New York University/Hospital for Joint Disease: Seminar in Advanced Rheumatology

NEW YORK – Early discontinuation of glucocorticoid therapy may greatly increase the risk of relapse in antineutrophil cytoplasmic antibody–associated vasculitis, Dr. Yusuf Yazici said at a rheumatology meeting sponsored by New York University.

He discussed a study that addressed the controversial question of whether low-dose glucocorticoids contribute to maintaining remission of the disease.

Patients successfully treated for antineutrophil cytoplasmic antibody–associated vasculitis (AAV) face high rates of relapse, up to 38% at 30 months. Although glucocorticoids are often used to prevent relapse in AAV, high-quality evidence to guide treatment is lacking, Dr. Yazici said during an update on the treatment of vasculitis.

"Our aim is always to get patients off steroid therapy, but maybe that is a misguided aim," said Dr. Yazici, director of the Seligman Center for Advanced Therapeutics and Behçet’s Syndrome Evaluation, Treatment and Research Center at the New York University Hospital for Joint Diseases.

Dr. Yazici cited findings from a meta-analysis of studies investigating the treatment of AAV that included a predefined glucocorticoid dose and protocol for tapering (Arthritis Care Res. 2010;62:1166-73). Thirteen studies involving 983 patients were identified for inclusion, including five observational and eight randomized controlled trials. None of the studies directly compared glucocorticoid regimens.

To elucidate the role of glucocorticoid therapy in relapse, the authors divided the studies into those that had a zero glucocorticoid target dose (i.e., aimed to get patients completely off glucocorticoid therapy, n = 695) and those having a nonzero glucocorticoid target dose (i.e., low glucocorticoid maintenance dose allowed, n = 288).

The investigators found that 36% of the overall group relapsed. Upon further examination, the relapse rate was 43% for those in the zero glucocorticoid target dose group, compared with 14% in those allowed to continue glucocorticoids – approximately a threefold increase.

Even for those who discontinue glucocorticoids, timing is important. When the investigators divided patients in the zero target dose into those who had to reach zero within 12 months (the early zero group) and those who were allowed to reach zero after 12 months (the late zero group), there was a 48% relapse rate for the early zero group, compared with a 29% rate for the late zero group. While the early zero glucocorticoid target dose group had significantly more relapses than the nonzero group (P less than .001), the late zero glucocorticoid target dose group was similar to the nonzero group. By grouping the late zero and nonzero groups, the authors concluded that early discontinuation of glucocorticoid was associated with a 20% increased risk of relapse (28% vs. 48%).

This study has several significant messages, said Dr. Yazici. "Small differences in [glucocorticoid] management may have a major impact on relapse rates. It may not be a bad thing to keep AAV patients on steroids a little longer. This is the first study that has looked into this," he noted.

The results suggest that glucocorticoid dose should be monitored, and that patients with AAV should be kept on 5.0-7.5 mg of glucocorticoids for at least a year after reaching disease remission. For clinical trials, failure to consider concomitant glucocorticoid dosing can affect outcomes, especially remission and relapse, as well as sample size determination, said Dr. Yazici.

Dr. Yazici has served as a consultant or speaker for, or has received research support from, BMS, Celgene, Centocor, Genentech, Merck, Novartis, Roche, and UCB.

NEW YORK – Early discontinuation of glucocorticoid therapy may greatly increase the risk of relapse in antineutrophil cytoplasmic antibody–associated vasculitis, Dr. Yusuf Yazici said at a rheumatology meeting sponsored by New York University.

He discussed a study that addressed the controversial question of whether low-dose glucocorticoids contribute to maintaining remission of the disease.

Patients successfully treated for antineutrophil cytoplasmic antibody–associated vasculitis (AAV) face high rates of relapse, up to 38% at 30 months. Although glucocorticoids are often used to prevent relapse in AAV, high-quality evidence to guide treatment is lacking, Dr. Yazici said during an update on the treatment of vasculitis.

"Our aim is always to get patients off steroid therapy, but maybe that is a misguided aim," said Dr. Yazici, director of the Seligman Center for Advanced Therapeutics and Behçet’s Syndrome Evaluation, Treatment and Research Center at the New York University Hospital for Joint Diseases.

Dr. Yazici cited findings from a meta-analysis of studies investigating the treatment of AAV that included a predefined glucocorticoid dose and protocol for tapering (Arthritis Care Res. 2010;62:1166-73). Thirteen studies involving 983 patients were identified for inclusion, including five observational and eight randomized controlled trials. None of the studies directly compared glucocorticoid regimens.

To elucidate the role of glucocorticoid therapy in relapse, the authors divided the studies into those that had a zero glucocorticoid target dose (i.e., aimed to get patients completely off glucocorticoid therapy, n = 695) and those having a nonzero glucocorticoid target dose (i.e., low glucocorticoid maintenance dose allowed, n = 288).

The investigators found that 36% of the overall group relapsed. Upon further examination, the relapse rate was 43% for those in the zero glucocorticoid target dose group, compared with 14% in those allowed to continue glucocorticoids – approximately a threefold increase.

Even for those who discontinue glucocorticoids, timing is important. When the investigators divided patients in the zero target dose into those who had to reach zero within 12 months (the early zero group) and those who were allowed to reach zero after 12 months (the late zero group), there was a 48% relapse rate for the early zero group, compared with a 29% rate for the late zero group. While the early zero glucocorticoid target dose group had significantly more relapses than the nonzero group (P less than .001), the late zero glucocorticoid target dose group was similar to the nonzero group. By grouping the late zero and nonzero groups, the authors concluded that early discontinuation of glucocorticoid was associated with a 20% increased risk of relapse (28% vs. 48%).

This study has several significant messages, said Dr. Yazici. "Small differences in [glucocorticoid] management may have a major impact on relapse rates. It may not be a bad thing to keep AAV patients on steroids a little longer. This is the first study that has looked into this," he noted.

The results suggest that glucocorticoid dose should be monitored, and that patients with AAV should be kept on 5.0-7.5 mg of glucocorticoids for at least a year after reaching disease remission. For clinical trials, failure to consider concomitant glucocorticoid dosing can affect outcomes, especially remission and relapse, as well as sample size determination, said Dr. Yazici.

Dr. Yazici has served as a consultant or speaker for, or has received research support from, BMS, Celgene, Centocor, Genentech, Merck, Novartis, Roche, and UCB.

NEW YORK – Early discontinuation of glucocorticoid therapy may greatly increase the risk of relapse in antineutrophil cytoplasmic antibody–associated vasculitis, Dr. Yusuf Yazici said at a rheumatology meeting sponsored by New York University.

He discussed a study that addressed the controversial question of whether low-dose glucocorticoids contribute to maintaining remission of the disease.

Patients successfully treated for antineutrophil cytoplasmic antibody–associated vasculitis (AAV) face high rates of relapse, up to 38% at 30 months. Although glucocorticoids are often used to prevent relapse in AAV, high-quality evidence to guide treatment is lacking, Dr. Yazici said during an update on the treatment of vasculitis.

"Our aim is always to get patients off steroid therapy, but maybe that is a misguided aim," said Dr. Yazici, director of the Seligman Center for Advanced Therapeutics and Behçet’s Syndrome Evaluation, Treatment and Research Center at the New York University Hospital for Joint Diseases.

Dr. Yazici cited findings from a meta-analysis of studies investigating the treatment of AAV that included a predefined glucocorticoid dose and protocol for tapering (Arthritis Care Res. 2010;62:1166-73). Thirteen studies involving 983 patients were identified for inclusion, including five observational and eight randomized controlled trials. None of the studies directly compared glucocorticoid regimens.

To elucidate the role of glucocorticoid therapy in relapse, the authors divided the studies into those that had a zero glucocorticoid target dose (i.e., aimed to get patients completely off glucocorticoid therapy, n = 695) and those having a nonzero glucocorticoid target dose (i.e., low glucocorticoid maintenance dose allowed, n = 288).

The investigators found that 36% of the overall group relapsed. Upon further examination, the relapse rate was 43% for those in the zero glucocorticoid target dose group, compared with 14% in those allowed to continue glucocorticoids – approximately a threefold increase.

