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

门脉高压性胃病王子强综述徐章审校（东风汽车公司中心医院郧阳）门脉高压症（ＰＶＨ）发生上消化道出血时，一般均归因于食管静脉曲张破裂（ＥＶＢ），但急诊胃镜检查结果ＥＶＢ仅占１３～４１％，而胃粘膜糜烂溃烂溃疡性病变所致的出血却占２９～５７％［１］。对ＰＶＨ...     

一氧化氮与门脉高压性胃病

一氧化氮在门脉高压性胃病的发生中起重要作用 ,其机制可能与其对胃粘膜屏障、胃粘膜血流量以及高动力学循环等作用有关 ,一氧化氮合酶抑制剂对改善门脉高压性胃病可能有一定的作用。本文对一氧化氮与门脉高压性胃病的关系进行综述。     

门脉高压性胃病的研究进展

门脉高压性胃病(Portal hypertensive gastropathy,PHG),表现为胃黏膜组织内小血管扩张,而无明显炎症.血管扩张、黏膜充血、水肿是PHG的特征性损害,炎症浸润和腺体萎缩是次要征象.PHG常见于肝硬化,其发病机制与多种因素有关,诊断主要依赖于内镜检查,多数是在肝硬化合并出血、寻找是否存在食管胃静脉曲张、及曲张静脉内镜治疗过程中发现其改变,常规检查依从性差,有其局限性,对症治疗是一种普遍方法,目前其有效的治疗尚需进一步研究.关注PHG可以减少出血和肝性脑病,提高患者生活质量.     

门脉高压性胃病的研究进展

门脉高压性胃病 (ＰＨＧ )系由门脉高压 (ＰＨＴ)引起的胃粘膜非炎症性病变 ,是引起非静脉曲张破裂出血的较常见原因。关于ＰＨＧ的发病率报道差别较大。肝硬化中半数以上可见ＰＨＧ。本文就ＰＨＧ的发病机理、内镜下表现、食管曲张静脉治疗的影响、ＰＨＧ的治疗现状进地简要综述。1　ＰＨＧ的发病机理肝硬化ＰＨＴ时 ,由于门静脉压力高于胃静脉压力 ,使胃静脉血回流障碍 ,导致胃微循环发生改变。随着肝硬化的加重 ,门静脉压力升高 ,胃壁单位面积内动静脉分流密度渐进性增加 ,并与门静脉压力上升呈正相关。其可能机制是门静脉压力上升 ,毛细…     

门脉高压性胃病的进展

门脉高压性胃病（ponalhypertensivegastropathy，PHG）是指门脉高压症伴发的胃黏膜病变，主要发生于肝硬化门脉高压症病人，也见于非肝硬化门脉高压症病人，临床主要表现为消化道出血等症状，严重时危急生命。1984年Sarfeh等提出PHG与非PHG在形态、功能、治疗上都有不同，因其病理组织学上炎性改变依据不足，可称其为门脉高压性胃病。PHG常与食管静脉曲张同时存在，而PHG出血可占门脉高压消化道出血的10％～60％。食管胃底静脉曲张、肝功能损害越重，则门脉高压性胃病并发消化道出血的发生率越高。在上消化道出血患者，食管静脉曲张程度较轻者以PHG合并出血为主，食管静脉曲张程度较重者则以曲张静脉破裂出血为主。     

门脉高压性胃病发病机制的研究进展

门脉高压性胃病(PHG)是门静脉高压症伴发的一种特殊类型的胃黏膜病变,是肝硬化常见并发症之一.PHG临床上多表现为上消化道出血,在肝硬化患者上消化道出血的病因中,PHG仅次于食管胃底静脉曲张,故越来越受到重视.目前PHG的发病机制尚未完全明确,此文就近年来PHG发病机制的研究进展作一综述.     

门脉高压性胃病研究进展

门脉高压性胃病（portal hypertensive gastropathy,PHG）是各种原因引起门静脉高压导致的胃黏膜非炎性病变,常见于肝硬化门脉高压症,可并发消化道出血,是肝脏疾病中除食管胃底静脉曲张引起消化道出血的第二大原因,严重者可危及生命。近年来,国内外对有关PHG的发病机制、诊断和治疗进行了相关研究,本文对研究进展进行了综述。     

门脉高压性胃病临床研究进展

肝硬化患者常常发生门脉高压症,继发胃肠道血流动力学和黏膜改变,导致门脉高压性胃病（PHG）。近年来,PHG引起的上消化道出血逐渐受到重视,在肝硬化上消化道出血病因中仅次于食管胃静脉曲张破裂出血,对其研究也越来越多。     

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.     

