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

Author:

Siafarikas Christos1,Kapelios Chris J.2,Papatheodoridi Margarita3ORCID,Vlachogiannakos John3ORCID,Tentolouris Nikolaos1,Papatheodoridis George3ORCID

Affiliation:

1. 1st Propaedeutic Department of Internal Medicine Medical School of National and Kapodistrian University of Athens, General Hospital of Athens “Laiko” Athens Greece

2. Heart Failure and Heart Transplantation Unit Onassis Cardiac Surgery Center Athens Greece

3. Department of Gastroenterology Medical School of National and Kapodistrian University of Athens, General Hospital of Athens “Laiko” Athens Greece

Abstract

AbstractType 2 diabetes mellitus (T2DM) and liver cirrhosis are clinical entities that frequently coexist, but glucose‐lowering medication options are limited in cirrhotic patients. Sodium–glucose linked transporter 2 (SGLT2) inhibitors are a class of glucose‐lowering medication that act independently of insulin, by causing glycosuria in the proximal convoluted tubule. In this review, we aimed to briefly present the main data and to provide insight into the pathophysiology and potential usefulness of SGLT2 inhibitors in cirrhotic patients with or without T2DM. SGLT2 inhibitors have been proven useful as antidiabetic treatment in patients with metabolic liver disease, with most robust data from patients with metabolic dysfunction‐associated steatotic liver disease (MASLD), where they also showed improvement in liver function parameters. Moreover, it has been suggested that SGLT2 inhibitors may have effects beyond their antidiabetic action. Accordingly, they have exhibited cardioprotective effects, expanding their indication in patients with heart failure without T2DM. Since decompensated liver cirrhosis and congestive heart failure share common pathophysiological features, namely renin–angiotensin–aldosterone axis and sympathetic nervous system activation as well as vasopressin secretion, SGLT2 inhibitors could also be beneficial in patients with decompensated cirrhosis, even in the absence of T2DM.

Publisher

Wiley

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