血管内皮生长因子在门脉高压患者胃黏膜的表达

目的探讨血管内皮生长因子(VEGF)在肝硬化门脉高压(PHT)患者胃黏膜的表达及其在门脉高压性胃病(PHG)发病中的作用。方法分别采集PHG、PHT和正常对照组胃黏膜组织。应用免疫组化法检测胃黏膜VEGF蛋白的表达。PHG程度按改良的McMrmark’s分级由有经验的消化科医师盲法评估。结果PHG组(49.56%±12.26%)和PHT组(48.56%±12.23%)胃黏膜VEGF表达较正常对照组(5.11%±2.14%)显著性增高(P<0.05),但前两组间VEGF的表达无统计学差异(P>0.05)。VEGF阳性表达主要见于胃小凹颈部黏膜细胞浆内。VEGF与PHG积分呈显著性正相关(H=10.592,P<0.05)。结论肝硬化门脉高压患者胃黏膜组织VEGF表达增高。PHT胃黏膜淤血、缺氧与VEGF增加存在互动关系,VEGF在PHG发病过程中的作用可能是有限的。     

门脉高压性胃病与幽门螺杆菌相关性研究

为了解门脉高压性胃病(PHG)与幽门螺杆菌(HP)的关系,采用尿素酶试验、血清HP抗体检测和14C呼吸试验等方法检测50例肝硬化PHG患者HP的感染率,并与非PHG肝硬化(NPHG)、十二指肠球部溃疡(DU)、功能性消化不良(FD)三组患者比较.PHG组HP感染率为36%,与NPHG组(38%)、FD组(44%)分别比较差异无显著性(P＞0.05),与DU组(94%)比较差异有显著性(P＜0.01).说明HP感染对PHG发病影响不大.     

门脉高压综合征与门脉高压性胃病155例临床分析

目的观察门脉高压综合征食管静脉曲张及脾肿大的严重程度与门脉高压性胃病(PHG)发病率的关系。方法对155例肝硬化住院病人行临床及胃镜检查,将PHG的发病率与食管静脉曲张及脾肿大的严重程度进行比较。结果PHG在食管静脉曲张轻、中、重度的发病率分别为37.0%(10/27)、60.0%(18/30)与51.0%(50/98),差异无显著性(P>0.05)。在脾肿大轻、中、重度的发病率分别为51.7%(47/91)、48.7%(19/39)及48.0%(12/25),差异无显著性(P>0.05)。结论门脉高压综合征食管静脉曲张及脾肿大的严重程度与门脉高压性胃病的发病率之间无相关性。     

门脉高压性胃病患者胃黏膜中ET-1与HIF-1的表达及其意义

目的 探讨门脉高压性胃病(PHG)患者胃黏膜中内皮素-1(ET-1)和缺氧诱导因子-1(HIF-1)的表达及其相关性,为PHG的发病机制提供一定理论依据.方法 随机选择从2010年11月至2011年6月期间的PHG患者60例、门静脉高压症(PHT)无PHG患者30例和正常对照者20例,PHG组中分为轻型34例、重型26...     

血红素加氧酶-1在门静脉高压性胃病患者胃黏膜的表达

目的 探讨血红素加氧酶-1(HO-1)在肝硬化门静脉高压性胃病(PHG)患者胃黏膜的表达情况及其意义.方法 分别采集22例正常受试者(对照组)、20例门静脉高压(PHT)患者(PHT组)和22例PHG患者(PHG组)的胃黏膜标本,观察胃黏膜组织学变化,测定门静脉血流量(PVF).应用免疫组织化学法和Western blot方法检测HO-1蛋白在胃黏膜组织的表达情况,并分析HO-1蛋白与PVF、内镜下PHG严重程度的相关性,以及内镜下PHG严重程度与临床参数的相关性.结果 PHG组和PHT组患者胃黏膜中HO-1蛋白表达明显高于对照组(P＜0.05),而PHG组与PHT组之间比较差异无统计学意义(P＞0.05).PHG患者胃组织HO-1蛋白表达与内镜下PHG严重程度积分呈显著正相关(r =0.459,P＜0.05).内镜下PHG严重程度积分与食管静脉曲张程度(r=0.059,P＞0.05)、Child-Pugh分级(r=-0.001,P＞0.05)均无显著性相关.PHG组与PHT组患者的胃黏膜组织HO-1蛋白表达与PVF无显著性相关(r=0.071,P＞0.05).结论 HO-1蛋白在PHG患者胃黏膜中呈高表达,参与了PHG患者胃黏膜血液循环紊乱的发生.     

