氟伐他汀联合非诺贝特治疗混合性高脂血症的可行性探讨

目的观察氟伐他汀联合非诺贝特治疗混合性高脂血症的临床效果。方法选择2007年1月至2008年12月南通市老年康复医院心内科门诊混合性高脂血症患者180例,随机分为氟伐他汀组、非诺贝特组、联合用药组各60例;氟伐他汀组每晚口服40mg氟伐他汀、非诺贝特组每晚口服非诺贝特200mg、联合用药每日清晨口服非诺贝特200mg,晚口服氟伐他汀20mg,均用至12周。观察血脂参数变化、疗效评价、药物主要不良反应。结果三组TC、LDL-C、TG治疗前无差异(P>0.05),氟伐他汀组治疗后TC、LDL-C均有显著性下降(P<0.05),TG变化不明显(P>0.05);非诺贝特组治疗后TG有显著性下降(P<0.05),TC、LDL-C变化不明显(P>0.05);联合用药组TC、LDL-C、TG均有显著性下降(P<0.05)。联合用药组临床控制(显效、好转)83.3%(50/60)高于氟伐他汀组的68.3%(41/60)和非诺贝特组的65.0%。三组患者血清CK、肝肾功能等参数均无明显变化,未出现肌病症状,无1例退出或终止。结论氟伐他汀联合非诺贝特对混合性高脂血症具有良好的安全性与耐受性,具有临床应用可行性。     

非诺贝特与辛伐他丁治疗高脂血症的临床疗效对比研究

目的探讨非诺贝特及辛伐他丁对混合型高脂血症的疗效作用差异,为临床用药提供指导。方法将在我院接受治疗的54例混合型高脂血症患者随机分为联合治疗组、非诺贝特组和辛伐他丁组各18例,联合治疗组组患者使用非诺贝特联合辛伐他丁进行治疗,非诺贝特组使用非诺贝特进行治疗,辛伐他丁组使用辛伐他丁进行治疗,检测血清总胆固醇（TC）、三酰甘油（TG）、高、低密度脂蛋白（HDL-C、LDL-C来评价药物疗效差异。结果非诺贝特组LDL-C的含量与联合治疗组比较具有显著性差异（＊＊P〈0.01）,辛伐他丁组与联合治疗组比较TG、HDL-C含量具有显著性差异（＊P〈0.05或＊＊P〈0.01）;与非诺贝特组比较,辛伐他丁组TG、HDL-C、LDL-C含量具有显著性差异（#P〈0.05）。结论非诺贝特较辛伐他丁其降低TG、升高HDL-C作用较强,对TC也具有一定的降低作用,辛伐他丁较非诺贝特其降低TC、降低LDL-C作用较强。     

应用瑞舒伐他汀联合非诺贝特治疗不稳定心绞痛合并高血脂症的疗效分析

目的探讨应用瑞舒伐他汀联合非诺贝特治疗不稳定心绞痛合并高血脂症的疗效。方法 84例不稳定心绞痛合并高血脂症患者分别用瑞舒伐他汀治疗(对照组,42例)与瑞舒伐他汀联合非诺贝特治疗(治疗组,42例),评价比较两组疗效。结果治疗组患者治疗前后的TC、TG及LDL-C改善程度优于对照组(P<0.05),治疗组患者治疗总有效率为90.48%,显著高于对照组的71.83%(P<0.05)。结论瑞舒伐他汀联合非诺贝特治疗不稳定心绞痛合并高血脂症的疗效确切,临床应用价值更高。     

非诺贝特与阿托伐他汀治疗高脂血症及高尿酸血症的效果比较

目的观察微粒化非诺贝特与阿托伐他汀对高脂血症合并高尿酸血症的治疗效果。方法55例高血脂症合并高尿酸血症患者随机分为两组。治疗组30例给予微粒化非诺贝特200mg／d;对照组25例给予阿托伐他汀10mg／d。两组患者均给治疗8周。比较两组临床疗效、血脂和血尿酸水平及不良反应。结果两组治疗后与治疗前比较,甘油三酯（TG）、总胆固醇（TC）差异均有统计学意义。治疗后治疗组与对照组TG差异有统计学意义。治疗组降低血尿酸效果好于对照组。两组均无严重不良反应。结论非诺贝特与阿托伐他汀均可用于高血酸症及高脂血症治疗,短时间内使血脂达标,减少脑血管病的危险因素。     

