Quantifying the benefit of nonselective beta-blockers in the prevention of hepatic decompensation: A Bayesian reanalysis of the PREDESCI trial

Rowe, Ian; Villanueva, Càndid; Shearer, Jessica; Albillos, Agustı́n; Genescà, Joan; García–Pagán, Joan Carles; Tripathi, Dhiraj; Hayes, Peter; Bosch, Jaime; Abraldes, Juan G.

doi:10.1097/hep.0000000000000342

Cited by 8 publications

(3 citation statements)

References 38 publications

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“…However, the mean dosages of propranolol and carvedilol actually achieved post-titration were 95 mg/day and 19 mg/day, respectively. After 2 years of clinical follow-up, patients treated with NSBB manifested significantly lower risk of decompensation (HR, 0.51; 95% CI, 0.26–0.97), predominantly a lower risk of developing ascites, recently confirmed in a Bayesian reanalysis 110 . Some caution should be made with applying these findings to all patients with compensated cirrhosis and CSPH because of the unique selection criteria of patients for this study; all patients had confirmed CSPH by HVPG and were not selected for inclusion by NILDA.…”

Section: Stage-specific Management Of Phmentioning

confidence: 79%

“…After 2 years of clinical follow-up, patients treated with NSBB manifested significantly lower risk of decompensation (HR, 0.51; 95% CI, 0.26-0.97), predominantly a lower risk of developing ascites, recently confirmed in a Bayesian reanalysis. [110] Some caution should be made with applying these findings to all patients with compensated cirrhosis and CSPH because of the unique selection criteria of patients for this study; all patients had confirmed CSPH by HVPG and were not selected for inclusion by NILDA. Additionally, the majority of patients had untreated hepatitis C prior to availability of all-oral direct antiviral therapy, and the effect of ongoing alcohol use was not assessed.…”

Section: Stage-specific Management Of Phmentioning

confidence: 99%

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AASLD Practice Guidance on risk stratification and management of portal hypertension and varices in cirrhosis

Kaplan,

Ripoll,

Thiele

et al. 2023

Hepatology

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Portal hypertension results from a series of maladaptive responses to chronic liver injury and cirrhosis. Initially, structural mechanisms because of accumulation of fibrous tissue, regenerative nodules, microthrombi, parenchymal extinction, and collapse lead to an increase in intrahepatic vascular resistance (1). In addition to architectural distortion, dynamic sinusoidal vasoconstriction contributes to 30% of the total increase in vascular tone. These structural changes lead to an increased portal pressure gradient; when this reaches values of about 10 mm Hg, it gives rise to formation of portal-systemic collaterals and compensatory splanchnic vasodilation, which, in turn, increases portal blood flow and, consequently, portal pressure (2). One of the first consequences of portal hypertension is the development of portosystemic collaterals, for which vascular endothelial growth factor (VEGF)-driven angiogenesis plays an important role (3). Gastroesophageal varices represent the most clinically relevant collaterals because of their increased risk of bleeding. Bleeding is directly dependent on increased wall tension at the varices, determined by portal pressure, variceal diameter, and thin wall thickness. Vasodilation occurs also in the systemic circulation resulting in a hyperdynamic circulatory state, driven by decreased effective arterial blood volume leading to activation of neurohumoral and vasoconstrictive systems, sodium and water retention, and increased cardiac output. This process eventually results in the development of ascites and, at late stages, hepatorenal syndrome because of compensatory renal vasoconstriction. Hepatic encephalopathy represents a multifactorial complication of portal hypertension, resulting from portosystemic shunting, impaired synthetic liver function, increased bacterial translocation, and muscle wasting (sarcopenia). Finally, imbalances on vasoconstrictors and vasodilators in the pulmonary circulation results in hepatopulmonary syndrome (increased vasodilation) and portopulmonary hypertension (increased vasoconstriction). CO, carbon monoxide; H 2 S, hydrogen sulfide; HVR, hepatic vascular resistance; NO, nitric oxide; ET, endothelin.

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Section: Stage-specific Management Of Phmentioning

confidence: 79%

Section: Stage-specific Management Of Phmentioning

confidence: 99%

AASLD Practice Guidance on risk stratification and management of portal hypertension and varices in cirrhosis

Kaplan,

Ripoll,

Thiele

et al. 2023

Hepatology

Self Cite

View full text Add to dashboard Cite

show abstract

“…19 Subsequent studies reinforce the value of NSBBs to prevent decompensation. 20,21 At present, CSPH can be confirmed non-invasively, mainly relying on liver stiffness measurement (LSM) by transient elastography. 18,22 LSM ≤15 KPa plus platelets ≥150x10 9 /L rule-out CSPH, and LSM of ≥25 KPa rule it in quite accurately.…”

mentioning

confidence: 99%