Myth Buster: Gout Can Occur in Patients With Rheumatoid Arthritis

WASHINGTON – Gout does occur in patients with rheumatoid arthritis, though at a lower rate than in the general population, Dr. Adlene Jebakumar said at the annual meeting of the American College of Rheumatology.

This finding comes from a review of a population-based cohort of 813 people diagnosed with rheumatoid arthritis (RA) between 1980 and 2007. Diagnoses were made either clinically including typical monosodium urate crystal positivity in synovial fluid or 1977 criteria developed by an ACR precursor organization, the American Rheumatology Association criteria. All subjects were longitudinally followed through their complete community medical records until April 2012 or they died or moved away.

Of the study cohort, 537 (66%) were rheumatoid factor positive; 33% had rheumatoid nodules, and 53% had erosive joint disease. During 9,771 total person-years of follow-up (mean 12 years per RA patient), 22 patients developed gout as defined by clinical criteria. The great toe was the most common site of gout (12 of 22 patients). The 25-year cumulative incidence of gout diagnosed by clinical criteria was 5.3%. Typical intracellular monosodium urate crystals were present in 9 of 22 patients with acute gout; all had developed gout after the RA incidence date. The 25-year cumulative incidence of gout diagnosed by clinical criteria including presence of urate crystals is 1.3%. The prevalence of gout in RA on Jan 1, 2008, was 1.9% (11 of 582 patients) as opposed to expected prevalence of 5.2% (or 30 patients) based on National Health and Nutrition Examination Survey data using age and sex-specific prevalence rates.

Risk factors for gout in RA were: older age (hazard ratio, 1.5/10-year increase; P = .04), male sex (HR, 3.18; P = .03) and obesity (HR, 3.5; P = .03). The presence of erosive RA joint disease reduced the risk of gout (HR, 0.24; P = .03). Gout has become more common in patients diagnosed with RA in recent years (1995-2007) than in previous years (1980-1994; HR, 5.6; P = .007).

Dr. Eric L. Matteson noted in an interview that when an RA patient develops a hot and tender big toe, rheumatologists are likely to presume it is an RA flare. In part, this is because there is a myth in rheumatology that patients with RA cannot get gout, Dr. Eric L. Matteson noted in an interview. The literature contains reports of only 30 such cases. In fact, as the study findings show, that hot and tender toe may be gout. The best course of action is to aspirate the toe joint and look at the synovial fluid for crystals.

The treatment of gout in an RA patient can involve administration of prednisone, anakinra, allopurinol, or febuxostat. Drug-drug interactions between the agents used to treat gout and those for RA may be a problem in some cases.

Some of the treatments used in RA may explain why there are so few gout flares in RA patients. High doses of aspirin, which are an RA treatment, significantly lower uric acid levels. In what he described as being speculation, Dr. Matteson, chair of the department of rheumatology at the Mayo Clinic, Rochester, Minn., suggested that the "push away" from use of NSAIDs long term and in high doses to help manage RA may be resulting in more gout flares in these patients.

Dr. Jebakumar and Dr. Matteson reported having no relevant financial conflicts of interest.

WASHINGTON – Gout does occur in patients with rheumatoid arthritis, though at a lower rate than in the general population, Dr. Adlene Jebakumar said at the annual meeting of the American College of Rheumatology.

This finding comes from a review of a population-based cohort of 813 people diagnosed with rheumatoid arthritis (RA) between 1980 and 2007. Diagnoses were made either clinically including typical monosodium urate crystal positivity in synovial fluid or 1977 criteria developed by an ACR precursor organization, the American Rheumatology Association criteria. All subjects were longitudinally followed through their complete community medical records until April 2012 or they died or moved away.

Of the study cohort, 537 (66%) were rheumatoid factor positive; 33% had rheumatoid nodules, and 53% had erosive joint disease. During 9,771 total person-years of follow-up (mean 12 years per RA patient), 22 patients developed gout as defined by clinical criteria. The great toe was the most common site of gout (12 of 22 patients). The 25-year cumulative incidence of gout diagnosed by clinical criteria was 5.3%. Typical intracellular monosodium urate crystals were present in 9 of 22 patients with acute gout; all had developed gout after the RA incidence date. The 25-year cumulative incidence of gout diagnosed by clinical criteria including presence of urate crystals is 1.3%. The prevalence of gout in RA on Jan 1, 2008, was 1.9% (11 of 582 patients) as opposed to expected prevalence of 5.2% (or 30 patients) based on National Health and Nutrition Examination Survey data using age and sex-specific prevalence rates.

