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“临床病理讨论”(clinical-pathological conference, CPC)是北京协和医院建院几十年坚持不断、难能可贵的传统学术活动,是发挥协和多学科综合优势协作诊治疑难复杂重症“临床特色”的重要体现。几十年持之以恒在全院范围内,开展对涉及多学科的疑难复杂重症病例进行讨论分析,总结经验教训,这种活动是提高临床诊治水平的基础。
CPC —般分为以下几个部分:首先,由对患者进行诊治的相关科室对CPC患者生前所经历的多个科室的诊断治疗过程进行复习、重新审视和全面分析。在CPC讨论中各科室根据临床资料引经据典,从本学科专业角度对患者的诊断治疗过程进行分析和总结,气氛热烈、发言踊跃,与会者可持以不同的学术观点进行针锋相对的辩论。第二,由病理科报告患者尸检结果,明确患病的疾病种类及患者的死亡原因。面对与临床有时并不完全一致的诊断,尸检报告的全面病理分析是对某种罕见及疑难复杂疾病的重新认识和思考,是对临床诊断思路正确与否的重新验证。最后,相关科室专家就病理确诊的某种罕见及疑难复杂疾病的国内外研究现状进行评述,结合本例患者的救治过程总结成功的经验、分析教训,获得今后临床诊治同类疾病需要加以改进和提高的启示。
CPC这种学术交流形式是提高临床诊疗水平极其有效的途径,也是培养临床医生,尤其是年轻的临床医学工作者不可多得的、宝贵的学习机会。这正是协和人能够坚持至今,并十分珍惜的重要原因。CPC这种在临床实践中的学习总结,是临床医生提高分析思维能力、改进临床救治水平的最佳课堂;也是临床医学在实践中不断总结、进步、发展、提高的最佳范例;更是对患者将生命贡献给医学发展的最高崇敬。
每次的协和CPC都是全院最受关注、参加人数最多的学术活动。近年来由于尸检数量的急剧下降,CPC的次数也在急剧减少。但是医务处仍组织了不少有价值的CPC; 此外,还创新性地组织了依靠活体标本进行的CPC,为在新的社会情况下继续保持协和优良的学术传统开辟了一条新的途径。本期刊登的CPC即为此创新性范例,医务处孙阳处长专门撰文点评,介绍协和CPC学术活动的新模式和新方法。
CPC是协和的传统和优势,CPC需要不断地发展和创新。本刊今后将继续组织更多的具有指导意义和创新性的CPC,呈现在广大读者面前。
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[1] Funke H, Assmann G. Strategies for the assessment of genetic coronary artery disease risk[J]. Cur Opin Lipidol, 1999, 10:285-291. DOI: 10.1097/00041433-199906000-00011
[2] Scarabin PY, Arveiler D, Amouyel P, et al. Plasma fibrinogen explains much of the difference in risk of coronary heart disease between France and Northern Ireland. The PRIME study[J]. Atherosclerosis, 2003, 166: 103-109. DOI: 10.1016/S0021-9150(02)00309-X
[3] Behague I, Poirier 0, Nicaud V, et al. β fibrinogen gene polymorphisms are associated with plasma fbrinogen and coronary artery disease in patients with myocardial infarction [J]. Girculation, 1996, 93:440-449 DOI: 10.1161/01.CIR.93.3.440
[4] Carter AM, Mansfield MW, Stickland MH, et al. β fibrinogen gene 455 G/A polymorphism and fibrinogen levels: risk factors for coronary artery disease in subjects with NIDDM [J]. Diabetes Care, 1996, 9:1265-1268. https://care.diabetesjournals.org/content/19/11/1265
[5] de Maat MPM, Kastelein JJP, Jukema JW, et al. 455G/A polymorphism of the b-fibrinogen gene is associated with the progression of coronary atherosclerosis in symptomatic men: proposed role for an acute phase reaction pattern of fibrinogen[J]. Arterioscler Thromb Vasc Biol, 1998, 18:265-271. DOI: 10.1161/01.ATV.18.2.265
[6] Zito F, Di Castelnuovo A, Amore C, et al. Bel I polymorphism in the fibrinogen b-chain gene is associated with the risk of familial myocardial infarction by increasing plasma fibrinogen levels: a case-control study in a sample of GISSI-2 patients[J]. Arterioscler Thromb Vasc Biol, 1997, 17: 3489-3494. DOI: 10.1161/01.ATV.17.12.3489
[7] Tybjaerg-Hansen A, Agerholm-Larsen B, Humphries SE, et al. A common mutation (G 455-A) in the b-fibrinogen promoter is an independent predictor of plasma fbrinogen, but not of ischemic heart disease: a study of9, 127 individuals based on the Copenhagen City Heart Study[J]. J Clin Invest, 1997, 99:3034-3039. DOI: 10.1172/JCI119499
[8] Wang XL, Wang J, MeCredie RM, et al. Polymorphisms of factor V, factor VⅡ, and fibrinogen genes: relevance to severity of coronary artery disease[J]. Arterioscler Thromb Vasc Biol, 1997, 17:246-251. DOI: 10.1161/01.ATV.17.2.246
[9] Boekholdt SM, Bijsterveld NR, Moons AH, et al. Genetic variation in coagulation and fibrinolytic proteins and their relation with acute myocardial infarction: a systematic review [J]. Circulation, 2001, 104:3063-3068. DOI: 10.1161/hc5001.100793
[10] Lane A, Green F, Scarabin PY, et al. Factor VⅡ Arg/Gln353 polymorphism determines factor VⅡ coagulant activity in patients with myocardial infarction (MI) and control subjects in Belfast and in France but is not a strong indication of MI risk in the ECTIM study[J]. Atherosclerosis, 1996, 119:119-127. DOI: 10.1016/0021-9150(95)05638-6
