Prognostic indicators in alcoholic cirrhotic men

The relationships between portal pressure, liver function and clinical variables on one hand and development of variceal hemorrhage and death on the other were investigated in 58 men with newly diagnosed alcoholic cirrhosis. Portal pressure was determined during hepatic vein catheterization as wedged minus free hepatic vein pressure, and median pressure was 14 mm Hg (range = 3 to 26 mm Hg). Fourteen of 31 patients (45%) had esophageal varices at upper gastrointestinal endoscopy (the size being considered large in nine patients). During follow-up (median = 31 months; range = 2 to 51 months), 12 patients (21%) developed variceal hemorrhage. Applying Cox's regression analysis, information about previous variceal bleeding (p = 0.0046), large varices at endoscopy (p = 0.012), hepatic vein pressure gradient (p = 0.0056) and indocyanine green clearance (p = 0.038) all contained significant prognostic information regarding development of variceal hemorrhage, even when easily obtained variables with known prognostic information were included [modified Child-Turcotte's criteria and incapacitation index (a weighted sum of days without normal health)]. During follow-up, 17 patients (29%) died. Applying Cox's regression analysis, large varices at endoscopy (p = 0.012) and hepatic vein pressure gradient (p = 0.019) contained significant prognostic information regarding death, in addition to the information contained in the modified Child-Turcotte's criteria and incapacitation index. In conclusion, prediction of prognosis in alcoholic cirrhotic men may be significantly improved by information about size of esophageal varices and level of portal pressure.     

Assessment of portal hypertension in humans

Patients suspected of having portal hypertension (either by clinical history, physical examination, or previous diagnosis) should undergo ultrasonography and upper gastrointestinal endoscopy. Ultrasonography, preferably using the duplex technique, can disclose the patency of the portal venous system, the presence of signs of portal hypertension (splenomegaly, portocollateral vessels, repermeabilization of the umbilical vein, and so forth) and provide additional information about liver, biliary, or pancreatic diseases that may be the cause of portal hypertension. Endoscopy can assess the presence and size of gastroesophageal varices, the appearance of the variceal wall, and the presence and severity of portal hypertensive gastropathy. Patients showing a patent portal vein should have hepatic vein catheterization to evaluate the presence of presinusoidal, sinusoidal, or postsinusoidal portal hypertension. Patients in whom presinusoidal portal hypertension is suspected (those having esophageal varices with an HVPG below 10 mm Hg) should have liver biopsy and percutaneous transhepatic measurement of portal pressure. In sinusoidal portal hypertension, the results of endoscopy and HVPG measurement are decisive for the therapeutic management of the patients. The authors' results indicate that, before starting prophylactic therapy with beta-blockers, all patients should undergo at least an hepatic vein catheterization to assess HVPG; it would be preferable to have a variceal pressure measurement also. These measurements must be repeated 3 to 4 weeks after the final dose of therapy has been reached to assess the risk of variceal bleeding or rebleeding.     

Predicting portal hypertension and variceal bleeding using non-invasive measurements of metabolic variables

Background & aim. This study assessed the involvement of metabolic factors (anthropometric indices, insulin resistance (IR) and adipocytokines) in the prediction of portal hypertension, esophageal varices and risk of variceal bleeding in cirrhotic patients.Material and methods. Two prospective and retrospective cohorts of cirrhotic patients were selected (n = 357). The first prospective cohort (n = 280) enrolled consecutively in three centers, underwent upper gastrointestinal endoscopy, seeking evidence of esophageal varices. Clinical, anthropometric, liver function tests, ultrasonographic, and metabolic features were recorded at the time of endoscopy, patients were followed-up every 6 months until death, liver transplantation or variceal bleeding. The second retrospective cohort (n = 48 patients) had measurements of the hepatic venous pressure gradient (HVPG). Statistical analyses of the data were with the SPSS package.Results. The presence of esophageal varices was independently associated with lower platelet count, raised HOMA index and adiponectin levels. This relationship extended to subset analysis in patients with Child A cirrhosis. HOMA index and adiponectin levels significantly correlated with HVPG. Beside Child-Pugh class, variceal size and glucagonemia, HOMA index but not adiponectin and leptin plasma levels were associated with higher risk of variceal bleeding.Conclusion. In patients with cirrhosis, HOMA score correlates with HVPG and independently predict clinical outcomes. Three simple markers i.e. platelet count, IR assessed by HOMA-IR and adiponectin significantly predict the presence of esophageal varices in cirrhotic patients.     

