Effects of pindolol on serum lipoproteins and postheparin lipolytic activities in hypertensive patients

Thirty-four hyperlipoproteinemic, hypertensive patients received 5 mg of pindolol twice daily for 12 weeks. During pindolol administration, there were significant decreases in serum triglyceride levels and increases in high-density lipoprotein cholesterol (HDL-C) levels, while total cholesterol levels did not change. Serum levels of very-low-density lipoprotein (VLDL) triglyceride and VLDL cholesterol decreased over time as HDL-C increased. There was a significant increase in low-density lipoprotein cholesterol at week 12. Apolipoprotein (apo) A-I, A-II, and B levels did not change during pindolol administration, but apo C-II, C-III, and E levels decreased significantly. Lipoprotein lipase activity in heparin-treated plasma was significantly higher after pindolol administration. The results suggest that the reduction in triglyceride levels and increase in HDL-C after pindolol are partly a response to an increase in the hydrolysis of VLDL resulting from an increase in lipoprotein lipase activity.     

血糖调节异常者血脂代谢的初步研究

目的初步评价血糖调节受损患者血脂代谢异常情况。方法检测糖耐量正常(NGT)、单纯空腹血糖异常(IFG)、单纯糖耐量异常(IGT)、空腹血糖异常合并糖耐量异常(IFG IGT)和糖尿病(DM)患者空腹血糖和餐后2 h血糖及空腹血清总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白A-I(apo A-I)和载脂蛋白B(apo B)水平,计算非高密度脂蛋白胆固醇(non-HDL-C)和血浆致动脉硬化指数(AIP),比较各组间血清脂质成分的差异。结果IFG组血清TC、LDL-C、non-HDL-C和apo B水平较NGT组明显升高(P<0.01),而TG、HDL-C、AIP差异无统计学意义(P>0.05)。IGT组血清TC、TG、LDL-C、non-HDL-C、apo A-I、apo B和AIP水平较NGT组显著升高(P<0.01),前6项指标与IFG IGT组差异无统计学意义(P>0.05)。IFG IGT组与NGT组比较,各指标差异均有统计学意义(P<0.01);HDL-C、non-HDL-C和AIP水平与IFG组比较差异有统计学意义(P<0.01)。DM组表现出典型的DM性脂代谢紊乱伴AIP水平显著异常。non-HDL-C和apo B间存在良好的相关性(P<0.01)。结论血糖调节受损者不同程度的存在血脂代谢异常,主要表现为TC、TG、LDL-C、non-HDL-C和apo B水平的升高和HDL-C、apo A-I的降低,伴不同程度AIP水平的改变。     

Metabolic effects of fluvastatin extended release 80 mg and atorvastatin 20 mg in patients with type 2 diabetes mellitus and low serum high-density lipoprotein cholesterol levels: a 4-month, prospective, open-label, randomized, blinded—end point (probe) trial

Background

Diabetic dyslipidemia is characterized by greater triglyceridation of all lipoproteins and low levels of plasma high-density lipoprotein cholesterol (HDL-C). In this condition, the serum level of low-density lipoprotein cholesterol (LDL-C) is only slightly elevated. The central role of decreased serum HDL-C level in diabetic cardiovascular disease has prompted the establishment of a target of ≥50 mg/dL in patients with diabetes mellitus (DM).

Objective

The aim of the study was to assess the effects of once-daily administration of fluvastatin extended release (XL) 80 mg or atorvastatin 20 mg on serum HDL-C levels in patients with type 2 DM and low levels of serum HDL-C.

Methods

This 4-month, prospective, open-label, randomized, blinded—end point (PROBE) trial was conducted at Endocrinology and Diabetology Service, L. Sacco-Polo University Hospital (Milan, Italy). Patients aged 45 to 71 years with type 2 DM receiving standard oral antidiabetic therapy, with serum HDL-C levels <50 mg/dL, and with moderately high serum levels of LDL-C and triglycerides (TG) were enrolled. After 1 month of lifestyle modification and dietary intervention, patients who were still showing a decreased HDL-C level were randomized, using a 1:1 ratio, to receive fluvastatin XL 80-mg tablets or atorvastatin 20-mg tablets, for 3 months. Lipoprotein metabolism was assessed by measuring serum levels of LDL-C, HDL-C, TG, apolipoprotein (apo) A-I (the lipoprotein that carries HDL), and apo B (the lipoprotein that binds very low-density lipoprotein cholesterol, intermediate-density lipoprotein, and LDL on a molar basis). Patients were assessed every 2 weeks for treatment compliance and subjective adverse events. Serum creatine phosphokinase and liver enzymes were assessed before the run-in period, at the start of the trial, and at 1 and 3 months during the study.

