Statin use and risk of prostate cancer: results from a population-based epidemiologic study.
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ABSTRACT:
SUBMITTER: Agalliu I
PROVIDER: S-EPMC2585510 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundEpidemiologic studies suggest that statin use may be inversely associated with risk of prostate cancer, but prior studies have focused predominantly on non-Hispanic white populations.MethodsWe evaluated the association between statin use and prostate cancer risk in the Southern Community Cohort Study (SCCS). Study participants were 32,091 men aged 40-79 at baseline, 67% of whom were non-Hispanic black. Between study enrollment (2002-2009) and December 31, 2010, 570 prostate cancer cases were diagnosed, including 324 low-grade cancers (Gleason score <7 or Gleason pattern 3 + 4) and 107 high-grade cancers (Gleason score >7 or Gleason pattern 4 + 3). Analyses of overall prostate cancer were conducted using Cox regression and analyses of grade-specific cancer were conducted using competing risks models.ResultsTen percent of non-Hispanic black men and 22% of non-Hispanic white men reported use of statins at study enrollment. As compared to non-use, statin use was associated with a non-significant 14% lower risk of prostate cancer in multivariable models (Hazard Ratio [HR]:0.86; 95% Confidence Interval [CI]: 0.63-1.18). This association was stronger for high-grade cancer (HR: 0.62; 95%CI: 0.30, 1.28) than low-grade cancer (HR:0.98; 95%CI: 0.65-1.48). Results were similar by race/ethnicity (p-interaction: 0.41) and did not vary by history of prostate-specific antigen [PSA] screening (p-interaction: 0.65).ConclusionsResults suggest no strong association between statin use and prostate cancer risk overall, and further suggest that if a modest protective effect does exist, it does not vary by race/ethnicity and may be restricted to high-grade tumors, although power to detect differences by subgroup was limited.
| S-EPMC4536142 | biostudies-literature
Project description:BackgroundConflicting evidence suggests that statins act chemopreventively against prostate cancer (PCa). Whether the association of statin use with PCa risk is Gleason score-dependent, time-, dose-respondent is not well studied.MethodsWe conducted a cohort study at a tertiary hospital in the Southeastern US using longitudinal data of electronic medical records (EMR) from 1994 to 2016. Only cancer-free men aged >18 years at baseline with follow-up time of ≥12 months were included. Time-dependent Cox proportional hazards regression was used to estimate adjusted hazard ratios (aHRs) with 95% confidence intervals (CIs).ResultsAmong 13 065 men, 2976 were diagnosed with PCa over median follow-up of 6.6 years. Statin use was associated with lower risk of both Gleason low- (score <7: aHR, 0.85; 95% CI, 0.74-0.96) and high-grade PCa (score ≥7: aHR, 0.54; 95% CI, 0.42-0.69). The protective association was observed only when statins had been used for a relatively longer duration (≥11 months) or higher dose (≥121 defined daily doses), and were more pronounced for PCa of higher Gleason score (<7: aHR, 0.85, 95% CI, 0.74-0.96; 7 [3 + 4]: aHR, 0.62, 95% CI, 0.43-0.90; 7 [4 + 3]: aHR, 0.49, 95% CI, 0.29-0.82; 8: aHR, 0.60, 95% CI, 0.37-0.96; 9-10: aHR, 0.24, 95% CI, 0.11-0.54). Lipophilic statins (aHR, 0.83; 95% CI, 0.72-0.95) might be more protective than hydrophilic statins (aHR, 0.91, 95% CI, 0.63-1.33) against PCa.ConclusionStatin use might be associated with reduced PCa risk only when used for a relatively longer duration, and the risk reduction was higher for PCa of higher Gleason score.
