Background: To update the current evidence on whether hepatitis C virus (HCV) infection represents a possible risk factor for renal cell cancer (RCC), prostate cancer (PCa) and bladder cancer (BC).
Methods: We searched literatures on Pubmed, Web of Science and Embases before February 2020. A systematic review and meta-analysis were performed.
Results: Finally, we extracted 12 studies based on the eligible criteria. Across 11 studies for HCV and RCC, the incorporated RR was 1.28 (95% CI 1.05-1.55), which meant that participants with HCV infection were associated with a higher risk of RCC. The pooled RR in hazard ratio (HR) subgroup (HR 1.59, 95% CI 1.22-2.08), cohort studies (CS) subgroup (RR 1.47, 95% CI 1.18-1.82), and North America subgroup (RR 1.71, 95% CI 1.40-2.09) detected a stronger association between HCV and RCC risk. Although an inverse association was seen for PCa (RR 0.75, 95% CI 0.54-1.03) across 7 studies, it was not statistically significant (P = 0.075). There was no significant association between HCV and BC with an incorporated RR of 0.92 (95% CI, 0.82-1.03) across 5 studies.
Conclusions: Our study demonstrated that HCV infection was significantly associated with increased RCC risk. There appeared to be an inverse association for HCV in PCa risk but no statistically significant. No significant association was found between HCV and BC risk. Prospective, large-scale and well-designed cohort studies are required to validate the association between HCV and RCC, and to investigate the role of HCV on PCa.

Figure 1

Figure 2
This is a list of supplementary files associated with this preprint. Click to download.
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Posted 23 Jun, 2020
Posted 23 Jun, 2020
Background: To update the current evidence on whether hepatitis C virus (HCV) infection represents a possible risk factor for renal cell cancer (RCC), prostate cancer (PCa) and bladder cancer (BC).
Methods: We searched literatures on Pubmed, Web of Science and Embases before February 2020. A systematic review and meta-analysis were performed.
Results: Finally, we extracted 12 studies based on the eligible criteria. Across 11 studies for HCV and RCC, the incorporated RR was 1.28 (95% CI 1.05-1.55), which meant that participants with HCV infection were associated with a higher risk of RCC. The pooled RR in hazard ratio (HR) subgroup (HR 1.59, 95% CI 1.22-2.08), cohort studies (CS) subgroup (RR 1.47, 95% CI 1.18-1.82), and North America subgroup (RR 1.71, 95% CI 1.40-2.09) detected a stronger association between HCV and RCC risk. Although an inverse association was seen for PCa (RR 0.75, 95% CI 0.54-1.03) across 7 studies, it was not statistically significant (P = 0.075). There was no significant association between HCV and BC with an incorporated RR of 0.92 (95% CI, 0.82-1.03) across 5 studies.
Conclusions: Our study demonstrated that HCV infection was significantly associated with increased RCC risk. There appeared to be an inverse association for HCV in PCa risk but no statistically significant. No significant association was found between HCV and BC risk. Prospective, large-scale and well-designed cohort studies are required to validate the association between HCV and RCC, and to investigate the role of HCV on PCa.

Figure 1

Figure 2
This is a list of supplementary files associated with this preprint. Click to download.
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