Liver involvement in dengue virus infection: a narrative review

Dengue fever, caused by the dengue virus (DENV), is the most prevalent viral haemorrhagic fever worldwide. Despite being primarily a non-hepatotropic virus, liver involvement occurs in up to 60-90% of DENV infections. This narrative review examines the patterns, pathophysiology, clinical implications and the management of hepatic involvement in DENV infection. Liver involvement in dengue can vary from mild subclinical elevations of transaminases to dengue-induced severe hepatitis (DISH) and even acute liver failure (ALF), which occurs in a minority but carries a high mortality rate. Patients with pre-existing liver conditions, including metabolic dysfunction-associated steatotic liver disease, alcohol-related liver disease and cirrhosis, face an increased risk of severe dengue-related hepatic complications. Pathophysiology involves direct viral hepatocyte injury, immune-mediated damage, and hypoperfusion-induced hepatic ischemia. Elevated liver enzymes, particularly Aspartate Transaminase (AST) and Alanine Transaminase (ALT), serve as early markers of disease severity and correlate with critical phase illness and plasma leakage in DENV infection. Gallbladder involvement, manifesting as wall thickening and acalculous cholecystitis, is also common. Management remains largely supportive, focusing on maintaining hydration and tissue perfusion. N-acetylcysteine shows promise in dengue-associated ALF (D-ALF), particularly when administered early, though clinical trial evidence is lacking. While liver transplantation is generally contraindicated due to bleeding risks and hemodynamic instability, rare successful cases have been reported. Further research is needed to develop targeted therapies and establish clear transplantation criteria for D-ALF.