The level of triglycerides, total cholesterol and HDL cholesterol in various stages of human immunodeficiency virus (HIV) infection

In 63 HIV-infected individuals the levels of concentration plasma triglicerides, total cholesterol and HDL cholesterol were determined by the level of immunological deficiency defined according to the CD4 lymphocytes count. The analyzed markers of lipid disorder allow to draw the following conclusions: 1. Along with the increase of immunological deficiency and clinical development of the HIV infection the disorders, which are indicated by the increase in trigliceride levels and decreased plasma concentrations for HDL cholesterol, intensify as well. 2. HIV-infected persons, particularly those treated with protease inhibitors, should have carefully monitored lipid metabolism.     

甲状腺功能亢进症患者血清抵抗素水平与血糖、血脂及甲状腺激素的关系

目的 探讨甲状腺功能亢进症（简称甲亢）患者血清抵抗素水平与血糖、血脂、甲状腺激素(TH)的关系。方法 甲亢组50例,来源于2008、2009年就诊于哈医大二院内分泌科患者,均为新确诊尚未服药病例;以同时间到医院体检的40例健康者为对照组,两组均排除糖尿病、肥胖、高血压、高血脂。ELISA法测定血清抵抗素水平;化学发光法测定空腹胰岛素、游离三碘甲状腺原氨酸（FT3）、游离甲状腺素(FT4)、促甲状腺激素(TSH);葡萄糖氧化酶-过氧化物酶(GOD-PAP)法测定空腹血糖;胆固醇氧化酶法测定总胆固醇(T-CH);磷酸甘油氧化酶(GPO)法测定甘油三酯(TG);均相酶比色法测定高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)。同时测定身高、体重、腰围、臀围,计算体重指数(BMI)、胰岛素抵抗指数(HOMA-IR)。组间比较采用t检验,相关分析采用Pearson相关检验,用多元逐步回归方法比较抵抗素与血糖、血脂、TH的关系。结果 甲亢组血糖[(5.2±0.7)mmol/L]、抵抗素[(132.1±41.3)μg/L]、FT3[(19.8±8.7) pmol/L]、FT4[(54.1±29.6)pmol/L]、胰岛素[(7.9±2.8)mU/L]、胰岛素抵抗指数[(2.3±1.0)]明显高于对照组[(4.7±0.5)mmol/L,(65.1±5.9)μg/L、(4.1±0.6)pmol/L、( 14.3±2.2)pmol/L、(6.4±2.7)mU/L、(1.5±1.2);t值分别为4.64、10.17、11.42、8.49、4.48、9.42,P＜ 0.01或＜0.05]。甲亢组T-CH[(3.7±0.8)mol/L]、LDL-C[( 1.8±0.6)mol/L]、TSH[(0.01±0.01 )mU/L]明显低于对照组[(4.6±0.7) mol/L、(2.3±0.7)mol/L、( 1.80±0.90)mU/L;t值分别为5.30、3.33、14.48,P均＜0.01）]。相关分析显示,甲亢组抵抗素与FT3、FT4、HOMA-IR呈正相关(r=0.719、0.790、0.396,P＜0.01或＜0.05),与T-CH、LDL负相关(r=-0.364、- 0.519,P＜0.05或＜0.01)。多元逐步回归显示,甲亢组抵抗素与FT3、FT4、HOMA-IR正相关（r=0.756,P均＜0.01）。结论 抵抗素水平的调节受甲状腺激素影响,甲亢患者血抵抗素可能与胰岛素抵抗及糖脂代谢紊乱有关。     

Association between serum total cholesterol level and renal outcome in systemic lupus erythematosus

OBJECTIVE: To determine whether an elevated serum total cholesterol level in a first-available sample obtained at a systemic lupus erythematosus (SLE) clinic is associated with worse renal outcome in patients with SLE. METHODS: Survival analysis methods were used on prospectively gathered data on 1,060 patients with SLE who were registered in the University of Toronto Lupus Databank. The effect of total cholesterol and 15 additional variables on the outcomes of renal deterioration, end-stage renal disease (ESRD), and death was assessed using Cox proportional hazards methods. RESULTS: In 474 (45%) of the 1,060 patients, the total cholesterol level exceeded 5.2 mmoles/liter. In the entire study group, the median total cholesterol level was 5.1 mmoles/liter (range 1.6-17.1). During a mean followup period of 8.8 years, 93 patients (9%) experienced renal deterioration, 42 patients (4%) had ESRD, and 161 deaths occurred, 48 (30%) of which were associated with renal dysfunction (renal death), and 113 (70%) of which were not associated with renal dysfunction (nonrenal death). Kaplan-Meier survival estimates for each outcome were statistically significantly different between patients with normal versus those with elevated total cholesterol levels (cutoff 5.2 mmoles/ liter), with a worse outcome observed among those with an elevated total cholesterol concentration. In multivariate analyses, total cholesterol level (hazard ratio [HR] 1.17, 95 confidence interval [95% CI] 1.01-1.36), serum creatinine level (HR 1.06, 95% CI 1.04-1.07), proteinuria (HR 2.44, 95% CI 1.25-4.76), the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (HR 1.44, 95% CI 1.16-1.80), and corticosteroid dose (HR 1.01, 95% CI 1.00-1.02) were associated with renal deterioration. Significant predictors of ESRD were baseline proteinuria (HR 6.24, 95% CI 1.96-19.88) and serum creatinine level (HR 1.15, 95% CI 1.08-1.22). The total cholesterol level was correlated with death (HR 1.20, 95% CI 1.11-1.29), retaining statistical significance for renal death (HR 1.33, 95% CI 1.20-1.47) but not for nonrenal death (HR 1.12, 95% CI 0.99-1.25). CONCLUSION: Those results indicate that an elevated serum total cholesterol level in a first-available sample obtained at an SLE clinic is associated with adverse renal outcomes and mortality.     

