ABSTRACT
Even though the relationship between antiarrhythmic drug usage and subsequent prostate cancer (PCa) risk has recently been highlighted, relevant findings in the previous literature are still inconsistent. In addition, very few studies have attempted to investigate the association between sodium channel blockers or potassium channel blockers for arrhythmia and the subsequent PCa risk. Therefore, this cohort study aimed to find the relationship between antiarrhythmic drug usage and the subsequent PCa risk using a population-based dataset. The data used in this study were derived from the Longitudinal Health Insurance Database 2005, Taiwan, China. We respectively identified 9988 sodium channel blocker users, 3663 potassium channel blocker users, 65 966 beta-blocker users, 23 366 calcium channel blockers users, and 7031 digoxin users as the study cohorts. The matched comparison cohorts (one comparison subject for each antiarrhythmic drug user) were selected from the same dataset. Each patient was tracked for a 5-year period to define those who were subsequently diagnosed with PCa. After adjusting for sociodemographic characteristics, comorbidities, and age, Cox proportional hazard regressions found that the hazard ratio (HR) of subsequent PCa for sodium channel blocker users was 1.12 (95% confidence interval [CI]: 0.84-1.50), for potassium channel blocker users was 0.89 (95% CI: 0.59-1.34), for beta-blocker users was 1.08 (95% CI: 0.96-1.22), for calcium channel blocker users was 1.14 (95% CI: 0.95-1.36), and for digoxin users was 0.89 (95% CI: 0.67-1.18), compared to their matched nonusers. We concluded that there were no statistical associations between different types of antiarrhythmic drug usage and subsequent PCa risk.
ABSTRACT
Prior studies suggested that the use of androgen deprivation therapy (ADT) in patients with prostate cancer (PC) might cause the impairment of cognitive function which is one of the common symptoms of dementia; however, the association between ADT and cognitive impairment still remains controversial. This retrospective cohort study aimed to investigate the relationship between ADT and subsequent risk of dementia using a population-based dataset. Data for this study were taken from the Taiwan (China)Longitudinal Health Insurance Database 2005. We included 755 PC patients who received ADT in the study cohort and 559 PC patients who did not receive ADT in the comparison cohort. Each patient was individually tracked for a 5-year period to define those who subsequently received a diagnosis of dementia. Results show that the incidence rates of dementia per 100 person-years were 2.35 (95% confidence interval [95% CI]: 1.82-2.98) and 1.85 (95% CI: 1.35-2.48) for PC patients who received ADT and those who did not receive ADT, respectively. The adjusted hazard ratio (HR) for dementia for PC patients who received ADT was 1.21 (95% CI: 0.82-1.78, P = 0.333) compared to those who did not receive ADT. In addition, the adjusted HRs for dementia for PC patients receiving ADT with gonadotropin-releasing hormone (GnRH) agonists and without GnRH agonists were 1.39 (95% CI: 0.80-2.40, P = 0.240) and 1.13 (95% CI: 0.75-1.71, P = 0.564), respectively, compared to PC patients not receiving ADT. We concluded that there was no difference in the risk of subsequent dementia between PC patients who did and those who did not receive ADT.