肝硬化患者门静脉高压性胃病发病因素的研究

背景：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—Pugh A、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。     

Is there ileopathy in portal hypertension?

BACKGROUND AND AIMS: Portal hypertensive gastropathy and colopathy are well described endoscopic abnormalities in patients with portal hypertension. Endoscopic abnormalities in the ileum in patients with portal hypertension have not been well described. The aim of the present study was to evaluate endoscopic abnormalities in the ileum of patients with portal hypertension. METHODS: Patients with portal hypertension of various etiologies were included in the study. Upper gastrointestinal endoscopy was performed to record esophageal varices, gastric varices and portal hypertensive gastropathy. Colonoscopy with retrograde intubation of the ileum was performed and the presence of colorectal varices, colopathy and mucosal findings in the ileum were noted. RESULTS: Forty-one patients (age 16-80 years, 33 men) were studied. Esophageal varices were present in all. Portal hypertensive gastropathy was present in 27/41 (66%) patients. Rectal varices were noted in 22/41 (54%) patients and 17/41 (42%) patients had features suggestive of colopathy. Ileum could be intubated in 38 patients (93%). Endoscopic abnormalities in the ileum were noted in 13/38 (34%) patients. Ileopathy as evident by endoscopic mucosal abnormalities was observed in 10/38 (26%) patients. Ileal varices were present in 8/38 (21%) patients. Three of these had ileal varices alone while the remaining five patients also had associated ileopathy The presence of ileopathy was significantly associated with the presence of portal hypertensive gastropathy and colopathy but not with esophageal, gastric or rectal varices. CONCLUSIONS: Ileopathy occurs in one-third of patients with portal hypertension and is significantly associated with the presence of portal hypertensive gastropathy and colopathy.     

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.     

Mucosal abnormalities of the small bowel in patients with cirrhosis and portal hypertension: a capsule endoscopy study

BACKGROUND: The frequency of small-bowel mucosal changes in patients with portal hypertension is not known. The objective of the study is to better define the mucosal abnormalities of portal hypertensive enteropathy (PHE) and to determine whether these findings are associated with the severity of liver disease, esophageal varices, portal gastropathy, portal colonopathy, or other clinical characteristics. METHODS: We compared the medical records of 37 patients with cirrhosis and portal hypertension with 34 control patients who underwent capsule endoscopy over a 3-year period. RESULTS: Mucosal changes were found to be significantly more common in the cirrhotic patients than in the control patients (67.5% vs. 0, p < 0.001). The lesions included telangiectasias or angiodysplastic-like lesions in 9 (24.3%) patients, red spots in 23 (62.2%), and varices in 3 (8.1%). Active bleeding was seen during endoscopic examinations in 4 (10.8%) patients. A comparison of patients with and those without PHE showed that grade 2+ or larger esophageal varices, portal gastropathy, portal colonopathy, and Child-Pugh class C cirrhosis were all significantly associated with PHE. There were no differences between these two groups of patients with regard to the etiology of cirrhosis, gender, or history of esophageal variceal bleeding. CONCLUSIONS: Mucosal abnormalities in portal jejunopathy include edema, erythema, and vascular lesions findings. A standardized grading system to classify the endoscopic appearance and the severity of portal enteropathy is proposed. The clinical import of these changes remains to be explained.     

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.     

乙型肝炎肝硬化患者门脉高压性胃病的胃镜检查特点分析

目的探讨肝硬化门脉高压性胃病(PHG)的胃镜特点及其与肝功能分级和食道静脉曲张的关系。方法对108例乙型肝炎肝硬化患者进行常规胃镜检查,对其并发PHG情况进行回顾性分析。结果在108例患者中,发现PHG42例(38.9%),食管静脉曲张91例(84.3%);肝功能Child-Pugh分级与PHG病变程度呈正相关(r=0.385,P=0.000),食管静脉曲张程度与PHG病变程度亦呈正相关(r=0.249,P=0.009)。结论随着肝功能分级及食管静脉曲张程度的加重,PHG的严重程度也逐渐加重。     

295例食管静脉曲张病因及内镜下表现分析

目的 回顾性分析我院295例食管静脉曲张（EV）患者的病因和内镜下表现。方法 2014年1月～2016年6月新疆维吾尔自治区人民医院消化内镜中心诊断存在EV的住院患者295例,使用GE E9彩色多普勒超声、GE 64排螺旋CT和Olympus Gif-260型胃镜行相关检查。收集其临床资料,记录性别、年龄、病因和内镜下表现。结果 在295例EV患者中,肝硬化258例（87.46%）,其中主要有乙型肝炎肝硬化94例（31.86%）,隐源性肝硬化58例（19.66%）,丙型肝炎肝硬化37例（12.54%）,原发性胆汁性肝硬化23例（7.80%）。非肝硬化相关病因37例（12.54%）;内镜下食管静脉曲张轻度61例,中度68例,重度166例,重度EV常常合并红色征（89.8%）,其合并胃静脉曲张及门脉高压性胃病明显增多,EV程度与胃静脉曲张、门脉高压性胃病和消化性溃疡显著相关（r=0.310、r=0.174、r=-0.173,P＜0.05）。结论 门静脉高压导致EV的主要病因仍是肝硬化,主要病因是乙型肝炎和隐源性肝硬化,但非肝硬化相关病因也占重要比重。随着EV程度的加重,胃静脉曲张和门脉高压性胃病的发病率升高,应注意区别防治。     

