Survival improvement in Child-Pugh C cirrhotic patients with hepatocellular carcinoma diagnosed during 1990-2002.

OBJECTIVES: The aim of this study was to describe the evolution of diagnostic modalities, treatment and survival in cases of hepatocellular carcinoma (HCC) between 1990 and 2002 in Calvados. METHODS: All cases registered as HCC in the Calvados Tumour Registry from 1990 to 2002 were retrospectively reviewed. Incidence rates were standardized in comparison to the world reference population. The Kaplan-Meier method was used for survival analysis, and the log-rank test and Cox's model were used to compare patient survival according to demographic and tumour characteristics, as well as diagnosis period. Multivariate analysis were performed to determine independent prognostic factors and to assess the impact of the diagnosis period on survival. RESULTS: From 1990 to 2002, 729 cases registered as HCC were retrospectively validated. Standard incidence rates were 11.1/100,000 in men and 1.9/100,000 in women. Mean age was 66.6+/-11.8 years. Cirrhosis was present in 90.4% of cases. The cause of cirrhosis was alcohol in 66.8% of cases, HCV in 12.5%, HBV in 2.9%, haemochromatosis in 3.5%, and "other" in 13.1%. Curative treatment was possible in 14.7% of cases. Median survival was 7.15 months. On multivariate analysis, male gender, age greater than 70 years, Child-Pugh C (advanced-stage) cirrhosis, portal or suprahepatic venous thrombosis, alpha-fetoprotein (AFP) level greater than 200 ng/mL and non-curative treatment were poor prognostic factors. However, the diagnosis period was a good prognostic factor, associated with survival improvement over time in Child-Pugh C patients independent of tumour size, but not in Child-Pugh A and B. CONCLUSION: From 1990 to 2002, improvement in the survival of Child-Pugh C cirrhosis patients with HCC was observed that was apparently essentially attributable to better management of cirrhosis, and an improved balance between treatment and the degree of portal hypertension and hepatocellular insufficiency.