Treatment of primary hypercholesterolaemia with simvastatin. New Zealand multicentre evaluation

OBJECTIVE: To assess the efficacy of simvastatin in a large patient cohort. DESIGN: In an open multicentre study, after a four week placebo phase, patients were treated with simvastatin for 24 weeks; a subgroup continued therapy for a further 24 weeks. Efficacy of simvastatin (a) with prolonged use over three years, and (b) in combination with bezafibrate was assessed in an open single site study. SETTING: Lipid or cardiology specialist hospital outpatient clinics. PATIENTS: For the open multicentre study, 228 patients with primary hypercholesterolaemia (total cholesterol level greater than 6.5 mmol/L) were recruited, of whom 224 met entry criteria and completed the study. Forty-seven of these patients continued therapy for one year. In the open single site study, 22 patients (with low density lipoprotein [LDL] cholesterol levels greater than 4.3 mmol/L) participated in studies of long term use (n = 9) or of combined therapy (n = 13). INTERVENTION: Therapy in the open multicentre study began with 10 mg of simvastatin per day, doubling to 20 mg after six weeks and then 40 mg after 12 weeks of therapy if total cholesterol levels persisted above 5.2 mmol/L. In the study of long term use, simvastatin (40 mg daily) was taken continuously over three years. In the study of combination therapy, bezafibrate (600 mg daily) was taken in addition to simvastatin (40 mg daily) for 10 months. MAIN OUTCOME MEASURES: Plasma lipid and lipoprotein concentrations. RESULTS: In the multicentre study, total plasma cholesterol levels were reduced by 32.8% from 9.11 +/- 1.84 (in mmol/L, mean +/- SD) to 6.12 +/- 1.25 (P less than 0.001), and LDL cholesterol levels by 41.4% from 6.90 +/- 1.92 to 4.04 +/- 0.31 (P less than 0.001). The effect of therapy was sustained in those patients continuing therapy to 48 weeks. The study of long term use found no significant attenuation of effect over three years of monotherapy. Combined simvastatin/bezafibrate therapy reduced the LDL cholesterol concentration by a further 19.9% (P less than 0.001) from levels achieved on simvastatin alone. CONCLUSIONS: Simvastatin is an effective, well tolerated lipid lowering drug, without significant attenuation of effect with prolonged use. Simvastatin plus bezafibrate appears to be a potentially useful drug combination.     

辛伐他汀治疗肾移植术后高脂血症的临床应用研究

目的 探讨他汀类药物对肾移植术后血脂异常的疗效。方法 将36例术后1年以上的高脂血症患者（血浆胆固醇总量水平＞6.35 mmol/L,低密度脂蛋白＞3.1 mmol/L）作为研究对象。所有患者均采取低脂饮食，测定患者血总胆固醇（TC）、高密度脂蛋白（HDL）、低密度脂蛋白（LDL）、甘油三酯（TG）、载脂蛋白A（apoA）、载脂蛋白B（apoB）、肌酐（Cr），谷草转氨酶（GOT）及谷丙转氨酶（GPT）等各参数数值；然后给予辛伐他汀10 mg，每晚一次口服，测定用药后1，3，6，12个月后以上各参数值的变化。结果 肾移植术后高脂血症患者LDL较TC增高更为明显；用药后患者TC,LDL,TG,apoB分别于用药后第1,3,6,12个月时均出现显著性下降（P<0. 01），LDL的下降尤为明显；HDL于用药后第12个月时出现显著增高（P<0.05）；其余各项指标无显著变化；结论 辛伐他汀可有效、安全地用于治疗肾移植术后血脂异常。 【关键词】 肾移植 辛伐他汀 高脂血症     

辛伐他汀治疗高脂血症56例的疗效观察

目的探讨辛伐他汀治疗混合型高脂血症的临床效果.方法56例混合型高脂血症患者口服辛伐他汀治疗,20mg,1次/d,于服药后4,8周检测血脂并比较分析.结果服用辛伐他汀4、8周后,血清胆固醇(TC)分别降低24.54%,24.39%(P＜0.001),甘油三酯(TG)分别降低21.03%、20.66%(P＜0.01),低密度脂蛋白胆固醇(LDL-C)分别下降33.33%、34.48%(P＜0.001),载脂蛋白A1(Apo-A1)分别增加了14.50%、19.85%(P＜0.01),即辛伐他汀在降低TC、TG的同时也能降低LDL-C,并有升高Apo-A1的作用.结论辛伐他汀在治疗混合型高脂血症中能有效降低血清胆固醇和甘油三酯,是一种理想的调脂药物.     

