Meta analysis of propranolol effects on gastrointestinal hemorrhage in cirrhotic patients

Cheng, Jin-Wei; Zhu, Liang; Gu, Min; Song, Zhe-Ming

doi:10.3748/wjg.v9.i8.1836

Cited by 38 publications

(18 citation statements)

References 27 publications

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“…The annual incidence of esophageal varices in patients with cirrhosis is approximately 5%,1 and a third of these will bleed 2, 3. Current therapy with propranolol results in a reduction in the first variceal bleed and mortality compared with placebo 4, 5. There have been two recent meta‐analyses with 16 trials studied in total 6, 7.…”

mentioning

confidence: 99%

Randomized controlled trial of carvedilol versus variceal band ligation for the prevention of the first variceal bleed

et al. 2009

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Current therapy for preventing the first variceal bleed includes beta-blocker and variceal band ligation (VBL). VBL has lower bleeding rates, with no differences in survival, whereas betablocker therapy can be limited by side effects. Carvedilol, a non-cardioselective vasodilating beta-blocker, is more effective in reducing portal pressure than propranolol; however, there have been no clinical studies assessing the efficacy of carvedilol in primary prophylaxis. The goal of this study was to compare carvedilol and VBL for the prevention of the first variceal bleed in a randomized controlled multicenter trial. One hundred fifty-two cirrhotic patients from five different centers with grade II or larger esophageal varices were randomized to either carvedilol 12.5 mg once daily or VBL performed every 2 weeks until eradication using a multibander device. T he most serious complication of portal hypertension is variceal hemorrhage. The annual incidence of esophageal varices in patients with cirrhosis is approximately 5%, 1 and a third of these will bleed. 2,3 Current therapy with propranolol results in a reduction in the first variceal bleed and mortality compared with placebo. 4,5 There have been two recent metaanalyses with 16 trials studied in total. 6,7 The one showed variceal band ligation (VBL) to be more effective than beta-blockers in primary prevention of variceal hemorrhage, although there was no difference in survival. 7 The other showed similar overall results, although when trials with unclear bias control and follow-up less than 20 months were excluded, the difference in bleeding was not present. 6 Carvedilol is a potent non-cardioselective betablocker, with weak vasodilating properties due to alpha-1 blockade. 8 A fall in both intrahepatic and portocollateral resistance contributes to the enhanced effects on portal pressure reduction through blockade of alpha-1 receptors as has been shown with prazosin. 9-11 A reduction in the hepatic venous pressure gradient (HVPG) of 8%-43% was observed with carvedilol in nine published hemodynamic studies involving 158 patients. [12][13][14][15][16][17][18][19][20] Carvedilol was also found to have a greater portal hypotensive effect than propranolol in randomized controlled hemodynamic studies. 15,17

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mentioning

confidence: 99%

Randomized controlled trial of carvedilol versus variceal band ligation for the prevention of the first variceal bleed

et al. 2009

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“…Since then, beta blockers are the drug of choice in the chronic treatment of portal hypertension. Non Selective beta blockers are capable of decreasing the incidence of digestive bleeding and reducing mortality, decreasing bleeding and rebleeding in 20% of patients in primary and secondary prophylaxis, besides decreasing mortality (CHENG;ZHU et al, 2003). The effect over beta receptors 2 is more important and significative in chronic and continous use of BBNS (BOSCH;BERZIGOTTI et al, 2008).…”