| S-EPMC6885894 | biostudies-literature
Project description:There is extensive debate regarding the protective effect of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins) on colorectal cancer (CRC). We aimed to assess the association between CRC risk and exposure to statins using a large cohort with prescription data. We carried out a case-control study in Catalonia using the System for Development of Primary Care Research (SIDIAP) database that recorded patient diseases history and linked data on reimbursed medication. The study included 25 811 cases with an incident diagnosis of CRC between 2010 and 2015 and 129 117 frequency-matched controls. Subjects were classified as exposed to statins if they had ever been dispensed statins. Analysis considering mean daily defined dose, cumulative duration and type of statin were performed. Overall, 66 372 subjects (43%) were exposed to statins. There was no significant decrease of CRC risk associated to any statin exposure (OR = 0.98; 95% CI: 0.95-1.01). Only in the stratified analysis by location a reduction of risk for rectal cancer was observed associated to statin exposure (OR = 0.87; 95% CI: 0.81-0.92). This study does not support an overall protective effect of statins in CRC, but a protective association with rectal cancer merits further research.
| S-EPMC6753123 | biostudies-literature
Project description:BackgroundPatients living with chronic obstructive pulmonary disease (COPD) are at an increased risk of lung cancer. A common comorbidity of COPD is cardiovascular disease; as such, COPD patients often receive statins. This study sought to understand the association between statin exposure and lung cancer risk in a population-based cohort of COPD patients.MethodsWe identified a population-based cohort of COPD patients based on having filled at least three prescriptions for an anticholinergic or short-acting beta-agonist (SABA). We used an array of methods of defining medication exposure including three conventional methods (ever statin exposure, cumulative duration of use, and cumulative dose) and two novel methods (recency-weighted cumulative duration of use and recency-weighted cumulative dose). To assess residual confounding, a negative control exposure was used to test the validity of our results. All exposure variables were time-dependent.ResultsThe population-based cohort of COPD had 39,879 patients with mean age of 70.6 (SD: 11.2) years and, of which, 53.5% were female. There were 12,469 patients who received at least one statin prescription. Results from the reference case multivariable analysis indicated a reduced risk from statin exposure (HR: 0.85 (95% CI: 0.73-1.00) in COPD patients, but this result not statistically significant. Using the two recency-weighted modelling approaches, statin exposure was associated with a statistically significant reduction in lung cancer risk (recency-weighted cumulative dose, HR: 0.85 (95% CI: 0.77-0.93) and recency-weighted cumulative duration of use, HR: 0.97 (95% CI: 0.96-0.99). Multivariable analysis incorporating the negative control exposure was not statistically significant (HR: 0.89 (95% CI: 0.75-1.10).ConclusionsThe results of this population-based analysis indicate that statin use in COPD patients may reduce the risk of lung cancer. While the effect was not statistically significantly across all exposure definitions, the overall results support the hypothesis that COPD patients might benefit from statin therapy.
| S-EPMC7236956 | biostudies-literature
Project description:To test the hypothesis that hydroxymethyl glutaryl coenzyme A reductase inhibitors (statins) may decrease the risk of community acquired pneumonia.Population based case-control study.Group Health, a large integrated healthcare delivery system. Population Immunocompetent, community dwelling Group Health members aged 65 to 94; two matched controls for each case with pneumonia. Information on comorbid illnesses and functional and cognitive status, potential confounders of the association between statin use and risk of pneumonia, came from medical record review and computerised pharmacy data.Adjusted estimates of risk of pneumonia in relation to current statin use.1125 validated cases of pneumonia and 2235 matched controls were identified. Compared with controls, cases were more likely to have chronic lung and heart disease, especially severe disease, and functional or cognitive impairment. Current statin use was present in 16.1% (181/1125) of cases and 14.6% (327/2235) of controls (adjusted odds ratio 1.26, 95% confidence interval 1.01 to 1.56). Among cases admitted to hospital and matched controls, current statin use was present in 17.2% (68/395) of cases and 14.2% (112/788) of controls (adjusted odds ratio 1.61, 1.08 to 2.39, compared with non-use). In people in whom statins were indicated for secondary prevention, the adjusted odds ratio for risk of pneumonia in relation to current statin use was 1.25 (0.94 to 1.67); in those with no such indication, it was 0.81 (0.46 to 1.42).Statin use was not associated with decreased risk of pneumonia among immunocompetent, community dwelling older people. Findings of previous studies may reflect "healthy user" bias.