Natural history of portal hypertension in patients with cirrhosis

All patients with cirrhosis will eventually develop portal hypertension and esophagogastric varices. Bleeding from ruptured esophagogastric varices is the most severe complication of cirrhosis and is the cause of death in about one third of patients. The rate of development and growth of esophageal varices is poorly defined but in general seem to be related to the degree of liver dysfunction. Once varices have formed, they tend to increase in size and eventually to bleed. In unselected patients, the incidence of variceal bleeding is about 20% to 30% at 2 years. Variceal size is the single most important predictor of a first variceal bleeding episode. Several prognostic indexes based on endoscopic and clinical parameters have been developed to predict the risk of bleeding; however, their degree of accuracy is unsatisfactory. Death caused by uncontrolled bleeding occurs in about 6% to 8% of patients; the 6-week mortality rate after a variceal hemorrhage is 25% to 30%. There are no good prognostic indicators of death caused by uncontrolled bleeding or death within 6 weeks. Untreated patients surviving a variceal hemorrhage have a 1- to 2-year risk of rebleeding of about 60% and a risk of death of about 40% to 50%. The risk of bleeding is greatest in the first days after a bleeding episode and slowly declines thereafter. All patients surviving a variceal hemorrhage must be treated to prevent rebleeding. Varices can also be found in the stomach of cirrhotic patients, alone or in association with esophageal varices. Gastric varices bleed less frequently but more severely than esophageal varices. Portal hypertensive gastropathy is a common feature of cirrhosis, and its prevalence parallels the severity of portal hypertension and liver dysfunction. Portal hypertensive gastropathy can progress from mild to severe and vice-versa or even disappear completely. Acute bleeding from portal hypertensive gastropathy seems to be relatively uncommon, and less severe than bleeding from varices.     

Nodules in antrum after variceal eradication a new finding in patients with portal hypertension

Portal hypertension is known to cause esophageal varices, gastric varices and portal hypertensive gastropathy (PHG). The prevalence of gastric varices and PHG is known to increase after eradication of esophageal varices. PHG includes the presence of a mucosal mosaic pattern, cherry red spots, and/or black-brown spots and gastric vascular ectasia (GAVE). Patients with portal hypertension in whom esophageal varices were eradicated were on follow up endoscopy for detection of recurrence of esophageal varices. Their status of PHG was assessed and patients antral nodules were enrolled. Twenty patients with antral nodules were identified over one year. Fifteen out of 20 patients had cirrhosis as etiology of portal hypertension, three had non-cirrhotic portal hypertension and two had extra-hepatic portal vein thrombosis. GAVE was seen more commonly (n=8, 40%) in patients with PHG with nodules. PHG with antral nodules is a novel endoscopic finding present both in cirrhotic and non-cirrhotic portal hypertension with unknown pathogenesis, and is seen more commonly in patients with eradicated varices who are on long-term follow up.     

Impaired gastric mucosal energy metabolism in congestive gastropathy in cirrhotic patients

To clarify the characteristics of congestive gastropathy, we investigated gastric mucosal hemodynamics and energy metabolism in cirrhotic patients, using a reflectance spectrophotometry system and high performance liquid chromatography. The index of the gastric mucosal blood volume of cirrhotic patients with esophageal varices was significantly higher, and the index of gastric mucosal blood oxygenation significantly lower, than those in controls, thus indicating congestion and hypoxia in the gastric mucosa. Energy charge levels in the gastric mucosa of cirrhotic patients with esophageal varices were also significantly decreased. The energy charge level showed a strong linear correlation with the index of mucosal blood oxygenation in the antral (r=0.996,P<0.01) and body (r=0.994,P<0.01) mucosa of the stomach. These findings suggest that congestive gastropathy in a portal hypertensive state causes hypoxia in the gastric mucosa, leading to a mucosal energy deficit that may increase mucosal susceptibility to aggressive factors.     