The hemodynamic response to medical treatment of portal hypertension as a predictor of clinical effectiveness in the primary prophylaxis of variceal bleeding in cirrhosis

In the prevention of variceal rebleeding, it is already established that hemodynamic response to drug treatment (decrease in hepatic venous pressure gradient [HVPG] to 12 mm Hg or by >20%) is predictive of clinical effectiveness. In primary prophylaxis very few clinical data are available. We assessed the role of the hemodynamic response to beta-blockers or beta-blockers plus nitrates in predicting clinical efficacy of prophylaxis. A total of 49 cirrhotic patients with varices at risk of bleeding, without prior variceal bleeding, were investigated by hepatic vein catheterization before and after 1 to 3 months of chronic treatment with nadolol or nadolol plus isosorbide mononitrate, and were followed during treatment for up to 5 years. A total of 30 patients (61%) were good hemodynamic responders, and among them in 12 (24%) HVPG was 相似文献   

Hepatic venous pressure gradient measurement: is it mandatory in the management of portal hypertension?

Abstract   Portal hypertension can be evaluated by hepatic vein catheterization and measurement of wedged and free hepatic vein pressures. The hepatic venous pressure gradient (HVPG) is the difference between both pressures and its normal value is lower than 5 mmHg. The technique is safe and reliable provided several requirements are fulfilled to get accurate results. HVPG measurement is useful to determine the site of increased resistance either presinusoidal, sinusoidal or postsinusoidal. If HVPG is normal in the presence of clinical signs of portal hypertension, evaluation of the portal venous system and direct measurement of portal vein pressure is required. HVPG measurement may also be used as a prognostic marker to evaluate the risks of developing complications such as ascites or variceal bleeding; in addition, it has been suggested that it could provide prognostic information for variceal rebleeding or survival. Primary and secondary prophylaxis of variceal bleeding can be achieved with a pharmacological treatment using beta blockers and/or nitrates. Repeated HVPG measurements are probably useful to monitor the treatment; it has been suggested that decreasing HVPG by 20% or below 12 mmHg is a reasonable target to define a good hemodynamic response and hopefully a low risk of bleeding; endoscopic therapy can be used in non-responders. Repeated hemodynamic evaluation, however, is invasive and must be performed in specialized liver units; therefore, future clinical trials must demonstrate unequivocally the clinical usefulness of this approach prior to recommending repeated HVPG measurement on a routine basis.     

Prognosis in patients with cirrhosis and mild portal hypertension

OBJECTIVE: Sixty to 70% of upper gastrointestinal bleeding episodes in patients with cirrhosis are caused by oesophageal varices. Prophylaxis is indicated in patients with varices and a hepatic venous pressure gradient (HVPG) above 12 mmHg. The study of the natural history of patients with lower HVPG has been sparse. In this study, long-term survival and the risk of complications in mild portal hypertension were analysed. MATERIAL AND METHODS: Sixty-one patients with cirrhosis and HVPG below 10 mmHg were included in the study. Data were collected from medical files and National Patient Registries. Variceal bleeding, hepatic encephalopathy and death related to cirrhosis were registered. Thirty-nine patients were graded as Child class A, 19 as class B and 3 as class C. Median survival time was 11 years. RESULTS: Twenty-eight patients (46%) developed one or more complications: variceal bleeding in 10 (16%) and hepatic encephalopathy in 18 patients (30%). Twenty-three patients (38%) died from complications of cirrhosis. Two patients (3%) died from variceal bleeding, another two (3%) from gastrointestinal bleeding of unidentified source. Survival rate was significantly decreased compared with that in the background population. CONCLUSIONS: The frequency of complications in patients with mild portal hypertension is considerable, and guidelines for follow-up or medical prophylaxis are warranted. The risk of bleeding from oesophageal varices is low and bleeding-related deaths rare.     