Even for those who discontinue glucocorticoids, timing is important. When the investigators divided patients in the zero target dose into those who had to reach zero within 12 months (the early zero group) and those who were allowed to reach zero after 12 months (the late zero group), there was a 48% relapse rate for the early zero group, compared with a 29% rate for the late zero group. While the early zero glucocorticoid target dose group had significantly more relapses than the nonzero group (P less than .001), the late zero glucocorticoid target dose group was similar to the nonzero group. By grouping the late zero and nonzero groups, the authors concluded that early discontinuation of glucocorticoid was associated with a 20% increased risk of relapse (28% vs. 48%).

This study has several significant messages, said Dr. Yazici. "Small differences in [glucocorticoid] management may have a major impact on relapse rates. It may not be a bad thing to keep AAV patients on steroids a little longer. This is the first study that has looked into this," he noted.

The results suggest that glucocorticoid dose should be monitored, and that patients with AAV should be kept on 5.0-7.5 mg of glucocorticoids for at least a year after reaching disease remission. For clinical trials, failure to consider concomitant glucocorticoid dosing can affect outcomes, especially remission and relapse, as well as sample size determination, said Dr. Yazici.

Dr. Yazici has served as a consultant or speaker for, or has received research support from, BMS, Celgene, Centocor, Genentech, Merck, Novartis, Roche, and UCB.

NEW YORK – The 18%-20% of systemic lupus erythematosus patients who test positive for platelet C4d face a much greater likelihood of having a future cardiovascular event, stroke, or death than those who are not platelet C4d positive, according to Dr. Susan M. Manzi, who presented the results at a rheumatology meeting sponsored by New York University.

"The only factor that predicted mortality greater than being positive for P-C4d [platelet C4d] was having cancer," said Dr. Manzi, chair of the department of medicine and codirector of the Lupus Center of Excellence at West Penn Allegheny Health System, Pittsburgh.

In the study of 356 patients with systemic lupus erythematosus (SLE), which was carried out between July 2001 and August 2009, 70 tested positive for P-C4d (20%) and 286 tested negative. This confirms a previous study that found that P-C4d was present in 18% of SLE patients and that P-C4d was highly specific for SLE (Arthritis Rheum. 2006;54:670-4). "P-C4d carries a 95% specificity for SLE," said Dr. Manzi, who is also vice chair and professor of medicine at Temple University, Philadelphia.

Patients who were P-C4d positive had twice as many cardiovascular events (36 vs. 18, P = .001). The odds ratio of having a cardiovascular event was 2.09 for positive P-C4d (P = .02), which was much higher than for smoking (OR 1.36), SLE disease duration (0.99), or the presence of renal disease (1.42). The odds ratio for aPL antibodies was 2.30 (P = 0.004).

The results for stroke were even more striking. Thirteen patients with P-C4d had stroke, compared with three in those who tested negative for P-C4d (P = .002). There was nearly a fivefold increased risk of stroke in this group (OR 4.96, CI 1.75-14.06, P = .003). Almost three times as many patients had a pulmonary embolism in the P-C4d group, compared with controls (11 vs. 4, P = .007).

Fourteen SLE patients (4%) died during the follow-up. Of those, more P-C4d-positive patients died compared with those who tested negative for P-C4d (11% vs. 2%, P = .002). Causes of death included infection (4), cardiac arrest (2), congestive heart failure (1), cancer (2), hemorrhage (1), and unspecified (4). The risk of all-cause mortality was increased almost eightfold in those who were P-C4d positive (OR 7.92, CI 2.13-29.48, P = .002). Only cancer (OR 19.74) surpassed being P-C4d as a risk for all-cause mortality in multivariate regression analysis.

"Usually when we measure complement in the circulation, we measure the parent protein C4 in the plasma. When complement is activated, it breaks down into fragments and we see that one fragment, C4d, can covalently bind to cell surfaces. So, as we study how these fragments of complement activation bind to cells, we are exploring their potential use as disease biomarkers and prognostic indicators," Dr. Manzi said.

Dr. Manzi serves on the advisory boards of Bristol-Myers Squibb, Human Genome Sciences, and Cephalon. She receives funding for research from Amgen USA, Aspreva Pharmaceuticals, Bristol-Myers Squibb, Cephalon, Genentech, Human Genome Sciences, and Immunomedics.

NEW YORK – The 18%-20% of systemic lupus erythematosus patients who test positive for platelet C4d face a much greater likelihood of having a future cardiovascular event, stroke, or death than those who are not platelet C4d positive, according to Dr. Susan M. Manzi, who presented the results at a rheumatology meeting sponsored by New York University.

"The only factor that predicted mortality greater than being positive for P-C4d [platelet C4d] was having cancer," said Dr. Manzi, chair of the department of medicine and codirector of the Lupus Center of Excellence at West Penn Allegheny Health System, Pittsburgh.

In the study of 356 patients with systemic lupus erythematosus (SLE), which was carried out between July 2001 and August 2009, 70 tested positive for P-C4d (20%) and 286 tested negative. This confirms a previous study that found that P-C4d was present in 18% of SLE patients and that P-C4d was highly specific for SLE (Arthritis Rheum. 2006;54:670-4). "P-C4d carries a 95% specificity for SLE," said Dr. Manzi, who is also vice chair and professor of medicine at Temple University, Philadelphia.

Patients who were P-C4d positive had twice as many cardiovascular events (36 vs. 18, P = .001). The odds ratio of having a cardiovascular event was 2.09 for positive P-C4d (P = .02), which was much higher than for smoking (OR 1.36), SLE disease duration (0.99), or the presence of renal disease (1.42). The odds ratio for aPL antibodies was 2.30 (P = 0.004).

The results for stroke were even more striking. Thirteen patients with P-C4d had stroke, compared with three in those who tested negative for P-C4d (P = .002). There was nearly a fivefold increased risk of stroke in this group (OR 4.96, CI 1.75-14.06, P = .003). Almost three times as many patients had a pulmonary embolism in the P-C4d group, compared with controls (11 vs. 4, P = .007).

Fourteen SLE patients (4%) died during the follow-up. Of those, more P-C4d-positive patients died compared with those who tested negative for P-C4d (11% vs. 2%, P = .002). Causes of death included infection (4), cardiac arrest (2), congestive heart failure (1), cancer (2), hemorrhage (1), and unspecified (4). The risk of all-cause mortality was increased almost eightfold in those who were P-C4d positive (OR 7.92, CI 2.13-29.48, P = .002). Only cancer (OR 19.74) surpassed being P-C4d as a risk for all-cause mortality in multivariate regression analysis.

"Usually when we measure complement in the circulation, we measure the parent protein C4 in the plasma. When complement is activated, it breaks down into fragments and we see that one fragment, C4d, can covalently bind to cell surfaces. So, as we study how these fragments of complement activation bind to cells, we are exploring their potential use as disease biomarkers and prognostic indicators," Dr. Manzi said.

Dr. Manzi serves on the advisory boards of Bristol-Myers Squibb, Human Genome Sciences, and Cephalon. She receives funding for research from Amgen USA, Aspreva Pharmaceuticals, Bristol-Myers Squibb, Cephalon, Genentech, Human Genome Sciences, and Immunomedics.

NEW YORK – The 18%-20% of systemic lupus erythematosus patients who test positive for platelet C4d face a much greater likelihood of having a future cardiovascular event, stroke, or death than those who are not platelet C4d positive, according to Dr. Susan M. Manzi, who presented the results at a rheumatology meeting sponsored by New York University.

"The only factor that predicted mortality greater than being positive for P-C4d [platelet C4d] was having cancer," said Dr. Manzi, chair of the department of medicine and codirector of the Lupus Center of Excellence at West Penn Allegheny Health System, Pittsburgh.

In the study of 356 patients with systemic lupus erythematosus (SLE), which was carried out between July 2001 and August 2009, 70 tested positive for P-C4d (20%) and 286 tested negative. This confirms a previous study that found that P-C4d was present in 18% of SLE patients and that P-C4d was highly specific for SLE (Arthritis Rheum. 2006;54:670-4). "P-C4d carries a 95% specificity for SLE," said Dr. Manzi, who is also vice chair and professor of medicine at Temple University, Philadelphia.

Patients who were P-C4d positive had twice as many cardiovascular events (36 vs. 18, P = .001). The odds ratio of having a cardiovascular event was 2.09 for positive P-C4d (P = .02), which was much higher than for smoking (OR 1.36), SLE disease duration (0.99), or the presence of renal disease (1.42). The odds ratio for aPL antibodies was 2.30 (P = 0.004).

