發(fā)布時(shí)間：2018-05-22 17:05

  本文選題：肝硬化 + 門靜脈血栓�。� 參考：《南昌大學(xué)》2016年碩士論文

【摘要】：背景:門靜脈血栓(portal vein thrombosis,PVT)是肝硬化(Liver Cirrhosis,LC)失代償期的常見并發(fā)癥之一,其形成的原因及具體機(jī)制迄今尚不十分明確,故探討門靜脈血栓形成的危險(xiǎn)因素有助于早期發(fā)現(xiàn)、預(yù)防及有效治療肝硬化并門靜脈血栓患者。目前針對血栓最常用的方法是抗凝治療,但因肝硬化患者肝功能差,使用抗凝藥物可增加肝硬化患者門脈高壓癥引起的食管胃底靜脈曲張破裂,從而導(dǎo)致上消化道出血等并發(fā)癥風(fēng)險(xiǎn),故臨床上使用抗凝藥物治療門靜脈血栓時(shí)非常慎重,有時(shí)即使發(fā)現(xiàn)了門靜脈血栓也會(huì)因考慮到出血風(fēng)險(xiǎn)而暫不使用抗凝藥物治療。但也有報(bào)道稱抗凝藥物治療不會(huì)增加肝硬化并PVT患者出現(xiàn)上消化道出血的發(fā)病率,同時(shí)有臨床相關(guān)試驗(yàn)表明在行內(nèi)鏡下曲張靜脈序貫治療的患者中給予抗凝藥物治療并不增加上消化道出血的風(fēng)險(xiǎn)。故目前對肝硬化并門靜脈血栓形成者是否給予抗凝藥物治療,學(xué)術(shù)界意見仍不統(tǒng)一。目的:1、通過分析肝硬化合并PVT患者的臨床相關(guān)資料,闡述門靜脈血栓形成的相關(guān)因素與獨(dú)立危險(xiǎn)因素,期望早期發(fā)現(xiàn)并預(yù)防門靜脈血栓。2、分析抗凝藥物治療對肝硬化并PVT者食管胃底曲張靜脈破裂出血的影響,探討肝硬化并PVT者食管胃底曲張靜脈破裂出血的危險(xiǎn)因素及預(yù)防措施,進(jìn)而更好的指導(dǎo)臨床抗凝藥物治療。方法:選取自2012年1月至2012年12月間在我院住院確診的肝硬化患者共239例,其中33例肝硬化合并PVT患者為血栓組,另外206例單純肝硬化無PVT患者作為對照組。33例肝硬化合并PVT患者中,有10例進(jìn)行了抗凝藥物治療,為抗凝組,另23例未經(jīng)抗凝藥物治療,則為未抗凝組;而在這33例合并門靜脈血栓的肝硬化患者中,出現(xiàn)食管胃底曲張靜脈破裂出血患者10例為出血組,而無出血的23例即為未出血組。分別記錄患者的一般信息(年齡、性別)和臨床資料(病因、是否有脾切除史與糖尿病史,脾臟厚度、門靜脈主干寬度、食管胃底靜脈曲張程度、有無門脈高壓性胃病與肝源性潰瘍、腹水程度、child-pugh評分、有無行內(nèi)鏡下曲張靜脈序貫治療、有無服用心得安治療),以及實(shí)驗(yàn)室檢查結(jié)果(白細(xì)胞(wbc)、血小板(plt)、紅細(xì)胞(rbc)、血紅蛋白(hb)、纖維蛋白原(fib)、d-二聚體、總膽紅素(tbil)、直接膽紅素(dbil)、白蛋白(alb)、肌酐(cr)等數(shù)據(jù)),從而探討肝硬化并pvt形成的相關(guān)因素及獨(dú)立危險(xiǎn)因素。對于使用抗凝藥物治療的肝硬化合并pvt患者觀察近1年內(nèi)是否出現(xiàn)上消化道出血,分析抗凝治療對食管胃底曲張靜脈破裂出血的影響,并進(jìn)一步闡述肝硬化并pvt患者發(fā)生食管胃底曲張靜脈破裂出血的危險(xiǎn)因素及預(yù)防措施。結(jié)果:1、239例肝硬化患者中,33例合并門靜脈血栓,陽性率為13.80%。2、血栓組與對照組在年齡、性別、病因方面比較均無統(tǒng)計(jì)學(xué)意義,具有可比性;比較白細(xì)胞、紅細(xì)胞、血紅蛋白、纖維蛋白原、總膽紅素、直接膽紅素、肌酐、凝血酶原時(shí)間、活化凝血酶原時(shí)間、脾臟厚度、child-pugh評分以及是否行內(nèi)鏡下曲張靜脈序貫治療、是否口服心得安藥物等,在兩組間無顯著差異(p0.05);血栓組白蛋白計(jì)數(shù)低于對照組(30.37±4.19g/lvs32.34±6.08g/lp=0.023),且血栓組血小板計(jì)數(shù)與門靜脈主干寬度明顯高于對照組(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),有顯著差異;血栓組在糖尿病患病率與脾切除病史方面均高于對照組(24.24%vs7.28%,p0.01;54.54%vs16.50%,p0.01),有極其顯著的差異。行非條件logistic回歸模型分析發(fā)現(xiàn)血小板計(jì)數(shù)與門靜脈主干寬度是形成門靜脈血栓的獨(dú)立危險(xiǎn)因素,(p=0.009,0.001;or分別值為1.006,16.85)。3、肝硬化并門靜脈血栓者引起食管胃底靜脈曲張破裂出血的相關(guān)因素進(jìn)行分析發(fā)現(xiàn):白細(xì)胞、紅細(xì)胞、血小板、血紅蛋白、總膽紅素、白蛋白含量、肌酐、凝血酶原時(shí)間、纖維蛋白原等不存在統(tǒng)計(jì)學(xué)差異,p值均大于0.05;而靜脈曲張程度是其危險(xiǎn)因素,p0.05;內(nèi)鏡下曲張靜脈序貫治療是其保護(hù)因素,行內(nèi)鏡下曲張靜脈序貫治療出血率與未行相應(yīng)治療出血率分別為30%及73.9%,有顯著差異(p0.05)。4、抗凝組與未抗凝組觀察1年發(fā)現(xiàn)出血率分別為40%及26.1%,兩組比較無顯著差異(p0.05)。結(jié)論:1、血小板計(jì)數(shù)、白蛋白計(jì)數(shù)、門靜脈主干寬度、糖尿病及脾切除病史是肝硬化并PVT的危險(xiǎn)因素,且血小板計(jì)數(shù)、門靜脈主干寬度是肝硬化患者PVT形成的獨(dú)立危險(xiǎn)因素,即血小板計(jì)數(shù)越高、門靜脈主干內(nèi)徑越寬肝硬化患者出現(xiàn)PVT的發(fā)生率越高。2、肝硬化并PVT者是否出現(xiàn)食管胃底曲張靜脈破裂出血與曲張靜脈程度密切相關(guān),即曲張靜脈程度越嚴(yán)重則越易出現(xiàn)曲張靜脈破裂出血,對其行曲張靜脈內(nèi)鏡下序貫治療可顯著降低肝硬化并PVT者曲張靜脈破裂出血的風(fēng)險(xiǎn)。3、肝硬化并PVT者進(jìn)行抗凝藥物治療可能不會(huì)增加食管胃底靜脈曲張破裂出血的發(fā)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.
【學(xué)位授予單位】：南昌大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2016
【分類號】：R575.21

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