BACKGROUND AND AIM: The risk factors for aggravation of esophageal varices (EV) in patients with hepatocellular carcinoma (HCC) are poorly understood. The aim of this study was to evaluate the effects of HCC on the appearance of the red color (RC) sign on EV and also investigate whether risk factors for the appearance of the RC sign differed between patients with and without HCC. METHODS: A total of 243 patients with cirrhosis (127 with HCC, 116 without HCC) without the RC sign, with no previous variceal hemorrhage, and not on prophylactic treatment for EV were enrolled. The endpoint was defined as being either when the RC sign was first noted, or when variceal bleeding occurred. In patients without HCC, follow-up was discontinued if HCC was discovered. The risk factors were analyzed by Cox proportional hazards regression. RESULTS: In patients with HCC, portal vein tumor thrombus was a statistically independent risk factor (risk ratio [RR] 4.58, 95% confidence interval [CI] 1.32-15.86), although the presence of HCC was not. A large HCC (> or =50 mm) tended to be a risk factor, but this was not statistically significant (RR 2.50, 95%CI 0.98-6.39). Child-Pugh classification and low platelet count were common risk factors regardless of whether HCC was present or not. CONCLUSIONS: Portal vein tumor thrombus, but not the presence of HCC, was a significant risk factor for aggravation of EV in patients with HCC. Cirrhotic patients with portal vein tumor thrombus should receive more aggressive management of portal hypertension to prevent aggravation of EV.
BACKGROUND AND AIM: The risk factors for aggravation of esophageal varices (EV) in patients with hepatocellular carcinoma (HCC) are poorly understood. The aim of this study was to evaluate the effects of HCC on the appearance of the red color (RC) sign on EV and also investigate whether risk factors for the appearance of the RC sign differed between patients with and without HCC. METHODS: A total of 243 patients with cirrhosis (127 with HCC, 116 without HCC) without the RC sign, with no previous variceal hemorrhage, and not on prophylactic treatment for EV were enrolled. The endpoint was defined as being either when the RC sign was first noted, or when variceal bleeding occurred. In patients without HCC, follow-up was discontinued if HCC was discovered. The risk factors were analyzed by Cox proportional hazards regression. RESULTS: In patients with HCC, portal vein tumor thrombus was a statistically independent risk factor (risk ratio [RR] 4.58, 95% confidence interval [CI] 1.32-15.86), although the presence of HCC was not. A large HCC (> or =50 mm) tended to be a risk factor, but this was not statistically significant (RR 2.50, 95%CI 0.98-6.39). Child-Pugh classification and low platelet count were common risk factors regardless of whether HCC was present or not. CONCLUSIONS: Portal vein tumor thrombus, but not the presence of HCC, was a significant risk factor for aggravation of EV in patients with HCC. Cirrhoticpatients with portal vein tumor thrombus should receive more aggressive management of portal hypertension to prevent aggravation of EV.