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。     

Observation of thoracic duct morphology in portal hypertension by endoscopic ultrasound

Background:Thoracic duct dilation has been demonstrated in portal hypertension and hepatic cirrhosis by lymphangiography and laparotomy and at autopsy. It is thought to be secondary to increased hepatic lymph flow and has been described in the absence of ascites or esophageal varices. The aim of the present study was to observe thoracic duct morphology by endoscopic ultrasound in various subsets of patients with portal hypertension and hepatic cirrhosis and also to validate existing radiologic/surgical data. Methods:The thoracic duct of 33 patients with cirrhosis and portal hypertension was studied by endoscopic ultrasound. Patients were divided into four groups: 1, patients with ascites and esophageal varices; 2, esophageal varices without ascites; 3, without esophageal varices or ascites; 4, extrahepatic portal hypertension due to pancreatic malignancy. The thoracic duct diameter was also measured in 14 control subjects (group 5). Results:When the thoracic duct diameter for the five groups was compared with analysis of variance, significance was p < 0.0001; by pairwise comparison, group 1 differed from the other four groups (p < 0.05). Thoracic duct dilation (5.61 mm) was seen in group 1 patients, whereas no dilation was present in groups 2 through 4. Additionally, thoracic duct diameter in 33 portal hypertensive and/or cirrhotic patients was significantly different from that in the 14 control subjects (p = 0.003). Conclusion:The thoracic duct can be reliably identified by EUS in patients with hepatic cirrhosis and portal hypertension. Dilation of the duct is seen only in patients with hepatic cirrhosis, ascites, and esophageal varices. No thoracic duct dilation is present in extrahepatic portal hypertension. Contrary to existing radiologic/surgical data, thoracic duct dilation is not seen in all patients with hepatic cirrhosis and portal hypertension signifying advanced disease. A dilated thoracic duct by endoscopic ultrasound should be considered yet another sign of portal hypertension. (Gastrointest Endosc 1998;48:588-92.)     

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.     

The prevalence and spectrum of colonic lesions in patients with cirrhotic and noncirrhotic portal hypertension

Portal hypertension diffusely affects the gastrointestinal tract. The frequency and profile of distinct colonic mucosal lesions (portal colopathy) and rectal varices (RV; veins >4 cm above the anal verge) is not well studied. Fifty consecutive patients with portal hypertension (25 with cirrhosis, 10 with noncirrhotic portal fibrosis [NCpf], and 15 with extrahepatic portal vein obstruction [EHPVO]) were assessed clinically and by upper and lower gastrointestinal (GI) endoscopy. Colorectal lesions were seen in 35 (70%) patients, significantly more often in bleeders than in nonbleeders. Rectal varices were detected in 22 (44%) patients; larger and more often seen in EHPVO (80%) than in cirrhosis (28%) and NCPF (30%) (P < .01) patients. Portal colopathy was seen in 26 (52%) patients, with nearly similar frequency in cirrhotics, NCPF, and EHPVO patients. Previous sclerotherapy or presence of gastric varices had little influence on the development of these lesions. An association (P < .01) was, however, seen between the presence of colopathy and portal gastropathy. Overt bleeding was seen in 8% and 4% of patients with RV and colopathy, respectively. In conclusion, our results demonstrate that colorectal lesions are present in about two thirds of patients with portal hypertension. Patients with portal hypertension and lower GI bleeding should be colonoscoped. Patients with extrahepatic portal vein obstruction may in turn benefit from baseline sigmoidoscopic examination to define the presence and size of rectal varices.     

Portal hypertensive colopathy

The aim of this paper was, first, to show in a case control study that in alcoholic cirrhotic patients colonic vascular ectasias (VE) are a complication of portal hypertension and, second, to establish in a histomorphometric study that colonic vascular ectasias and rectal varices (RV) are only endoscopic features of a new entity: portal hypertensive colopathy, the pathologic basis of which is colonic mucosal capillary ectasia. In the case control study, for each case, three age- and sex-matched controls selected from consecutive patients were used. Sixteen alcoholic cirrhotic patients, 12 men, 4 women (mean age ±sd: 62±10 years) had colonic vascular ectasias. The prevalence of esophageal varices (88% vs 44%,P<0.005), esophageal varices (5 mm) (44% vs 12.5%,P<0.01), previous history of bleeding from esophageal varices (44% vs 8%,P<0.005), and rectal varices (63% vs 6%,P<0.001) was significantly greater in cases with colonic vascular ectasias than in controls without colonic vascular ectasias. The relative risk of colonic vascular ectasias in alcoholic cirrhotic patients with esophageal varices versus cirrhotic patients without esophageal varices was 14.4 (95% confidence interval 2.8–75.3). In the histomorphometric study, cirrhotic patients with vascular ectasias and/or rectal varices had a significantly higher mean diameter of vessels (20.3±1.5 m vs 18.7±1.6 m,P<0.05) and a higher mean cross-sectional vascular area (2143±396 m² vs 1676±345 m²,P<0.05) than cirrhotic patients without vascular ectasias and/or rectal varices. These results suggest that colonic vascular ectasias seem to be a complication of portal hypertension and that colonic vascular ectasias and rectal varices are endoscopic features of a new entity the portal hypertensive colopathy.     