| S-EPMC2697311 | biostudies-other
Project description:AIMS:To examine the association between statin use before and after intracranial haemorrhage (ICH) and the risk of poststroke epilepsy (PSE). METHODS:Patients with new-onset ICH between 2004 and 2012 were identified from the Taiwan National Health Insurance Research Database. The main outcome was the occurrence of epilepsy after stroke. Multivariable Cox regression modelling was used to estimate the association between statin use and the risk of PSE, with poststroke medication exposures being treated as time-dependent variables. RESULTS:A total of 7435 patients with ICH were enrolled with a median follow-up of 17.6 months. Within the study cohort, 709 patients developed PSE. Poststroke, but not prestroke, stain use was associated with a reduced risk of PSE (adjusted hazard ratio 0.62, 95% confidence interval 0.42-0.90, P = 0.01). In subanalyses, a trend of a dose-response relationship was observed. A significant PSE risk reduction was correlated with a higher cumulative statin dose. Moreover, the risk of PSE was lower in patients receiving moderate-to-high-intensity statin therapy (adjusted hazard ratio 0.37, 95% confidence interval 0.18-0.75, P = 0.01). Lipophilic and hydrophilic statins were similar with regard to their associations with the reduced risk of PSE. CONCLUSIONS:Statin therapy may reduce the risk of PSE after ICH, especially with moderate-to-high therapy intensity. Further research is needed to understand the mechanisms underlying the potential protective effects of statins against PSE in this patient population.
| S-EPMC6089806 | biostudies-other
Project description:DNA repair pathways are crucial to prevent accumulation of DNA damage and maintain genomic stability. Alterations of this pathway have been reported in many cancers. An increase in oxidative DNA damage or decrease in DNA repair capacity with aging or due to germline genetic variation may affect prostate cancer risk.Pooled data from two population-based studies (1,457 cases and 1,351 controls) were analyzed to examine associations between 28 single-nucleotide polymorphisms (SNPs) in nine DNA repair genes (APEX1, BRCA2, ERCC2, ERCC4, MGMT, MUTYH, OGG1, XPC, and XRCC1) and prostate cancer risk. We also explored whether associations varied by smoking, by family history or clinical features of prostate cancer.There were no associations between these SNPs and overall risk of prostate cancer. Risks by genotype also did not vary by smoking or by family history of prostate cancer. Although two SNPs in BRCA2 (rs144848, rs1801406) and two SNPs in ERCC2 (rs1799793, rs13181) showed stronger associations with high Gleason score or advanced-stage tumors when comparing homozygous men carrying the minor versus major allele, results were not statistically significantly different between clinically aggressive and non-aggressive tumors.Overall, this study found no associations between prostate cancer and the SNPs in DNA repair genes. Given the complexity of this pathway and its crucial role in maintenance of genomic stability, a pathway-based analysis of all 150 genes in DNA repair pathways, as well as exploration of gene-environment interactions may be warranted.
| S-EPMC2811225 | biostudies-literature
Project description:The role of metformin in prostate cancer chemoprevention remains unclear. REDUCE, which followed biopsy-negative men with protocol-dictated PSA-independent biopsies at 2- and 4-years, provides an opportunity to evaluate the link between metformin use and prostate cancer diagnosis with minimal confounding from screening biases. In diabetic men from REDUCE, we tested the association between metformin use, use of other antidiabetic medications, versus no antidiabetic medication use, and prostate cancer diagnosis as well as prostate cancer grade (low-grade Gleason 4-6 and high-grade Gleason 7-10) using logistic regression. Of the 540 diabetic men with complete data, 205 (38%) did not report use of any antidiabetic medications, 141 (26%) reported use of at least one antidiabetic medication other than metformin, and 194 (36%) reported use of metformin. During the 4-year study, 122 men (23%) were diagnosed with prostate cancer. After adjusting for various clinical and demographic characteristics, we found that metformin use was not significantly associated with total (OR, 1.19; P = 0.50), low- (OR, 1.01; P = 0.96), or high-grade (OR, 1.83; P = 0.19) prostate cancer diagnosis. Likewise, there was no significant association between the use of non-metformin antidiabetic medications and prostate cancer risk in both crude (OR, 1.02; P = 0.95) and multivariable analysis (OR, 0.85; P = 0.56). Furthermore, the interactions between antidiabetic medication use and BMI, geographic location, coronary artery disease, smoking, and treatment group were not significant (all P > 0.05). Among diabetic men with a negative prestudy biopsy who all underwent biopsies largely independent of PSA, metformin use was not associated with reduced risk of prostate cancer diagnosis.
