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。     

慢性乙型肝炎患者血清抗HP体检测及其与年龄变化、病毒载量和病毒基因型的关系分析

目的 探讨幽门螺杆菌(HP)在慢性乙型肝炎中的作用.方法 采用病例对照研究的方法分析376例慢性乙型病毒性肝炎患者的HP感染状况与年龄、乙型肝炎病毒(HBV)DNA定量和分型的关系.结果 HP感染率随年龄变化无明显差异(P＞0.05),HP感染率在慢性乙型肝炎组(56.2%)、乙型肝炎肝硬化组(69.9%)、乙型肝炎合并肝癌组(75.0%)明显高于健康对照组(43.4%)(P＜0.01),各组与慢性胃炎组(57.9%)相比较无明显差异(P＞0.05),其中肝硬化组和合并肝癌组HP感染率均高于肝炎组(P＜0.05).不同病毒载量慢性乙型肝炎患者的HP感染率均明显高于健康对照组(P＜0.01),但不同病毒载量之间无明显差异(P＞0.05).慢性乙型肝炎患者B基因型、C基因型和D基因型HP感染率分别为61.3%、63.3%和50.0%,三组之间比较无统计学意义(P＞0.05).结论 慢性乙型肝炎患者HP感染率明显增加,且HP感染率随着肝病病变程度的进展而增加.     

乙型肝炎后肝硬化合并消化性溃疡与幽门螺杆菌感染的相关性

目的探讨乙型肝炎后肝硬化合并消化性溃疡与幽门螺杆菌感染的相关性。方法选择2014年1月至2016年1月深圳市盐田区人民医院收治的乙型肝炎后肝硬化患者180例为观察组,单纯性消化性溃疡患者130例作为对照组1组,600例健康体检者作为对照2组。比较各组HP感染率、观察组不同肝功能分级患者HP感染率以及观察组和对照1组不同类型消化性溃疡患者HP的感染率。结果观察组和对照2组患者的HP感染率分别为44.4%(80/180)和49.3%(296/600),均低于对照1组的77.7%(101/130),差异有统计学意义(χ~2=29.200、34.638,P0.001)。观察组中Child-Pugh A级、B级和C级患者的HP感染率分别为37.2%(29/78)、45.0%(27/60)和57.1%(24/42),差异无统计学意义(χ~2=0.762,P=0.284)。观察组初发溃疡患者的HP感染率为64.5%(40/62),复发溃疡患者的HP感染率为70.4%(38/54),差异无统计学意义(χ~2=0.449,P=0.503);胃溃疡患者HP感染率为58.7%(27/46),十二指肠溃疡患者HP感染率为72.9%(52/70),分别低于对照1组患者的68.6%(35/51)和83.5%(66/79),但差异无统计学意义(χ~2分别为0.336、0.610,P值分别为1.415、0.087)。结论乙型肝炎后肝硬化患者HP感染率与正常人群差异无统计学意义,乙型肝炎后肝硬化合并消化性溃疡患者HP感染率低于单纯性消化性溃疡患者,HP感染并非乙型肝炎后肝硬化合并消化性溃疡的主要因素。     

