肝硬化门脉高压性胃病与幽门螺杆菌感染的相关性研究

目的研究幽门螺杆菌(Hp)在肝硬化门脉高压性胃病(PHG)发生、发展中的作用及临床意义。方法随机选取肝硬化患者57例,行上消化道内镜检查,采用快速尿素酶试验、Warthin-Starry银染色及抗Hp-IgG法测定来判断Hp感染。结果肝硬化门脉高压组Hp感染率为31.3%,显著低于慢性胃炎组(65.5%,P<0.05)和消化性溃疡组(83.3%,P<0.05);Hp感染和肝功能Child-Pugh分级无显著性相关(P>0.05);Hp感染率随食管静脉曲张程度的增加而下降(无食管静脉曲张者Hp阳性率为57.1%,有食管静脉曲张者Hp阳性率为21.0%,P<0.05;轻度食管静脉曲张者Hp阳性率为32.4%,中重度食管静脉曲张者Hp阳性率为10.75%,(P<0.05)。结论Hp感染不是PHG的主要致病因素;肝硬化门脉高压影响Hp感染率;Hp感染与患者肝功能分级无关。     

肝硬化门脉高压非曲张静脉破裂出血

目的 探讨肝硬化门脉高压(PVH)非曲张静脉破裂出血病因及与年龄、门脉高压程度之间的关系，分析其发病机理。方法选择经内镜证实肝硬化门脉高压非曲张静脉破裂出血97例，纪录内镜检查结果、静脉曲张程度、胃粘膜损害情况，并取病理活检、Hp检查，评定肝功能情况。结果门脉高压性胃病(PHG)占58．76％，溃疡病占39．18％，其中胃溃疡19．50％，十二指肠疡16．5％，复合性溃疡3．09％，不明原因2．06％，Hp感染率37．11％，随年龄增大，门脉高压程度增加，非曲张静脉性出血递增，出血量可以很大，以PHG居多，其产生机理认为主要与胃粘膜淤血、动静脉短路建立与开放、粘膜缺氧及PGE降低等有关，而与Hp感染关系不大。讨论肝硬化门脉高压时主要因PHG或溃疡导致出血，以PHG居多，其产生机现认为主要与门脉高压、胃粘膜淤血、动静脉短路建立与开放、粘膜缺氧、PGE2降低等有关，而与Hp感染关系不大。     

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。     

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。     

幽门螺杆菌感染与肝硬化

探讨幽门螺杆菌(Hp)在肝硬化中的感染率并对其与肝功能、门脉高压、传播途径作相关分析。对30例胃十二指肠疾病患者和30例肝硬化患者进行胃镜检查、Hp快速尿素酶试验、14C呼吸试验同时记录年龄、饮食结构、习惯;肝功能指标(白蛋白、凝血酶原时间),门脉高压(腹水、脾大、食道静脉曲张),血常规(记录Hb)的相关资料。结果显示:Hp在肝硬化的感染率低于胃十二指肠疾病。Hp在肝硬化感染中的现象:分餐和低唾液可能是感染率低的一个主要因素,Hh减少、肝功能差、门脉高压增加与Hp感染率低有重要相关。肝硬化的低感染率与肝功能失代偿期、门脉高压和贫血不适宜Hp生存有关。口一口传播途径与Hp减少有重要相关性。     

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.     

门脉高压性胃病患者胃黏膜Ghrelin的表达

目的研究Ghrelin在门脉高压性胃病(PHG)胃黏膜上的表达。方法用免疫组化方法检测36例门脉高压患者和15例对照组(内镜检查胃黏膜大致正常)胃黏膜Ghrelin的表达。结果门脉高压组胃黏膜Ghrelin表达阳性细胞面积(18.89%±5.47%)与对照组(8.51%±5.31%)比较,差异有显著性(P<0.001);PHG组胃黏膜Ghrelin表达阳性细胞面积(20.82%±6.35%)与单纯门脉高压症(PHT)组(17.51%±4.40%)比较有增高趋势,但无显著性差异(P>0.05)。结论Ghrelin可能参与了门脉高压时高动力循环的形成和发展,分泌Ghrelin的内分泌细胞对PHG时胃黏膜损害具有相当的抵抗力。     

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。     

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)。     

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。     

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.     

Colonization by Helicobacter pylori and its relationship to histological changes in the gastric mucosa in portal hypertension

Abstract In order to investigate the relationship between Helicobacter pylori infection of the gastric mucosa and mucosal changes in portal hypertension, gastric fundic and antral biopsies were obtained from 66 patients with portal hypertension and 49 controls with non-ulcer dyspepsia (NUD). Gastric mucosa from portal hypertensive patients exhibited typical vascular dilatation and congestion, while mild dilatation of lamina propria blood vessels was not uncommon in NUD patients with histological evidence of gastritis. Colonization of the gastric mucosa by H. pylori infection was significantly less in portal hyptertension (51.5%) compared to controls (75.5%; P <0.01). The difference was more apparent in patients with marked vascular dilatation (18.8% colonization) compared to patients with minimal vascular dilatation (66.7%). H. pylori infection was significantly associated with active superficial gastritis ( P <0.001), and with atrophic gastritis ( P <0.001), in both study groups. H. pylori -negative superficial gastritis was significantly more common in portal hypertension (25/66 patients) than in controls (7/49; P <0.05). H. pylori infection was not more common in patients who had undergone repeated sclerotherapy. The results suggest that the gastric mucosa of portal hypertension does not provide a hospitable environment for H. pylori colonization, particularly when mucosal congestion is marked. H. pylori infection does not add significantly to the gastropathy of portal hypertension.     

