肥胖和高血压患者餐后甘油三酯代谢异常与胰岛素抵抗的关系

目的　探讨高血压病与肥胖患者餐后甘油三酯 (TG)代谢异常与胰岛素抵抗的关系。方法　 19例健康人 ,19例单纯肥胖患者 ,2 1例高血压非肥胖患者 ,2 3例高血压合并肥胖患者禁食 12h后 ,进行标准脂肪负荷试验 ,以TG 8h曲线下面积 (TG AUC)和TG峰反应 (TGPR)作为标准脂肪负荷后TG反应水平的指标。以胰岛素敏感性指数 (ISI)及胰岛素曲线下面积 (IS AUC)作为胰岛素敏感性的判定指标。结果　 (1)高血压合并肥胖、高血压非肥胖、单纯肥胖组TG AUC ,TGPR均显著高于正常组 [TG AUC分别为 :(2 4 5 1± 10 6 8)mmol/L、(17 5 8± 7 6 8)mmol/L、(15 2 6± 4 93)比 (8 74± 2 34)mmol/L ,P <0 0 5 ;TGPR分别为 :(5 2 1± 2 2 7)mmol/L、(3 4 6± 1 82 )mmol/L、(3 0 2± 1 0 1)比 (1 5 4±0 5 6 )mmol/L ,P <0 0 5 ],高血压合并肥胖组TG AUC ,TGPR显著高于高血压非肥胖和单纯肥胖组 (P<0 0 1) ,高血压非肥胖组与单纯肥胖组之间无显著性差异。 (2 )高血压合并肥胖、高血压非肥胖、单纯肥胖组ISI(绝对值 ) ,IS AUC均显著高于正常组 ,高血压合并肥胖组IS AUC ,ISI显著高于高血压非肥胖和单纯肥胖组 (P <0 0 1) ,高血压非肥胖组与单纯肥胖组之间无显著性差异。 (3)高血压合并肥胖、高血压非肥胖和肥胖组中具     

高血压患者脂肪酸粘附蛋白2基因多态性与餐后甘油三酯代谢异常的关系

目的研究原发性高血压患者(EH)餐后甘油三酯代谢异常与脂肪酸粘附蛋白2基因(FABP2)变异的关系.方法 50例EH患者和30例健康人禁食10～12小时后,进行标准脂肪负荷试验,以甘油三酯(TG)8小时曲线下面积(TG-AUC)和TG峰反应(TGPR)作为标准脂肪负荷后TG反应水平的指标.用聚合酶链反应(PCR)对FABP2基因54密码子HhaI酶切位点限性片段长度多态性进行分析.结果 (1)EH组TG-AUC,TGPR均显著高于对照组(TG-AUC 20.02±6.25比9.61±2.27 mmol/L,P<0.05;TGPR 4.15±2.82比2.05±1.31 mmol/L,P<0.01).(2) EH组FABP2基因54密码子Thr型(Thr54)基因频率与正常组无显著差别(0.28比0.25, P>0.05).(3)EH组中Thr纯合型(Thr 54/Thr 54)和Thr杂合型(Ala 54 /Thr 54)患者TG-AUC、TGPR显著高于野生型(Ala 54 /Ala 54)者,纯合型患者TG-AUC、TGPR显著高于杂合型(TG-AUC28.2±6.11、21.9±6.16比13.9±6.07 mmol/L,P<0.05;TGPR 7.56±2.67、4.20±1.62比2.34±1.47 mmol/L,P<0.05).结论高血压病患者存在餐后TG代谢障碍和消除延迟,FABP2基因54密码子Thr改变是餐后甘油三酯代谢异常的影响因素之一.     