Factors influencing development of portal hypertensive gastropathy in patients with portal hypertension.

Portal hypertensive gastropathy (PGP) is an important cause of bleeding in portal hypertension patients. Although hyperdynamic congestion seems to be the underlying mechanism, the factors that influence the development of PGP are not understood. To investigate these, 107 patients [cirrhosis, 35; noncirrhotic portal fibrosis (NCPF), 24; extrahepatic portal vein obstruction (EHPVO), 46; Budd-Chiari syndrome, 2] were prospectively studied. Eighty-three patients had Child's A, 17 had Child's B, and 7 had Child's C liver disease. Before sclerotherapy, although intravariceal pressure was similar, 4 cirrhosis patients (3.7%) but no NCPF or EHPVO patients had PGP. After sclerotherapy, 21 additional patients (20.3%) developed PGP during a follow-up of 23.2 +/- 3.4 months (range, 1-52). The incidence of PGP was higher in cirrhotic patients (37.1%) than in NCPF (16.7%; P less than 0.05) or EHPVO (8.7%; P less than 0.01) patients. The probability of developing PGP among all patients at the end of 52 months of follow-up was 30%, more in cirrhosis than in EHPVO (55% vs. 15%; P less than 0.005). Only 2 patients bled from PGP during follow-up. Development of PGP correlated with severity of liver disease, being more common in Child's C than Child's A patients (87% vs. 13%; P less than 0.001). PGP was seen more often in patients with gastroesophageal varices than in patients with esophageal varices alone (42% vs. 11%; P less than 0.01). In conclusion, the results show that development of PGP is significantly influenced by sclerotherapy, severity of liver disease, etiology of portal hypertension, coexisting gastric varices and is not directly correlated with intravariceal pressure.     

Rectosigmoid Varices and Other Mucosal Changes in Patients with Portal Hypertension

A prospective study was performed to evaluate the prevalence of anorectal varices and their clinical significance as well as to study other proctosigmoidoscopic changes in 75 patients with portal hypertension of diverse etiology. Sixty-seven patients (89.3%) had lower gastrointestinal varices with no significant difference (p greater than 0.05) in prevalence between cirrhosis (92.1%), noncirrhotic portal fibrosis (87%), and extrahepatic portal venous obstruction (85.7%). The rectum was the most common site of lower gastrointestinal varices. External anal and sigmoid colonic varices almost always occurred in the presence of rectal and/or internal anal varices. There was no correlation between the presence of rectosigmoid varices and the severity of esophagogastric mucosal changes or portal hypertension. There was no suggestion that esophageal variceal sclerotherapy influenced the presence of anorectal varices. Seven patients (9.3%) had recent hematochezia, including three patients in whom it occurred in the absence of any upper gastrointestinal hemorrhage. Varices were the cause of bleeding in at least five patients. An abnormal mucosal vascular pattern in the form of telangiectasias or spiders was seen, irrespective of etiology of portal hypertension, in nine patients (12%). Hemorrhoids were present in 31 patients (41.3%) with an age-related difference (p less than 0.05) between patients with cirrhosis (55.3%) and extrahepatic portal venous obstruction (21.4%).     

Portal hypertension and portal hypertensive gastropathy in patients with liver cirrhosis: a haemodynamic study

BACKGROUND/AIM: The relationships between the levels of portal hypertension and the morphologic alterations of gastric mucosa in patients with liver cirrhosis--generally described as portal hypertensive gastropathy--are poorly defined. PATIENTS: In total, 62 patients with cirrhosis of different aetiologies, were examined by endoscopy and measurement of portal hypertension by hepatic venous pressure gradient. RESULTS: Portal hypertensive gastropathy was observed in 49 cases; six patients showed gastric antral vascular ectasia always associated with gastric lesions described as severe portal hypertensive gastropathy with different localizations. Hepatic venous pressure gradient showed severe portal hypertension in 37 cases, and averaged 17.7 +/- 4.3 mmHg. It was much higher in patients with severe lesions (p=0.0004). Hepatic venous pressure gradient in patients with endoscopic signs of isolated antral gastropathy was lower (p=0.04) than in those with isolated lesions in body-fundus. No relationship was found between hepatic function, as assessed by the Child-Pugh score, and portal hypertensive gastropathy. CONCLUSIONS: The present data suggest that the severity of portal hypertensive gastropathy is related to portal hypertension, but portal hypertension is not the sole determinant of the occurrence of endoscopic abnormalities of gastric mucosa. The derangement of liver function does not appear to play any role in the occurrence of portal hypertensive gastropathy.     

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.