吉非贝齐与非诺贝特降脂疗效比较

高脂血症２１０例，其中１０９例（男性６０例，女性４９例；年龄５８±ｓ８ａ）采用吉非贝齐６００ｍｇ，ｐｏ，ｂｉｄ共治疗１２ｗｋ；另１组１０１例（男性６６例，女性３５例；年龄５９±８ａ）采用非诺贝特１００ｍｇ．ｐｏ，ｔｉｄ共１２ｗｋ。结果：降三酰甘油，降总胆固醇及升高高密度脂蛋白胆固醇，吉非贝齐组依次为５３．０％，１９．４％及２６．８％，（Ｐ值均为＜０．０１），非诺贝特依次为４１．０％，２２．０％及２２．０％（Ｐ值均＜０．０１），２组组间比较无差异（Ｐ＞０．０５）；前者有４例，后者有５例一过性ＧＰＴ（ＡＬＴ）升高。     

非诺贝特对缺血性脑血管疾病病人血清脂质成分的影响

目的：探索非诺贝特对缺血性脑血管疾病（ＩＣＶＤ）病人血脂成分的影响。方法：缺血性脑血管疾病伴血清脂质成分异常病人５４例（男性３２例，女性２２例；年龄５４±ｓ１２ａ）。非诺贝特０．１ｇ，ｐｏ，ｔｉｄ，４Ｗｋ为一个疗程。结果：治疗后血清ＨＤＬ一ｃｈ及ＨＤＬ２－ｃｈ、ＨＤＬ２－ｃｈ明显提高（Ｐ＜０．０１或Ｐ＜０．０５），其升高的，总有效率，依次为１００％，９６％及７７％。ＴＣ，ＴＧ及ＬＤＬ－ｃｈ显著下降（Ｐ＜０．０１或Ｐ＜０．０５），其降低的总有效率依次为９５％，１００％及７６％，不良反应轻微。结论：非诺贝特能迅速调整血脂成分及含量，可延缓或减轻动脉硬化的形成，是治疗ＩＣＶＤ病人较满意的药物。     

非诺贝特对缺血性脑血管疾病病人血清脂质成分的影响

探索非诺贝特对缺血性脑血管疾病病人血脂成分的影响。方法：缺血性脑血管疾病伴血清脂质成分异常病人５４例（男性３２例，女性２２例；年龄５４±ｓ１２ａ）。非诺贝特０．１ｇ，ｐｏ，ｔｉｄ，４ｗｋ为一个疗程。结果：治疗后血清ＨＤＬ－ｃｈ及ＨＤＬ２－ｃｈ，ＨＤＬ３－ｃｈ明显提高（Ｐ〈０．０１或Ｐ〈０．０５），其升高的产生的总有效率，依次为１００％，９６％及７７％，ＴＣ，ＴＧ及ＬＤＬ－ｃｈ显下降（Ｐ〈０．０１     

醋柳黄酮治疗高脂血症和高粘血症

目的：比较醋柳黄酮与丹参治疗高脂、高粘血症病人的疗效。方法：治疗组３５例（全部男性，年龄５２±ｓ８ａ）用醋柳黄酮２０ｍｇ，ｐｏ，ｔｉｄ。对照组３４例（全部男性，年龄５１±９ａ）用丹参１０ｍＬ，ｐｏ，ｂｉｄ。疗程均为６ｗｋ。结果：治疗组血胆固醇（ＴＣ）、三酰甘油（ＴＧ）、载脂蛋白Ｂ１００（ＡｐｏＢ１００）、血浆凝血因子Ｉ、血液粘度、血小板聚集率和血栓指数均较治疗前有显著（Ｐ＜０．０５）或极显著（Ｐ＜０．０１）下降。对照组在１０·ｓ－１血液粘度较治疗前有极显著下降（Ｐ＜０．０１），在１００·ｓ－１血液粘度和血栓指数较治疗前有显著下降（Ｐ＜０．０５）。结论：醋柳黄酮治疗后，大部分指标（除１０·ｓ－１血液粘度指标外）下降，优于丹参。     