Treatment of primary hypercholesterolaemia with pravastatin: efficacy and safety over three years.

OBJECTIVE: To assess the efficacy, safety and tolerability of pravastatin over three years of treatment. DESIGN: An open, multicentre randomised study. SETTING: Subjects receiving tertiary care at three hospital lipid clinics. PATIENTS: Subjects with primary hypercholesterolaemia (type IIa) or combined hyperlipidaemia (type IIb), already stabilised on a cholesterol-lowering diet, with low density lipoprotein (LDL) cholesterol levels of greater than 4.7 mmol/L and triglyceride levels of less than 4.5 mmol/L. Sixty-one subjects were randomly assigned to the treatment groups: 60 completed 12 weeks and 46 completed 30-36 months of treatment. INTERVENTIONS: Subjects were randomly assigned to receive either pravastatin 20 mg/day, pravastatin 40 mg/day or cholestyramine 16 g/day for a period of 12 weeks. Subsequently, dose titration of pravastatin up to 40 mg/day was permitted, if required, and all groups received supplementary therapy with other lipid-lowering drugs. MAIN OUTCOME MEASURES: Lipids, lipoproteins, haematological and biochemical safety parameters were measured at regular intervals. Adverse events were monitored. RESULTS: There were significant reductions in total and LDL cholesterol levels with all treatments over 12 weeks (P < 0.001). The mean reductions (+/- SD) in LDL cholesterol were 26% +/- 14% in the group taking pravastatin 20 mg/day (n = 21), 30% +/- 8% in the group taking pravastatin 40 mg/day (n = 21) and 34% +/- 13% in the group taking resin (n = 18). The percentage changes in LDL cholesterol were independent of age, baseline cholesterol level or lipid phenotype. High density lipoprotein (HDL) cholesterol levels were significantly increased, by 8%-18% with all treatments (P < 0.001). Triglyceride levels were reduced by high-dose pravastatin only (7% +/- 29%), but were found to increase with resin (45% +/- 63%). During long-term treatment over 36 months, still greater reductions in total and LDL cholesterol were found in patients taking pravastatin (n = 35), but not in those taking resin (n = 11). There was an apparent decrease in effect beyond 18 months in both groups, possibly related to reduced compliance with diet or cholestyramine intake. Eight subjects allocated to pravastatin and seven allocated to resin withdrew (one and two subjects respectively because of drug-induced adverse events). Adverse events during 12 weeks' monotherapy with pravastatin included central nervous system (CNS) symptoms (12%), gastrointestinal (GIT) symptoms (7%) and an acute hepatitic reaction (one subject). Of those in the resin therapy group, 22% developed GIT symptoms. Myalgia occurred in three subjects using a combination of pravastatin and clofibrate, but this resolved fully upon clofibrate withdrawal. CONCLUSIONS: Pravastatin was found to be a relatively effective, safe and well tolerated lipid-lowering drug. Still greater LDL reduction was achieved with pravastatin combination therapy and this was essentially maintained over three years.     