Portal pressure, presence of gastroesophageal varices and variceal bleeding

This study was performed to examine the relationships between portal pressure measurements and the presence of esophagogastric varices, the size of varices and the occurrence of hemorrhage from varices in 93 patients with alcoholic cirrhosis, using standardized measurements of portal pressure by hepatic vein catheterization. The mean hepatic vein pressure gradient (HVPG) was significantly higher in 49 patients who had bled from varices than in 44 cirrhotic patients who had not (20.4 +/- 5.1 vs. 16.0 +/- 5.2; p less than 0.001). None of the 49 patients who had bled from varices had an HVPG less than 12 mm Hg. Among the 87 patients who had been examined by endoscopy for varices, all 72 with varices had an HVPG greater than 12 mm Hg. Six of 15 cirrhotic patients without varices had HVPG less than 12 mm Hg. The mean HVPG in the 15 patients without varices (15.1 +/- 6.8 mm Hg) was lower than the 72 patients with varices (19.3 +/- 4.8 mm Hg; p less than 0.01). Of the 72 patients with varices, 40 had large varices, 28 had small varices, and in four patients variceal size could not be assessed adequately. The mean HVPG was similar in the patients with large or small varices (19.8 +/- 4.8 vs. 18.3 +/- 5.0 mm Hg; p greater than 0.10). There was a positive relationship between the presence of large varices and the occurrence of bleeding from varices.(ABSTRACT TRUNCATED AT 250 WORDS)     

Correlation of HVPG Level with CTP Score,MELD Score,Ascites, Size of Varices,and Etiology in Cirrhotic Patients

Background/Aim:

This study intends to determine the correlation of a patient''s hepatic venous pressure gradient (HVPG) measurement with six factors: Child–Turcotte–Pugh (CTP) score, model for end-stage liver disease (MELD) score, presence of ascites, size of varices, presence of variceal bleeding, and an etiology of cirrhosis. The study also aims to identify the predictors of higher HVPG measurements that can indirectly affect the prognosis of cirrhotic patients.

Patients and Methods:

Thirty patients diagnosed with cirrhosis were enrolled prospectively and each patient''s HVPG level was measured by the transjugular catheterization of the right or middle hepatic vein. The wedged hepatic venous pressure (WHVP) and free hepatic venous pressure (FHVP) were measured using a 7F balloon catheter. The HVPG level was calculated as the difference between the WHVP and FHVP measurements.

Results:

The mean HVPG level was higher in alcoholic than in nonalcoholic cirrhosis (19.5 ± 7.3 vs 15.2 ± 4.5 mm Hg, P = 0.13). The mean HVPG was also higher in bleeders compared with nonbleeders (18.5 ± 5.3 vs 10.7 ± 3.1 mmHg, P = 0.001). Patients with varices had a higher mean HVPG level than those without varices (17.4 ± 5.8 vs 11.7 ± 3.9 mmHg, P = 0.04). The difference among the three categories of varices (small, large, and no varices) was statistically significant (P = 0.03). In addition, the mean HVPG level was higher in patients with ascites than in those without ascites (18.7 ± 4.7 vs 11 ± 5.3 mmHg, P = 0.002), and it was significantly higher in patients in CTP class C (21.8 ± 5.5 mmHg) as compared with those in CTP class B (16.9 ± 2.9 mmHg) and CTP class A (10.5 ± 4.1 mmHg; P ≤ 0.001).

Conclusion:

HVPG levels were significantly higher in patients in CTP class C as compared with those in CTP classes A and B, thereby indicating that an HVPG measurement correlates with severity of liver disease. A high HVPG level signifies more severe liver disease and can predict the major complications of cirrhosis.     

Prognosis in patients with cirrhosis and mild portal hypertension

Objective. Sixty to 70% of upper gastrointestinal bleeding episodes in patients with cirrhosis are caused by oesophageal varices. Prophylaxis is indicated in patients with varices and a hepatic venous pressure gradient (HVPG) above 12 mmHg. The study of the natural history of patients with lower HVPG has been sparse. In this study, long-term survival and the risk of complications in mild portal hypertension were analysed. Material and methods. Sixty-one patients with cirrhosis and HVPG below 10 mmHg were included in the study. Data were collected from medical files and National Patient Registries. Variceal bleeding, hepatic encephalopathy and death related to cirrhosis were registered. Thirty-nine patients were graded as Child class A, 19 as class B and 3 as class C. Median survival time was 11 years. Results. Twenty-eight patients (46%) developed one or more complications: variceal bleeding in 10 (16%) and hepatic encephalopathy in 18 patients (30%). Twenty-three patients (38%) died from complications of cirrhosis. Two patients (3%) died from variceal bleeding, another two (3%) from gastrointestinal bleeding of unidentified source. Survival rate was significantly decreased compared with that in the background population. Conclusions. The frequency of complications in patients with mild portal hypertension is considerable, and guidelines for follow-up or medical prophylaxis are warranted. The risk of bleeding from oesophageal varices is low and bleeding-related deaths rare.     

