pravastatin prevent CIN with CVD and CKD

他汀类药物在心血管病一级预防的应用指征赵佳;李刚【摘要】目前心血管疾病(CVD)是人类主要致残、致死原因,如何有效防治CVD已成为医学界疾病防治工作的重中之重,大量循证医学证据证实了他汀类药物在CVD 防治中起到了举足轻重的作用.他汀类药物不但能够有效地降低冠心病患者的病死率和发病率,而且对那些尚未出现心血管疾病的高危人群一级预防也会产生显著的效果.一级预防的高危人群包括高血压患者、糖尿病患者和多数老年患者.本文将阐述不同人群他汀类药物作为一级预防应用的必要性及指征.【期刊名称】《临床荟萃》【年(卷),期】2018(033)006【总页数】4页(P465-468)【关键词】心血管疾病;他汀;一级预防;糖尿病;高血压【作者】赵佳;李刚【作者单位】河北北方学院研究生学院,河北张家口 075000;河北省人民医院老年心脏科,河北石家庄 050000【正文语种】中文【中图分类】R54据统计全球每年约有1 730余万人死于心血管疾病(CVD)[1]。

即便是在诊疗技术如此发达的今天，CVD仍是人类健康的“头号杀手”。

最近，越来越多的证据阐明了他汀类药物在CVD一级预防中的重要作用[2-5]，《新英格兰医学杂志》于2012年在创刊200周年之际所发表的首篇纪念文章—《冠状动脉粥样硬化性心脏病和心肌梗死的故事》中便汇总了60年间能够使心血管病病死率下降的一系列科学进展，其中他汀类药物便榜上有名，因此至今为止他汀类药物在CVD的一级预防证据不断得到保障，在CVD的一级预防中的地位也不断提升。

自2013至今北美和欧洲的5个指南协会，其中包括英国国家卫生研究院和护理协会、美国心脏病学会、美国预防服务工作组、加拿大心血管协会及欧洲动脉粥样硬化协会都阐明表示他汀类药物可以作为CVD高发人群的一级预防药物[6]。

那么什么是他汀类药物呢？他汀类药物是一类参与胆固醇生物合成的降血脂类的药物，主要作用机制是抑制三羟基三甲基戊二酰辅酶A(HMG-CoA)还原酶，从而降低胆固醇的生物合成。

他汀在慢性肾功能不全患者中的应用王锦溪【摘要】慢性肾功能不全患者的总体死亡风险和心血管疾病死亡风险较之普通人群都有显著提高,该类患者血脂的质和量都存在异常.他汀具有降低胆固醇、抗炎、抗氧化以及稳定现有斑块等作用.现就他汀在慢性肾功能不全患者中的疗效观察进行综述,并且介绍他汀在临床应用方面的最新进展.%Patients at all stages of chronic kidney disease ( CKD ) have a significantly elevated risk of all-cause and cardiovascular mortality compared with the general population. The lipid profile shows both qualitative and quantitative abnormalities in patients with CKD. The use of statins results in lipid-lowering, anti-inflammation, anti-oxidation, and the stabilization of existing plaques. This review focuses on evidence showing the benefits of statin therapy in patients with CKD, and presents the latest progress of statins in clinical therapy.【期刊名称】《心血管病学进展》【年(卷),期】2013(034)001【总页数】3页(P66-68)【关键词】他汀;血脂异常;慢性肾功能不全【作者】王锦溪【作者单位】首都医科大学第二临床医学院,北京,100050【正文语种】中文【中图分类】R972+.6;R692.5慢性肾功能不全(CKD)的发病率在逐年递增，处于病程中各个阶段的CKD患者的总体死亡风险和心血管疾病(CVD)死亡风险较之普通人群都有显著提高。

中国临床神经外科杂志2021年4月第26卷第4期Chin J Clin Neurosurg,April 2021,Vol.26,No.4【摘要】目的探讨慢性硬膜下血肿脂联素（APN ）、基底膜蛋白多糖（PL ）的表达变化。

方法2019年5月至2020年5月钻孔引流术治疗CSDH 共32例，所有病人入院后均服用阿托伐他汀钙片，直至复查CT 示血肿完全吸收。

术前、术后3d 、术后3周各取静脉血5ml ，术中采集血肿液5ml ，采用酶联免疫吸附法检测APN 和PL 的浓度。

结果血肿液APN 浓度[（12.3±1.9）ng/ml]较外周血[（13.8±0.7）ng/ml]明显降低（P <0.05），而PL 浓度[（10.9±4.3）ng/ml]较外周血[（7.6±2.3）ng/ml]明显增高（P <0.05）。

术后3d 外周血APN 浓度[（14.1±0.7）ng/ml]较术前无明显变化（P >0.05），术后3周外周血APN 浓度[（15.3±0.8）ng/ml]较术前明显增高（P <0.05）。

血肿液APN 浓度与血肿液PL 浓度呈明显负相关（r =-0.585，P <0.01）；血肿液APN 浓度与血肿量呈明显负相关（r =-0.486，P <0.01）；血肿液PL 浓度与血肿量呈明显正相关（r =0.557，P <0.01）。