Results

One hundred patients were enrolled (50 patients per treatment group; fluvastatin XL group: 33 men, 17 women; mean [SD] age, 58 [12] years; atorvastatin group: 39 men, 11 women; mean [SD] age, 59 [11] years). In the fluvastatin group after 3 months of treatment, mean (SD) LDL-C decreased from 149 (33) to 95 (25) mg/dL (36%; P < 0.01), TG decreased from 437 (287) to 261 (164) mg/dL (40%; P < 0.01), and HDL-C increased from 41 (7) to 46 (10) mg/dL (12%; P < 0.05). In addition, apo A-I increased from 118 (18) to 124 (15) mg/dL (5%; P < 0.05) and apo B decreased from 139 (27) to 97 (19) mg/dL (30%; P < 0.05). In the atorvastatin group, LDL-C decreased from 141 (25) to 84 (23) mg/dL (40%; P < 0.01) and TG decreased from 411 (271) to 221 (87) mg/dL (46%; P < 0.01). Neither HDL-C (41 [7] vs 40 [6] mg/dL; 2%) nor apo A-I (117 [19] vs 114 [19] mg/dL; 3%) changed significantly. However, apo B decreased significantly, from 131 (20) to 92 (17) mg/dL (30%; P < 0.05). Mean changes in HDL-C (+5 [8] vs −1 [2] mg/dL; P < 0.01) and apo A-I (+6 [18] mg/dL vs −3 [21] mg/dL; P < 0.01) were significantly greater in the fluvastatin group than in the atorvastatin group, respectively. However, the decreases in LDL-C (54 [31] vs 57 [32] mg/ dL), TG (177 [219] vs 190 [65] mg/dL), and apo B (42 [26] vs 39 [14] mg/dL) were not significantly different between the fluvastatin and atorvastatin groups, respectively. No severe adverse events were reported.

Conclusions

Fluvastatin XL 80 mg and atorvastatin 20 mg achieved mean serum LDL-C (≤ 100 mg/dL) and apo B target levels (≤ 100 mg/dL) in the majority of this population of patients with type 2 DM, but mean serum HDL-C level was increased significantly only with fluvastatin—16 patients (32%) in the fluvastatin group compared with none in the atorvastatin group achieved HDL-C levels ≥50 mg/dL. The increase in HDL-C in the fluvastatin-treated patients was associated with an increase in apo A-I, suggesting a potential pleiotropic and selective effect in patients with low HDL-C levels.     

血清非高密度脂蛋白胆固醇测定在非酒精性脂肪肝中的应用

目的探讨非酒精脂肪肝患者非高密度脂蛋白胆固醇（non-HDL-C）水平及临床应用价值。方法检测973名职工健康体检者的总蛋白（TP），白蛋白（Alb）、球蛋白（Glo）、天门冬氨酸氩基转移酶（AST）、丙氨酸氨基转移酶（ALT）、总胆红素（TBil）、直接胆红素（DBil）、间接胆红素（IBil）、葡萄糖（Glu）、总胆固醇（TC）、三酰甘油（TG）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、载脂蛋白A-I（apo A-I）、载脂蛋白B（apo B）、计算non-HDL-C及apo B/apo A-I、LDI-C／HDL-C、apo B／HDL-C、TC／HDL-C比值，并对其中89例非酒精性脂肪肝与202名体检健康者进行比较结果脂肪肝检出率为9．15％，男性检出率为12．50％，显著高于女性的5．99％（P〈0．05）；与对照组比较，59例男性患者的ALT、IBil、TG、HDL-C、LDL-C、apo A-I、non-HDL-C水平及apo B／apo A-I、LDL-C／HDL-C、apo B／HDL-C、TC／HDL-C比值差异具有统计学意义（P〈0.5，P〈0.01）,30例女性患者的AST、TBil、DBil、IBil、Glu、TC、TG、LDL-C、apo A-I、non-HDL-C水平及apo B／apo A-I、LDL-C/HDL-C、apo B/HDL-C、TC／HDL-C比值差并具有统计学意义（P〈0．05，P〈0．01）。non-HDL-C与TC、LDL-C、TG、HDL-C、apo A-I、apo B、apo B/apo A-I、TC／HDL均显著相关[相关系数（r）=0．4113～0．9893，P〈0．01]。结论非酒精性脂肪肝普遍具有代谢异常和肝脏受损等特点，non-HDL-C的检测有助于全面了解非酒精性脂肪肝脂炎代谢状况。     

