肝硬化者并门静脉血栓形成的危险因素及抗凝治疗对其所致食管胃底曲张静脉破裂出血的影响

发布时间：2018-05-22 17:05

本文选题：肝硬化 + 门静脉血栓　；参考：《南昌大学》2016年硕士论文

【摘要】：背景:门静脉血栓(portal vein thrombosis,PVT)是肝硬化(Liver Cirrhosis,LC)失代偿期的常见并发症之一,其形成的原因及具体机制迄今尚不十分明确,故探讨门静脉血栓形成的危险因素有助于早期发现、预防及有效治疗肝硬化并门静脉血栓患者。目前针对血栓最常用的方法是抗凝治疗,但因肝硬化患者肝功能差,使用抗凝药物可增加肝硬化患者门脉高压症引起的食管胃底静脉曲张破裂,从而导致上消化道出血等并发症风险,故临床上使用抗凝药物治疗门静脉血栓时非常慎重,有时即使发现了门静脉血栓也会因考虑到出血风险而暂不使用抗凝药物治疗。但也有报道称抗凝药物治疗不会增加肝硬化并PVT患者出现上消化道出血的发病率,同时有临床相关试验表明在行内镜下曲张静脉序贯治疗的患者中给予抗凝药物治疗并不增加上消化道出血的风险。故目前对肝硬化并门静脉血栓形成者是否给予抗凝药物治疗,学术界意见仍不统一。目的:1、通过分析肝硬化合并PVT患者的临床相关资料,阐述门静脉血栓形成的相关因素与独立危险因素,期望早期发现并预防门静脉血栓。2、分析抗凝药物治疗对肝硬化并PVT者食管胃底曲张静脉破裂出血的影响,探讨肝硬化并PVT者食管胃底曲张静脉破裂出血的危险因素及预防措施,进而更好的指导临床抗凝药物治疗。方法:选取自2012年1月至2012年12月间在我院住院确诊的肝硬化患者共239例,其中33例肝硬化合并PVT患者为血栓组,另外206例单纯肝硬化无PVT患者作为对照组。33例肝硬化合并PVT患者中,有10例进行了抗凝药物治疗,为抗凝组,另23例未经抗凝药物治疗,则为未抗凝组;而在这33例合并门静脉血栓的肝硬化患者中,出现食管胃底曲张静脉破裂出血患者10例为出血组,而无出血的23例即为未出血组。分别记录患者的一般信息(年龄、性别)和临床资料(病因、是否有脾切除史与糖尿病史,脾脏厚度、门静脉主干宽度、食管胃底静脉曲张程度、有无门脉高压性胃病与肝源性溃疡、腹水程度、child-pugh评分、有无行内镜下曲张静脉序贯治疗、有无服用心得安治疗),以及实验室检查结果(白细胞(wbc)、血小板(plt)、红细胞(rbc)、血红蛋白(hb)、纤维蛋白原(fib)、d-二聚体、总胆红素(tbil)、直接胆红素(dbil)、白蛋白(alb)、肌酐(cr)等数据),从而探讨肝硬化并pvt形成的相关因素及独立危险因素。对于使用抗凝药物治疗的肝硬化合并pvt患者观察近1年内是否出现上消化道出血,分析抗凝治疗对食管胃底曲张静脉破裂出血的影响,并进一步阐述肝硬化并pvt患者发生食管胃底曲张静脉破裂出血的危险因素及预防措施。结果:1、239例肝硬化患者中,33例合并门静脉血栓,阳性率为13.80%。2、血栓组与对照组在年龄、性别、病因方面比较均无统计学意义,具有可比性;比较白细胞、红细胞、血红蛋白、纤维蛋白原、总胆红素、直接胆红素、肌酐、凝血酶原时间、活化凝血酶原时间、脾脏厚度、child-pugh评分以及是否行内镜下曲张静脉序贯治疗、是否口服心得安药物等,在两组间无显著差异(p0.05);血栓组白蛋白计数低于对照组(30.37±4.19g/lvs32.34±6.08g/lp=0.023),且血栓组血小板计数与门静脉主干宽度明显高于对照组(113.00(51.00,340.50)vs55.00(36.75,89.25),p0.01;1.40(1.20,1.60)vs1.20(1.10,1.40)p0.01),有显著差异;血栓组在糖尿病患病率与脾切除病史方面均高于对照组(24.24%vs7.28%,p0.01;54.54%vs16.50%,p0.01),有极其显著的差异。行非条件logistic回归模型分析发现血小板计数与门静脉主干宽度是形成门静脉血栓的独立危险因素,(p=0.009,0.001;or分别值为1.006,16.85)。3、肝硬化并门静脉血栓者引起食管胃底静脉曲张破裂出血的相关因素进行分析发现:白细胞、红细胞、血小板、血红蛋白、总胆红素、白蛋白含量、肌酐、凝血酶原时间、纤维蛋白原等不存在统计学差异,p值均大于0.05;而静脉曲张程度是其危险因素,p0.05;内镜下曲张静脉序贯治疗是其保护因素,行内镜下曲张静脉序贯治疗出血率与未行相应治疗出血率分别为30%及73.9%,有显著差异(p0.05)。4、抗凝组与未抗凝组观察1年发现出血率分别为40%及26.1%,两组比较无显著差异(p0.05)。结论:1、血小板计数、白蛋白计数、门静脉主干宽度、糖尿病及脾切除病史是肝硬化并PVT的危险因素,且血小板计数、门静脉主干宽度是肝硬化患者PVT形成的独立危险因素,即血小板计数越高、门静脉主干内径越宽肝硬化患者出现PVT的发生率越高。2、肝硬化并PVT者是否出现食管胃底曲张静脉破裂出血与曲张静脉程度密切相关,即曲张静脉程度越严重则越易出现曲张静脉破裂出血,对其行曲张静脉内镜下序贯治疗可显著降低肝硬化并PVT者曲张静脉破裂出血的风险。3、肝硬化并PVT者进行抗凝药物治疗可能不会增加食管胃底静脉曲张破裂出血的发病率。
[Abstract]:Background: portal vein thrombosis (PVT) is one of the common complications of decompensated cirrhosis (Liver Cirrhosis, LC). The reasons for its formation and its specific mechanism are not yet very clear. Therefore, the study of the risk factors for the formation of portal vein thrombosis is helpful for the early detection, prevention and effective treatment of patients with cirrhosis and portal vein thrombosis. At present, anticoagulant therapy is the most commonly used method for thrombus, but the use of anticoagulant drugs can increase the rupture of esophageal and gastric fundus varices caused by portal hypertension in patients with cirrhosis due to the poor function of liver cirrhosis, which leads to the risk of upper gastrointestinal bleeding, so it is very careful to treat the portal vein thrombosis with anticoagulant drugs. Sometimes it is also reported that anticoagulant therapy does not increase liver