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[3] Brooker JC, Saunders BP, Shah SG, et al. Treatment with argon plasma coagulation reduces recurrence after piecemeal resection of large sessile colonic polyps: a randomized trial and recommendations. Gastrointest Endosc, 2002, 55:371.
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[4] 李益农，陆星华．消化内镜学．北京：科学出版社，1998，504.
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[5] Kelly S, Harris KM, Berry E, et al. A systematic review of the staging performance of endoscopic ultrasound in gastro oesophageal carcinoma. Gut. 2001, 49:534.
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[6] Seitz U, Bapye, Bohnack S, et al. Advances intuerapeutic endoscopic treatment of come bile duct stones, World Surg, 1998, 21133.
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[7] Kim MH, Lee SK, Lee MH, et al. Endoscopic retrograde cholangiopancreato graphy and needle knife sphincterotomy in patients with Billroth II gastrectomy: a comparative study of the forward viewing endoscope and the side viewing duodenoscope. Endoscopy, 1997, 29:82.
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[8] 李兆申．胰腺疾病的内镜治疗．中华消化杂志，1999，19:12.
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[9] Kasarskis EJ, Scarlata D, Hill R, et al. A retrospective study of percutaneous endoscopic gastrostomy in ALS patients during the BDNF and CNTT trials. J Neurol Sci, 1999, 169:118.
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（厉有名 陈卫星）
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内科学新进展 [:1700627006]
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内科学新进展 第四章 血液系统疾病
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内科学新进展 [:1700627007]
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第一节 弥漫性血管内凝血研究的若干进展
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摘 要 弥漫性血管内凝血（DIC）不是一种独立的疾病。许多疾病或病理状态均可引致，见于临床各科。发生的机理极为复杂，多种致病因素激活凝血因子Ⅻ，导致内源凝血途径激活；组织因子释入血液，引致外源凝血途径激活；血小板在血管内皮处黏附、聚集并释放一系列物质，促进DIC形成、发展以及纤溶亢进等引致凝血—抗凝—纤维蛋白溶解失衡。此外，AT-Ⅲ、蛋白C、S系统及TFP等凝血抑制物被消耗，也是加重的原因。临床表现颇为悬殊，以广泛的严重出血、顽固性休克、多发性脏器栓塞和功能衰竭、溶血性贫血等为主要的表现，常危及生命。临床上，DIC分为：①高凝血期；②消耗性低凝血期；③继发性纤溶期。目前，国内DIC的诊断是根据第七届中华血液学会全国血栓与止血学术会议制定的标准（1999年），但尚有一些不同意见。于2001年，国际血栓与止血学会DIC分会提出DIC诊断积分系统。国际上对DIC实验室筛检项目，有不同评论。存在易于发生DIC的基础疾病时，应该动态观察临床表现和实验室指标。DIC需要与原发性纤溶、血栓性血小板减少性紫癜以及严重肝病等做鉴别。DIC的治疗应该根据不同病期，治疗措施包括：①治疗原发病和消除诱因，如纠正产科意外、大手术时减少组织损伤；休克时尽快改善微循环，纠正休克等；②阻断血管内凝血过程；③阻断继发性纤溶亢进；④恢复正常血小板和血浆凝血因子水平等。目前，肝素是最主要的抗凝治疗药物，包括普通肝素和低分子量肝素。用药期间必须作凝血指标监测。此外，补充凝血因子、AT-Ⅲ和血小板以及溶栓治疗等。目前，国外已报道新的抗凝血酶药物和新的丝氨酸蛋白酶抑制剂。
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Abstract Disseminated intravascular coagulation（DIC）is not an isolated disorder and happens in response to a variety of clinical and pathological events. The mechanisms of DIC are complicated which are initiated upon the activation of coagulation factor Ⅻ by multiple pathological factors. Intrinsic coagulation pathway is then activated followed by the release of tissue factor exposed to the circulation and trigger the extrinsic pathway. Thus, platelets adhere and aggregate on the endothelium yielding a series of substances leading to the formation and development of DIC, fibrinolysis activation, and imbalance of coagulation-anticoagulation-fibrinolysis system. Besides that, subsequent consumption and exhaustion of coagulation inhibitors including AT-Ⅲ, Protein C and S System, TFP also contribute to the aggravation of DIC. As we know, DIC is manifested to a large variety including extensive hemorrhage, refractory shock, multiple organ thrombosis, organ failure, hemolytic anemia and carries a high mortality rate. Clinically, DIC is divided into 3 stages: ①hypercoagulatin stage; ②consumptive hypocoagulation stage; ③secondary fibrinosis stage. At present, the domestic diagnostic criterion of DIC was established according to the 7th National Thrombosis and Homeostasis Congress in 1999. The Scientific Subcommittee on Disseminated Intravascular Coagulation of the International Society on Thrombosis and Homeostasis proposed the DIC scoring system in 2001. Comments on DIC laboratory screening assay are different globally. When predisposing condition of DIC exists, continuous monitoring of clinical manifestation and laboratory markers are required. DIC is distinguished from primary fibrinolysis, thrombotic thrombocytic purpura and severe liver disease. The management of therapy is determined according to clinical stages which includes: ①the treatment of primary disease and eliminate predisposing conditions such as therapy of obstetrical calamities, alleviate tissue injury during surgery, ameliorate microcirculation, overcome shock, etc; ②blockade of intravascular coagulation; ③blockade of secondary fibrinoysis; ④and elevate platelets and coagulation factor in plasma to a normal level. Heparin is the most effective anticoagulants involving normal heparin and low molecular heparin. Coagulation markers monitoring is required. Moreover, supplement of coagulation factors, AT-Ⅲ, platelets and thrombolysis therapy are recommended. Novel antithrombin and inhibitor of serine proteases have been reported recently abroad.
