Ki Tae Suk1, Eun Jin Kim, Dong Joon Kim, Hyo Sun Kim, Chang Seok Bang, Tae Young Park, Gwang Ho Baik, Sung Eun Kim, Ji Won Park, Sang Hoon Park, Myung Seok Lee, Hyoung Su Kim, Myoung Kuk Jang, Seung Ha Park, Eunhee Choi, Chang H Kim, Hotaik Sung, Choong Kee Park. 1. *Department of Internal Medicine, Hallym University College of Medicine, Chuncheon †Department of Internal Medicine, Hallym University Sacred Heart Hospital, Anyang ‡Department of Internal Medicine, Hallym University Gangnam Sacred Heart Hospital §Department of Internal Medicine, Hallym University Gangdong Sacred Heart Hospital, Seoul ∥Department of Internal Medicine, Inje University Haeundae-Paik Hospital, Busan ¶Institute of Lifestyle Medicine, Yonsei University Wonju College of Medicine, Wonju, South Korea #Department of Internal Medicine, University Hospitals Case Medical Center, Cleveland **Department of Molecular and Cellular Physiology, University of Cincinnati College of Medicine, Cincinnati, OH.
Abstract
BACKGROUND & GOALS: Early identification of hepatocellular carcinoma (HCC) is associated with improved survival for patients with chronic liver disease (CLD). We evaluated the prognostic significance of hemodynamic stage (HS) and clinical stage (CS) in predicting HCC in CLD patients. METHODS: Between January 2006 and May 2014, 801 patients with CLD who underwent hepatic venous pressure gradient (HVPG) measurement were prospectively enrolled. HS was classified by HVPG (mm Hg) as follows: HS-1 (HVPG≤6), HS-2 (6<HVPG≤10), HS-3 (10<HVPG≤12), HS-4 (12<HVPG≤20), and HS-5 (20<HVPG). CS was classified as follows: CS-0 (no cirrhosis), CS-1 (cirrhosis without varix), CS-2 (cirrhosis with varix), CS-3 (varix bleeding without other complications), CS-4 (first nonbleeding decompensating event), and CS-5 (any second decompensating event). The HCC development and risk factors for HCC were evaluated in all patients and patients with cirrhosis, respectively. RESULTS: HCC developed in 53 patients (6.6%). The incidence densities of HCC according to HS-1 to HS-5 and CS-0 to CS-5 were 4, 16, 36, 45, and 49/1000 person years and 0, 15, 25, 33, 36, and 53/1000 person years of observation, respectively. Ascites aggravation [P=0.008, odd ratio (OR)=2.33], HVPG>12 mm Hg (P=0.033, OR=2.17), CS>2 (P=0.039, OR=2.36), and alpha-fetoprotein (AFP; P=0.017, OR=1.01) were significant predictors of HCC development in all patients. For patients with cirrhosis, ascites aggravation (OR=2.51), HVPG >12 mm Hg (OR=2.46), and CS >2 (OR=2.62) were correlated with HCC development. Areas under receiver operating characteristic curves of the prediction-model, CS, HVPG score, and AFP were 0.797, 0.707, 0.701, and 0.653, respectively. CONCLUSIONS: HCC development correlates with advancing liver fibrosis or disease as measured by HS and CS. In addition, ascites aggravation and elevated AFP appears to be associated with increased incidence of HCC.
BACKGROUND & GOALS: Early identification of hepatocellular carcinoma (HCC) is associated with improved survival for patients with chronic liver disease (CLD). We evaluated the prognostic significance of hemodynamic stage (HS) and clinical stage (CS) in predicting HCC in CLD patients. METHODS: Between January 2006 and May 2014, 801 patients with CLD who underwent hepatic venous pressure gradient (HVPG) measurement were prospectively enrolled. HS was classified by HVPG (mm Hg) as follows: HS-1 (HVPG≤6), HS-2 (6<HVPG≤10), HS-3 (10<HVPG≤12), HS-4 (12<HVPG≤20), and HS-5 (20<HVPG). CS was classified as follows: CS-0 (no cirrhosis), CS-1 (cirrhosis without varix), CS-2 (cirrhosis with varix), CS-3 (varix bleeding without other complications), CS-4 (first nonbleeding decompensating event), and CS-5 (any second decompensating event). The HCC development and risk factors for HCC were evaluated in all patients and patients with cirrhosis, respectively. RESULTS: HCC developed in 53 patients (6.6%). The incidence densities of HCC according to HS-1 to HS-5 and CS-0 to CS-5 were 4, 16, 36, 45, and 49/1000 person years and 0, 15, 25, 33, 36, and 53/1000 person years of observation, respectively. Ascites aggravation [P=0.008, odd ratio (OR)=2.33], HVPG>12 mm Hg (P=0.033, OR=2.17), CS>2 (P=0.039, OR=2.36), and alpha-fetoprotein (AFP; P=0.017, OR=1.01) were significant predictors of HCC development in all patients. For patients with cirrhosis, ascites aggravation (OR=2.51), HVPG >12 mm Hg (OR=2.46), and CS >2 (OR=2.62) were correlated with HCC development. Areas under receiver operating characteristic curves of the prediction-model, CS, HVPG score, and AFP were 0.797, 0.707, 0.701, and 0.653, respectively. CONCLUSIONS: HCC development correlates with advancing liver fibrosis or disease as measured by HS and CS. In addition, ascites aggravation and elevated AFP appears to be associated with increased incidence of HCC.