[11] Doggen CJM, Cats VM, Bertina RM, et al. A genetic propensity to high factor VⅡ is not associated with the risk of myocardial infarctin in men[J]. Thromb Haemost, 1998, 80:281-285. DOI: 10.1055/s-0037-1615188
[12] Domenico G, Carla Russo, Paolo F, et al. Polymorphisms in the Factor VⅡ gene and the risk of myocardial infarction in patients with coronary artery disease[J]. N Engl J Med, 2000, 343:774-780. DOI: 10.1056/NEJM200009143431104
[13] lacoviello L, Di Castelnuovo A, de Knjf P, et al. Polymorphisms in the coagulation factor VⅡ gene and the risk of myocardial infarction[J]. N Engl J Med, 1998, 338:79-85. DOI: 10.1056/NEJM199801083380202
[14] Rosendaal FR, Siscovick DS, Schwartz SM, et al. Factor V Leiden (resistance to activated protein C) increases the risk of myocardial infarction in young women [J]. Blood, 1997, 89:2817-2821. DOI: 10.1182/blood.V89.8.2817
[15] Salomaa V, Matei C, Aleksic N, et al. Soluble thrombomodulin as a predictor of incident coronary heart disease and symptomless carotid artery atherosclerosis in the Atherosclerosis Risk in Communities (ARIC) Study: a case-cohort study[J]. Lancet, 1999, 353:1729-1734. DOI: 10.1016/S0140-6736(98)09057-6
[16] Norland L, Holm J, Zoller B, et al. A common thrombomodulin amino acid dimorphism is associated with myocardial infarction[J]. Thromb Haemost, 1997, 77:248-251. DOI: 10.1055/s-0038-1655947
[17] Thompson SG, Kienast J, Pyke SDN, et al. Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris[J]. N Engl J Med, 1995, 332:635-641. DOI: 10.1056/NEJM199503093321003
[18] Ludwig M, Wihn KD, Scheuning WD, et al. Alleleie dimorphism in the human tissue-type plasminogen activator (TPA) gene as a result of an Alu insertion/deletion event [J]. Hum Genet, 1992, 88:388-392. DOI: 10.1007/BF00215671
[19] Ladenvall P, Johansson L, Jansson JH, et al. Tissue-type plasminogen activator-7, 35 1C/T enhancer polymorphism is associated with a first myocardial infarction[J]. Thromb Haemost, 2002, 87: 105-109. DOI: 10.1055/s-0037-1612951
[20] Sobel BE, Woodcock-Mitchell J, Schneider DJ, et al. Increased plasminogen activator inhibitor type 1 in coronary artery atherectomy specimens from type 2 diabetic compared with non-diabetic patients: a potential factor predisposing to thrombosis and its persistence[J]. Circulation, 1998, 97: 2213-2221. DOI: 10.1161/01.CIR.97.22.2213
[21] Margaglione M, Cappucci G, ColaizzoD, et al. The PAI-1 gene locus 4G/5G polymorphism is associated with a family history of coronary artery disease[J]. Arterioscler Thromb Vase Biol, 1998, 18:152-156. DOI: 10.1161/01.ATV.18.2.152
[22] Weis EJ, Bray PF, Tayback M, et al. A polymorphism of a platelet glycoprotein receptor as an inherited risk factor for coronary thrombosis[J]. N Engl J Med, 1996, 334:1090-1094. DOI: 10.1056/NEJM199604253341703
[23] Herrmann SM, Poirier 0, Marques-Vidal P, et al. The Leu 33/Pro polymorphism (PIA1/PIA2) of the glycoprotein Ila (GPⅡa) receptor is not related to myocardial infarction in the ECTIM Study[J]. Thomb Haemost, 1997, 77:1179-1181. DOI: 10.1055/s-0038-1656134
[24] Gonzalez-Conejero R, Lozano ML, Rivera J, et al. Polymorphisms of platelet membrane glycoprotein lba associated with arterial thrombotie disease[J]. Blood, 1998, 92: 2771-2776. DOI: 10.1182/blood.V92.8.2771
[25] The W llcome Trust Case Control Consortium. Genome-wide association study of 14, 000 cases of seven common diseases and 3, 000 shared controls[J]. Nature, 2007, 447: 661-677.
[26] Hardy J, Singleton A, Genomewide association studies and human disease[J]. N Engl J Med, 2009, 360: 1759-1768.
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