超敏C反应蛋白与老年高血压患者合并颈动脉粥样硬化的关系

该文研究目的是了解炎症标记物超敏C反应蛋白(hsCRP)与老年高血压患者颈动脉粥样硬化发生之间的关系,进一步加深对高血压导致外周血管病变的认识。入选154例[男81例,女73例,年龄60~83岁,血压(152±21/87±12)mm Hg]老年高血压患者进行颈动脉超声测量颈动脉内中膜厚度(IMT)、观察有无斑块形成,定量检测血清hsCRP,并进行血清hsCRP与颈动脉内中膜增厚、斑块(颈动脉粥样硬化)之间的相关性分析。结果:合并颈动脉粥样硬化的高血压患者血清hsCRP明显高于无颈动脉硬化患者[(4·9±4·8)vs(3·1±3·9)mg/L,P<0·05]。有颈动脉斑块的患者血清…     

餐后高甘油三酯血症与冠心病的关系

为探讨餐后高甘油三酯血症与冠心病的关系 ,6 1例研究对象被分为冠心病组 (n =30 )和对照组 (n =31)两组 ,均口服标准脂肪餐 (含脂肪 5 3.4g/m2 体表面积 ) ,分别测定其空腹及餐后 2、4、6、8及 10h的甘油三酯浓度及高密度脂蛋白胆固醇浓度。发现两组病人餐后甘油三酯浓度达高峰时间均为 6h ,冠心病组的高峰浓度 (6 .15±3.0 0mmol/L)及餐后甘油三酯代谢的曲线下面积 [2 5 .96± 14.33mmol/ (h·L) ]明显高于对照组 [4 .5 9± 2 .0 9mmol/L及 14.6 9± 6 .5 8mmol/ (h·L) ,P <0 .0 0 5 ]。Logistic多元回归分析提示 ,餐后甘油三酯代谢的曲线下面积是冠心病的独立危险因素。相关分析表明餐后甘油三酯代谢的曲线下面积与两组餐后 6h及 8h甘油三酯浓度存在明显的正相关关系。以上提示冠心病病人存在异常的餐后高甘油三酯血症 ,该异常是冠心病的独立危险因素。测定餐后 6h及 8h甘油三酯浓度可以代替餐后甘油三酯代谢的曲线下面积 ,从而简化脂肪餐负荷试验。     

超敏C反应蛋白与老年高血压患者合并颈动脉粥样硬化的关系

目的了解炎症标记物超敏C反应蛋白(hsCRP)与老年高血压患者颈动脉粥样硬化发生之间的关系,进一步加深对高血压导致外周血管病变的认识。方法对入选154例老年高血压患者进行颈动脉超声测量颈动脉内中膜厚度(IMT)、观察有无斑块形成,定量检测血清hsCRP,并进行血清hsCRP与颈动脉内中膜增厚、斑块(颈动脉粥样硬化)之间的相关性分析。结果合并颈动脉粥样硬化的高血压患者血清hsCRP明显高于无颈动脉硬化患者[(4.94±4.76)vs(3.12±3.90)mg/L,P<0.05]。有颈动脉斑块的患者血清hsCRP显著高于颈动脉内中膜正常与增厚患者,分别为(5.38±4.96)vs(3.12±3.90)mg/L,(5.38±4.96)vs(3.55±3.81)mg/L,P<0.05。结论血清hsCRP水平与高血压患者颈动脉粥样硬化的发生有一定相关性,合并颈动脉粥样硬化尤其有颈动脉斑块的患者血清hsCRP显著高于无颈动脉病变患者。     