结论本文结果提示APN 和PL 在CSDH 发生、发展过程中具有一定作用，APN 可作为CSDH 阿托伐他汀治疗反应的评估指标。

【关键词】慢性硬膜下血肿；脂联素；基底膜蛋白多糖【文章编号】1009-153X （2021）04-0278-03【文献标志码】A【中国图书资料分类号】R 651.1+5;Q 786Expression of adiponectin and perlecan in chronic subdural hematomaCAO Li-hui 1,LIU Xiao 2,DAI Yong-jian 3,TANG Zhen-gang 3,LIU Yue 2.1.Postgraduate Training Base of Hubei University of Medicine,Jinzhou Medical University,Shiyan 442000,China;2.Department of Neurosurgery,Xiangyang No.1People's Hospital,Hubei University of Medicine,Xiangyang 441000,China;3.Department of Neurosurgery,Shiyan People's Hospital,Hubei University of Medicine,Shiyan 442000,China【Abstract 】Objective To explore the expression of adiponectin (APN)and perlecan (PL)in the chronic subdural hematoma (CSDH).Methods The hemotoma and peripheral blood levels of APN and PL were detected in 32patients with CSDH who underwent drilling drainage from May 2019to May 2020and received atorvastatin calcium tablets until the hemotomas were completely absorbed using the enzyme-linked immunosorbent assay.Results The APN concentration in hematoma [(12.3±1.9)ng/ml]was significantly lower that [(13.8±0.7)ng/ml]in peripheral blood before the operation (P <0.05),and PL concentration in hemotoma [(10.9±4.3)ng/ml]was significantly higher than that [(7.6±2.3)ng/ml]in peripheral blood before the operation (P <0.05).The APN concentration in peripheral blood 3days after the surgery [(14.1±0.7)ng/ml;P >0.05]did not significantly changed and significantly increased 3weeks after thesurgery [(15.3±0.8)ng/ml;P <0.05]compared with before the surgery.The hematoma APN concentration was significantly negatively correlated with the hematoma PL concentration (r =0.585,P <0.01).The concentration of hematoma APN was significantly negativelycorrelated with the amount of hematoma (r =-0.486,P <0.01).The hematoma PL concentration was significantly positively correlated with the amount of hematoma (r =0.557,P <0.01).Conclusions Our results suggest that APN and PL have a certain role in the pathogenesisand development of CSDH,and the APN can be used as an assessment indicator of atorvastatin treatment for the CSDH.【Key words 】Chronic subdural hematoma;Adiponectin;Perlecan●实验研究●慢性硬膜下血肿（chronic subdural hematoma ，CSDH ）以老年男性居多，长期酗酒和服用抗凝药物是CSDH 的易患因素[1]。

避免药害事件发生英语作文Title: Preventing Medication-Related Incidents。

In today's healthcare landscape, medication-related incidents have become a significant concern. Theseincidents encompass a wide range of errors, from prescribing and dispensing mistakes to administrationerrors and adverse drug reactions. Such mishaps can lead to patient harm, prolongation of hospital stays, and increased healthcare costs. Thus, it's crucial to implementstrategies to prevent medication-related incidents and ensure patient safety. This essay explores various approaches to mitigate these incidents.Firstly, enhancing healthcare professionals' education and training is paramount. Clinicians must receive comprehensive education on pharmacology, including medication indications, contraindications, interactions, and adverse effects. Continuous training programs should be implemented to update healthcare providers on newmedications and evidence-based practices. Additionally, interprofessional education can foster collaboration among healthcare team members, reducing communication errors and enhancing patient care coordination.Secondly, improving medication management systems can significantly reduce the risk of errors. Healthcare facilities should invest in electronic prescribing systems with built-in clinical decision support tools. These systems can alert prescribers to potential drug interactions, allergies, and dosage errors, thus preventing medication errors at the point of prescribing. Moreover, barcoding technology and automated dispensing cabinets can enhance medication accuracy during the dispensing and administration processes.Furthermore, promoting patient engagement and medication literacy is crucial in preventing medication-related incidents. Patients should be empowered to actively participate in their medication management process. Healthcare providers should educate patients about their medications, including proper administration techniques,potential side effects, and the importance of adherence. Clear and accessible medication labels and instructions can also help patients understand their treatment regimen and avoid errors.Moreover, fostering a culture of safety within healthcare organizations is essential. Healthcare leaders should prioritize patient safety initiatives and establish systems for reporting and analyzing medication errors. By encouraging open communication and non-punitive reporting of errors, healthcare organizations can identify system weaknesses and implement corrective actions to prevent future incidents. Additionally, recognizing and celebrating successes in medication safety initiatives can reinforce a culture of continuous improvement.In addition to these proactive measures, regulatory agencies play a vital role in safeguarding medication safety. Government agencies should enforce stringent regulations for medication approval, manufacturing, and distribution. Regular inspections of pharmaceutical facilities can ensure compliance with quality standards andGood Manufacturing Practices (GMP). Pharmacovigilance programs should be established to monitor the safety of medications post-market and promptly identify and address adverse drug reactions.Furthermore, promoting research and innovation in medication safety is essential. Investment in technologies such as artificial intelligence and predictive analytics can help identify patients at higher risk of medication-related incidents. Additionally, research studies on human factors and ergonomics can inform the design of healthcare systems and processes to reduce the likelihood of errors.In conclusion, preventing medication-related incidents requires a multifaceted approach involving education, technology, patient engagement, organizational culture, regulation, and research. By implementing these strategies collaboratively, healthcare stakeholders can minimize the occurrence of medication errors and enhance patient safety. Ultimately, prioritizing medication safety is essential for delivering high-quality, patient-centered care.。

不同剂量阿托伐他汀对不稳定性心绞痛患者血清高敏C反应蛋白和胱抑素－C的影响张旭;周麟;兰健【期刊名称】《航空航天医学杂志》【年(卷),期】2016(027)003【摘要】Objective To investigate the effects of different doses atorvastatin on plasma levels of high sensitivive C-reactive protein( hs-CRP) and Cystain C( Cys-c) in patients with unstable angina.Methods 165 patients with un-stable angina were randomized to control group (n=55),conventional -dose group (20 mg/d,n=55) and high-dose group (40 mg/d,n=55).Plasma levels of hs-CRP and Cys-c before and after treatment weredetected.Course of treatment is 12 weeks.Results Atorvastatin could decrease the Plasma levels of hs-CRP and Cys-c in the conven-tional-dose group and high-dose group,especially in the high-dose group.Conclusions Atorvastatin decreased in-flammatory response in the patients of unstable angina and may stabilize atherosclerotic plaque.%目的：探讨不同剂量阿托伐他汀对不稳定性心绞痛（ unstable angina，UA）患者血清高敏C反应蛋白（high sensitivive C－reactive protein，hs－CRP）和胱抑素－C（Cystain C，Cys－c）的影响。

