NEW YORK – Evidence is emerging that treating hyperuricemia and gout could help control comorbid cardiovascular disease, according to Dr. Michael H. Pillinger, director of the rheumatology fellowship program at New York University and director of rheumatology at the Manhattan VA Hospital, New York.
Patients with gout tend to have an average of three to four comorbidities, including hypertension, hyperlipidemia, kidney disease, diabetes, and coronary artery disease. Now there is some limited evidence indicating that lowering uric acid may help to reduce cardiovascular mortality, Dr. Pillinger said at a rheumatology meeting sponsored by New York University.
Dr. Michael H. Pillinger
Data presented at last year’s American College of Rheumatology’s annual meeting show that cardiovascular mortality dropped by nearly half among patients taking urate-lowering therapy. The study, which looked at a database of about 45,000 Taiwanese hyperuricemia patients, also showed that stroke mortality decreased significantly when urate levels were lowered. And the researchers observed a larger decrease in mortality when patients on the drug actually achieved urate lowering than when they did not. "This would suggest that there really is a relationship between uric acid and cardiovascular disease," Dr. Pillinger said.
More research will be needed to know for sure whether lowering uric acid could benefit cardiovascular disease, he said. And other questions remain as well: For example, is it hyperuricemia or gout that conveys the risk for coronary artery disease? That’s unclear, because most of the current studies have been done comparing only hyperuricemia to cardiac outcomes, he said.
Another Taiwanese database study, published last year, compared patients with hyperuricemia and those with gout vs. control patients. After adjusting for comorbidities, the researchers concluded that only gout was a risk for cardiovascular mortality (Rheumatology [Oxford] 2010;49:141-6). But Dr. Pillinger said he’s not convinced that the data should have been adjusted, because if gout or hyperuricemia themselves contribute to the comorbidities, then such an adjustment may lead to an underestimation of the impact of uric acid.
To shed more light on the role of gout and hyperuricemia in cardiovascular disease, researchers at NYU have been recruiting patients to a study assessing coronary artery disease in men with hyperuricemia, in those with gout, and in control patients. Preliminary data from the prospective cohort study indicate that coronary artery disease increases in a stepwise fashion from hyperuricemia to gout, Dr. Pillinger said.
The researchers are also starting to look at how hyperuricemic patients with lower levels of uric acid (6.9-9.0 mg/dL), compared with those who have higher levels (greater than 9.0 mg/dL). In that preliminary subanalysis, patients with the highest levels of uric acid had the highest risk for coronary artery disease and MI. "I think this is beginning to suggest that there’s at least an intermediate risk from having elevated uric acid," Dr. Pillinger said.
Some studies have also shown that treatment of the inflammation associated with gout could help in cardiovascular disease. Researchers performed an analysis of nearly 1,300 patients in the New York VA gout cohort. About half of the patients were on chronic colchicine therapy and half were not taking colchicine. The cross-sectional study, which was presented at the 2010 ACR annual meeting, found that patients who took colchicine had more than a 50% decrease in MI rates, compared with those who were not on the drug. Patients also had a lower risk of death and a lower C-reactive protein level, but these results did not achieve statistical significance. "This is very provocative," Dr. Pillinger said.
Dr. Pillinger said that he had no relevant conflicts of interest to report.