高血压病患者脂餐后甘油三酯代谢变化与血管内皮功能的关系

目的本研究旨在探讨高血压病(EH)患者脂餐后甘油三酯(TG)变化及其与血管内皮功能之间的关系.方法38例EH患者和20例健康人禁食10～12h后,采用高分辨率彩色血管超声、以肱动脉反应性充血前、后血管内径变化百分比反映血管内皮依赖性扩张功能.随后进行标准脂肪负荷试验,以TG8h曲线下面积(TG-AUC)和TG峰反应(TGPR)作为标准脂肪负荷后TG反应水平的指标.结果(1)EH组的肱动脉反应性充血前、后血管内径变化百分比显著小于对照组[(10.36±3.43)%比(15.48±4.36)%P<0.05];(2)EH组餐后TG水平的TGPR[(4.68±1.74)mmol/L比(1.84±0.67)mmol/L]及TG-AUC[(23.59±6.48)mmol/L比(9.49±3.47)mmol/L]均显著大于对照组(P<O.05);(3)EH合并餐后TG代谢障碍组(n=26)的肱动脉反应性充血前、后血管内径变化百分比较EH餐后TG代谢正常组(n=12)有明显降低[(10.98±1.32)%比(13.14±1.09)%,P<0.05].结论68.4%的EH患者伴有脂餐后TG代谢障碍和消除延迟,餐后TG代谢异常会加重EH患者血管内皮功能障碍.     

正常人餐后甘油三酯动态代谢对血清一氧化氮和血浆内皮素1的影响

为探讨正常人脂肪负荷后甘油三酯动态代谢对血清一氧化氮和血浆内皮素 1浓度的影响 ,取 2 0例正常人标准脂肪餐前 (0h)、餐后 2、4、6和 8h外周静脉血 ,分离血清 ,测定甘油三酯、总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、载脂蛋白AⅠ和载脂蛋白B水平 ,放射免疫法测定血浆内皮素 1浓度 ,比色法测定血清一氧化氮相对浓度 ,计算一氧化氮 /内皮素 1比值。结果发现 ,餐后 2h血清甘油三酯浓度显著高于餐前 (2 .19± 0 .16比 1.161.16± 0 .11mmol/L ,P <0 .0 5 ) ,4h达到高峰 (3.34± 0 .37mmol/L) ,8h恢复至餐前水平。餐后 2h血浆一氧化氮浓度存在一过性升高 (61.5 8± 5 .97比 42 .5 0± 7.42ng/L ,P <0 .0 5 ) ,6、8h又显著降低 (37.60± 5 .71比 61.5 8± 5 .97ng/L ;30 .76± 5 .0 1比 61.5 8± 5 .97ng/L ,P <0 .0 5 )。餐后 2h内皮素 1浓度较餐前显著降低(99.0 8± 16.5 5比 114.2 2± 16 .45ng/L ,P <0 .0 5 ) ,餐后 6、8h较 2h显著升高 (113.82± 19.80比 99.0 8± 16 .5 5ng/L ,12 1.0 2± 19.5 5比 99.0 8± 16.5 5ng/L ,P <0 .0 5 ) ,餐后 8h较 4h高 (12 1.0 2± 19.5 5比 10 3.45± 19.87ng/L ,P <0 .0 5 )。同样 ,一氧化氮 /内皮素 1比值在餐后 2h存在高峰 (0 .78± 0 .13比 0 .46±     

高血压患者脂肪酸粘附蛋白2基因多态性与餐后甘油三酯代谢异常的关系

目的　研究原发性高血压患者 (EH)餐后甘油三酯代谢异常与脂肪酸粘附蛋白 2基因 (FABP2 )变异的关系。方法　 5 0例EH患者和 30例健康人禁食 10～ 12小时后 ,进行标准脂肪负荷试验 ,以甘油三酯 (TG) 8小时曲线下面积(TG AUC)和TG峰反应 (TGPR)作为标准脂肪负荷后TG反应水平的指标。用聚合酶链反应 (PCR)对FABP2基因5 4密码子HhaI酶切位点限性片段长度多态性进行分析。结果　 (1)EH组TG AUC ,TGPR均显著高于对照组 (TG AUC :2 0 0 2± 6 2 5比 9 6 1± 2 2 7mmol/L ,P <0 0 5 ;TGPR :4 15± 2 82比 2 0 5± 1 31mmol/L ,P <0 0 1)。 (2 )EH组FABP2基因 5 4密码子Thr型 (Thr5 4 )基因频率与正常组无显著差别 (0 2 8比 0 2 5 ,P >0 0 5 )。 (3)EH组中Thr纯合型 (Thr 5 4 /Thr 5 4 )和Thr杂合型 (Ala 5 4 /Thr5 4 )患者TG AUC、TGPR显著高于野生型 (Ala 5 4 /Ala 5 4 )者 ,纯合型患者TG AUC、TGPR显著高于杂合型 (TG AUC :2 8 2± 6 11、2 1 9± 6 16比 13 9± 6 0 7mmol/L ,P <0 0 5 ;TGPR :7 5 6± 2 6 7、4 2 0± 1 6 2比 2 34± 1 4 7mmol/L ,P <0 0 5 )。结论　高血压病患者存在餐后TG代谢障碍和消除延迟 ,FABP2基因 5 4密码子Thr改变是餐后甘油三酯代谢异常的影响因素之一     

