门静脉血栓形成对肝硬化病程发展影响

目的探讨门静脉血栓（PVT）形成对肝硬化病程的影响。方法回顾我院2003年～2011年肝硬化伴PVT形成的患者资料。18例肝硬化伴PVT形成患者人选血栓组;随机选择同阶段肝硬化门静脉高压症的无门静脉血栓形成患者19例作为对照组,比较两组患者的门静脉宽度、脾脏厚度、食管胃底静脉曲张、腹水及上消化道大出血发生等情况。结果血栓组的门静脉宽度及脾脏厚度大于对照组,差异有统计学意义（P〈0．05）。血栓组食管胃底重度静脉曲张、上消化道大出血和大量腹水比例两组比较,差异有统计学意义（P〈0．05）。结论脾肿大和门静脉增宽是PVT形成的主要危险因素,PVT形成加重门静脉高压的程度,从而增加上消化道出血几率,使腹水难以消退,增加相关并发症发生率并使相关症状加重,预防门静脉血栓形成有助于延缓肝硬化病情发展。     

肝硬化门静脉高压症患者胃动力障碍的多因素分析

目的研究肝硬化门静脉高压症(PHT)患者胃半排空时间、肝功能分级以及胃肠激素水平,评估胃排空与肝功能分级及胃肠激素水平的关系。方法选取2013年1月至2015年12月住院的36例肝硬化PHT患者,对其进行胃排空核素扫描,检测肝功能、凝血功能、血浆硫化氢(H2S)、胃泌素(GAS)、血管活性肠肽(VIP)、胃动素(MTL)水平,并行腹部B超/CT检查。根据肝功能Child-Pugh分级将患者分为A级、B级、C级3组。根据肝硬化PHT患者的内镜下表现,分为食管胃底静脉曲张组和无食管胃底静脉曲张组;食管胃底静脉组中,根据静脉曲张程度分为轻度、中度、重度3组。14例同期健康体检者作为健康对照组。结果与健康对照组相比,肝硬化PHT组的胃半排空时间明显延迟(P0.01)。肝硬化PHT组中:肝功能Child-Pugh A级、B级、C级3组的胃半排空时间差异无统计学意义(P0.05);无食管胃底静脉曲张组与食管胃底静脉曲张组的胃半排空时间的差异无统计学意义(P0.05);食管胃底静脉曲张轻度、中度和重度3组的胃半排空时间的差异无统计学差异(P0.05)。肝硬化PHT组的血浆H2S水平明显低于健康对照组(P0.01),血浆VIP、MTL水平明显高于健康对照组(P0.01),而血浆GAS水平与健康对照组相比,差异无统计学意义(P0.05)。结论肝硬化PHT患者的胃半排空时间明显延迟,与肝功能分级及食管胃底静脉曲张程度无关。肝硬化PHT患者的血浆H2S水平降低,血浆VIP、MTL水平升高。H2S与胃半排空时间呈负相关,其可能参与肝硬化PHT患者胃动力障碍的发生。     

正确认识经颈静脉肝内门体分流术治疗肝硬化门静脉高压并发症的地位

门静脉高压常引起食管胃底静脉曲张甚至破裂出血、腹水、脾功能亢进、肝肾综合征、肝肺综合征等,统称为门静脉高压症,尤其是食管胃底静脉曲张出血和顽固性腹水最为常见.静脉曲张出血是肝硬化门静脉高压致死性的并发症,50%的肝硬化患者诊断时存在食管胃底静脉曲张,其中多数发生于肝功能Child-Pugh分级为A级或C级的患者.     