降纤酶、缬沙坦和舒降之对食饵性兔动脉粥样硬化影响的比较

目的 :对比降纤酶、缬沙坦和舒降之对食饵性兔动脉粥样硬化的影响及探讨其可能的机制。方法 :随机将 4 4只兔分为正常对照组 (普通饲料 )、动脉粥样硬化模型组 (胆固醇饲料 )、降纤酶组 (胆固醇饲料 +降纤酶注射液1u·kg-1·4d-1)、缬沙坦组 (胆固醇饲料 +缬沙坦 5mg·kg-1·d-1)和舒降之组 (胆固醇饲料 +舒降之 5mg·kg-1·d-1)。 10周后检测血清总胆固醇 (TC)、甘油三酯 (TG)、低密度脂蛋白胆固醇 (LDL -C)、纤维蛋白原 (Fbg)、组织型纤溶酶原激活剂 (t -PA)和纤溶酶原激活剂抑制物 - 1(PAI - 1)活性、炎症因子C -反应蛋白 (CRP)等 ,观察各组动物主动脉病理学形态及血管内膜厚度。结果 :① 3组药物对兔动脉粥样硬化均有不同程度抑制效果 ,其程度大小依次为舒降之、缬沙坦、降纤酶 (P <0 .0 5 ) ;②降纤酶、舒降之对血脂有干预作用 (P <0 .0 5 ) ;③ 3组药物均可降低Fbg、升高t-PA /PAI- 1比值 (P <0 .0 1) ,其程度大小为降纤酶、舒降之、缬沙坦 (P <0 .0 5 ) ;④舒降之、缬沙坦可明显降低CRP水平 (P <0 .0 5 ) ,而降纤酶无影响。结论 :3组不同类型药物对兔动脉粥样硬化均有干预作用 ,但影响程度不一 ;舒降之作用最强 ,得益于其对血脂、纤溶和炎症等多方面的影响 ,降纤酶改善纤溶活性明显 ,而缬沙坦有?     

辛伐他汀治疗混合性高脂血症患者的疗效和耐受性

目的：观察辛伐他汀治疗混合性高脂血症患者的疗效和耐受性。方法;采用开放性、自身对比研究,对１２３例混合性高脂血症患者给予辛伐他汀１０ｍｇ,每晚一次口服,共治疗６周。结果：６周后,血清总胆固醇、低密度脂蛋白胆固醇均较治疗前明显下降（分别降低２３．８％、２９．５％,Ｐ〈０．０５）,血甘油三酯也显著降低（平均降低２７．１％,Ｐ〈０．０５）,高密度脂蛋白胆固醇明显上升（平均升高２３．６％,Ｐ〈０．０５）。未出现严重不良反应。结论：辛伐他汀对混合性高脂血症患者疗效明显,耐受性好。     

急性心肌梗死患者血脂水平的增龄变化特点

目的探讨急性心肌梗死（AMI）患者血脂水平的增龄变化特点。方法收集本院2007年5月至2011年7月符合入选标准的AMI患者1214例。依据年龄40—89岁间每10岁分为一组,比较各年龄组及不同性别间患者的血脂水平差异。结果在7个年龄组中进行两两间TC或LDL—C水平比较,40～69岁各年龄组的TC水平[分别为（4．71±1．08）、（4．80±1．30）、（4．69±1．03）mmol／L]均高于70～89岁各年龄组[分别为（4．41±0．96）、（4．38±1．03）mmol／L],均P〈0．05（t值分别为2．381、2．323、4．382、3．965、3．317、3．096）。59岁以下的3个年龄组间的TG水平差异无统计学意义,该3组的TG水平均高于60岁以上各年龄组;在50—89岁患者TG水平随年龄组的增加而逐渐降低。7个年龄组间的HDL—C水平两两比较,40—59岁各年龄组的HDL—C水平[分别为（1．03-4-0．23）、（1．05±0．26）mmol／L]均低于60～89岁各年龄组[分别为（1．11±0．28）、（1．11±0．28）、（1．16±0．34）mmol／L],均P〈0．05（t值分别为-2．777、-2．789、-3．731、-2．543、-2．566、-3．644）。AMI患者TC（r=-0．123,P〈0．01）、LDL—C（r=-0．139,P〈0．01）和TG（r=-0．287,P〈0．01）与年龄呈负相关,HDL—C与年龄呈正相关（r=0．125,P〈0．01）。1214例AMI患者中,50～89岁各年龄组的女性TC水平高于同年龄组男性,50～69岁各年龄组的女性LDL—C水平高于同年龄组男性,40～79岁各年龄组的女性HDL—C水平高于同年龄组男性,均P〈0．05（t值分别为-2．878、-3．007、-3．352、-3．333）。结论总体上看,〈60岁的AMI患者的TC、LDL和TG高于≥60岁老年AMI患者,而HDL偏低。同年龄组女性TC、LDL、HDL水平有高于男性的趋势。     

Low-density lipoprotein cholesterol and the risk of dementia with stroke.