The results for stroke were even more striking. Thirteen patients with P-C4d had stroke, compared with three in those who tested negative for P-C4d (P = .002). There was nearly a fivefold increased risk of stroke in this group (OR 4.96, CI 1.75-14.06, P = .003). Almost three times as many patients had a pulmonary embolism in the P-C4d group, compared with controls (11 vs. 4, P = .007).

Fourteen SLE patients (4%) died during the follow-up. Of those, more P-C4d-positive patients died compared with those who tested negative for P-C4d (11% vs. 2%, P = .002). Causes of death included infection (4), cardiac arrest (2), congestive heart failure (1), cancer (2), hemorrhage (1), and unspecified (4). The risk of all-cause mortality was increased almost eightfold in those who were P-C4d positive (OR 7.92, CI 2.13-29.48, P = .002). Only cancer (OR 19.74) surpassed being P-C4d as a risk for all-cause mortality in multivariate regression analysis.

"Usually when we measure complement in the circulation, we measure the parent protein C4 in the plasma. When complement is activated, it breaks down into fragments and we see that one fragment, C4d, can covalently bind to cell surfaces. So, as we study how these fragments of complement activation bind to cells, we are exploring their potential use as disease biomarkers and prognostic indicators," Dr. Manzi said.

Dr. Manzi serves on the advisory boards of Bristol-Myers Squibb, Human Genome Sciences, and Cephalon. She receives funding for research from Amgen USA, Aspreva Pharmaceuticals, Bristol-Myers Squibb, Cephalon, Genentech, Human Genome Sciences, and Immunomedics.

NEW YORK – The 18%-20% of systemic lupus erythematosus patients who test positive for platelet C4d face a much greater likelihood of having a future cardiovascular event, stroke, or death than those who are not platelet C4d positive, according to Dr. Susan M. Manzi, who presented the results at a rheumatology meeting sponsored by New York University.

"The only factor that predicted mortality greater than being positive for P-C4d [platelet C4d] was having cancer," said Dr. Manzi, chair of the department of medicine and codirector of the Lupus Center of Excellence at West Penn Allegheny Health System, Pittsburgh.

In the study of 356 patients with systemic lupus erythematosus (SLE), which was carried out between July 2001 and August 2009, 70 tested positive for P-C4d (20%) and 286 tested negative. This confirms a previous study that found that P-C4d was present in 18% of SLE patients and that P-C4d was highly specific for SLE (Arthritis Rheum. 2006;54:670-4). "P-C4d carries a 95% specificity for SLE," said Dr. Manzi, who is also vice chair and professor of medicine at Temple University, Philadelphia.

Patients who were P-C4d positive had twice as many cardiovascular events (36 vs. 18, P = .001). The odds ratio of having a cardiovascular event was 2.09 for positive P-C4d (P = .02), which was much higher than for smoking (OR 1.36), SLE disease duration (0.99), or the presence of renal disease (1.42). The odds ratio for aPL antibodies was 2.30 (P = 0.004).

The results for stroke were even more striking. Thirteen patients with P-C4d had stroke, compared with three in those who tested negative for P-C4d (P = .002). There was nearly a fivefold increased risk of stroke in this group (OR 4.96, CI 1.75-14.06, P = .003). Almost three times as many patients had a pulmonary embolism in the P-C4d group, compared with controls (11 vs. 4, P = .007).

Fourteen SLE patients (4%) died during the follow-up. Of those, more P-C4d-positive patients died compared with those who tested negative for P-C4d (11% vs. 2%, P = .002). Causes of death included infection (4), cardiac arrest (2), congestive heart failure (1), cancer (2), hemorrhage (1), and unspecified (4). The risk of all-cause mortality was increased almost eightfold in those who were P-C4d positive (OR 7.92, CI 2.13-29.48, P = .002). Only cancer (OR 19.74) surpassed being P-C4d as a risk for all-cause mortality in multivariate regression analysis.

"Usually when we measure complement in the circulation, we measure the parent protein C4 in the plasma. When complement is activated, it breaks down into fragments and we see that one fragment, C4d, can covalently bind to cell surfaces. So, as we study how these fragments of complement activation bind to cells, we are exploring their potential use as disease biomarkers and prognostic indicators," Dr. Manzi said.

Dr. Manzi serves on the advisory boards of Bristol-Myers Squibb, Human Genome Sciences, and Cephalon. She receives funding for research from Amgen USA, Aspreva Pharmaceuticals, Bristol-Myers Squibb, Cephalon, Genentech, Human Genome Sciences, and Immunomedics.

NEW YORK – The 18%-20% of systemic lupus erythematosus patients who test positive for platelet C4d face a much greater likelihood of having a future cardiovascular event, stroke, or death than those who are not platelet C4d positive, according to Dr. Susan M. Manzi, who presented the results at a rheumatology meeting sponsored by New York University.

"The only factor that predicted mortality greater than being positive for P-C4d [platelet C4d] was having cancer," said Dr. Manzi, chair of the department of medicine and codirector of the Lupus Center of Excellence at West Penn Allegheny Health System, Pittsburgh.

In the study of 356 patients with systemic lupus erythematosus (SLE), which was carried out between July 2001 and August 2009, 70 tested positive for P-C4d (20%) and 286 tested negative. This confirms a previous study that found that P-C4d was present in 18% of SLE patients and that P-C4d was highly specific for SLE (Arthritis Rheum. 2006;54:670-4). "P-C4d carries a 95% specificity for SLE," said Dr. Manzi, who is also vice chair and professor of medicine at Temple University, Philadelphia.

Patients who were P-C4d positive had twice as many cardiovascular events (36 vs. 18, P = .001). The odds ratio of having a cardiovascular event was 2.09 for positive P-C4d (P = .02), which was much higher than for smoking (OR 1.36), SLE disease duration (0.99), or the presence of renal disease (1.42). The odds ratio for aPL antibodies was 2.30 (P = 0.004).

The results for stroke were even more striking. Thirteen patients with P-C4d had stroke, compared with three in those who tested negative for P-C4d (P = .002). There was nearly a fivefold increased risk of stroke in this group (OR 4.96, CI 1.75-14.06, P = .003). Almost three times as many patients had a pulmonary embolism in the P-C4d group, compared with controls (11 vs. 4, P = .007).

Fourteen SLE patients (4%) died during the follow-up. Of those, more P-C4d-positive patients died compared with those who tested negative for P-C4d (11% vs. 2%, P = .002). Causes of death included infection (4), cardiac arrest (2), congestive heart failure (1), cancer (2), hemorrhage (1), and unspecified (4). The risk of all-cause mortality was increased almost eightfold in those who were P-C4d positive (OR 7.92, CI 2.13-29.48, P = .002). Only cancer (OR 19.74) surpassed being P-C4d as a risk for all-cause mortality in multivariate regression analysis.

"Usually when we measure complement in the circulation, we measure the parent protein C4 in the plasma. When complement is activated, it breaks down into fragments and we see that one fragment, C4d, can covalently bind to cell surfaces. So, as we study how these fragments of complement activation bind to cells, we are exploring their potential use as disease biomarkers and prognostic indicators," Dr. Manzi said.

Dr. Manzi serves on the advisory boards of Bristol-Myers Squibb, Human Genome Sciences, and Cephalon. She receives funding for research from Amgen USA, Aspreva Pharmaceuticals, Bristol-Myers Squibb, Cephalon, Genentech, Human Genome Sciences, and Immunomedics.

NEW YORK – The 18%-20% of systemic lupus erythematosus patients who test positive for platelet C4d face a much greater likelihood of having a future cardiovascular event, stroke, or death than those who are not platelet C4d positive, according to Dr. Susan M. Manzi, who presented the results at a rheumatology meeting sponsored by New York University.

"The only factor that predicted mortality greater than being positive for P-C4d [platelet C4d] was having cancer," said Dr. Manzi, chair of the department of medicine and codirector of the Lupus Center of Excellence at West Penn Allegheny Health System, Pittsburgh.

In the study of 356 patients with systemic lupus erythematosus (SLE), which was carried out between July 2001 and August 2009, 70 tested positive for P-C4d (20%) and 286 tested negative. This confirms a previous study that found that P-C4d was present in 18% of SLE patients and that P-C4d was highly specific for SLE (Arthritis Rheum. 2006;54:670-4). "P-C4d carries a 95% specificity for SLE," said Dr. Manzi, who is also vice chair and professor of medicine at Temple University, Philadelphia.

