Naveed Z Janjua1, Mei Chong2, Margot Kuo2, Ryan Woods3, Jason Wong4, Eric M Yoshida5, Morris Sherman6, Zahid A Butt4, Hasina Samji4, Darrel Cook2, Amanda Yu2, Maria Alvarez2, Mark Tyndall4, Mel Krajden7. 1. British Columbia Centre for Disease Control, Vancouver, BC, Canada; School of Population and Public Health, University of British Columbia, Vancouver, BC, Canada. Electronic address: naveed.janjua@bccdc.ca. 2. British Columbia Centre for Disease Control, Vancouver, BC, Canada. 3. British Columbia Cancer Agency, Vancouver, BC, Canada. 4. British Columbia Centre for Disease Control, Vancouver, BC, Canada; School of Population and Public Health, University of British Columbia, Vancouver, BC, Canada. 5. Division of Gastroenterology, Department of Medicine, University of British Columbia, Vancouver, BC, Canada. 6. Division of Gastroenterology, Department of Medicine, University of Toronto, Toronto, Ontario, Canada. 7. British Columbia Centre for Disease Control, Vancouver, BC, Canada; Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada.
Abstract
BACKGROUND & AIMS: Evidence is limited on hepatocellular carcinoma (HCC) risk after sustained virological response (SVR) to interferon-based treatment of hepatitis C virus (HCV) infection. We evaluated the effect of SVR on the risk of HCC and estimated its incidence in post-SVR HCV patients from a large population-based Canadian cohort. METHODS: The British Columbia Hepatitis Testers Cohort includes individuals tested for HCV between 1990-2013 linked with data on their medical visits, hospitalizations, cancers, prescription drugs and mortality. Patients receiving interferon-based HCV treatments were followed from the end of treatment to HCC diagnosis, death or December 31, 2012. We examined HCC risk among those who did and did not achieve SVR using multivariable proportional hazard models with the Fine and Gray modification for competing risks. RESULTS: Of 8147 individuals who received HCV treatment and were eligible for analysis, 4663 (57%) achieved SVR and 3484 (43%) did not. Each group was followed for a median of 5.6years (range: 0.5-12.9) for an HCC incidence rate of 1.1/1000 person-years (PY) among the SVR and 7.2/1000 PY among the no SVR group. The HCC incidence rate was higher among those with cirrhosis (SVR: 6.4, no SVR: 21.0/1000 PY). In the multivariable model, SVR was associated with a lower HCC risk (subdistribution hazard ratio [SHR]=0.20, 95% CI: 0.13-0.3), while cirrhosis (SHR=2.61, 95% CI: 1.68-4.04), age ⩾50years, being male and genotype 3 infection were associated with a higher HCC risk. Among those who achieved SVR, cirrhosis, age ⩾50years and being male were associated with a higher HCC risk. CONCLUSION: SVR after interferon-based treatment substantially reduces but does not eliminate HCC risk, which is markedly higher among those with cirrhosis and age ⩾50years at treatment initiation. Treatment of patients at an advanced fibrosis stage with new highly effective drugs will warrant continued surveillance for HCC post-SVR. LAY SUMMARY: We assessed the effect of successful hepatitis C treatment with older interferon-based treatment on the occurrence of liver cancer (hepatocellular carcinoma) and found that successful treatment prevents liver cancer. However, more people with cirrhosis and older age continued to develop liver cancer after successful treatment. Thus, treatment with new drugs among those with cirrhosis will require continued monitoring for liver cancer.
BACKGROUND & AIMS: Evidence is limited on hepatocellular carcinoma (HCC) risk after sustained virological response (SVR) to interferon-based treatment of hepatitis C virus (HCV) infection. We evaluated the effect of SVR on the risk of HCC and estimated its incidence in post-SVR HCVpatients from a large population-based Canadian cohort. METHODS: The British Columbia Hepatitis Testers Cohort includes individuals tested for HCV between 1990-2013 linked with data on their medical visits, hospitalizations, cancers, prescription drugs and mortality. Patients receiving interferon-based HCV treatments were followed from the end of treatment to HCC diagnosis, death or December 31, 2012. We examined HCC risk among those who did and did not achieve SVR using multivariable proportional hazard models with the Fine and Gray modification for competing risks. RESULTS: Of 8147 individuals who received HCV treatment and were eligible for analysis, 4663 (57%) achieved SVR and 3484 (43%) did not. Each group was followed for a median of 5.6years (range: 0.5-12.9) for an HCC incidence rate of 1.1/1000 person-years (PY) among the SVR and 7.2/1000 PY among the no SVR group. The HCC incidence rate was higher among those with cirrhosis (SVR: 6.4, no SVR: 21.0/1000 PY). In the multivariable model, SVR was associated with a lower HCC risk (subdistribution hazard ratio [SHR]=0.20, 95% CI: 0.13-0.3), while cirrhosis (SHR=2.61, 95% CI: 1.68-4.04), age ⩾50years, being male and genotype 3 infection were associated with a higher HCC risk. Among those who achieved SVR, cirrhosis, age ⩾50years and being male were associated with a higher HCC risk. CONCLUSION: SVR after interferon-based treatment substantially reduces but does not eliminate HCC risk, which is markedly higher among those with cirrhosis and age ⩾50years at treatment initiation. Treatment of patients at an advanced fibrosis stage with new highly effective drugs will warrant continued surveillance for HCC post-SVR. LAY SUMMARY: We assessed the effect of successful hepatitis C treatment with older interferon-based treatment on the occurrence of liver cancer (hepatocellular carcinoma) and found that successful treatment prevents liver cancer. However, more people with cirrhosis and older age continued to develop liver cancer after successful treatment. Thus, treatment with new drugs among those with cirrhosis will require continued monitoring for liver cancer.
Authors: Jinping Liu; Wei Tang; Anuradha Budhu; Marshonna Forgues; Maria O Hernandez; Julián Candia; Yujin Kim; Elise D Bowman; Stefan Ambs; Yongmei Zhao; Bao Tran; Xiaolin Wu; Christopher Koh; Pallavi Surana; T Jake Liang; Maria Guarnera; Dean Mann; Manoj Rajaure; Tim F Greten; Zhanwei Wang; Herbert Yu; Xin Wei Wang Journal: Cell Date: 2020-06-10 Impact factor: 41.582
Authors: Ana Zaida Gomez-Moreno; Daniel Pineda-Tenor; Maria Angeles Jimenez-Sousa; Juan Jose Sánchez-Ruano; Tomas Artaza-Varasa; Jose Saura-Montalban; Pablo Ryan; Salvador Resino Journal: PLoS One Date: 2017-09-07 Impact factor: 3.240
Authors: María Ángeles Jiménez-Sousa; Ana Zaida Gómez-Moreno; Daniel Pineda-Tenor; Luz Maria Medrano; Juan José Sánchez-Ruano; Amanda Fernández-Rodríguez; Tomas Artaza-Varasa; José Saura-Montalbán; Sonia Vázquez-Morón; Pablo Ryan; Salvador Resino Journal: PLoS One Date: 2018-05-09 Impact factor: 3.240
Authors: Yun Bin Lee; Joon Yeul Nam; Jeong-Hoon Lee; Young Chang; Hyeki Cho; Young Youn Cho; Eun Ju Cho; Su Jong Yu; Hwi Young Kim; Dong Ho Lee; Jeong Min Lee; Seong Gyu Hwang; Yoon Jun Kim; Jung-Hwan Yoon Journal: Sci Rep Date: 2018-09-12 Impact factor: 4.379