CONTEXT: Next to Alzheimer disease, vascular dementia is the second most common form of dementia in the elderly, yet few specific risk factors have been identified. OBJECTIVE: To investigate the relationship of plasma lipids and lipoproteins to dementia with stroke. DESIGN AND SETTING: Prospective longitudinal community-based study over a 7-year period (1991-1998). PARTICIPANTS: A total of 1111 nondemented participants (mean [SD] age, 75.0 [5.9] years) were followed up for an average of 2.1 years (range, 1-7.8 years). MAIN OUTCOME MEASURE: Incident dementia with stroke according to standardized criteria, by baseline levels of total plasma cholesterol and triglycerides, low-density lipoprotein (LDL) cholesterol, LDL levels corrected for lipoprotein(a), high-density lipoprotein cholesterol, lipoprotein(a), and apolipoprotein E genotype. RESULTS: Two hundred eighty-six (25.7%) of the 1111 subjects developed dementia during follow-up; 61 (21.3%) were classified as having dementia with stroke and 225 (78.7%) as having probable Alzheimer disease. Levels of LDL cholesterol were significantly associated with an increased risk of dementia with stroke. Compared with the lowest quartile, the highest quartile of LDL cholesterol was associated with an approximately 3-fold increase in risk of dementia with stroke, adjusting for vascular risk factors and demographic variables (relative risk [RR], 3.1; 95% confidence interval [CI], 1.5-6.1). Levels of LDL corrected for lipoprotein(a) were an even stronger predictor of dementia with stroke in the adjusted multivariate analysis. Compared with the lowest quartile, the RR of dementia with stroke for the highest quartile of lipoprotein(a)-corrected LDL cholesterol was 4.1 (95% CI, 1.8-9.6) after adjusting for vascular factors and demographic variables. Lipid or lipoprotein levels were not associated with the development of Alzheimer disease in our cohort. CONCLUSIONS: Elevated levels of LDL cholesterol were associated with the risk of dementia with stroke in elderly patients. Further study is needed to determine whether treatment of elevated LDL cholesterol levels will reduce the risk of dementia with stroke.     

辛伐他汀治疗老年高脂血症的疗效和安全性

目的观察辛伐他汀治疗老年高脂血症，特别是高胆固醇血症的疗效和安全性。方法选取58名老年高脂血症患者应用辛伐他汀20mg／d治疗，每3个月检查血脂、血尿常规、肝肾功能、肌酸激酶等生化指标1次．随访至少24个月，观察其调脂疗效和不良反应。结果辛伐他汀能使总胆固醇（TC）平均下降26．30％，低密度脂蛋白胆固醇（LDL—C）平均下降28．63％，甘油三酯（TG）平均下降16．38％，高密度脂蛋白胆固醇（HDL—C）平均上升8．16％；在随访期间，未发现有明显的不良反应出现。结论辛伐他汀有明显降低TC、LDL—C的作用，对TG也有一定降低作用，HDL—C则有一定升高作用；该药长期应用具有良好的安全性。     

