微粒化非诺贝特治疗高脂血症疗效评价

评价微粒化非诺贝特治疗高脂血症(Ⅱ_b型12例、Ⅳ型22例)的疗效及耐受性,服用微粒化非诺贝特200mg,每晚一次,观察8周,治疗前后比较,治疗8周后,Ⅱ_b型TC下降15％(P<0.05),Ⅱ_b和Ⅳ型TG分别下降55.5％、67.6％(P<0.01、P<0.01),尿酸下降31.9％。结论:微粒化非诺贝特治疗Ⅱ_b、Ⅳ型高脂血症有效,且有部分降低尿酸作用。     

微粒化非诺贝特治疗高脂血症疗效和耐受性

上海市多中心、开放性、自身比较，观察微粒化非诺贝特２００ｍｇ，每晚一次，治疗１３１例高脂血症病人４～８周的疗效和耐受性。男性７６例，女性５５例，平均年龄５６．２±９．７３岁，所属高血脂类型：Ⅱａ型２６例，Ⅱｂ型５３例，Ⅳ型５２例。治疗８周之后，Ⅱａ和Ⅱｂ型患者血清总胆固醇明显降低（平均降低２０％，Ｐ＜０．０１），Ⅱｂ和Ⅳ型患者血清甘油三酯明显降低（平均降低６０％～６３％，Ｐ＜０．０１），未出现严重不良反应，结论：微粒化非诺贝特特别适用于治疗Ⅱｂ和Ⅳ型高脂血症患者。４例合并有高尿酸血症者，治疗８周后，血尿酸平均降低５９％。     

非诺贝特与氟伐他汀治疗原发性高脂血症的对比观察

原发性高脂血症患者46例随机分成二组，一组23人，口服非诺贝特每次100mg，每日三次，另一组23人，口服氟伐他汀200mg每晚一次，疗程均为四周。与服药前比，服非诺贝特四周后血清TC、TG、LDL－C分别下降12．77％，43．32％，12．54％，HDL－C升高22．22％；服氟伐汀四清TC、TG、LDL－C分别下降16．57％，22．35％，12．80％，HDL－C升高15．13％，两组间比较，非诺贝特降TG优于氟伐他汀，氟伐他汀降TC优于非诺贝特，均有明显的统计学差异（P＜0．05）。     

微粒化非诺贝特调脂效应的临床观察(摘要)

为了评价微粒化非诺贝特的疗效及耐受性，选择３０例原发性高脂血症患者，服微粒化非诺贝特２００ｍｇ，每日一次，疗程为２个月，仅１例胃部不适及１１例心慌，不影响服药。取空腹１２ｈ肘静脉血自凝，纤维蛋白原用１０％草酸钾防凝，４ｈ内分离血清，置于－３０℃低温贮...     

微粒化非诺贝特降脂疗效的临床观察

采用前后比较的方法观察微粒化非诺贝特２００ｍｇ，每晚一次，治疗５６例高脂血症患者８周的调脂疗效和安全性。５６例高脂血症的分型为：Ⅱｂ型１４例，Ⅳ型４２例。治疗８周末，Ⅱｂ型患者血清总胆固醇降低；Ⅱｂ型和Ⅳ型患者血清甘油三酯明显降低，分别为５５％和４３％；此外，两型高脂血症患者的ＨＤＬ－Ｃ水平均有明显升高，ＡｐｏＢ水平明显降低，说明该药具有全面调脂作用。     

自身交叉试验比较非诺贝特与辛伐他汀降脂疗效及对ApoA, …

目的：观察辛伐他汀和微粒化非诺贝特治疗原发性高脂血症病人降脂疗效及对ＡｐｏＡ，ＡｐｏＢ的影响。方法：３０例原发性旨血症患者随机被分为微粒化非诺贝特（Ｆ，２００ｍｇ／日）组和辛伐他汀（５ｍｇ／日）组，进行自身交叉试验。结果：治疗４周后，两者降ＴＣ、ＴＧ均有显著的疗效，但Ｓ组以降低ＴＣ和ＡｐｏＢ为主（分别为２０．７％和２０％），Ｆ组以降ＴＧ和升ＨＤＬ为主（分别为４９．７％和２９．５％），并有显著降尿酸     