The New EnglandJournal of Medicine©Copyright, 1996, by the Massachusetts Medical Societ yTHE EFFECT OF PRAVASTATIN ON CORONARY EVENTSAFTER MYOCARDIAL INFARCTION IN PATIENTSWITH AVERAGE CHOLESTEROL LEVELSF RANK M. S ACKS, M.D., M ARC A. P FEFFER, M.D., P H.D., L EMUEL A. M OYE, M.D., P H.D., J EAN L. R OULEAU, M.D.,J OHN D. R UTHERFORD, M.D., T HOMAS G. C OLE, P H.D., L ISA B ROWN, M.P.H., J. W AYNE W ARNICA, M.D., J. M ALCOLM O. A RNOLD, M.D., C HUAN-C HUAN W UN, P H.D., B ARRY R. D AVIS, M.D., P H.D., AND E UGENE B RAUNWALD, M.D., FOR THE C HOLESTEROL AND R ECURRENT E VENTS T RIAL I NVESTIGATORS*A BSTRACTBackground In patients with high cholesterol lev-els, lowering the cholesterol level reduces the risk ofcoronary events, but the effect of lowering cholester-ol levels in the majority of patients with coronarydisease, who have average levels, is less clear.Methods In a double-blind trial lasting five years,we administered either 40 mg of pravastatin per dayor placebo to 4159 patients (3583 men and 576 wom-en) with myocardial infarction who had plasma totalcholesterol levels below 240 mg per deciliter (mean,209) and low-density lipoprotein (LDL) cholesterollevels of 115 to 174 mg per deciliter (mean, 139). Theprimary end point was a fatal coronary event or anonfatal myocardial infarction.Results The frequency of the primary end pointwas 10.2 percent in the pravastatin group and 13.2percent in the placebo group, an absolute differenceof 3 percentage points and a 24 percent reduction inrisk (95 percent confidence interval, 9 to 36 percent;Pϭ0.003). Coronary bypass surgery was needed in7.5 percent of the patients in the pravastatin groupand 10 percent of those in the placebo group, a 26percent reduction (Pϭ0.005), and coronary angio-plasty was needed in 8.3 percent of the pravastatingroup and 10.5 percent of the placebo group, a 23percent reduction (Pϭ0.01). The frequency of strokewas reduced by 31 percent (Pϭ0.03). There were no significant differences in overall mortality or mortal-ity from noncardiovascular causes. Pravastatin low-ered the rate of coronary events more among wom-en than among men. The reduction in coronary events was also greater in patients with higher pretreat-ment levels of LDL cholesterol.Conclusions These results demonstrate that the benefit of cholesterol-lowering therapy extends to the majority of patients with coronary disease who have average cholesterol levels. (N Engl J Med 1996; 335:1001-9.)©1996, Massachusetts Medical Society.From the Departments of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston (F.M.S., M.A.P., L.B., E.B.); the Univer-sity of T exas School of Public Health, Houston (L.A.M., C.-C.W., B.R.D.); the University of Sherbrooke, Sherbrooke, Que., Canada (J.L.R.); the Uni-versity of T exas Southwestern Medical Center, Dallas (J.D.R.); Washington University, St. Louis (T.G.C.); Foothills Hospital, Calgary, Alta., Canada (J.W.W.); and Victoria Hospital, London, Ont., Canada (J.M.O.A.). Address reprint requests to Dr. Sacks at Brigham and Women’s Hospital, 75 Francis St., Boston, MA 02115.Other contributing authors were Pierre Theroux, M.D., Montreal Heart Institute, Montreal; David T. Nash, M.D., State University of New Y ork Health Sciences Center, Syracuse; and C. Morton Hawkins, D.Sc., Univer-sity of T exas School of Public Health, Houston.*Participants in the Cholesterol and Recurrent Events trial are listed in the Appendix.HE plasma levels of total cholesterol andlow-density lipoprotein (LDL) cholesterolare important risk factors for coronary heartdisease.1-4However, the relation between plasma cholesterol and coronary events appears to be stronger if levels are at elevated, rather than average, values.1-4Angiography in clinical trials has demon-strated that lowering cholesterol levels slows the pro-gression and promotes the regression of coronary ath-erosclerosis.5 These beneficial changes are also directly related to the pretreatment level of LDL cholester-ol,5,6 with little benefit occurring in patients with av-erage base-line levels.7 Clinical trials have shown that lowering elevated LDL cholesterol levels prevents both first and recurrent coronary events.8-11 However, it has not been clear whether coronary events can be prevented by cholesterol-lowering therapy in patients who do not have hypercholesterolemia. This issue is of importance because the large majority of patients with coronary disease have cholesterol levels that are, like those of the general population,12 in the average, not the elevated, range.13-16The Cholesterol and Recurrent Events (CARE) Ttrial and its entry criteria (a plasma total cholesterol level of less than 240 mg per deciliter [6.2 mmol per liter] and an LDL cholesterol level of 115 to 174 mg per deciliter [3.0 to 4.5 mmol per liter]) were de-signed specifically to study the effectiveness in a typ-ical population of lowering LDL cholesterol levels to prevent coronary events after myocardial infarction.METHODSStudy Design and PatientsThe design of the CARE trial has been described in detail else-where. 17 Patients were recruited from 80 participating centers, 13in Canada and 67 in the United States. Men and postmenopausal women were eligible if they had had an acute myocardial infarction between 3 and 20 months before randomization, were 21 to 75years of age, and had plasma total cholesterol levels of less than 240mg per deciliter, LDL cholesterol levels of 115 to 174 mg per dec-iliter, fasting triglyceride levels of less than 350 mg per deciliter (4.0mmol per liter), fasting glucose levels of no more than 220 mg per deciliter (12.2 mmol per liter), left ventricular ejection fractions of no less than 25 percent, and no symptomatic congestive heart fail-ure. Criteria for a qualifying myocardial infarction included typical symptoms and an elevated serum level of creatine kinase. 