辛伐他汀与非诺贝特治疗2型糖尿病合并高血脂临床观察

目的:探讨辛伐他汀与非诺贝特治疗2型糖尿病合并高血脂症临床的疗效.方法:将120例2型糖尿病合并高血脂症患者随机分为3组;辛伐他汀组、非诺贝特组、辛伐他汀与非诺贝特组;分别用药观察2型糖尿病合并高血脂症的疗效.结果:各组治疗后血清TC、LDL-C、TG均比治疗前下降,HDL-C比治疗前上升.联合用药组:TC、LDL-C、TG三项水平下降的幅度及升高HDL-C的幅度均高于单独用药的两组.结论:辛伐他汀与非诺贝特治疗2型糖尿病合并高血脂症临床的疗效满意.     

对混合性高脂血症实施阿托伐他汀与非诺贝特治疗的临床效果

目的：观察混合性高脂血症实施阿托伐他汀与非诺贝特治疗的临床效果。方法：选取2012年3月～2015年2月东莞市黄江医院收治的混合性高脂血症患者106例作为研究对象,按照计算机数字法分为对照组（n=53）和治疗组（n=53）,对照组采用阿托伐他汀治疗,治疗组采用阿托伐他汀联合非诺贝特治疗,比较两组治疗效果。结果：经过1个疗程的治疗,两组TG、TC、LDL-C、HDL-C等血脂指标与治疗前相比,差异明显（P＜0.05）,治疗组TG、LDL-C改善情况优于对照组（P＜0.05）,治疗总有效率96.2%明显高于对照组79.3%,组间差异具有统计学意义（P＜0.05）。结论：混合性高脂血症实施阿托伐他汀与非诺贝特治疗效果确切,协同作用良好,可显著改善临床症状,提高调脂效果,具有临床推广价值。     

辛伐他汀和微粒化非诺贝特对混合型高脂血症的疗效比较 (附56例分析)

目的比较辛伐他汀和微粒化非诺贝特对混合型高脂血症的疗效.方法56例混合型高脂血症患者随机分为两组,一组接受辛伐他汀(20mg qn,n=28)治疗,一组接受微粒化非诺贝特(200mg qd,n=28)治疗,疗程6周,观察治疗前后血脂成份的变化.结果两组治疗后均能明显降低总胆固醇(TC)、甘油三脂(TG)、低密度脂蛋白胆固醇(LDL-C),升高高密度脂蛋白胆固醇(HDL-C),但辛伐他汀降低TC、LDL-C、LDL-C/HDL-C的幅度比微粒化非诺贝特高(P＜0.05),而微粒化非诺贝特降低TG的幅度比辛伐他汀大(P＜0.05),辛伐他汀治疗后TC、LDL-C恢复至正常水平的百分比显著比微粒化非诺贝特高(P＜0.05),而TG降至正常水平的百分比,微粒化非诺贝特比辛伐他汀高(P＜0.05).结论本研究提示对于甘油三脂轻至中度升高的混合型高脂血症患者,他汀类调脂药为首选药物;而对于严重的高甘油三脂血症者,非诺贝特则是合适的选择.大剂量辛伐他汀(20mg)与微粒化非诺贝特(200mg)均有报告认为能全面调脂[1],但两种药作用机制不同,调脂侧重点不同,如何选择是临床医生面临的困境.本研究旨在比较大剂量辛伐他汀及微粒化非诺贝特对混合型高脂血症的疗效,指导临床用药.     