老年糖尿病患者颈动脉病变与血脂关系的研究

目的探讨老年糖尿病患者血脂水平与颈动脉血管并发症的关系.方法老年糖尿病患者150例为糖尿病组,年龄60～89岁;106例同期健康体检者为对照组,年龄60～88岁.受试者均测定空腹血压、血糖、胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、极低密度脂蛋白(VLDL)、载脂蛋白AI(apoAI)和载脂蛋白B(apoB)同时行彩色多普勒颈动脉超声检查.结果 (1)糖尿病组血糖、TC、TG、VLDL、apoB[(9.81±3.25)mmol/L、(5.27±1.10)mmol/L、(5.32±3.78)mmol/L、(0.86±0.84)mmol/L、(2.58±0.89)mmol/L]水平高于对照组[(6.96±0.09)mmol/L、(4.58±0.94)mmol/L、(3.03±1.57)mmol/L、(0.57±0.30)mmol/L、(2.09±0.59)mmol/L],两组比较差异有显著性(P＜0.05),糖尿病组纤维蛋白原为(4.67±1.64) g/L,高于对照组(3.24±1.07) g/L,P＜0.01;(2)老年糖尿病患者的颈动脉超声显示颈动脉血管壁回声不均匀,内中膜增厚,可有多支血管斑块形成及不同程度的狭窄.结论脂代谢异常是血管并发症形成的基础,颈动脉粥样硬化斑块是糖尿病患者早期主要血管病变之一,颈动脉超声能提示老年糖尿病患者的血管病变程度,为治疗、预防提供依据.     

原发性高血压患者颈动脉粥样硬化的临床意义

该文探讨原发性高血压与颈动脉粥样硬化的关系。方法:对251例原发性高血压患者,其中男性29例,女性122例,年龄(59.6±9.8)岁。高血压等级标准分为3组,Ⅰ级高血压52例;Ⅱ级高血压02例;Ⅲ级高血压97例。再根据病程分为3组;A组(<5年)98例,年龄(57.5±9.4)岁;B组(5~10年)70例,年龄(60.5±10.3)岁;C组(>10年)83例,年龄(62.5±9.3)岁。和93例健康对照者进行颈动脉超声检测,测量血管内径、内中膜厚度I MT)、血流频谱参数及观察斑块的存在与否,了解其与原发性高血压的关系。结果:原发性高血压患者颈动脉I MT较对照组明显增加(P<0.01),斑块发生率…     

脂餐负荷后血清甘油三酯反应水平与颈动脉内中膜厚度的关系

探讨餐后血浆富含甘油三酯脂蛋白蓄积与劝脉粥样硬化的关系。方法４２例经冠状动脉造影证实的男性冠心病患者接受了标准口服脂肪餐负荷试验,分别于餐前及虎后２、４、６、８小时测定血清甘油三酯浓度及空腹血清载脂蛋白Ｂ、高密度脂蛋白胆固浓度。     

Lipid-lowering therapy does not affect the postprandial drop in high density lipoprotein-cholesterol (HDL-c) plasma levels in obese men with metabolic syndrome: a randomized double blind crossover trial