17 The lip-id levels, as measured at two or three specified visits to the clinic at least eight weeks after hospitalization for myocardial infarction and after four weeks of treatment with the National Cholesterol Edu-cation Program (NCEP) Step 1 diet, 18 were averaged for eligibility.After stratification according to clinical center, we randomly as-signed the eligible patients to receive either 40 mg of pravastatin (Pravachol, Bristol-Myers Squibb) once daily, or a matching place-bo, by means of a telephone call to the data center. After random-ization, visits to the clinic took place quarterly. Patients continued to take all prescribed medication, for cardiac and other conditions,that they had been receiving at base line (Table 1).Plasma total cholesterol, high-density lipoprotein (HDL) cho-lesterol, and triglyceride levels were measured by the core labora-tory at base line, at 6 and 12 weeks after randomization, at the end of each quarter during the first year, and semiannually there-after. LDL cholesterol levels were calculated. 19 For any patient in either group with an LDL cholesterol level of 175 mg per deci-liter (4.5 mmol per liter) or more, intensified (NCEP Step 2) di-etary counseling was initiated. 18 If the LDL level remained at 175mg per deciliter or more, cholestyramine was prescribed, in a daily dose of 8 to 16 g, as needed, to decrease the level to less than 175 mg per deciliter. T o maintain blinded conditions, a pa-tient in the other treatment group who was matched for age and sex and had an LDL cholesterol level in the highest decile was provided with parallel dietary counseling and cholestyramine treatment. If counseling and treatment were unsuccessful, the pa-tient with a persistently elevated LDL cholesterol level was re-ferred to his or her physician for treatment. The primary end point of the trial was death from coronary heart disease (includ-ing fatal myocardial infarction, either definite or probable; sud-den death; death during a coronary intervention; and death from other coronary causes) or a symptomatic (unless during noncar-diac surgery) nonfatal myocardial infarction confirmed by serum creatine kinase measurements. In each group, we measured the time elapsed to the primary end point. Deaths were reviewed by the end-points committee without knowledge of the patient’s treatment assignment or plasma lipid levels.The protocol was approved by the Safety and Data Monitoring Committee and the institutional review boards of all participating centers.Statistical AnalysisThe size of the sample was designed to provide an 80 percent power to detect a 20 percent reduction in the number of primary*Plus–minus values are means Ϯ SD. Except for the use of oral hypoglycemic agents, differences between the groups were not significant. CABG denotes coronary-artery bypass grafting, PTCA percutaneous transluminal coronary angio-plasty, ACE angiotensin-converting enzyme, VLDL very-low-density lipoprotein, LDL low-density lipoprotein, and HDL high-density lipoprotein.†The body-mass index is the weight in kilograms divided by the square of the height in meters.‡P Ͻ 0.05 for the comparison with the placebo group.§T o convert values for cholesterol to millimoles per liter,multiply by 0.02586. T o convert values for triglycerides to millimoles per liter, multiply by 0.01129.T ABLE 1. B ASE -L INE C HARACTERISTICS OF P ATIENTS IN THE P LACEBO AND P RAVASTATIN G ROUPS .*C HARACTERISTICP LACEBO (N ؍ 2078)P RAVASTATIN (N ؍ 2081)General Age (yr)59 Ϯ 959 Ϯ 9Sex (%)Female Male 14861486Race (%)White Other928937Country of residence (%)United States Canada66346634Hypertension (%)4342Current smoker (%)2121Diabetes (%)1514Body-mass index†28 Ϯ 428 Ϯ 4Blood pressure (mm Hg)Systolic Diastolic129 Ϯ 1879 Ϯ 10129 Ϯ 1879 Ϯ 10 Cardiovascular statusMonths from myocardial infarctionto randomization10 Ϯ 510 Ϯ 5Type of myocardial infarction (%)Q wave Other 61386138Angina (%)2021Congestive heart failure (%)44CABG (%)2826PTCA (%)3234CABG or PTCA (%)5454Thrombolysis (%)4042Ejection fraction (%)53 Ϯ 1253 Ϯ 12 Medication use Aspirin (%)8383Beta-blocker (%)3941Nitrate (%)3332Calcium-channel blocker (%)3840ACE inhibitor (%)1415Diuretic agent (%)1111Insulin (%)2.6 2.4Oral hypoglycemic agent (%)75‡Estrogen (% of women)10.38.4Plasma lipids §Cholesterol (mg/dl)T otal VLDL LDL HDL209 Ϯ 1727 Ϯ 16139 Ϯ 1539 Ϯ 9209 Ϯ 1727 Ϯ 16139 Ϯ 1539 Ϯ 9Triglycerides (mg/dl)155 Ϯ 61156 Ϯ61events with pravastatin. All analyses were performed on an inten-tion-to-treat basis, and P values were two-sided. The effect of therapy on the rate of the primary end point of the trial was as-sessed with use of log-rank P values. 20 All other hypothesis tests and all reductions in risk were assessed with a Cox proportional-hazards model. 21 The size of the trial did not provide adequate power to assess therapeutic efficacy against the primary end point within subgroups. Therefore, treatment effects were analyzed in several prespecified subgroups with a more broadly defined end point: major coronary events (including fatal coronary heart dis-ease, nonfatal myocardial infarction, bypass surgery, and angio-plasty).RESULTSBetween December 4, 1989, and December 31,1991, 4159 patients were randomly assigned to study groups, 2078 to the placebo group and 2081 to the pravastatin group. The characteristics of the patients before randomization were similar in the two groups (Table 1). In the last year of follow-up, 86 percent of the placebo group and 94 percent of the treat-ment group were taking their study medication.This included the 6 percent of patients in each treat-ment group who were taking cholestyramine ac-cording to the protocol. Of the patients, 8 percent in the placebo group and 2 percent in the treatment group discontinued the study medication and start-ed treatment to lower lipid levels with open-label drug therapy, as prescribed by their personal physi-cians. The final study visit was between January 1and February 14, 1996, at which time the median