内源性高甘油三酯血症患者血浆VLDL、LDL及HDL对血小板聚集功能的影响

目的　研究内源性高甘油三酯血症 (HTG)患者血浆极低密度脂蛋白 (VL DL )、低密度脂蛋白 (L DL )及高密度脂蛋白 (HDL )对血小板聚集功能的影响。方法　对 2 1例内源性高甘油三酯血症患者与 2 1例正常对照者用一次性密度梯度超速离心法分离血浆 VL DL、L DL及 HDL。测定这三种脂蛋白的 2 34nm吸光度 (A2 34 )、电泳迁移率 (REM)及硫代巴比妥酸反应物质 (TBARS)含量。分别将这三种脂蛋白加入由正常人新鲜血浆构成的反应系统中 ,用血小板聚集仪分别测定 ADP诱导的血小板 5 min最大聚集率。结果　内源性 HTG患者血浆 TG含量平均升高 2 .73倍 ,HDL - C下降 1.71倍 ,同时 L PO升高 1.2 2倍 ;HTG组 VL DL、L DL及 HDL的 REM、A2 34 、TBARS含量均较对照组显著增加 (P<0 .0 1) ,表明内源性 HTG患者血浆 VL DL、L DL及 HDL均发生了氧化修饰生成Ox- VL DL、Ox- L DL及 Ox- HDL。血小板聚集率在分别加入 HTG组患者的 VL DL、L DL及 HDL后均比加入正常组相应脂蛋白明显增加 (P<0 .0 5及 P<0 .0 1)。相关分析表明 ,HTG- L DL及 HTG- HDL A2 34 、REM及 TBARS含量与血小板聚集率呈正相关 (P<0 .0 1)。结论　 HTG患者血浆 VL DL、L DL及 HDL发生了氧化修饰 ,并使血小板聚集增加     

姜黄素对高脂血症大鼠血脂和血管内皮生长因子水平的影响

目的观察姜黄素对高脂血症大鼠血脂及血管内皮生长因子（VEGF）水平的影响。方法将健康4周龄雄性sD大鼠50只随机分为正常对照组、模型对照组、低剂量姜黄素组、高剂量姜黄素组和辛伐他汀组,正常对照组给予普通饲料喂养,余各组给予高脂饲料喂养。低剂量姜黄素组、高剂量姜黄素组和辛伐他汀组于每13上午同一时间分别给予姜黄素50、100mg·kg-1、辛伐他汀20mg·kg-1灌胃。12周后颈动脉取血测定各组大鼠血清血脂、VEGF水平。结果模型对照组较正常对照组大鼠血清总胆固醇（TC）、三酰甘油（TG）、低密度脂蛋白（LDL）水平均显著升高,高密度脂蛋白（HDL）、VEGF水平均显著降低（P〈0．01）;各给药组较模型对照组大鼠TC、TG、LDL水平均显著降低,HDL、VEGF水平均显著升高（P〈0．01）;高剂量姜黄素组较低剂量姜黄素组大鼠血清TC、TG、LDL水平显著降低（P〈0．01）,HDL、VEGF水平显著升高（P〈0．01）;辛伐他汀组较高剂量姜黄素组大鼠血清TC、LDL水平显著降低,TG水平显著升高（P〈0．01）,血清HDL、VEGF水平比较差异均无统计学意义（P〉0．05）。结论姜黄素能有效降低高脂血症大鼠血清TC、TG、LDL水平,同时升高血清HDL、VEGF水平,且作用强度与剂量有关。姜黄素具有调节血脂、促进受损血管内皮修复的作用。     

Successful management of primary hypercholesterolaemia with simvastatin and low-dose colestipol.