肝硬化门静脉高压自发性脾肾分流患者临床特征分析

目的:分析肝硬化门静脉高压合并自发性脾肾分流患者临床特征。方法:回顾性分析我院17例肝硬化门静脉高压合并脾肾分流患者作为分流组,记录其Child-Pugh评分,门静脉内径、脾静脉内径,总胆红素水平及有无食管胃底静脉曲张、肝性脑病及腹水的发生;随机抽取同期住院20例肝硬化门静脉高压未合并脾肾分流患者作为对照组,分析其临床特征。结果:分流组患者门静脉及脾静脉内径分别为(14.14±0.93)mm、(15.82±1.03)mm,对照组患者分别为(15.35±1.22)mm、(12.56±1.90)mm,两组相比较差异均有统计学意义(P0.05);脾肾分流患者总胆红素水平为(32.94±7.56)μmol/L,总胆红素异常率为88.23%,对照组分别为(37.45±22.61)μmol/L和55.00%,两组总胆红素水平相比无统计学意义(P0.05)。分流组患者总胆红素异常率高于对照组(P0.05);分流组食管胃底静脉曲张、肝性脑病、腹水发生率分别为88.24%、47.06%、23.53%,对照组分别为55.00%、10.00%、30.00%,两组相比较,食管胃底静脉曲张及肝性脑病发生率有统计学意义(P0.05),腹水发生率相比无统计学意义(P0.05)。结论:肝硬化门静脉高压合并脾肾分流患者存在不同程度的总胆红素升高,多合并食管胃底静脉曲张,其肝性脑病的发生率明显升高。     

肝硬化门静脉血栓形成37例临床分析

目的探讨门静脉血栓（PVT）形成对肝硬化病程的影响。方法回顾我院2003～2010年肝硬化伴PVT形成的患者资料。18例肝硬化伴PVT形成患者入选血栓组;随机选择同阶段肝硬化门静脉高压症的无门静脉血栓形成患者19例作为对照组,比较两组患者的门静脉宽度及脾脏厚度,食管胃底静脉曲张、腹水及上消化道大出血发生等情况。结果血栓组的门静脉宽度及脾脏厚度大于对照组,差异有统计学意义（P〈0.05）。血栓组患者的上消化道大出血发生率、重度食管胃底静脉曲张程度、大量腹水患者数量明显高于对照组。结论 PVT形成加重门静脉高压的程度,从而增加上消化道出血机率,使腹水难以消退,预防门静脉血栓形成有助于延缓肝硬化病情发展。     

门静脉高压脾切除门奇静脉离断术后再出血的食管胃静脉曲张分类研究

目的：探讨门静脉（门脉）高压患者脾切除门奇静脉离断术（脾切断流术）后再发上消化道出血的平均时间、内镜下食管和胃静脉曲张的分类特点及门脉高压性胃病的发病率。方法：190例肝硬化门脉高压出血患者分为脾切断流术后再出血组（40例）和未行手术组（150例）,统计手术患者术后至首次出血的平均时间间隔,每组患者分别行内镜检查,观察并对比其曲张静脉的分型特点及门脉高压性胃病发生率。结果：脾切断流术后再发出血时间平均为24个月,再出血患者内镜皆提示存有食管和（或）胃静脉曲张,2组患者内镜下的曲张静脉分型构成比有明显差异,脾切断流术者以单纯食管静脉曲张及食管胃静脉曲张（GOV）1型为主,未发现孤立性胃静脉曲张（IGV）1型及IGV2型,60．0％患者存在门脉高压性胃病,其发病率及严重程度均高于未行手术组患者。结论：脾切断流术治疗门脉高压近期止血疗效确切,但术后曲张静脉并未有效消退,须强调手术的规范性,并在再出血高发时段定期内镜随访．及时掌握食管胃曲张静脉及门脉高压性胃病的发展情况,早期干预治疗,从而改善患者预后。     

肝硬化上消化道出血92例临床分析

目的探讨肝硬化上消化道出血的原因及其与肝功能损害程度的关系。方法对92例肝硬化上消化道出血患者行急诊胃镜检查,发现病因。结果在92例肝硬化并发上消化道出血患者中,食管胃底静脉曲张破裂出血占52．2％,门脉高压性胃病出血占22．8％,肝源性溃疡出血占20．7％;肝功能A级与B级和C级患者出血原因差异显著。结论食管胃底静脉曲张破裂出血是肝硬化上消化道出血的主要原因,门脉高压性胃病和肝源性溃疡也是不可忽视的出血原因。     