cirrhosis and the incidence of upper gastrointestinal bleeding in PVT patients, and there are clinical trials showing that anti - endoscopic variceal sequential therapy is given to patients who have been treated with endoscopic varicose vein sequential therapy. Anticoagulant therapy does not increase the risk of bleeding in the upper gastrointestinal tract. Therefore, there are still no academic opinions on whether or not anticoagulant therapy is given to patients with cirrhosis and portal vein thrombosis. Objective: 1. Through the analysis of the clinical data of patients with liver cirrhosis with PVT, the related factors and independent risk factors of portal venous thrombosis and the expectation of independent risk factors are described. Early detection and prevention of portal vein thrombosis.2, analysis of anticoagulant therapy on cirrhosis and PVT patients with esophageal and gastric fundus variceal bleeding, to explore the risk factors and preventive measures of PVT patients with esophageal and gastric fundus variceal bleeding, and to better guide the clinical anticoagulant therapy. Methods: from January 2012 to 20 239 cases of liver cirrhosis confirmed in our hospital in December 12 years, of which 33 cases of cirrhosis with PVT patients were thrombus group, and 206 cases of simple cirrhosis without PVT as the control group.33 cases of cirrhosis combined with PVT, 10 cases were treated with anticoagulant, the other 23 cases were not treated with anticoagulant, then the unanticoagulant group; In these 33 patients with portal vein thrombosis, 10 cases of bleeding patients with esophageal and gastric fundus variceal bleeding were seen as bleeding group, and 23 cases without bleeding were unbleeding group. The general information (age, sex) and clinical data were recorded respectively (etiology, the history of splenectomy and diabetes, spleen thickness, the main portal vein). The width, the degree of varicose esophagus and gastric fundus vein, the portal hypertensive gastropathy and hepatogen ulcers, the degree of ascites, the Child-Pugh score, the endoscopic variceal sequential therapy, the treatment of propranolol, the results of the laboratory examination (WBC), the platelet (PLT), the RBC, the Hb, the fibrinogen (FIB), and the d- Two polymer, total bilirubin (TBIL), direct bilirubin (DBIL), albumin (ALB), creatinine (CR), and so on, to explore the related factors and independent risk factors for the formation of liver cirrhosis and Pvt. For the patients with PVT with anticoagulant therapy, the upper digestive tract bleeding was observed in the last 1 years, and the anticoagulant therapy for esophagogastric fundus was analyzed. The risk factors and preventive measures for bleeding of esophageal and gastric fundus varicose veins in patients with liver cirrhosis and PVT were further discussed. Results: of the 1239 cases of cirrhosis, 33 cases with portal vein thrombosis were combined with 13.80%.2, and there was no statistical difference between the thrombus group and the control group in age, sex and etiology. The comparison of white blood cells, red blood cells, hemoglobin, fibrinogen, total