***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: This guidance provides a data -supported approach to risk stratification , diagnosis , and management of patients with cirrhosis and portal hypertension ( PH ) . A guidance document is different from a guideline . Guidelines are developed by a multidisciplinary panel of experts who rate the quality ( level ) of the evidence and the strength of each recommendation using the Grading of Recommendations Assessment , Development , and Evaluation system . A guidance document is developed by a panel of experts in the topic , and guidance statements , not recommendations , are put forward to help clinicians underst and and implement the most recent evidence . This guidance focuses on PH , varices , and variceal hemorrhage ( VH ) , and statements are based on the following : ( 1 ) review of the recent literature using PubMed , giving more weight to large , well- design ed , prospect i ve trials and well-performed meta-analyses ; ( 2 ) several consensus conferences among experts ; and ( 3 ) the authors ’ years of experience caring for patients with cirrhosis and varices . Management of ascites and encephalopathy is addressed in other documents Abstract Portal vein thrombosis may occur in cirrhosis ; nevertheless , its prevalence , and predictors are still elusive . To investigate this issue , the Italian Society of Internal Medicine undertook the “ Portal vein thrombosis Relevance On Liver cirrhosis : Italian Venous thrombotic Events Registry ” ( PRO-LIVER ) . This prospect i ve multicenter study includes consecutive cirrhotic patients undergoing Doppler ultrasound examination of the portal area to evaluate the prevalence and incidence of portal vein thrombosis over a 2-year scheduled follow-up . Seven hundred and fifty-three ( 68 % men ; 64 ± 12 years ) patients were included in the present analysis . Fifty percent of the cases were cirrhotic out patients . Viral ( 44 % ) etiology was predominant . Around half of the patients had a  mild-severity disease  according to the Child – Pugh score ; hepatocellular carcinoma was present in 20 % . The prevalence of ultrasound-detected portal vein thrombosis was 17 % ( n = 126 ) ; it was asymptomatic in 43 % of the cases . Notably , more than half of the portal vein thrombosis patients ( n = 81 ) were not treated with anticoagulant therapy . Logistic step-forward multivariate analysis demonstrated that previous portal vein thrombosis ( p < 0.001 ) , Child – Pugh Class B + C ( p < 0.001 ) , hepatocellular carcinoma ( p = 0.01 ) , previous upper gastrointestinal bleeding ( p = 0.030 ) and older age ( p = 0.012 ) were independently associated with portal vein thrombosis . Portal vein thrombosis is a frequent complication of cirrhosis , particularly in patients with moderate – severe liver failure . The apparent undertreatment of patients with portal vein thrombosis is a matter of concern and debate , which should be addressed by planning interventional trials especially with newer oral anticoagulants . Clinical trials.gov identifier NCT01470547 The prognostic value of portal hemodynamics , measured by pulsed echo-Doppler , was prospect ively evaluated , together with clinical , biochemical and endoscopic parameters , in a series of 50 consecutive patients with compensated cirrhosis . After a mean follow-up of 6 years , 25 patients had died , all from complications of liver disease . Among conventional variables , the step-wise Cox model showed that only the Child-Pugh score independently predicted death ( chi 2 = 18.66 ; p < 0.001 ) . When hemodynamic parameters were added to the Child-Pugh score in the same model , portal blood velocity was shown to add prognostic significance ( improvement in chi 2 = 14.06 ; p = 0.0002 ; Wald test ) . The present study shows that a portal blood velocity below the lower limit of controls ( 10 cm/s ) characterizes patients with shorter survival , and suggests that this non-invasive parameter should be associated to the Child-Pugh score in the evaluation of patients with cirrhosis Background The effect of an angiotensin II blockade in lowering the portal pressure in patients with liver cirrhosis and