Portal hypertensive gastropathy:A systematic review of thepathophysiology,clinical presentation,natural history andtherapy

AIM: To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy(PHG) based on a systematic literature review.METHODS: Computerized search of the literature was performed via Pub Med using the following medical subject headings or keywords: "portal" and "gastropathy"; or "portal" and "hypertensive"; or "congestive" and "gastropathy"; or "congestive" and "gastroenteropathy". The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS: PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG.PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt or liver transplantation is highly successful ultimate therapies because they reduce the underlying portal hypertension.CONCLUSION: PHG is important to recognize in patients with cirrhotic or non-cirrhotic portal hypertension because it can cause acute or chronic GI bleeding that often requires pharmacologic therapy.

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 S o Paulo Endoscopy Service, Brazil, we performed this singlecenter 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 sequentialpatients 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 endosco- pists 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, redpoint lesions and cherry-red spots with no subdivisions,which were associated with a high rate of inter-observer reliability.

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.

Helicobacter pylori and portal hypertensive gastropathy

To the Editor:H. pylori lives in the gastric epithelial cells, sometimes in gastric glands.Whetherornottheproliferationandbiologicalbehavior of H. pylori can be influenced by the status of the gastric mucosa is still unknown. Portal hypertensive gastropathy (PHG) is a blood drainage obstructive disease. In this pathologic environment, gastric mucosa may be further impaired when patients are infected with H. pylori. The role of H. pylori in the pathogenesis of PHG and

The role of endotoxin in the pathogenesis of gastric mucosal damage in cirrhotic rats with portal hypertensive gastropathy

Objective:To study the role and the mechanism of endotoxin in the pathogenesis of gastric mucosa during portal vein hypertension gastrography(PHG) in the rats with cirrhosis.Methods: Rat model for PHG was established by injection of tetrachloride.The animals were injected with endotoxin i.p.at 3 mg/kg and endotoxin antagonist BPI21 i.v.at 2.0 mg/kg.The plasma level of endotoxin as well as the gastric mucosal level of tumor necrosis factor alpha(TNF-α) was measured with azobenzene and ELISA respectively.Furthermore,the pathological changes of the gastric mucosa were studied with HE stainning.Results:In rats with PHG,increased endotoxin and TNF-αas well as the gastric pathological lesion were observed.Injection of endotoxin remarkably increased plasma level of endotoxin as well as the gastric mucosal level of tumor necrosis TNF-αand induced more serious gastric lesion.Animals injected with endotoxin antagonist BPI21 showed improved gastric mucosal lesion,accompanied by the declining TNF-αlevel.Conclusions:Our results suggestes that endotoxin may play a pathogenetic role in PHG by inducing the expression of TNF-α.

Accuracy of virtual chromoendoscopy in differentiating gastric antral vascular ectasia from portal hypertensive gastropathy:A proof of concept study

BACKGROUND Accurate detection of gastric antral vascular ectasia(GAVE)is critical for proper management of cirrhosis-related gastrointestinal bleeding.However,endoscopic diagnosis of GAVE can be challenging when GAVE overlaps with severe portal hypertensive gastropathy(PHG).AIM To determine the added diagnostic value of virtual chromoendoscopy to high definition white light for real-time endoscopic diagnosis of GAVE and PHG.METHODS We developed an I-scan virtual chromoendoscopy criteria for diagnosis of GAVE and PHG.We tested our criteria in a cross-sectional cohort of cirrhotic adults with GAVE and PHG when high-definition white light endoscopy(HDWLE)diagnosis was in doubt.We then compared the accuracy of I-scan vs HDWLE alone to histology.RESULTS Twenty-three patients were included in this study(65.2%Caucasians and 60.9%males).Chronic hepatitis C was the predominant cause of cirrhosis(43.5%)and seven adults(30.4%)had confirmed GAVE on histology.I-scan had higher sensitivity(100%vs 85.7%)and specificity(75%vs 62.5%)in diagnosing GAVE compared to HDWLE.This translates into a higher,albeit not statistically significant,accuracy of I-scan in detecting GAVE compared to HDWLE alone(82%vs 70%).I-scan was less likely to lead to an accurate diagnosis of GAVE in patients on dialysis(P<0.05)and in patients with elevated creatinine(P<0.05).Iscan had similar accuracy to HDWLE in detecting PHG.CONCLUSION This pilot work supports that virtual chromoendoscopy may obviate the need for biopsies when the presence of GAVE is in doubt.Larger studies are needed to assess the impact of virtual chromoendoscopy on success of endoscopic therapy for GAVE.

