The effects of transjugular intrahepatic portosystemic shunt on portal hypertensive gastropathy

In addition to variceal bleeding, haematemesis may occur due to haemorrhagic gastritis in patients with portal hypertension. This has been known as portal hypertensive gastropathy (PHG). We have evaluated the effects of the transjugular intrahepatic portosystemic shunt (TIPS) on portal venous pressure (PVP) and endoscopic gastric mucosal changes observed in patients with portal hypertension. We performed TIPS in 12 patients with complications due to portal hypertension as follows: variceal bleeding in nine patients (bleeding from oesophageal varices in seven and gastric varices in two), refractory ascites in three and haemorrhage from severe PHG in one. Endoscopic examinations were performed before and after TIPS for all patients. Changes of PVP and gastric mucosal findings on endoscopy were analysed. Before TIPS, PHG was seen in 10 patients. Portal venous pressure decreased from an average of 25.1 ± 8.8 to 17.1 ± 6.2 mmHg after TIPS ( P < 0.005). On endoscopy, PHG improved in nine of 10 patients. Oesophagogastric varices improved in eight of 11 patients. In one patient with massive haematemesis, haemorrhage from severe PHG completely stopped after TIPS. Because TIPS effectively reduced PVP, this procedure appeared to be effective for the treatment of uncontrollable PHG.     

内镜下聚桂醇治疗食管静脉曲张对门脉高压性胃病的影响

[目的]探讨内镜下聚桂醇治疗食管静脉曲张对门脉高压性胃病(PHG)的影响.[方法]对连续100例门脉高压食管静脉曲张出血后接受内镜下硬化剂聚桂醇治疗的患者开展临床随访研究,评估聚桂醇治疗后对PHG的影响.[结果]注射聚桂醇前33例患者存有PHG(33％);初次注射聚桂醇治疗后PHG患者为74例,其中新增轻度PHG患者41例;2次及以上注射聚桂醇治疗后PHG患者达88例,经注射聚桂醇后PHG发生率明显增高(P＜0.01).注射聚桂醇的次数与PHG的发生相关(P＜0.01).[结论]内镜下硬化剂聚桂醇治疗术(EIS)治疗食管静脉曲张,在控制出血和消退曲张静脉的同时,具有产生和加重PHG的可能,但大多为轻度PHG.患者经硬化剂治疗后控制出血,全身状况好转后应择期手术治疗或长期应用降门脉压药物,控制和改善PHG,预防食管静脉曲张和PHG出血.     

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。     

Effect of transjugular intrahepatic portosystemic shunt formation on portal hypertensive gastropathy and gastric circulation

OBJECTIVES: The aim of this study was to investigate the effect of a transjugular intrahepatic portosystemic shunt (TIPS) on portal hypertensive gastropathy (PHG) and gastric hemodynamics. METHODS: A total of 16 patients with cirrhosis and portal hypertensive gastropathy were prospectively studied. Of these, 12 patients underwent TIPS for esophageal varices and four for refractory ascites. Gastric mucosal blood flow (GMBF) was assessed by laser Doppler flowmeter, and total blood flow (TBF) in submucosa and mucosa by near-infrared endoscopy. Portal venous pressure was obtained by a transducer during the TIPS procedure. The severity of portal hypertensive gastropathy was classified as none, mild, or severe. The examinations were performed before and 2 wk after the procedure. RESULTS: TIPS significantly reduced portal venous pressure. PHG improved in all four patients with severe PHG and in five of 12 patients with mild PHG after treatment. Gastric mucosal blood flow increased from 49.0 to 55.6 ml/min/100 g after TIPS. In contrast, TBF decreased from 0.35/s to 0.27/s after treatment. Liver function tests showed no significant changes before and after the procedure. CONCLUSIONS: It is considered that TIPS may have a beneficial effect on PHG at least for a short time. The mechanism by which PHG improves may be closely related to the improvement of the injured gastric perfusion in cirrhotic patients with PHG.     

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.     

