Benefit of prophylactic endoscopic sclerotherapy of esophageal varices A retrospective analysis

Svoboda, Petr; Kantorová, I; Ochmann, J; Kozumplík, L

doi:10.1007/s004649900724

Cited by 2 publications

(3 citation statements)

References 24 publications

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“…Table 1. Human studies evaluating the effects of ACEi and ARBs on liver fibrosis and portal hypertension in liver disease [65,98,[102][103][104][105][106][107][108][109][110][111][112][113][114][115][116][119][120][121][122]. Italicized studies indicate meta-analyses.…”

Section: Ras Inhibition In Cirrhotic Portal Hypertensionmentioning

confidence: 99%

“…Other studies of ARB use have failed to show an effect on portal pressure, but these are fewer than the supporting studies [ 103 , 109 , 110 , 111 , 112 , 113 ]. In contrast, research on ACEi in portal hypertension is too sparse to impact clinical practice ( Table 1 ) [ 114 , 115 , 116 ]. A large, multicenter study evaluating RASi ability to mitigate portal hypertension is needed with subgroup analyses of compensation status and RASi type.…”

Section: Modulation Of Classical Rasmentioning

confidence: 99%

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The Renin–Angiotensin System in Liver Disease

McGrath,

Wentworth

2024

IJMS

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The renin–angiotensin system (RAS) is a complex homeostatic entity with multiorgan systemic and local effects. Traditionally, RAS works in conjunction with the kidney to control effective arterial circulation, systemic vascular resistance, and electrolyte balance. However, chronic hepatic injury and resulting splanchnic dilation may disrupt this delicate balance. The role of RAS in liver disease, however, is even more extensive, modulating hepatic fibrosis and portal hypertension. Recognition of an alternative RAS pathway in the past few decades has changed our understanding of RAS in liver disease, and the concept of opposing vs. “rebalanced” forces is an ongoing focus of research. Whether RAS inhibition is beneficial in patients with chronic liver disease appears to be context-dependent, but further study is needed to optimize clinical management and reduce organ-specific morbidity and mortality. This review presents the current understanding of RAS in liver disease, acknowledges areas of uncertainty, and describes potential areas of future investigation.

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Section: Ras Inhibition In Cirrhotic Portal Hypertensionmentioning

confidence: 99%

Section: Modulation Of Classical Rasmentioning

confidence: 99%

The Renin–Angiotensin System in Liver Disease

McGrath,

Wentworth

2024

IJMS

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“…Studies in patients with cirrhosis demonstrated beneficial effects of ACE inhibitors (enalapril for one week, enalapril for three months, captopril for three weeks) and AT 1 receptor blockers (losartan for three months) on HVPG without serious adverse events [187][188][189][190][191]. Particularly patients with a HVPG > 16 mm Hg or a portal venous velocity < 12 cm/s responded to these agents [188,191].…”

Section: Liver Hemodynamics and Raas Inhibitionmentioning

confidence: 99%

Impact of Inhibitors of the Renin-Angiotensin-Aldosterone System on Liver Fibrosis and Portal Hypertension

Töx

Steffen²

2006

CMC

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Morbidity and mortality of chronic liver disease are primarily caused by liver cirrhosis and portal hypertension, both of them secondary disorders of progressive liver fibrosis. The main fibrogenic cell type in the liver, the hepatic stellate cell (HSC), is activated and stimulated by several factors, among which the renin-angiotensin-aldosterone system (RAAS) plays a major role. Angiotensin II induces various profibrotic pathways via the angiotensin II receptor type 1 (AT(1) receptor) not only in heart and kidney, but also in liver tissue. Stimulation of the AT(1) receptor promotes the transformation of the quiescent HSC into the myofibroblast like activated HSC and the synthesis of transforming growth factor-beta1 (TGF-beta), the major profibrotic cytokine in the liver. In addition, aldosterone has been suggested to induce profibrotic effects in chronic heart and liver disease. This review focuses on the concept that inhibitors of the RAAS retard or even reverse liver fibrosis and reduce portal hypertension. Angiotensin converting enzyme (ACE) inhibitors, AT(1) receptor antagonists, and aldosterone antagonists have been demonstrated to reduce the proliferation of HSC, to decrease the synthesis of profibrotic molecules, and to have the potential to improve liver fibrosis. However, side-effects such as systemic hypotension may impair the clinical application of RAAS inhibitors in patients with liver cirrhosis and portal hypertension. Also, efficacy may be limited by the downregulation of AT(1) receptors in advanced fibrosis, which has been observed in animal and human studies. Randomized clinical studies are essential to evaluate, whether this approach is beneficial in patients with chronic liver disease and progressive fibrosis.

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Benefit of prophylactic endoscopic sclerotherapy of esophageal varices A retrospective analysis

Abstract: We recommend prophylactic sclerotherapy with 1% polidocanol in patients with advanced varices in liver cirrhosis of varied etiology. We emphasize the need to perform these procedures in a department with adequate experience, where at least 100-200 sclerotherapies per year are performed.

Cited by 2 publications

References 24 publications

The Renin–Angiotensin System in Liver Disease

The Renin–Angiotensin System in Liver Disease

Impact of Inhibitors of the Renin-Angiotensin-Aldosterone System on Liver Fibrosis and Portal Hypertension

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