Patients who were P-C4d positive had twice as many cardiovascular events (36 vs. 18, P = .001). The odds ratio of having a cardiovascular event was 2.09 for positive P-C4d (P = .02), which was much higher than for smoking (OR 1.36), SLE disease duration (0.99), or the presence of renal disease (1.42). The odds ratio for aPL antibodies was 2.30 (P = 0.004).

The results for stroke were even more striking. Thirteen patients with P-C4d had stroke, compared with three in those who tested negative for P-C4d (P = .002). There was nearly a fivefold increased risk of stroke in this group (OR 4.96, CI 1.75-14.06, P = .003). Almost three times as many patients had a pulmonary embolism in the P-C4d group, compared with controls (11 vs. 4, P = .007).

Fourteen SLE patients (4%) died during the follow-up. Of those, more P-C4d-positive patients died compared with those who tested negative for P-C4d (11% vs. 2%, P = .002). Causes of death included infection (4), cardiac arrest (2), congestive heart failure (1), cancer (2), hemorrhage (1), and unspecified (4). The risk of all-cause mortality was increased almost eightfold in those who were P-C4d positive (OR 7.92, CI 2.13-29.48, P = .002). Only cancer (OR 19.74) surpassed being P-C4d as a risk for all-cause mortality in multivariate regression analysis.

"Usually when we measure complement in the circulation, we measure the parent protein C4 in the plasma. When complement is activated, it breaks down into fragments and we see that one fragment, C4d, can covalently bind to cell surfaces. So, as we study how these fragments of complement activation bind to cells, we are exploring their potential use as disease biomarkers and prognostic indicators," Dr. Manzi said.

Dr. Manzi serves on the advisory boards of Bristol-Myers Squibb, Human Genome Sciences, and Cephalon. She receives funding for research from Amgen USA, Aspreva Pharmaceuticals, Bristol-Myers Squibb, Cephalon, Genentech, Human Genome Sciences, and Immunomedics.

NEW YORK – The 18%-20% of systemic lupus erythematosus patients who test positive for platelet C4d face a much greater likelihood of having a future cardiovascular event, stroke, or death than those who are not platelet C4d positive, according to Dr. Susan M. Manzi, who presented the results at a rheumatology meeting sponsored by New York University.

"The only factor that predicted mortality greater than being positive for P-C4d [platelet C4d] was having cancer," said Dr. Manzi, chair of the department of medicine and codirector of the Lupus Center of Excellence at West Penn Allegheny Health System, Pittsburgh.

In the study of 356 patients with systemic lupus erythematosus (SLE), which was carried out between July 2001 and August 2009, 70 tested positive for P-C4d (20%) and 286 tested negative. This confirms a previous study that found that P-C4d was present in 18% of SLE patients and that P-C4d was highly specific for SLE (Arthritis Rheum. 2006;54:670-4). "P-C4d carries a 95% specificity for SLE," said Dr. Manzi, who is also vice chair and professor of medicine at Temple University, Philadelphia.

Patients who were P-C4d positive had twice as many cardiovascular events (36 vs. 18, P = .001). The odds ratio of having a cardiovascular event was 2.09 for positive P-C4d (P = .02), which was much higher than for smoking (OR 1.36), SLE disease duration (0.99), or the presence of renal disease (1.42). The odds ratio for aPL antibodies was 2.30 (P = 0.004).

The results for stroke were even more striking. Thirteen patients with P-C4d had stroke, compared with three in those who tested negative for P-C4d (P = .002). There was nearly a fivefold increased risk of stroke in this group (OR 4.96, CI 1.75-14.06, P = .003). Almost three times as many patients had a pulmonary embolism in the P-C4d group, compared with controls (11 vs. 4, P = .007).

Fourteen SLE patients (4%) died during the follow-up. Of those, more P-C4d-positive patients died compared with those who tested negative for P-C4d (11% vs. 2%, P = .002). Causes of death included infection (4), cardiac arrest (2), congestive heart failure (1), cancer (2), hemorrhage (1), and unspecified (4). The risk of all-cause mortality was increased almost eightfold in those who were P-C4d positive (OR 7.92, CI 2.13-29.48, P = .002). Only cancer (OR 19.74) surpassed being P-C4d as a risk for all-cause mortality in multivariate regression analysis.

"Usually when we measure complement in the circulation, we measure the parent protein C4 in the plasma. When complement is activated, it breaks down into fragments and we see that one fragment, C4d, can covalently bind to cell surfaces. So, as we study how these fragments of complement activation bind to cells, we are exploring their potential use as disease biomarkers and prognostic indicators," Dr. Manzi said.

Dr. Manzi serves on the advisory boards of Bristol-Myers Squibb, Human Genome Sciences, and Cephalon. She receives funding for research from Amgen USA, Aspreva Pharmaceuticals, Bristol-Myers Squibb, Cephalon, Genentech, Human Genome Sciences, and Immunomedics.

NEW YORK – The 18%-20% of systemic lupus erythematosus patients who test positive for platelet C4d face a much greater likelihood of having a future cardiovascular event, stroke, or death than those who are not platelet C4d positive, according to Dr. Susan M. Manzi, who presented the results at a rheumatology meeting sponsored by New York University.

"The only factor that predicted mortality greater than being positive for P-C4d [platelet C4d] was having cancer," said Dr. Manzi, chair of the department of medicine and codirector of the Lupus Center of Excellence at West Penn Allegheny Health System, Pittsburgh.

In the study of 356 patients with systemic lupus erythematosus (SLE), which was carried out between July 2001 and August 2009, 70 tested positive for P-C4d (20%) and 286 tested negative. This confirms a previous study that found that P-C4d was present in 18% of SLE patients and that P-C4d was highly specific for SLE (Arthritis Rheum. 2006;54:670-4). "P-C4d carries a 95% specificity for SLE," said Dr. Manzi, who is also vice chair and professor of medicine at Temple University, Philadelphia.

Patients who were P-C4d positive had twice as many cardiovascular events (36 vs. 18, P = .001). The odds ratio of having a cardiovascular event was 2.09 for positive P-C4d (P = .02), which was much higher than for smoking (OR 1.36), SLE disease duration (0.99), or the presence of renal disease (1.42). The odds ratio for aPL antibodies was 2.30 (P = 0.004).

The results for stroke were even more striking. Thirteen patients with P-C4d had stroke, compared with three in those who tested negative for P-C4d (P = .002). There was nearly a fivefold increased risk of stroke in this group (OR 4.96, CI 1.75-14.06, P = .003). Almost three times as many patients had a pulmonary embolism in the P-C4d group, compared with controls (11 vs. 4, P = .007).

Fourteen SLE patients (4%) died during the follow-up. Of those, more P-C4d-positive patients died compared with those who tested negative for P-C4d (11% vs. 2%, P = .002). Causes of death included infection (4), cardiac arrest (2), congestive heart failure (1), cancer (2), hemorrhage (1), and unspecified (4). The risk of all-cause mortality was increased almost eightfold in those who were P-C4d positive (OR 7.92, CI 2.13-29.48, P = .002). Only cancer (OR 19.74) surpassed being P-C4d as a risk for all-cause mortality in multivariate regression analysis.

"Usually when we measure complement in the circulation, we measure the parent protein C4 in the plasma. When complement is activated, it breaks down into fragments and we see that one fragment, C4d, can covalently bind to cell surfaces. So, as we study how these fragments of complement activation bind to cells, we are exploring their potential use as disease biomarkers and prognostic indicators," Dr. Manzi said.

Dr. Manzi serves on the advisory boards of Bristol-Myers Squibb, Human Genome Sciences, and Cephalon. She receives funding for research from Amgen USA, Aspreva Pharmaceuticals, Bristol-Myers Squibb, Cephalon, Genentech, Human Genome Sciences, and Immunomedics.

NEW YORK – The 18%-20% of systemic lupus erythematosus patients who test positive for platelet C4d face a much greater likelihood of having a future cardiovascular event, stroke, or death than those who are not platelet C4d positive, according to Dr. Susan M. Manzi, who presented the results at a rheumatology meeting sponsored by New York University.

"The only factor that predicted mortality greater than being positive for P-C4d [platelet C4d] was having cancer," said Dr. Manzi, chair of the department of medicine and codirector of the Lupus Center of Excellence at West Penn Allegheny Health System, Pittsburgh.