Section: Artigos De Revisãomentioning

confidence: 99%

Cirrhotic Portal Hypertension: New Insights in an Old Syndrome

2015

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Liver Cirrhosis is currently understood as a pathological systemic process, inflammatory, vascular and, overall, dynamic and bidirectional. The intrahepatic circulation is the site of pronounced and determinant alterations characterized by the increase of mechanical resistance to the portal blood flow and the increase of the hepatic vascular tone. Compensated cirrhosis and decompensated cirrhosis can be described according to the presence and severity of portal hypertension. The most accurate method for diagnosis and stratification of portal hypertension is the measurement of the hepatic venous pressure gradient (HVPG). The standard pharmacological treatment available for cirrhotic portal hypertension consists, currently in the use of a non-selective beta-blocker(NSBB). A significant proportion of patients do not respond to treatment. Moreover, it seems to be a therapeutic window of the non-selective beta blockers in which very early stages of compensated cirrhosis and decompensated patients are not benefiting from that medication. The discovery of new drugs that might interfere in the disease's evolution and treat portal hypertension, allows a glimpse of a new horizon in hepatic cirrhosis. KEY WORDS:Cirrhotic Portal Hypertension; Pharmacological Therapy; Hepatic Venous Pressure Gradient.HIPERTENSÃO PORTA CIRRÓTICA: NOVAS PERSPECTIVAS SOBRE UMA SÍNDROME ANTIGA RESUMO: A cirrose Hepática é, atualmente, compreendida como um processo patológico sistêmico, inflamatório, vascular e, em geral, dinâmico e bidirecional. A circulação intra-hepática é o local de alterações pronunciadas e determinantes, caracterizadas pelo aumento da resistência mecânica ao fluxo sanguíneo portal e pelo aumento do tónus vascular hepático. A cirrose compensada e a descompensada podem ser descritas de acordo com a presença e gravidade da hipertensão porta. O método mais preciso para o diagnóstico e estratificação da hipertensão porta é a medida do gradiente de pressão venosa hepática (HVPG). O tratamento farmacológico disponível para a hipertensão porta cirrótica, nos dias atuais, consiste na utilização de um beta bloqueador não seletivo (NSBB). Uma proporção significativa dos pacientes não responde ao tratamento. Além disso, parece haver uma janela terapêutica dos beta-bloqueadores não seletivos, em que fases muito iniciais da cirrose compensada e pacientes descompensados não se beneficiam da medicação. Logo, a descoberta de novas drogas que possam interferir na evolução da doença e tratar a hipertensão porta, permite vislumbrar um novo horizonte na cirrose hepática.

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“…Propranolol has been shown to significantly reduce rebleeding and mortality in these patients and should be commenced soon after stabilisation 55. The combination of β-blockers and nitrates is superior to β-blocker monotherapy but is associated with more side effects and is poorly tolerated 56…”

Section: Variceal Haemorrhagementioning

confidence: 99%

Upper gastrointestinal haemorrhage: an update

Jafar

Sharma

2014

Frontline Gastroenterol

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Upper gastrointestinal (GI) haemorrhage is a common cause for admission to hospital and is associated with a mortality of around 10%. Prompt assessment and resuscitation are vital, as are risk stratification of the severity of bleeding, early involvement of the multidisciplinary team and timely access to endoscopy, preferably within 24 h. The majority of bleeds are due to peptic ulcers for whichHelicobacter pyloriand non-steroidal anti-inflammatory agents are the main risk factors. Although proton pump inhibitors (PPIs) are widely used before endoscopy, this is controversial. Pre-endoscopic risk stratification with the Glasgow Blatchford score is recommended as is the use of the Rockall score postendoscopy. Endoscopic therapy, with at least two haemostatic modalities, remains the mainstay of treating high-risk lesions and reduces rebleeding rates and mortality. High-dose PPI therapy after endoscopic haemostasis also reduces rebleeding rates and mortality. Variceal oesophageal haemorrhage is associated with a higher rebleeding rate and risk of death. Antibiotics and vasopressin analogues are advised in suspected variceal bleeding; however, endoscopic variceal band ligation remains the haemostatic treatment of choice. Balloon tamponade remains useful in the presence of torrential variceal haemorrhage or when endoscopy fails to secure haemostasis, and can be a bridge to further endoscopic attempts or placement of a transjugular intrahepatic portosystemic shunt. This review aims to provide an update on the latest evidence-based recommendations for the management of acute upper GI haemorrhage.

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Meta analysis of propranolol effects on gastrointestinal hemorrhage in cirrhotic patients

Abstract: Propranolol can markedly reduce the risks of both primary and recurrent gastrointestinal hemorrhage, and also the total mortality.

Cited by 38 publications

References 27 publications

Randomized controlled trial of carvedilol versus variceal band ligation for the prevention of the first variceal bleed

Randomized controlled trial of carvedilol versus variceal band ligation for the prevention of the first variceal bleed

Cirrhotic Portal Hypertension: New Insights in an Old Syndrome

Upper gastrointestinal haemorrhage: an update

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