Introduction The postprandial lipid metabolism in metabolic syndrome patients is disturbed and may add to the increased cardiovascular risk in these patients. It is not known whether postprandial high density lipoprotein‐cholesterol (HDL‐c) metabolism is also affected and whether this can be influenced by statin and/or ezetimibe treatment. Methods Prospective, randomized, double blind, crossover trial comparing simvastatin 80 mg with simvastatin/ezetimibe 10 mg/10 mg treatment for 6 weeks on postprandial HDL‐c metabolism in 15, nonsmoking, male, obese metabolic syndrome patients (Adult Treatment Panel III, ATPIII). Only study medication was allowed. HDL‐c concentrations, cholesteryl ester transfer (CET), CET protein (CETP) mass and adiponectin were measured before and after oral fat loading. ClinicalTrials.gov NCT00189085. Results Plasma HDL‐c levels remained stable during continuous fasting following an overnight fast. Pre‐fat load HDL‐c concentrations without treatment, after simvastatin and simvastatin/ezetimibe treatment were 1·15 ± 0·04, 1·16 ± 0·05 and 1·11 ± 0·04 mmol/l. Fat load induced a 11% drop in HDL‐c plasma levels; 1·02 ± 0·05 mmol/l (P < 0·001) which was not affected by either therapy. Triglyceride levels during fat load were similar after both treatments. Total CET increased from 9·73 ± 0·70 to 12·20 ± 0·67 nmol/ml/h (P = 0·004). Four hours after fat loading CETP mass was increased while adiponectin levels were decreased, irrespective of treatment. Discussion HDL‐c levels decrease as CET increases after fat loading in obese metabolic syndrome patients. This is not influenced by either simvastatin or simvastatin/ezetimibe treatment. After fat loading, CETP mass and CET increased, and adiponectin decreased pointing towards a potential role for intra‐abdominal fat. Decreased postprandial HDL‐c levels may contribute to the increased cardiovascular risk in metabolic syndrome patients on top of already low HDL‐c levels.     

Two years of growth hormone replacement therapy in a group of patients with Sheehan’s syndrome

To investigate the effects of GH replacement on lipid profile, carotid artery intima-media thickness (IMT), glucose metabolism and visceral fat in patients with Sheehan’s syndrome, ten patients, mean age 44.8 ± 9.5 yr, compared with 10 controls matched for age and body mass index were studied. Total cholesterol, Triglycerides (TG), HDL-c, LDL-c, Apolipoprotein A and B (apoA and apoB) and Lipoprotein (a), serum IGF-1, ultrasonography of the carotid arteries, oral glucose tolerance test (OGTT), HOMA insulin resistance index, insulin sensitivity index (ISI)-composite and abdominal CT scan were performed. When compared to a control group, patients presented lower HDL concentrations (p = 0.05) and 2-h OGTT insulin levels (p < 0.04) and increased TG levels (p < 0.04). After 24 months of GH replacement a reduction in the relation ApoB/ApoA (p = 0.04) was observed, as well as an increase in HDL (p < 0.004). A decrease in carotid artery IMT and in visceral fat over time was found, p < 0.03 and p < 0.04 respectively, though without any significant differences during post hoc comparisons of means, which may be explained by the small number of cases studied, but there was a tendency, p = 0.08 and p = 0.09 respectively. The 2-h OGTT insulin levels increased (p < 0.02) as well as the prevalence of glucose intolerance (prevalence = 42.8%, p < 0.05). GH replacement therapy promoted favorable effects on carotid artery IMT, lipid profile and visceral fat in patients with Sheehan’s syndrome. On the other hand, patients developed abnormal glucose tolerance probably due to an increase in insulin resistance, demonstrated by higher insulin levels, despite favorable changes in body composition.     