上海地区老年男性血脂参考值及其分布

目的分析60岁以上老年男性血清脂类水平的参考值及其分布。方法752名健康老年男性按年龄分组,先按年龄5岁为组距分组并分析各血清脂类水平,根据统计结果重新分组。结果按不同年龄段之间的差异分为3组,其中随年龄增长,致动脉粥样硬化的脂类下降,抗动脉粥样硬化脂类成分上升。在不同年龄组间三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、载脂蛋白A-I(apo A-I)、载脂蛋白B(apo B)、非高密度脂蛋白胆固醇(non-HDL-C)差异有统计学意义,调查人群各指标的95%范围分别为:胆固醇(Chol)3.18～6.60 mmol/L,TG 0.66～3.66 mmol/L,HDL-C>0.92 mmol/L,低密度脂蛋白胆固醇(LDL-C)1.22～4.16 mmol/L,apo A-I0.91～1.65 g/L,apo B 0.56～1.34 g/L,non-HDL-C 1.87～5.13 mmol/L,LDL/LDL-apo B>1.07。结论老年人群的血脂合适范围较一般人群升高,特别是TG水平,在临床应用时应按不同年龄段选用恰当的合适范围。     

Post hoc analysis of data from the Multiple Outcomes of Raloxifene Evaluation (MORE) trial on the effects of three years of raloxifene treatment on glycemic control and cardiovascular disease risk factors in women with and without type 2 diabetes

BACKGROUND: The long-term effects of the selective estrogen-receptor modulator raloxifene hydrochloride on glycemic control and markers of cardiovascular disease risk in postmenopausal women with type 2 diabetes mellitus are unknown. OBJECTIVE: The aim of this analysis was to compare the effects of 3-year treatment with raloxifene 60 mg/d versus placebo on glycemic control and markers of cardiovascular disease risk in osteoporotic postmenopausal women with and without type 2 diabetes. METHODS: In this analysis, we included women from the Multiple Outcomes of Raloxifene Evaluation trial (a multicenter, double-masked trial) who were randomized to receive raloxifene 60 mg/d (n = 2557) or placebo (n = 2576). Baseline and 36-month fasting plasma glucose (FPG) and total cholesterol (TC) were measured for all participants. Glycated hemoglobin (HbA1c), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TGs), apolipoprotein (apo) A-I, apo B, and fibrinogen were assessed in approximately 1800 participants from selected larger sites. RESULTS: At baseline, 202 of all 5133 women (3.9%) had type 2 diabetes. Of the approximately 1800 women who were assessed for HbA1c, LDL-C, TGs, apo A-I, apo B, and fibrinogen, 70 (3.9%) had type 2 diabetes at baseline. Compared with placebo, raloxifene did not significantly affect HbA1c, FPG, HDL-C, or TGs in women with or without diabetes. Raloxifene produced statistically significant reductions in TC, LDL-C, and fibrinogen both in women with diabetes (all P < or = 0.004) and without diabetes (all P < 0.001). Raloxifene significantly increased apo A-I (P < 0.001) and reduced apo B (P < 0.001) in women without diabetes. In the raloxifene-treated group, body weight increased by a mean 0.31 kg (P < 0.001) in women without diabetes. CONCLUSIONS: In osteoporotic postmenopausal women with or without type 2 diabetes, raloxifene 60 mg/d did not affect glycemic control and had favorable effects on TC, LDL-C, and fibrinogen levels.     

