfibrate combination therapy must be undertaken cautiously and only after careful risk-benefit analysis. a higher incidence of myopathy has been reported with statin monotherapy. Moreover. Reducing the residual cardiovascular risk in patients treated with statins requires addressing multiple lipid goals. there were 5 major clinical trials of statin therapy with clinical end points have been published.12%. Fibrates improve atherogenic dyslipidemia characterized by high triglyceride and/ or low HDL cholesterol levels and elevated concentrations of small dense LDL particles. consideration can be given to combining a fibrate or nicotinic acid with an LDL-lowering drug.17. an LDL-C goal of <70mg/dL is a therapeutic option. especially in patients with the metabolic syndrome.18. Patient counseling on the risks and warning signs of myopathy is extremely important.19. Recommendation: The authors recommend the use of Fenogal (lidose technology) to be included to optimize medical therapy in patients with dyslipidemia. Even systolic and diastolic blood pressures. Therapeutic lifestyle changes remain an essential modality in clinical management.
Insulin Resistance and cardiovascular events with low HDL cholesterol. Micronised Fenofibrate: an Updated Review of its Clinical Efficacy in the Management of Dyslipidaemia. Am J Cardiovasc Drugs. Fraioli A. CG Ericson et al. Effects of Adding Fenofibrate (200 mg/ day) to Simvastatin (10 mg/day) in Patients with Combined Hyperlipidemia and Metabolic Syndrome. Adkins JC. Pigna G. Grundy SM. Hernández G. 02-5215. Update on the Clinical Utility of Fenofibrate in Mixed Dyslipidemias: Mechanisms of Action and Rational Prescribing. Kardiol Pol. F Venandria. Staels B. 106:3369 15. Fiévet C. Grundy SM. 2004 Oct.48(1):47-54 . et al. Garcia-Garcia AB. Shek A.11:257-263 3. Ormrod D. Casals E. Drugs 1996 Nov. SJ Robins. The Veterans Affairs HDL Intervention Trial (VAHIT). Am J Cardiol. Comparison of Atorvastatin Versus Fenofibrate in Reaching Lipid Targets and Influencing Biomarkers and Endothelial Damage in Patients with Familial Combined Hyperlipidemia. Zambón D. 2003 Apr 15. 2004 Jun. Drugs. Cater NB. Vázquez M.51(6):982-1018 7. Montali A. Vega GL. Barradell LB. Evaluation. Keating GM. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection. Cleeman JI. Grundy SM. Bezafibrate. et al. and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report. Becker D. Kłosiewicz-Latoszek L. Nutrition and Heath Status of Filipino Adults [Excerpts from the National Nutrition and Health Survey (NNHes)]: 2003-2004 for the Multisectoral Task Force on NNHes: 2003-2004. 2009. Clark L. Szostak WB. Type 2 Diabetes Mellitus.9(6):401-9 19. Wiśniewska B. Letizia C. Circulation. Beneficial Effects of the Addition of Fenofibrate to Statin Therapy in Patients with Acute Coronary Syndrome After Percutaneous Coronary Interventions. Goa KL. Białobrzeska-Paluszkiewicz J. Grundy SM. Derosa G.12(2):91-96 4. and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Executive Summary. M Farnier. Vasc Rsk and Hlt Mgmt 2008. HB Rubins. Becker D. FNRI-DOST 11. U De Faire. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection. Statin-fibrate Combination Therapy. and Coronary Heart Disease: A 12-month. NIH Publication No. Ciccarelli L. MC Chag et al. Filipchuk N. Merz CN. 2002. Grzybowska B. Micronised Fenofibrate: a Review of its Pharmacodynamic Properties and Clinical Efficacy in the Management of Dyslipidaemia. Retardation of Coronary Atherosclerosis : The Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT) and Other Angiographic Trials. Roggeri DE. Double-blind. HD Shah. Meguro S.60(6):567-77 12. Randomized. Ma PT.110:227-239 10. Rodriguez-Villar C. Vnitr Lek. An Update of its Pharmacology and use in the Management of Dyslipidemia. Randomized Crossover Study of Gemfibrozil Versus Lovastatin in Familial Combined Hyperlipidemia: Additive Effects of Combination Treatment on Lipid Regulation.4(5):991-1000 2. Sanllehy C. Mastrantoni M. et al. Comparison of Combined Statin-Fibrate Treatment to Monotherapy in Patients with Mixed Hyperlipidemia. May 2001 8.26(5):1513-1517 14. Antonini TM.52(1):80-4 17. Exp Clin Cardiol 2007. Coordinating Committee of the National Cholesterol Education Program. a MJ.91(8):956-60 22.26(10):1599-607 20. KH Parikh. Antonini R. Keating GM. Faulds D. Implications of Recent Clinical Trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines.9(6):401-9 18. September 2002 9. Gemfibrozil: A Reappraisal of its Pharmacological properties and Place in the Management of Dyslipidaemia. Spencer CM. Evaluation.102(suppl):34L-40L 16. Plosker GL. 2009.54(4):615-33 13. Maddaloni M. Clin Ther. After the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) Study: Implications for Fenofibrate. NIH Publication No. Clark L. 1997 Oct. Comparison of Fluvastatin + Fenofibrate Combination Therapy and Fluvastatin Monotherapy in the Treatment of Combined Hyperlipidemia. Sol JM. Metabolism 1999 Jan. Cardiovascular Drugs and Therapy 1997. J Widimsky.56(11):1534-41 5. Cicero AE. Kardiol Pol.Bibliography: 1. Bertone G. Fenofibric Acid: In Combination Therapy in the Treatment of Mixed Dyslipidemia. et al. Drugs 1996 Jun. Diabetes Care 2003. Laguna JC. 2006. Ros E. Am J Cardiovasc Drugs. Controlled Trial. Piccinni MN.52(5):725-53 6. Arca M. Luigi P. Unconvincing Results of Fenofibrates in Diabetic Patients. FM Sacks. Am J Cardiol 2008.60(6):567-77 21. C Duante et al. Barradell LB. Circulation 2004. Stolarska I. The FIELD study Presented and Published. 2004 Jun. Combination Therapy of Statins and Fibrates in the Management of Cardiovascular Risk. Metabolism 2007 Nov. 01-3670. Yang LP.
73 0.47 0.17 0.13 0.93 0.33 0.03 0.03 1.03 3.27 0.07 0.10 62.17 0.03 0.33 1.30 0.93 0.10 0.73 0.07 1.03 19.03 1.07 0.07 0.10 0.63 0.56 .03 1.Appendix A.60 0.53 0.20 2.17 0. 1 104 5 1 52 2 1 49 8 3 5 3 3 10 58 6 62 2 58 5 18 9 21 2 1 4 14 31 588 1 46 10 1 22 3 1877 % 0.10 0.70 0.60 0.47 1. Previous Medication of Patients for Dyslipidemia Medications Afordel Atorvastatin Cholestad Ciprofibrate Crestor Ezetemibe Ezetrol Fenofibrate Fenoflex Fenogal Fibrafen Fibrate Fluvastatin Forcad Gemfibrozil Lescol Lipanthyl Lipigem Lipitor Lipway Lopid Niacin Nubrex Omacor Orlistat Pravastatin Reducel Rosuvastatin Simvastatin Vamstat Vidastat Vytorin Ximvast Zocor Unrecalled None indicated No.
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