In the study of 356 patients with systemic lupus erythematosus (SLE), which was carried out between July 2001 and August 2009, 70 tested positive for P-C4d (20%) and 286 tested negative. This confirms a previous study that found that P-C4d was present in 18% of SLE patients and that P-C4d was highly specific for SLE (Arthritis Rheum. 2006;54:670-4). "P-C4d carries a 95% specificity for SLE," said Dr. Manzi, who is also vice chair and professor of medicine at Temple University, Philadelphia.

Patients who were P-C4d positive had twice as many cardiovascular events (36 vs. 18, P = .001). The odds ratio of having a cardiovascular event was 2.09 for positive P-C4d (P = .02), which was much higher than for smoking (OR 1.36), SLE disease duration (0.99), or the presence of renal disease (1.42). The odds ratio for aPL antibodies was 2.30 (P = 0.004).

The results for stroke were even more striking. Thirteen patients with P-C4d had stroke, compared with three in those who tested negative for P-C4d (P = .002). There was nearly a fivefold increased risk of stroke in this group (OR 4.96, CI 1.75-14.06, P = .003). Almost three times as many patients had a pulmonary embolism in the P-C4d group, compared with controls (11 vs. 4, P = .007).

Fourteen SLE patients (4%) died during the follow-up. Of those, more P-C4d-positive patients died compared with those who tested negative for P-C4d (11% vs. 2%, P = .002). Causes of death included infection (4), cardiac arrest (2), congestive heart failure (1), cancer (2), hemorrhage (1), and unspecified (4). The risk of all-cause mortality was increased almost eightfold in those who were P-C4d positive (OR 7.92, CI 2.13-29.48, P = .002). Only cancer (OR 19.74) surpassed being P-C4d as a risk for all-cause mortality in multivariate regression analysis.

"Usually when we measure complement in the circulation, we measure the parent protein C4 in the plasma. When complement is activated, it breaks down into fragments and we see that one fragment, C4d, can covalently bind to cell surfaces. So, as we study how these fragments of complement activation bind to cells, we are exploring their potential use as disease biomarkers and prognostic indicators," Dr. Manzi said.

Dr. Manzi serves on the advisory boards of Bristol-Myers Squibb, Human Genome Sciences, and Cephalon. She receives funding for research from Amgen USA, Aspreva Pharmaceuticals, Bristol-Myers Squibb, Cephalon, Genentech, Human Genome Sciences, and Immunomedics.

NEW YORK – Tumor necrosis factor inhibitors reduced the risk of myocardial infarction, stroke and cardiovascular-related death in patients with rheumatoid arthritis, according to Dr. Jeffrey D. Greenberg, who presented the findings at a rheumatology meeting sponsored by New York University. Methotrexate was not associated with a reduced risk of cardiovascular events, and prednisone use was associated with a dose-dependent increased risk.

The findings come from CORRONA (Consortium of Rheumatology Researchers of North America), a registry of patients with RA or psoriatic arthritis. The study population involved 10,156 patients followed for a median of 23 months. A subset analysis was performed, and 88 patients were identified who had experienced nonfatal myocardial infarction (n = 26), transient ischemic attack or stroke (n = 45), or cardiovascular-related death (n = 17) (Ann. Rheum. Dis. 2011;70:576-82).

In an editorial accompanying Dr. Greenberg’s report (Ann. Rheum. Dis. 2011 70:561-2), Dr. Johan Askling of Karolinska University Hospital, Stockholm, and Dr. Will Dixon of the University of Manchester (England) praiseed Dr. Greenberg’s study in terms of its methodology and transparency. However, they point out that other studies, such as those published by the British Society for Rheumatology Biologics Register (BSRBR), have not supported a cardiovascular protective effect for TNF inhibitors.

Nonbiologic disease-modifying antirheumatic drugs (DMARDs) other than methotrexate served as the reference cohort for all therapeutic comparisons. Relative to nonbiologic DMARDs, methotrexate use was associated with a nonsignificant reduction in risk (HR 0.83, 95% CI 0.44-1.57). In contrast, patients using a TNF inhibitor had a 61% reduced risk of the primary composite cardiovascular end point (HR 0.39, 0.18-0.74).

Dr. Greenberg also showed significant reductions in risk for those taking TNF inhibitors compared with those taking nonbiological DMARDs as measured by a composite end point that included CV deaths (HR = 0.39, 0.19-0.82) and a composite end point that excluded CV deaths (HR = 0.35, 0.16-0.74), and nonfatal MI (HR = 0.24, 0.06-0.95). There was a trend toward reduced risk for nonfatal TIA/stroke (HR = 0.44, 0.18-1.09). "These data indicate that TNF antagonists may represent a therapeutic strategy to attenuate the heightened cardiovascular risk experienced by RA patients," Dr. Greenberg said.

"As expected, there was a dose-dependent increased risk of cardiovascular events with steroids," said Dr. Greenberg of New York University. Prednisone doses between 1-2.5 mg and 3-7 mg almost doubled the risk (HR 1.90 and 1.89, respectively) while doses greater than 7 mg tripled the risk (HR 3.00, 1.44-6.25) (P = .04).

Dr. Greenberg advocates a three-step strategy to decrease cardiovascular risk in RA.

The first is to adhere to recommended cardiovascular disease prevention, screening, and guidelines. This includes management of "traditional" cardiovascular risk factors such as blood pressure, diabetes, lipids, smoking, and obesity, he said.

The second component – as supported by his study’s results – is to minimize use of NSAIDs and corticosteroids, and to utilize steroid-sparing options if possible.

The third component is to aim for tighter control of RA disease activity. For patients at increased CV risk, "I would treat RA aggressively," said Dr. Greenberg. Even so, he acknowledged that it has not been proved that the strategy would alter the natural course of developing cardiovascular disease. It remains to be determined what measures should be targeted, he said, suggesting options such as a specific disease activity score, C-reactive protein levels, or other inflammatory biomarkers.

Indeed, the lack of CV risk assessment tools and evidence-based practice guidelines for improving cardiovascular risk management in RA patients is getting a lot of attention.

Dr. Sherine E. Gabriel and researcher Cynthia S. Crowson of the Mayo Clinic, Rochester, Minn., discussed the limitations of both the SCORE and Framingham Risk Scores (Ann. Rheum. Dis. 2011;70:719-21). While applauding the European League Against Rheumatism (EULAR) for formulating guidelines to improve cardiovascular management in patients with RA, the researchers point out several areas of weakness. Cardiovascular disease risk, for example, is not necessarily associated with longer disease duration. In fact, studies show there is an increased risk of cardiovascular events early in the course of RA, they noted. The risks also are unclear for patients who are RF negative or ACPA negative. Further, RA patients may respond atypically to traditional cardiovascular risk factors.

Dr. Greenberg has done consulting for Centocor, CORRONA, Novartis Pharmaceutical Corp, Roche Laboratories, and UCB. He has received research and grant support from the Arthritis Foundation and the National Institutes of Health. He receives consulting fees from, or owns stock shares in, AstraZeneca, CORRONA, Genentech, Novartis, and Pfizer.

NEW YORK – Tumor necrosis factor inhibitors reduced the risk of myocardial infarction, stroke and cardiovascular-related death in patients with rheumatoid arthritis, according to Dr. Jeffrey D. Greenberg, who presented the findings at a rheumatology meeting sponsored by New York University. Methotrexate was not associated with a reduced risk of cardiovascular events, and prednisone use was associated with a dose-dependent increased risk.

The findings come from CORRONA (Consortium of Rheumatology Researchers of North America), a registry of patients with RA or psoriatic arthritis. The study population involved 10,156 patients followed for a median of 23 months. A subset analysis was performed, and 88 patients were identified who had experienced nonfatal myocardial infarction (n = 26), transient ischemic attack or stroke (n = 45), or cardiovascular-related death (n = 17) (Ann. Rheum. Dis. 2011;70:576-82).

In an editorial accompanying Dr. Greenberg’s report (Ann. Rheum. Dis. 2011 70:561-2), Dr. Johan Askling of Karolinska University Hospital, Stockholm, and Dr. Will Dixon of the University of Manchester (England) praiseed Dr. Greenberg’s study in terms of its methodology and transparency. However, they point out that other studies, such as those published by the British Society for Rheumatology Biologics Register (BSRBR), have not supported a cardiovascular protective effect for TNF inhibitors.

