Background/Purpose: To assess if gout is associated with a higher risk of incident chronic pain in older adults, 65 years or older.

Methods: This study used the 2006-2012 Medicare claims data. We used multivariable-adjusted Cox regression analyses to examine the association of pre-existing diagnosis of gout with incident (new) diagnosis of chronic pain, adjusting for demographics, medical comorbidity and use of common medications for cardiovascular disease and gout. Sensitivity analyses substituted Charlson-Romano score with a categorical variable or each Charlson-Romano comorbidity. Gout was identified by the presence of two claims for gout at least 4 weeks apart, with International Classification of Diseases, ninth revision, common modification (ICD-9-CM) code of 274.xx. Study outcome was was incident (new) chronic pain, with an absence of this diagnosis in the baseline period of ³1 year, that occurred in patients with or without pre-existing gout diagnosis that preceded the diagnosis of chronic pain. We identified chronic pain by the occurrence of at least two claims 4-weeks apart containing any of the following ICD-9-CM codes [12]. 307.80, 307.89, 338.0, 338.2, 338.4, 719.41, 719.45 – 719.47, 719.49, 720.0, 720.2, 720.9, 721.0 – 721.4, 721.6, 721.8, 721.9, 722, 723.0, 723.1, 723.3 – 723.9, 724.0 – 724.6, 724.70, 724.79, 724.8, 724.9, 729.0 – 729.2, 729.4, 729.5. This approach has been shown to be valid, with positive predictive value of 95%, sensitivity of 70% and specificity of 99%. We used multivariable-adjusted Cox proportional hazard models to assess the association of gout with incident GCA, adjusting for potential confounders/covariates including demographics (age, race, gender), comorbidities (Charlson-Romano comorbidity index), and medications commonly used for cardiac diseases (statins, beta-blockers, diuretics, and angiotensin converting enzyme (ACE)-inhibitors) and gout (allopurinol and febuxostat; Model 1).  

Results: There were 1,321,521 eligible people, of whom 424,518 developed incident chronic pain. Crude incidence rates of chronic pain were as follow: gout, 158.1 per 1,000 person-years and no gout, 64.5 per 1,000 person-years. In multivariable-adjusted Cox regression analyses, gout was associated with higher hazard ratio of chronic pain, 2.02 (95% CI, 1.98, 2.05), confirmed in sensitivity analyses 1.96 (95% CI, 1.93, 1.99) (model 2) and 1.77 (95% CI, 1.74, 1.80) (model 3).

No meaningful differences were found by gender and race in subgroup analyses; slightly lower hazard of gout with chronic pain was seen in oldest people (Table 1).

Conclusion: Gout was associated with a doubling of the risk of chronic pain. Efforts must be made to optimize gout control and gout inflammation, so that long-term sequalae of gout, including chronic pain can be avoided and when present, treated early and appropriately.