duration of follow-up was 5.0 years (range, 4.0 to 6.2). Data were obtained to classify myocardial in-farctions as confirmed or unconfirmed for all pa-tients in whom a myocardial infarction was report-ed. Vital status was ascertained for the first four years for all patients and, at the end, for all but one patient.Pravastatin therapy lowered the mean LDL cho-lesterol level of 139 mg per deciliter (3.6 mmol per liter) by 32 percent and maintained mean levels of 97 to 98 mg per deciliter (2.5 mmol per liter)throughout the five-year follow-up. During follow-up, the LDL cholesterol level was 28 percent lower in the pravastatin group than in the placebo group,the total cholesterol level was 20 percent lower, the HDL cholesterol level was 5 percent higher, and the triglyceride level was 14 percent lower (P Ͻ 0.001 for all comparisons).Patients treated with pravastatin had a 24 percent lower incidence of the primary end point, fatal cor-onary heart disease or confirmed myocardial infarc-tion, than patients in the placebo group (95 percent confidence interval, 9 to 36 percent; P ϭ 0.003) (Ta-ble 2 and Fig. 1). Two hundred seventy-four pa-tients (13.2 percent) had a primary event in the pla-cebo group, as compared with 212 (10.2 percent) in the pravastatin group. One hundred seventy-three*Risk reductions and P values were based on Cox proportional-hazards analysis; P values are iden-tical to those derived by log-rank analysis. Patient-specific data were used to compute P values andconfidence intervals (CI). CHD denotes coronary heart disease, MI myocardial infarction, CABG coronary-artery bypass grafting, and PTCA percutaneous transluminal coronary angioplasty.†This combined variable was the specified primary end point. Nonfatal myocardial infarctions were confirmed by the core laboratory.‡This variable comprises all nonfatal myocardial infarctions reported by investigators.T ABLE 2. C ARDIOVASCULAR E VENTS A CCORDING TO S TUDY G ROUP .*E VENTP LACEBO (N ؍2078)P RAVASTATIN (N ؍2081)R ISK R EDUCTIONWITH P RAVASTATIN(95% CI)P V ALUENO . OF PATIENTSINCIDENCE(%)NO . OF PATIENTSINCIDENCE(%)percentDeath from CHD or non-fatal MI†27413.221210.224 (9 to 36)0.003Death from CHD 119 5.796 4.620 (Ϫ5 to 39)0.10Nonfatal MI 1738.3135 6.523 (4 to 39)0.02Fatal MI38 1.824 1.237 (Ϫ5 to 62)0.07Fatal MI or confirmed non-fatal MI20710.01577.525 (8 to 39)0.006Clinical nonfatal MI‡23111.11828.723 (6 to 36)0.01CABG 20710.01567.526 (8 to 40)0.005PTCA21910.51728.323 (6 to 37)0.01CABG or PTCA 39118.829414.127 (15 to 37)Ͻ0.001Unstable angina 35917.331715.213 (Ϫ1 to 25)0.07Stroke783.8542.631 (3 to 52)0.03Figure 1. Kaplan–Meier Estimates of the Incidence of Coronary Events in the Pravastatin and Placebo Groups.15105012345I n c i d e n c e (%)0252015105012345I n c i d e n c e (%)N O. AT R ISK Placebo Pravastatin2078208120092015195619631881191518101856854900N O. AT R ISK Placebo Pravastatin2078208119561969185718771739180016341716754819PlaceboPravastatinChange in risk,Ϫ27%P Ͻ0.001Change in risk,Ϫ24%P ϭ0.003PlaceboPravastatinFatal Coronary Heart Disease or Nonfatal Myocardial InfarctionCoronary Bypass Surgery or AngioplastyYearsYears*Major coronary events were the primary end point (death from coronary heart disease or nonfatalmyocardial infarction [MI]), coronary-artery bypass grafting (CABG), or percutaneous transluminal coronary angioplasty (PTCA). P values for the interaction between subgroup and treatment were Ͼ0.10 except for sex (P ϭ0.05), LDL cholesterol level (Ͻ125, 125–150, and Ͼ150 mg per deciliter;P ϭ0.03), and triglyceride level (P ϭ0.08). LDL denotes low-density lipoprotein, and HDL high-density lipoprotein.†The median values for all 4159 patients were as follows: total cholesterol, 209 mg per deciliter;LDL cholesterol, 137 mg per deciliter; HDL cholesterol, 37 mg per deciliter; LDL:HDL ratio, 3.7;and triglycerides, 144 mg per deciliter. T o convert values for cholesterol to millimoles per liter, mul-tiply by 0.02586. T o convert values for triglycerides to millimoles per liter, multiply by 0.01129.‡The type of myocardial infarction could not be determined for three patients.T ABLE 3. M AJOR C ORONARY E VENTS IN S UBGROUPS D EFINED BY B ASE -L INE V ARIABLES .*V ARIABLE †N O . OF P ATIENTSN O . (%) OF P ATIENTSWITH E VENTR ISK R EDUCTION (95% CI)P V ALUEPLACEBOPRAVASTATINPLACEBOPRAVASTATINpercentSexFemale Male 2901788286179580 (28)469 (26)46 (16)384 (21)46 (22 to 62)20 (8 to 30)0.0010.001AgeϽ60 yr у60 yr 1003107510271054258 (26)291 (27)217 (21)213 (20)20 (4 to 33)27 (12 to 38)0.02Ͻ0.001Hypertension Present Absent 89911798751206263 (29)286 (24)200 (23)230 (19)23 (8 to 36)24 (9 to 36)0.0050.002Diabetes Present Absent 30417742821799112 (37)437 (25)81 (29)349 (19)25 (0 to 43)23 (11 to 33)0.05Ͻ0.001Smoking Current Other33417443371744111 (33)437 (25)81 (24)349 (20)33 (11 to 50)22 (10 to 33)0.006Ͻ0.001Left ventricular ejec-tion fraction р40%Ͼ40%35317253531728112 (32)436 (25)84 (24)346 (20)28 (4 to 45)23 (11 to 33)0.02Ͻ0.001Previous CABG Yes No56415145271554116 (21)433 (29)88 (17)342 (22)22 (Ϫ3 to 41)25 (13 to 35)0.08Ͻ0.001Previous PTCA Yes No66814107011380188 (28)361 (26)153 (22)277 (20)25 (7 to 39)23 (10 to 34)0.009Ͻ0.001Previous CABG orPTCA Yes No11189601127954269 (24)280 (29)218 (19)212 (22)22 (7 to 35)25 (10 to 37)0.0060.002Type of MI‡Q wave Other12777991279801334 (26)215 (27)251 (20)179 (22)27 (14 to 38)19 (1 to 34)Ͻ0.0010.04T otal cholesterol р209 mg/dl Ͼ209 mg/dl 1040103810321049260 (25)289 (28)211 (20)219 (21)19 (3 to 33)27 (13 to 39)0.02Ͻ0.001LDL cholesterol р137 mg/dl Ͼ137 mg/dl 1048103010421039269 (26)280 (27)210 (20)220 (21)23 (8 to 36)24 (10 to 36)0.0040.002LDL cholesterol Ͻ125 mg/dl 125–150 mg/dl Ͼ150–175 mg/dl 4411172465410118348893 (21)311 (27)145 (31)89 (22)239 (20)102 (21)Ϫ3 (Ϫ38 to 23)26 (13 to 38)35 (17 to 50)0.85Ͻ0.0010.008HDL cholesterol р37 mg/dl Ͼ37 mg/dl 1025105310331048290 (28)259 (25)236 (23)194 (19)21 (6 to 33)27 (12 to 39)0.008Ͻ0.001LDL:HDL