BACKGROUND AND AIM: Gamma-glutamyl transpeptidase-to-platelet ratio (GPR) can evaluate the degree of liver fibrosis. We investigated whether GPR can predict the development of hepatocellular carcinoma (HCC) in chronic hepatitis B (CHB) patients. METHODS: We retrospectively evaluated 1109 CHB patients that were enrolled between 2006 and 2012, and all patients had available data for the assessment of GPR at enrollment. Three risk groups were defined according to tertile stratification: GPR < 0.05, low-risk (n = 370 [33.4%]); GPR 0.05-0.24, intermediate-risk (n = 370 [33.4%]); and GPR > 0.24, high-risk (n = 369 [33.2%]). The predictive accuracy of GPR, fibrosis-4 (FIB-4), and aspartate transaminase-to-platelet ratio index (APRI) in predicting HCC development was tested. RESULTS: The median age of the study population (746 men and 363 women) was 50 years. During the follow-up period (median, 32 months; interquartile range, 19-57 months), 69 (6.2%) patients developed HCC. Together with age, male gender, diabetes mellitus, antiviral therapy, serum albumin, and alpha-fetoprotein, the relative risk of HCC development significantly increased from low-risk to high-risk GPR groups (hazard ratio [HR], up to 29.5; adjusted HR, up to 10.6; all P < 0.05). In addition, FIB-4 was calculated to be a significantly high relative risk of HCC development (HR, up to 20.1; adjusted HR, up to 7.3; all P < 0.05), whereas APRI was not (P = 0.168). The cumulative incidence of HCC development was significantly different among three risk groups (P < 0.001, log-rank test). CONCLUSIONS: This study suggests that GPR can be used as a noninvasive marker to assess the risk of HCC development in CHB patients.
BACKGROUND AND AIM: Gamma-glutamyl transpeptidase-to-platelet ratio (GPR) can evaluate the degree of liver fibrosis. We investigated whether GPR can predict the development of hepatocellular carcinoma (HCC) in chronic hepatitis B (CHB) patients. METHODS: We retrospectively evaluated 1109 CHB patients that were enrolled between 2006 and 2012, and all patients had available data for the assessment of GPR at enrollment. Three risk groups were defined according to tertile stratification: GPR < 0.05, low-risk (n = 370 [33.4%]); GPR 0.05-0.24, intermediate-risk (n = 370 [33.4%]); and GPR > 0.24, high-risk (n = 369 [33.2%]). The predictive accuracy of GPR, fibrosis-4 (FIB-4), and aspartate transaminase-to-platelet ratio index (APRI) in predicting HCC development was tested. RESULTS: The median age of the study population (746 men and 363 women) was 50 years. During the follow-up period (median, 32 months; interquartile range, 19-57 months), 69 (6.2%) patients developed HCC. Together with age, male gender, diabetes mellitus, antiviral therapy, serum albumin, and alpha-fetoprotein, the relative risk of HCC development significantly increased from low-risk to high-risk GPR groups (hazard ratio [HR], up to 29.5; adjusted HR, up to 10.6; all P < 0.05). In addition, FIB-4 was calculated to be a significantly high relative risk of HCC development (HR, up to 20.1; adjusted HR, up to 7.3; all P < 0.05), whereas APRI was not (P = 0.168). The cumulative incidence of HCC development was significantly different among three risk groups (P < 0.001, log-rank test). CONCLUSIONS: This study suggests that GPR can be used as a noninvasive marker to assess the risk of HCC development in CHB patients.