文成县居民2013年血脂异常患病情况及相关因素调查

目的 研究文成县社区居民血脂异常患病情况的现状及其主要危险因素,为制定干预策略提供科学依据。 方法 2013年采用多阶段随机抽样方法抽取文成县4 003名18岁及以上常住居民为调查对象。进行问卷调查(一般情况、吸烟、饮酒、体力活动、膳食及精神因素等)、体格检查(体重、身高和血压的测量)及血生化检测(甘油三酯、高密度脂蛋白胆固醇、低密度脂蛋白、总胆固醇和血糖的检测),采用χ²检验分析血脂异常的人群分布,采用多因素非条件 logistic 回归分析探讨血脂异常的危险因素。 结果 文成县18岁及以上居民血脂异常患病率为45.32％,男女性血脂异常患病率为40.12％、48.86％。以2000年中国人口构成进行标化后血脂异常标化患病率为44.21%:男为39.43%,女为46.40%。女性显著高于男性(χ²=29.76,P=0.000),居民血脂异常患病率随着年龄的增加而增加(χ²_趋势=29.25,P=0.000)。高甘油三酯血症、高低密度脂蛋白胆固醇、高胆固醇血症、低高密度脂蛋白血症患病率分别为22.2％、14.9%、12.4%、8.9％。多因素非条件 logistic 回归分析结果表明,血脂异常与性别(OR=1.317,95%CI:1.115~1.554, P=0.001)、年龄(OR=1.010,95%CI:1.005~1.016, P=0.000)、职业(OR=1.053,95%CI:1.021~1.086, P=0.001)、文化程度(OR=1.146,95%CI:1.055~1.246, P=0.001)、高血压(OR=13.094,95%CI:11.053~15.512, P=0.000)、超重(OR=1.220,95%CI:1.022~1.457, P=0.028)、肥胖(OR=2.376,95%CI:1.524~3.704, P=0.000)有关。 结论 文成县社区居民18 岁及以上人群血脂异常患病率已经达到较高水平,血脂异常与性别、年龄、职业、文化程度、高血压、超重和肥胖有关。     

家族性高胆固醇血症性黄瘤病LDL-R基因的突变

目的　研究3个家族性高胆固醇血症黄瘤病家系低密度脂蛋白受体基因突变方式，初步探讨基因型与临床表型的关系。方法　对3例先证者及25个家系成员进行血脂测定、临床检查后，采用聚合酶链反应-变性高效液相色谱，结合扩增产物直接序列分析检测低密度脂蛋白受体基因，结果与GenBank比对，分析突变的病理意义。结果　3例先证者出生时即有黄瘤，之后多处出现黄瘤，并有角膜环，可确诊为家族性高胆固醇血症黄瘤病。先证者1低密度脂蛋白受体基因发现D601N错义突变；先证者2多次出现早发冠心病症状，低密度脂蛋白受体基因发现C122Y错义突变。先证者3低密度脂蛋白受体基因未发现突变位点。28例家系成员共确诊4例杂合子患者。结论　低密度脂蛋白受体基因两个外显子的突变可能是导致家族性高胆固醇血症黄瘤病的原因。     

Platelet dysfunction in vascular pathologies and how can it be treated

Cardiovascular diseases are one of the leading causes of morbidity and mortality in industrialized countries, and although many processes play a role in the development of vascular disease, thrombosis is the primary event that precipitates stroke and acute coronary syndromes. The blood platelets are of significant importance in medicine. These cells are involved in many physiological processes, particularly haemostasis through their ability to aggregate and form clots in response to activation. In addition, these dynamic cells display activities that extend beyond thrombosis, including an important role in initiating and sustaining vascular inflammation. The expansion of knowledge from basic and clinical research has highlighted the critical position of platelets in several inflammatory diseases such as arthritis and atherosclerosis. Platelets are emerging as important mediators of inflammation and provide important signals to mediate phenotype of other blood and vascular cells. The important role of platelets in arterial thrombosis and the onset of acute myocardial infarction after atherosclerotic plaque rupture make inhibition of platelet aggregation a critical step in preventing thrombotic events associated with stroke, heart attack, and peripheral arterial thrombosis. However, the use of platelet inhibitors for thrombosis prevention must seek a delicate balance between inhibiting platelet activation and an associated increased bleeding risk. The aim of this review is to up-date the knowledge on platelets physiology and dysfunction in pathologies, such as diabetes mellitus, hypercholesterolemia, and hypertension, emphasizing the link between platelets and the inflammation-related atherosclerosis. The review evaluates the opportunities offered by the novel platelet inhibitors to efficiently alleviate the thrombotic events.     