OBJECTIVE: To examine whether a small dose of bile acid sequestrant used in combination with a hydroxymethylglutaryl coenzyme A reductase inhibitor is more effective in reducing serum and low-density lipoprotein (LDL) cholesterol levels than inhibitor used alone. DESIGN: A randomised, double-blind study. SETTING: Subjects receiving tertiary care at a hospital lipid clinic. PATIENTS: Subjects with severe primary hypercholesterolaemia (types IIa and IIb), already stabilised on a cholesterol-lowering diet, with serum cholesterol levels of 7.0 mmol/L or more and triglyceride levels of 6.0 mmol/L or less. Sixty-four subjects were randomly assigned to the treatment groups; three withdrew before any outcome observations; 61 completed the trial and their results were analysed. INTERVENTIONS: Subjects were randomly assigned to receive either colestipol placebo or colestipol 5 g or 10 g each morning in fixed dosage for 18 weeks. They simultaneously received incremental doses of simvastatin: placebo for six weeks, then 20 mg/night for six weeks, then 40 mg/night for a final six weeks. MAIN OUTCOME MEASURES: Lipids, lipoproteins, and haematological and biochemical safety parameters were measured at the end of each treatment period. Adverse events were monitored. RESULTS: Respective maximum reductions (95% confidence intervals) in serum cholesterol, LDL cholesterol and apolipoprotein B (apo-B) values in subjects taking combination therapy were 41% (38%-45%), 50% (46%-53%) and 43% (39%-46%), compared with lesser reductions of 32% (26%-37%), 38% (31%-45%) and 37% (32%-41%) in those taking simvastatin monotherapy. The percentage changes in LDL cholesterol with combination therapy were independent of baseline cholesterol level or lipid phenotype. Combination therapy reduced serum triglyceride levels by up to 24% (15%-32%) and increased high-density lipoprotein (HDL) cholesterol levels by up to 9% (3%-15%). Three subjects withdrew within a few weeks because of severe gastrointestinal side effects related to colestipol; 19 experienced milder gastrointestinal side effects, 15 were taking combination therapy. CONCLUSIONS: A combination of low-dose colestipol and simvastatin was found to be more effective in reducing serum and LDL cholesterol than simvastatin used alone. Such combination therapy offers the possibility of improved cholesterol lowering without the need for full dosage of either drug.     

1型糖尿病患者临床特点与胰岛素剂量关系的研究

目的研究胰岛素剂量与1型糖尿病患者的临床特点是否相关。方法94例初诊1型糖尿病(DM)病人随诊4a,记录每日胰岛素剂量、家族史,定期测量血糖、糖化血红蛋白、血脂、血尿酸、尿蛋白排泄量、体重指数、腰臀比等指标。结果胰岛素剂量、总胆固醇、甘油三酯、低密度脂蛋白与1型糖尿病病程的相关系数有统计意义(P<0.05)。确诊后4a胰岛素剂量与各自变量的相关系数中,腰臀比、甘油三酯、2型糖尿病家族史与胰岛素剂量的相关系数有统计意义(P<0.01)。结论在1型DM患者,胰岛素剂量与腰臀比、甘油三酯、2型糖尿病家族史相关。     

临床常用剂量下的舒降之、血脂康、美百乐镇对原发性高脂血症调脂作用的比较

目的:验证舒降之、血脂康、美百乐镇的调脂作用并做比较研究.方法:60例高脂血症患者随机分为3组,舒降之20mg每晚顿服;美百乐镇10mg每晚顿服;血脂康0.6g早晚各1次口服;服药前及服药后4、8、12周测定血脂.结果:舒降之组治疗后4周TC、LDL-C有下降(P＜0.05),12周比4周下降更明显(P＜0.05).美百乐镇组治疗后4周TC、LDL-C有下降(P＜0.05),12周与4周无明显变化(P＞0.05).两组的TG、HDL-C治疗前后均无明显变化(P＞0.05).血脂康组治疗后4周TC、LDL-C、TG有下降(P＜0.05),TC、LDL-C 12周比4周下降更明显(P＜0.05);HDL治疗前后无明显变化(P＞0.05).舒降之组治疗后8周、12周LDL-C分别下降(40%,45%),明显大于血脂康组(31%与36%)和美百乐镇组(31%与35%)(P＜0.05).血脂康组治疗后8周、12周TG分别下降(33%,35%),明显大于舒降之组(25%,26%)和美百乐镇组(18%,19%)(P＜0.05).3组TC、TG、HDL-C总有效率无显著差异(P＞0.05).结论:舒降之、血脂康、美百乐镇降脂疗效确切,但3种药疗效判断及调整治疗的时间窗不同.舒降之降LDL-C能力强,血脂康降TG能力强且较经济实用.     