肝硬化门静脉高压性胃病的胃镜表现及相关因素分析

目的探讨门静脉高压性胃病(PHG)胃镜下胃黏膜特征及其与食管胃静脉曲张、溃疡病及肝硬化并发症之间的关系。方法回顾性分析2012年8月-2018年6月陆军军医大学大坪医院867例肝硬化患者临床资料,统计其胃镜下食管胃静脉曲张、PHG、溃疡病发生的情况,收集肝硬化并发自发性细菌性腹膜炎、肝性脑病、原发性肝癌的数据资料。计数资料组间比较采用χ2检验,相关性分析采用Spearman相关性检验。结果肝硬化患者PHG发生率高达66.2%(574/867),轻度PHG胃黏膜改变以红点灶(68.6%)和蛇皮征(56.8%)为主,而重度PHG以弥漫红斑为主(76.5%)。PHG在不同程度的食管静脉曲张中发生率差异显著(χ2=304.712,P<0.05),并且随着食管静脉曲张加重,PHG程度亦越来越重(r=0.515,P<0.05)。不同程度胃静脉曲张的患者PHG发生率差异有统计学意义(χ2=81.004,P<0.05),且PHG程度与胃静脉曲张程度相关(r=0.292,P<0.05)。不同部位静脉曲张患者PHG的发生率差异显著(χ2=41.361,P<0.05),当患者仅出现胃静脉曲张时,PHG发生率(34.8%)最低,且均为轻度;而食管和胃均出现静脉曲张时,PHG发生率(85.6%)最高。未合并PHG患者中有71例(24.2%)因呕血和(或)黑便就诊住院,而574例PHG患者中有316例(55.1%)因此而住院,二者差异显著(χ2=74.562,P<0.05)。结论不同PHG严重程度的患者胃黏膜特征差异显著,PHG的发生和严重程度与食管胃静脉曲张程度密切相关,且是肝硬化消化道出血重要原因,应积极治疗和预防PHG以降低消化道出血风险和相关并发症。     

Natural history of portal hypertensive gastropathy in patients with liver cirrhosis. The New Italian Endoscopic Club for the study and treatment of esophageal varices (NIEC)

BACKGROUND & AIMS: The clinical importance of portal hypertensive gastropathy (PHG) as a source of gastrointestinal bleeding in patients with cirrhosis is poorly defined. We investigated the natural history of this condition in a large series of patients. METHODS: All patients with cirrhosis seen at 7 hospitals during June and July 1992 were followed up with clinical and endoscopic examinations every 6 months for up to 3 years. Gastropathy was classified according to the classification of the New Italian Endoscopic Club. RESULTS: The prevalence of gastropathy was 80% and was correlated with the duration of disease, presence and size of esophagogastric varices, and a previous history of endoscopic variceal sclerotherapy. During 18+/-8 months of follow-up, gastropathy was stable in 29% of patients, deteriorated in 23%, improved in 23%, and fluctuated with time in 25%. The evolution of gastropathy with time was identical in patients with and without previous or current sclerotherapy. Acute bleeding from gastropathy occurred in 8 of 315 patients (2.5%). The bleeding-related mortality rate was 12.5%. Chronic bleeding occurred in 34 patients (10.8%). CONCLUSIONS: PHG is common in patients with cirrhosis, and its prevalence parallels the severity of portal hypertension. Gastropathy can progress from mild to severe and vice versa or even disappear completely. Bleeding from this lesion is relatively uncommon and rarely severe. Sclerotherapy of esophageal varices does not seem to influence the natural history of this condition.     