门脉高压性胃病与HBV感染关系探讨

为探讨门脉高压性胃病 (PHG)与乙肝病毒 (HBV)感染的关系 ,对 5 8例乙肝后肝硬化并 PHG患者(PHG组 )行内窥镜检查 ,同时取其胃粘膜组织行免疫组织化学 (ABC法 )检查。结果显示 PHG组胃粘膜组织HBs Ag和 HBc Ag阳性率分别为 31.0 3%和 2 5 .86 % ,与对照组比较 ,P<0 .0 1;PHG病变的程度与 HBV抗原阳性率呈正比。认为 PHG及其病变程度可能与 HBV感染有关     

肝硬化门脉高压性胃病与幽门螺杆菌关系的探讨

目的探讨肝硬化门脉高压性胃病(PHG)与幽门螺杆菌(Hp)感染的关系及临床意义。方法对72例PHG和50例慢性胃炎患者进行了胃镜、病理检查和Hp检测,并进行对比分析。结果伴有PHG 的肝硬化门脉高压患者的Hp感染率为23.07%,不伴有PHG者为25.0%,两者差异无显著性(P>0.05), 轻度PHG患者Hp感染率为23.80%,重度为20.0%,差异无显著性(P>0.05)。门脉高压患者的Hp感染率显著低于慢性胃炎组(23.60%比72.0%,P<0.01),但门脉高压患者慢性活动性胃炎的发生与Hp的感染密切相关,活动性胃炎的Hp感染率(53.84%)比非活动性胃炎Hp感染率(16.94%)显著升高(P< 0.01)。结论肝硬化门脉高压性胃病的Hp感染率降低,可能与肝硬化患者胃内环境不适合Hp的生存有关。门脉高压患者胃黏膜的活动性炎症,可能是由Hp感染引起,与肝硬化门脉高压关系不大。     

其它肝脏疾病：肝硬化

血管内皮生长因子在门脉高压患者胃黏膜的表达——白云等（河北 邢台市人民医院）；《胃肠病学和肝病学杂志》，2007，16（1）：63-65[目的：探讨血管内皮生长因子（VEGF）在肝硬化门脉高压（PHT）患者胃黏膜的表达及其在门脉高压性胃病（PHG）发病中的作用。方法：分别采集PHG、PHT和正常对照组胃黏膜组织。应用免疫组化法检测胃黏膜VEGF蛋白的表达。     

门脉高压性胃病肝郁脾虚证与胃动素水平关系的研究

[目的]从胃动素(MTL)水平探讨门脉高压性胃病(PHG)肝郁脾虚证的病理生理基础,为PHG肝郁脾虚证的中医辨病辨证提供理论依据。[方法]入选对象120例,分为:PHG组(P组)、慢性乙型肝炎组(H组)、慢性胃炎组(G组)、正常对照组(C组),每组30例。详细询问每例患者的病史、临床症状,进行肝郁脾虚证的评分;在早晨空腹状态下采肘前静脉血,检测血浆MTL水平。[结果]①P组MTL水平最高,并与其他各组比较差异有统计学意义(P0.01);②P组McCormick分度重度患者MTL水平比轻度者为高(P0.01);③P组肝郁脾虚证积分与血浆MTL水平呈正相关(P0.01);④P组肝功能Child-Pugh分级,C级MTL水平均明显高于B级和A级,各级之间比较差异有统计学意义(P0.01)。[结论]①MTL参与PHG的形成,促进其发展,在PHG的形成与发展中起重要作用;②症状越重,积分越高,MTL水平升高越明显,PHG胃黏膜改变越重;③肝功能损害越明显,MTL水平越高,PHG胃黏膜改变越重;④MTL可作为PHG肝郁脾虚证的检测指标。     