肝硬化门静脉高压患者胃镜与B超表现相关性研究

目的 通过对肝炎肝硬化门静脉高压患者胃镜、B超检测结果行相关性分析，为临床判断肝硬化程度、早期预防并发症提供参考。方法 选择肝炎肝硬化门静脉高压患者192例，根据食管静脉曲张程度分为轻、中、重度3组。比较胃底静脉曲张在各组中发生比例，并测量门静脉主干宽度、脾静脉宽度、脾脏厚度，研究其与食管静脉曲张程度相关性。结果 3组患者胃底静脉曲张发生比例存在显著差异，食管静脉曲张程度越重，伴胃底静脉曲张比例越高；随食管静脉曲张程度不同，门静脉主干内径、脾静脉内径及脾脏厚度之间存在差异，脾脏厚度与脾静脉内径之间存在直线相关关系。结论 门静脉主干内径、脾静脉内径、脾脏厚度可为判断门静脉高压提供参考，综合上述3点并结合胃镜检查结果可较准确判断有无食管静脉曲张及程度。     

97例肝硬化患者胃镜结果分析

目的：通过97例肝硬化患者的胃镜检查,对上消化道黏膜病变程度与Child-Pugh分级的关系进行探讨。方法：将97例肝硬化患者根据Child．Pugh分级,分为A级、B级两组,观察其食管静脉曲张轻、中、重程度、门脉高压性胃病、溃疡、食管炎及十二指肠球炎发生率,并做统计学处理。结果：97例肝硬化患者食管静脉曲张检出率90．7％,门脉高压性胃病检出率54．6％,胃溃疡检出率17．5％,十二指肠溃疡检出率9．3％,十二指肠球炎检出率27．8％,反流性食管炎检出率10．3％。食管静脉曲张严重程度（x^2=10．95）和反流性食管炎发生率（X^2=6．12）与Child．Pugh级别呈正相关（P〈0．01）,而门脉高压性胃病、胃溃疡、十二指肠溃疡、十二指肠球炎发病率与之无明显关系（P均〉0．05）。结论：肝硬化患者食管静脉曲张严重程度和反流性食管炎发生率随Child·Pugh分级而上升,门脉高压性胃病、胃溃疡、十二指肠溃疡、十二指肠球炎发病率则与Child-Pugh分级无明显关系。     

胃肠超声造影对胃底静脉曲张的诊断价值

食管胃静脉曲张是肝硬化门静脉高压的常见并发症。近年来,超声造影在胃肠疾病诊断中的应用日益受到关注。目的：探讨胃肠超声造影对胃底静脉曲张的诊断价值。方法：收集2009年3月-2011年9月于河北省玉田县医院接受胃镜和口服胃肠超声造影检查的肝硬化门静脉高压患者79例,回顾性分析胃肠超声造影的声像图特征,并以胃镜检查结果为“金标准”,评价其对胃底静脉曲张的诊断价值。结果：79例肝硬化门静脉高压患者中41例经胃镜检查证实胃底静脉曲张,其中33例胃肠超声造影显示特征性声像图表现,曲张静脉内径（12．6±8．9）mm,血液流速（13．9±2．7）cm／s。胃肠超声造影诊断胃底静脉曲张的敏感性、特异性、准确率分别为80．5％（33／41）、100％（38／38）、89．9％（71／79）。结论：胃肠超声造影在胃底静脉曲张的诊断中具有较高应用价值,有望成为肝硬化门静脉高压患者胃底静脉曲张的初步筛查手段推广使用。     

Natural history of portal hypertension

A rise in pressure in the portal vein is a frequent occurrence in patients with cirrhosis. One common manifestation affecting at least 50% of cirrhosis patients is the development of gastroesophageal varices and portal hypertensive gastropathy. Bleeding from gastric or esophageal varices will occur in approximately 1/4 of cirrhotic patients with an associated high mortality. Large esophageal varices that have red color signs and isolated gastric varices in the fundus of the stomach are most likely to hemorrhage. The greatest risk of bleeding is during the first year following the index endoscopy. Once varices have bled they are almost certain to rebleed in the absence of therapy. Similarly, severe portal hypertensive gastropathy is likely to cause chronic blood loss. Knowledge of the natural history of gastroesophageal varices allows for the development of effective treatment strategies.     