Clinical significance and prediction factors of gastric varices in patients with hepatocellular carcinoma

BACKGROUND/AIMS: Hepatocellular carcinoma is part of the natural history of liver cirrhosis. Gastrointestinal bleeding and hepatic failure are the leading causes of death in hepatocellular carcinoma patients. With gastrointestinal bleeding, variceal bleeding is the most prominent, and most variceal bleeding is of esophageal origin. Gastric varices bleeding is often a massive and severe bleeding episode. The role of gastric varices among patients with hepatocellular carcinoma remains to be clarified. In this study, we aimed to evaluate the prevalence, clinical significance and prediction of gastric varices in patients with hepatocellular carcinoma. METHODOLOGY: From 1998 to 2000, we reviewed 304 patients with hepatocellular carcinoma receiving upper gastrointestinal endoscopic examinations. Patients' clinical characteristics, physical findings, laboratory data, image studies, endoscopic examinations and treatment were reviewed. RESULTS: Among 304 patients with HCC, twenty-one (6.9%) had gastric varices among 304 patients with hepatocellular carcinoma. The location of gastric varices were the posterior wall in 12 (57%), the lesser curvature in 1 (5%), the greater curvature in 4 (19%) and the fundus in 4 (19%). Three (14%) of these 21 patients with hepatocellular carcinoma and gastric varices had clinical evidence of bleeding. One of them died due to uncontrollable bleeding. Child-Pugh classification, hepatic encephalopathy, portal vein or splenic vein dilatation, ascites, splenomegaly, albumin level, prothrombin time and platelet count were significantly different between hepatocellular carcinoma patients with gastric varices and without gastric varices under the univariate analysis. Ascites (Odds ratio: 5.45; 95% confidence interval: 2.12-14.01) and portal vein or splenic vein dilatation (Odds ratio: 4.38; 95% confidence interval: 1.77-10.86) were the two most important predictors under the stepwise logistic regression analysis. CONCLUSIONS: The prevalence of gastric varices in patients with hepatocellular carcinoma is 6.9% and the risk of bleeding is low in this study. The Predictors of gastric varices among hepatocellular carcinoma are related to liver cirrhosis, Child-Pugh classification, hepatic encephalopathy, portal vein or splenic vein dilatation, ascites, splenomegaly, albumin level, prothrombin time and platelet count.     

Pharmacological reduction of portal pressure and long-term risk of first variceal bleeding in patients with cirrhosis

OBJECTIVES: A reduction in hepatic venous pressure gradient (HVPG) of > or =20% of baseline or to < or =12 mmHg (responders) is associated with a reduced risk of first variceal bleeding. The aim of this study was to evaluate whether this protective effect is maintained in the long term and if it extends to other portal hypertension complications. METHODS: Seventy-one cirrhotic patients with esophageal varices and without previous variceal bleeding who entered into a program of prophylactic pharmacological therapy and were followed for up to 8 yr were evaluated. All had two separate HVPG measurements, at baseline and after pharmacological therapy with propranolol +/- isosorbide mononitrate. RESULTS: Forty-six patients were nonresponders and 25 were responders. Eight-year cumulative probability of being free of first variceal bleeding was higher in responders than in nonresponders (90% vs 45%, p= 0.026). The lack of hemodynamic response and low platelet count were the only independent predictors of first variceal bleeding. Additionally, reduction of HVPG was independently associated with a decreased risk of spontaneous bacterial peritonitis (SBP) or bacteremia. No significant differences in the development of ascites, hepatic encephalopathy, or survival were observed. CONCLUSIONS: The hemodynamic response in cirrhotic patients is associated with a sustained reduction in the risk of first variceal bleeding over a long-term follow-up. Reduction of HVPG also correlate with a reduced risk of SBP or bacteremia.     

Splanchnic hemodynamics in cirrhotic patients with esophageal varices and gastrointestinal bleeding.