高胆固醇血症红细胞形态扫描电镜观察

 目的 探讨高胆固醇血症红细胞形态变化及发病机制.方法 以扫描电镜观察20例高胆固醇血症(>6 mmol/L)临床亚健康人血红细胞形态.结果 所选20例高胆固醇血症(>6 mmol/L)临床亚健康人血红细胞均有不同程度形态变异.结论 高胆固醇血症红细胞不仅存在膜组分的变化,同时膜蛋白和膜骨架受损及膜内外环境的劣化可能是导致其形态变异、功能受限的原因所在.     

大鼠高胆固醇血症与听觉器官线粒体DNA4834缺失的关系

目的　探讨大鼠高胆固醇血症对听觉器官线粒体DNA483 4 缺失以及听力下降的影响。方法　 6 0只大鼠分为实验组 (38只 )和对照组 (2 2只 ) ,实验组大鼠以高胆固醇饲料喂养 ,时间为 6个月 ,建立高胆固醇血症大鼠模型 ;对照组则在相同条件下以普通饲料喂养。通过听性脑干电反应(auditorybrainstemresponses,ABR)检查实验前后ABR阈上升程度。取左侧耳蜗 (实验组 2 1个 ,对照组10个 )和左侧蜗神经核 (实验组 2 7个 ,对照组 13个 ) ,提取DNA ,通过套式聚合酶链反应 (nestpolymerasechainreaction ,nestPCR)扩增检测听觉器官线粒体DNA483 4 (mitochondrialDNA ,mtDNA483 4 )缺失 ,比较两组动物的ABR阈上升程度和听觉器官的mtDNA483 4 缺失率并进行统计分析。结果　①高胆固醇饲料喂养可造成实验组大鼠血清胆固醇水平明显升高 (t检验 ,P <0 0 5 ) ;②两组大鼠随年龄增加ABR阈均上升 ,高胆固醇血症大鼠的ABR阈上升更加明显 ,和对照组的差异具有显著性 (t检验 ,P<0 0 5 ) ;③所有标本都扩增到正常mtDNA编码tRNA和NADH基因 ,实验组听觉器官mtDNA483 4 缺失发生率较对照组明显增高 ,其差异具有显著性 (χ2 检验 ,P <0 0 5 )。结论　长期高胆固醇血症可以加剧大鼠的听力下降 ,听觉器官mtDNA483 4 缺失可能是其作用     

家族性高胆固醇血症低密度脂蛋白受体基因突变的研究

目的 分析中国儿童家族性高胆固醇血症低密度脂蛋白受体基因突变,并建立筛查该基因突变的方法。方法 以一家两患儿及其父母的基因组DNA为模板,用聚合酶链反应（PCR）及增该基因的启动子和全部18个外显子。用温度梯度凝胶电泳（TGGE）分析检测PCR产物,对电泳结果异常者进行DNA测序。结果 平行TGGE发现,两患儿第13外显子存在一纯合突变,其父母此外显存在杂合突变。DNA测充证实两患儿第13外显子发生Ala^606→Thr纯合错义突变,其父母均为此Ala^606→Thr杂合突变。结论 此家系家族性高胆固醇血症患者的LDL受体 基因存在Ala^606→Thr突变。TGGE结合DNA测序法的建立可用本症的基因诊断。     

