Abstract
A protective effect of statins on primary liver cancer (PLC) risk has been suggested. However, issues about the dose–response relationship, the protective effect of individual statins, and PLC risk reduction among at-risk populations remain unsolved. Therefore, a meta-analysis was conducted. PubMed and EMBASE were searched for studies providing the risk ratio (RR) on statins and PLC risk. Summary RRs were calculated using a random-effects model. Twenty-five studies were identified. Stain use was significantly associated with a reduced risk of PLC (RR = 0.60, 95% confidence interval (CI) = 0.53–0.69). The summary RR for every additional 50 cumulative defined daily doses per year was 0.87 (95% CI = 0.83–0.91). Evidence of a non-linear dose–response relationship between statins and PLC risk was found (Pnon-linearity < 0.01). All individual statins significantly reduced PLC risk, and the risk reduction was more evident with rosuvastatin. The inverse association between statins and PLC risk remained among populations with common risk factors. Subgroup analyses revealed more significant reduction in PLC risk by statins in high- versus non-high-risk populations (Pinteraction = 0.02). Overall, these findings add to our understanding of the association between statins and PLC risk. Whether statin use is causally associated with a reduced risk of PLC should be further studied.
Highlights
Recent meta-analysis[11] included around half of studies currently available
Findings from the overall meta-analysis supported an inverse association between statin use and Primary liver cancer (PLC) risk, which are consistent with previous meta-analyses[11,24,25]
Our two-stage dose–response analysis indicated that higher statin dose was associated with a lower risk of PLC
Summary
Recent meta-analysis (involving a total of 12 studies)[11] included around half of studies currently available. Studies were considered for inclusion if they were observational studies (cohort, nested case-control or case-control studies) or post hoc analyses of randomized controlled trials (RCTs) where risk estimate on the association of statin use with PLC risk was available. On the basis of specific statin dose, distribution of cases and person years or controls, and adjusted RRs with 95% CIs, a two-stage dose–response meta-analysis was conducted to determine whether higher statin dose was associated with a lower risk of PLC.
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