血脂与脑梗死患者颈动脉粥样硬化的关系

目的了解血脂与脑梗死患者颈动脉粥样硬化的关系。方法对344例脑梗死疑似患者进行三酰甘油(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白A-I(apo A-I)、载脂蛋白B(apo B)、脂蛋白(a)[Lp(a)]检测,同时用计算机断层扫描(CT)、B超检测颈动脉病变。结果344例脑梗死疑似患者中有303例经临床及CT检查诊断为脑梗死,其余41例作为对照组。303例确诊患者中颈动脉管壁内膜-中层厚度(IMT)>0.9 mm或有斑块者206例,占68.0%;其余97例无病变,占32.0%。脑梗死患者LDL-C水平无论有无颈动脉病变均高于对照组(P<0.05)。无脑梗死的颈动脉粥样硬化患者apoA-I水平低于对照组(P<0.05)。结论LDL-C、apo A-I是发生脑梗死和颈动脉硬化病变重要的危险因素和诊疗的观察指标,B超检测颈动脉粥样硬化再结合血脂检查,对于脑血管疾病的预防、早期诊断、指导治疗以及观察疗效具有一定的临床价值。     

Effects of enalapril on serum lipoproteins in mild essential hypertension

The effect of the angiotensin converting enzyme inhibitor enalapril on serum lipids, apolipoproteins, and lipoproteins was studied in 21 patients with mild essential hypertension. The drug was administered at a dosage of 2.5 to 10 mg daily for 12 weeks. Enalapril significantly decreased the very low-density lipoprotein (VLDL) fraction at eight and 12 weeks. The apolipoprotein (apo) A-I and A-II fractions were significantly increased by 10% and 7.8%, respectively, at 12 weeks. The apo B fraction and the apo B/apo A-I ratio were significantly decreased at eight weeks (8% and 17%, respectively) and at 12 weeks (11% and 19%, respectively). Unchanged were the total cholesterol level, the lipoprotein cholesterol level, the triglyceride level, apo C-II, apo C-III, apo E, and the apo A-I/apo A-II ratio. This study confirmed that enalapril is an effective antihypertensive drug with a favorable effect on the lipid profile.     

Effects of polydextrose on serum lipids, lipoproteins, and apolipoproteins in healthy subjects

The subjects were 61 healthy volunteers who received 15 gm of polydextrose daily for two months. A significant increase in the incidence of soft feces and diarrhea and in the volume of feces was reported during polydextrose treatment. These had returned to normal one month after treatment. Serum levels of total cholesterol, triglycerides, and low-density lipoprotein cholesterol did not change during treatment. Levels of apolipoprotein (apo) A-I and A-II were significantly lowered at one month and high-density lipoprotein cholesterol (HDL-C) and apo A-I were significantly decreased at two months; these returned to normal after treatment. Levels of HDL2-C decreased and HDL3-C levels increased significantly during treatment. The results indicate that polydextrose selectively affected the metabolism of HDL and its major proteins, apo A-I and A-II.     

Lipid biomarkers, hormone therapy and the risk of venous thromboembolism in women

Summary.  Background: Published reports of a relationship between lipids and incident venous thromboembolism (VTE) are conflicting. Objectives: To clarify the relationship between lipids and VTE risk in healthy women, including potential effect modification by hormone therapy (HT). Patients/methods: Among 27 081 initially healthy women followed prospectively for incident VTE, we measured a full panel of lipid biomarkers, including total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides and apolipoproteins A-I (apo A-I) and B₁₀₀. Results: During a median follow-up of 11.4 years, VTE occurred in 355 women. We observed no relationship between any of the lipids and VTE risk. However, when unprovoked VTE was considered separately ( n  = 161), both HDL-C and apo A-I were positively associated with risk. Fully adjusted hazard ratios (HR) and 95% confidence intervals (CI) for extreme tertiles of HDL-C and apo A-I were 1.75 (1.13–2.73) and 1.70 (1.10–2.62), respectively. After stratifying by HT use, this relationship was present only among HT users; the HRs for unprovoked VTE for extreme tertiles of HDL-C and apo A-I were 3.58 (1.69–7.58) and 2.88 (1.29–6.42) among users, but only 0.79 (0.39–1.62) and 0.89 (0.50–1.57) among non-users. The interactions were statistically significant (each P _interaction <0.05). Conclusions: We observed little evidence that lipid levels predict risk of incident VTE among non-users of HT. High levels of HDL-C and apo A-I associate with unprovoked VTE risk among HT users. This observation likely reflects prothrombotic effects of HT that are concomitant with HDL-C and apo A-I levels, rather than direct effects of those lipids.     