Portal hypertensive colopathy in patients with liver cirrhosis

AIM: In patients with liver cirrhosis and portal hypertension, portal hypertensive colopathy is thought to be an important cause of lower gastrointestinal hemorrhage. In this study, we evaluated the prevalence of colonic mucosal changes in patients with liver cirrhosis and its clinical significance. METHODS: We evaluated the colonoscopic findings and liver function of 47 patients with liver cirrhosis over a 6-year period. The main cause of liver cirrhosis was post-viral hepatitis (68%) related to hepatitis B (6%) or C (62%) infection. All patients underwent upper gastrointestinal endoscopy to examine the presence of esophageal varices, cardiac varices, and congestive gastropathy, as well as a full colonoscopy to observe changes in colonic mucosa. Portal hypertensive colopathy was defined endoscopically in patients with vascular ectasia, redness, and blue vein. Vascular ectasia was classified into two types: type 1, solitary vascular ectasia; and type 2, diffuse vascular ectasia. RESULTS: Overall portal hypertensive colopathy was present in 31 patients (66%), including solitary vascular ectasia in 17 patients (36%), diffuse vascular ectasia in 20 patients (42%), redness in 10 patients (21%) and blue vein in 6 patients (12%). As the Child-Pugh class increased in severity, the prevalence of portal hypertensive colopathy rose. Child-Pugh class B and C were significantly associated with portal hypertensive colopathy. Portal hypertensive gastropathy, esophageal varices, ascites and hepatocellular carcinoma were not related to occurrence of portal hypertensive colopathy. Platelet count was significantly associated with portal hypertensive colopathy, but prothrombin time, serum albumin level, total bilirubin level and serum ALT level were not related to occurrence of portal hypertensive colopathy. CONCLUSION: As the Child-Pugh class worsens and platelet count decreases, the prevalence of portal hypertensive colopathy increases in patients with liver cirrhosis. A colonoscopic examination in patients with liver cirrhosis is indicated, especially those with worsening Child-Pugh class and/or decreasing platelet count, to prevent complications such as lower gastrointestinal bleeding.     

The natural history of portal hypertensive gastropathy in patients with liver cirrhosis and mild portal hypertension

BACKGROUND: Portal hypertensive gastropathy is a potential cause of bleeding in patients with liver cirrhosis. Studies on its natural history have often included patients submitted to endoscopic or pharmacological treatment for portal hypertension. PATIENTS AND METHODS: A total of 222 cirrhotic patients with mild degree of portal hypertension (i.e., with no or small varices at entry, without previous gastrointestinal bleeding and medical, endoscopic, or angiographic treatment) were followed up with upper endoscopy every 12 months for 47 +/- 28 months. RESULTS: Upon enrollment 48 patients presented portal hypertensive gastropathy (43 mild and 5 severe) and the presence of esophageal varices was the only independent predictor of the presence of this gastric lesion at multivariate analysis. The incidence of portal hypertensive gastropathy was 3.0% (1.1-4.9%) at 1 yr and 24% (18.1-29.9%) at 3 yr, while the progression was 3% (1-6.9%) at 1 yr and 14% (4.2-23.8%) at 3 yr. The presence of esophageal varices and the Child-Pugh class B or C at enrollment were predictive of the incidence of portal hypertensive gastropathy, while only Child-Pugh class B or C was correlated with the progression from mild to severe, at multivariate analysis. During follow-up 16 patients bled from portal hypertensive gastropathy (9 acutely and 7 chronically) and one patient died of exsanguination from this lesion. CONCLUSIONS: The natural history of portal hypertensive gastropathy is significantly influenced by the severity of liver disease and severity of portal hypertension. Acute bleeding from portal hypertensive gastropathy is infrequent but may be severe.     