原发性高血压患者微量白蛋白尿与无症状性脑血管损害的研究

目的探讨原发性高血压(EH)患者微量白蛋白尿(MAU)与无症状性脑血管损害及颈动脉粥样硬化的关系。方法根据24h尿蛋白滤过率(UAER)测定结果,将162例EH患者分为正常白蛋白尿(NAU)组101例和MAU组61例。应用高频多普勒超声检测颈动脉内膜中层厚度(IMT)及颈动脉粥样硬化斑块;头颅MRI评价腔隙性脑梗死。采用logistic回归分析颈动脉IMT增厚和腔隙性脑梗死相关的危险因素。结果162例EH患者中MAU的阳性率为37.7%;与NAU组比较,MAU组颈动脉IMT明显增厚[(1.00±0.26)mmvs(0.86±0.20)mm,P<0.01],腔隙性脑梗死的发生率明显增高(62.3%vs44.6%,P<0.05);MAU与颈动脉IMT增厚及腔隙性脑梗死的发生独立相关(OR=2.639,95%CI:1.240～5.615,P<0.05及OR=2.369,95%CI:1.156～4.856,P<0.05)。结论MAU是高血压患者发生腔隙性脑梗死和颈动脉IMT增厚的一个预测指标,可作为判断无症状性脑血管损害及颈动脉粥样硬化的早期指标。     

代谢综合征的颈动脉粥样硬化特征

目的　观察代谢综合征患者颈动脉形态和功能的变化特点。方法　 171例住院病人分为代谢综合征组 (MS ,84例 ) ,高血压病组 (EH ,6 8例 )、糖尿病组 (DM ,19例 ) ,比较三组患者血脂改变及颈动脉超声检测结果。结果　MS组患者血浆甘油三酯 (TG)、低密度脂蛋白、载脂蛋白B水平较EH组明显升高 ( 2 5 3± 2 15比 1 72± 1 6 6 ,3 2 7± 0 99比 2 91± 0 92 ,1 0 7± 0 2 6比 0 97±0 2 0 ,P <0 0 1,0 0 5 ,0 0 1) ,MS组TG水平明显高于DM组 ( 2 5 3± 2 15比 1 6 7± 0 89,P <0 0 1) ;与EH、DM组比较 ,MS组患者颈动脉系血流阻力指数明显升高 ,颈总动脉内膜明显增厚 ( 0 88± 0 2 2比 0 80± 0 2 4 ,0 88± 0 2 2比 0 72± 0 2 9,P值均 <0 0 5 ) ;MS组颈动脉粥样斑块发生率及斑块指数明显升高。结论　代谢综合征颈动脉粥样硬化程度较单纯高血压病和糖尿病颈动脉病变更严重     

陈旧性心肌梗死患者颈动脉粥样硬化与危险因素的关系

为探讨陈旧性心肌梗死患者颈动脉粥样硬化情况，对38例陈旧性心肌梗死患者的颈动脉内中膜厚度及斑块进行超声检测，与32例健康者作对照。结果发现，陈旧性心肌梗死患者的颈动脉内中膜厚度、斑块指数及斑块发生率明显高于对照组。多因素回归分析显示，年龄、总胆固醇、收缩压与颈动脉内中膜厚度密切相关。     

Increased serum visfatin in patients with metabolic syndrome and carotid atherosclerosis

Objective Visfatin is a newly identified adipocytokine and recent studies indicated that visfatin may have potential proinflammatory effect. However, its pathophysiological role in the metabolic syndrome (MetS) is not fully understood. In this study we investigated whether serum visfatin levels is altered in patients with the MetS, and compared the levels of visfatin between patients with and without carotid plaques. Design and method A total of 139 patients with MetS and 105 controls were included. The patients were further divided into two groups: 40 with carotid plaques and 99 without carotid plaques. Serum visfatin was measured by using enzyme immunoassay method and carotid intimal‐media thickness (IMT) was measured by ultrasound in all subjects. Results Serum visfatin was elevated in both MetS patients with and without carotid plaques compared to controls (log visfatin: 1·14 ± 0·14 vs. 0·99 ± 0·17 ng/ml vs. 0·93 ± 0·23 ng/ml, P < 0·001 and P < 0·05 vs. control group, respectively), and in patients with carotid plaques more than in patients without carotid plaques (P < 0·001). Multiple stepwise regression analysis revealed that only LDL‐cholesterol correlated with visfatin, and visfatin independently correlated with max IMT in the patients with MetS. A log visfatin > 1·08 ng/ml had 70% sensitivity and 67% specificity for detecting patients with carotid plaques. Conclusions/interpretation Our results showed that serum visfatin was increased in patients with MetS, especially in those with carotid plaques. Visfatin may be an inflammatory marker of MetS.     