Nonbiologic disease-modifying antirheumatic drugs (DMARDs) other than methotrexate served as the reference cohort for all therapeutic comparisons. Relative to nonbiologic DMARDs, methotrexate use was associated with a nonsignificant reduction in risk (HR 0.83, 95% CI 0.44-1.57). In contrast, patients using a TNF inhibitor had a 61% reduced risk of the primary composite cardiovascular end point (HR 0.39, 0.18-0.74).

Dr. Greenberg also showed significant reductions in risk for those taking TNF inhibitors compared with those taking nonbiological DMARDs as measured by a composite end point that included CV deaths (HR = 0.39, 0.19-0.82) and a composite end point that excluded CV deaths (HR = 0.35, 0.16-0.74), and nonfatal MI (HR = 0.24, 0.06-0.95). There was a trend toward reduced risk for nonfatal TIA/stroke (HR = 0.44, 0.18-1.09). "These data indicate that TNF antagonists may represent a therapeutic strategy to attenuate the heightened cardiovascular risk experienced by RA patients," Dr. Greenberg said.

"As expected, there was a dose-dependent increased risk of cardiovascular events with steroids," said Dr. Greenberg of New York University. Prednisone doses between 1-2.5 mg and 3-7 mg almost doubled the risk (HR 1.90 and 1.89, respectively) while doses greater than 7 mg tripled the risk (HR 3.00, 1.44-6.25) (P = .04).

Dr. Greenberg advocates a three-step strategy to decrease cardiovascular risk in RA.

The first is to adhere to recommended cardiovascular disease prevention, screening, and guidelines. This includes management of "traditional" cardiovascular risk factors such as blood pressure, diabetes, lipids, smoking, and obesity, he said.

The second component – as supported by his study’s results – is to minimize use of NSAIDs and corticosteroids, and to utilize steroid-sparing options if possible.

The third component is to aim for tighter control of RA disease activity. For patients at increased CV risk, "I would treat RA aggressively," said Dr. Greenberg. Even so, he acknowledged that it has not been proved that the strategy would alter the natural course of developing cardiovascular disease. It remains to be determined what measures should be targeted, he said, suggesting options such as a specific disease activity score, C-reactive protein levels, or other inflammatory biomarkers.

Indeed, the lack of CV risk assessment tools and evidence-based practice guidelines for improving cardiovascular risk management in RA patients is getting a lot of attention.

Dr. Sherine E. Gabriel and researcher Cynthia S. Crowson of the Mayo Clinic, Rochester, Minn., discussed the limitations of both the SCORE and Framingham Risk Scores (Ann. Rheum. Dis. 2011;70:719-21). While applauding the European League Against Rheumatism (EULAR) for formulating guidelines to improve cardiovascular management in patients with RA, the researchers point out several areas of weakness. Cardiovascular disease risk, for example, is not necessarily associated with longer disease duration. In fact, studies show there is an increased risk of cardiovascular events early in the course of RA, they noted. The risks also are unclear for patients who are RF negative or ACPA negative. Further, RA patients may respond atypically to traditional cardiovascular risk factors.

Dr. Greenberg has done consulting for Centocor, CORRONA, Novartis Pharmaceutical Corp, Roche Laboratories, and UCB. He has received research and grant support from the Arthritis Foundation and the National Institutes of Health. He receives consulting fees from, or owns stock shares in, AstraZeneca, CORRONA, Genentech, Novartis, and Pfizer.

NEW YORK – Tumor necrosis factor inhibitors reduced the risk of myocardial infarction, stroke and cardiovascular-related death in patients with rheumatoid arthritis, according to Dr. Jeffrey D. Greenberg, who presented the findings at a rheumatology meeting sponsored by New York University. Methotrexate was not associated with a reduced risk of cardiovascular events, and prednisone use was associated with a dose-dependent increased risk.

The findings come from CORRONA (Consortium of Rheumatology Researchers of North America), a registry of patients with RA or psoriatic arthritis. The study population involved 10,156 patients followed for a median of 23 months. A subset analysis was performed, and 88 patients were identified who had experienced nonfatal myocardial infarction (n = 26), transient ischemic attack or stroke (n = 45), or cardiovascular-related death (n = 17) (Ann. Rheum. Dis. 2011;70:576-82).

In an editorial accompanying Dr. Greenberg’s report (Ann. Rheum. Dis. 2011 70:561-2), Dr. Johan Askling of Karolinska University Hospital, Stockholm, and Dr. Will Dixon of the University of Manchester (England) praiseed Dr. Greenberg’s study in terms of its methodology and transparency. However, they point out that other studies, such as those published by the British Society for Rheumatology Biologics Register (BSRBR), have not supported a cardiovascular protective effect for TNF inhibitors.

Nonbiologic disease-modifying antirheumatic drugs (DMARDs) other than methotrexate served as the reference cohort for all therapeutic comparisons. Relative to nonbiologic DMARDs, methotrexate use was associated with a nonsignificant reduction in risk (HR 0.83, 95% CI 0.44-1.57). In contrast, patients using a TNF inhibitor had a 61% reduced risk of the primary composite cardiovascular end point (HR 0.39, 0.18-0.74).

Dr. Greenberg also showed significant reductions in risk for those taking TNF inhibitors compared with those taking nonbiological DMARDs as measured by a composite end point that included CV deaths (HR = 0.39, 0.19-0.82) and a composite end point that excluded CV deaths (HR = 0.35, 0.16-0.74), and nonfatal MI (HR = 0.24, 0.06-0.95). There was a trend toward reduced risk for nonfatal TIA/stroke (HR = 0.44, 0.18-1.09). "These data indicate that TNF antagonists may represent a therapeutic strategy to attenuate the heightened cardiovascular risk experienced by RA patients," Dr. Greenberg said.

"As expected, there was a dose-dependent increased risk of cardiovascular events with steroids," said Dr. Greenberg of New York University. Prednisone doses between 1-2.5 mg and 3-7 mg almost doubled the risk (HR 1.90 and 1.89, respectively) while doses greater than 7 mg tripled the risk (HR 3.00, 1.44-6.25) (P = .04).

Dr. Greenberg advocates a three-step strategy to decrease cardiovascular risk in RA.

The first is to adhere to recommended cardiovascular disease prevention, screening, and guidelines. This includes management of "traditional" cardiovascular risk factors such as blood pressure, diabetes, lipids, smoking, and obesity, he said.

The second component – as supported by his study’s results – is to minimize use of NSAIDs and corticosteroids, and to utilize steroid-sparing options if possible.

The third component is to aim for tighter control of RA disease activity. For patients at increased CV risk, "I would treat RA aggressively," said Dr. Greenberg. Even so, he acknowledged that it has not been proved that the strategy would alter the natural course of developing cardiovascular disease. It remains to be determined what measures should be targeted, he said, suggesting options such as a specific disease activity score, C-reactive protein levels, or other inflammatory biomarkers.

Indeed, the lack of CV risk assessment tools and evidence-based practice guidelines for improving cardiovascular risk management in RA patients is getting a lot of attention.

Dr. Sherine E. Gabriel and researcher Cynthia S. Crowson of the Mayo Clinic, Rochester, Minn., discussed the limitations of both the SCORE and Framingham Risk Scores (Ann. Rheum. Dis. 2011;70:719-21). While applauding the European League Against Rheumatism (EULAR) for formulating guidelines to improve cardiovascular management in patients with RA, the researchers point out several areas of weakness. Cardiovascular disease risk, for example, is not necessarily associated with longer disease duration. In fact, studies show there is an increased risk of cardiovascular events early in the course of RA, they noted. The risks also are unclear for patients who are RF negative or ACPA negative. Further, RA patients may respond atypically to traditional cardiovascular risk factors.

Dr. Greenberg has done consulting for Centocor, CORRONA, Novartis Pharmaceutical Corp, Roche Laboratories, and UCB. He has received research and grant support from the Arthritis Foundation and the National Institutes of Health. He receives consulting fees from, or owns stock shares in, AstraZeneca, CORRONA, Genentech, Novartis, and Pfizer.

NEW YORK – Tumor necrosis factor inhibitors reduced the risk of myocardial infarction, stroke and cardiovascular-related death in patients with rheumatoid arthritis, according to Dr. Jeffrey D. Greenberg, who presented the findings at a rheumatology meeting sponsored by New York University. Methotrexate was not associated with a reduced risk of cardiovascular events, and prednisone use was associated with a dose-dependent increased risk.

