Abstract
Extract Hepatopulmonary syndrome (HPS) and portopulmonary hypertension (PoPH) represent distinct pulmonary vascular complications associated with portal hypertension and end-stage liver disease. While HPS results from intrapulmonary vasodilatations leading to hypoxemia, PoPH arises from pulmonary arterial remodelling, ultimately causing right heart failure [1, 2]. Both conditions substantially increase morbidity and mortality among liver transplantation candidates. Liver transplantation remains the only curative treatment for HPS, whereas its role in the management of PoPH remains uncertain and continues to be debated [3, 4].