特拉唑嗪对原发性高血压病人的血压、血脂及糖代谢的影响

目的：观察特拉唑嗪对３８例（男性２２例，女性１６例；年龄５６±ｓ８ａ）原发性高血压Ｉ期病人血压、血脂及糖代谢的影响。方法：特拉唑嗪首剂于晚上睡前服１ｍｇ，以后根据血压情况逐渐增量，最大剂量为１０ｍｇ／ｄ，８ｗｋ为一个疗程。结果：特拉唑嗪治疗后，血压下降（Ｐ＜０．０１），糖负荷曲线略降低，胰岛素水平（Ｉｎｓ）及胰岛素抵抗（ＩＳＲ）降低（Ｐ＜０．０１），心率及血脂无改变（Ｐ＞０．０５）。结论：特拉唑嗪对原发性高血压Ｉ期者，在改善血压的同时，不影响脂代谢，对糖代谢、胰岛素及ＩＳＲ有益。     

海绵体内注射前列地尔治疗心理性不射精

目的：观察前列地尔阴茎海绵体内注射（ＩＣＩ）治疗心理性不射精的疗效。方法：６０例男性病人（年龄３１±ｓ４ａ），甲组３０例用前列地尔１５～２０μｇ加电按摩，乙组３０例单用电按摩。每周２次，疗程４ｗｋ，前２ｗｋ男性治疗，后２ｗｋ夫妇治疗。用男女性功能电脑诊断与测评系统评估疗效。结果：甲组的性欲减退、性合作缺乏、性操作焦虑和性快感缺乏等４项指数较治疗前有显著改善（Ｐ＜０．０５或０．０１），与乙组比较上述４项指数以及夫妇双方对射精疗效的主观评价均有显著差异（Ｐ＜０．０５或０．０１）。结论：前列地尔作ＩＣＩ加电按摩治疗不射精效果满意。     

巴曲抗栓酶对肺原性心脏病病人血栓前状态的作用

目的：研究巴曲抗栓酶对肺原性心脏病（肺心病）病人的纤溶作用。方法：所有肺心病病人接受常规治疗（包括吸氧、抗生素及平喘药物），治疗组２０例（男性１６例，女性４例；年龄５７±ｓ７ａ）静脉滴注巴曲抗栓酶５ＢＵ加入０．９％氯化钠注射液１００ｍＬ，２次／ｗｋ，共２ｗｋ．对照组１０例（男性９例、女性１例；年龄５５±３ａ）不用巴曲抗栓酶。结果：巴曲抗栓酶组治疗后ＰＬＧ，ＰＡＩ比治疗前下降（Ｐ＜０．０５）．ＴＰＡ，Ｄ－ｄｉｍｅｒ比治疗前增加（Ｐ＜０．０５）。对照组治疗后仅ＰＬＧ比治疗前降低（Ｐ＜０．０５）。２组病人ＴＰＡ、ＰＡＩ比较有差异（Ｐ＜０．０５）。结论：巴曲抗栓酶对肺心病病人血栓前状态运用有一定价值。     

硝苯地平控释片对无痛性心肌缺血病人左心功能的影响

目的：观察硝苯地平控释片（Ｎｉｆ－ＣＲ）治疗无痛性心肌缺血（ＳＭＩ）时对左心功能的影响。方法：３６例ＳＭＩ病人（男性２３例，女性１３例；年龄５６±ｓ７ａ）采用Ｎｉｆ－ＣＲ２０ｍｇ，ｐｏ，ｑ１２ｈ×３ｗｋ。结果：（１）舒张压从１２５±２．３ｋＰａ下降至９．７±２．３ｋＰａ（Ｐ＜０．０５）；缺血型ＳＴ段压低明显改善（从１．６±０．７ｍｍ升至１．０±０．６ｍｍ）（Ｐ＜０．０１）。（２）核素心功能检测，ＬＶＥＦ，ＳＶ，ＥＲ，ＰＦＲ及ＲＣＯ均显著改善（Ｐ＜０．０５或Ｐ＜０．０１）。（３）治疗后ＰＲＡ和ＡＮＧⅡ水平降低（Ｐ＜０．０５）。结论：Ｎｉｆ－ＣＲ的持久血药浓度可改善左心功能，降低血压。不良反应小。     