替普瑞酮对门脉高压大鼠胃黏膜保护作用初探

目的观察预防性使用替普瑞酮对实验性门脉高压大鼠胃黏膜的保护作用。方法128只大鼠均分为正常对照组、正常干预组、单纯造模组和造模干预组,后2组腹腔注射硫代乙酰胺制作门脉高压大鼠模型。正常干预组和造模干预组同步给予口服替普瑞酮治疗。观察各组在8、12、16、20周末胃凝胶黏液层厚度和胃黏膜损伤指数。结果门脉高压大鼠胃凝胶层厚度明显下降,胃黏膜损伤指数增高。造模干预组治疗16周和20周后胃凝胶层厚度分别为(34.89±9.84)μm和(32.34±4.24)μm,明显高于单纯造模组[(20.24±8.27)μm和(15.52±5.92)μm,P<0.01];胃黏膜损伤指数分别为13.8±6.5和20.5±4.6,与单纯造模组(30.7±8.6和35.6±9.5)比较差异有显著性(P<0.01)。结论替普瑞酮对门脉高压胃黏膜可能具有一定的保护作用。     

Assessment of the agreement between wedge hepatic vein pressure and portal vein pressure in cirrhotic patients

BACKGROUND: Measuring wedged hepatic venous pressure and hepatic venous pressure gradient as indices of portal pressure is being increasingly used in assessing the prognosis and response to pharmacological treatment for portal hypertension in cirrhotic patients. AIM: To re-evaluate the agreement and correlation between wedged hepatic pressures and directly measured portal pressures. METHODS: Medline search for studies comparing direct portal with wedged hepatic pressure measurement and assessment of correlation and agreement of the pooled data. RESULTS: Eleven suitable studies included 320 patients. Coefficient of determination (r2) was 0.87 in all patients, 0.87 in 102 patients with alcoholic liver disease, 0.83 in 88 patients with non-alcoholic liver disease and 0.75 in 53 patients with hepatitis C-related liver disease. Coefficient of determination was 0.85 in the 194 patients in whom a wedge catheter and 0.90 in the 113 patients in whom a balloon catheter was used. Agreement according to the method of Bland and Altman was also found to be good, with only 4-8% of the measurements outside 2 standard deviations. CONCLUSIONS: Wedged hepatic pressure measurement correlates well with direct portal pressure measurement and the agreement is sufficiently good to use this as a surrogate measurement.     

门静脉高压症脾切除术后患者血浆内皮素变化与门静脉血栓形成的关系

为探讨门静脉高压症患者脾切除术后血浆内皮素 (ET)水平变化及其临床意义 ,采用放免法测定了30例肝硬变门静脉高压症行脾切除术患者 (观察组 )术前及术后 1周血浆 ET水平 ,并设对照组比较。结果显示 ,观察组术前血浆 ET水平 (6 7.2 4± 2 4 .6 3pg/ml)明显高于对照组 (33.2 1± 11.0 5 pg/ml) ,P<0 .0 0 1;术后 1周明显下降 (37.2 4± 14 .4 7pg/ml) ,P<0 .0 0 1,与对照组 (32 .4 8± 10 .6 2 pg/m l)比较无显著差异 ,P>0 .0 5。脾切除术后门静脉血栓形成者 ET水平 (5 7.90± 2 1.70 pg/m l)明显高于非血栓形成者 (33.15± 8.2 9pg/ml) ,P<0 .0 0 1。认为ET在肝硬变、门静脉高压症发生中起重要作用 ,ET增高与门静脉血栓形成有关。脾切除术后血浆 ET明显下降 ,对改善肝脏功能、降低门静脉压力具有重要意义     