氟伐他汀和非诺贝特治疗糖尿病合并高血脂的效果

目的研究非诺贝特和氟伐他汀在糖尿病合并高血脂的治疗效果。方法选取我院2011年6月至2012年6月的糖尿病合并高血脂患者290例,按照随机方法将其分为联合用药组(70例)、非诺贝特组(65例)、氟伐他汀组(55例),其中联合用药组采用氟伐他汀和非诺贝特进行用药治疗,非诺贝特组采用每晚口服210mg非诺贝特进行治疗;氟伐他汀组采用每晚口服39mg氟伐他汀进行治疗。三组糖尿病合并高血脂患者治疗中均选用常规降糖,不改变生活习惯,不做任何的降脂治疗,分别于治疗9周后,对三组糖尿病合并高血脂患者的三酰甘油(TG)、低密度脂蛋白(LDL)、血清总胆固醇(TC)、空腹血糖(FPG)、餐后两小时血糖(2hPG)和高密度脂蛋白(HDL)水平进行检测。结果三组患者在治疗的9个月后的各检测指标改善具有显著性差异,联合用药组的指标变化比单独选用非诺贝或氟伐他汀的效果显著(P<0.05)。结论非诺贝和氟伐他汀特具有调脂调糖作用,联合治疗糖尿病合并高血脂的效果更好。     

探讨应用瑞舒伐他汀联合非诺贝特治疗不稳定心绞痛合并高血脂症的疗效

目的:探讨应用瑞舒伐他汀联合非诺贝特治疗不稳定心绞痛合并高血脂症的疗效。方法:选择2016年11月-2017年12月来我院就诊的不稳定心绞痛合并高血脂症80例患者作为试验对象,按照随机数字表法分成试验组与对照组,对照组40例运用瑞舒伐他汀进行治疗,试验组40例采取瑞舒伐他汀联合非诺贝特进行治疗。对比两组治疗前后相关参数(TG、TC、LDL-C)变化率、治疗总有效率、治疗后随访3个月内冠状动脉心脏病发生率、不良反应发生率。结果:试验组治疗前后TG、TC、LDL-C变化率、治疗总有效率都明显高于对照组(P0.05)。试验组随访3个月内不稳定型心绞痛发作明显低于对照组(P0.05),不良反应发生率与对照组比较差异无统计学意义(P0.05)。结论:瑞舒伐他汀联合非诺贝特治疗不稳定型心绞痛合并高脂血症,治疗效果显著,可以降低心绞痛发生率。     

氟伐他汀联合非诺贝特治疗糖尿病合并高血脂的临床疗效观察

目的探讨氟伐他汀联合非诺贝特治疗糖尿病合并高血脂的临床疗效。方法 60例糖尿病合并高血脂患者随机分为治疗组及对照组各30例,两组患者均予常规降血糖治疗,对照组予氟伐他汀40mg,每晚一次,口服;治疗组同时加用非诺贝特200mg,每晚一次,口服。疗程8周。比较两组的疗效及两组患者治疗前后血脂和血糖的变化情况。结果治疗后治疗组患者的有效率达96.7%,明显高于对照组的疗效,差异具有显著性(x2=8.537,P0.05)。治疗8周后,两组患者的TC、TG、LDL-C、2hPG水平均较治疗前明显下降(P0.05),且治疗组患者的TC、TG、LDL-C、2hPG水平较对照组降低更显著(P0.05)。而两组患者的HDL-C水平均较治疗前明显升高(P0.05),且治疗组患者的HDL-C水平较对照组升高更显著(P0.05)。结论氟伐他汀联合非诺贝特治疗糖尿病合并高血脂的临床疗效确切,能够显著降低血脂及血糖水平,值得临床推广和应用。     

Safety and efficacy of colesevelam hydrochloride in combination with fenofibrate for the treatment of mixed hyperlipidemia