肥胖大鼠血脂和体脂肪变化及心室肌细胞内钙离子强度与心律失常发生的关系

目的 观察高脂饮食诱导肥胖(DIO)大鼠血脂和体脂肪变化,探讨心室肌细胞内钙离子强度与心律失常发生的关系.方法 健康雄性SD大鼠60只,体质量200～250 g.将大鼠按体质星随机分为对照组(15只)和高脂饮食组(45只),高脂饮食组采用高脂饮食诱导法建立肥胖大鼠模型.喂养12周后,在高脂饮食组筛选体质量增加明显的大鼠进入肥胖组(15只).两组各选8只大鼠舌下注射0.1 ms/kg BaCl2,诱导心律失常.应用标准Ⅱ导联心电图连续监测1 h,评价大鼠心律失常发生率及严重程度.采集两组大鼠腹主动脉血,分离血清,测血清总胆同醇,甘油三酯,低密度脂蛋白胆固醇和高密度脂蛋白胆固醇.分离大鼠肾周脂肪,睾周脂肪和肠系膜脂肪,称重,计算体脂比.酶解法分离大鼠单个心室肌细胞,应用激光共聚焦技术记录细胞内钙离子强度([Ca2+]i).结果 肥胖组大鼠体脂比[(7.71±0.74)%]明显高于对照组[(4.69±0.37)%],两组比较差异有统计学意义(t＝3.650,P＜0.05),血清总胆固醇,甘油三酯和低密度脂蛋白水平,肥胖组[(1.26±0.04),(0.58±0.10),(0.51±0.04)mmol/L]与对照组[(0.92±0.08),(0.29±0.03),(0.31±0.04)mmol/L]比较显著增高(t值分别为3.801,2.778,3.536,P＜0.05),肥胖组大鼠心律失常发生率高于对照组(X2＝5.333,P＜0.05),心律失常评分肥胖组(2.5±0.6)高于对照组(0),肥胖组大鼠心室肌细胞内钙离子强度(247.96±20.03)明显高于对照组(174.25±23.13),两组比较差异有统计学意义(t=2.409,P＜0.05).结论 肥胖大鼠心律失常发生率增加,血脂升高,心肌细胞内钙离子积聚是引发肥胖源性心律失常的主要机制之一.     

血清胆红素与冠状动脉病变严重程度及血脂水平的关系

目的　探讨血清胆红素水平与冠状动脉病变严重程度及血脂水平的相关性。方法　经冠状动脉造影 (CAG)确诊的冠心病 (CHD)患者 5 6例 ,其中急性冠状动脉综合征 (ACS)患者 4 3例 ,包括急性心肌梗死 (AMI) 15例 ,不稳定性心绞痛 (UAP) 2 8例 ;稳定性心绞痛 (SAP) 13例 ;另设CAG排除CHD患者 2 0例作为对照组。运用比色法及酶法测定血清总胆红素 (TB)、直接胆红素 (DB)、总胆固醇 (TC)、低密度脂蛋白胆固醇 (LDL C)及甘油三酯 (TG)水平 ,间接胆红素 (IB)水平通过计算得出。以冠状动脉病变支数、冠状动脉病变积分、冠状动脉狭窄程度三者作为评价冠状动脉病变严重程度的的指标。结果　CHD组中SAP、UAP、AMI患者血清TB及IB水平明显低于对照组 ,而DB水平在CHD组与对照组之间差异无显著性意义 ,血清TB、IB、DB水平与冠状动脉病变支数、冠状动脉病变积分、冠状动脉病变程度呈明显负相关 ;与LDL C水平呈负相关 ,与TG ,TC无明显相关性。结论　人体内胆红素代谢紊乱可能和心血管事件发生相关 ,且其水平在一定程度上与冠状动脉病变严重性及血脂水平有关。     