ratio Ͻ3.7у3.71043103510361045251 (24)298 (29)190 (18)240 (23)26 (11 to 39)21 (7 to 34)0.0020.006Triglycerides Ͻ144 mg/dl у144 mg/dl1049102910311050281 (27)268 (26)195 (19)235 (22)32 (18 to 43)15 (Ϫ1 to 29)Ͻ0.0010.0703530252015105012345I n c i d e n c e (%)N O. AT R ISK Placebo 441410411384396363378343354322153160117211831089110610221055 9511010891963426443465488434451410426375407344387144189PravastatinChange in risk,ϩ3%P ϭ0.85Pravastatin Placebo03530252015105012345Change in risk,Ϫ26%P Ͻ0.001PravastatinPlacebo0353*******105012345PravastatinPlaceboLDL, Ͻ125 mg/dlLDL, 125 –150 mg/dlLDL, Ͼ150 mg/dlYearsYearsYearsChange in risk,Ϫ35%P ϭ0.008with impaired left ventricular ejection, in all of whom the efficacy of lowering cholesterol levels had been questioned, had a reduction in risk. These re-sults demonstrate that for patients with coronary disease in North America, the average cholesterol level is too high and can contribute to the recur-rence of cardiovascular events.These results also suggest that the pretreatment LDL cholesterol level, at least within the CARE tri-al’s eligibility range of 115 to 174 mg per deciliter, has an influence on the success of cholesterol-lower-ing therapy in preventing coronary events. In the upper part of the range, Ͼ150 to 175 mg per deci-liter, the reduction in risk (35 percent) was similar to that achieved with reductase inhibitors in patients with hypercholesterolemia.8-10 In the middle of the range, 125 to 150 mg per deciliter, the risk reduc-tion remained substantial (26 percent); this range is at the center of the distribution of LDL cholesterol values in contemporary populations with coronary heart disease.13-16However, there was no reduction in coronary events among patients with base-line LDL cholesterol levels below 125 mg per deciliter. These results are consistent with those of epidemio-logic studies that show a stronger relation between LDL cholesterol levels and coronary events at hyper-cholesterolemic, as compared with average, levels,1-4 as well as those of angiographic studies that show that improvement in coronary-artery stenosis in pa-tients receiving lipid-lowering therapy is proportion-al to the base-line LDL cholesterol level.5-7 Although our finding cannot be considered definitive and re-quires confirmation, it suggests that an LDL choles-terol level of 125 mg per deciliter may be an approx-imate lower boundary for a clinically important influence of the LDL cholesterol level on coronary heart disease.Stroke, a specified end point in the CARE trial,17 was reduced significantly (by 31 percent) in the pra-vastatin group. A reduction in cerebrovascular end points was found in post hoc analyses of data from several previous trials conducted in hypercholester-olemic populations.8,10,22,23A meta-analysis of trials of pravastatin in patients with atherosclerosis showed a significant, 62 percent reduction in stroke.10 Die-tary therapy that replaced saturated fat with polyun-saturated fat reduced the incidence of stroke by 45 percent (Pϭ0.055).22The incidence of stroke and transient ischemic attacks considered together was lowered significantly (by 24 percent) by nicotinic acid23and lowered by 30 percent by simvastatin.8 Ultrasound measurements of carotid atherosclerosis demonstrated slowing of the progression of disease by treatment with pravastatin24,25and lovastatin.26 This evidence from clinical trials therefore suggests that high plasma LDL cholesterol levels are a treat-able cause of cerebrovascular atherosclerosis and clin-ical cerebrovascular events. The potential for benefit from cholesterol-lowering treatment should contin-ue to be evaluated in patients with coronary disease, as well as in other groups of patients at high risk for stroke, such as those with a history of stroke, tran-sient ischemic attack, carotid-artery bruit, or hyper-tension.The overall incidence of fatal or nonfatal cancer was not increased in the pravastatin group as com-pared with the placebo group. The incidence of gas-trointestinal, liver, and lymphatic cancers was also not increased, thus providing no confirmation in humans of findings from testing in animals.27The increased incidence of breast cancer in patients given pravastatin was surprising; it has not been reported in previous or ongoing trials with pravastatin or oth-er related drugs, and testing in animals has not iden-tified breast cancer as one that is increased by such therapy. There is also no known potential biologic basis, such as an increase in estrogen levels,28 to sug-gest a causal link. In evaluating this finding, it should be noted that although there was one case of breast cancer among the women given placebo, five cases would have been expected on the basis of the rate of breast cancer in the general population for women of similar race and age.29 Importantly, interim results of the Long-T erm Intervention with Pravastatin in Ischemic Disease (LIPID) trial,30 from four years of treatment of 1508 women, show no increase in breast cancer (Barter P, Safety and Data Monitoring Committee, LIPID study: personal communication). The totality of evidence suggests that these findings in the CARE trial could be an anomaly and may be best interpreted in the context of the trial’s very low event rates and statistical testing of many adverse events.The Scandinavian Simvastatin Survival Study was a study of secondary prevention in patients with hy-percholesterolemia and coronary disease in which the reduction in coronary events was 37 percent.8 In the 544 CARE patients who, on the basis of lipid levels and other characteristics, would have been el-igible for the Scandinavian study, the reduction in coronary events (as defined in that study) was 43 percent in the pravastatin group as compared with the placebo group (Pϭ0.048). Therefore, we con-clude that the difference in overall risk reduction in the two trials was caused mainly by the difference