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MAUI, HAWAII – Urate-lowering therapy doesn’t have to be suspended while gout patients are treated for acute attacks, according to rheumatologist Orrin Troum of Santa Monica, Calif.
In fact, there are arguments against it; stopping allopurinol or other urate-lowering therapies (ULTs) during an attack doesn’t seem to help, and there’s a chance that patients might have another attack when it’s reintroduced. Still, the practice persists despite evidence and recommendations to the contrary, Dr. Troum said at the 2015 Rheumatology Winter Clinical Symposium.
Gout is a curable or at least eminently manageable condition, but it remains a tricky problem to treat. Part of that is because referring physicians might be using an out-of-date playbook before sending patients for a rheumatology consult; another issue is that optimal care requires follow-up visits, which might not always be possible.
Gout management guidelines from the European League Against Rheumatism (Ann. Rheum. Dis. 2006;65:1312-24) and the American College of Rheumatology (Arthritis Care Res. 2012;64:1431-46) now largely concur on how best to handle the condition, which might help bring uniformity to gout management if their message filters through to other branches of medicine, said rheumatologist and copresenter Martin Bergman of the department of rheumatology at Drexel University in Philadelphia.
Another persistent misconception is that ULT can’t be started during an acute attack. “There are some very good studies showing” that it can so long as antiflare drugs are on board and patients follow up to check for hypersensitivity reactions and other potential ULT problems, said Dr. Bergman, also chief of rheumatology at Taylor Hospital in Ridley Park, Pa.
Starting low and going slow, a key concept with ULT, hasn’t fully taken hold outside the rheumatology community, either. With allopurinol, that means starting at 100 mg/day – and 50 mg/day in those with chronic kidney disease – then titrating up slowly over several follow-up visits to an effective serum uric acid (SUA)–lowering dose. The idea is to lower serum uric acid slowly, to avoid precipitating an acute attack.
Even so, patients are still sometimes started on 300 mg/day, and although more than half will need more than 300 mg/day to reach SUA targets, that dose is still sometimes considered to be the maximum allowable.
Overall, the consensus on both sides of the Atlantic is that gout patients need to have serum urate levels below 6 mg/dL, and below 5 mg/dL if they have tophi.
“So the next question is, ‘How low do you go?’ ” It’s recently been found that “lifelong maintenance on very low levels of uric acid might actually increase the risk of neurodegenerative diseases, such as Parkinson’s, multiple sclerosis, and dementia.” Uric acid is a strong antioxidant that, perhaps, has protective effects in the central nervous system, Dr. Troum said.
It might be best to go below 5 mg/dL in severe gout for only 3-5 years, then loosen the target to 5-6 mg/dL (Nat. Rev. Rheumatol. 2014;10:271-83), he added.
Among other recent developments, it’s now known that psoriasis and psoriatic arthritis substantially increase the risk of gout (Ann. Rheum. Dis. 2014 March 20 [doi:10.1136/annrheumdis-2014-205212]), so it’s important to check for gout crystals when aspirating inflamed joints in those conditions. It remains unclear, however, if psoriasis or gout should take precedence when crystals are found, Dr. Bergman said.
Also, it makes sense to screen patients for their HLA-B genotype. Carriers of the variant allele HLA-B*5801 are at high risk for severe cutaneous adverse reactions with allopurinol, so another ULT is probably a better option. The variant is most common in individuals of Korean, Han Chinese, or Thai descent (Clin. Pharmacol. Ther. 2013;93:153-8).
Dr. Troum is an adviser, consultant, speaker, or grant recipient for several companies, including AbbVie, Amgen, Bristol-Myers Squibb, Centocor, Novartis, Pfizer, and Roche. He holds shares in Theralogix. Dr. Bergman is an adviser, speaker, or consultant for several companies, as well, including AbbVie, Celgene, Amgen, and Roche. He holds shares in Bristol-Myers Squibb, Pfizer, and Johnson & Johnson.