黄芩苷对动脉粥样硬化大鼠凝血酶激活纤溶抑制物水平及血脂、凝血纤溶指标的影响

目的 观察黄芩苷对动脉粥样硬化(AS)模型大鼠的凝血酶激活纤溶抑制物(TAFI)水平及血脂、凝血纤溶指标的影响,探讨黄芩苷在干预AS进程中的机制.方法 40只健康雄性Wistar大鼠随机分为正常对照组、模型组、黄芩苷治疗组、辛伐他汀组,每组10只.正常对照组给予普通饲料喂养,其余3组在给予高脂饲料喂养的基础上行主动脉球囊损伤术,喂养4个月,以复制大鼠AS模型.用全自动生化仪测定血浆总胆固醇(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),用全自动血凝仪测定凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、纤维蛋白原(Fib),发色底物法测定血浆TAFI的活性.结果 与正常对照组相比,其余各组大鼠的TC、TG、LDL-C、Fib和TAFI活性均明显升高 (P<0.01或P<0.05),PT、APTT明显缩短(P<0.01或P<0.05);实验结束时,与模型组相比,黄芩苷治疗组与辛伐他汀组的TC、TG、LDL-C、Fib和TAFI活性明显低于模型组(P<0.01或P<0.05),PT、APTT明显延长(P<0.01或P<0.05);与辛伐他汀组比较,黄芩苷治疗组TC、TG、LDL-C、Fib、PT、APTT改善程度稍低(P<0.05),而TAFI活性则无明显统计学差异(P>0.05).结论 黄芩苷可能通过降血脂、改善凝血纤溶系统平衡、下调TAFI水平等途径干预了AS的形成.     

Long-term changes in serum cholesterol level does not influence the progression of coronary calcification

BackgroundA number of reports controversially describe the influence of cholesterol level and lipid-lowering treatment (LLT) on the progression of coronary calcium (CC). We tested the hypothesis that long-term changes in serum cholesterol (CL) would affect the progression of CC.MethodsThe study population comprised 510 patients with stable angina pectoris, mean age of 63 ± 9 years. At baseline 372 patients received statin and/or fibrate (LLT group) while 138 patients did not (No-LLT at baseline group). Spiral CT every 24 months was used to track the progression of CC over a median 5.6 year follow-up.ResultsCL decreased during follow-up in both groups, but more pronouncedly in patients with LLT. The changes in total calcium score (TCS) were similar in both groups (p = 0.3). Changes in CL during follow-up were not associated with CC: TCS increased by 501 ± 63 from baseline in the 1st (upper) quartile, and by 350 ± 44, 403 ± 41 and 480 ± 56 in the 2nd, 3rd, and 4th quartiles of CL longitudinal changes (p = 0.2), respectively. Baseline TCS and its changes were not correlated with baseline CL and its changes. New calcified lesions were diagnosed in 132 (28.2%) out of the 467 patients available for this analysis, without significant difference between groups (p = 0.4). Multivariate analysis demonstrated that only baseline TCS (p < 0.001), body mass index (p = 0.007) and age (p = 0.006) were independent predictors for the TCS changes.ConclusionsLongitudinal CL changes do not seem to have a measurable effect on the rate of progression of CC.     

Effects of exercise, dietary cholesterol, and dietary fat on blood lipids

Exercise, a low fat diet, or a diet low in saturated fat content can each lower plasma total cholesterol and low-density lipoprotein (LDL) cholesterol. We investigated whether these factors together could prevent the lipid-raising effects of dietary cholesterol. Ten healthy, athletic, normolipidemic male volunteers were studied. Two diets of 4 weeks duration each were compared in a randomized, blind crossover design. Diets were identical except for cholesterol content: one contained 600 mg/d; the other 200 mg/d. Both diets contained 15% of calories as protein, 55% as carbohydrate, 30% as fat, and the polyunsaturated fat to saturated fat ratio was 1.5. Exercise level and body weight were kept constant in each subject. As compared with plasma values obtained following the 200-mg/d cholesterol diet, mean values following the 600-mg/d cholesterol diet significantly increased for LDL cholesterol and apolipoprotein B by 10% and 13%, respectively. Mean plasma triglycerides, high-density lipoprotein 2 and 3, and apolipoprotein A-1 levels did not change significantly. Individual responses, however, were highly variable. Three subjects increased LDL cholesterol by more than 25%; 2 subjects increased LDL cholesterol by 10% to 25%; and 5 subjects had 5% or less change in LDL cholesterol. A dietary cholesterol increase can significantly elevate plasma LDL cholesterol and apolipoprotein B in certain normolipidemic, healthy men even when they are exercising regularly and consuming a moderately fat restricted, low saturated fat diet. Dietary cholesterol restriction may therefore be justifiable even when other life-style and dietary measures to minimize blood cholesterol are undertaken.     

Effect of dietary protein level and cholesterol supplementation prior to acute starvation on serum and liver lipids in the rat

The effect of acute starvation on serum and liver lipids has been studied in rats receiving high and low protein diets, with or without cholesterol and cholic acid supplementation. The rats which had consumed the low protein diet alone, showed during starvation an increase in the concentration of all serum lipid fractions, while rats on the high protein diet had a marked and significant decrease. The groups on the diet supplemented with cholesterol and cholic acid had higher initial values that dropped rapidly during starvation. This change, however, was more pronounced in the group receiving the high protein-cholesterol supplemented diet. The animals on the low protein cholesterol supplemented diet maintained higher serum lipid levels throughout the experiment. Changes in liver lipids were also observed among the dietary groups studied. It was concluded, therefore, that serum and liver lipids change differently with starvation in animals on a low protein diet than in animals on a high protein diet. No mechanism for such differences can be postulated at present.