Postprandial reverse cholesterol transport in type 2 diabetic patients: effect of a lipid lowering treatment

Deterioration of reverse cholesterol transport (RCT), an important anti-atherogenic process, may contribute to the largely unexplained severity of cardiovascular risk in type 2 diabetic patients. Among other relevant metabolic perturbations is the impairment in type 2 patients of the postprandial increase in RCT which, in normal subjects, is associated with the transfer to HDL of PL from lipolyzed chylomicrons. We have explored the possibility that improvement of postprandial lipolysis by bezafibrate might also restore the stimulated level of postprandial RCT. Twelve male patients (HbA1c 7.6 +/- 1.6% triglycerides (TG) 4.5 +/- 2.4 mmol/l) were treated for 4 weeks with 400 mg bezafibrate and compared with seven age-matched controls. Lipoproteins were analyzed over 8 h after a 1000 Kcal fat load (80% lipid), serum mediated cholesterol efflux was evaluated using 3H-cholesterol labelled Fu5AH cells. Fasting efflux was lower in patients (17.9 +/- 3.3 vs 19.9 +/- 3.0 a. units, P < 0.05) and decreased postprandially in most instead of increasing, so that area under the time-curve (AUC) was 23% lower than in controls (140 +/- 23 vs 170 +/- 25 units x h, P < 0.001) The patients' HDL failed to acquire PL and gained TG in proportion to lipemia (r = 0.660, P < 0.001). Bezafibrate restored fasting efflux (19.6 +/- 3.6 units, P < 0.005 vs pretreatment) but not postprandial increase of efflux or HDL-PL. AUC of efflux was however improved to 155 +/- 23 units h (P < 0.02). Postprandial efflux related mainly to HDL-PL in controls and patients before treatment. HDL-TG emerged as a significant negative correlate common to all groups (r = -0.674, P < 0.001 8 h after the meal). Impairment of reverse cholesterol transport in diabetic patients might therefore be due to combined postprandial deficit of PL transfer and excess accumulation of TG in HDL. The significant improvement due to fibrate treatment might thus be related to the reduction of HDL-TG contents associated with the improvement of postprandial hyperlipemia.     

Subclinical atherosclerosis and endothelial dysfunction in young South-Asian patients with systemic lupus erythematosus

Patients with systemic lupus erythematosus (SLE), especially Asian Indians, are at increased risk of developing premature atherosclerosis. To find out the prevalence and predictors of carotid intima-medial thickness (IMT) and brachial artery flow-mediated dilatation (FMD). Endothelial dysfunction was assessed by FMD in brachial artery and IMT was measured in common carotid artery in SLE patients and healthy controls. Sixty SLE patients (mean age 31 ± 9 years) and 38 healthy controls (mean age 34 ± 6 years) were included. The IMT was higher in SLE patients as compared to controls (0.49 ± 0.08 mm vs. 0.39 ± 0.05 mm, p < 0.0001). SLE and damage were independent predictors of abnormal IMT. FMD was impaired in SLE patients compared to controls (9.97% vs. 18.97%, p < 0.00001). None of the classical cardiovascular risk factors were predictors of FMD or abnormal IMT. Indian patients with SLE have higher prevalence of subclinical atherosclerosis and endothelial dysfunction. Presence of damage was associated with abnormal IMT in SLE patients.