The role of Spleen Stiffness measurement as predictor of HCC recurrence after curative resection in cirrhotic patients

Introduction: Hepatocellular carcinoma (HCC) is a frequent complication in patients with chronic liver diseases and one of the most common malignancies worldwide. Liver resection is the gold standard treatment option for patients with solitary tumors; however, tumor recurrence complicates 70% of cases of hepatic resection at 5 years. Recently it has been demonstrated that the degree of portal hypertension (PH) measured by HVPG is directly correlated with the risk of developing HCC. We recently documented that spleen (SSM) and liver (LSM) stiffness measurement are accurate non-invasive markers of portal hypertension in cirrhosis. Aims: The aim of our study was to identify the role of SSM and LSM as predictors of HCC recurrence after curative resection. Materials and methods/Results: 157 patients with HCC who underwent curative resection between 2008 and 2014 were prospectively enrolled to assess early (24 months) recurrence. The results of LSM and SSM assessed with TE (Fibroscan®, Echosens) together with clinical and histological data were collected before surgery and their association with early or late recurrence was assessed by uni and multivariate logistic regression analysis. Forty-nine (49) patients with early and 22 with late HCC recurrence were identified during follow-up period. At univariate analysis, early recurrences were associated with etiology, number of nodules, HCC diameter and grading, infiltrated resection margins and satellitosis. Multivariate analysis showed that only viral (HCV, HBV) etiology, tumor diameter and margin infiltration were independently associated with early recurrence with an area under the curve (AUC) of 0.73. At univariate analysis late recurrence was associated only with SSM (p = 0.0027) with an AUC of 0.70. Conclusions: Early HCC recurrence is associated with HCC clinical and pathological features; late recurrence was best predicted by the assessment of SSM, thus suggesting a role of portal hypertension in the development of HCC late recurrence