冠心病患者血浆载脂蛋白M水平及其相关性研究

目的　监测冠心病患者血浆中载脂蛋白M (ApoM )的水平 ,了解ApoM与其他脂蛋白或载脂蛋白的关系。方法　应用Dot Blotting技术检测 70例冠心病患者及 85例健康志愿者血浆中ApoM的水平 ,酶法及比浊法检测冠心病患者血浆中载脂蛋白AI(ApoAI)、载脂蛋白B(ApoB)、脂蛋白a(Lpa)、总三酸甘油酯 (TG)、高密度脂蛋白胆固醇 (HDL C)、低密度脂蛋白胆固醇 (LDL C)以及空腹血糖 (Glu) ;比较冠心病患者和健康志愿者血浆中ApoM的水平 ,对ApoM与其他脂蛋白的关系进行相关性分析。结果　冠心病患者血浆中ApoM的水平为 (3 .3 55± 0 .12 2 2 )ODu·mm- 2 ,明显高于健康志愿者 (2 .0 97± 0 .0 5988)ODu·mm- 2 (P <0 .0 1) ,与ApoAI(r=-0 .2 42 3 ,P =0 .0 43 3 )、LDL C ApoB(r =-0 .2 481,P =0 .0 3 83 )、LDL C(r =-0 .2 60 8,P =0 .0 2 92 )相关。健康志愿组血浆ApoM与HDL C (r =0 .3 4 69,P =0 .0 0 95)、HDL C ApoAI(r =0 .414 6,P =0 .0 0 16)相关。结论　ApoM可能参与了体内的胆固醇代谢 ,并与冠心病的形成与发展有关     

痛风患者代谢指标及胰岛素抵抗的研究

[目的]了解痛风患者的代谢指标及胰岛素抵抗(IR)的情况,并探讨痛风患者胰岛素抵抗的影响因素.[方法]106例痛风患者为研究对象,测定空腹血糖(FPG)、空腹胰岛素(FINS)、血脂、血尿酸(Ua)及餐后2 h血糖(2hPG)、胰岛素(2hINS),分析痛风组与尿酸正常组的上述代谢指标,稳态模型(HOMA)计算胰岛素抵抗指数(IRI).并对影响痛风患者IR的诸多因素进行多元线性逐步回归分析.[结果]痛风患者体重指数(BMI)、空腹胰岛素、甘油三酯(TG)、低密度脂蛋白(LDL)及IRI分别为:(25.0±2.0)kg/m2、(14.26±3.53)mU/L、(2.35±0.71)mmol/L、(3.07±0.64)mmol/L、3.36±0.83,上述指标较尿酸正常组明显增高,痛风患者高密度脂蛋白(HDL)(1.47±0.55)mmol/L较尿酸正常组明显降低,2组间上述指标比较差异有显著性意义(P＜0.05,P＜0.01).痛风患者IR的Pearson相关分析结果示:IRI与年龄、BMI、TG、TC、LDL、UA呈正相关(P＜0.05或P＜0.01),与HDL呈负相关(P＜0.01).多元线性逐步回归分析提示BMI、UA、TG是影响痛风患者IR的独立危险因素.[结论]痛风患者存在IR,且BMI、UA、TG是影响痛风患者IR的重要因素.     

内源性睾酮对血浆脂质,脂蛋白和载脂蛋白水平的影响

对１０２例冠心病患者及９９名健康人进行了血浆睾酮、雌二醇、空腹血糖（ＢＳ）、总胆固醇（ＴＣ）、甘油三酯（ＴＧ）、高密度脂蛋白－胆固醇（ＨＤＬ－Ｃ）、低密度脂蛋白（ＬＤＬ－Ｃ）、脂蛋白（ａ）［Ｌｐ（ａ）］、载脂蛋白（Ａｐｏ）ＡＩ，ＡｐｏＢ１００测定。观察到血浆睾酮与ＴＧ和Ｌｐ（ａ）呈负相关，而与血浆ＨＤＬ－Ｃ和ＨＤＬ３－Ｃ呈正相关。血浆睾酮水平低下组，其ＴＧ和Ｌｐ（ａ）浓度明显高于血浆睾酮水平正常组     

3-Hydroxy-3-methylglutaryl--coenzyme A reductase inhibitors in the treatment of hypercholesterolemia