微粒化非诺贝特与苯扎贝特治疗老年高脂血症和高尿酸血症的比较

目的 比较两种苯氧芳酸衍生物微粒化非诺贝特(力平脂)与苯扎贝特(必降脂)治疗高脂血症和高尿酸血症的疗效。方法 随机分成两组，每组各30例。力平脂组男性21例，女性9例，年龄73．2±4．92岁，剂量200毫克；必降脂组男性23例，女性7例．年龄71.5±4．29，剂量400毫克，均每晚口服一次，持续八周。结果 两组药物治疗均有显的降低总胆固醇和甘油三脂的作用，其中力平脂也有明显的降低血尿酸的作用。均未出现严重的不良反应。结论 微粒化非诺贝特适用于治疗老年高脂血症合并有高尿酸血症的患，安全、有效。     

国产与进口微粒化非诺贝特治疗高脂血症的成本-效果分析

目的对国产与进口微粒化非诺贝特治疗高脂血症的成本-效果进行评价。方法选取2011年8月至2012年8月在我院住院部及门诊部治疗的高脂血症病例,排除肝胆、胰腺及其他影响血脂代谢的疾病,从中随机抽取32例患者给予国产非诺贝特胶囊（Ⅱ）（即国产微粒化非诺贝特）治疗（其中Ⅳ型26例,1Ib型6例）为A组。抽取32例患者给予进口微粒化非诺贝特治疗（其中Ⅳ型26例,Ⅱb型6例）为B组。两组患者治疗3个月后进行回访。运用药物经济学成本-效果分析法计算治疗成本并进行分析和评价。结果国产和进口微粒化非诺贝特在治疗高脂血症时的总有效率分别为5．1％和4．5％,无统计学差异（P〉0．05）;不良反应发生率分别为9．3％和6．3％,无统计学差异（P〉0．05）。以临床总有效率计算成本-效果分别为2．64和5．41,有统计学差异（P〈0．05）。结论国产微粒化非诺贝特治疗高脂血症较进口微粒化非诺贝特更具有成本一效果优势。     

非诺贝特对糖尿病肾病的前瞻性研究

将伴有高脂血症的早期糖尿病肾病患100例随机分组,保持原治疗方案不变,治疗组每天加服微粒化非诺贝特0．2g,对照组不加服。结果6个月以后发现治疗组血胆固醇、甘油三酯、LDL－C、脂蛋白（a)、纤维蛋白原、尿酸及β2微球蛋白、尿微量白蛋白排泄率明显降低,HDL－C明显上升。而对照组无显变化。结论：微粒化非诺贝特除了可调整脂代谢紊乱外,对早期糖尿病肾病亦有良好疗效。     

非诺贝特对糖尿病肾病的前瞻性研究

将伴有高脂血症的早期糖尿病肾病患者100例随机分组,保持原治疗方案不变,治疗组每天加服微粒化非诺贝特0.2g,对照组不加服.结果6个月以后发现治疗组血胆固醇、甘油三酯、LDL-C、脂蛋白(a)、纤维蛋白原、尿酸及β2微球蛋白、尿微量白蛋白排泄率明显降低,HDL-C明显上升.而对照组无显著变化.结论微粒化非诺贝特除了可调整脂代谢紊乱外,对早期糖尿病肾病亦有良好疗效.     

微粒化非诺贝特调节老年代谢综合征患者血脂及尿酸代谢的研究

目的观察微粒化非诺贝特(非诺贝特)对老年代谢综合征患者血脂及尿酸代谢的影响,并探讨其潜在机制。方法入选131例老年代谢综合征患者,同时伴有高TG及高尿酸血症,每日顿服非诺贝特胶囊200 mg,疗程为4周。观察治疗前和治疗4周后主要血脂参数、血尿酸、24 h尿尿酸的变化及不良反应。结果非诺贝特治疗4周后:(1)患者血清TG下降最为显著,与基线比较下降49%,血清HDL-C水平升高18%,此外患者血清TC和LDL-C水平也有一定程度的下降(分别为11%和14%);(2)患者血尿酸水平由(472.5±74.8)μmol/L降至(325.0±82.1)μmol/L,下降幅度为31.2%。其中男性患者血尿酸水平下降32.6%,女性患者下降29.7%,差异均有统计学意义(P<0.01)。(3)患者24 h尿尿酸排泄明显增多,由(2 885.2±502.7)μmol/L增加至(3 701.7±768.2)μmol/L,排泄增加28.8%,其中男性24 h尿尿酸排泄高于女性(P<0.01)。结论非诺贝特具有同时改善老年代谢综合征患者的血脂及尿酸代谢异常的双重疗效,能明显促进尿尿酸排泄,且该作用与性别无关。     