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.     

Role of chronic Helicobacter pylori infection in hyperdynamic circulation of cirrhotic patients

BACKGROUND/AIMS: Hyperdynamic circulation observed in portal hypertension is characterized by generalized vasodilatation, increased cardiac index, and increased systemic and regional blood flows, and mediated at least partly by increased nitric oxide activities. Recent studies have demonstrated that Helicobacter pylori (H. pylori) infection can stimulate nitric oxide synthase expression and activities. This study investigated if chronic H. pylori infection might be involved in the development of hyperdynamic circulation in cirrhotic patients. METHODOLOGY: Fifty-eight patients with cirrhosis and thirty-six healthy subjects entered this study. The serologic evidence of H. pylori infection was determined with ELISA in both groups. In addition, in cirrhotic patients hemodynamic studies were performed by Swan-Ganz catheterization and thermodilution technique. RESULTS: No significant differences in age (65.5 +/- 0.8 vs. 63.7 +/- 1.1 years), sex (male/female: 43/15 vs. 29/7) and seroprevalence of H. pylori (74.1% vs. 80.6%) were observed between cirrhotic patients and healthy subjects (P > 0.05). The seropositive rate of H. pylori in patients with cirrhosis was not associated with severity of cirrhosis and size of esophageal varices (P > 0.05). There were no significant differences in systemic vascular resistance and hepatic venous pressure gradient between cirrhotic patients with and those without chronic H. pylori infection (P > 0.05). CONCLUSIONS: The seroprevalence of H. pylori in cirrhotic patients is similar to that of healthy controls, and not related to the severity of cirrhosis and degree of portal hypertension. Chronic H. pylori infection does not play a major role in the hyperdynamic circulation observed in cirrhotic patients.     

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     

胃肠外疾病患者幽门螺杆菌感染分析

目的检测幽门螺杆菌（Helicobacterpylori，H．pylori）在胃肠外疾病患者中的感染率及其分布特征，探讨其与胃肠外疾病发病的相关性，以期在疾病预防及临床治疗中发挥指导作用。方法对1530例特发性血小板减少性紫癜、糖尿病、结缔组织病、肝硬化、过敏性紫癜及其他胃肠外疾病患者进行14C-尿素呼气试验检测。结果1530例胃肠外疾病患者中有1140例14C-UBT结果阳性，感染率74．5％。特发性血小板减少性紫癜、糖尿病、结缔组织病、过敏性紫癜组H．pylori感染率均高于健康人（P〈0．05），肝硬化患者H．pylori感染率与健康人无明显差异。特发性血小板减少性紫癜、糖尿病、结缔组织病等合并慢性胃炎或消化性溃疡的病例H．pylori感染率较单纯慢性胃炎或消化性溃疡患者高（P〈0．05），而肝硬化及过敏性紫癜组则无明显差异。在特发性血小板减少性紫癜等胃肠外疾病患者中联合抗日．pylori治疗疗效优于单纯治疗原发病。结论H．pylori感染可能在消化道以外疾病的发生发展过程中起重要作用，但是否为相关胃肠外疾病发病的独立危险因素需要进一步证实。     

A low prevalence of H pylori and endoscopic findings in HIV-positive Chinese patients with gastrointestinal symptoms

AIM： To compare the prevalence of H pylori infection, peptic ulcer, cytomegalovirus （CNV） infection and Candida esophagitis in human immunodeficiency virus （HIV）- positive and HIV-negative patients, and evaluate the impact of CD4 lymphocyte on H pylori and opportunistic infections.
METHODS： A total of 151 patients （122 HIV-positive and 29 HIV-negative） with gastrointestinal symptoms were examined by upper endoscopy and biopsy. Samples were assessed to determine the prevalence of Hpylori infection, CMV, candida esophagitis and histologic chronic gastritis.
RESULTS： The prevalence of Hpylori was less common in HIV-positive patients （22.1%） than in HIV-negative controls （44.8%; P 〈 0.05）, and the prevalence of H pylori displayed a direct correlation with CD4 count stratification in HIV-positive patients. In comparison with HIV-negative group, HIV-positive patients had a lower incidence of peptic ulcer （20.7% vs 4.1%; P 〈 0.01）, but a higher prevalence of chronic atrophy gastritis （6.9% vs 24.6%; P 〈 0.05）, Candida esophagitis and CMV infection. Unlike HIV-negative group, H pylori infection had a close relationship to chronic active gastritis （P 〈 0.05）. In HIV-positive patients, chronic active gastritis was not significantly different between those with Hpylori infection and those without.
CONCLUSION： The lower prevalence of H pylori infection and peptic ulcer in HIV-positive patients with gastrointestinal symptoms suggests a different mechanism of peptic ulcerogenesis and a different role of H pylori infection in chronic active gastritis and peptic ulcer. The pathogen of chronic active gastritis in HIV-positive patients may be different from the general population that is closely related to Hpylori infection.