OBJECTIVE: The aim of this study was to evaluate the amount of low-density lipoprotein cholesterol (LDL-C) reduction achieved by adding the specifically engineered bile acid sequestrant (SE-BAS) colesevelam HCl to a stable dose of fenofibrate in patients with mixed hyperlipidemia. RESEARCH DESIGN AND METHODS: Patients with mixed hyperlipidemia (n = 129) were enrolled in a randomized, double-blind, placebo-controlled, parallel-group study investigating the efficacy of fenofibrate plus colesevelam HCl versus fenofibrate monotherapy. After a 4- to 8-week washout period, subjects received fenofibrate 160 mg/day for 8 weeks and were then randomized to receive colesevelam HCl 3.75 g/day or placebo, in addition to fenofibrate 160 mg/day, for 6 weeks. MAIN OUTCOMES MEASURES: The primary efficacy endpoint was mean percent change in LDL-C during randomized treatment. Secondary endpoints included absolute and percent changes in mean levels of LDL-C, triglycerides (TGs), high-density lipoprotein cholesterol (HDL-C), non-HDL-C, total cholesterol (TC), and apolipoproteins (apo) A-I and B during randomized treatment and from washout to end of randomized treatment. RESULTS: Of the 129 patients randomized to treatment, 119 completed the study. After 6 weeks of treatment, fenofibrate plus colesevelam HCl produced a mean percent change in LDL-C of -10.4% versus +2.3% with fenofibrate monotherapy (p < 0.0001). Fenofibrate plus colesevelam HCl was significantly more effective than fenofibrate alone at reducing levels of non-HDL-C, TC, and apo B (p < or = 0.0002). Colesevelam HCl did not significantly affect the TG-lowering effects of fenofibrate. Both treatment regimens were safe and well tolerated. CONCLUSIONS: Compared with fenofibrate monotherapy in patients with mixed hyperlipidemia, fenofibrate/colesevelam HCl combination therapy significantly reduced mean LDL-C, non-HDL-C, TC, and apo B levels without significantly affecting the TG-lowering or HDL-C-raising effects of fenofibrate. Fenofibrate/colesevelam HCl combination therapy is a safe, useful alternative for the treatment of mixed hyperlipidemia.     

普伐他汀与非诺贝特治疗高脂血症的疗效

目的:探讨普伐他汀和非诺贝特联合应用治疗混合性高脂血症的疗效及安全性。方法:102例混合性高脂血症患者,随机分为普伐他汀组(10mg/d,n=51)和联合治疗组(普伐他汀10mg/d 非诺贝特200mg/d,n=51),共治疗6个月。观察治疗前后主要血脂参数的变化、总有效率、与治疗安全性有关的指标以及不良反应。结果:联合治疗组血脂参数的变化率最显著,血清总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)和甘油三酯(TG)分别下降30%、36%和55%,而血清高密度脂蛋白胆固醇(HDL-C)升高24%,联合治疗组TG和HDL-C的总有效率明显高于普伐他汀组(P<0.01)。结论:普伐他汀与非诺贝特联合治疗混合性高脂血症患者能更全面调节血脂异常,疗效优于单用普伐他汀治疗。     

Micronised fenofibrate: an updated review of its clinical efficacy in the management of dyslipidaemia

Micronised fenofibrate is a synthetic phenoxy-isobutyric acid derivative (fibric acid derivative) indicated for the treatment of dyslipidaemia. Recently, a new tablet formulation of micronised fenofibrate has become available with greater bioavailability than the older capsule formulation. The micronised fenofibrate 160mg tablet is bioequivalent to the 200mg capsule. The lipid-modifying profile of micronised fenofibrate 160mg (tablet) or 200mg (capsule) once daily is characterised by a decrease in low-density lipoprotein cholesterol (LDL-C) and total cholesterol (TC) levels, a marked reduction in plasma triglyceride (TG) levels and an increase in high-density lipoprotein cholesterol (HDL-C) levels. Micronised fenofibrate 200mg (capsule) once daily produced greater improvements in TG and, generally, in HDL-C levels than the hydroxymethylglutaryl coenzyme A reductase inhibitors simvastatin 10 or 20 mg/day, pravastatin 20 mg/day or atorvastatin 10 or 40 mg/day. Combination therapy with micronised fenofibrate 200mg (capsule) once daily plus fluvastatin 20 or 40 mg/day or atorvastatin 40 mg/day was associated with greater reductions from baseline than micronised fenofibrate alone in TC and LDL-C levels. Similar or greater changes in HDL-C and TG levels were seen in combination therapy, compared with monotherapy, recipients. Micronised fenofibrate 200mg (capsule) once daily was associated with significantly greater improvements from baseline in TC, LDL-C, HDL-C and TG levels than placebo in patients with type 2 diabetes mellitus enrolled in the double-blind, randomised Diabetes Atherosclerosis Intervention Study (DAIS) [> or =3 years follow-up]. Moreover, angiography showed micronised fenofibrate was associated with significantly less progression of coronary atherosclerosis than placebo. Micronised fenofibrate has also shown efficacy in patients with metabolic syndrome, patients with HIV infection and protease inhibitor-induced hypertriglyceridaemia and patients with dyslipidaemia secondary to heart transplantation. Micronised fenofibrate was generally well tolerated in clinical trials. The results of a large (n = 9884) 12-week study indicated that gastrointestinal disorders are the most frequent adverse events associated with micronised fenofibrate therapy. Elevations in serum transaminase and creatine phosphokinase levels have been reported rarely with micronised fenofibrate. In conclusion, micronised fenofibrate improves lipid levels in patients with primary dyslipidaemia; the drug has particular efficacy with regards to reducing TG levels and raising HDL-C levels. Micronised fenofibrate is also effective in diabetic dyslipidaemia; as well as improving lipid levels, the drug reduced progression of coronary atherosclerosis in patients with type 2 diabetes mellitus. The results of large ongoing studies (e.g. FIELD with approximately 10 000 patients) will clarify whether the beneficial lipid-modifying effects of micronised fenofibrate result in a reduction in cardiovascular morbidity and mortality.     