The findings come from CORRONA (Consortium of Rheumatology Researchers of North America), a registry of patients with RA or psoriatic arthritis. The study population involved 10,156 patients followed for a median of 23 months. A subset analysis was performed, and 88 patients were identified who had experienced nonfatal myocardial infarction (n = 26), transient ischemic attack or stroke (n = 45), or cardiovascular-related death (n = 17) (Ann. Rheum. Dis. 2011;70:576-82).

In an editorial accompanying Dr. Greenberg’s report (Ann. Rheum. Dis. 2011 70:561-2), Dr. Johan Askling of Karolinska University Hospital, Stockholm, and Dr. Will Dixon of the University of Manchester (England) praiseed Dr. Greenberg’s study in terms of its methodology and transparency. However, they point out that other studies, such as those published by the British Society for Rheumatology Biologics Register (BSRBR), have not supported a cardiovascular protective effect for TNF inhibitors.

Nonbiologic disease-modifying antirheumatic drugs (DMARDs) other than methotrexate served as the reference cohort for all therapeutic comparisons. Relative to nonbiologic DMARDs, methotrexate use was associated with a nonsignificant reduction in risk (HR 0.83, 95% CI 0.44-1.57). In contrast, patients using a TNF inhibitor had a 61% reduced risk of the primary composite cardiovascular end point (HR 0.39, 0.18-0.74).

Dr. Greenberg also showed significant reductions in risk for those taking TNF inhibitors compared with those taking nonbiological DMARDs as measured by a composite end point that included CV deaths (HR = 0.39, 0.19-0.82) and a composite end point that excluded CV deaths (HR = 0.35, 0.16-0.74), and nonfatal MI (HR = 0.24, 0.06-0.95). There was a trend toward reduced risk for nonfatal TIA/stroke (HR = 0.44, 0.18-1.09). "These data indicate that TNF antagonists may represent a therapeutic strategy to attenuate the heightened cardiovascular risk experienced by RA patients," Dr. Greenberg said.

"As expected, there was a dose-dependent increased risk of cardiovascular events with steroids," said Dr. Greenberg of New York University. Prednisone doses between 1-2.5 mg and 3-7 mg almost doubled the risk (HR 1.90 and 1.89, respectively) while doses greater than 7 mg tripled the risk (HR 3.00, 1.44-6.25) (P = .04).

Dr. Greenberg advocates a three-step strategy to decrease cardiovascular risk in RA.

The first is to adhere to recommended cardiovascular disease prevention, screening, and guidelines. This includes management of "traditional" cardiovascular risk factors such as blood pressure, diabetes, lipids, smoking, and obesity, he said.

The second component – as supported by his study’s results – is to minimize use of NSAIDs and corticosteroids, and to utilize steroid-sparing options if possible.

The third component is to aim for tighter control of RA disease activity. For patients at increased CV risk, "I would treat RA aggressively," said Dr. Greenberg. Even so, he acknowledged that it has not been proved that the strategy would alter the natural course of developing cardiovascular disease. It remains to be determined what measures should be targeted, he said, suggesting options such as a specific disease activity score, C-reactive protein levels, or other inflammatory biomarkers.

Indeed, the lack of CV risk assessment tools and evidence-based practice guidelines for improving cardiovascular risk management in RA patients is getting a lot of attention.

Dr. Sherine E. Gabriel and researcher Cynthia S. Crowson of the Mayo Clinic, Rochester, Minn., discussed the limitations of both the SCORE and Framingham Risk Scores (Ann. Rheum. Dis. 2011;70:719-21). While applauding the European League Against Rheumatism (EULAR) for formulating guidelines to improve cardiovascular management in patients with RA, the researchers point out several areas of weakness. Cardiovascular disease risk, for example, is not necessarily associated with longer disease duration. In fact, studies show there is an increased risk of cardiovascular events early in the course of RA, they noted. The risks also are unclear for patients who are RF negative or ACPA negative. Further, RA patients may respond atypically to traditional cardiovascular risk factors.

Dr. Greenberg has done consulting for Centocor, CORRONA, Novartis Pharmaceutical Corp, Roche Laboratories, and UCB. He has received research and grant support from the Arthritis Foundation and the National Institutes of Health. He receives consulting fees from, or owns stock shares in, AstraZeneca, CORRONA, Genentech, Novartis, and Pfizer.

NEW YORK – Tumor necrosis factor inhibitors reduced the risk of myocardial infarction, stroke and cardiovascular-related death in patients with rheumatoid arthritis, according to Dr. Jeffrey D. Greenberg, who presented the findings at a rheumatology meeting sponsored by New York University. Methotrexate was not associated with a reduced risk of cardiovascular events, and prednisone use was associated with a dose-dependent increased risk.

The findings come from CORRONA (Consortium of Rheumatology Researchers of North America), a registry of patients with RA or psoriatic arthritis. The study population involved 10,156 patients followed for a median of 23 months. A subset analysis was performed, and 88 patients were identified who had experienced nonfatal myocardial infarction (n = 26), transient ischemic attack or stroke (n = 45), or cardiovascular-related death (n = 17) (Ann. Rheum. Dis. 2011;70:576-82).

In an editorial accompanying Dr. Greenberg’s report (Ann. Rheum. Dis. 2011 70:561-2), Dr. Johan Askling of Karolinska University Hospital, Stockholm, and Dr. Will Dixon of the University of Manchester (England) praiseed Dr. Greenberg’s study in terms of its methodology and transparency. However, they point out that other studies, such as those published by the British Society for Rheumatology Biologics Register (BSRBR), have not supported a cardiovascular protective effect for TNF inhibitors.

Nonbiologic disease-modifying antirheumatic drugs (DMARDs) other than methotrexate served as the reference cohort for all therapeutic comparisons. Relative to nonbiologic DMARDs, methotrexate use was associated with a nonsignificant reduction in risk (HR 0.83, 95% CI 0.44-1.57). In contrast, patients using a TNF inhibitor had a 61% reduced risk of the primary composite cardiovascular end point (HR 0.39, 0.18-0.74).

Dr. Greenberg also showed significant reductions in risk for those taking TNF inhibitors compared with those taking nonbiological DMARDs as measured by a composite end point that included CV deaths (HR = 0.39, 0.19-0.82) and a composite end point that excluded CV deaths (HR = 0.35, 0.16-0.74), and nonfatal MI (HR = 0.24, 0.06-0.95). There was a trend toward reduced risk for nonfatal TIA/stroke (HR = 0.44, 0.18-1.09). "These data indicate that TNF antagonists may represent a therapeutic strategy to attenuate the heightened cardiovascular risk experienced by RA patients," Dr. Greenberg said.

"As expected, there was a dose-dependent increased risk of cardiovascular events with steroids," said Dr. Greenberg of New York University. Prednisone doses between 1-2.5 mg and 3-7 mg almost doubled the risk (HR 1.90 and 1.89, respectively) while doses greater than 7 mg tripled the risk (HR 3.00, 1.44-6.25) (P = .04).

Dr. Greenberg advocates a three-step strategy to decrease cardiovascular risk in RA.

The first is to adhere to recommended cardiovascular disease prevention, screening, and guidelines. This includes management of "traditional" cardiovascular risk factors such as blood pressure, diabetes, lipids, smoking, and obesity, he said.

The second component – as supported by his study’s results – is to minimize use of NSAIDs and corticosteroids, and to utilize steroid-sparing options if possible.

The third component is to aim for tighter control of RA disease activity. For patients at increased CV risk, "I would treat RA aggressively," said Dr. Greenberg. Even so, he acknowledged that it has not been proved that the strategy would alter the natural course of developing cardiovascular disease. It remains to be determined what measures should be targeted, he said, suggesting options such as a specific disease activity score, C-reactive protein levels, or other inflammatory biomarkers.

Indeed, the lack of CV risk assessment tools and evidence-based practice guidelines for improving cardiovascular risk management in RA patients is getting a lot of attention.

Dr. Sherine E. Gabriel and researcher Cynthia S. Crowson of the Mayo Clinic, Rochester, Minn., discussed the limitations of both the SCORE and Framingham Risk Scores (Ann. Rheum. Dis. 2011;70:719-21). While applauding the European League Against Rheumatism (EULAR) for formulating guidelines to improve cardiovascular management in patients with RA, the researchers point out several areas of weakness. Cardiovascular disease risk, for example, is not necessarily associated with longer disease duration. In fact, studies show there is an increased risk of cardiovascular events early in the course of RA, they noted. The risks also are unclear for patients who are RF negative or ACPA negative. Further, RA patients may respond atypically to traditional cardiovascular risk factors.