The effect of micronised fenofibrate on paraoxonase activity in patients with coronary heart disease

OBJECTIVE: To evaluate the effect of micronised fenofibrate on serum paraoxonase (PON) and lipoprotein levels in coronary heart disease patients with type IIb hyperlipidemia. PATIENTS AND METHODS: Fifty-two patients were investigated for the three-month effect of 200 mg per day micronised fenofibrate on the serum enzyme activity and concentration of PON and their relationship with serum lipids, high-density lipoprotein (HDL-C) parameters. RESULTS: Serum paraoxonase activity was lower in CHD patients with type IIb hyperlipoproteinemia. During the three-month study it was observed that following treatment with micronised fenofibrate, serum triglyceride and cholesterol levels decreased, while HDL-C increased significantly (p<0.001). Low-density lipoprotein (p<0.05) and apolipoprotein B-100 (p<0.01) decreased, while HDL constituent apolipoprotein A-I (p<0.05) increased after micronised fenofibrate treatment. The HDL-associated paraoxonase specific activity increased significantly (p<0.05). To assess whether the increased PON activity was due to elevated HDL and apoA-I level, we standardized PON activity for HDL and apoA-I concentrations. The standardized values for HDL (PON/HDL) increased (p<0.05) while the PON/apoA-I ratio did not change significantly. CONCLUSION: Three months of treatment with micronised fenofibrate is thought to normalize lipid profile and improve antioxidant status by increasing serum paraoxonase activity in these patients.     

Efficacy and safety of micronised fenofibrate in a randomised double-blind study comparing four doses from 200 mg to 400 mg daily with placebo in patients with hypercholesterolemia

The aim of this study was to evaluate the efficacy on LDL-cholesterol (LDL-C) of micronised fenofibrate given for three months at doses ranging from 200 to 400 mg once daily, compared with placebo. A double-blind, randomised, parallel-group, multi-centre trial was performed in four centers of France in 340 hypercholesterolemic patients (163M, 177F) aged 18-75 years. After a 2-3 month single-blind run-in period on placebo and diet, patients with LDL-C greater than or equal to 4.65 mmol/l (180 mg/dl) maintained on the same diet throughout the study were randomly allocated to placebo or to 200, 267, 340 or 400 mg micronised fenofibrate, given once daily with the evening meal for 3 months. LDL-C, total cholesterol (TC), total triglycerides (TG) and apolipoprotein B (Apo B) significantly decreased compared with placebo in all four fenofibrate groups. For all randomised patients, the decrease in the fenofibrate groups ranged from 31.6-38.8% for LDL-C, 24.5-31.9% for TC, 26.7-40.8% for TG, and 27.3-35.0% for Apo B. An increase in HDL-cholesterol of 4.1-8.2% was observed in the fenofibrate groups, but did not reach statistical significance. Lipid values in the placebo group remained unchanged. The therapeutic goal of LDL-C<3.36 mmol/l (130 mg/dl) was reached in 27% in the 200 mg group and increased to 56% in the 300 mg group. There were no major clinical or biological adverse events in the dose interval from 200 mg to 400 mg of micronised fenofibrate per day. This study showed treatment for 3 months with micronised fenofibrate at doses up to 400 mg per day is effective and can reduce LDL-cholesterol up to 30% allowing further evaluation of these doses on longer trials.     

Effects of micronized fenofibrate and vitamin E on in vitro oxidation of lipoproteins in patients with type 1 diabetes mellitus