portal hypertension is controversial . This prospect i ve study was undertaken to evaluate the portal hypotensive effect of captopril compared to that of propranolol , and to determine the factors that contribute to a successful reduction in the portal pressure after longterm captopril administration in patients with liver cirrhosis . Methods The hepatic venous pressure gradient ( HVPG ) and portal venous velocity ( PVV ) were measured both before and 3 months after initiation of the administration of captopril  ( n = 29 ) or propranolol  ( n = 29 ) in cirrhotic patients with a variceal bleeding episode . Patients who showed a reduction in the HVPG of more than 20 % of the baseline were defined as being responders . Results At 3 months , the mean reduction in the HVPG  after captopril was less than that after propranolol ( −3.0 ± 9.3 % vs −28.5 % ± 4.1 % ; P ≪ 0.05 ) . However , of the 29 patients receiving captopril  , 9 were classified as being responders . On multivariate analysis with parameters including age , cause , Child-Pugh score , HVPG , and PVV , only low PVV was found to be a significant independent factor for responders ( PVV ≪ 12 cm/s ; odds ratio [ OR ] , 12.2 ; 95 % confidence interval [ CI ] , 1.47–102.40 ) in the captopril group . Conclusions Longterm captopril administration reduces the portal pressure effectively in cirrhotic patients with a low PVV . This suggests that the reduction in portal pressure  after captopril administration is a result of improved portal venous outflow brought about by a decrease in the intrahepatic vascular resistance . When the PVV is below 12 cm/s , a captopril trial might be useful in preventing variceal bleeding in portal hypertensive patients The effects of different types of adrenoceptor blocking agents on portal venous blood flow were studied in 10 patients with liver cirrhosis by using a duplex Doppler system . Oral atenolol ( selective beta 1 blocker ) , propranolol ( non-selective beta blocker ) , and labetalol ( non-selective adrenoceptor blocker ) were compared . The drugs were administered at r and om at an interval of 3 days or more . Hemodynamic measurements were done before and after 1 h , 2 h , and 3 h of therapy .  Atenolol and propranolol  produced significant decrease in the portal vein cross-sectional area , portal blood velocity , and estimated volume of the portal blood flow . The portal blood velocity decreased by 13.1 + /- 7.2 % 3 h after atenolol and by 16.2 + /- 6.5 % 3 h after propranolol administration ( p less than 0.05 ) . Labetalol had no significant influence on portal venous hemodynamics . These results support the hypothesis that a decrease in portal venous flow induced by beta blockers is at least partly mediated with alpha-adrenergic receptors BACKGROUND / AIMS The portal pressure response to propranolol varies significantly in individual patients with cirrhosis . At present , propranolol responders can be identified only by measuring the hepatic venous pressure gradient . The aims of this study were : 1 ) to investigate whether the noninvasive monitoring of portal blood flow by pulsed Doppler ultrasound and forearm blood flow by strain-gauge plethysmography can predict the hepatic venous pressure gradient response to propranolol in patients with cirrhosis , and 2 ) to analyze the factors that may influence this response . METHODS Hemodynamic measurements were undertaken in 80 patients with cirrhosis before and after receiving propranolol ( 0.15 mg/kg i.v . , n = 60 ) or placebo ( n = 20 ) . RESULTS No changes were observed in the placebo group . Propranolol lowered ( p < 0.01 ) hepatic venous pressure gradient from 17.6 + /- 3.8 to 14.7 + /- 3.8 mmHg , portal blood flow from 1122 + /- 363 to 897 + /- 332 ml/min and forearm blood flow from 7.52 + /- 3.1 to 6.12 + /- 2.3 ml/min% . Changes in hepatic venous pressure gradient were correlated ( p < 0.01 ) with those of portal blood flow ( r = 0.82 ) and forearm blood flow ( r = 0.54 ) . The reduction in hepatic venous pressure gradient was > 20 % in 23 patients ( " responders " ) . The accuracy of portal Doppler flowmetry in identifying responders was higher than that of forearm