bilirubin, direct bilirubin, creatinine, prothrombin time, activation of prothrombin time, spleen thickness, Child-Pugh score and whether or not endoscopic varicose vein sequential treatment, and whether oral propranolol or not, were not significantly different between the two groups (P0.05). The albumin count of the thrombus group was lower than that of the control group (30.37 + 4.19g/lvs32.34 + 6.08g/lp=0.023), and the blood platelet count and the main trunk width of the portal vein were significantly higher than that of the control group (113 (51.00340.50) vs55.00 (36.75,89.25), P0.01; 1.40 (1.20,1.60) vs1.20 (1.10,1.40) P0.01), and there were significant differences. The incidence of diabetes and splenectomy in the thrombosis group was significantly higher than that in the control group. The history was higher than that of the control group (24.24%vs7.28%, P0.01; 54.54%vs16.50%, P0.01), and there was an extremely significant difference. The analysis of the unconditional logistic regression model found that the platelet count and the breadth of the portal vein were independent risk factors for the formation of portal vein thrombosis (p=0.009,0.001; or value 1.006,16.85).3, cirrhosis and portal vein thrombosis The analysis of related factors causing bleeding of esophageal variceal variceal rupture found that there were no statistical differences between white blood cells, red blood cells, platelets, hemoglobin, total bilirubin, albumin, creatinine, prothrombin time, fibrinogen and so on, the p value was more than 0.05, and the degree of varicosity was a risk factor, P0.05; endoscopy Zhang Jing Pulse sequential therapy was a protective factor. Endoscopic variceal venous sequential therapy was 30% and 73.9%, respectively, 30% and 73.9%. There were significant differences (P0.05).4. The bleeding rates of the anticoagulant group and the non anticoagulant group were 40% and 26.1%, respectively, and there was no significant difference between the two groups (P0.05). Conclusion: 1, platelet count, albumin meter The number, the breadth of the portal vein, the history of diabetes and splenectomy is a risk factor for cirrhosis and PVT, and the platelet count, the width of the portal vein, is an independent risk factor for the formation of PVT in the patients with cirrhosis, that is, the higher the platelet count, the greater the diameter of the portal vein, the higher the incidence of PVT in the patients with cirrhosis, the higher the incidence of.2, the liver cirrhosis, and the PVT. The bleeding of the varicose veins is closely related to the occurrence of rupture of the varicose veins of the esophagus and stomach fundus varicose veins. That is, the more severe the varicose vein is, the more prone to variceal bleeding. The endoscopic sequential therapy of varicose veins can significantly reduce the risk of.3 in the liver cirrhosis and PVT variceal bleeding, and the patients with cirrhosis and PVT are treated with anticoagulant therapy. It may not increase the incidence of bleeding of esophageal and gastric varices.
【学位授予单位】：南昌大学
【学位级别】：硕士
【学位授予年份】：2016
【分类号】：R575.21

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