Twenty cirrhotic patients with esophageal varices and an episode of gastrointestinal bleeding within the previous week underwent hemodynamic studies which used an indicator dilution technique based on selective catheterization of the splanchnic arteries and hepatic vein. Portasystemic shunting of splenic arterial flow averaged 95% (range 80 to 100%) in 17 patients with proved variceal bleeding, but only 8% in 3 who bled from another site. Superior mesenteric shunting averaged 70% (range 27 to 100%) in those who bled from varices, and no shunting was detectable in the nonvariceal bleeders. In at least 4 patients shunting was essentially complete from both beds. In 11 others, however, more than one-third of mesenteric flow still perfused the liver. The pressure gradient from the wedge to free position in the hepatic vein and the hepatic blood flow bore no relationship to the degree of shunting. These data indicated the variability of the splanchnic hemodynamic pattern that may exist in alcoholic patients with esophageal varices. If hemodynamic factors are important in determining the response to surgery, indicator dilution studies to quantitate portasystemic shunting may be a vital part of preoperative evaluation.     

Endoscopic, Ultrasonographic, and US-Doppler Parameters as Indicators of Variceal Bleeding in Patients with Schistosomiasis

Bleeding from esophagogastric varices is a potentially deadly complication in patients with hepatosplenic schistosomiasis. The aim of this study is to establish indicators of variceal bleeding. We studied 40 patients with compensated hepatosplenic schistosomiasis and varices, analyzing four endoscopic (variceal size, red color signs, fundic varices, and congestive gastropathy), nine ultrasonographic (right and left hepatic lobe size, periportal and gallbladder wall thickness, portal and splenic veins diameter, spleen longitudinal axis and volume, and presence of collateral circulation), and five US-Doppler parameters (portal and splenic veins velocity and flow and portal vein congestion index). Patients were divided in two groups according to previous history of variceal bleeding. The group with bleeding episodes was again divided in two groups: with and without treatment, namely endoscopic sclerotherapy. All endoscopic parameters and two ultrasonographic (periportal thickness and portal vein diameter) were statistically different between the groups with and without previous bleeding. The likelihood index, adopted to determine the best parameters related to previous bleeding showed that the most important combinations are: gastropathy and red signs followed by portal vein diameter and variceal size. In conclusion, although aware of the limits of the statistical analysis due to the small number of patients, our results demonstrated that endoscopic and US parameters (isolated or combined) can identify patients with a high risk of variceal bleeding, allowing physicians to optimize prophylactic therapy.     

Aminopyrine breath test in the prognostic evaluation of patients with cirrhosis.

This prospective study assessed the role of aminopyrine breath test in the prognosis of patients with cirrhosis, and evaluated whether the test provided useful information not included in the Pugh score. During a period of 36 months, 125 patients with biopsy proven liver cirrhosis were included, and followed for up to 48 months (median 17 months). During follow up 43 patients died (20 of liver failure). Survival was univariately related to aminopyrine breath test (p less than 0.02), Pugh score (p less than 0.01), presence of ascites (p less than 0.01), and sex (p less than 0.05). Using Cox's regression analysis, Pugh score, aminopyrine breath test, and sex, were independent significant predictors of survival. From the Cox's model a prognostic index was computed. According to a receiver operating characteristic curve analysis, the prognostic index predicting death showed an improvement in area under the curve when compared with a prognostic index calculated excluding aminopyrine breath test, but the improvement did not reach statistical significance (p = 0.12). A similar prognostic index was calculated to predict death from liver failure. Cox's regression analysis selected aminopyrine breath test, Pugh score, and aetiology as the best set of predictor covariates. According to a receiver operating characteristic curve analysis, a prognostic index cut off value of 2.6 had a 94% sensitivity and a 88% specificity. The prognostic index significantly improved prognostic accuracy when compared with a prognostic index calculated from Pugh score and aetiology, but excluding aminopyrine breath test (p = 0.05). These data disclose that the aminopyrine breath test offers additional prognostic information to the Pugh score, and the prognosis of patients with cirrhosis.     