plethysmography ( 88.3 vs. 68.3 % , p < 0.05 ) . Multivariate analysis proved that previous variceal bleeding was the only factor independently associated with a lack of response to propranolol ( relative risk 3.42 , 95 % CI 1.5 - 7.4 , p < 0.01 ) . Hepatic venous pressure gradient reduction by propranolol was higher in non-bleeders than in bleeders ( -19.9 + /- 9.4 vs. -11.3 + /- 8.6 % , p < 0.01 ) . CONCLUSIONS Portal Doppler ultrasound can be used as a reliable surrogate indicator of the hepatic venous pressure gradient response to acute propranolol administration . In addition , our study indicates that this response is mainly influenced by previous variceal hemorrhage The drugs currently under investigation in the prevention of recurrent gastrointestinal bleeding in cirrhosis are likely to decrease the portal pressure by means of a primary reduction of portal blood flow . The hemodynamic effects of β‐blocking agents and vasodilatory drugs were noninvasively measured in eight patients with cirrhosis by means of pulsed echo‐doppler equipment . Portal caliber , blood velocity and flow were recorded hourly after a single dose of propranolol ( 40 mg p.o . ) or atenolol ( 100 mg p.o . ) , and every 5 min after treatment with isosorbide dinitrate ( 5 mg sublingually ) . The drugs were administered at r and om with an interval of 2 days or more . The portal caliber decreased after atenolol , but did not change after propranolol and isosorbide . The blood velocity decreased by 29 ± 2 % 3 hr after propranolol , by 26 ± 2 % 3 hr after atenolol and by 31 ± 3 % 15 min after isosorbide . The portal blood flow decreased by 0.29 ± 0.03 liters per min after propranolol , by 0.34 ± 0.06 after atenolol and by 0.26 ± 0.03 after isosorbide , without any difference among the various treatments . β‐blockers and vasodilatory drugs have comparable effects on portal blood flow . β1‐selective and nonselective β‐blockers are similarly effective in keeping with the hypothesis that changes in portal blood flow are mainly due to the block of β1‐receptors Only some patients show a substantial hepatic venous pressure gradient ( HVPG ) reduction after propranolol , which makes it desirable to investigate drugs with greater portal hypotensive effect . The aim of this study was to investigate whether carvedilol , a nonselective beta-blocker with anti-alpha1-adrenergic activity , may cause a greater HVPG reduction than propranolol .  Thirty-five cirrhotic patients had hemodynamic measurements before and after the r and om administration of carvedilol ( n = 14 ) , propranolol ( n = 14 ) , or placebo ( n = 7 ) . Carvedilol markedly reduced HVPG , from 19.5 + /- 1.3 to 15.4 + /- 1 mm Hg ( P < .0001 ) . This HVPG reduction was greater than after propranolol ( -20.4 + /- 2 vs. -12.7 + /- 2 % , P < .05 ) . Moreover , carvedilol decreased HVPG greater than 20 % of baseline values or to < /=12 mm Hg in a greater proportion of patients ( 64 % vs. 14 % , P < .05 ) . Both drugs caused similar reductions in hepatic and azygos blood flows , suggesting that the greater HVPG decrease by carvedilol was because of reduced hepatic and portocollateral resistance .  Propranolol caused greater reductions in heart rate and cardiac output than carvedilol , whereas carvedilol caused a greater decrease in mean arterial pressure ( -23.1 vs. -11 % , P < .05 ) . Thus , carvedilol has a greater portal hypotensive effect than propranolol in patients with cirrhosis , suggesting a greater therapeutic potential . However , it causes arterial hypotension , which calls for careful evaluation before its long-term use BACKGROUND Patients with liver cirrhosis and large oesophageal varices run a high risk of digestive haemorrhage due to the rupture of oesophageal varices , an event associated with a high mortality . At present , the only treatment for the prevention of first bleeding from oesophageal varices on which there is general agreement is drug-based . In order to tailor drug treatment to the requirements of individual patients more 
    Output:
    
Based on the systematic review and meta- analysis , we found that the use of NSBBs increased a 4.62-fold risk of PVT in cirrhotic patients