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Seegers等（1950年）首先描述有关弥漫性血管内凝血（disseminated intravascular coagulation, DIC）的临床及病理现象。DIC不是一种独立的疾病。其特点为循环血液首先处于高凝状态，微循环中存在广泛的血小板及（或）纤维蛋白性血栓，并由此引起循环功能及其他的内脏功能障碍，常引起不可逆性脏器损害，功能衰竭导致死亡。临床上以广泛严重的出血、顽固性休克、多发性脏器栓塞和功能衰竭、溶血性贫血等为主要表现。通常，起病急骤、病情复杂、发展迅猛，常危及生命。几十年来已被广泛地研究，新的、高度敏感的诊断技术已应用于临床，并有大量的、详细的文献综述，近年来已较少见。
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一、病因学
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许多疾病或病理状态均可引致，见于临床各科。
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（1）临床上最常见的易于引发急性DIC的疾病如下：①产科意外：胎盘早期剥离、前置胎盘、羊水栓塞、死胎滞留、子宫破裂、感染性流产、重症妊娠高血压综合征、高渗盐水引产等；②感染性疾病，如革兰氏阴性或阳性细菌、病毒、真菌、原虫及立克次体等引起的感染；③恶性肿瘤，如血液系统恶性肿瘤（急性早幼粒细胞白血病尤为多见）以及各种实体肿瘤等；④内科疾病，如心血管病（原发性肺动脉高压、恶性高血压、严重心力衰竭等）；消化系统疾病（肝硬化、急性出血性胰腺炎、伪膜性肠炎等）；肺部疾患（肺梗死、呼吸窘迫综合征等）；肾脏疾病（急性肾小球肾炎、急性肾小管坏死及肾皮质坏死等）以及糖尿病酮症、系统性红斑狼疮、药物过敏、中暑等；⑤肝病和阻塞性黄疸、急性肝功能不全。
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（2）其他：休克、输血及输液反应、中毒以及各种物理、化学、生物等因素皆可诱发。有的报道以感染为多见，但有一组大宗病例报道，＞50％的病例是产科病人。而热休克、自身免疫性疾病及溶血性贫血等较少见。
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二、发病机理
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发病机理极为复杂，主要是在某些严重疾病基础上，受到一些因素影响，机体内凝血系统激活、血小板活化、纤维蛋白沉积，导致微血管内弥散性微血栓形成，多种凝血因子及血小板消耗性降低，并伴以继发性纤维蛋白溶解（纤溶）亢进。凝血—抗凝血及纤维蛋白溶解的作用相互关联，相互影响。细胞因子TNF-α或IL-1等介导下，凝血系统激活；纤溶酶形成及tPA释放。此外，内皮细胞一旦被损伤，其对止血—凝血机理的调控作用即被破坏、丧失。总之，多种致病因素激活凝血因子Ⅻ导致内源凝血途径激活是发病机制中的重要一环；组织、细胞受损时，组织因子释入血液，引，致外源凝血途径激活是触发DIC的重要因素之一；致病因素使血小板在血管内皮处黏附、聚集并释放一系列物质，促进DIC形成、发展以及纤溶激活、亢进，以致凝血—抗凝失调进一步加重，在病程进展中起十分重要的作用。此外，AT-Ⅲ、蛋白C、S系统及TFP等凝血抑制物被消耗，也是加重的原因。基本可以分为五种类型：①大量的组织凝血活酶流入血中，如暴发性肝炎、急性早幼粒细胞白血病（如107个白血病细胞可释放55～280U组织凝血活酶）、产科意外等；②单核细胞产生的组织因子，如白血病、败血症时；③血管内皮细胞抗凝机制受损，如血栓调节蛋白和肝素样物质减少；④补体系统和免疫复合物从不同途径激活凝血；⑤其他的促凝物质直接作用于凝血途径，促发血液凝固，如腺癌分泌的黏蛋白或蛇毒等。
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三、病理生理
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由于病因及发病机理不同，病理生理作用可极为复杂，临床表现及实验室检查结果变化也大。DIC病理生理见图4-1。
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