基于诺模图模型预测内镜下治疗肝硬化胃静脉曲张的疗效

目的通过诺模图(Nomogram)模型预测内镜下组织黏合剂治疗肝硬化患者胃静脉曲张的疗效。方法选择2014年8月至2017年9月因肝硬化食管胃底静脉曲张破裂出血至复旦大学附属中山医院就诊且接受内镜下组织黏合剂治疗的158例患者。随访12个月,主要结局指标为再出血。分析肝硬化胃静脉曲张内镜下治疗后再出血的影响因素。构建诺模图模型,比较其与Child分级、计算机体层摄影血管造影(CTA)和肝静脉压力梯度(HVPG)预测肝硬化胃静脉曲张内镜下治疗后再出血的准确性。统计学分析采用单因素和多因素Cox回归分析,以及Kaplan-Meier曲线和log-rank检验。结果随访中,在内镜下治疗后2、6和12个月分别出现再出血18例(11.4%)、37例(23.4%)和49例(31.0%)。单因素Cox回归分析结果显示,性别、酒精性肝硬化、糖尿病、Child-Pugh分级(A级与B或C级)、CTA腔外血管(有与无)、HVPG(<16 mmHg与≥16 mmHg,1 mmHg=0.133 kPa)、门脉系统广泛栓塞、食管静脉曲张、食管胃静脉曲张2型、组织黏合剂注射点(≤3点与>3点)和组织黏合剂注射量(≤3 mL与>3 mL)均为胃静脉曲张内镜下治疗后再出血的影响因素(HR=0.575、2.018、1.562、3.433、2.945、1.859、2.743、0.324、1.840、1.477、1.716,95%CI 0.305~1.084、0.902~4.514、0.814~2.792、1.753~6.724、1.663~5.217、1.012~3.415、0.852~8.830、0.079~1.335、1.012~3.317、0.839~2.602、0.935~3.152,P均<0.2)。多因素Cox回归分析结果显示,Child-Pugh分级、CTA腔外血管和HVPG均为胃静脉曲张内镜下治疗后再出血的独立危险因素(HR=2.665、2.886、2.095,95%CI 1.339~5.300、1.580~5.271、1.099~3.995,P均<0.05)。Kaplan-Meier曲线显示,Child-Pugh分级(A级与B或C级)、CTA腔外血管(有与无)和HVPG(<16 mmHg与≥16 mmHg)均能有效预测胃静脉曲张内镜下治疗后1年累积未再出血率,差异均有统计学意义(P均<0.05)。ROC曲线分析显示,联合Child-Pugh分级、CTA腔外血管和HVPG(<16 mmHg与≥16 mmHg)的模型可能比Child-Pugh分级和HVPG有更好的预测价值(AUC=0.746、0.673和0.585,95%CI 0.662~0.829、0.583~0.762和0.486~0.683,P<0.01、P=0.001、P=0.089)。根据诺模图评分的下四分位数和上四分位数将患者分为低、中、高危组,结果显示诺模图可以有效区分胃静脉曲张内镜下治疗后再出血的高危人群,差异有统计学意义(P<0.01)。结论CTA腔外血管、HVPG和Child-Pugh分级是肝硬化胃静脉曲张内镜下治疗疗效的独立预测指标,基于此3项指标建立的诺模图模型的预测准确性可能优于Child-Pugh分级和HVPG。     

Correlation of hepatic venous pressure gradient with variceal bleeding, size of esophageal varices, etiology, ascites and degree of liver dysfunction in cirrhosis of liver

An elevated hepatic venous pressure gradient (HVPG) has been associated with risk of variceal bleeding, and outcome and survival after variceal bleeding. In this pilot study, we measured HVPG in 40 patients with liver cirrhosis and studied its relationship with etiology of liver disease, esophageal variceal size, history of variceal bleeding or ascites, biochemical liver tests and Child-Pugh class. There was no procedurerelated complication. The mean (SD) HVPG was similar in patients who had history of variceal bleeding as compared to those who did not (15.4 [2.8] mmHg vs. 13.9 [2.7] mmHg, p=0.1); HVPG had no significant association with etiology of cirrhosis (p=0.4). HVPG levels were significantly higher in patients with larger esophageal varices (grade III/IV vs. I/II: 15.2 [2.7] mmHg vs.13.1 [2.8] mmHg, p=0.04), poorer Child-Pugh class (B or C versus A), and presence of ascites (p=0.04). Thus, HVPG correlated with variceal size, Child-Pugh class, and presence of ascites, but not with variceal bleeding status.     