Combination therapy of low-dose atorvastatin and fenofibrate in mixed hyperlipidemia

Mixed hyperlipidemia is a major cause of coronary artery disease. Monotherapy with statins is considered the gold standard for treatment of mixed hyperlipidemia. But greater benefit may be expected by combination therapy. Combination may allow lower doses of statins and less adverse effects. Hence, this preliminary study was designed to evaluate the efficacy and safety of low-dose atorvastatin in combination with fenofibrate in patients with mixed hyperlipidemia. Ninety patients were assigned into three groups and received atorvastatin (10-40 mg/day) or fenofibrate (160-200 mg/day) or combination of low-dose atorvastatin (5 mg/day) and fenofibrate (160 mg/day). There was a significant decrease in low-density lipoprotein (LDL), triglycerides (TG) and total cholesterol (TC), and a significant increase in high-density lipoprotein (HDL) in all the groups at the end of therapy. Combination therapy produced maximum decrease in LDL, TG and TC, and maximum increase in HDL when compared with monotherapies. No significant difference was reported in safety profile between the two groups. To conclude, the results suggest that combination therapy with low-dose atorvastatin and fenofibrate is more efficacious, with no increase in adverse effects when compared with monotherapies with individual drugs for mixed hyperlipidemia. The results are preliminary and suggestive only, as the study was open and nonrandomized.     

Combined treatment with fibrates and small doses of atorvastatin in patients with mixed hyperlipidemia

Combined statin and fibrate therapy is often imperative for the improvement of the serum lipid profile in patients with mixed hyperlipidemia. However, the potential risk of myopathy has limited the widespread use of such therapy. Preferably this treatment should involve low optimally tolerable doses of hypolipidemic drugs. Thus, we undertook a study to determine the safety and efficacy of combination therapy with fibrates and small doses of atorvastatin. Twenty-two patients with mixed hyperlipidemia were started on a fibrate regimen (micronised fenofibrate 200mg/day or ciprofibrate 100 mg/day). Because after 12 weeks of therapy the fibrate failed to normalise the serum lipid profile, small doses of atorvastatin (5 mg/day) were added for a further 12 weeks. The administration of the fibrates resulted in a significant decrease in total and LDL-cholesterol levels, as well as in triglycerides, and an increase in HDL-cholesterol levels. The addition of atorvastatin (5 mg/day) resulted in a further decrease in total and LDL-cholesterol levels. Consequently, the hypolipidemic therapy target was achieved in most of the patents. Combination therapy was well tolerated and no significant increases in serum liver and muscle enzymes were noticed. We conclude that the careful administration of small doses of atorvastatin in patients with mixed dyslipidemia receiving fibrates is associated with a significant amelioration of lipid abnormalities.     

Colesevelam

Colesevelam hydrochloride (Cholestagel, WelChol is an orally administered, non-absorbable, polymeric, bile-acid-binding agent with a higher affinity for glycocholic acid in vitro and greater capacity for binding bile acids in vivo than other bile-acid-binding agents.In randomized controlled trials in patients with primary hypercholesterolemia, colesevelam monotherapy reduced mean serum low-density lipoprotein-cholesterol (LDL-C) levels by 9-19%. In combination with an HMG-CoA reductase inhibitor (statin) or fenofibrate, colesevelam induced additive reductions in LDL-C 10-16% greater than those achieved by monotherapy with a statin (in patients with primary hypercholesterolemia) or fenofibrate (in patients with mixed hyperlipidemia). Colesevelam was generally well tolerated, with a relatively low incidence of gastrointestinal adverse events and a high compliance rate. Thus, colesevelam provides a useful addition to primary therapy with statins in the treatment of primary hypercholesterolemia, or fenofibrate in the treatment of mixed hyperlipidemia.     