门脉高压性胃病临床研究进展

肝硬化患者常常发生门脉高压症,继发胃肠道血流动力学和黏膜改变,导致门脉高压性胃病（PHG）。近年来,PHG引起的上消化道出血逐渐受到重视,在肝硬化上消化道出血病因中仅次于食管胃静脉曲张破裂出血,对其研究也越来越多。     

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。     

Effects of Esophageal Varice Eradication on Portal Hypertensive Gastropathy and Fundal Varices: A Retrospective and Comparative Study

Esophageal varice eradication results in gastric hemodynamic changes. The aim of this study was to detect the influence of variceal eradication on portal hypertensive gastropathy (PHG) and fundal varices and to compare the results of two therapeutic methods (endoscopic variceal ligation and endoscopic sclerotherapy). A total of 114 consecutive patients with cirrhosis and portal hypertension who underwent elective endoscopic variceal ligation (EVL) (85 patients) or endoscopic sclerotherapy (EST) (29 patients) for obliteration of esophageal varices were selected for this study. Both groups were compared for PHG and fundal varice formation before and after eradication. Fifty-eight (68.2%) patients in the EVL and 18 (62.1%) patients in the EST group had PHG before esophageal varice eradication (P > 0.05). PHG grade after eradication of esophageal varices by both EVL and EST was significantly higher compared to pre-eradication. PHG grade and aggregation were similar in both groups. Thirty-seven patients (34 F₁, 3 F₂) in the EVL group and 13 patients (10 F₁, 3 F₂) in the EST group had fundal varices before variceal eradication (P > 0.05). Fundal varices were detected in 46 (35 F₁, 11F₂) and 19 (11F₁, 8F₂) patients in the EVL and EST groups after eradication, respectively. There was a statistically significant increment in occurrence of fundal varices after eradication with EVL and EST groups. There was no significant difference regarding fundal varice development after esophageal variceal eradication in both groups. After varical eradication, PHG was found in 57 (87.7%) and 39 (79.6%) patients with and without fundal varices, respectively (P > 0.05). Esophageal eradication with EVL and EST increases both the incidence and the severity of PHG and fundal varice formation. Both methods have comparable influences on PHG and fundal varices.     

Prevalence of portal hypertensive duodenopathy in cirrhosis: clinical and haemodynamic features

OBJECTIVES: To estimate the prevalence of portal hypertensive duodenopathy (PHD) in patients with cirrhosis and portal hypertension, and to evaluate its relationship with clinical and haemodynamic parameters. PATIENTS AND METHODS: Endoscopy reports and clinical history of 549 consecutive patients with cirrhosis and portal hypertension were evaluated retrospectively. A diagnosis of PHD was obtained in those patients with a congestive vascular pattern of the duodenum. RESULTS: PHD was found in 46 patients (8.4%). Previous endoscopic band ligation and coexistence of severe gastropathy were significantly more frequent in PHD group. Systemic and hepatic haemodynamic evaluations were performed in 20 patients with PHD and 160 without PHD: the mean hepatic venous pressure gradient was higher in those cases with PHD (22.5 (5.4) vs. 19.8 (5.5) mmHg, P=0.045). Hypertensive colopathy was found in seven out of the 10 patients with PHD and a colonoscopic evaluation. In five of six patients PHD disappeared after liver transplant. CONCLUSIONS: PHD is an uncommon finding of portal hypertension in cirrhotic patients. It is associated with previous endoscopic band ligation, to manifestations of portal hypertension in other sites of the gastrointestinal tract and to greater values of hepatic venous pressure gradient. The clinical relevance of this syndrome remains to be determined.     

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.     

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.     

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.     

Effects of endoscopic injection sclerotherapy on portal hypertensive gastropathy: a prospective study.

The effect of endoscopic injection sclerotherapy (EIS) for esophageal varices on portal hypertensive gastropathy (PHG) was investigated in 137 patients who underwent EIS from July 1987 to March 1990. Two groups, PHG(+) (N = 35) and PHG(-) (N = 102) were distinguished by endoscopic findings obtained before EIS. PHG was classified into four grades by endoscopy scored as 0, 1, 2, or 3. The PHG score significantly worsened after EIS (p < 0.01), and PHG became worse 6 to 9 months after the eradication of varices followed by gradual improvement. Recurrent small veins, which required additional EIS, appeared more frequently in the PHG(+) group (p < 0.05). New gastric varices appeared or gastric varices enlarged after EIS more frequently in the PHG(+) group (7 patients, 20.0%) than in the PHG(-) group (12 patients, 11.8%), but this was not statistically significant. Thus, frequent endoscopy after EIS is needed with special attention directed to development of PHG and gastric varices, especially for patients with PHG prior to treatment.     

