降血脂药——普罗布考

目的：为了临床和患者了解新药普罗布考，本文做一全面综述。方法：从普罗布考的作用、副作用、给药及药代动力学几方面介绍。结果：普罗布考可降低血清总胆固醇２０％￣２５％，对纯合子型家族性高胆固醇血症及皮肤和腱黄瘤和明显疗效，及抗氧化作用是α－ＶＥ的５￣６倍，其抗动脉粥样硬化和抗经皮经腔冠状动脉成形术（ＰＴＣＡ）后再狭窄作用明显强于洛伐他汀、普伐他汀和消胆胺。另外其副作用小。结论：普罗布考将在血脂调节、抗     

微粒化非诺贝特对冠心病脂餐后血清甘油三酯反应水平的影响

目的　探讨微粒化非诺贝特 (力平之 ,法国利博福尼制药公司 ,批号 772 89)对冠心病(CHD)患者脂餐后血清甘油三酯 (TG)浓度、达峰时间及反应水平的影响。以CHD脂餐后TG的动态变化指标进行研究。方法　将 116例研究对象分为CHD组 (62例 )和对照组 (5 4例 ) ,均口服标准脂肪餐 ,并予CHD组患者服用力平之 2 0 0mg ,每晚 1次 ,共 8周。检测其空腹及餐后 2、4、6、8h的TG浓度。结果　GHD组餐后TG浓度峰值时间是 6h ,峰值浓度明显高于对照组 (P <0 .0 1) ,8h复原能力下降。治疗8周后 ,患者空腹及餐后TG浓度、餐后TG曲线下面积 (TG AUC)、餐后TG峰反应 (TGPR)明显降低 (P <0 .0 1)。结论　力平之适用于CHD空腹及餐后高TG血症患者。     

服用ω—3多不饱和脂肪酸浓缩剂一年可降低应用辛伐他汀而持续有高甘油三酯血症冠心病患者的甘油三酯

有人报道ω-3脂肪酸(例如存在于鱼油者)可延长心肌梗死生存者的寿命。此种脂肪酸能降低血清甘油三酯,但是至今在检验其对冠脉疾病终点的试验所用的剂量,对降低甘油三酯的效应极低。 PN Durrington等进行一项研究观察Omacor,一种来自鱼油的ω-3长链多不饱和脂肪酸浓缩剂(占总量的84％,而鱼油中平均为35％)的降甘油三酯效果、安全性和耐受性。作者们按斯堪的纳维亚辛伐他汀生存研究(Scandinavian simvastatin survival study)相同的辛伐他汀剂量给予冠心病患者服用而仍持续有高甘油三酯血症,并口服Omacor 1年。     

浅析影响视力的因素和预防对策及重要性

随着社会的发展工作和学习压力的不断增大,视力低下状况越发严重,近年来越来越多的学生受到近视、斜视、弱视、散光等问题的严重困扰。据临床资料统计,学生的视力低下率逐年升高,以达到31%～35%,而且更趋于中小学生,分析其影响视力的原因,认识保护视力的重要性,做好预防对策和工作,是降低学生视力低下的重要的保证。     

上海松江区新桥镇居民高同型半胱氨酸血症分布及影响因素分析

目的:了解上海松江区新桥镇居民同型半胱氨酸(Hcy)水平及分布情况,分析人群高同型半胱氨酸血症(HHcy)的检出情况及其相关因素.方法:采用整群抽样的方法随机选取2个家庭医生团队的服务人群,且在2017年10月—2018年9月在上海松江区新桥镇社区卫生服务中心参与体检的6265名社区居民作为研究对象,年龄中位数为63岁...     

新生儿体重相关影响因素的研究

目的分析新生儿出生体重的相关影响因素。方法选取唐山市妇幼保健医院2002全年出生的4144例单胎活产新生儿,对其出生体重的相关影响因素进行分析比较。结果新生儿体重男性明显高于女性（P〈0.01）,文化程度高的产妇其新生儿体重高于文化程度低的产妇的新生儿（P〈0.01）,不同孕次的产妇新生儿出生体重比较差异有统计学意义（P〈0.05）,不同产次的新生儿平均出生体重比较差异无统计学意义（P〉0.05）,未发现产妇年龄和新生儿出生体重有相关关系（r=0.0072,P=0.6235）。结论本次研究发现,产妇的文化程度、孕次、新生儿性别等可能是出生体重的影响因素。     