A cost-effectiveness study of hepatic venous pressure gradient measurement in the secondary prevention of variceal bleeding

OBJECTIVE: variceal rebleeding is common following a first episode of hemorrhage in cirrhotic patients. The objective of this study was to determine the cost-effectiveness of monitoring hepatic venous pressure gradient (HVPG) to guide secondary prophylaxis. METHODS: we created a Markov decision model to calculate cost-effectiveness for two strategies: Group 1: HVPG monitoring to decide treatment -when portal pressure was reduced by at least 20 percent or HVPG was less than 12 mmHg after beta-blocker administration, patients received beta-blockers; when portal pressure did not meet these criteria therapy was endoscopic band ligation. Group 2: in this group there was no monitoring of HVPG. Patients with large varices received treatment with beta-blockers combined with EBL; patients with small varices received beta-blockers plus isosorbide mononitrate. RESULTS: there was no recurrent variceal bleeding in group 1 for good responders, and for 17% of poor responders. In group 2 a 25% rebleeding rate was detected in patients with small varices and 13% for those with big varices. Overall cost in group 1 was 14,100.49 euros, and 14,677.16 in group 2. CONCLUSIONS: HVPG measurement is cost-effective for the secondary prophylaxis of variceal bleeding.     

Somatostatin treatment and risk stratification by continuous portal pressure monitoring during acute variceal bleeding.

BACKGROUND AND AIMS: During acute variceal bleeding, several factors may lead to elevations of hepatic venous pressure gradient (HVPG), which may precipitate further hemorrhage. Whether somatostatin can suppress these increments is unknown. This study monitored somatostatin effects on HVPG during acute bleeding and assessed whether the changes affect outcome. METHODS: In 40 patients with acute variceal bleeding treated with sclerotherapy, a catheter was placed into a main hepatic vein for 24-hour serial measurements of HVPG. After baseline measurements, patients received somatostatin (N = 25) or placebo (N = 15) under double blind conditions. RESULTS: Somatostatin but not placebo produced a sustained decrease in HVPG (from 20.7 +/- 3.7 mm Hg to 17.7 +/- 2.7, P < 0.01). In patients receiving placebo, HVPG increased after a test meal (P = 0.018) and after blood transfusion (P = 0.034). Somatostatin completely prevented these increments. HVPG decreased significantly only in patients without further bleeding. One of 27 patients with HVPG <20 mm Hg at baseline or decreased >10% rebled vs. 9 of 13 who had neither of these 2 criteria (P < 0.0001). Both criteria had independent prognostic value for further bleeding. CONCLUSIONS: During acute variceal bleeding, somatostatin produces a significant and sustained decrease in HVPG and prevents secondary elevations. Monitoring HVPG may stratify further bleeding risk and discriminate treatment response.     

Transhepatic Embolisation of Gastro-oesophageal Varices in the Management of Variceal Haemorrhage

Summary The difficulty of controlling variceal haemorrhage has led to the recent development of methods designed to sclerose the bleeding vessels. This study describes the application of percutaneous transhepatic portal catheterization with emboiisation and sclerosis of varices in eight consecutive patients admitted with bleeding oesophago-gastric varices. Portal hypertension was documented and varices demonstrated in each case. Bleeding ceased rapidly in seven patients, two patients rebled 1–3 weeks after the procedure, and five patients were subsequently discharged from hospital. In no instance was death related to continued gastrointestinal haemorrhage. Initial experience with transhepatic embolisation of bleeding oesophago-gastric varices indicates that this technique is effective in controlling variceal haemorrhage.     

Evaluation of portal hypertension in the cirrhotic patient: hepatic vein pressure gradient and beyond

Portal hypertension (PH) is a major complication of liver cirrhosis, as it predisposes to the development of serious clinical manifestations such as ascites, hepatic encephalopathy and variceal bleeding. Till now, the measurement of hepatic vein pressure gradient (HVPG) is the gold standard method to ascertain the presence and significance of PH, as many studies have shown its correlation with the appearance of varices and the possibility of variceal bleeding. However, the invasiveness of this procedure makes it difficult to be used in daily clinical practice. Several noninvasive methods with adequate capability of evaluating liver fibrosis, including elastographic techniques, are currently used as alternatives to HVPG in order to assess the presence and the severity of PH. The aim of this paper is to express an overview of the literature about the actual role of HVPG and all available noninvasive tests on the prediction of development of PH complications, to highlight their advantages and their potential limitations, and to provide the latest trends on clinical practice.