scholarly journals Aspirin decreases hepatocellular carcinoma risk in hepatitis C virus carriers: a nationwide cohort study

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Yen-Hsiang Liao ◽  
Ren-Jun Hsu ◽  
Tzu-Hwei Wang ◽  
Chen-Ta Wu ◽  
Sheng-Yao Huang ◽  
...  

Abstract Background Aspirin has been found to lower the occurrence rates of some cancers through the inhibition of the cyclooxygenase enzyme. For example, there is a well-known association between aspirin use and the occurrence of hepatocellular carcinoma (HCC) in hepatitis B virus (HBV) carriers. However, the association, if any, between aspirin use and HCC in hepatitis C virus (HCV) carriers is unknown. Therefore, this study compared the occurrence rates of HCC in HCV carriers treated with or without aspirin. Methods The participants in this retrospective cohort study consisted of people newly diagnosed with HCV in Taiwan from 2000 to 2012. Those who were treated with aspirin were defined as the control group, whereas those not treated with aspirin were defined as the comparison cohort. We used a 1:1 propensity score matching by age, sex, comorbidities, drugs, diagnosis year, and index year with covariate assessment. Results Our study sample consisted of 2980 aspirin-treated HCV carriers and 7771 non-aspirin-treated HCV carriers. After propensity score matching, each cohort consisted of 1911 HCV carriers. The adjusted hazard ratio (aHR) of HCC incidence in the aspirin users (aHR = 0.56, 95% CI = 0.43–0.72, p < 0.001) was significantly lower than that in the non-aspirin users. A Kaplan-Meier analysis showed that among the HCV carriers, the aspirin users had a lower cumulative incidence rate of HCC over the first 10 years of aspirin treatment (p < 0.0001). Conclusions The HCC incidence rate was lower in the aspirin-using HCV carriers than in the non- aspirin-using HCV carriers, indicating that the effects of aspirin might occur through inhibition of the cyclooxygenase enzyme pathway. Moreover, protection from HCC was provided by less than a year of aspirin treatment, while treatment with aspirin for 1 to 2 years exhibited the greatest protective effect. We therefore encourage aspirin treatment to prevent HCC in HCV carriers.

2019 ◽  
Author(s):  
Yen-Hsiang Liao ◽  
Ren-Jun Hsu ◽  
Tzu-Hwei Wang ◽  
Chen-Ta Wu ◽  
Sheng-Yao Huang ◽  
...  

Abstract Background Aspirin has been found to lower the occurrence rates of some cancers through the inhibition of the cyclooxygenase enzyme. For example, there is a well-known association between aspirin use and the occurrence of hepatocellular carcinoma (HCC) in hepatitis B virus (HBV) carriers. However, the association, if any, between aspirin use and HCC in hepatitis C virus (HCV) carriers is unknown. Therefore, this study compared the occurrence rates of HCC in HCV carriers treated with or without aspirin. Methods The participants in this retrospective cohort study consisted of people newly diagnosed with HCV in Taiwan from 2000 to 2012. Those who were treated with aspirin were defined as the control group, whereas those not treated with aspirin were defined as the comparison cohort. We used a 1:1 propensity score matching by age, sex, comorbidities, drugs, diagnosis year, and index year with covariate assessment. Results Our study sample consisted of 2980 aspirin-treated HCV carriers and 7771 non-aspirin-treated HCV carriers. After propensity score matching, each cohort consisted of 1911 HCV carriers. The adjusted hazard ratio (aHR) of HCC incidence in the aspirin users (aHR=0.56, 95% CI=0.43-0.72, p < 0.001 ) was significantly lower than that in the non-aspirin users. A Kaplan-Meier analysis showed that among the HCV carriers, the aspirin users had a lower cumulative incidence rate of HCC over the first 10 years of aspirin treatment ( p < 0.0001 ). Conclusions The HCC incidence rate was lower in the aspirin-using HCV carriers than in the non- aspirin-using HCV carriers, indicating that the effects of aspirin might occur through inhibition of the cyclooxygenase enzyme pathway. Moreover, protection from HCC was provided by less than a year of aspirin treatment, while treatment with aspirin for 1 to 2 years exhibited the greatest protective effect. We therefore encourage aspirin treatment to prevent HCC in HCV carriers.


2019 ◽  
Author(s):  
Yen-Hsiang Liao ◽  
Wen-Lin Hsu ◽  
Tzu-Hwei Wang ◽  
Chen-Ta Wu ◽  
Sheng-Yao Huang ◽  
...  