OBJECTIVE: The primary objective was to compare the antioxidant activity of micronised fenofibrate 200 mg to 400 IU of vitamin E and placebo, on the LDL and VLDL particles of patients with type 1 diabetes. The secondary objective was to investigate the possible synergy between micronized fenofibrate and vitamin E and to compare the efficacy of these treatments on lipids. METHODS: A double-blind, placebo-controlled trial in which patients were randomised into three treatment groups after a wash-out period of 8 weeks: the placebo group (Pla/Pla-group) in which patients received placebo during two consecutive periods of 8 weeks, the vitamin E group (Vit E/Vit E-group) in which patients received Vitamin E during two consecutive periods, and the fenofibrate/Vitamin E group (Fen/Fen + Vit E-group) in which patients received fenofibrate during the first period, followed by fenofibrate and vitamin E during the consecutive period. Blood samples taken at each visit, were analysed for routine biochemistry, blood lipids and copper mediated lipid peroxidation in vitro. RESULTS: The lag time of the non-HDL lipoprotein oxidation increased in the group given fenofibrate. The lag-time increased further when fenofibrate and vitamin E were given in association. (This reached significance in the intention-to-treat population, P = 0.034). The AUC of TBARS formation in the Vit E/Vit E group decreased after the first period, but this effect was not enhanced by continuing vitamin E for another 8 weeks. The AUC of TBARS formation did not change significantly after the administration of fenofibrate. Only after the second period, when vit E was given in association, the AUC of TBARS formation decreased significantly (P = 0.004). Fenofibrate caused a significant decrease in total and LDL-cholesterol and triglycerides (P < 0.05). In contrast, vitamin E had no effect on lipids. CONCLUSIONS: The combination of micronized fenofibrate 200 mg/day and vitamin E 400 IU/day tended to increase the resistance of non-HDL lipoproteins to copper-mediated oxidation, shown by a prolongation of the lag-time. Vitamin E administration only, decreased the oxidation of non-HDL lipoproteins shown by a reduction of TBARS formation. This protective effect of vitamin E tended to be amplified by micronized fenofibrate.     

Comparison of the efficacy of atorvastatin and micronized fenofibrate in the treatment of mixed hyperlipidemia.

OBJECTIVE: To evaluate and compare the influences of micronized fenofibrate and atorvastatin on serum lipid profile, including lipoprotein(a) levels, and on fibrinogen levels in a large group of patients with primary mixed hyperlipidemia (serum total and low-density lipoprotein cholesterol levels > 240 and 160 mg/dl, respectively, and serum triglyceride level > 200 mg/dl). METHODS: This was a 16-week, open-label, parallel-design study conducted in our lipid clinic. After a 6-week dietary baseline phase, we implemented a treatment phase, during which patients received 10 mg/day atorvastatin (n = 45) or 200 mg/day micronized fenofibrate (n = 46) for 16 weeks. Patients were assigned to one of the drugs in sequential orders. Serum lipid profiles, including levels of lipoprotein(a) and fibrinogen, as well as muscle and liver enzymes, were measured during screening, and during weeks -4, -2, 0, 8, and 16 of the treatment period. RESULTS: Atorvastatin was more effective than was micronized fenofibrate at lowering levels of total and low-density lipoprotein cholesterol, whereas fenofibrate was more effective at lowering levels of triglycerides, and raising levels of high-density lipoprotein cholesterol and apolipoprotein A1. However, micronized fenofibrate could significantly decrease plasma fibrinogen levels, whereas atorvastatin evoked a small increase. CONCLUSION: Both atorvastatin in small doses and micronized fenofibrate are effective for improving serum lipid profiles of patients with mixed hyperlipidemia. However, there are considerable differences between the two drugs concerning their influences on plasma fibrinogen levels.     

Both fenofibrate and atorvastatin improve vascular reactivity in combined hyperlipidaemia (fenofibrate versus atorvastatin trial--FAT).