瑞巴派特对门脉高压性胃病胃黏膜中瘦素表达的影响

目的:观察瑞巴派特对门脉高压性胃病胃黏膜中瘦素表达的影响,评价其对门脉高压性胃病的胃黏膜保护作用．方法:将患者随机分为正常对照组、正常干预组、空白对照组及试验组各15例,其中正常干预组及试验组给予口服瑞巴派特治疗．治疗前后内镜检查对比,用RT-PCR法分别检测治疗前后胃黏膜组织中瘦素mRNA的表达水平．结果:0 wk时,正常对照组瘦素mRNA表达量为0．344±0．202,空白对照组0．816±0．132,实验组0．803±0．143,与正常对照组相比,空白对照组与实验组的瘦素mRNA的表达有差异 (P<0．05);4 wk时,空白对照组瘦素mRNA表达量为0．867±0．170,试验组为1．120±0．237,正常干预组为0．397±0．199,与空白对照组相比, 试验组瘦素mRNA的表达增多;与正常干预组相比,试验组在治疗后其瘦素mRNA的表达显著升高(P<0．01)．内镜检查前后对比:药物治疗4 wk时试验组14例中胃黏膜的内镜表现不同程度改善12例(12/14),而空白对照组无一例改善．结论:瑞巴派特可通过增加胃黏膜中的瘦素表达,对门脉高压性胃病的胃黏膜起保护作用．     

垂体后叶素对门脉高压性胃病胃粘膜灌注的影响

目的 探讨垂体后叶素对门脉高压性胃病（ＰＨＧ）大鼠胃粘膜血流量（ＧＭＢＦ）和血浆胰高粘素的影响。方法 部分结扎大鼠门脉主干２ｗｋ后,采用激光多普勒血流计（ＬＤＦ）测定大鼠ＧＭＢＦ,观察了垂体后叶素输注前和输注后３０ｍｉｎ ＧＭＢＦ,门脉压力（ＰＶＰ）的变化;测定了输注垂体后叶素３０ｍｉｎ后血浆胰高糖素的含量。结果 输注垂体后叶素１０ｍｉｎ ＰＨＧ大鼠的ＧＭＢＦ开始降低（Ｐ〈０．０５）,１５ｍｉｎ显     

慢性重型肝炎伴胃粘膜病变及门脉高压性胃病的研究

目的　观察慢性重型肝炎患者上消化道粘膜病变特点。方法　将列入观察对象的患者分为 2个组 :A组为肝硬化伴门静脉高压转重而符合慢性重型肝炎诊断者 ;B组为慢性肝炎病情转重者。同期住院的急性黄疸型肝炎病人作为对照观察。结果　A组慢重肝患者有 68 6% ( 13 1/ 191)胃体粘膜出现门脉高压性胃病 (PHG)改变 ;B组PHG为 2 4 6% ( 43 / 175 ) (P <0 0 5 ) ;A组胃粘膜病变 (GML)的检出率为 42 4% ( 81/ 191) ,与B组的45 1% ( 79/ 175 )无明显差异 (P >0 0 5 ) ;但与对照组相比差异显著 (P <0 0 1)。结论　重度PHG的发生与肝脏功能密切相关。门脉压变化影响胃粘膜微循环 ,对PHG形成有一定作用。慢性重型肝炎发生GML构成多脏器功能损伤表现之一。其发生机制可能与凝血因子合成障碍 ;门脉高压的作用 ;高胃泌素血症 ;肿瘤坏死因子(TNF)的作用有关。多种因素中某一因素可能在某一时期起主导作用。临床应重视整体治疗 ,如积极的支持疗法 ,改善肝功 ,补充凝血因子 ,纠正低氧血症 ,调节酸硷平衡。出现消化道症状及时进行胃镜检查 ,针对性处理     

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例.经胃镜取胃黏膜,采用免疫组化方法检测ET-1蛋白和HIF-1蛋白的含量.结果 PHG组和PHT无PHG组的ET-1、HIF-1表达均较正常对照组增强,差异有统计学意义(P<0.05).PHG组中重型患者的ET-1表达较轻型增强,差异无统计学意义(P>0.05),PHG组重型患者的HIF-1表达较轻型增强,差异有统计学意义(P<0.05).结论 ET-1、HIF-1可能参与PHG的发病过程,与胃黏膜病理损害有关.     

肝硬化门脉高压性胃病患者胃粘膜炎症与一氧化氮合酶表达

目的 定位、定量研究肝硬化门脉高压性胃症（ＰＨＧ）患者胃粘膜炎症及其与一氧化氮合酶（ｉＮＯＳ／ｃＮＯＳ）表达的关系。方法 肝硬化患者６０例,其中伴有ＰＨＧ者３５例,无胃粘膜病变者２５例。胃粘膜活检３块,Ｂｏｕｉｎ固定,ＨＥ染色及免疫组化ＳＰ法ＭＰＶ显微分光光度计测定ｉＮＯＳ／ｃＮＯＳ表达。结果 肝硬化ＰＨＧ发生率５８．２％,其中７１．４％患者伴有胃粘膜炎症（Ｐ〈０．０５）;胃粘膜炎症者胃粘膜血管ｉ     

