Abstract

BackgroundGout affects 1-4% of the population in the industrialized world. Increased levels of serum urate is the strongest risk factor and “path variable” for gout development. Parkinson’s disease (PD) is the second most common neurodegenerative disease in the world affecting 1% of the population over the age 60 in North America and Western Europe. A reduced risk of PD has been reported in association with smoking, caffeine consumption and higher serum urate levels.ObjectivesTo determine the incidence of PD in all patients with gout compared to matched controls in the region of western Sweden (VGR).MethodsAll incident and prevalent gout cases from 2001 through 2019 were identified in the health care consumption database VEGA covering all health care in VGR. A case of gout was defined as having received a diagnosis of gout (M10) from a physician. Up to 5 controls from the census register were included matched by age, gender and municipality at year of first gout diagnosis (index-year). A case of PD was defined as having been given a diagnosis of PD (G20.9) at a visit to a physician. A PD diagnosis in the index-year and the 1 to 19 years before was considered prevalent in cases and controls and they were censored from the study. Cases and controls were followed until first of; end of study (2019-12-31), incident PD diagnosis, migration or death. Data on comorbidities at baseline/indexyear were retrieved from VEGA and information on education, death and migration were retrieved from registers at the National Board of Health and Welfare. Effect of gout on risk of PD was calculated using time dependent COX regression on whole population and stratified by sex, adjusted for age, sex, educational level, risk factors for gout (diabetes, obesity, chronic kidney disease (CKD)) and PD (cerebrovascular disease (CeVD), chronic obstructive pulmonary disease (COPD) as a proxy for smoking and malignant melanoma (MM)).ResultsWe identified 48907 cases of gout (67% male) and 198717 (65% male) matched controls with a mean (SD) age of 68 (15) and 67 (15) respectively. In the case population we found 205 prevalent cases of PD compared to 2205 in the controls (prevalence ratio = 0.91 (95% CI:0.87-0.94)). They were all removed from further analysis. All comorbidities, (hypertension, ischemic heart disease, heart failure, CeVD, diabetes, dyslipidemia, obesity, CKD, COPD, and MM were significantly more common in the gout cases vs controls. During a median follow-up time of 5.8 years we identified 364 (0.7%) incident cases of PD in the gout population compared to 1965 (1.0%) in the controls. Adjusting for only age and sex in time dependent COX regression, (Model 1, Table 1) the relative risk reduction in gout patients for incident PD overall was 25% (HR 0.75; 95% CI:0.70-0.84). In age-adjusted models stratified by sex results were similar, HR 0.77 (95% CI:0.68-0.87) for men and HR = 0.69 (95% CI:0.54-0.87) for women. Adjusting also for known risk factors for gout and PD gave similar point estimates (model 2, Table 1).Table 1.Time dependent COX regression on risk of incident gout in the total population and stratified by age and sex. Model 1 adjusted for age and sex, model 2 adjusted for age, sex, educational level, diabetes, obesity, CKD, CeVD, COPD, MM. HR = hazard ratio, CI confidence intervalModel 1Model 2HR 95% CIp-valueHR 95% CIp-valueTotal population0.75 (0.70-0.84)<.00010.75 (0.67-0.84)<.0001Men0.77 (0.68-0.87)<.00010.77 (0.68-0.88)<.0001Women0.68 (0.53-0.86)0.00140.68 (0.53-0.86)0.0016Age group 18-69Total population0.78 (0.65-0.95)0.01130.78 (0.65-0.95)0.0137Men0.80 (0.65-0.99)0.04150.82 (0.66-1.01)0.0631Women0.67 (0.41-1.08)0.09670.61 (0.37-1.00)0.0505Age group 70+Total population0.71 (0.62-0.82)<.00010.72 (0.63-0.84)<.0001Men0.73 (0.62-0.85)<.00010.73 (0.62-0.86)0.0002Women0.68 (0.51-0.89)0.00490.70 (0.53-0.93)0.0130ConclusionGout is associated with a significant risk reduction for incident PD. This may have implications for management of urate lowering therapy in persons with increased risk for PD and for the understanding of PD pathogenesis.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

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