乙型肝炎肝硬化合并上消化道出血与幽门螺杆菌感染关系的临床研究

目的:探讨乙型肝炎肝硬化合并上消化道出血与幽门螺杆菌(HP)感染的关系,为临床诊疗提供理论依据。方法:选取2011年1月至2015年1月就诊于本院的乙型肝炎肝硬化合并上消化道出血者87例,根据患者年龄所在的区段将其分为A组(40-50岁)、B组(51~60岁)、C组(大于60岁)3组,均采用碳14呼气试验对所有患者进行HP感染检测,观察3组患者HP检测的阳性率及不同性别、不同肝功能级别以及不同类型的乙型肝炎肝硬化上消化道出血组间HP感染阳性率的差异。结果:87例乙型肝炎肝硬化合并上消化道出血患者中,55例(63.2%)HP检测阳性,男、女性的感染阳性率分别为64.2%和61.8%,差异无统计学意义(P0.05);A组患者18例(50.0%)HP检测阳性,B组患者21例(70.0%)阳性,C组患者16例(76.2%)阳性,患者随着年龄的增大,HP检测的阳性率逐渐升高,且C组与A、B两组比较,差异有统计学意义(P0.05),A、B两组间比较,差异无统计学意义(P0.05);乙型肝炎肝硬化合并门脉高压性胃病出血患者HP阳性5例(31.2%),乙型肝炎肝硬化合并食管胃静脉曲张破裂出血患者HPP阳性15例(71.4%),乙型肝炎肝硬化合并消化道溃疡出血患者32例(82.1%)阳性,乙型肝炎肝硬化合并原因不明出血患者3例(27.3%)阳性,乙型肝炎肝硬化合并消化道溃疡出血患者的HP感染率最高,但与乙型肝炎肝硬化合并食管胃静脉曲张破裂出血比较,差异无统计学意义(P0.05),乙型肝炎肝硬化合并食管胃静脉曲张破裂出血和消化道溃疡出血的幽门螺杆菌检测阳性率明显高于乙型肝炎肝硬化合并门脉高压性胃病出血和原因不明出血,差异有统计学意义(P0.05);Child-Pugh分级肝功能A级患者HP检测30例(63.8%)阳性,B级患者14例(60.9%)阳性,C级患者11例(64.7%)阳性,三种级别肝功能的乙型肝炎肝硬化合并上消化道出血幽门螺杆菌检测阳性率无明显差异(P0.05)。结论:HP感染与乙型肝炎肝硬化合并上消化道出血关系密切,根治HP感染,是乙型肝炎肝硬化上消化道出血的一项有效的预防措施。     

肝炎肝硬化患者胃粘膜幽门螺杆菌DNA检测及意义探讨

目的 检测肝硬化门脉高压性胃病(PHG)胃粘膜幽门螺杆菌(HP)感染与PHG的关系。方法 经胃镜检查病理涂片及尿素酶试验确定为HP感染的PHG患者用定量聚合酶链反应方法(QPCR)检测其胃粘膜HP DNA含量,并以慢性浅表性胃炎作对照。结果 38例PHG患者HP DNA含量与患病时间无明显关系,与病变部位及程度关系密切,重度PHG及胃底部HP DNA含量明显较高。结论 PHG时粘膜血流障碍易于HP生长,严重的HP感染可加重PHG。     

肝炎后肝硬化门脉高压性肝病相关因素的临床研究

为探讨肝炎后肝硬化门脉高压性胃病(PHG)形成的相关因素,对68例肝炎后肝硬化门脉高压患者按胃镜下有无PHG分组对照研究,比较两组患者性别、年龄、实验室检查、B超及胃镜检查资料。发现两组的肝功能分级、门静脉内径、食管静脉曲张程度差异有显著性(P<0.05),而与性别、年龄、血氨水平及脾静脉内径无相关性(P>0.05)。PHG组幽门螺杆菌(Hp)感染率较对照组低(P<0.05)。     

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.     

HP和CagA^＋HP与中国人慢性萎缩性胃炎、胃腺癌、消化性溃疡的关系

目的　探讨幽门螺旋杆菌 (HP)及产细胞毒素型幽门螺旋杆菌 (CagA+HP)在中国人慢性萎缩性胃炎、胃腺癌、十二指肠球部溃疡及胃溃疡患者中的感染情况及意义。方法　将 492例患者分为 5组进行观察。无症状对照组 (AC组 )、慢性萎缩性胃炎组 (CAG组 )、胃腺癌组 (GCa组 )、十二指肠球部溃疡组 (DU组 )及胃溃疡组 (GU组 ) ,分别计算各组HP及CagA+HP的感染率以及患者中CagA+HP占HP感染的比例 (CagA+HP/HP) ,并作组间比较。结果　HP感染率在CAG及GCa组略高于AC组 ,但无统计学意义 ,DU及GU组HP感染率明显高于AC组 [(P <0 .0 1;CagA+HP感染率及 (CagA+HP/HP) ] ,各相关疾病观察组均显著高于AC组的 2 4.2 %及 33 .8% (P <0 .0 1)。结论　HP相关性疾病如慢性萎缩性胃炎、胃腺癌及消化性溃疡时 ,以CagA+HP感染为主 ,CagA+HP感染率较无症状对照组更高 ,显然 ,在各相关性疾病的发生中CagA+HP占有极其重要的地位 ,这为疾病的防治乃至HP根治提供了重要的证据。     