Reliability in endoscopic diagnosis of portal hypertensive gastropathy

AIM: To analyze reliability among endoscopists in diagnosing portal hypertensive gastropathy (PHG) and to determine which criteria from the most utilized classifications are the most suitable.METHODS: From January to July 2009, in an academic quaternary referral center at Santa Casa of São Paulo Endoscopy Service, Brazil, we performed this single-center prospective study. In this period, we included 100 patients, including 50 sequential patients who had portal hypertension of various etiologies; who were previously diagnosed based on clinical, laboratory and imaging exams; and who presented with esophageal varices. In addition, our study included 50 sequential patients who had dyspeptic symptoms and were referred for upper digestive endoscopy without portal hypertension. All subjects underwent upper digestive endoscopy, and the images of the exam were digitally recorded. Five endoscopists with more than 15 years of experience answered an electronic questionnaire, which included endoscopic criteria from the 3 most commonly used Portal Hypertensive Gastropathy classifications (McCormack, NIEC and Baveno) and the presence of elevated or flat antral erosive gastritis. All five endoscopists were blinded to the patients’ clinical information, and all images of varices were deliberately excluded for the analysis.RESULTS: The three most common etiologies of portal hypertension were schistosomiasis (36%), alcoholic cirrhosis (20%) and viral cirrhosis (14%). Of the 50 patients with portal hypertension, 84% were Child A, 12% were Child B, 4% were Child C, 64% exhibited previous variceal bleeding and 66% were previously endoscopic treated. The endoscopic parameters, presence or absence of mosaic-like pattern, red point lesions and cherry-red spots were associated with high inter-observer reliability and high specificity for diagnosing Portal Hypertensive Gastropathy. Sensitivity, specificity and reliability for the diagnosis of PHG (%) were as follows: mosaic-like pattern (100; 92.21; High); fine pink speckling (56; 76.62; Unsatisfactory); superficial reddening (69.57; 66.23; Unsatisfactory); red-point lesions (47.83; 90.91; High); cherry-red spots (39.13; 96.10; High); isolated red marks (43.48; 88.31; High); and confluent red marks (21.74; 100; Unsatisfactory). Antral elevated erosive gastritis exhibited high reliability and high specificity with respect to the presence of portal hypertension (92%) and the diagnosis of portal hypertensive gastropathy (88.31%).CONCLUSION: The most suitable endoscopic criteria for the diagnosis of PHG were mosaic-like pattern, red-point lesions and cherry-red spots with no subdivisions, which were associated with a high rate of inter-observer reliability.     

汉防己甲素对肝硬化大鼠胃黏膜微循环及超微结构的影响

目的:观察汉防己甲素降低大鼠肝硬化门脉高压(PHT)的疗效和对胃黏膜微循环及其超微结构的影响.方法:制作肝硬化PHT模型,成模后分为模型(M)组、汉防己甲素(T)组、普萘洛尔组(P)及正常对照(N)组,治疗15 d后进行各指标的测定.结果:与M组比较,T组门静脉压力(PVP)明显降低(P<0.01),ALT,HA及PCⅢ指标下降(P<0.05),平均动脉压(MAP)和心率(HR)无明显变化;P组引起了PVP明显降低(P<0.01)和HR的减慢(P<0.05),MAP,ALT,HA及PCⅢ无明显变化;T组、P组光镜下胃黏膜毛细血管最大直径及面积明显减小(P<0.01),透射电镜下胃黏膜超微结构的损伤明显减轻.结论:汉防己甲素能有效、安全地降低大鼠肝硬化门脉压力,可有效改善其胃黏膜微循环及超微的变化,为临床治疗门脉高压性胃病提供实验依据.     

Effect of early propranolol administration on portal hypertensive gastropathy in cirrhotic rats

AIM： To investigate any protective effect of early propranolol administration in the development of portal hypertensive gastropathy in cirrhotic rats. METHODS： For the development of liver cirrhosis and portal hypertensive gastropathy, 60 rats underwent ligation of the left adrenal vein and complete devascularization of the left renal vein, followed by phenobarbital and carbon tetrachloride （CCl4） administration. After two weeks of CCl4 administration, the rats were randomly separated into two groups. In group A, propranolol was continuously administered intragastrically throughout the study, whereas in group B normal saline （placebo） was administered instead. Hemodynamic studies and vascular morphometric analysis of gastric sections were performed after complete induction of cirrhosis. RESULTS： Vascular morphometric studies showed higher numbers of vessels in all mucosal layers in the control group. Statistical analysis revealed a significantly higher total vascular surface in the control group compared to the propranolol group, but with no statistically significant difference between the mean vascular surfaces between the groups. Our study clearly shows that the increased mucosal blood flow is manifested by a marked increase of vessel count. CONCLUSION： Early propranolol＇s administration in portal hypertensive cirrhotic rats seems to prevent intense gastric vascular congestion that characterizes portal hypertensive gastropathy.