in the base-line LDL cholesterol levels of the two groups of subjects, although other characteristics, such as a greater use of aspirin by the CARE patients, may also have contributed. The results of the CARE trial should be considered representative of what can be achieved by lipid-lowering treatment, over and above other strategies currently employed in the modern, comprehensive treatment of patients with a history of myocardial infarction and average choles-terol levels.We calculated the overall clinical benefit that couldcular disease in relation to cholesterol level among men with and without preexisting cardiovascular disease. N Engl J Med 1990;322:1700-7.4.Kannel WB. Range of serum cholesterol values in the population devel-oping coronary artery disease. Am J Cardiol 1995;76:69C-77C.5.Rossouw JE. Lipid-lowering interventions in angiographic trials. Am J Cardiol 1995;76:86C-92C.6.Sacks FM, Gibson CM, Rosner B, Pasternak RC, Stone PH, Harvard Atherosclerosis Reversibility Project Research Group. The influence of pre-treatment low density lipoprotein cholesterol concentrations on the effect of hypocholesterolemic therapy on coronary atherosclerosis in angiograph-ic trials. Am J Cardiol 1995;76:78C-85C.7.Sacks FM, Pasternak RC, Gibson CM, Rosner B, Stone PH. Effect on coronary atherosclerosis of decrease in plasma cholesterol concentrations in normocholesterolaemic patients. Lancet 1994;344:1182-6.8.Scandinavian Simvastatin Survival Study Group. Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994;344:1383-9.9.Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart dis-ease with pravastatin in men with hypercholesterolemia. N Engl J Med 1995;333:1301-7.10.Byington RP, Jukema JW, Salonen JT, et al. Reduction in cardiovascu-lar events during pravastatin therapy: pooled analysis of clinical events of the Pravastatin Atherosclerosis Intervention Program. Circulation 1995; 92:2419-25.11.Holme I. Cholesterol reduction and its impact on coronary artery dis-ease and total mortality. Am J Cardiol 1995;76:10C-17C.12.Johnson CL, Rifkind BM, Sempos CT, et al. Declining serum total cholesterol levels among US adults: the National Health and Nutrition Ex-amination Surveys. JAMA 1993;269:3002-8.vie CJ, Milani RV. National Cholesterol Education Program’s rec-ommendations and implications of “missing” high-density lipoprotein cho-lesterol in cardiac rehabilitation programs. Am J Cardiol 1991;68:1087-8.14.Buring JE, O’Connor GT, Goldhaber SZ, et al. Decreased HDL2 and HDL3 cholesterol, Apo A-I and Apo A-II, and increased risk of myocardial infarction. Circulation 1992;85:22-9.15.Genest J Jr, McNamara JR, Ordovas JM, et al. Lipoprotein choles-terol, apolipoprotein A-I and B and lipoprotein (a) abnormalities in men with premature coronary heart disease. J Am Coll Cardiol 1992;19:792-802.16.Rubins HB, Robins SJ, Collins D, et al. Distribution of lipids in 8,500 men with coronary artery disease. Am J Cardiol 1995;75:1196-201. 17.Sacks FM, Pfeffer MA, Moye L, et al. Rationale and design of a sec-ondary prevention trial of lowering normal plasma cholesterol levels after acute myocardial infarction: the Cholesterol and Recurrent Events trial (CARE). Am J Cardiol 1991;68:1436-46. [Erratum, Am J Cardiol 1992; 69:574.]18.Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Summary of the second report of the National Cho-lesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel II). JAMA 1993;269:3015-22.19.Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concen-tration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972;18:499-502.20.Kalbfleisch JD, Prentice RL. The statistical analysis of failure time da-ta. New Y ork: John Wiley, 1980.21.Cox DR. Regression models and life-tables. J R Stat Soc [B] 1972;34: 187-220.22.Dayton S, Pearce ML, Hashimoto S, Dixon WJ, T omiyasu U. A con-trolled clinical trial of a diet high in unsaturated fat in preventing compli-cations of atherosclerosis. Circulation 1969;40:Suppl II:II-1–II-63.23.The Coronary Drug Project Research Group. Clofibrate and niacin in coronary heart disease. JAMA 1975;231:360-81.24.Crouse JR III, Byington RP, Bond MG, et al. Pravastatin, Lipids, and Atherosclerosis in the Carotid Arteries (PLAC-II). Am J Cardiol 1995;75: 455-9. [Erratum, Am J Cardiol 1995;75:862.]25.Salonen R, Nyyssonen K, Porkkala E, et al. Kuopio Atherosclerosis Prevention Study (KAPS): a population-based primary prevention trial of the effect of LDL lowering on atherosclerotic progression in carotid and femoral arteries. Circulation 1995;92:1758-64.26.Furberg CD, Adams HP Jr, Applegate WB, et al. Effect of lovastatin on early carotid atherosclerosis and cardiovascular events. Circulation 1994;90:1679-87.27.Newman TB, Hulley SB. Carcinogenicity of lipid-lowering drugs. JAMA 1996;275:55-60.28.Dobs AS, Sarma PS, Schteingart D. Long-term endocrine function in hypercholesterolemic patients treated with pravastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Metabolism 1993;42: 1146-52.29.Ries LA, Miller BA, Hankey BF, Kosary CL, Haras A, Edwards BK, eds. SEER cancer statistics review, 1973-1991: tables and graphs. Bethes-da, Md.: National Cancer Institute, 1994. (NIH publication no. 94-2789.)30.The Lipid Study Group. Design features and baseline characteristics of the LIPID (Long-T erm Intervention with Pravastatin in Ischemic Disease) Study: a randomized trial in patients with previous acute myocardial infarc-tion and/or unstable angina pectoris. Am J Cardiol 1995;76:474-9. 31.Pfeffer MA, Sacks FM, Moye LA, et al. Cholesterol and Recurrent Events [CARE]: a secondary prevention trial for normolipidemic patients. Am J Cardiol 1995;76:98C-106C.MASSACHUSETTS MEDICAL SOCIETY REGISTRY ON CONTINUING MEDICAL EDUCATION T o obtain information about continuing medical education courses in New England, callbetween 9 a.m. and 12 noon, Monday through Friday, (617) 893-4610, or in Massachusetts, 1-800-322-2303, ext. 1342.。