功能性消化不良及十二指肠溃疡的若干因素分析

目的　对功能性消化不良 (functionaldyspepsia ,FD)及十二指肠溃疡 (duodenalulcer,DU)患者的多种因素进行比较 ,探讨其意义及在发病中的作用。方法　对 186例FD及 77例DU患者进行年龄、性别、生活习惯、文化程度、幽门螺杆菌 (Helicobacterpylori,Hp)感染率、焦虑及抑郁情绪进行比较 ,用焦虑自评量表 (SAS)和抑郁自评量表 (SDS)进行评定。结果　FD以女性多见 ,年龄偏大 ,DU以男性多见 ,年龄较轻 ,吸烟、饮酒者多。FD的Hp感染率 ( 3 8 17% )显著低于DU( 80 3 3 % )。FD与焦虑、抑郁的关系较DU明显。结论　FD与DU的发生与性别、年龄、生活习惯有一定关系 ,FD是一种心身疾病 ,DU的心理异常可能是继发性的一种身心反应。     

幽门螺杆菌感染与HBV相关肝硬化常见死亡原因的关系

目的探讨幽门螺杆菌(H.pylori)感染与HBV相关肝硬化(HBC)常见致死因素的关系。方法回顾性分析2008年10月-2014年10月于大连医科大学附属第一医院及烟台毓璜顶医院就诊的235例HBC患者的临床资料,统计H.pylori的感染率;比较其中155例伴有食管和(或)胃底静脉曲张患者H.pylori的感染率;比较其中97例伴有门静脉高压性胃病(PHG)患者H.pylori的感染率;比较其中32例血氨检测的患者H.pylori阳性与阴性组静脉血氨水平。计量资料组间比较采用t检验和方差分析,计数资料组间比较采用χ2检验。结果 235例HBC患者的H.pylori阳性率为80.85%(190/235);伴有食管和(或)胃底静脉曲张的患者,胃镜下见食管的曲张静脉呈蛇形迂曲隆起或串珠状改变,胃底的曲张静脉呈孤立瘤样改变,伴或不伴有胃黏膜糜烂,其中轻度、中度、重度曲张者H.pylori阳性率分别为50.55%(46/91)、43.59%(17/39)和76.00%(19/25),差异具有统计学意义(χ2=6.913,P0.05);伴有PHG的患者,胃镜可见胃黏膜呈蛇皮样改变,可伴有樱桃红斑、猩红疹及糜烂出血表现,其中轻度及重度PHG患者H.pylori阳性率分别为43.33%(26/60)和67.57%(25/37),差异具有统计学意义(χ2=5.391,P0.05);检测血氨的患者H.pylori阳性组血氨平均浓度[(62.76±13.43)μmol/L]明显高于阴性组[(47.20±12.51)μmol/L],差异具有统计学意义(t=3.39,P0.01)。结论 HBC患者中H.pylori的感染率高,且H.pylori感染很可能增加食管和(或)胃底静脉曲张以及PHG的严重程度以及升高血氨水平,进而有增加肝硬化主要致死因素上消化道出血及肝性脑病发生风险的可能性。     

门脉高压性胃病患者幽门螺杆菌感染率调查

目的探讨幽门螺杆菌（Hp）与肝硬化并发胃和十二指肠病变的关系。方法采用快速尿素酶试验和改良的Giemsa染色法检测Hp感染。结果在264例肝硬化患者,Hp阳性183例（69．4％）,在262例慢性胃炎（EG）患者,Hp阳性172例（66．4％,19〉0．05）;在79例肝硬化伴有PHG患者,Hp阳性60例（75．9％）,在114例肝硬化不伴PHG患者,Hp阳性75例（65．8％）,在37例肝硬化伴轻型PHG患者,Hp阳性26例（70．2％）,在42例肝硬化伴重型PHG患者,Hp阳性34例（80．9％,P〉0．05）;在56例肝硬化伴十二指肠溃疡（DU）患者,Hp阳性48例（85．7％）,在109例肝硬化不伴消化性溃疡（Pu）患者,Hp阳性67例（61．4％,P〈0．05）;在125例DU患者,Hp阳性112例（89．6％）;在28例肝硬化伴胃溃疡（GU）患者,Hp阳性20例（71．4％）,在47例GU患者,Hp阳性43例（91．5％）。结论肝硬化伴DU患者Hp感染率较高。     

肝硬化患者中幽门螺杆菌感染的研究

目的 研究幽门螺杆菌（Hp)在肝硬化患者中的感染情况。方法 肝硬化组656例，对照组600例，接受胃镜检查，采用血清学方法，快速尿素酶试验，组织学染色进行Hp检测。结果 肝硬化组Hp感染率为70％，对照组为71％。两者比较无显著性差异，而在肝硬化组中Hp阳性患者的消化性溃疡发生率，门脉高压性胃病发生率及严重程度，上消化道出血率均高于Hp阴性组。结论 在肝硬化患者中Hp感染可能与消化性溃疡，门 脉高压性胃病及上消化道出血的发生相关。     

Active peptic ulcer disease in patients with hepatitis C virus-related cirrhosis: the role of Helicobacter pylori infection and portal hypertensive gastropathy.

