Evolution of care in cirrhosis: Preventing hepatic decompensation through pharmacotherapy

Abstract

Cirrhosis is a leading cause of morbidity and mortality, impacting more than 120 million people worldwide. Although geographic differences exist, etiologic factors such as alcohol use disorder, chronic viral hepatitis infections, and non-alcoholic fatty liver disease are prevalent in nearly every region. Historically, significant effort has been devoted to modifying these risks to prevent disease progression. Nevertheless, more than 11% of patients with compensated cirrhosis experience hepatic decompensation each year. This transition signifies the most important prognostic factor in the natural history of the disease, corresponding to a decline in median survival to below 2 years. Over the past decade, the need for pharmacotherapies aimed at reducing the risk for hepatic decompensation has been emphasized, and non-selective beta-blockers have emerged as the most effective option to date. However, a critical therapeutic gap still exists, and additional therapies have been proposed, including statins, rifaximin, and sodium-glucose cotransporter-2 inhibitors. Based on the results of innovative retrospective analyses and small-scale prospective trials, these pharmacotherapies represent promising options, but further studies, including randomized controlled trials, are necessary before they can be incorporated into clinical use. This report highlights the potential impact of these agents and others in preventing hepatic decompensation and discusses how this paradigm shift may pave the way for guideline-directed medical therapy in cirrhosis.

Optimizing cardiac status in the preliver transplant candidate

“…The nonselective beta blocker carvedilol, for example, is frequently used for primary and secondary prevention of variceal bleeding and may be used safely in renal dysfunction. Angiotensinconverting enzyme inhibitors (ACEi), angiotensin receptor blockers (ARBs), mineralocorticoid receptor antagonists (MRAs) and sodium-glucose cotransporter-2 inhibitors (SGLT2i) all attenuate activation of the renin-angiotensin-aldosterone system (RAAS) and decrease portal pressure [18,19], but should be discontinued peri-operatively due to increased risk for hypotension and renal failure (ACEi, ARBs, MRAs) as well as ketoacidosis and urinary tract infections (SGLT2i).…”

Sodium–glucose linked transporter 2 inhibitors in liver cirrhosis: Beyond their antidiabetic use

“…Cirrhosis and especially decompensated cirrhosis are accompanied by high rates of morbidity and mortality causing 1 million deaths per year worldwide 5 . Despite the significant healthcare and socioeconomic burden, the management of patients with decompensated cirrhosis remains suboptimal and non‐specific 6 . Regardless of the indications for liver transplantation, the currently recommended measures mainly focus on treating the complications of decompensated cirrhosis.…”

“…5 Despite the significant healthcare and socioeconomic burden, the management of patients with decompensated cirrhosis remains suboptimal and non-specific. 6 Regardless of the indications for liver transplantation, the currently recommended measures mainly focus on treating the complications of decompensated cirrhosis. In particular, the management of ascites is based on sodium intake restriction often along with mineralocorticoid receptor antagonists (MRAs), with or without the addition of loop diuretics.…”

Analysis of Factors Influencing Prognosis and Assessment of 60 Cases of Decompensated Cirrhotic Patients with Portal Hypertension

“…Cirrhosis, as a major cause of morbidity and mortality in hepatic diseases, affects over 120 million people worldwide. 1 Decompensated cirrhosis serves as a turning point in the prognosis, primarily manifested by complications such as ascites, hepatic encephalopathy, spontaneous bacterial peritonitis, or variceal bleeding. Accurate staging of decompensated cirrhosis can significantly reduce the risk of mortality.…”