MAUI, HAWAII – Urate-lowering therapy doesn’t have to be suspended while gout patients are treated for acute attacks, according to rheumatologist Orrin Troum of Santa Monica, Calif.
In fact, there are arguments against it; stopping allopurinol or other urate-lowering therapies (ULTs) during an attack doesn’t seem to help, and there’s a chance that patients might have another attack when it’s reintroduced. Still, the practice persists despite evidence and recommendations to the contrary, Dr. Troum said at the 2015 Rheumatology Winter Clinical Symposium.
Gout is a curable or at least eminently manageable condition, but it remains a tricky problem to treat. Part of that is because referring physicians might be using an out-of-date playbook before sending patients for a rheumatology consult; another issue is that optimal care requires follow-up visits, which might not always be possible.
Gout management guidelines from the European League Against Rheumatism (Ann. Rheum. Dis. 2006;65:1312-24) and the American College of Rheumatology (Arthritis Care Res. 2012;64:1431-46) now largely concur on how best to handle the condition, which might help bring uniformity to gout management if their message filters through to other branches of medicine, said rheumatologist and copresenter Martin Bergman of the department of rheumatology at Drexel University in Philadelphia.
Another persistent misconception is that ULT can’t be started during an acute attack. “There are some very good studies showing” that it can so long as antiflare drugs are on board and patients follow up to check for hypersensitivity reactions and other potential ULT problems, said Dr. Bergman, also chief of rheumatology at Taylor Hospital in Ridley Park, Pa.
Starting low and going slow, a key concept with ULT, hasn’t fully taken hold outside the rheumatology community, either. With allopurinol, that means starting at 100 mg/day – and 50 mg/day in those with chronic kidney disease – then titrating up slowly over several follow-up visits to an effective serum uric acid (SUA)–lowering dose. The idea is to lower serum uric acid slowly, to avoid precipitating an acute attack.
Even so, patients are still sometimes started on 300 mg/day, and although more than half will need more than 300 mg/day to reach SUA targets, that dose is still sometimes considered to be the maximum allowable.
Overall, the consensus on both sides of the Atlantic is that gout patients need to have serum urate levels below 6 mg/dL, and below 5 mg/dL if they have tophi.
“So the next question is, ‘How low do you go?’ ” It’s recently been found that “lifelong maintenance on very low levels of uric acid might actually increase the risk of neurodegenerative diseases, such as Parkinson’s, multiple sclerosis, and dementia.” Uric acid is a strong antioxidant that, perhaps, has protective effects in the central nervous system, Dr. Troum said.
It might be best to go below 5 mg/dL in severe gout for only 3-5 years, then loosen the target to 5-6 mg/dL (Nat. Rev. Rheumatol. 2014;10:271-83), he added.
Among other recent developments, it’s now known that psoriasis and psoriatic arthritis substantially increase the risk of gout (Ann. Rheum. Dis. 2014 March 20 [doi:10.1136/annrheumdis-2014-205212]), so it’s important to check for gout crystals when aspirating inflamed joints in those conditions. It remains unclear, however, if psoriasis or gout should take precedence when crystals are found, Dr. Bergman said.
Also, it makes sense to screen patients for their HLA-B genotype. Carriers of the variant allele HLA-B*5801 are at high risk for severe cutaneous adverse reactions with allopurinol, so another ULT is probably a better option. The variant is most common in individuals of Korean, Han Chinese, or Thai descent (Clin. Pharmacol. Ther. 2013;93:153-8).
Dr. Troum is an adviser, consultant, speaker, or grant recipient for several companies, including AbbVie, Amgen, Bristol-Myers Squibb, Centocor, Novartis, Pfizer, and Roche. He holds shares in Theralogix. Dr. Bergman is an adviser, speaker, or consultant for several companies, as well, including AbbVie, Celgene, Amgen, and Roche. He holds shares in Bristol-Myers Squibb, Pfizer, and Johnson & Johnson.