BACKGROUND & AIM: The relationship between Helicobacter pylori infection and peptic ulcer disease in cirrhosis remains controversial. The purpose of the present study was to investigate the role of H pylori infection and portal hypertension gastropathy in the prevalence of active peptic ulcer among dyspeptic patients with compensated hepatitis C virus (HCV)-related cirrhosis. METHODS: Patients undergoing upper endoscopy with compensated HCV-related cirrhosis were enrolled. Child-Pugh's score was determined at the entry. Variceal size was measured endoscopically and the severity of portal hypertensive gastropathy was graded. H pylori infection status was determined by urea breath testing and/or histology. RESULTS: A total of 178 patients positive for HCV (A and B Child-Pugh's score) were prospectively included. The prevalence of H pylori infection was 43%. An active peptic ulcer was found in 14 patients (8%) and was significantly more common among those with H pylori infection (16% versus 2% in H pylori uninfected patients, odds ratio: 8.0). No association was observed between H pylori infection and variceal size, or hypertensive gastropathy. CONCLUSIONS: Patients with compensated cirrhosis and H pylori infection showed higher risk of developing a peptic ulcer. Clinical relevance of this result would be that dyspeptic patients with HCV-related cirrhosis may benefit from preventive screening and eradication of H pylori, especially those with features of insufficient hemostasis.     

肝硬化门脉高压症患者的十二指肠损害

目的探讨肝硬化门脉高压症患者十二指肠损害的发生率及其与肝硬化病程、门脉高压性胃病、肝功能分级的关系。方法对72例肝硬化门脉高压症患者进行胃镜检查,观察十二指肠粘膜病变,同时检测14C呼气试验。另选72例接受胃镜检查的非肝硬化门脉高压患者为对照组。结果肝硬化门脉高压症患者十二指肠糜烂发生率为41.7%,随肝硬化病程延长和肝功能分级差而增高,而幽门螺杆菌感染率与对照组无显著性相差(P>0.05)。糜烂主要发生于十二指肠降部,糜烂轻重程度与肝功能分级无关(P>0.05)。结论肝硬化门脉高压症患者十二指肠糜烂与非特异性十二指肠炎不同,是门脉高压导致十二指肠的一种病变。     

门脉高压性胃病与幽门螺杆菌感染的关系

目的探讨门脉高压性胃病（ｐｏｒｔａｌｈｙｐｅｒｔｅｎｓｉｖｅｇａｓｔｒｏｐａｔｈｙ，ＰＨＧ）与幽门螺杆菌（Ｈｅｌｉｃｏｂａｃｔｅｒｐｙｌｏｒｉ，Ｈｐ）感染之间的关系．方法ＰＨＧ患者６８例，通过内镜检查诊断，胃粘膜活检（每例４块）用Ｗａｒｔｈｉｎ＿Ｓｔａｒｒｙ银染色法检测Ｈｐ．结果ＰＨＧ患者的Ｈｐ阳性率为６０３％（４１／６８），合并消化性溃疡的ＰＨＧ患者Ｈｐ阳性率为５３７％（２２／４１），单纯性ＰＨＧ患者Ｈｐ阳性率为４６３％（１９／４１）．结论ＰＨＧ患者的胃粘膜病变与Ｈｐ感染有密切关系     

77例门脉高压性胃病临床分析

目的探讨门脉高压性胃病（PHG）的临床特征。方法回顾性分析77例PHG患者的临床资料,分析Child-Pugh分级、食管胃底静脉曲张（EV）、门静脉和脾静脉直径及幽门螺杆菌（HP）感染对PHG的影响。结果在77例PHG患者中,病变主要位于胃底者56例（72.7%）;按照Tanoue分类法I级25例,Ⅱ级35例,III级17例;PHG严重程度与Child-Pugh分级程度呈正相关（r=18.129,P〈0.05）;PHG严重程度与EV程度有统计学相关（r=22.121,P〈0.05）;PHG严重程度与门静脉和脾静脉直径均成正相关（r=13.101,P〈0.05;r=10.290,P〈0.05）;PHG严重程度与HP感染与否无显著相关性（r=0.668,P〉0.05）。结论 PHG发生于患者肝功能、EV程度、门静脉和脾静脉直径有一定的相关性。     