Abstract Background Aspirin lowered some cancer occurrence rate, through the inhibition of the cyclooxygenase enzyme. The association of aspirin-use and hepatocellular carcinoma (HCC) occurrence rate in hepatitis B virus (HBV) carriers is well known. However, the association in hepatitis C virus (HCV) carriers is not known. Our purpose is comparing the HCC occurrence rate in HCV carriers with or without Aspirin treatment. Methods In this retrospective cohort study, the participants were ones newly-diagnosed with HCV from 2000 to 2012 in Taiwan. These HCV carriers with aspirin treatment were defined as the control group, whereas those without aspirin were defined as a compared cohort. We used a 1:1 propensity score matching by age, sex, comorbidities, drugs, diagnosis year and index year with covariate assessment. Results Our study sample consisted of 2980 aspirin-treated HCV carriers and 7771 non-aspirin-treated HCV carriers. After propensity score matching, each cohort consisted of 1911 HCV carriers. The adjusted hazard ratio (aHR) of HCC incidence in aspirin users (aHR=0.56, 95% CI=0.43-0.72, p < 0.001 ) was significantly lower than that in non-aspirin users. The Kaplan-Meier curves show that among the HCV carriers, aspirin users had a lower cumulative incidence rate of HCC in the first 10-year aspirin treatment course ( p < 0.0001 ). Conclusions The HCC incidence rate was lower in the aspirin users than non- aspirin users among HCV carriers, supporting the aspirin effect may be acting through inhibition of the cyclooxygenase enzyme pathway. Moreover, the patients got HCC protection by aspirin within 1-year treatment course and had best HCC prevention during 1- to 2-year aspirin treatment course. We encourage aspirin treatment to prevent HCC in HCV carriers.


2017 ◽  
Vol 05 (03) ◽  
Author(s):  
Jennifer Wu ◽  
Tsivia Hochman ◽  
Judith D Goldberg ◽  
Jafar Al Mondhiry ◽  
Bennal Perkins ◽  
...  

2018 ◽  
Vol 12 (1) ◽  
pp. 26-32 ◽  
Author(s):  
Arnolfo Petruzziello

Introduction:Hepatocellular carcinoma (HCC) is one of the most prevalent primary malignant tumors and accounts for about 90% of all primary liver cancers. Its distribution varies greatly according to geographic location and it is more common in middle and low- income countries than in developed ones especially in Eastern Asia and Sub Saharan Africa (70% of all new HCCs worldwide), with incidence rates of over 20 per 100,000 individuals.Explanation:The most important risk factors for HCC are Hepatitis B Virus (HBV) infection, Hepatitis C Virus (HCV) infection, excessive consumption of alcohol and exposition to aflatoxin B1. Its geographic variability and heterogeneity have been widely associated with the different distribution of HBV and HCV infections worldwide.Chronic HBV infection is one of the leading risk factors for HCC globally accounting for at least 50% cases of primary liver tumors worldwide. Generally, while HBV is the main causative agent in the high incidence HCC areas, HCV is the major etiological factor in low incidence HCC areas, like Western Europe and North America.Conclusion:HBV-induced HCC is a complex, stepwise process that includes integration of HBV DNA into host DNA at multiple or single sites. On the contrary, the cancerogenesis mechanism of HCV is not completely known and it still remains controversial as to whether HCV itself plays a direct role in the development of tumorigenic progression.


2011 ◽  
Vol 140 (5) ◽  
pp. S-924-S-925 ◽  
Author(s):  
Hillary Lin ◽  
Nghiem B. Ha ◽  
Deawodi Ladzekpo ◽  
Aijaz Ahmed ◽  
Walid Ayoub ◽  
...  

2020 ◽  
Vol 9 (3) ◽  
pp. 796 ◽  
Author(s):  
Naim Abu Freha ◽  
Tamar Wainstock ◽  
Tzvi Najman Menachem ◽  
Eyal Sheiner

This study aimed to investigate the long-term effect of maternal hepatitis B virus (HBV) or hepatitis C virus (HCV) carrier status on offspring endocrine morbidity. A population-based cohort study included all singleton deliveries between the years 1991–2014 at the Soroka University Medical Center, Beer-Sheva, Southern Israel. The mothers were subdivided into three groups, HBV carriers, HCV carriers and non-carriers. Data regarding the long-term endocrine morbidity of their offspring were compared between the groups. The study included 242,905 (99.7%) non-carrying mothers, 591 (0.2%) mothers who were carriers for HBV and 186 (0.1%) mothers who were carriers for HCV. The Kaplan–Meier’s survival curve demonstrated a significantly higher cumulative endocrine morbidity in children born to mothers with HCV (log-rank test, p = 0.002). Specifically, higher rates of hypoglycemia were noted among the offspring born to mothers who were carriers of HCV (1.1%; p = 0.001) compared with the offspring of mothers who were either carriers of HBV (0.2%) or non-carriers (0.1%). A Cox regression model controlled for maternal age, gestational age, maternal diabetes, hypertensive disorders of pregnancy, found maternal HCV carrier status to be independently associated with pediatric endocrine morbidity in the offspring (adjusted hazard ratio = 5.05, 95% CI: 1.625–15.695, p = 0.005). Maternal HCV carrier status is an independent risk factor for long-term endocrine morbidity.


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