N-acetylcysteine modulates angiogenesis and vasodilation in stomach such as DNA damage in blood of portal hypertensive rats

AIM: To evaluate the antioxidant effect of N-acetylcysteine(NAC) on the stomach of rats with portal hypertension.METHODS: Twenty-four male Wistar rats weighing ± 250 g were divided into four experimental groups(n =6 each): Sham-operated(SO),SO + NAC,partial portal vein ligation(PPVL),and PPVL + NAC. Treatment with NAC in a dose of 10 mg/kg(i.p.) diluted in 0.6 m L of saline solution was administered daily for 7 d starting 8 d after the surgery. Animals from the PPVL and SO group received saline solution(0.6 m L) for the same period of time as the PPVL + NAC and SO + NAC group. On the 15 th day the animals were anesthetized and we evaluated portal pressure by cannulating mesenteric artery. After,we removed the stomach for further analysis. We performed immunohistochemical analysis for endothelial nitric oxide synthase(e NOS),vascular endothelial growth factor(VEGF),and nitrotirosine(NTT) proteins in stomach. We also evaluated e NOS and VEGF by Western blot analysis and assessed DNA damage in blood samples by the comet assay.RESULTS: The portal hypertension group exhibited increases in portal pressure when compared to SO group(29.8 ± 1.8 vs 12.0 ± 0.3 mm Hg)(P < 0.001). The same was observed when we compared the e NOS(56.8 ± 3.7 vs 13.46 ± 2.8 pixels)(P < 0.001),VEGF(34.9 ± 4.7 vs 17.46 ± 2.6 pixels)(P < 0.05),and NTT(39.01 ± 4.0 vs 12.77 ± 2.3 pixels)(P < 0.05) expression by immunohistochemistry of the PPVL animals with the SO group. The expression of e NOS(0.39 ± 0.03 vs 0.25 ± 0.03 a.μ)(P < 0.01) and VEGF(0.38 ± 0.04 vs 0.26 ± 0.04 a.μ)(P < 0.01) were also evaluated by Western blot analysis,and we observed an increase of both proteins on PPVL animals. We also evaluated the DNA damage by comet assay,and observed an increase on damage index and damage frequency on those animals. NAC decreased portal pressure values in PPVL + NAC animals(16.46 ± 2 vs 29.8 ± 1.8 mm Hg)(P < 0.001) when compared to PPVL. The expression of e NOS(14.60 ± 4.1 vs 56.8 ± 3.7 pixels)(P < 0.001),VEGF(19.53 ± 3.2 vs 34.9 ± 4.7 pixels)(P < 0.05) and NTT(21.84 ± 0.7 vs 39.01 ± 4.0 pixels)(P < 0.05) evaluated by immunohistochemistry were also reduced in PPVL + NAC animals. Also,when evaluated by Western blot e NOS expression(0.32 ± 0.03 vs 0.39 ± 0.03 a.μ)(P < 0.05) and VEGF expression(0.31 ± 0.09 vs 0.38 ± 0.04 a.μ)(P < 0.01). Furthermore,NAC modulated DNA damage in PPVL + NAC animals.CONCLUSION: In view of these results,we believe NAC is able to protect the stomach from the alterations induced by the PPVL procedure.