门静脉高压性胃肠病的诊治进展

门静脉高压性胃病和肠病通常指继发于门静脉高压的胃肠道黏膜病变,可导致消化道出血。其发病机制不明,可能与血流动力学改变及其分子机制有关,药物治疗、内镜治疗、手术治疗是主要的治疗手段。本文就门静脉高压性胃肠病的发病机制、内镜表现、治疗方案等方面进行文献回顾,以期为临床诊治提供参考。     

Stability of a rat model of prehepatic portal hypertension caused by partial ligation of the portal vein

AIM： To study the stability of portal hypertension （PHT） caused by partial ligation of the portal vein ligation （PVL） in a rat model.
METHODS： Thirty male adult Wistar rats were divided into two groups： 10 in Group Ⅰ received a sham operation; and 20 in Group Ⅱreceived partial PVL. Portal vein pressure （PVP） was measured at four time periods： before ligation, 2 wk, 6 wk and 10 wk postsurgery. Portal venography, blood sampling and liver and spleen pathological examinations were conducted at 10 wk after surgery.
RESULTS： The PVP was 9.15± 0.58 cmH2O before ligation, and increased to 17.32 ±0.63 cmH2O 2 wk after PVL. By repeat measurement of the PVP in each rat, it was shown to remain elevated for 10 wk. There were no significant differences in the pressure measurements at 2 wk, 6 wk and 10 wk. Varices were found mainly in the mesenteric vein 2 wk after PVL, which were more obvious later, while these manifestations were similar at week 6 and week 10. Portal venography demonstrated the varices and collaterals. There was no significant change in liver pathology. The volume of the spleen was enlarged 2-fold after ligation, and the sinus of the spleen was enlarged due to congestion. Significant sinus endothelial cell proliferation was observed, but no evidence of hypersplenia was found on hemogram and biochemical examination.
CONCLUSION： These findings suggest that a satisfactory prehepatic PHT rat model can be obtained by partial ligation of the portal vein, and this PHT rat model was stable for at least 10 wk.     

肝硬化门静脉血栓形成的临床分析

目的　探讨肝硬化 (LC)门静脉血栓 (PVT)形成对LC病程发展的影响。方法　检索我院自 1 995至 2 0 0 2年肝硬化PVT形成患者 ,血栓诊断依据彩色多普勒和 (或 )CT。 4 8例肝硬化PVT形成患者入选血栓组 ;同阶段LC门脉高压症的非血栓病例中选择 5 2例作为对照组。对两组患者的肝功能Child Pugh分级、凝血功能、门静脉、脾静脉宽度及脾脏面积、厚度进行比较。行t检验 ,χ2 检验 ,Logistic回归分析。结果　肝硬化PVT形成除继发于脾切除等手术后 ,75 .0 %隐匿发病 ,85 .4 %的血栓发生于门静脉主干 ,脾脏增大与门静脉增宽是PVT形成的危险因素 (P =0 .0 0 3、0 .0 1 0 )。血栓组门静脉及脾静脉宽度分别为 (1 .4 8± 0 .2 6 )cm ,(1 .2 3± 0 .38)cm ,与对照组比较差异有显著性 [(1 .37± 0 .2 2 )cm ,(1 .0 5± 0 .30 )cm ,P =0 .0 37,0 .0 31 ]。血栓组脾面积平均值为 (96 .6 4± 33.4 )cm2 ,脾厚径为 (6 .0 7± 1 .2 0 )cm ,分别大于对照组的 (80 .81± 2 8.9)cm2 ,(5 .2 3± 1 .0 8)cm(P =0 .0 36 ,0 .0 0 1 )。血栓组食管胃底静脉曲张程度重于非血栓组 ,大出血、大量腹水比例高 (P <0 .0 5 )。血栓形成后 1年内死亡率为1 6 .6 % ,较非血栓组增高 (P =0 .0 2 3)。两组肝功能Child Pugh分级、凝血功能、血小板计     