Risk factors for gout in RA were: older age (hazard ratio, 1.5/10-year increase; P = .04), male sex (HR, 3.18; P = .03) and obesity (HR, 3.5; P = .03). The presence of erosive RA joint disease reduced the risk of gout (HR, 0.24; P = .03). Gout has become more common in patients diagnosed with RA in recent years (1995-2007) than in previous years (1980-1994; HR, 5.6; P = .007).

Dr. Eric L. Matteson noted in an interview that when an RA patient develops a hot and tender big toe, rheumatologists are likely to presume it is an RA flare. In part, this is because there is a myth in rheumatology that patients with RA cannot get gout, Dr. Eric L. Matteson noted in an interview. The literature contains reports of only 30 such cases. In fact, as the study findings show, that hot and tender toe may be gout. The best course of action is to aspirate the toe joint and look at the synovial fluid for crystals.

The treatment of gout in an RA patient can involve administration of prednisone, anakinra, allopurinol, or febuxostat. Drug-drug interactions between the agents used to treat gout and those for RA may be a problem in some cases.

Some of the treatments used in RA may explain why there are so few gout flares in RA patients. High doses of aspirin, which are an RA treatment, significantly lower uric acid levels. In what he described as being speculation, Dr. Matteson, chair of the department of rheumatology at the Mayo Clinic, Rochester, Minn., suggested that the "push away" from use of NSAIDs long term and in high doses to help manage RA may be resulting in more gout flares in these patients.

Dr. Jebakumar and Dr. Matteson reported having no relevant financial conflicts of interest.

WASHINGTON – Gout does occur in patients with rheumatoid arthritis, though at a lower rate than in the general population, Dr. Adlene Jebakumar said at the annual meeting of the American College of Rheumatology.

This finding comes from a review of a population-based cohort of 813 people diagnosed with rheumatoid arthritis (RA) between 1980 and 2007. Diagnoses were made either clinically including typical monosodium urate crystal positivity in synovial fluid or 1977 criteria developed by an ACR precursor organization, the American Rheumatology Association criteria. All subjects were longitudinally followed through their complete community medical records until April 2012 or they died or moved away.

Of the study cohort, 537 (66%) were rheumatoid factor positive; 33% had rheumatoid nodules, and 53% had erosive joint disease. During 9,771 total person-years of follow-up (mean 12 years per RA patient), 22 patients developed gout as defined by clinical criteria. The great toe was the most common site of gout (12 of 22 patients). The 25-year cumulative incidence of gout diagnosed by clinical criteria was 5.3%. Typical intracellular monosodium urate crystals were present in 9 of 22 patients with acute gout; all had developed gout after the RA incidence date. The 25-year cumulative incidence of gout diagnosed by clinical criteria including presence of urate crystals is 1.3%. The prevalence of gout in RA on Jan 1, 2008, was 1.9% (11 of 582 patients) as opposed to expected prevalence of 5.2% (or 30 patients) based on National Health and Nutrition Examination Survey data using age and sex-specific prevalence rates.

Risk factors for gout in RA were: older age (hazard ratio, 1.5/10-year increase; P = .04), male sex (HR, 3.18; P = .03) and obesity (HR, 3.5; P = .03). The presence of erosive RA joint disease reduced the risk of gout (HR, 0.24; P = .03). Gout has become more common in patients diagnosed with RA in recent years (1995-2007) than in previous years (1980-1994; HR, 5.6; P = .007).

Dr. Eric L. Matteson noted in an interview that when an RA patient develops a hot and tender big toe, rheumatologists are likely to presume it is an RA flare. In part, this is because there is a myth in rheumatology that patients with RA cannot get gout, Dr. Eric L. Matteson noted in an interview. The literature contains reports of only 30 such cases. In fact, as the study findings show, that hot and tender toe may be gout. The best course of action is to aspirate the toe joint and look at the synovial fluid for crystals.

The treatment of gout in an RA patient can involve administration of prednisone, anakinra, allopurinol, or febuxostat. Drug-drug interactions between the agents used to treat gout and those for RA may be a problem in some cases.

Some of the treatments used in RA may explain why there are so few gout flares in RA patients. High doses of aspirin, which are an RA treatment, significantly lower uric acid levels. In what he described as being speculation, Dr. Matteson, chair of the department of rheumatology at the Mayo Clinic, Rochester, Minn., suggested that the "push away" from use of NSAIDs long term and in high doses to help manage RA may be resulting in more gout flares in these patients.

Dr. Jebakumar and Dr. Matteson reported having no relevant financial conflicts of interest.