Gastric permeability to sucrose is increased in portal hypertensive gastropathy

BACKGROUND: Portal hypertensive gastropathy (PHG) is frequently found among patients with hepatic cirrhosis and at present the only way to detect and follow PHG is via endoscopy. OBJECTIVE: To assess gastric and intestinal permeability and investigate its relationship to endoscopic findings and indices of portal hypertension and hepatic function. DESIGN AND METHODS: Thirty-one non-diabetic patients with hepatic cirrhosis and PHG (PHG+) were studied and compared with 17 cirrhotic patients without PHG (PHG-). All patients underwent endoscopy for the assessment of PHG and Helicobacter pylori status, ultrasound determination of the diameters of spleen and portal vein, and, subsequently, an oral load of sucrose, lactulose, and mannitol. Sugar concentrations were determined in 6-h urine specimens and expressed as a percentage of the orally administered dose or as lactulose/mannitol ratio. RESULTS: The urinary sucrose excretion was significantly elevated in patients with PHG compared to those without (PHG+, 0.20% +/- 0.03; PHG-, 0.07% +/- 0.01; P< 0.001). No difference was found for the small intestinal probes lactulose and mannitol. Gastric sucrose permeability correlated positively with the endoscopic lesion score (P < 0.001), but not with other parameters of portal hypertension or hepatic function. H. pylori status did not influence gastric permeability. The sensitivity of this test reached 100% for PHG scores > 2. CONCLUSIONS: Gastric permeability to sucrose is increased in patients with PHG, independently of the presence of H. pylori. Sucrose permeability may be useful for the follow-up of patients with PHG.     

病毒性肝炎患者的胃镜表现

目的：探讨病毒性肝炎患者的胃镜表现。方法：２６４例肝炎病人中肝硬变１７３例,慢性肝炎６１例,急性肝炎３０例,分别观察其胃镜下胃粘膜改变的特征及其与临床的关系。结果：门脉高压性胃病、消化道溃疡及糜烂性胃炎、浅表性胃炎、Ｈｐ阳性等均为病毒性肝炎患者的常见胃镜表现。门脉高压性胃病多发性在胃底、胃体;溃疡多发生于胃窦及球部。门脉高压性胃病及胃粘膜糜烂的范围和程度与食道静脉曲张程度相关。结论：病毒性肝炎患者     

Frequency and factors influencing portal hypertensive gastropathy and duodenopathy in cirrhotic portal hypertension

Portal hypertensive gastropathy and duodenopathy are distinct clinical and endoscopic entities. Data on factors influencing the development of these lesions are still emerging. Data on portal hypertensive duodenopathy are scarce. We prospectively studied 230 patients with liver cirrhosis and oesophageal varices attending the liver clinic of the Sanjay Gandhi Post Graduate Institute of Medical Sciences. One hundred and forty-two patients had no history of upper gastrointestinal bleeding, while the remainder had bled in the past. Endoscopic appearances were recorded before starting patients on a sclerotherapy programme. Forty-four patients were re-evaluated after variceal eradication. The frequency of portal hypertensive gastropathy (PHG) and duodenopathy (PHD) was 61 and 14%, respectively. Mild PHG was present in 85% and was severe in the rest. Portal hypertensive duodenopathy was mild in 50%, while in the other half it was severe. There was no relationship of PHG and PHD to: (i) a history of upper gastrointestinal bleed; (ii) size of oesophageal varices; (iii) aetiology of liver cirrhosis; or (iv) liver function status as assessed by Child Pugh's scores (P=NS for all). The prevalence of PHG was higher in those patients with oesophagogastric varices (74 of 107; 69%) compared with patients with oesophageal varices alone (68 of 123; 55%; P<0.05). However, no such increase in frequency of PHD was noted in patients with oesophagogastric varices. Sclerotherapy increased the frequency of PHG. Twenty-four patients had PHG before starting sclerotherapy, while it was noted in 33 patients 1–3 months after variceal eradication (P< 0.05). In contrast, there was no increase in the prevalence of portal hypertensive duodenopathy after sclerotherapy (P=NS). There was no correlation between endoscopic and histological changes of PHG and PHD. In conclusion, PHG is quite frequent in patients with cirrhosis and its frequency increases with the presence of oesophagogastric varices and after sclerotherapy. However, the frequency of PHD is low and is not affected by the factors studied.