Portal hypertension and gastrointestinal bleeding:Diagnosis,prevention and management

Bleeding from esophageal varices is a life threatening complication of portal hypertension.Primary prevention of bleeding in patients at risk for a first bleeding episode is therefore a major goal.Medical prophylaxis consists of non-selective beta-blockers like propranolol or carvedilol.Variceal endoscopic band ligation is equally effective but procedure related morbidity is a drawback of the method.Therapy of acute bleeding is based on three strategies:vasopressor drugs like terlipressin,antibiotics and endoscopic therapy.In refractory bleeding,self-expandable stents offer an option for bridging to definite treatments like transjugular intrahepatic portosystemic shunt(TIPS).Treatment of bleeding from gastric varices depends on vasopressor drugs and on injection of varices with cyanoacrylate.Strategies for primary or secondary prevention are based on non-selective beta-blockers but data from large clinical trials is lacking.Therapy of refractory bleeding relies on shuntprocedures like TIPS.Bleeding from ectopic varices,portal hypertensive gastropathy and gastric antral vascular ectasia-syndrome is less common.Possible medical and endoscopic treatment options are discussed.

门脉高压性胃病患者中医证型分布特点及其与胃镜下黏膜病变的相关性

目的:明确门脉高压性胃病(portal hypertension gastropathy,PHG)患者中医证型分布特点,探究PHG中医证型与胃镜下黏膜病变特点之间的相关性。方法:采用临床调查方式对符合标准的180例PHG患者中医证型、胃黏膜病变特点等资料进行统计学分析。结果:PHG患者中医证型主要为湿热蕴结证、瘀血阻络证;胃黏膜糜烂、充血、水肿、出血以湿热蕴结证患者多见,瘀血阻络证以PHG重度患者多见;肝气郁结证及瘀血阻络证与肝肾阴虚证、水湿内阻证及脾肾阳虚证相比,食管静脉曲张发病率差异有统计学意义(P<0.05)。结论:PHG中医证型与胃黏膜病变相关,湿热、瘀血是其主要病理因素。

门脉高压性胃病患者内镜下诊治临床特征分析

目的分析门脉高压性胃病患者的临床症状、内镜下表现及其与食管静脉曲张内镜下治疗的关系,为疾病预防性诊治提供依据。方法对肝硬化食管静脉曲张患者进行胃镜检查,记录食管静脉曲张和门脉高压性胃病的程度,收集患者的性别、体质量、血生化指标、肝功能评分数据,行部分患者内镜下食管静脉曲张硬化剂或套扎治疗后随访,并对临床数据进行统计学分析。结果纳入肝硬化食管静脉曲张患者162例,检出门脉高压性胃病为53.7%,且血清白细胞、血红蛋白、血小板和血氨水平在门脉高压性胃病与不伴门脉高压性胃病组间差异有统计学意义(P<0.01)。在87例门脉高压性胃病患者中,严重程度组间比较肝功能评分差异有统计学意义(P<0.01)。门脉高压性胃病导致非食管胃静脉曲张破裂伴出血患者发生率为77.2%。内镜下治疗35例患者中,门脉高压性胃病中-重度占比由28.6%增至71.4%,与治疗前比较,差异有统计学意义(P<0.01)。结论肝硬化食管静脉曲张患者伴门脉高压性胃病发病率较高,已成为肝硬化患者主要的出血原因之一。重视食管静脉曲张内镜下治疗后对疾病的影响,将为门脉高压性胃病引起的消化道出血的诊治提供一定的依据。

1例内镜序贯腹腔镜治疗食管静脉曲张伴门脉高压性胃病并文献复习

门脉高压性胃病(PHG)是门静脉高压的常见并发症,轻度慢性渗血较为常见,而急性出血较为少见,且较为严重,不易与食管静脉曲张破裂出血鉴别,预后较差。本研究报道1例女性患者,因急性消化道出血住院,急诊胃镜及门静脉CT血管造影(CTA)发现门静脉高压并食管静脉曲张合并PHG出血,行内镜下食管静脉曲张套扎术、药物保守治疗,控制急性出血,3个月后食管静脉曲张好转,PHG加重,进一步行腹腔镜脾切除术联合贲门周围血管离断术,术后随访预后较好,生命质量提高。食管静脉曲张同时合并PHG急性出血是门静脉高压少见的严重并发症,临床医师需重视治疗时机、治疗方式的选择。