胃静脉曲张:临床及内镜特征初探

目的 初步观察胃静脉曲张的临床及内镜特征。方法 回顾分析10年来我院资料完整的胃静脉曲张（GV）85例,并与同期仅有食管静脉曲张（EV）196例对照。结果 GV的检出率占同期静脉曲张的30．2％,其中胃食管静脉曲张I型（GOV－1）占74．1％,GOV－Ⅱ型占22．4％,单纯胃静脉曲张I型（IGV－I）占2．4％,IGV－Ⅱ型占1．2％。GOV型GV的病因以肝硬化门脉高压最多见,IGV型GV主要见于非肝硬化节段性门脉高压;GV的各型的检出率与肝功能Child分级无关,GV合并门脉高压性胃病（PHC）发生率高于EV（P＜0．01）。GOV－Ⅱ较GOV－I合并PHG的检出率高、程度重,GOV－Ⅱ较GOV－I合并EV的程度重;而GV的出血率显著低于EV（P＜0．01）。结论 Sarin分类法简单、实用,适合国内推广应用。GV并非少见,检出率占全部静脉曲张的30．2％,其中,GOV－I最多见,GOV－Ⅱ次之,IGV较少,而GV出血较EV少见。     

Portal ductopathy: clinical importance and nomenclature

Non-cirrhotic portal hypertension(PHT)accounts for about 20%of all PHT cases,portal vein thrombosis(PVT) resulting in cavernous transformation being the most common cause.All known complications of PHT may be encountered in patients with chronic PVT.However,the effect of this entity on the biliary tree and pancreatic duct has not yet been fully established.Additionally,a dispute remains regarding the nomenclature of common bile duct abnormalities which occur as a result of chronic PVT.Although many clinical...     

丹参等活血化淤中药对门脉高压血流动力学影响的临床与实验研究

目的探讨丹参、当归等及硝苯啶对门脉高压血流动力学的影响。方法采用血管插管测定胆管结扎肝硬化犬门脉系统压力变化；超声多普勒观测肝硬化患者门脉血流动力学变化。结果（１）静脉滴注丹参、当归后，肝硬化犬门静脉压（Ｐｐｖ）、嵌塞肝静脉压（ＷＨＶＰ）、肝静脉压力梯度（ＨＶＰＧ）显著降低（Ｐ＜０．０５～０．０１），平均动脉压（ＭＡＰ）、心率（ＨＲ）无明显变化（Ｐ＞０．０５），硝苯啶则使Ｐｐｖ，ＷＨＶＰ，ＭＡＰ．ＨＲ显著降低（Ｐ＜０．０５）。（２）丹参、丹参＋硝苯啶．丹参＋水＋硝苯啶口服药１０－１２周，能显著降低肝硬化患者门静脉内径（Ｄｐｖ）、脾静脉内径（Ｄｓｖ）．门静脉血流量（Ｑｐｖ），脾静脉血流量（Ｑｓｖ）（Ｐ＜０．０５－０．０１，当归作用较弱。结论对比表明，丹参、当归等中药较硝苯啶对门脉压力作用为慢，但较持久，无副反应。     

How can portal vein cavernous transformation cause chronic incomplete biliary obstruction?

Biliary disease in the setting of non-cirrhotic portal vein thrombosis (and similarly in portal vein cavernous transformation) can become a serious problem during the evolution of disease. This is mostly due to portal biliary ductopathy. There are several mechanisms that play a role in the development of portal biliary ductopathy, such as induction of fibrosis in the biliary tract (due to direct action of dilated peribiliary collaterals and/or recurrent cholangitis), loss of biliary motility, chronic cholestasis (due to fibrosis or choledocholithiasis) and increased formation of cholelithiasis (due to various factors). The management of cholelithiasis in cases with portal vein cavernous transformation merits special attention. Because of a heterogeneous clinical presentation and concomitant pathophysiological changes that take place in biliary anatomy, diagnosis and therapy can become very complicated. Due to increased incidence and complications of cholelithiasis, standard treatment modalities like sphincterotomy or balloon sweeping of bile ducts can cause serious problems. Cholangitis, biliary strictures and hemobilia are the most common complications that occur during management of these patients. In this review, we specifically discuss important issues about bile stones related to bile duct obstruction in non-cirrhotic portal vein thrombosis and present evidence in the current literature.