胃静脉曲张的病因及临床特点

目的探讨胃静脉曲张的病因及临床特点。方法回顾性分析北京协和医院2000年1月至2005年4月胃静脉曲张患者的病因及并发出血的情况,胃静脉曲张出血与红色征、曲张静脉类型、程度的关系,以及各型曲张静脉发生门脉高压性胃病的情况。结果我院5年间共诊治胃静脉曲张407例,占同期全部食管、胃静脉曲张的47.1%。胃静脉曲张的病因中,肝硬化占74.4%。孤立性胃静脉曲张的病因中脾静脉阻塞占37.2%,肝硬化占33%。407例胃静脉曲张患者中出血121例(29.7%)。在1型和2型胃静脉曲张、1型孤立性胃静脉曲张患者中,出血组红色征的阳性率、静脉曲张的程度均显著高于未出血组(P<0.01)。门脉高压所致的304例胃静脉曲张患者中发生门脉高压性胃病60例(19.7%),与食管静脉曲张发生门脉高压性胃病(22.3%)无差异,但孤立性胃静脉曲张很少出现门脉高压性胃病(9.6%,P<0.05)。结论胃静脉曲张最常见的病因是各种原因引起的肝硬化,而孤立性胃静脉曲张最常见的病因是脾静脉阻塞。红色征、静脉曲张程度是胃静脉曲张出血的危险因素。胃静脉曲张对门脉高压性胃病无影响。     

Gastroduodenal and intestinal permeability in primary biliary cirrhosis

OBJECTIVES: To evaluate gastrointestinal permeability in primary biliary cirrhosis (PBC), using a sensitive method to detect epithelial damage, and to correlate it with the Mayo score, histological stage, ascites, spontaneous bacterial peritonitis, endoscopic signs of portal hypertension and Helicobacter pylori infection. METHODS: Fifty consecutive patients with PBC and 39 patients with cirrhosis of other aetiologies (non-PBC) were enrolled in the study. Coeliac disease was initially ruled out in all participants. Permeability was assessed using sucrose (gastro-duodenum) and lactulose-mannitol (intestine). RESULTS: Sucrose excretion was above the limit in both PBC and non-PBC patients. Twenty-two per cent of PBC patients had an increased result for the lactulose-mannitol test compared to 12.8% of non-PBC cirrhotic patients. PBC patients had high sucrose excretion levels irrespective of the presence of any oesophageal varices, which significantly increased the gastroduodenal permeability in non-PBC patients only when associated with hypertensive gastropathy. Sucrose excretion was significantly enhanced by hypertensive gastropathy in non-PBC patients (P < 0.001) but not in PBC patients. No significant correlation was found in either group between gastrointestinal permeability and the other parameters. CONCLUSIONS: Gastrointestinal permeability is increased in PBC. Portal hypertension contributes to altered gastric mucosal permeability in non-PBC cirrhosis, whereas different epithelial dysfunction can be hypothesized in PBC.     

Non-variceal upper gastrointestinal bleeding in cirrhotic patients in Nile Delta

Background and Study Aims

Acute upper gastrointestinal bleeding (AUGIB) in cirrhotic patients occurs mainly from esophageal and gastric varices; however, quite a large number of cirrhotic patients bleed from other sources as well. The aim of the present work is to determine the prevalence of non-variceal UGIB as well as its different causes among the cirrhotic portal hypertensive patients in Nile Delta.

Methods

Emergency upper gastrointestinal (UGI) endoscopy for AUGIB was done in 650 patients. Out of these patients, 550 (84.6 %) patients who were proved to have cirrhosis were the subject of the present study.

Results

From all cirrhotic portal hypertensive patients, 415 (75.5 %) bled from variceal sources (esophageal and gastric) while 135 (24.5 %) of them bled from non-variceal sources. Among variceal sources of bleeding, esophageal varices were much more common than gastric varices. Peptic ulcer was the most common non-variceal source of bleeding.

Conclusions

Non-variceal bleeding in cirrhosis was not frequent, and sources included peptic ulcer, portal hypertensive gastropathy, and erosive disease of the stomach and duodenum.

