Gout and Dementia May Be Linked
By Lorraine L. Janeczko
NEW YORK—Gout may be linked with a higher risk of developing dementia in the elderly, according to new research.
"Gout may be a marker of other chronic conditions, and perhaps clinicians may discuss the possibility of dementia with their patients who have gout," Dr. Jasvinder Singh of the University of Alabama in Birmingham, who worked on the study, told Reuters Health by phone. "But as with any epidemiological study, ours has several limitations, and more studies, including clinical trials, need to be conducted to understand the pathogenic pathways involved in the increased risk."
Dr. Singh presented the results at EULAR 2018, the annual meeting of the European League Against Rheumatism, in Amsterdam, the Netherlands, on June 14.
He and coauthor Dr. J. D. Cleveland, also at the University of Alabama at Birmingham, conducted an observational cohort study based on Medicare claims data.
They used multivariable-adjusted Cox proportional hazard models to determine the link between gout and incident dementia, adjusting for demographics, comorbidities and medications commonly used for cardiac diseases and gout.
Of the 1.23 million Medicare beneficiaries, 65,324 had incident dementia. The crude incidence rates in those without and with gout were 7.36 and 13.58 per 1,000 person-years, respectively.
In multivariable-adjusted analyses, gout was independently linked with a significantly higher hazard of incident dementia (hazard ratio, 1.17), which was confirmed in sensitivity analyses.
Being older than 75 years was associated with a 6.3-fold higher hazard of dementia. Dementia risk was also higher for females, those who were black and those with more medical comorbidity.
In subgroup analyses, gout was significantly linked with dementia in patients without key comorbidities: coronary artery disease, cardiovascular disease, hypertension, hyperlipidemia or diabetes, but not in those with each comorbidity, except coronary artery disease.
Dr. Singh acknowledged several limitations of the study, including that they examined data from people 65 years and above only, so the findings cannot be generalized to the wider population. Possible misclassification, diagnostic code errors, and other biases may also have arisen from reviewing records and claims data instead of examining and diagnosing people, he added.
"Any epidemiological study will always be subject to residual confounding bias," Dr. Singh explained, "meaning that we may not have measured some factor that can be causing both gout and dementia."
He noted that the study has several strengths, including that the Medicare data are quite representative of adults 65 and above and that they had a large sample size.
Dr. Alexander So, a professor of rheumatology at Lausanne University Hospital in Switzerland, told Reuters Health by email, "This study contributes to the current debate on how gout and the underlying condition hyperuricemia may impact cognitive function. Is hyperuricemia neuroprotective? Is gout deleterious to cognitive function? This data would suggest the latter."
Dr. So, who was not involved in the study, said studies will need to address whether the association is due to increased vascular disease, what type of dementia is involved and whether the link is really secondary to diabetes and hypertension.
"For the moment," he observed, "this data will not impact clinical practice, but it reinforces the notion that gout patients are at risk for many comorbid conditions such as hypertension, cardiac diseases - and now, possibly dementia."
Dr. Singh said, "The most important question in my mind is, does gout actually cause dementia? If so, how can we establish causality?"
"What is the mechanism? Uric acid, inflammation, mitochondrial dysfunction, oxidative stress, biochemical changes, inflammation, some factor we have not yet measured?" he wondered. "Because if we understand the mechanism, we can think of ways to either slow down the process or prevent it."
The study received no commercial funding.
Ann Rheum Dis 2018.
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