脂必妥(74例)与多烯康(36例)降脂疗效比较

目的：比较脂必妥与多烯康的降脂疗效。方法：脂必妥组７４例（男性４９例，女性２５例；年龄５６±ｓ８ａ）给脂必妥３片（０．３５ｇ／片），ｐｏ，ｔｉｄ×８ｗｋ；多烯康组３６例（男性２５例，女性１６例；年龄５５±８ａ）给多烯康胶丸４粒（０．４５ｇ／粒），ｐｏ，ｔｉｄ×８ｗｋ。结果：脂必妥治疗后ＴＣ，ＴＧ，ＬＤＬ－ｃｈ和ＡｐｏＢ１００下降极显著（Ｐ＜０．０１）。ＨＤＬ－ｃｈ和ＨＤＬ－ｃｈ／ＴＣ比值显著升高（Ｐ＜０．０５，Ｐ＜０．０１）。而对照组治疗后ＴＣ无显著下降（Ｐ＞０．０５），ＨＤＬ－ｃｈ亦无显著升高（Ｐ＞０．０５）。但组间对比ＨＤＬ－ｃｈ及ＨＤＬ－ｃｈ／ＴＣ比例２组升幅差异均不显著（Ｐ＞０．０５）。脂必妥用于２７例高尿酸血症治疗８ｗｋ后血清尿酸显著下降（Ｐ＜０．０１）。２组均无严重副作用。结论：调脂作用，脂必妥优于多烯康。     

通脉宁心对血脂,血浆血栓烷B2和6—酮—前列腺素F1a的影响

用通脉宁心治疗高脂血症患３０例（男性１４例，女性１６例；平均年龄５４±ｓ１０ａ）。剂理１０ｇ，ｔｉｄ，ｐｏ。８ｗｋ为一个疗程。结果：该药歙血清中甘油三酯及血浆中血栓烷Ｂ２较治疗前明显降低（Ｐ＜０．０１；Ｐ＜０．０５）；对高密度脂蛋白及６－酮－前列腺素Ｆ１ａ的升高不显（Ｐ均＞０．０５）。     

微粒化非诺贝特与辛伐他汀治疗糖尿病合并高脂血症的比较

目的 :观察微粒化非诺贝特与辛伐他汀治疗 2型糖尿病 (NIDDM )合并高脂血症的疗效。方法 :4 0例 (男性 2 2例 ,女性 18例 ,年龄 55a±s 8a)NIDDM病人用微粒化非诺贝特胶囊 0 .2 g ,po ,qd× 8wk。另 38例 (男性 2 1例 ,女性 17例 ,年龄 54a± 9a)NIDDM病人用辛伐他汀片 5mg ,po ,qd× 8wk。结果 :非诺贝特组依次降低TC ,TG ,LDL C为18% ,4 6% ,2 2 %及升高HDL C 2 0 % ;辛伐他汀组依次下降 2 5% ,2 8% ,2 3%及升高 18%。非诺贝特组较辛伐他汀组TG下降更显著 (P <0 .0 1)。结论 :微粒化非诺贝特是NIDDM合并高脂血症病人有效的调脂药物 ,比辛伐他汀降低TG更有效     

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。     

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.     

The effects of the addition of micronised fenofibrate on uric acid metabolism in patients receiving indapamide

OBJECTIVE: Hyperuricaemia is associated with indapamide administration. In contrast, micronised fenofibrate can significantly decrease serum uric acid levels. However, there are no data on the effect of combination therapy of indapamide with micronised fenofibrate on uric acid metabolism. METHODS:We studied 20 non-diabetic hypertensive patients with mixed dyslipidaemia in whom serum metabolic parameters, including uric acid levels in serum and urine, were measured before and after eight weeks of indapamide administration (2.5 mg once daily). This study was continued for a further eight weeks, when the indapamide was combined with micronised fenofibrate (200 mg once daily). RESULTS: Indapamide significantly decreased mean systolic and diastolic blood pressure (BP) from 153 +/- 9/97 +/- 8 mmHg to 138 +/- 8/93 +/- 4 mmHg (p< 0.05 for both comparisons). A significant increase in serum uric acid levels occurred after indapamide administration (from a mean value of 5.6 +/- 1.3 mg/dl (0.33 +/- 0.07 mmol/l) to 6.4 +/- 1.1 mg/dl (0.38 +/- 0.06 mmol/l), p < 0.01]. This effect was associated with a decrease in the fractional excretion of uric acid (from a mean value of 9.5 +/- 5% to 7 +/- 5.5%, p < 0.05). The addition of micronised fenofibrate significantly decreased plasma fibrinogen levels as well as total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B (ApoB) and triglycerides, and increased high-density lipoprotein cholesterol and ApoA, levels. Fenofibrate administration was followed by a significant decrease in serum uric acid levels to 4.7 +/- 1.2 mg/dl (0.28 +/- 0.07 mmol/l), p < 0.01, owing to a substantial increase in fractional urate excretion to 11 +/- 3%, p < 0.01. CONCLUSION:The addition of micronised fenofibrate can correct the hyperuricaemic effect of indapamide administration.     