脾体积对肝硬化门静脉高压性胃病及其严重程度的预测价值

目的探讨脾体积(SV)对肝硬化患者门静脉高压性胃病(PHG)及重度PHG的预测价值。方法回顾性分析2018年1月—2022年8月湖北医药学院附属襄阳市第一人民医院收治的168例肝硬化患者临床资料,以胃镜检查结果为“金标准”,将患者分为无PHG组(n=115)和PHG组(n=53),轻度PHG组(n=26)和重度PHG组(n=27),所有患者均行电子胃镜、腹部磁共振及相关血清学检查,获取相关指标及参数。正态分布的计量资料两组间比较采用成组t检验;非正态分布的计量资料两组间比较采用Mann-Whitney U检验。计数资料两组间比较采用χ^(2)检验。通过多因素Logistic回归分析筛选出PHG、重度PHG的独立危险因素,利用受试者工作特征曲线(ROC曲线)比较相关指标或参数的预测价值。ROC曲线下面积的比较采用Delong检验。结果单因素分析显示:PHG组和非PHG组性别、有无腹水、Hb、PLT、AST、TBil、Alb、PT、INR、Child-Pugh分级、FIB-4评分、King评分、Lok评分、脾长径(SD)、SV、血小板/脾长径(PSDR)、血小板/脾体积(PSVR)比较,差异均有统计学意义(P值均<0.05);轻度PHG组和重度PHG组Hb、PLT、Alb、SD、SV、PSDR、PSVR比较,差异均有统计学意义(P值均<0.05)。多因素Logistic回归分析显示:FIB-4评分(OR=1.280,95%CI:1.009~1.625)和SV(OR=1.007,95%CI:1.001~1.013)是PHG发生的独立危险因素(P值均<0.05);SV(OR=0.990,95%CI:0.980~1.000)是重度PHG发生的独立影响因素(P<0.05)。ROC曲线分析结果显示:在预测PHG发生时,SV的曲线下面积为0.884,高于FIB-4评分的0.825(P<0.05),其最佳临界值为406.82,敏感度为0.774,特异度为0.870;在预测重度PHG发生时,SV的曲线下面积为0.782,最佳临界值为714.63,敏感度为0.593,特异度为0.962。结论SV对PHG和重度PHG的发生均具有较好的预测价值。

门脉高压性胃肠病研究进展

门脉高压性胃肠病是指继发于门静脉高压的胃肠道黏膜血管病变。其发病机制尚未明确。主要依赖内镜诊断,内镜下描述差异较大,诊断标准尚未统一,且临床表现缺乏特异性,常与其他疾病混淆。治疗相对困难,需要根据患者的具体表现来确定,主要包括药物治疗、内镜治疗及外科手术治疗。

1078例食管胃静脉曲张内镜下表现特点

摘要：目的对1078例食管胃静脉曲张（GOV）患者的内镜下表现特点进行分析。方法随机抽取2011年11月-2012年6月解放军第302医院内窥镜中心诊断食管胃静脉曲张4210例患者中1078例常规检查患者进行分析。食管静脉曲张严重程度分为：轻度（EV1）、中度（EV2）和重度（EV3）。门脉高压性胃病（PHG）分为轻度和重度。对胃静脉曲张提出新的分型方法：GVl、GV2、GV3、GV4和IGV。等级资料采用秩和检验。结果1078例患者中，Ev333例（30．89％）；EV伴GV728例（67．53％）：其中GVl占42．31％，GV2占14．42％，GV占19．78％，GV4占23．49％；IGV17例（1．58％）。无PHG542例（50．28％），轻度PHG324例（30．06％），重度PHG212例（19．66％）。PHG发生率与GOV的分型无明显关系（P〉0．05）。PHG的发生率与Ev的严重程度有关（P=O．0023）。结论GOV的内镜表现主要为EV伴GV占大多数，其中食管静脉曲张延伸至胃小弯最为常见，而食管静脉曲张只延伸至贲门也为数不少，可作为胃静脉曲张的分型之一。门脉高压性胃病的发生率随食管静脉曲张严重程度的增加而升高。