冠心病的新危险因素研究进展

冠状动脉粥样硬化心脏病 (简称冠心病 ,ＣＨＤ)的危险因素如 ,糖尿病、高血压、高胆固醇血症、吸烟等已得到大家的公认 ,而且已经进行有效的防治 ,诸如控制高血压、戒烟、降低胆固醇、控制血糖等治疗 ,但仍有一部分病人病变继续发展。因此大家都在探索新的危险因子 ,以期更好的控制疾病的发生与发展。目前 ,又发现了许多新的危险因子 ,如高同型半胱氨酸血症、血浆纤溶酶原激活物抑制剂 (ＰＡＩ 1)、Ⅶ因子、纤维蛋白原、小而密的低密度脂蛋白、感染等 ,本文就近年研究进展做一综述。1　高同型半胱氨酸血症血浆同型半胱氨酸 (Ｈｃｙ)是一种含…     

高尿酸血症和痛风的流行病学及影响因素研究

目的:分析高尿酸血症和痛风的流行病学及影响因素。方法:研究阶段为2016年1月～2018年1月,共纳入950例研究对象进行调查,开展问卷调查、体格检查及实验室检查。结果:950例研究对象中有76例高尿酸血症患者,患病率为8%,男性高尿酸血症患病率明显高于女性(P0.05)。男性血尿酸平均水平为(326.02±68.35)μmol/L,经方差分析总体差异有统计学意义(F男=7.342,P=0.000),经SNK比较50～岁与其他年龄段不同(P0.05);女性平均(294.62±72.63)μmol/L,经方差分析总体差异有统计学意义(F女=8.305,P=0.000),经SNK比较30～岁、50～岁与其他年龄段不同(P0.05)。高胆固醇血症、高三酰甘油血症、饮酒、性别、高血压、体重是高尿酸血症的危险因素(P0.05)。结论:男性高尿酸血症和痛风明显高于女性,另外高胆固醇血症、高三酰甘油血症、饮酒、性别、高血压、体重增加发生高尿酸血症和痛风的可能性,提示临床需重点关注。     

HDL-C levels and cardiovascular disease: more is not always better!

HMG-CoA reductase inhibitors have consistently demonstrated a relative risk reduction of death and myocardial infarction ranging between 29 and 35%. Nevertheless, in spite of significant improvement in prevention, cardiovascular disease remains the main cause of morbidity and mortality in industrialized countries. This significant residual risk observed in approximately 70% of patients under optimal anti-atherosclerotic therapies, warrants the exploration and development of alternative cardiovascular drugs. Specifically, HDL-C levels have been inversely correlated with the incidence of cardiovascular disease and an estimated 1 mg/dl higher HDL-C is associated with a 2% lower risk for men and a 3% lower risk for women. However, HDL-C-C pharmacological induced increases presented contradicting results regarding atherosclerotic development and in some cases increased cardiovascular mortality. In this review, we will focus on the structure and metabolism of HDL-C and patents related to HDL-C levels and cardiovascular disease along with the possible role of HDL-C increasing therapies in the future primary and secondary prevention of cardiovascular disease.     

慢性乙型肝炎患者HBV DNA水平的影响因素分析

乙型肝炎病毒(HBV)的持续性复制在慢性乙型肝炎(乙肝)的发展过程中起着重要的作用。它可以引起肝脏的氧化应激和炎症反应水平增高,从而增加肝纤维化、肝硬化及肝癌的风险[1]。HBV的生物学活性及复制水平受到宿主各种因素的制约,而血清HBV DNA水平在一定程度上反映了HBV的生物学活性和复制水平[2]。高密度脂蛋白胆固醇(HDL-C)具有抗炎等生物学活性,同时可能作为宿主非特异性免疫反应的一部分影响HBV的生物学活性和复制水平[3]。本研究旨在探讨HBV与HDL-C可能存在的关系。     

Beyond LDL-C--the importance of raising HDL-C

Epidemiological studies have established that low levels of high-density lipoprotein cholesterol (HDL-C) are associated with an increased risk of coronary heart disease (CHD). Recent studies have demonstrated that low HDL-C levels, and high triglycerides and total cholesterol levels are independent predictors of CHD, and that the combination of these lipid abnormalities increases the risk of coronary events. In lipid-modifying intervention studies, agents that raise HDL-C levels have been shown to reduce the incidence of major coronary events. The VA-HIT study consisted of patients with low-density lipoprotein cholesterol (LDL-C) levels similar to those recommended by several guidelines but with low levels of HDL-C. This trial demonstrated that raising HDL-C levels with gemfibrozil reduced the risk of CHD-related events. While the mechanisms by which HDL-C exerts its anti-atherogenic effects have yet to be fully elucidated, its role in the reverse transport of cholesterol and the beneficial effects on endothelial function are plausible explanations for these actions. Although LDL-C reduction is the primary goal in the treatment of dyslipidaemia, current guidelines recognise low HDL-C levels as a major risk factor for CHD. Indeed, the NCEP ATP III guidelines suggest that the treatment of isolated low HDL-C levels in CHD patients or individuals with CHD risk equivalents should be considered. The differing abilities of statins to raise HDL-C levels may be an important factor when making treatment decisions. New lipid-modifying drugs with beneficial effects on both HDL-C and LDL-C levels would be desirable additions to the currently available therapeutic options.     