A new class of drugs, which inhibit de novo cholesterol biosynthesis, significantly reduces the blood cholesterol concentrations in hypercholesterolemic patients. Four separate inhibitors have lowered plasma total cholesterol and low-density lipoprotein (LDL) levels in humans by 20% to 40%: mevastatin (Compactin), lovastatin (mevinolin), pravastatin (CS-514, Eptastatin, and SQ 31000), and simvastatin (Synvinolin, MK-733). In addition to lowering total and LDL cholesterol concentrations, the plasma concentration of the potentially atherogenic B apolipoprotein is also reduced by 20% to 40%. The reduction in the levels of circulating atherogenic lipoprotein particles occurs as a result of decreased synthesis and enhanced removal of LDLs by the LDL receptor pathway in hepatocytes. Moreover, the levels of high-density lipoprotein cholesterol, which are inversely related to atherosclerosis, increase in concentration with treatment by these drugs. If the short-term safety of these drugs extends to ongoing long-term studies and if cardiovascular morbidity and mortality are affected by their use, this class of hypolipidemic agent will markedly facilitate the effective treatment of hypercholesterolemia.     

冠心病患者红细胞膜ATP酶活性及血脂水平的变化

观察２１例冠心病患者及正常对照组的空腹血浆甘油三酯（ＴＧ）、总胆固醇（ＴＣ）、低密度脂蛋白胆固醇（ＬＤＬＣ）、高密度脂蛋白胆固醇（ＨＤＬＣ）,红细胞膜Ｎａ＋Ｋ＋ＡＴＰ酶、Ｃａ２＋ＡＴＰ酶,Ｍｇ２＋ＡＴＰ酶及红细胞内Ｃａ２＋浓度（［Ｃａ２＋］）的变化。发现冠心病组ＴＧ,ＴＣ,ＬＤＬＣ及红细胞内［Ｃａ２＋］高于对照组;而血浆ＨＤＬＣ,红细胞膜Ｎａ＋Ｋ＋ＡＴＰ酶与Ｃａ２＋ＡＴＰ酶活性低于后者;Ｍｇ２＋ＡＴＰ酶无变化;Ｎａ２＋Ｋ＋ＡＴＰ酶,Ｃａ２＋ＡＴＰ酶分别与血浆ＴＧ,ＴＣ和ＬＤＬＣ呈负相关,与血浆ＨＤＬＣ呈正相关。根据测定结果,对其发病机制进行了讨论     

肥胖危险因素与血清瘦素的相关性研究

目的　探讨瘦素 (leptin ,LP)与肥胖、体重指数、性别、胰岛素、血糖、血脂及 2型糖尿病的关系。方法　 6 0例肥胖与 5 0例非肥胖受试者禁食 1 0h ,于清晨排大、小便后精确测量其身高、体重 ,空腹测血瘦素、血糖、胰岛素、总胆固醇 (totalcholestero ,Tch)、甘油三酯 (triglycerides,TG)、低密度脂蛋白胆固醇 (lowdensitylipoproteincholestero ,LDL c)、高密度脂蛋白胆固醇 (highdensitylipoproteincholestero ,HDL c)。将肥胖组与非肥胖组分别根据性别及是否有 2型糖尿病进行两次分组 ,对瘦素及其他各参数作比较分析。结果　 (1 )肥胖组瘦素均较非肥胖组显著增高 ;(2 )女性瘦素水平显著高于男性 ;(3)肥胖组空腹胰岛素 (fastinginsulin ,FINS)水平显著高于非肥胖组 ,女性显著高于男性 ,血脂Tch、TG、LDL c水平肥胖组显著高于非肥胖组 ,HDL c水平肥胖组低于非肥胖组 ,肥胖组与非肥胖组空腹血糖水平无差异性 ;(4)肥胖组、非肥胖组中 2型糖尿病与非 2型糖尿病之间的瘦素水平、胰岛素水平均无显著差异性。结论　瘦素水平与肥胖关系密切 ,瘦素与体重指数 (bodymassindex ,BMI)呈正相关 (P <0 .0 1 ) ;女性瘦素水平显著高于男性 ,LP与性别有相关性 (P <0 .0 5 ) ;LP与胰岛素 (P <0 .0 1 )、Tch(P <0 .0 5 )、