Hypertriglyceridemia and cholesteryl ester transfer protein interact to dramatically alter high density lipoprotein levels, particle sizes, and metabolism. Studies in transgenic mice.

Several types of transgenic mice were used to study the influence of hypertriglyceridemia and cholesteryl ester transfer protein (CETP) expression on high density lipoprotein (HDL) levels, particle sizes, and metabolism. The presence of the CETP transgene in hypertriglyceridemic human apo CIII transgenic mice lowered HDL-cholesterol (HDL-C) 48% and apolipoprotein (apo) A-I 40%, decreased HDL size (particle diameter from 9.8 to 8.8 nm), increased HDL cholesterol ester (CE) fractional catabolic rate (FCR) 65% with a small decrease in HDL CE transport rate (TR) and increased apo A-I FCR 15% and decreased apo A-I TR 29%. The presence of the CETP transgene in hypertriglyceridemic mice with human-like HDL, human apo A-I apo CIII transgenic mice, lowered HDL-C 61% and apo A-I 45%, caused a dramatic diminution of HDL particle size (particle diameters from 10.3 and 9.1 to 7.6 nm), increased HDL CE FCR by 107% without affecting HDL CE TR, and increased apo A-I FCR 35% and decreased apo A-I TR 48%. Moreover, unexpectedly, hypertriglyceridemia alone in the absence of CETP was also found to cause lower HDL-C and apo A-I levels primarily by decreasing TRs. Decreased apo A-I TR was confirmed by an in vivo labeling study and found to be associated with a decrease in intestinal but not hepatic apo A-I mRNA levels. In summary, the introduction of the human apo A-I, apo CIII, and CETP genes into transgenic mice produced a high-triglyceride, low-HDL-C lipoprotein phenotype. Human apo A-I gene overexpression caused a diminution of mouse apo A-I and a change from monodisperse to polydisperse HDL. Human apo CIII gene overexpression caused hypertriglyceridemia with a significant decrease in HDL-C and apo A-I levels primarily due to decreased HDL CE and apo A-I TR but without a profound change in HDL size. In the hypertriglyceridemic mice, human CETP gene expression further reduced HDL-C and apo A-I levels, primarily by increasing HDL CE and apo A-I FCR, while dramatically reducing HDL size. This study provides insights into the genes that may cause the high-triglyceride, low-HDL-C phenotype in humans and the metabolic mechanisms involved.     

Familial hypercholesterolaemia: optimum treatment strategies

Familial hypercholesterolaemia (FH) is a hereditary metabolic disorder characterised by defects in the low-density lipoprotein (LDL) receptor, elevated LDL cholesterol (LDL-C) levels and an extremely high risk for premature cardiovascular disease. Heterozygous FH occurs in about one of every 500 individuals in the United States and Europe. The high prevalence of FH and associated morbidity and mortality strongly support aggressive screening and treatment. There are two major barriers to effective management of FH: 1) the failure to screen for this disease in people who may be at increased risk for it; and 2) the inability of most available therapies to enable achievement of LDL-C goals. More aggressive screening, coupled with new genetic screening techniques, and more powerful 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors have the potential to overcome these limitations. Automated genetic assays are now available for detection of common LDL receptor mutations in individuals at risk for FH, and they have been used effectively to identify patients with this condition. Recent clinical trial results with the new synthetic statin rosuvastatin (Crestor; AstraZeneca, Alderley Park, Macclesfield, Cheshire, UK; licensed from Shionogi & Co, Ltd, Osaka, Japan) in patients with heterozygous FH have shown that it decreased LDL-C by 58% and increased high-density lipoprotein cholesterol (HDL-C) by 12%. Rosuvastatin was significantly superior to high-dose atorvastatin in improving these lipid parameters as well as total cholesterol, apolipoprotein (apo) B, apo A-I, and the LDL-C/HDL-C ratio. Thus, new screening tools and medical therapies have the potential to significantly improve management and reduce cardiovascular disease risk for patients with FH.     