The Effects of the Addition of Micronised Fenofibrate on Uric Acid Metabolism in Patients Receiving Indapamide

Summary

Objective: Hyperuricaemia is associated with indapamide administration. In contrast, micronised fenofibrate can significantly decrease serum uric acid levels. However, there are no data on the effect of combination therapy of indapamide with micronised fenofibrate on uric acid metabolism.

Methods: We studied 20 non-diabetic hypertensive patients with mixed dyslipidaemia in whom serum metabolic parameters, including uric acid levels in serum and urine, were measured before and after eight weeks of indapamide administration (2.5?mg once daily). This study was continued for a further eight weeks, when the indapamide was combined with micronised fenofibrate (200?mg once daily).

Results: Indapamide significantly decreased mean systolic and diastolic blood pressure (BP) from 153±9/97±8mmHgto 138 ± 8/93 ± 4mmHg (p < 0.05 for both comparisons). A significant increase in serumuric acid levels occurred after indapamide administration [from a mean value of5.6± 1.3mg/dl (0.33 ± 0.07 mmol/l) to 6.4 ± 1.1?mg/dl (0.38 ± 0.06mmol/l), p< 0.01]. This effect was associated with a decrease in the fractional excretion of uric acid (from a mean value of 9.5 ± 5% to 7 ± 5.5%, p < 0.05). The addition of micronised fenofibrate significantly decreased plasma fibrinogen levels as well as total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B (ApoB) and triglycerides, and increased high-density lipoprotein cholesterol and ApoA1 levels. Fenofibrate administration was followed by a significant decrease in serum uric acid levels to 4.7± 1.2?mg/dl (0.28 ± 0.07 mmol/l), p < 0.01, owing to a substantial increase in fractionalurate excretion to 11 ± 3%, p < 0.01.

Conclusion: The addition of micronised fenofibrate can correct the hyperuricaemic effect of indapamide administration.     

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.     

微粒化非诺贝特治疗糖尿病血脂异常及其对血清C-反应蛋白的影响

目的:观察微粒化非诺贝特治疗糖尿病(DM)血脂异常及其对血清C-反应蛋白(C-RP)的影响。方法:选择1999年1月~2004年12月门诊及住院的2型糖尿病(T2DM)患者共86例,将上述患者随机分成治疗组44例,对照组42例。治疗组给予微粒化非诺贝特200 mg,每晚服用,连续8周;对照组给予辛伐他汀10 mg,每晚服用,连续8周。分别于治疗前和治疗后8周检查血脂常规、C-RP、肝功能、血常规、血糖等指标。结果:治疗组与对照组治疗8周后,血清甘油三脂(TG)明显降低(P<0.01)、高密度脂蛋白胆固醇(HDL-C)显著增加(P<0.01),两组比较有显著差异(P<0.01);两组血清总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、C-RP均有显著下降(P<0.01),但两组比较无显著差异(P>0.05)。结论:微粒化非诺贝特治疗糖尿病血脂异常有确切调脂及抗炎作用。     

国产与进口辛伐他汀治疗原发性高胆固醇血症的临床疗效比较

目的 :比较国产与进口辛伐他汀的临床疗效、安全性。方法 :将 1 5 9例病人随机分为国产辛伐他汀组 (n =1 0 0 )及进口辛伐他汀组 (n =5 9) ,分别口服国产及进口辛伐他汀 ,每晚 1 0mg ,服用 8wk。观察用药 4wk及 8wk病人血脂的变化。结果 :服药 4wk和 8wk后 2组病人血清总胆固醇 (TC)、三酰甘油 (TG)、低密度脂蛋白胆固醇 (LDL C)水平及TC -HDL C/HDL C明显降低 ,高密度脂蛋白胆固醇 (HDL C)明显升高 ,服药 4wk即有明显疗效 ,不良反应轻 ,2组比较调脂疗效差异无显著意义 (P >0 .0 5 )。结论 :国产辛伐他汀调血脂作用疗效肯定、使用安全 ,与进口辛伐他汀比较基本相当。     

普伐他汀对高脂血症患者血脂及血液流变性的影响

目的探讨普伐他汀对高脂血症患者血脂及血液流变性的影响。方法对服用普伐他汀12周的54例高脂血症患者检测治疗前后的血脂及血液流变的各参数。结果（1）治疗后患者的血清总胆固醇、三酰甘油、低密度脂蛋白明显下降（P＜0.05）,而高密度脂蛋白明显升高。（2）治疗后患者全血低切粘度、血浆粘度、红细胞聚集指数、红细胞压积和血沉明显下降（P<0.05）。结论普伐他汀不仅能明显降低血脂,而且能改善患者的血液流变性。