***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 
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    ***EXAMPLES*** 
    Input: Background / Aims Angiotensin receptor blockers ( ARBs ) inhibit activated hepatic stellate cell contraction and are thought to reduce the dynamic portion of intrahepatic resistance . This study compared the effects of combined treatment using the ARB c and esartan and propranolol versus propranolol monotherapy on portal pressure in patients with cirrhosis in a prospect i ve , r and omized controlled trial . Methods Between January 2008 and July 2009 , 53 cirrhotic patients with clinical ly significant portal hypertension were r and omized to receive either c and esartan and propranolol combination therapy ( 26 patients ) or propranolol monotherapy ( 27 patients ) . Before and 3 months after the administration of the planned medication , the hepatic venous pressure gradient ( HVPG ) was assessed in both groups . The dose of propranolol was subsequently increased from 20 mg bid until the target heart rate was reached , and the c and esartan dose was fixed at 8 mg qd . The primary endpoint was the HVPG response rate ; patients with an HVPG reduction of > 20 % of the baseline value or to < 12 mmHg were defined as responders . Results The mean portal pressure declined significantly in both groups , from 16 mmHg ( range , 12 - 28 mmHg ) to 13.5 mmHg ( range , 6 - 20 mmHg ) in the combination group ( P<0.05 ) , and from 17 mmHg ( range , 12 - 27 mmHg ) to 14 mmHg ( range , 7 - 25 mmHg ) in the propranolol monotherapy group ( P<0.05 ) . However , the medication-induced pressure reduction did not differ significantly between the two groups [ 3.5 mmHg ( range , -3 - 11 mmHg ) vs. 3 mmHg ( range , -8 - 10 mmHg ) , P=0.674 ] . The response rate ( 55.6 % vs. 61.5 % , P=0.435 ) and the reductions in mean blood pressure or heart rate also did not differ significantly between the combination and monotherapy groups . Conclusions The addition of c and esartan ( an ARB ) to propranolol confers no benefit relative to classical propranolol monotherapy for the treatment of portal hypertension , and is thus not recommended BACKGROUND & AIMS Angiotensin II receptor antagonists have been proposed as new drugs for portal hypertension . This r and omized , placebo-controlled , double-blind study aim ed to assess the effect of the angiotensin II receptor antagonist irbesartan on portal and systemic hemodynamics and renal function in patients with cirrhosis . METHODS Thirty-six patients with cirrhosis and portal hypertension received 150 mg/d irbesartan or placebo for 1 week . Systemic hemodynamics , kidney and liver function parameters were recorded regularly ; hepatic venous pressure gradient and plasma renin were assessed on days 0 and 7 . RESULTS Irbesartan reduced the hepatic venous pressure gradient by 12.2 % + /- 6.6 % ( P < 0.05 ) and mean arterial pressure by 5.3 % + /- 4.0 % in 13 of 18 verum patients . In 4 ( 22 % ) verum patients , arterial hypotension , accompanied by significant renal impairment , required withdrawal of irbesartan . In these patients , baseline plasma renin ( P < 0.002 ) and cystatin C ( P < 0.001 ) levels were higher , and creatinine clearance ( P < 0.02 ) , serum sodium ( P < 0.01 ) , and albumin ( P < 0.05 ) were lower than in patients who tolerated irbesartan . Four of five patients with baseline renin > 900 microU/mL developed treatment-limiting hypotension . CONCLUSIONS The angiotensin II receptor antagonist irbesartan is not advisable in patients with advanced cirrhosis and high plasma renin because it may induce arterial hypotension and only moderately reduces portal pressure BACKGROUND / AIMS The role of angiotensin II ( AT-II ) type I receptor antagonists in the treatment of portal hypertension remains controversial . We tested the efficacy of Irbesartan ( Irb ) vs. Propranolol ( Pro ) in reducing portal pressure and evaluated its systemic haemodynamic effects . METHODS Thirty-four patients were r and omly assigned to receive either Irb 300 mg/day ( 19 patients ) or Pro 40 - 120 mg/day ( 15 patients ) for 2 months . RESULTS Irb was discontinued in five patients ( 26 % ) . No major side effect occurred in the Pro group . On an average , the portal pressure gradient decreased significantly more in the Pro than in the Irb group ( median -19.5 % , range -11/-31 % vs. -4.8 % , + 2.5/-10 % , P<0.001 ) . A clinical ly significant decrease was seen in one ( 7 % ) of the patients given Irb vs. five ( 33 % ) given Pro ( P<0.02 ) . The fall in mean arterial pressure was significantly higher with Irb than with Pro ( median -29 % , range -15/-45 % vs. -4.9 % , + 8/-19 % , P<0.02 ) . Irb significantly modified the blood creatinine clearance ( median -29 ml/m , range + 9/-61 ml/m , -30 , -24/-35 % P<0.0001 vs. basal ) . CONCLUSIONS Irb offers no advantage over Pro in the control of portal hypertension . Moreover , its therapeutic profile is limited by important side effects BACKGROUND / AIMS The renin-angiotensin system plays an important role in hepatic fibrogenesis and in portal hypertension . To examine the long-term effects of C and esartan cilexetil , an angiotensin type 1 ( AT1 ) receptor blocker , on portal-systemic haemodynamics and on liver fibrosis . METHODS Forty-seven compensated Child A and Child B ( 8) cirrhotic patients were r and omly assigned to receive C and esartan cilexetil , 8 mg/d ( N.24 ) and no treatment ( N.23 ) for 1 year . Portal-systemic haemodynamic parameters , serological levels of procollagen ( PIIINP ) , hyaluronic acid ( HA ) and transforming growth factor beta 1 ( TGFbeta1 ) were assessed at baseline and after 12 months . RESULTS No patients discontinued or decreased the drug . The hepatic venous pressure gradient ( HVPG ) decreased significantly in treated patients ( -8.4%+/-2.4 ) with a reduction > 20 % in 25 % of cases vs+5.6%+/-2.9 in the untreated group . HA plasma levels decreased significantly in C and esartan treated patients in whom HVPG diminished and rose in untreated patients in whom HVPG increased . CONCLUSIONS In selected cirrhotic patients , pharmacological inhibition of the AT1 receptor is well tolerated and induced a mild reduction of portal pressure . This haemodynamic effect might be related to liver fibrogenesis activity Administration of angiotensin II causes an increase in portal pressure , and plasma concentration of angiotensin II is elevated in patients with cirrhosis , suggesting that angiotensin II may be involved in the pathogenesis of portal hypertension in cirrhosis . We evaluated the effect of the orally active angiotensin II receptor antagonist , losartan , on portal pressure in patients with cirrhosis and portal hypertension . Thirty patients with severe ( hepatic venous pressure gradient [ HVPG ] > /= 20 mm Hg ) and 15 patients with moderate ( HVPG < 20 mm Hg ) portal hypertension at baseline measurement were treated with an oral dose of 25 mg losartan once daily for 1 week and compared with 15 ( HVPG > /= 20 mm Hg ) and 10 ( HVPG < 20 mm Hg ) , respectively , cirrhotic controls . On the seventh day , HVPG was determined again , and blood pressure , heart rate , body weight , and parameters of liver and kidney function were recorded . Losartan induced a significant ( P < .001 ) decrease of HVPG in the patients with severe ( -46.8 % + /- 15.5 % ) and moderate ( -44.1 % + /- 14.7 % ) portal hypertension , while no significant change was seen in the controls . Losartan caused a slight but significant ( P < .01 ) fall in mean arterial blood pressure ( -3.1 + /- 5.0 and -3.5 + /- 4.3 mm Hg , respectively ) . One patient treated with losartan had a short symptomatic hypotensive reaction after the first dose of losartan that did not recur despite continued treatment . No deterioration of liver or kidney function was observed . The present study indicates that angiotensin II blockade with orally administered losartan is safe and highly effective in the treatment of portal hypertension BACKGROUND & AIMS It has been suggested that losartan , an angiotensin II ( A-II ) type 1 receptor blocker , may have a pronounced portal pressure reducing effect , far greater than that of propranolol . This r and omized controlled trial compared the hemodynamic and renal effects of continued 6-week administration of losartan ( n = 25 ) vs. propranolol ( n = 15 ) in portal hypertensive patients with cirrhosis treated endoscopically after a variceal bleeding episode . METHODS Hepatic venous pressure gradient ( HVPG ) , systemic hemodynamics , renal function , and vasoactive factors were measured before and at 6 weeks of treatment . RESULTS Losartan did not reduce HVPG ( -2 % + /- 12 % , NS ) but significantly decreased mean arterial pressure ( MAP , -8 % + /- 10 % , P = 0.001 ) . On the contrary , propranolol significantly reduced HVPG ( -10 % + /- 11 % , P = 0.003 ) and cardiac output ( -16 % + /- 12 % , P = 0.001 ) but did not modify MAP ( 2.5 % + /- 10 % , NS ) . Losartan increased A-II levels , reduced aldosterone , and decreased glomerular filtration rate ( GFR ) in  Child B patients . Propranolol did not modify renal function . Adverse events related to therapy were mild and similar in both groups . CONCLUSIONS Unlike propranolol , long-term losartan administration does not significantly reduce HVPG in patients with cirrhosis treated after a variceal bleeding episode , and it caused hypotension and reduced GFR in patients with moderate liver failure . Therefore , losartan is not an alternative to propranolol in preventing variceal rebleeding OBJECTIVES : Angiotensin II receptor antagonists have been shown to moderately lower portal pressure in some patients with cirrhosis but may have adverse effects on kidney function . This study aim ed at comparing the effects of a combined treatment using irbesartan plus propranolol with propranolol monotherapy on portal pressure and kidney function in patients with cirrhosis . METHODS : Thirty-two patients were included ( Child A/B/C : 13/18/1 , etiology : 16 alcohol , 13 viral , 3 other ; bilirubin 1.4 ± 1.1 mg/dL , creatinine 0.86 ± 0.20 mg/dL , baseline hepatic venous pressure gradient 18.7 ± 5.3 mmHg ) . All patients received 20 mg propranolol b.i.d . Additionally , they r and omly received either placebo ( N = 15 ) or irbesartan ( step-up dosage titration up to 300 mg/d , N = 17 ) . Patients were followed at weekly intervals , re-evaluation of hepatic venous pressure gradient ( HVPG ) was performed after 8 wk . RESULTS : One patient in the propranolol/irbesartan group was excluded due to variceal bleeding . No other adverse events occurred . Portal pressure declined in both groups ( propranolol/irbesartan group 19.6 ± 1.5 mmHg to 16.6 ± 1.2 mmHg , P = 0.037 , propranolol/placebo group 17.8 ± 1.1 mmHg to 15.1 ± 1.2 mmHg , P = 0.019 ) . Sodium excretion significantly increased in the propranolol/irbesartan group ( from 122 ± 20 mmol/d to 230 ± 23 mmol/d , P = 0.045 ) , but not in the propranolol/placebo group . CONCLUSIONS : Combination treatment of propranolol plus irbesartan is well tolerated in cirrhotic patients when titrating the angiotensin II antagonist in a step-up manner , and it increases sodium excretion in patients with compensated or moderately decompensated cirrhosis . Addition of irbesartan has no effect on portal pressure BACKGROUND & AIMS The potential use of losartan , an angiotensin II type 1 receptor blocker , in the treatment of portal hypertension is still under debate . This r and omized controlled 
    Output:
    
Conclusions ARBs did not reduce portal pressure in patients with cirrhosis ; moreover , the risk of symptomatic hypotension may increase