MAUI, HAWAII – Urate-lowering therapy doesn’t have to be suspended while gout patients are treated for acute attacks, according to rheumatologist Orrin Troum of Santa Monica, Calif.
In fact, there are arguments against it; stopping allopurinol or other urate-lowering therapies (ULTs) during an attack doesn’t seem to help, and there’s a chance that patients might have another attack when it’s reintroduced. Still, the practice persists despite evidence and recommendations to the contrary, Dr. Troum said at the 2015 Rheumatology Winter Clinical Symposium.
Gout is a curable or at least eminently manageable condition, but it remains a tricky problem to treat. Part of that is because referring physicians might be using an out-of-date playbook before sending patients for a rheumatology consult; another issue is that optimal care requires follow-up visits, which might not always be possible.
Gout management guidelines from the European League Against Rheumatism (Ann. Rheum. Dis. 2006;65:1312-24) and the American College of Rheumatology (Arthritis Care Res. 2012;64:1431-46) now largely concur on how best to handle the condition, which might help bring uniformity to gout management if their message filters through to other branches of medicine, said rheumatologist and copresenter Martin Bergman of the department of rheumatology at Drexel University in Philadelphia.
Another persistent misconception is that ULT can’t be started during an acute attack. “There are some very good studies showing” that it can so long as antiflare drugs are on board and patients follow up to check for hypersensitivity reactions and other potential ULT problems, said Dr. Bergman, also chief of rheumatology at Taylor Hospital in Ridley Park, Pa.
Starting low and going slow, a key concept with ULT, hasn’t fully taken hold outside the rheumatology community, either. With allopurinol, that means starting at 100 mg/day – and 50 mg/day in those with chronic kidney disease – then titrating up slowly over several follow-up visits to an effective serum uric acid (SUA)–lowering dose. The idea is to lower serum uric acid slowly, to avoid precipitating an acute attack.
Even so, patients are still sometimes started on 300 mg/day, and although more than half will need more than 300 mg/day to reach SUA targets, that dose is still sometimes considered to be the maximum allowable.
Overall, the consensus on both sides of the Atlantic is that gout patients need to have serum urate levels below 6 mg/dL, and below 5 mg/dL if they have tophi.
“So the next question is, ‘How low do you go?’ ” It’s recently been found that “lifelong maintenance on very low levels of uric acid might actually increase the risk of neurodegenerative diseases, such as Parkinson’s, multiple sclerosis, and dementia.” Uric acid is a strong antioxidant that, perhaps, has protective effects in the central nervous system, Dr. Troum said.
It might be best to go below 5 mg/dL in severe gout for only 3-5 years, then loosen the target to 5-6 mg/dL (Nat. Rev. Rheumatol. 2014;10:271-83), he added.
Among other recent developments, it’s now known that psoriasis and psoriatic arthritis substantially increase the risk of gout (Ann. Rheum. Dis. 2014 March 20 [doi:10.1136/annrheumdis-2014-205212]), so it’s important to check for gout crystals when aspirating inflamed joints in those conditions. It remains unclear, however, if psoriasis or gout should take precedence when crystals are found, Dr. Bergman said.
Also, it makes sense to screen patients for their HLA-B genotype. Carriers of the variant allele HLA-B*5801 are at high risk for severe cutaneous adverse reactions with allopurinol, so another ULT is probably a better option. The variant is most common in individuals of Korean, Han Chinese, or Thai descent (Clin. Pharmacol. Ther. 2013;93:153-8).
Dr. Troum is an adviser, consultant, speaker, or grant recipient for several companies, including AbbVie, Amgen, Bristol-Myers Squibb, Centocor, Novartis, Pfizer, and Roche. He holds shares in Theralogix. Dr. Bergman is an adviser, speaker, or consultant for several companies, as well, including AbbVie, Celgene, Amgen, and Roche. He holds shares in Bristol-Myers Squibb, Pfizer, and Johnson & Johnson.
EXPERT ANALYSIS AT RWCS 2015
