Liver stiffness-based model for portal hypertension and hepatocellular cancer risk in HBV responsive to antivirals

BACKGROUND: In hepatitis B virus (HBV)-related cirrhosis the antiviral therapy reduces portal hypertension (PH) and risk of hepatocellular carcinoma (HCC). This study assessed the prognostic role of LS PS Score (liver stiffness value X spleen diameter/platelet count) in predicting these goals in cirrhotic patients responsive to antiviral therapy. METHODS: The correlation between LS PS, PH, esophageal varices (EVs) and HCC was evaluated in 121 cirrhotic patients treated with nucleos(t)ide analogues (NUCs). Sixty-one patients (50.4%) had PH at baseline. All were HBV DNA negative on-treatment. They were evaluated after a median of 8 years of therapy (1-17) for LS PS, PH, hepatic venous pressure gradient (HVPG), EVs and HCC. RESULTS: LSPS <= 0.62 and <= 1.4 identified patients without PH measured by HVPG (< 6 mmHg, NPV=100%) and EVs (PPV 63.3%, NPV 93.7%), respectively. After antiviral therapy LSPS <= 0.62 was detected in 51.3% of the patients (16.4% and 76.6% of subjects with and without PH at baseline, P< 0.0001). HCC developed in 26 patients (21.5%, 2.6%-year) with a higher incidence in patients with LS PS> 0.62 after antiviral therapy (36% vs. 7%, P< 0.001). On multivariate analysis LS PS post-therapy and PH at baseline were the only independent predictors of HCC (OR : 1.18; 95% CI : 1.02-1.28, P=0.02 and OR: 1.70; 95% CI: 1-2.86, P=0.04 respectively). CONCLUSIONS: LSPS is useful to identify patients with regression of PH and EVs, avoiding endoscopy. LSPS <= 0.62 at baseline or due to antiviral therapy is associated with a lower risk of HCC. Early antiviral treatment is recommended in order to maintain or to induce LSPS <= 0.62.