OBJECTIVE: It has been repeatedly proven that statins improve endothelial function in isolated hypercholesterolaemia but there is far less evidence in the case of combined hyperlipidaemia. Studies assessing the effects of fibrates on endothelium have been neglected. Therefore, we conducted a trial in which the effects of fenofibrate and atorvastatin monotherapy on both endothelium-dependent vascular reactivity and biochemical parameters were compared in patients with combined hyperlipidaemia. METHODS: 29 otherwise healthy males (aged 47.4+/-7.8 years) with combined hyperlipidaemia (total cholesterol 7.55+/-1.20 mmol/l, triglycerides 5.41+/-4.54 mmol/l) were included into the randomised, single-blind, cross-over study to receive either 200 mg of micronised fenofibrate or 10 mg of atorvastatin daily--each of the drugs for a period of 10 weeks. Analysed biochemical parameters were as follows: serum total-, LDL- and HDL-cholesterol, apolipoproteins A-I and B, triglycerides, fibrinogen, uric acid, C-reactive protein (CRP), insulin, and homocysteine. Endothelial function was investigated by duplex Doppler ultrasonography at the brachial artery. Two indices of endothelial-dependent postischaemic changes were used - the recently introduced index of peak blood flow (PBF) representing the level of reactive hyperaemia and traditional flow-mediated dilatation (FMD). RESULTS: We observed a small improvement in FMD after both fenofibrate and atorvastatin (from 2.26% to 2.98% and 2.87%, respectively; NS). PBF increased from 448 ml/min to 536 ml/min after fenofibrate (P=0.04) and to 570 ml/min after atorvastatin (P=0.03). The effects of both fenofibrate and atorvastatin on endothelial function did not differ significantly (P-values of 0.82 and 0.47 for FMD and PBF, respectively). Significant correlations (P<0.01) between the changes of vascular reactivity and biochemical indices were found between FMD and CRP (r=-0.60) and between both FMD and PBF, and insulinaemia (r=-0.48 and -0.56, respectively) only during treatment with fenofibrate. CONCLUSIONS: Both fenofibrate and atorvastatin significantly improved endothelium-dependent vascular reactivity without mutual difference. The PBF was superior to FMD for the detection of this improvement. The beneficial effect of both drugs did not correlate with the change of lipid profile during therapy. The improvement of vascular reactivity during treatment with fenofibrate (opposed to atorvastatin) was related to the reduction of indirect marker of chronic vessel wall inflammation and of insulin resistance. The PBF was more reproducible than FMD because of considerably lower intra-subject variability.     

Micronized fenofibrate, decreased triglyceride levels, total cholesterol and LDL fractions in serum

Elevated serum level of triglycerides is a classic indication for fibrates. Micronized fenofibrate is hypolipemic drug with proven safety and efficacy in a view of triglycerides reduction, but according to few papers published so far on the subject is also effective in decreasing elevated total and LDL cholesterol. The aim of study was to confirm results obtained from these few previous studies. Forty seven persons with lipid disturbances (25 males and 22 females, age range 34-71 yrs. mean 48.0) entered the study. Thirty two patients had a history myocardial infarction and fifteen persons without clinical symptoms of heart diseases. All of them were treated with micronized fenofibrate 200 mg daily. Micronized fenofibrate decreased serum concentration of total cholesterol by 13.4% (p < 0.01), LDL cholesterol by 21.2% (p < 0.001) and triglycerides by 39.5% (p < 0.001) in whole group of patients. Most beneficial effects were obtained in persons with mixed hyperlipidemia: reduction of total cholesterol, triglycerides and LDL cholesterol serum levels was 22.4% (p < 0.01), 52.5% (p < 0.0001), 25.4% (p < 0.01), respectively. In individuals with hypercholesterolemia a reduction of total cholesterol by 11% (p < 0.05) and LDL cholesterol by 15.4% (p < 0.05) was observed. In the group with hypertriglyceridemia or mixed hyperlipidemia reduction of serum triglycerides concentration by 33.5% (p < 0.05) was achieved. No significant change in serum HDL cholesterol level in any group was observed. The treatment with micronized fenofibrate was well tolerated. Our study shows that this drug is safe and seems to be effective in some cases with increased serum total and LDL cholesterol level as well.     

微粒化非诺贝特对原发性高血压颈动脉内膜中层厚度与脑血流动力学的影响

目的　探讨微粒化非诺贝特对原发性高血压患者颈动脉内膜中层厚度 (IMT)与脑循环动力学 (CVA)的影响。方法　分别对 2 0 7例原发性高血压患者应用微粒化非诺贝特进行为期 2 4个月的治疗和对照 ,观察治疗前后患者颈动脉超声、脑循环动力学及血脂等指标的变化。结果　治疗组 2 4个月后颈动脉IMT基本保持稳定 ,IMT/内径 (D)比率及颈动脉粥样硬化斑块发生率均比治疗前有明显降低 (P <0 0 5 ) ;脑循环动力学指标较治疗前明显改善。结论　在有效降压治疗的同时加用微粒化非诺贝特治疗 ,对原发性高血压患者延缓颈动脉粥样硬化的进展和改善脑循环动力学有良好效果。     

Rosuvastatin and fenofibrate alone and in combination in type 2 diabetes patients with combined hyperlipidaemia