血脂康对高脂血症患者血管内皮舒张功能的影响

目的比较高脂血症患者经血脂康治疗前后的血管内皮舒张功能的改变。方法应用高频血管探头检测56名高脂血症患者颈动脉内-中膜厚度(IMT)及在休息时、反应性出血、舌下含服硝酸甘油后的肱动脉内径,同时检测血浆胆固醇水平,肝功能及血清肌酸磷酸激酶(CK)等指标,服用血脂康10周后,复查上述指标,比较前后的变化。结果服血脂康10周后患者的血管内皮功能明显改善,血浆胆固醇水平明显降低,肝功能及血清肌酸激酶未见明显变化。结论血脂康在降低血脂的同时可逆转或延迟颈动脉IMT的进程,明显改善高脂血症患者的血管内皮功能,对患者的肝功能及血浆肌酸激酶无影响。     

家族性高胆固醇血症纯合子患者低密度脂蛋白受体缺陷的研究

目的：研究家族性高胆固醇血症纯合子患者的发病机理。方法：在临床研究和家系调查的基础上, 培养患者皮肤成纤维细胞, 采用放射性配体结合受体分析技术研究其低密度脂蛋白受体。结果：患者低密度脂蛋白受体对低密度脂蛋白的高亲和性结合为正常人的７８．２％，高亲和性内移和降解则分别为正常人的３．６％和１．７％。结论：本例家族性高胆固醇血症纯合子患者的发病机制为低密度脂蛋白受体内移功能障碍。     

Effect of raloxifene on the incidence of elevated low density lipoprotein (LDL) and achievement of LDL target goals in postmenopausal women

SUMMARY

Objective: To determine the extent to which raloxifene can maintain low density lipoprotein cholesterol (LDL-C) levels below 160?mg/dL or reduce elevated LDL-C levels to below lipidlowering goals in postmenopausal women.

Patients and methods: The Multiple Outcomes of Raloxifene Evaluation (MORE) osteoporosis treatment trial randomized 7705 postmenopausal women to placebo or raloxifene (60?mg or 120 mg) daily for a core treatment phase of 3 years. Changes in LDL-C and other serum lipids in a subset of women was a predefined secondary objective. This post-hoc analysis included the 2413 women who did not take lipid-lowering medications at any time during the trial and for whom LDL-C measurements were available. The threshold for high LDL-C (≥ 160?mg/dL) and LDL-C lipid-lowering goals were defined according to National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) guidelines.

Results: The percent of women with LDL-C < 160?mg/dL was comparable between treatment groups at baseline (placebo, 57.5%; raloxifene 60?mg, 56.4%; raloxifene 120?mg, 56.8%). At 3 years, the percent of these women whose LDL-C had increased to above 160?mg/dL was significantly less in the raloxifene 60?mg and 120?mg groups compared with placebo by 65% (95% CI, 44%–78%) and 64% (95% CI, 43%–77%), respectively. Among women with elevated (defined for these analyses as ≥ 160?mg/dL) LDL-C at baseline, the proportion having elevated LDL-C at 3 years was significantly less in the raloxifene 60?mg and 120?mg groups compared with placebo by 32% (95% CI, 24%–40%) and 40% (95% CI, 32%–48%), respectively. Fifty percent and 13% of these women achieved LDL-C goals of <160?mg/dL and <130?mg/dL, respectively (P <0.001 vs. placebo for both) in the raloxifene 60?mg group, with similar results for the raloxifene 120?mg group.

Conclusions: In postmenopausal women with osteoporosis not taking concurrent lipid-lowering therapy, raloxifene significantly reduced the incidence of LDL-C ≥ 160?mg/dL and significantly increased the proportion achieving LDL-C goals for lipid-lowering compared with placebo. Whether these and other effects of raloxifene on cardiovascular risk markers will improve cardiovascular outcomes requires further study.