Endoscopic Evaluation of Rectal Mucosal Reddening in Patients with Liver Cirrhosis

Background: Colonic mucosal lesions observed in patients with portal hypertension have been reported as portal hypertensive colopathy. We studied the rectal mucosa in patients with liver cirrhosis to evaluate the prevalence of mucosal reddening which looks like gastric red spots in the portal hypertensive gastropathy and to determine whether there is a correlation between this lesion and portal hypertension or the severity of liver disease. Methods: Seventy‐two patients with liver cirrhosis and 50 control subjects were examined. Colonoscopy was performed to evaluate the presence of mucosal reddening in the rectum. We investigated the relations between rectal mucosal reddening and esophageal varices, portal hypertensive gastropathy and the severity of liver cirrhosis. Results: Rectal mucosal reddening was observed in eight of 72 patients with liver cirrhosis but in none of the 50 control subjects; its prevalence in cirrhosis patients was significantly higher than that in the control subjects (P < 0.05). Cirrhosis patients with esophageal varices were more likely to have rectal mucosal reddening than cirrhosis patients without esophageal varices (P < 0.05). In addition, the occurrence of rectal mucosal reddening correlated with the severity of cirrhosis, based on Child–Pugh's classification (P < 0.05). Conclusion: We have shown that rectal mucosal reddening develops in patients with liver cirrhosis and is associated with the existence of esophageal varices and the severity of liver cirrhosis. These results suggest the possibility that portal hypertension and impaired liver function may play an important role in the pathogenesis of rectal mucosal reddening in patients with cirrhosis.     

Effect of laparoscopic splenectomy on portal hypertensive gastropathy in cirrhotic patients with portal hypertension

Aim:  This study investigated the relationship between portal hypertensive gastropathy (PHG) and splenomegaly, and the effect of laparoscopic splenectomy on PHG in cirrhotic patients with portal hypertension.
Methods:  Seventy patients with liver cirrhosis and portal hypertension were prospectively studied. Indication for laparoscopic splenectomy was bleeding tendency in 10 patients, induction of interferon in 45, treatment of hepatocellular carcinoma in seven, and treatment for endoscopic injection sclerotherapy-resistant esophagogastric varices in eight. The severity of PHG was classified into none, mild, or severe according to the classification by McCormack et al. The severity of liver disease was classified using the Child–Pugh score. All patients underwent upper gastrointestinal endoscopy before and 1 month after the operation.
Results:  The prevalence of PHG was significantly correlated with the severity of liver disease using the Child–Pugh score. The severity of PHG was significantly correlated with the resected spleen volume. One month after the operation, PHG was improved in 16 of 17 patients with severe PHG and in 12 of 32 with mild PHG. The Child–Pugh score showed a significant improvement (6.8 ± 1.4 to 6.2 ± 1.2) at 3 months after laparoscopic splenectomy ( P  < 0.0001).
Conclusions:  PHG may be associated with splenomegaly, and laparoscopic splenectomy may have a beneficial effect on PHG, at least for a short time.     

Small bowel capsule endoscopy and portal hypertensive enteropathy in cirrhotic patients: results from a tertiary referral centre