Effectiveness of simvastatin therapy in raising HDL-C in patients with type 2 diabetes and low HDL-C

OBJECTIVE: To evaluate the efficacy of high and moderate doses of simvastatin (80 and 40 mg), for raising high density lipoprotein-cholesterol (HDL-C), improving HDL sub-fractions, and affecting other parameters, including high sensitivity C-reactive protein (hs-CRP), in patients with type 2 diabetes mellitus (DM) and low HDL-C. RESEARCH DESIGN AND METHODS: This double-blind, placebo-controlled, randomized, 3-period, complete block, 6-week crossover study examined the efficacy of simvastatin in adult men and women (N = 151) with stable type 2 DM (HbA(1C) < 9%), low density lipoprotein-cholesterol (LDL-C) > 100 mg/dL (2.6 mmol/L), HDL-C < 40 mg/dL (< 1 mmol/L), and fasting triglyceride level > 150 (> 1.7 mmol/L) and < 700 mg/dL (< 7.9 mmol/L). This study included adult men (71%) and women (29%) of various races (89% white, 6% black, 1% Asian, 3% other) enrolled from 29 practice-based sites in the United States. MAIN OUTCOME MEASURES: Percentage change in HDL-C from baseline at the end of each 6-week treatment interval. RESULTS: Both simvastatin 80 and 40 mg significantly increased total HDL-C from baseline (mean increases of 8% +/- 1 [SE] and 5% +/- 1, respectively; p < 0.001) compared with placebo, and significantly reduced plasma concentrations of LDL-C (p < 0.001), triglycerides (p < 0.001), apolipoprotein B (p < 0.001), and hs-CRP (p < or = 0.012). Compared with simvastatin 40 mg, the 80 mg dose provided additional efficacy. Simvastatin 80 mg also significantly (p < 0.001) increased HDL(2) from baseline (14% +/- 3[SE]) and placebo phases (10 +/- 3). An exploratory analysis showed 87% (simvastatin 80 mg) and 82% (simvastatin 40 mg) of patients reached the NCEP ATP III treatment goals for LDL-C compared with 14% on placebo. CONCLUSIONS: Both simvastatin 80 and 40 mg raise HDL-C and improve other measures associated with elevated coronary risk in patients with type 2 DM and low HDL-C.     

Effectiveness of simvastatin therapy in raising HDL-C in patients with type 2 diabetes and low HDL-C

SUMMARY

Objective: To evaluate the efficacy of high and moderate doses of simvastatin (80 and 40?mg), for raising high density lipoprotein-cholesterol (HDL-C), improving HDL sub-fractions, and affecting other parameters, including high sensitivity C-reactive protein (hs-CRP), in patients with type 2 diabetes mellitus (DM) and low HDL-C.

Research design and methods: This double-blind, placebo-controlled, randomized, 3-period, complete block, 6-week crossover study examined the efficacy of simvastatin in adult men and women (N = 151) with stable type 2 DM (HbA_1C < 9%), low density lipoprotein-cholesterol (LDL-C) > 100?mg/dL (2.6?mmol/L), HDL-C < 40?mg/dL (< 1?mmol/L), and fasting triglyceride level > 150 (> 1.7?mmol/L) and < 700?mg/dL (< 7.9?mmol/L). This study included adult men (71%) and women (29%) of various races (89% white, 6% black, 1% Asian, 3% other) enrolled from 29 practice-based sites in the United States.

Main outcome measures: Percentage change in HDL-C from baseline at the end of each 6-week treatment interval.

Results: Both simvastatin 80 and 40?mg significantly increased total HDL-C from baseline (mean increases of 8% ± 1 [SE] and 5% ± 1, respectively; p < 0.001) compared with placebo, and significantly reduced plasma concentrations of LDL-C (?p < 0.001), triglycerides (?p < 0.001), apolipoprotein B (?p < 0.001), and hs-CRP (?p ≤ 0.012). Compared with simvastatin 40?mg, the 80?mg dose provided additional efficacy. Simvastatin 80?mg also significantly (?p < 0.001) increased HDL₂ from baseline (14% ± 3[SE]) and placebo phases (10 ± 3). An exploratory analysis showed 87% (simvastatin 80?mg) and 82% (simvastatin 40?mg) of patients reached the NCEP ATP III treatment goals for LDL-C compared with 14% on placebo.

Conclusions: Both simvastatin 80 and 40?mg raise HDL-C and improve other measures associated with elevated coronary risk in patients with type 2 DM and low HDL-C.     

