Tingting Huo1,2, Jingyu Cao3, Yaowen Tian1,4, Xuetao Shi1, Liqun Wu3, Mingzhi Zhang2, Linda L Wong5, Lei Zhao1,2,6,7. 1. Department of Hepatobiliary Surgery, Shandong Cancer Hospital and Institute, Jinan. 2. Department of Oncology, the First Affiliated Hospital of Zhengzhou University, China. 3. Department of Hepatobiliary Surgery, Affiliated Hospital of Qingdao University, China. 4. School of Medicine and Life Sciences, University of Jinan-Shandong Academy of Medical Sciences, China. 5. Department of Surgery, University of Hawaii School of Medicine, Honolulu. 6. Shandong Cancer Hospital Affiliated to Shandong University, China. 7. Shandong Academy of Medical Science, Jinan, China.
Abstract
Background: The aim of this study was to evaluate the effect of chronic hepatitis B infection on the risk of synchronous colorectal liver metastasis (synCRLM). Methods: A total of 4033 consecutive patients with newly diagnosed colorectal cancer (CRC) with hepatitis B testing were enrolled. The prevalence of synCRLM was compared between hepatitis B surface antigen (HBsAg)-positive and -negative patients; significant predictors for synCRLM were analyzed by logistic regression analysis; Fibrosis-4 Index for Liver Fibrosis (FIB-4), aspartate aminotransferase-to-platelet ratio index (APRI), and hepatitis B e antigen (HBeAg) status were compared between patients with or without synCRLM. Results: The prevalence of synCRLM was significantly higher in the HBsAg+ patients than that in the HBsAg- patients (15.57% vs 8.60%; P < .001, χ2 test). A logistic regression analysis indicated that HBsAg+ showed the highest hazard ratio (2.317 [95% confidence interval, 1.406-3.820]) for synCRLM. Both FIB-4 and APRI were significantly higher in those with HBsAg positivity but no synCRLM compared to those with HBsAg positivity and synCRLM (FIB-4: 1.23 [0.92-1.88] vs 1.09 [0.74-1.51], P = .045; APRI: 0.23 [0.227-0.387] vs 0.18 [0.171-0.309], P = .023, Mann-Whitney test; all shown as median [25th-75th percentile]); HBeAg positivity was detected in 26.32% of those with positive HBsAg and synCRLM compared to 18.45% of those with positive HBsAg but no synCRLM; the difference was not statistically significant. Conclusions: Concomitant chronic HBV infection significantly increases the risk of CRLM, and for HBsAg+ CRC patients, elevated FIB-4/APRI may be antimetastatic. Further study is needed to determine whether active HBV replication is prometastatic.
Background: The aim of this study was to evaluate the effect of chronic hepatitis B infection on the risk of synchronous colorectal liver metastasis (synCRLM). Methods: A total of 4033 consecutive patients with newly diagnosed colorectal cancer (CRC) with hepatitis B testing were enrolled. The prevalence of synCRLM was compared between hepatitis B surface antigen (HBsAg)-positive and -negative patients; significant predictors for synCRLM were analyzed by logistic regression analysis; Fibrosis-4 Index for Liver Fibrosis (FIB-4), aspartate aminotransferase-to-platelet ratio index (APRI), and hepatitis B e antigen (HBeAg) status were compared between patients with or without synCRLM. Results: The prevalence of synCRLM was significantly higher in the HBsAg+ patients than that in the HBsAg- patients (15.57% vs 8.60%; P < .001, χ2 test). A logistic regression analysis indicated that HBsAg+ showed the highest hazard ratio (2.317 [95% confidence interval, 1.406-3.820]) for synCRLM. Both FIB-4 and APRI were significantly higher in those with HBsAg positivity but no synCRLM compared to those with HBsAg positivity and synCRLM (FIB-4: 1.23 [0.92-1.88] vs 1.09 [0.74-1.51], P = .045; APRI: 0.23 [0.227-0.387] vs 0.18 [0.171-0.309], P = .023, Mann-Whitney test; all shown as median [25th-75th percentile]); HBeAg positivity was detected in 26.32% of those with positive HBsAg and synCRLM compared to 18.45% of those with positive HBsAg but no synCRLM; the difference was not statistically significant. Conclusions: Concomitant chronic HBV infection significantly increases the risk of CRLM, and for HBsAg+ CRCpatients, elevated FIB-4/APRI may be antimetastatic. Further study is needed to determine whether active HBV replication is prometastatic.