Author information
1Department of Gastroenterology and Hepatology, Hospital General Universitario Gregorio Marañon, Madrid, Spain.
2Instituto de Investigación Sanitaria Gregorio Marañón, Madrid, Spain.
3Centre for Biomedical Research in Liver and Digestive Diseases Network, Instituto de Salud Carlos III, Madrid, Spain.
4Department of Nuclear Medicine, Hospital General Universitario Gregorio Marañon, Madrid, Spain.
5Department of Diagnostic Radiology, Hospital General Universitario Gregorio Marañon, Madrid, Spain.
6Department of Interventional Radiology, Hospital General Universitario Gregorio Marañon, Madrid, Spain.
7Department of Hepatobiliary and Pancreatic Surgery, Hospital General Universitario Gregorio Marañon, Madrid, Spain.
8Faculty of Medicine, Complutense University of Madrid, Madrid, Spain.
9Faculty of Medicine, Complutense University of Madrid, Madrid, SpainCalle del Doctor Esquerdo 46, 28007 Madrid, Spain.
Abstract
Background: Transarterial radioembolization (TARE) is increasingly used in patients with hepatocellular carcinoma (HCC). This treatment can induce or impair portal hypertension, leading to hepatic decompensation. TARE also promotes changes in liver and spleen volumes that may modify therapeutic decisions and outcomes after therapy.
Objectives: We aimed to investigate the impact of TARE on the incidence of decompensation events and its predictive factors.
Design: In all, 63 consecutive patients treated with TARE between February 2012 and December 2018 were retrospectively included.
Methods: We assessed clinical (including Barcelona Clinic Liver Cancer stage, portal hypertension assessment, and liver decompensation), laboratory parameters, and liver and spleen volumes before and 6 and 12 weeks after treatment. A multivariate analysis was performed.
Results: In total, 18 out of 63 (28.6%) patients had liver decompensation (ascites, variceal bleeding, jaundice, or encephalopathy) within the first 3 months after therapy, not associated with tumor progression. Clinically significant portal hypertension (CSPH) and bilobar treatment independently predicted the development of liver decompensation after TARE. A significant volume increase in the non-treated hemi-liver was observed only in patients with unilobar treatment (median volume increase of 20.2% in patients with right lobe TARE; p = 0.007), especially in those without CSPH. Spleen volume also increased after TARE (median volume increase of 16.1%; p = 0.0001) and was associated with worsening liver function scores and decreased platelet count.
Conclusion: Bilobar TARE and CSPH may be associated with an increased risk of liver decompensation in patients with intermediate or advanced HCC. A careful assessment considering these variables before therapy may optimize candidate selection and improve treatment planning.