Effects of rosuvastatin versus atorvastatin, simvastatin, and pravastatin on non-high-density lipoprotein cholesterol, apolipoproteins, and lipid ratios in patients with hypercholesterolemia: additional results from the STELLAR trial

BACKGROUND: Non-high-density lipoprotein cholesterol (HDL-C), apolipoprotein (apo) B, and lipid and apolipoprotein ratios that include both atherogenic and antiatherogenic lipid components have been found to be strong predictors of coronary heart disease risk. OBJECTIVE: The goal of this study was to examine prospectively the effects of rosuvastatin, atorvastatin, simvastatin, and pravastatin across dose ranges on non-HDL-C, apo B, apo A-I, and total cholesterol (TC):HDL-C, low-density lipoprotein cholesterol (LDL-C):HDL-C, non-HDL-C:HDL-C, and apo B:apo A-I ratios in patients with hypercholesterolemia (LDL-C > or =160 mg/dL and <250 mg/dL and triglycerides <400 mg/dL) in the Statin Therapies for Elevated Lipid Levels compared Across doses to Rosuvastatin (STELLAR) trial. METHODS: In this randomized, Multicenter, parallel-group, open-label trial (4522IL/0065), patients > or =18 years of age received rosuvastatin 10, 20, 40, or 80 mg; atorvastatin 10, 20, 40, or 80 mg; simvastatin 10, 20, 40, or 80 mg; or pravastatin 10, 20, or 40 mg for 6 weeks. Pairwise comparisons were prospectively planned and performed between rosuvastatin 10, 20, and 40 mg and milligram-equivalent or higher doses of comparators. RESULTS: A total of 2268 patients were randomized to the rosuvastatin 10- to 40-mg, atorvastatin, simvastatin, and pravastatin groups. Fifty-one percent of patients were women, the mean (SD) age was 57 (12) years, and 19% had a documented history of atherosclerotic disease. Over 6 weeks, rosuvastatin significantly reduced non-HDL-C, apo B, and all lipid and apolipoprotein ratios assessed, compared with milligram-equivalent doses of atorvastatin and milligram-equivalent or higher doses of simvastatin and pravastatin (all, P < 0.002). Rosuvastatin reduced non-HDL-C by 42.0% to 50.9% compared with 34.4% to 48.1% with atorvastatin, 26.0% to 41.8% with simvastatin, and 18.6% to 27.4% with pravastatin. Rosuvastatin reduced apo B by 36.7% to 45.3% compared with 29.4% to 42.9% with atorvastatin, 22.2% to 34.7% with simvastatin, and 14.7% to 23.0% with pravastatin. The highest increase in apo A-I (8.8%) was observed in the rosuvastatin 20-mg group, and this increase was significantly greater than in the atorvastatin 40-mg and 80-mg groups (both, P < 0.002). CONCLUSION: Rosuvastatin 10 to 40 mg was more efficacious in improving the lipid profile of patients with hypercholesterolemia than milligram-equivalent doses of atorvastatin and milligram-equivalent or higher doses of simvastatin and pravastatin.     

高密度脂蛋白胆固醇、低密度脂蛋白胆固醇及其比值检测在中老年冠心病患者诊断和临床治疗中的意义

目的 探讨血清高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、LDL-C/HDL-C检测在中老年冠心病(CHD)患者中的意义.方法 分析经冠状动脉造影确诊为冠状动脉粥样硬化(药物治疗组)83例、CHD(支架植入组)163例及冠状动脉造影阴性(对照组)44例中老年病例的血清HDL-C、LDL-C、LDL-C/HDL-C比值与冠状动脉病变程度之间的关系.并比较各组间男女血脂水平的差异.结果 药物治疗组、支架植入组与对照组总胆固醇(T()、LDL-C、LDL C/HDL-C比值水平差异有统计学意义(P＜0.05或＜0.01).支架植入组TC、LDL-C、TC/HDLC比值水平明显高于药物治疗组及对照组(P＜0.05或＜0.01).支架植入组HDL-C显著低于药物治疗组及对照组(P＜0.05).药物治疗组女性HDL-C水平高于男性(P＜0.05),但女性TC/H DL-C比值、LDL-C/HDL-C比值低于男性(P ＜0.05).支架植入组女性TC和HDL-C高于男性(P＜0.05).对照组女性TC、HDL-C高于男性(P＜0.05),但女性TG/HDL C、LDLC/HDL-C低于男性(P＜0.05).结论 血清HDL-C、LDL-C、LDL-C/HDL-C比值与冠状动脉病变相关,对中老年CHD患者的诊断及临床治疗有使用价值.     

