Background Data on the risk of venous thromboembolism (VTE, including deep venous thrombosis and pulmonary embolism) in patients with gout are scarce.
Objectives 1) To estimate the overall risk of VTE in an incident gout cohort; 2) To estimate the temporal trends of VTE before and after gout diagnosis compared with the general population.
Methods We conducted a matched cohort study using a population based administrative health database that includes all outpatient visits, hospital admissions, vital statistics, and dispensed medications for all residents in British Columbia, Canada. Gout cases were defined using one ICD-9/10 code (274/M10) from a physician or hospital visit. To ensure incident gout, we required that all cases have ≥10 years of prior registration without a gout diagnosis. Gout cases were matched 1:1 with controls on age, sex, and cohort entry time. Prior VTE events were excluded after matching. VTE was defined using ICD-9/ICD-10 codes plus use of oral anti-coagulant. We calculated incidence rate ratios (IRRs) and age, sex, and entry time matched multivariable hazard ratios (HRs) for the risk of VTE. Sensitivity analyses were conducted to assess for unmeasured confounders (e.g., obesity).
Results Among 105,307 individuals with newly diagnosed gout (61% male, mean age of 58 yrs), we observed 1,212 VTE events (mean follow-up time of 5.3 yrs). The fully adjusted HR was 1.27 (95% CI, 1.16–1.39) (Table 1). Our results remained significant in the sensitivity analyses (OR of 2.0 between gout and unmeasured confounder and a 50% prevalence for obesity). There were 437 incident VTE events within 3 yrs prior to the gout diagnosis. Compared to controls, during the 3rd, 2nd, and 1st yrs before gout diagnosis, the fully adjusted HRs for VTE in patients with imminent gout were 1.51, 1.58 and 1.73. The corresponding HRs in the 1st, 2nd, 3rd, 4th, and 5th yrs after gout diagnosis were 1.54, 1.39, 1.38, 1.37, and 1.32, respectively.
Conclusions Patients with gout have an increased risk of VTE. The risk increases gradually before gout diagnosis, peaks in the year prior to gout diagnosis, and then progressively declines. Our findings suggest that hyperuricemia or gout associated inflammation may be a contributing factor for VTE.
Disclosure of Interest None declared