超低出生体质量早产儿病因及并发症分析

目的：分析超低出生体质量早产儿（ELBWI）相关的病因、并发症,以便更好地制定诊疗方案,改善患儿临床结局。方法：采用回顾性研究方法,选取我院NICU 1998年5月至2004年12月收治的ELBWI 32例（A组）和2012年1月至2014年6月收治的ELBWI 79例（B组）,对相关早产原因、并发症进行比较分析。结果：B组中母亲行体外受精胚胎移植术（IVF-ET）、不良孕育史的患儿比例高于A组（P<0.05）。B组酸中毒、早产儿视网膜病变（ROP）、动脉导管未闭（PDA）、低血糖、休克、低体温、硬肿症的发生率较Ａ组下降,新生儿呼吸窘迫综合征（NRDS）、支气管肺发育不良（BPD）的发生率较A组升高（P均<0.05）。B组中,胎龄＜２８周的患儿NRDS、脑室周围白质软化（PVL）、呼吸暂停、BPD、院内感染、酸中毒、新生儿坏死性小肠结肠炎（NEC）的发生率高于胎龄≥28周的患儿（P均<0.05）。结论：ELBWI相关的早产原因和并发症较多,近年来的主要并发症为NRDS、呼吸暂停、BPD等。积极避免早产高危因素,制定正确的诊疗方案,防止严重并发症的发生,是改善ELBWI临床结局的关键。     

胆固醇/高密度脂蛋白-胆固醇比值在脑梗死中的价值研究

目的:探讨胆固醇/高密度脂蛋白-胆固醇比值(TC/HDL-C比值)与脑梗死发病危险性的关系以及这一比值在脑梗死患者合并高血压或糖尿病时的变化。方法:选择197例脑梗死患者分为三组:单纯脑梗死组、合并高血压组、合并糖尿病组。58例健康者作为正常对照组,探讨这一比值的变化。结果:胆固醇(TC)水平及TC/HDL-C比值在脑梗死患者与正常对照组间有显著性差异(P<0.05);脑梗死患者的HDL-C水平较正常对照组降低,但两者差异无显著性(P>0.05);不同病例组间TC、HDL-C水平及TC/HDL-C比值无显著性差异(P>0.05)。结论:TC/HDL-C比值是脑梗死的危险因素,与高血压、糖尿病无关。     

血浆TC/HDL-C和LDL-C/HDL-C比值与冠心病严重程度的相关性分析

目的探讨血浆TC/HDL-C、LDL-C/HDL-C比值预测冠心病严重程度的价值。方法选择笔者所在医院2013年5月—2015年5月因胸痛、心前区不适行冠状动脉造影术的患者250例。按照诊断结果分为非冠心病组71例、单支病变组93例、多支病变组86例,分析三组血脂差异及冠状动脉不同病变程度(单支、多支)与血脂变化的相关性。结果非冠心病组TC、TG、LDL-C等指标均明显低于冠心病患者(单支和多支病变),组间比较,差异有高度统计学意义(P<0.01);而HDL-C指标对比结果,非冠心病组均明显高于冠心病患者(P<0.01);单支病变组TC、TG、LDL-C等指标与多支病变组比较,P>0.05;但单支病变组HDL-C指标明显高于多支病变组,组间比较,P<0.05;HDL-C与冠状动脉病变支数呈负相关,P<0.01;TC、TG、LDL-C指标与冠状动脉病变支数无明显相关性,P>0.05;非冠心病组TC/HDL-C、LDL-C/HDL-C、TG/HDL-C比值明显低于单支病变组和多支病变组,组间比较,差异有统计学意义(P<0.01);单支病变组TC/HDL-C、LDL-C/HDL-C、TG/HDL-C比值明显低于多支病变组,组间比较,差异有统计学意义(P<0.01);TC/HDL-C、LDL-C/HDL-C与冠状动脉病变支数呈正相关(P<0.01);TG/HDL-C与冠状动脉病变支数无明显相关性。结论 TC/HDL-C、LDL-C/HDL-C比值可作为临床预测心血管严重程度的可靠指标。     

Low levels of cadmium chloride damage the corneal endothelium

The effect of cadmium chloride on the integrity of the endothelium of isolated bullfrog (Rana catesbeiana) corneas was examined by spectrophotometric analysis of corneal uptake of the vital stain Janus green and by scanning electron microscopy (SEM). The uptake of Janus green by the endothelium was dose related between 1.0 and 100.0 μM CdCl₂. The effect of cadmium was significantly attenuated by the calcium channel blocker SKF 96365 and was augmented by the calcium ionophore A23187, indicating that cadmium influx through calcium channels is an important determinant of its cellular effect. The effect of cadmium was not altered by changes in the external calcium concentration, indicating that the mechanism does not involve competitive inhibition by calcium. SEM demonstrated significant structural damage to the corneal endothelium exposed to cadmium chloride, including focal disruption and denuding of the apical endothelial membrane. Received: 11 October 1996 / Accepted: 12 February 1997