Low-dose effect of simvastatin (MK-733) on serum lipids, lipoproteins, and apolipoproteins in patients with hypercholesterolemia

The effects of simvastatin (MK-733), a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on serum lipids, lipoproteins, and apolipoproteins were investigated in 29 patients (12 men, 17 women, aged 37 to 73) with moderate to severe hypercholesterolemia. It was given in doses of 2.5 mg/day for four months and 5 mg/day for the succeeding four months. Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and apolipoprotein (apo) B decreased by 18% (263 +/- 7 mg/dl to 216 +/- 7 mg/dl, P less than 0.01), 24% (180 +/- 7 mg/dl to 136 +/- 7 mg/dl, P less than 0.01), and 21% (133 +/- 4 mg/dl to 104 +/- 3 mg/dl, P less than 0.01), respectively, four months after treatment. Similar reductions (17%, 24%, and 23%, respectively, P less than 0.01) were observed at eight months. A significant reduction in triglyceride (TG) was observed (173 +/- 15 mg/dl to 136 +/- 11 mg/dl at eight months, P less than 0.01), as was a significant increase in serum high-density lipoprotein cholesterol (HDL-C) (48 +/- 2 mg/dl to 52 +/- 2 mg/dl at eight months, P less than 0.01). However, apo AI and apo AII remained unchanged. Atherogenic indices of (TC--HDL-C)/ HDL-C, LDL-C/HDL-C, and apo B/Apo AI ratios were significantly (P less than 0.01) reduced after treatment. No significant changes were observed in lipoprotein lipase, hepatic TG lipase, and lecithin: cholesterol acyltransferase (LCAT) activities. Simvastatin was well tolerated and no critical side effects were noted in the eight-month study period. These data indicate that simvastatin, even at a low dose of 2.5 to 5 mg daily, causes consistent reductions in serum TC, LDL-C, apo B, and TG, and a rise in HDL-C and antiatherogenic lipoproteins.     

北京地区晚发性阿尔兹海默病患者apo E基因多态性与血脂的相关性

目的探讨晚发型阿尔兹海默病(LOAD)患者载脂蛋白E(apo E)基因多态性与血脂水平之间的关系。方法采用基因芯片法检测150例LOAD患者(LOAD组)及150名体检健康者(正常对照组)apo E基因多态性,同时检测总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、小而密低密度脂蛋白胆固醇(sd-LDL-C)、高密度脂蛋白胆固醇(HDL-C)、载脂蛋白B(apo B)、脂蛋白(a)[Lp(a)]水平。采用多因素非条件Logistic回归分析筛选LOAD的相关危险因素。结果LOAD组E2/3和E3/3基因型频率均低于正常对照组(P<0.05),E3/4和E2/4基因型频率均高于正常对照组(P<0.01)。LOAD组ε3等位基因频率低于正常对照组(P<0.05),ε4等位基因频率高于正常对照组(P<0.01)。与正常对照组比较,LOAD组TC、LDL-C和sd-LDL-C水平明显升高(P<0.01),HDL-C水平明显降低(P<0.01),其他血脂项目差异均无统计学意义(P>0.05)。TC及LDL-C水平在LOAD组ε2、ε3和ε4表型患者中依次升高(P<0.05)。正常对照组ε4表型LDL-C水平明显高于ε2表型(P<0.05)。apo Eε4等位基因和LDL-C升高是LOAD发生的危险因素[比值比(OR)值分别为14.454、5.824,95%可信区间(CI)分别为5.793~16.368、2.582~7.973],HDL-C升高则是LOAD的保护因素(OR=0.020,95%CI为0.006~0.352)。结论apo E基因多态性与脂质代谢密切相关,ε4等位基因可能是LOAD发病的重要遗传因素之一。     

Effects of gamma-oryzanol on serum lipids and apolipoproteins in dyslipidemic schizophrenics receiving major tranquilizers