超声检查对肝硬化门脉高压性胃病的预测

以超声检查指标对门脉高压性胃病进行预测。经超声和胃镜检查 ,筛选出与门脉高压性胃病相关且对其判断贡献较大的指标 ,建立回归方程。门静脉内径、脾长径、脾指数、脾静脉内径、腹水、胆囊壁厚度与门脉高压性胃病呈正相关 ,经Logistic回归分析对门脉高压性胃病的综合判断符合率为 79 3%。超声检查指标对肝硬化患者门脉高压性胃病判断符合率较高 ,可由超声检查预测肝硬化门脉高压性胃病。

门脉高压性胃病的研究进展

门脉高压性胃病(portal hypertension gastopathy,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,其临床主要表现为消化系出血症,是上消化道出血的重要原因之一,严重时危急生命.近年来关于门脉高压性胃病的发病机制,内镜下和影像学诊断、治疗发展较快.本文就近年来门脉高压性胃病的研究作一综述.

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.

门脉高压性胃病患者血浆、尿中内皮素浓度变化及意义

本文应用放射免疫法测定 40例门脉高压性胃病 (PHG)患者血桨、尿中内皮素 (ET)含量。结果 ,PHG患者血桨ET(PEt)尿ET(UEt)及PEt/UEt显著高于非PHG肝硬化患者和正常人 (P <0 .0 5 ) ,且与食管静脉曲张程度、脾厚和门脉宽度成正比。轻、重度PHG上述三项指标差异均有显著性 (P <0 .0 5 ) ;提示 ,ET参与PHG的形成机制 ,可能主要与ET使门脉压增高有关。

肝硬化患者门静脉高压性胃病发病因素的研究

门静脉高压性胃病是肝硬化患者上消化道出血的原因之一,但其发病机制目前尚不完全清楚。目的:探讨肝硬化患者门静脉高压性胃病的发生与肝硬化分级、食管胃底静脉曲张程度、腹水量和胃肠激素血管活性肠肽(VIP)水平的关系。方法:45例肝硬化患者行胃镜检查观察食管胃底静脉曲张程度和胃黏膜改变,行腹部B超检查观察腹水量,同时检测血清白蛋白、总胆红素、胆碱酯酶、凝血酶原时间等肝功能指标和血浆VIP水平。结果:Child-PughA、B、C级肝硬化患者、不同程度食管胃底静脉曲张患者以及不同程度腹水患者之间的门静脉高压性胃病发生率均无显著差异(P>0.05)。但肝硬化伴门静脉高压性胃病患者的血浆VIP水平较无门静脉高压性胃病者显著升高(P<0.001)。结论:门静脉高压是门静脉高压性胃病的必要条件,而其他因素,如血浆VIP水平与门静脉高压性胃病的发生也有一定关系。

幽门螺杆菌、肝功及食管曲张静脉套扎治疗对肝硬化门脉高压性胃病的影响

目的 探讨幽门螺杆菌 (HP)感染、肝功能状态、食管胃底静脉曲张及食管曲张静脉套扎 (EVL)后对PHG的影响。方法 对 4 7例肝硬化患者 (伴PHG者 34例 ,不伴PHG者 13例 )分别行肝功能、胃内HP测定 ,胃镜下判断食管胃底曲张静脉及其程度。EVL患者术后 1～ 2月复查胃镜 ,观察PHG变化。结果 肝硬化患者HP感染率低于对照组 ,肝硬化伴或不伴PHG者HP感染率无显著差异 ,轻度PHG与重度PHG患者HP感染率无统计学差异。有食管、胃底静脉曲张者PHG发生率较高。EVL术后PHG加重或发病率增加。结论 PHG与HP感染无关 ,肝功能状态可影响PHG的发生及程度 ;食管胃底静脉曲张和PHG发生有密切关系 ,但静脉曲张程度与PHG程度无关 ;EVL术后可诱发或加重PHG。