不可切除胰腺癌的分子靶向药物治疗进展胡润，李俊蒽，姚沛，桂仁捷，段华新湖南师范大学附属第一医院，湖南省人民医院肿瘤科，长沙 410005通信作者：段华新，****************（ORCID： 0000-0001-9596-5013）摘要：胰腺癌作为消化系统最常见的恶性肿瘤之一，其发病率及死亡率正逐年上升，大多数胰腺癌患者因分期较晚而失去了手术机会。

尽管以吉西他滨、氟尿嘧啶为主的化疗方案在一定程度上延长了患者的生存期，但仍有部分患者因无法耐受化疗而失去治疗机会。

随着精准医疗时代的来临，分子靶向药物治疗展现出的优异疗效使其成为对抗肿瘤的重要治疗手段之一，但由于胰腺癌高度的异质性及复杂的免疫微环境，针对胰腺癌的分子靶向治疗并未取得显著效果，因此亟需探寻新的治疗靶点及药物攻克这一难题。

本综述基于胰腺癌常见分子靶点及肿瘤免疫相关靶点探究在不可切除胰腺癌中分子靶向药物治疗研究的最新进展，为胰腺癌患者提供新的治疗策略。

关键词：胰腺肿瘤；分子靶向治疗；免疫疗法基金项目：湖南省自然科学基金（2020JJ8084）Advances in molecular-targeted therapy for unresectable pancreatic cancerHU Run，LI Junen，YAO Pei，GUI Renjie，DUAN Huaxin.（Department of Oncology，The First Affiliated Hospital of Hunan Normal University， Hunan Provincial People’s Hospital， Changsha 410005， China）Corresponding author： DUAN Huaxin，****************（ORCID： 0000-0001-9596-5013）Abstract：Pancreatic cancer is one of the most prevalent malignant tumors of the digestive system， and its incidence and mortality rates are increasing year by year. Most patients with pancreatic cancer are unable to receive surgery due to the advanced stage. Although chemotherapy regimens based on gemcitabine and fluorouracil have prolonged the survival time of patients to some extent，some patients cannot tolerate chemotherapy and hence lose the opportunity for treatment. With the advent of the era of precision medicine， molecular-targeted therapy has exhibited an excellent therapeutic efficacy and has thus become one of the most important treatment techniques for tumors； however， due to the high heterogeneity of pancreatic cancer and its complicated tumor microenvironment， molecular-targeted therapy for pancreatic cancer has not achieved notable results. Therefore， it is imperative to seek new therapeutic targets and medications to overcome this issue. This article reviews the latest advances in the research on molecular-targeted therapy for unresectable pancreatic cancer based on common molecular targets and tumor immunity-related therapeutic targets， in order to provide new treatment strategies for patients with pancreatic cancer.Key words：Pancreatic Neoplasms； Molecular Targeted Therapy； ImmunotherapyResearch funding：Natural Science Foundation of Hunan Province of China （2020JJ8084）胰腺癌是一种起病隐匿、进展迅速、疗效及预后极差的恶性肿瘤，大多数患者确诊时已经属于晚期。

《2024年世界卫生组织慢性乙型肝炎患者的预防、诊断、关怀和治疗指南》推荐意见要点艾小委，张梦阳，孙亚朦，尤红首都医科大学附属北京友谊医院肝病中心，北京 100050通信作者：尤红，******************（ORCID：0000-0001-9409-1158）摘要：2024年3月世界卫生组织（WHO）发布了最新版《慢性乙型肝炎患者的预防、诊断、关怀和治疗指南》。

该指南在以下方面进行了更新：扩大并简化慢性乙型肝炎治疗适应证，增加可选的抗病毒治疗方案，扩大抗病毒治疗预防母婴传播的适应证，提高乙型肝炎病毒诊断，增加合并丁型肝炎病毒的检测等。

本文对指南中的推荐意见进行归纳及摘译。

关键词：乙型肝炎，慢性；预防；诊断；治疗学；世界卫生组织；诊疗准则Key recommendations in guidelines for the prevention，diagnosis，care and treatment for people with chronic hepatitis B infection released by the World Health Organization in 2024AI Xiaowei， ZHANG Mengyang， SUN Yameng， YOU Hong.（Liver Research Center， Beijing Friendship Hospital， Capital Medical University， Beijing 100050， China）Corresponding author： YOU Hong，******************（ORCID： 0000-0001-9409-1158）Abstract：In March 2024， the World Health Organization released the latest version of guidelines for the prevention， diagnosis，care and treatment for people with chronic hepatitis B infection. The guidelines were updated in several aspects，including expanding and simplifying the indications for chronic hepatitis B treatment，adding alternative antiviral treatment regimens，broadening the indications for antiviral therapy to prevent mother-to-child transmission，improving the diagnosis of hepatitis B virus，and adding hepatitis D virus （HDV）testing. This article summarizes and gives an excerpt of the recommendations in the guidelines.Key words：Hepatitis B， Chronic； Prevention； Diagnosis； Therapeutics； World Health Organization； Practice Guideline近年来，慢性乙型肝炎（CHB）在预防、诊断、治疗等方面取得重要进展。

・IDF代谢综合征全球共识定义（2005）・国际糖尿病联盟代谢综合征全球共识定义*宋秀霞译纪立农校一、用于临床工作的代谢综合征全球性定义1.国际糖尿病联盟（IDF）新定义：根据IDF定义，确认一个个体是否为代谢综合征，必须具备：（1）中心性肥胖：在欧洲裔人种中定义为男性腰围≥94cm，女性腰围≥80cm，在其他人种中采用种族特异性的腰围切点（见表1）。

（2）另加下列4因素中任意两项：①甘油三酯（TG）水平升高：> 150mg/dl（1.7mmol/L），或已接受针对此脂质异常的特殊治疗；②高密度脂蛋白胆固醇（HDL-C）水平降低：男性<40 mg/dl（1.03mmol/L），女性<50mg/dl（1.29mmol/L）或已接受针对此脂质异常的特殊治疗；③血压升高：收缩压≥130 mm Hg或舒张压≥85mm Hg，或此前已被诊断为高血压而接受治疗；④空腹血糖升高：空腹血糖≥100mg/dl（5.6 mmol/L），或已被诊断为2型糖尿病。

如果空腹血糖≥100 mg/dl（5.6mmol/L），则强烈推荐行口服葡萄糖耐量试验（OGTT）；但是OGTT在诊断代谢综合征时并非必需。

代谢综合征及其各个组分的发病机制很复杂，目前尚未充分了解，但中心性肥胖和胰岛素抵抗是被公认的重要的致病因素［1-5］。

中心性（或腹型）肥胖可以很容易地用腰围来评定，且与代谢综合征其他组分包括胰岛素抵抗独立相关［2，6］，是代谢综合征新定义中诊断此综合征的先决危险因素。

而在日常的临床工作中很难测量的胰岛素抵抗则非诊断的必要条件。

致动脉硬化性的血脂异常包括增高的TG和降低的HDL-C以及增高的载脂蛋白B（APO-B）、小而密的低密度脂蛋白胆固醇（LDL-C）和小的HDL颗粒。

其中的每一项都有独立的致动脉硬化作用［7］。

上述血脂异常在2型糖尿病和代谢综合征病人中均常见。

无论有无2型糖尿病，胰岛素抵抗患者常有低HDL-C和高TG水平［8］，两者均是冠心病（CHD）的危险因素［9，10］。