The subjects were 20 chronic schizophrenic patients with dyslipidemia (total cholesterol levels greater than or equal to 220 mg/dl, triglycerides greater than or equal to 150 mg/dl, or high-density lipoprotein cholesterol less than or equal to 40 mg/dl) who had been receiving neuroleptics for a mean of ten years. Each patient was given 100 mg of gamma-oryzanol three times daily for 16 weeks. Total cholesterol and low-density lipoprotein cholesterol levels, respectively, decreased significantly, from 204 and 124 mg/dl at baseline to 176 and 101 mg/dl at week 12. High-density lipoprotein cholesterol levels were 36.1 mg/dl at baseline and 35.9 mg/dl at week 12. Apolipoprotein (apo) B levels decreased significantly from 116 mg/dl to 101 mg/dl at week 16; apo A-II levels increased significantly from 31.7 mg/dl to 34.7 mg/dl; and the apo B/apo A-I ratio declined significantly from 0.99 to 0.84. No treatment side effects were recorded. It is concluded that gamma-oryzanol is safe and effective in the treatment of dyslipidemia.     

2型糖尿病患者大血管并发症与血脂血糖关系的临床观察

目的　探讨 2型糖尿病患者血脂、血糖水平与大血管并发症的关系。方法　采用免疫透射比浊法及酶法 ,分别测定空腹血糖 (FBS)、总胆固醇 (TC)、甘油三酯 (TG)、高密度脂蛋白 (HDL C)、低密度脂蛋白(LDL C)、载脂蛋白A1(apoA1)及载脂蛋白B(apoB)水平。结果　有大血管并发症组FBS、TC、LDL C、apoB水平及糖尿病病程与对照组比较有显著升高 (P <0 .0 5 )。结论　 2型糖尿病大血管并发症的发生与血脂代谢异常有关     

Activity of low-density lipoprotein receptors as estimated from concentrations of apolipoprotein B and C-II in serum

The correlation between low-density lipoprotein (LDL) receptor activity and concentrations of lipids and apolipoproteins in serum was examined in 12 subjects with heterozygous familial hypercholesterolemia (FH) and in four with non-FH type II hyperlipoproteinemia. Concentrations of high-density lipoprotein cholesterol and of apolipoproteins (apo) A-I, C-II, and C-III were significantly positively correlated with LDL receptor activity, whereas LDL receptor activity was significantly inversely correlated with LDL cholesterol and apo B concentrations, and with apo ratios B/A-I and B/A-II. Neither total serum cholesterol, triglyceride, phospholipid, apo A-I, nor apo E concentrations correlated significantly with LDL receptor activity. Multiple regression analysis, with LDL receptor activity as the dependent variable, revealed concentrations of apo B and apo C-II to be the principal determinant factors. To confirm this, we subsequently calculated the LDL receptor activities before and after administration of CS-514, an inhibitor of hydroxymethylglutaryl-CoA reductase (EC 1.1.1.88), which increases the hepatic LDL receptor activity and decreases the concentration of cholesterol in serum. This drug increased calculated LDL receptor activities significantly, with a significant decrease in serum cholesterol.     

血浆卵磷脂-胆固醇酰基转移酶与红细胞膜脂质成分的相关性探讨

目的 探讨缺血性脑血管病(ischemic cerebrovascular disorders,ICVD)患者血浆卵磷脂-胆固醇酰基转移酶(LCAT)活性与红细胞膜脂质成分含量的相关性。方法 采用酶学方法分别测定105例ICVD患者和65例健康对照者血浆LCAT活性,并同时检测血清高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白A1和载脂蛋白B(apoA1,apoB)、红细胞膜胆固醇(RBCM-CH)和红细胞膜磷脂(RBCM-PL)含量。结果 ICVD患者LCAT活性、HCL-C及apoA1含量明显低于对照组(P<0.05),LDL-C、apoB、RBCM-CH及RBCM-CH／RBCM-PL比值显著高于对照组(P<0.05),并且LCAT活性分别与HDL-C、及apoA1呈正相关(P<0.01、P<0.05),而与LDL-C和RBCM-CH呈负相关(P<0.05)。结论 ICVD患者脂质代谢方面的异常可能与血浆LCAT活性降低有关。