Efficacy of combination of atorvastatin and micronised fenofibrate in the treatment of severe mixed hyperlipidemia

OBJECTIVES: In patients with mixed lipid disorders, monotherapy may not effectively control all lipid abnormalities. We undertook this study to assess the efficacy of fenofibrate in combination with atorvastatin in patients with severe mixed dyslipidemia. METHODS: This was an 18-week, open-label study conducted in our lipid clinic. After a 6-week dietary baseline phase, patients received 200 mg/day micronised fenofibrate for 6 weeks. At the end of this period the subjects discontinued this treatment and received 40 mg/day atorvastatin for 6 weeks. Finally 200 mg/day of micronised fenofibrate was added to the statin therapy. RESULTS: Administration of micronised fenofibrate reduced serum triglycerides (P < 0.01) and total cholesterol and low-density lipoprotein (LDL) cholesterol (P < 0.05 for both parameters), while it evoked a significant increase in serum high-density lipoprotein (HDL) cholesterol levels (P < 0.05). Atorvastatin monotherapy induced a more pronounced decrease of total and LDL cholesterol. However, plasma triglycerides, although significantly lower than baseline values (P < 0.05), were higher than the values observed during treatment with fenofibrate. Moreover, serum HDL cholesterol concentrations were higher during fibrate therapy than during the statin one. During the combination therapy, the decrease in triglycerides was greater than that observed with fenofibrate alone, while the decrease in LDL cholesterol was more pronounced than that observed with atorvastatin alone. CONCLUSION: The combination of atorvastatin with micronised fenofibrate in patients with severe mixed dyslipidemia may have a favourable effect on some major coronary artery disease risk factors.     

Combined Treatment with Fibrates and Small Doses of Atorvastatin in Patients with Mixed Hyperlipidemia

Summary

Combined statin and fibrate therapy is often imperative for the improvement of the serum lipid profile in patients with mixed hyperlipidemia. However, the potential risk of myopathy has limited the widespread use of such therapy. Preferably this treatment should involve low optimally tolerable doses of hypolipidemic drugs. Thus, we undertook a study to determine the safety and efficacy of combination therapy with fibrates and small doses of atorvastatin. Twenty-two patients with mixed hyperlipidemia were started on a fibrate regimen (micronised fenofibrate 200mg/day or ciprofibrate 100mg/day). Because after 12 weeks of therapy the fibrate failed to normalise the serum lipid profile, small doses of atorvastatin (5mg/day) were added for a further 12 weeks.

The administration of the fibrates resulted in a significant decrease in total and LDL-cholesterol levels, as well as in triglycerides, and an increase in HDL-cholesterol levels. The addition of atorvastatin (5mg/day) resulted in a further decrease in total and LDL-cholesterol levels. Consequently, the hypolipidemic therapy target was achieved in most of the patients. Combination therapy was well tolerated and no significant increases in serum liver and muscle enzymes were noticed.

We conclude that the careful administration of small doses of atorvastatin in patients with mixed dyslipidemia receiving fibrates is associated with a significant amelioration of lipid abnormalities.     

微粒化非诺贝特治疗高脂血症的临床观察

目的 观察微粒化非诺贝特对高脂血症的疗效与安全性。方法 用开放、随机对照方式,应用非诺贝特和多烯康治疗高脂血症12周,观察病人治疗前后有关检查结果及副作用。结果 非诺贝特组服药12周后血清胆固醇（TC）、甘油三脂（TG）、低胆固醇胆脂蛋白（LDL－C）水平与0周比较分别降低18．9％（P＜0．01）、44％（P＜0．001）、13％（P＜0．05）;多烯康组则分别降低11％、19％、13．7％（P＜0．05）。非诺贝特组与多烯康组服药12周时降低血脂的总有效率分别为79．1％和48．8％,非诺贝特组显著优于多烯康组（P＜0．01）。结论 非诺贝特为高脂血症的有效治疗药物,安全性好,疗效优于多烯康。