     

Gastroesophageal reflux in cirrhotic patients with esophageal varices without endoscopic treatment

BACKGROUND: Portal hypertension in patients with liver cirrhosis causes manifestations such as esophageal varices, ascites and edema. Some studies have been conducted about the role of esophageal varices in the development of esophageal motor disorders and abnormal gastroesophageal reflux in these patients. Ascites could be a factor promoting gastroesophageal reflux and it has been questioned whether reflux would favor the rupture of varices. However there are a few studies using ambulatory esophageal pH recording in the evaluation of these patients. AIMS: Evaluate gastroesophageal reflux by pH recording in cirrhotic patients with esophageal varices and possible predictors. METHODS: Fifty one patients (28 men, 23 women, mean age of 54 years) with liver cirrhosis, diagnosed by clinical, laboratorial, image and histological findings were prospectively evaluated. All patients had esophageal varices confirmed by endoscopy and were submitted to a questionnaire about typical gastroesophageal reflux disease symptoms (heartburn and or acid regurgitation). pH recording was performed with the probe placed 5 cm above the superior lower esophageal sphincter limit, as determined by manometry. Abnormal reflux (% total time with pH < 4 >4.5%) was related to the size of varices, congestive gastropathy, ascites, severity of cirrhosis and typical gastroesophageal reflux disease symptoms. RESULTS: The caliber of the varices was considered to be small in 30 patients (59%), medium in 17 (33%) and large in 4 (8%), 21 (41%) congestive gastropathy. Ascites was observed in 17 (33%), 32 patients (63%) were classified as Child-Pugh A, 17 (33%) Child-Pugh B and 2 (4%) Child-Pugh C. Twenty seven patients (53%) presented with typical gastroesophageal reflux disease symptoms. Abnormal reflux at pH recording was found in 19 patients (37%). One of them presented with erosive esophagitis at endoscopy. There was no relation between ascites, variceal size, congestive gastropathy and Child-Pugh score and abnormal reflux. There was a correlation between typical gastroesophageal reflux disease symptoms and abnormal reflux. CONCLUSION: Abnormal gastroesophageal reflux was found in 37% of the patients with hepatic cirrhosis and esophageal varices. Only typical gastroesophageal reflux disease symptoms predicted these findings.     

Correlation of Doppler ultrasound of the portal system with endoscopic changes caused by portal hypertension in cirrhotic patients

BACKGROUND: The portal hypertension in cirrhotic patients is the main cause of this illness complication, that are clinically translated to visible collateral circulation in the abdominal wall, ascites and esophageal varices. AIM: To evaluate if the portal system echodoppler is able to estimate the presence of esophageal varices, gastric varices and congestive gastropathy in patients with hepatic cirrhosis. PATIENTS AND METHODS: One hundred and eighty six patients of the gastroenterology and hepatology ambulatory of the Clinical Hospital of the Federal University of Paraná, Curitiba, PR, Brazil, had been selected for evaluation. Of those, 145 had completed all the stages of the evaluation and 133 had been enclosed in the final analysis. All had been submitted to high digestive endoscopy for evaluation of esophagogastric varices and congestive gastropathy and then to Doppler ultrasound of the portal system with study of the systolic peak speed of the portal vein, diameter of the portal and splenic vein and spleen size, presence of the umbilical vein recanalization and hepatofugal flow. RESULTS: The patients with esophagogastric varices had significant difference of the spleen size when compared to patients without these change. However, none of the Doppler ultrasound parameters showed good accuracy and specificity in this group of cirrhotic patients. Congestive gastropathy patients had their diagnosis predict with significant manner not only by the portal and splenic vein diameter but also by the spleen size. Similarly to that described above, they do not have a good accuracy and specificity. These evaluations were validated by the construction of ROC (Receiver Operating Characteristic) curves, whose areas below the curves had always been less than 0,8. CONCLUSION: There was not a good correlation of the Doppler ultrasound parameters of the portal system to the presence of the main endoscopic alterations (esophagogastric varices and congestive gastropathy) in patients with hepatic cirrhosis.