Background and rationale. Portal hypertensive enteropathy (PHE) remains difficult to diagnose in patients with cirrhosis and portal hypertension. Limited test choices exist for the inspection of the small bowel in these patients. Small bowel capsule endoscopy (SBCE) is ideal in this situation but rarely performed. We aimed to determine the prevalence of PHE using SBCE in a cirrhotic patient population and correlate its presence with clinical and CT imaging findings.Material and methods. We retrospectively analysed data from cirrhotic patients who underwent SBCE at our unit. Studies were evaluated for the presence of cirrhosis-related findings in the oesophagus, stomach and small-bowel. The relationships between PHE and patients’ clinical characteristics were evaluated.Results. 53 patients with cirrhosis underwent SCBE. We used PillCam®SB on 36 patients and MiroCam® capsule on 17. Thirty patients were referred for iron deficiency anaemia, 15 for obscure gastrointestinal bleeding, and 4 for other indications. Four data sets were not available for review, leaving 49 patients. Mean age was 61.19 ± 14.54 years (M/F = 27/22). Six SBCE examinations were incomplete. Thirty three patients had evidence of portal hypertensive gastropathy (PHG) and 17 had evidence of oesophageal varices. In total, 29 patients had SCBE evidence of PHE (57%). 28/29 (96.5%) patients with PHE had also evidence of PHG. 13/17 (76.4%) patients with oesophageal varices had also evidence of PHE.Conclusions. The prevalence of PHE in our study was 57%. SBCE is a useful tool in evaluating PHE in cirrhotic patients irrespective of aetiology.     

Role of extravariceal collateral channels in the development of portal-hypertensive gastropathy before and after sclerotherapy

We investigated whether extravariceal collateral pattern contributed to the development of portal-hypertensive gastropathy (PHG) before and after sclerotherapy. Ninety-nine patients with cirrhosis and large esophageal varices were examined in this retrospective study. They were divided into four groups according to transhepatic portographic findings: group A (with neither paraesophageal veins nor gastrorenal shunt; n = 46), group B (with paraesophageal veins; n = 27), group C (with gastrorenal shunt; n = 14), and group D (with paraesophageal veins and gastrorenal shunt; n = 12). To assess PHG, endoscopic examinations were carried out before and 1 week and 1 month after sclerotherapy. The severity of PHG was classified according to a modified McCormack's classification and scored as: absence, 0; mild, 1; severe, 2. There were no significant differences in age, sex, cause of cirrhosis, severity of liver dysfunction, and extent of esophageal varices in the four groups. The PHG score before sclerotherapy was significantly higher in group A than in either group C (P < 0.05) or group D patients (P < 0.05). The calculated, integrated incremental change in PHG score after sclerotherapy was significantly higher in group A than in group C (P < 0.01) and group D patients (P < 0.01). Although the integrated change in PHG score was lower in group B than in group A patients, the difference was not significant (P = 0.68). These results suggest that gastrorenal shunt, but not paraesophageal veins, may play a protective role in the development of PHG before and after sclerotherapy. (Received Mar. 10, 1997; accepted July 25, 1997)     

Does the measurement of portal flow velocity have any value in the identification of patients with cirrhosis at risk of digestive bleeding?

Abstract: Upper gastrointestinal bleeding is a leading cause of death in patients with liver cirrhosis. In most cases haemorrhage originates from oesophageal varices or from congestive gastropathy, and the evaluation of the bleeding risk is based on oesophagogastroduodenoscopic data. The aim of this prospective study was to determine whether the measurement of portal flow velocity by Duplex-Doppler, compared with endoscopic data, can help in detecting patients with cirrhosis at risk of bleeding. One hundred and seventy-three patients underwent endoscopy to ascertain the size of the varices and the severity of congestive gastropathy. For each patient maximal portal flow velocity measurements were obtained. No difference in portal flow velocity was observed between patients with or without oesophageal varices or congestive gastropathy. During a 2-year observation period, 27 patients (15.6%) had at least one episode of acute digestive bleeding. Stepwise multiple logistic regression analysis demonstrated a correlation between oesophageal varices and congestive gastropathy endoscopic grading and the incidence of bleeding; only the former was entered into the final regression equation (p>0.001). No relationship between the max portal flow velocity value and incidence of bleeding was found. This study shows that portal flow velocity is unrelated to the degree of the endoscopic abnormalities in patients with liver cirrhosis and that it has no value in the identification of patients with cirrhosis at risk of upper gastrointestinal bleeding.