The aim of this study was to evaluate the effects of rosuvastatin and fenofibrate alone and in combination in type 2 diabetes associated with combined hyperlipidaemia. A total of 216 patients with total cholesterol >/=200 mg/dl (>/=5.17 mmol/l) and triglycerides >/=200 and <800 mg/dl (>/=2.26 and <9.03 mmol/l) were randomised to one of two placebo groups, rosuvastatin 5 mg or rosuvastatin 10 mg for 6 weeks (fixed-dose phase). During the subsequent 18-week dose-titration phase, one placebo group received titrated rosuvastatin 10, 20 and 40 mg (placebo/rosuvastatin); one placebo group received titrated fenofibrate 67 mg once, twice and three times daily (placebo/fenofibrate); and patients receiving 5 or 10 mg rosuvastatin received titrated fenofibrate as above (rosuvastatin 5mg/fenofibrate and rosuvastatin 10 mg/fenofibrate groups). Doses were increased at 6-week intervals if low-density lipoprotein (LDL) cholesterol remained >50 mg/dl (>1.3 mmol/l). At 24 weeks, the placebo/rosuvastatin group and placebo per fenofibrate group had triglyceride reductions of 30.3% versus 33.6%, respectively (P = NS), and LDL cholesterol was reduced by 46.7% in the rosuvastatin group and increased by 0.7% in the fenofibrate group (P < 0.001). The triglyceride reduction in the rosuvastatin 10 mg/fenofibrate group (47.1%) was significantly greater than in the placebo/rosuvastatin group (P = 0.001), with no significant differences in other lipid measures found between these two groups. No significant differences in effect on high-density lipoprotein (HDL) were observed among treatment groups. In the fixed-dose phase, rosuvastatin 5 and 10 mg reduced triglycerides by 24.5 and 29.5%, respectively, and decreased LDL cholesterol by 40.7 and 45.8%, respectively. All treatments were well tolerated. These results indicated that rosuvastatin produces marked reductions in triglycerides and LDL cholesterol when used alone or in combination with fenofibrate in type 2 diabetes patients with elevated cholesterol and triglyceride levels and may constitute a valuable treatment option in the diabetic population.     

Comparison of combined statin-fibrate treatment to monotherapy in patients with mixed hyperlipidemia

BACKGROUND: Statins are the preferred drugs for the treatment of hypercholesterolemia, and fibrates for hypertriglyceridemia. In patients with mixed hyperlipidemia, monotherapy with one of these agents may not be effective and combined treatment may be preferable. AIM: To compare retrospectively the efficacy and safety of combined statin-fibrate treatment in patients with mixed hyperlipidemia in whom previous monotherapy with one of these agents occurred ineffective. METHODS AND RESULTS: The initial study group consisted of 327 patients who received micronised fenofibrate and 93 patients who received simvastatin for 12 months. Both agents caused significant changes in lipid profile. Following fibrate therapy, total cholesterol (TC), LDL-cholesterol (LDL-C) and triglyceride (TG) levels decreased by 27.9%, 28.2% and 58%, respectively, and following simvastatin therapy by 33.6%, 42.8% and 37.5%, respectively. The HDL-cholesterol (HDL-C) level increased after fenofibrate by 14.8% and remained unchanged following simvastatin therapy. The TC/HDL-C ratio decreased following fenofibrate by 35.6%, and following simvastatin by 35.3%. In some patients the required reduction in lipid parameters was not achieved fenofibrate or simvastatin. Subsequently, 93 patients underwent combined therapy by adding a second agent (simvastatin in a dose of 20 mg/day or fenofibrate in a dose of 200 mg per day) which was continued for another 12 months. The addition of simvastatin to fenofibrate decreased TC, LDL-C and TG levels by 35.5%, 42.1% and 59.6%, respectively in comparison to before treatment volumes. HDL-C level was increased by 11.1%, and TC/HDL-C ratio decreased by 45.3%. The addition of fenofibrate to simvastatin decreased TC, LDL-C and TG levels by 39.3%, 48.9% and 51,6%, respectively. HDL-C level was increased by 13.4%, and TC/HDL-C ratio decreased by 49.3%. No clinical side effects nor an increase in the transaminase levels, requiring termination of the treatment, were observed. CONCLUSIONS: Combined therapy with 20 mg of simvastatin and 200 mg of micronised fenofibrate is highly effective and safe in patients with mixed hyperlipidemia.