| S-EPMC4651624 | biostudies-literature
Project description:BackgroundEmerging evidence suggests that statins may decrease the risk of cancers. However, available evidence on prostate cancer (PCa) is conflicting. We therefore examined the association between statin use and risk of PCa by conducting a detailed meta-analysis of all observational studies published regarding this subject.MethodsLiterature search in PubMed database was undertaken through February 2012 looking for observational studies evaluating the association between statin use and risk of PCa. Before meta-analysis, the studies were evaluated for publication bias and heterogeneity. Pooled relative risk (RR) estimates and 95% confidence intervals (CIs) were calculated using random-effects model (DerSimonian and Laird method). Subgroup analyses, sensitivity analysis and cumulative meta-analysis were also performed.ResultsA total of 27 (15 cohort and 12 case-control) studies contributed to the analysis. There was heterogeneity among the studies but no publication bias. Statin use significantly reduced the risk of both total PCa by 7% (RR 0.93, 95% CI 0.87-0.99, p = 0.03) and clinically important advanced PCa by 20% (RR 0.80, 95% CI 0.70-0.90, p<0.001). Long-term statin use did not significantly affect the risk of total PCa (RR 0.94, 95% CI 0.84-1.05, p = 0.31). Stratification by study design did not substantially influence the RR. Furthermore, sensitivity analysis confirmed the stability of results. Cumulative meta-analysis showed a change in trend of reporting risk from positive to negative in statin users between 1993 and 2011.ConclusionsOur meta-analysis provides evidence supporting the hypothesis that statins reduce the risk of both total PCa and clinically important advanced PCa. Further research is needed to confirm these findings and to identify the underlying biological mechanisms.
| S-EPMC3462187 | biostudies-literature
Project description:BackgroundIn addition to their potent lipid-lowering action, statins may modulate inflammation. However, data on statin use and the risk of inflammatory bowel diseases [IBD] have been inconsistent.MethodsWe searched the Nationwide Swedish Patient Register [inpatient and non-primary outpatient care] to identify adults diagnosed with Crohn's disease [CD, n = 7637] or ulcerative colitis [UC, n = 15 652] from 2006 to 2014. Each case was matched to 10 general population controls [n = 232 890]. Data on dispensed statin prescriptions were extracted from the Prescribed Drug Register. Conditional logistic regression models estimated odds ratios [ORs] for risk of IBD according to statin exposure while controlling for potential confounders, including indications for statin therapy.ResultsIn multivariable adjusted models, compared with no statin use, any statin use was associated with a lower risk of CD (OR = 0.71; 95% confidence interval [CI], 0.63-0.79), but not UC [OR = 1.03; 95% CI, 0.96-1.11]. The lowest OR for CD was seen for current statin use [OR = 0.67; 95% CI, 0.60-0.75]. For CD, the lowest category of cumulative statin dose [31-325 defined daily dose, DDD] was associated with an OR of 0.73 [95% CI, 0.61-0.88] and the highest category [>1500 DDD] with an OR of 0.66 [95% CI, 0.55-0.80], ptrend = 0.10. For UC, the lowest and highest dose categories yielded ORs of 1.12 [95% CI, 1.00-1.25] and 0.99 [95% CI, 0.88-1.13], respectively, ptrend = 0.13.ConclusionsStatin use was associated with a lower risk of CD, but not of UC. The association with CD risk appeared strongest for current statin use. Our findings suggest that statin use may influence the development of CD.
| S-EPMC8247597 | biostudies-literature