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Most of us are familiar with the relationship between diuretics and increased uric acid levels potentially precipitating attacks of gout. Perhaps fewer recall that beta blockers also increase uric acid levels. In contrast, calcium channel blockers (CCBs) and losartan have been observed to decrease serum uric acid levels. This begs the question: Do CCBs and losartan reduce the incidence of gout attacks? Unfortunately, no randomized trials have been conducted to evaluate this.
However, a very large case-control study was published recently (BMJ. 2012;344:d8190) exploring the benefit of these drug classes for preventing gout attacks. Using an impressive computerized medical record database including 4 million patients entered by U.K. general practitioners, investigators conducted a case-control study of adults, aged 20 to 89 years, to determine the relationship between antihypertensives and gout. Incident cases of gout (n = 24,768) were ascertained in individuals having a gout attack after an initial diagnosis and were matched with 50,000 controls. The antihypertensives evaluated included diuretics, beta blockers, CCBs, ACE-inhibitors, losartan, and non-losartan angiotensin receptor blockers (ARBs). Results were adjusted for covariates. Hypertension itself was associated with a higher relative risk for incident gout (RR 1.75; 95% CI: 1.69-1.82). CCBs were associated with a lower risk of incident gout (RR 0.87; 95% CI: 0.82-0.93). Increasing duration and dose of medication further reduced the risk. Losartan also was associated with a reduced risk of developing gout (RR 0.81; 95% CI: 0.70 to 0.94). In contrast, current use of diuretics, beta blockers, ACE-inhibitors, and non-losartan ARBs among those with hypertension were all associated with an increased risk of incident gout. Findings were similar among patients without hypertension and among those on anti-gout medications.
Since the majority of patients with gout have hypertension, most of these patients will eventually be taking an antihypertensive. Data from this study would suggest that the selection of antihypertensive is an important consideration for avoiding future gout attacks. Similarly to how we might select an ACE-I/ARB for the treatment of hypertension in patients with diabetes for renoprotection, we should consider selecting losartan and CCB’s in patients with gout to prevent future attacks.
Dr. Ebbert reported having no relevant conflicts of interest.
Most of us are familiar with the relationship between diuretics and increased uric acid levels potentially precipitating attacks of gout. Perhaps fewer recall that beta blockers also increase uric acid levels. In contrast, calcium channel blockers (CCBs) and losartan have been observed to decrease serum uric acid levels. This begs the question: Do CCBs and losartan reduce the incidence of gout attacks? Unfortunately, no randomized trials have been conducted to evaluate this.
However, a very large case-control study was published recently (BMJ. 2012;344:d8190) exploring the benefit of these drug classes for preventing gout attacks. Using an impressive computerized medical record database including 4 million patients entered by U.K. general practitioners, investigators conducted a case-control study of adults, aged 20 to 89 years, to determine the relationship between antihypertensives and gout. Incident cases of gout (n = 24,768) were ascertained in individuals having a gout attack after an initial diagnosis and were matched with 50,000 controls. The antihypertensives evaluated included diuretics, beta blockers, CCBs, ACE-inhibitors, losartan, and non-losartan angiotensin receptor blockers (ARBs). Results were adjusted for covariates. Hypertension itself was associated with a higher relative risk for incident gout (RR 1.75; 95% CI: 1.69-1.82). CCBs were associated with a lower risk of incident gout (RR 0.87; 95% CI: 0.82-0.93). Increasing duration and dose of medication further reduced the risk. Losartan also was associated with a reduced risk of developing gout (RR 0.81; 95% CI: 0.70 to 0.94). In contrast, current use of diuretics, beta blockers, ACE-inhibitors, and non-losartan ARBs among those with hypertension were all associated with an increased risk of incident gout. Findings were similar among patients without hypertension and among those on anti-gout medications.
Since the majority of patients with gout have hypertension, most of these patients will eventually be taking an antihypertensive. Data from this study would suggest that the selection of antihypertensive is an important consideration for avoiding future gout attacks. Similarly to how we might select an ACE-I/ARB for the treatment of hypertension in patients with diabetes for renoprotection, we should consider selecting losartan and CCB’s in patients with gout to prevent future attacks.
Dr. Ebbert reported having no relevant conflicts of interest.
Most of us are familiar with the relationship between diuretics and increased uric acid levels potentially precipitating attacks of gout. Perhaps fewer recall that beta blockers also increase uric acid levels. In contrast, calcium channel blockers (CCBs) and losartan have been observed to decrease serum uric acid levels. This begs the question: Do CCBs and losartan reduce the incidence of gout attacks? Unfortunately, no randomized trials have been conducted to evaluate this.
However, a very large case-control study was published recently (BMJ. 2012;344:d8190) exploring the benefit of these drug classes for preventing gout attacks. Using an impressive computerized medical record database including 4 million patients entered by U.K. general practitioners, investigators conducted a case-control study of adults, aged 20 to 89 years, to determine the relationship between antihypertensives and gout. Incident cases of gout (n = 24,768) were ascertained in individuals having a gout attack after an initial diagnosis and were matched with 50,000 controls. The antihypertensives evaluated included diuretics, beta blockers, CCBs, ACE-inhibitors, losartan, and non-losartan angiotensin receptor blockers (ARBs). Results were adjusted for covariates. Hypertension itself was associated with a higher relative risk for incident gout (RR 1.75; 95% CI: 1.69-1.82). CCBs were associated with a lower risk of incident gout (RR 0.87; 95% CI: 0.82-0.93). Increasing duration and dose of medication further reduced the risk. Losartan also was associated with a reduced risk of developing gout (RR 0.81; 95% CI: 0.70 to 0.94). In contrast, current use of diuretics, beta blockers, ACE-inhibitors, and non-losartan ARBs among those with hypertension were all associated with an increased risk of incident gout. Findings were similar among patients without hypertension and among those on anti-gout medications.
Since the majority of patients with gout have hypertension, most of these patients will eventually be taking an antihypertensive. Data from this study would suggest that the selection of antihypertensive is an important consideration for avoiding future gout attacks. Similarly to how we might select an ACE-I/ARB for the treatment of hypertension in patients with diabetes for renoprotection, we should consider selecting losartan and CCB’s in patients with gout to prevent future attacks.
Dr. Ebbert reported having no relevant conflicts of interest.