Dr. Greenberg has done consulting for Centocor, CORRONA, Novartis Pharmaceutical Corp, Roche Laboratories, and UCB. He has received research and grant support from the Arthritis Foundation and the National Institutes of Health. He receives consulting fees from, or owns stock shares in, AstraZeneca, CORRONA, Genentech, Novartis, and Pfizer.

NEW YORK – Tumor necrosis factor inhibitors reduced the risk of myocardial infarction, stroke and cardiovascular-related death in patients with rheumatoid arthritis, according to Dr. Jeffrey D. Greenberg, who presented the findings at a rheumatology meeting sponsored by New York University. Methotrexate was not associated with a reduced risk of cardiovascular events, and prednisone use was associated with a dose-dependent increased risk.

The findings come from CORRONA (Consortium of Rheumatology Researchers of North America), a registry of patients with RA or psoriatic arthritis. The study population involved 10,156 patients followed for a median of 23 months. A subset analysis was performed, and 88 patients were identified who had experienced nonfatal myocardial infarction (n = 26), transient ischemic attack or stroke (n = 45), or cardiovascular-related death (n = 17) (Ann. Rheum. Dis. 2011;70:576-82).

In an editorial accompanying Dr. Greenberg’s report (Ann. Rheum. Dis. 2011 70:561-2), Dr. Johan Askling of Karolinska University Hospital, Stockholm, and Dr. Will Dixon of the University of Manchester (England) praiseed Dr. Greenberg’s study in terms of its methodology and transparency. However, they point out that other studies, such as those published by the British Society for Rheumatology Biologics Register (BSRBR), have not supported a cardiovascular protective effect for TNF inhibitors.

Nonbiologic disease-modifying antirheumatic drugs (DMARDs) other than methotrexate served as the reference cohort for all therapeutic comparisons. Relative to nonbiologic DMARDs, methotrexate use was associated with a nonsignificant reduction in risk (HR 0.83, 95% CI 0.44-1.57). In contrast, patients using a TNF inhibitor had a 61% reduced risk of the primary composite cardiovascular end point (HR 0.39, 0.18-0.74).

Dr. Greenberg also showed significant reductions in risk for those taking TNF inhibitors compared with those taking nonbiological DMARDs as measured by a composite end point that included CV deaths (HR = 0.39, 0.19-0.82) and a composite end point that excluded CV deaths (HR = 0.35, 0.16-0.74), and nonfatal MI (HR = 0.24, 0.06-0.95). There was a trend toward reduced risk for nonfatal TIA/stroke (HR = 0.44, 0.18-1.09). "These data indicate that TNF antagonists may represent a therapeutic strategy to attenuate the heightened cardiovascular risk experienced by RA patients," Dr. Greenberg said.

"As expected, there was a dose-dependent increased risk of cardiovascular events with steroids," said Dr. Greenberg of New York University. Prednisone doses between 1-2.5 mg and 3-7 mg almost doubled the risk (HR 1.90 and 1.89, respectively) while doses greater than 7 mg tripled the risk (HR 3.00, 1.44-6.25) (P = .04).

Dr. Greenberg advocates a three-step strategy to decrease cardiovascular risk in RA.

The first is to adhere to recommended cardiovascular disease prevention, screening, and guidelines. This includes management of "traditional" cardiovascular risk factors such as blood pressure, diabetes, lipids, smoking, and obesity, he said.

The second component – as supported by his study’s results – is to minimize use of NSAIDs and corticosteroids, and to utilize steroid-sparing options if possible.

The third component is to aim for tighter control of RA disease activity. For patients at increased CV risk, "I would treat RA aggressively," said Dr. Greenberg. Even so, he acknowledged that it has not been proved that the strategy would alter the natural course of developing cardiovascular disease. It remains to be determined what measures should be targeted, he said, suggesting options such as a specific disease activity score, C-reactive protein levels, or other inflammatory biomarkers.

Indeed, the lack of CV risk assessment tools and evidence-based practice guidelines for improving cardiovascular risk management in RA patients is getting a lot of attention.

Dr. Sherine E. Gabriel and researcher Cynthia S. Crowson of the Mayo Clinic, Rochester, Minn., discussed the limitations of both the SCORE and Framingham Risk Scores (Ann. Rheum. Dis. 2011;70:719-21). While applauding the European League Against Rheumatism (EULAR) for formulating guidelines to improve cardiovascular management in patients with RA, the researchers point out several areas of weakness. Cardiovascular disease risk, for example, is not necessarily associated with longer disease duration. In fact, studies show there is an increased risk of cardiovascular events early in the course of RA, they noted. The risks also are unclear for patients who are RF negative or ACPA negative. Further, RA patients may respond atypically to traditional cardiovascular risk factors.

Dr. Greenberg has done consulting for Centocor, CORRONA, Novartis Pharmaceutical Corp, Roche Laboratories, and UCB. He has received research and grant support from the Arthritis Foundation and the National Institutes of Health. He receives consulting fees from, or owns stock shares in, AstraZeneca, CORRONA, Genentech, Novartis, and Pfizer.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

NEW YORK – When magnetic resonance imaging is used instead of plain x-rays in patients with early inflammatory back pain, the diagnostic accuracy for spondyloarthritis jumps from 25% to 70%, according to Dr. Maxime Dougados, who spoke at a rheumatology meeting sponsored by New York University.

"Seventy-five percent of the time, you cannot make the diagnosis with plain x-rays," said Dr. Dougados, professor of rheumatology at Paris-Descartes University/Cochin Hospital in Paris and the president-elect of EULAR. He presented the Ira Goldstein Memorial Lecture at the meeting, focusing on spondyloarthritis (SpA).

Dr. Dougados presented the as yet unpublished results from the DESIR cohort, a large French national multicenter database of long-term follow-up of 708 patients presenting with early inflammatory back pain that was initiated by the French Society of Rheumatology. Patients were recruited between December 2007 and April 2010 if they had inflammatory back pain lasting more than 3 months and less than 3 years. The group will be followed for 10 years in the ongoing study. At baseline, the mean age was 35 years, 54% were female and 57% were HLA-B27 positive (Joint Bone Spine 2011 March 30 [doi: 10.1016/j.jbspin.2011.01.013]).

Looking at radiological sacroiliac changes, the diagnosis was "obvious" for 25.6% of the cohort, "doubtful" for 21.3%, and "normal" for 53.1%. "These results indicate that at the first clinical visit, the interview is very important to pick up other clinical symptoms," said Dr. Dougados. In fact, about 80% were found to have non-axial clinical manifestations, including articular peripheral involvement, enthesopathy, dactylitis, anterior chest wall pain, uveitis, or psoriasis.

Using MRI, 70% of the cohort were determined to have "obvious" sacroiliitis, about 20% had a "doubtful" diagnosis and about 10% were thought to be "normal."

"These results indicate that you can detect early abnormalities of the sacroiliac joint on MRI even if x-rays are normal," he said.

According to Dr. Dougados, these imaging findings fit well with recent results from the DECLIC study, in which 163 rheumatologists were asked to diagnose 472 patients with early inflammatory back pain, including 161 patients with spondyloarthritis, according to four different sets of criteria. The specificity of the modified New York criteria, which relies on radiographic signs of sacroiliitis (unilateral grade III or bilateral grade II), fell well below that of the modified Amor criteria, the modified ESSG (European Spondyloarthropathy Study Group) criteria, and the ASAS (Assessment of Spondyloarthritis International Society) criteria. The latter three criteria include the option of diagnosing sacroiliitis with MRI.

In the new classification criteria from the ASAS, separate criteria are listed for patients with axial SpA with and without peripheral manifestations and patients with peripheral manifestations only. For axial SpA, one diagnostic pathway requires sacroiliitis on imaging plus one or more SpA feature. Sacroiliitis on MRI is given as much weight as is sacroiliitis on radiographs (Best Pract. Res. Clin. Rheumatol. 2010;24:589-604). The other pathway requires HLA-B27 positivity plus two or more SpA features. In patients with peripheral manifestations only, the requirements include peripheral arthritis, enthesitis or dactylitis plus one or more SpA features, including sacroiliitis on imaging.

Dr. Dougados also spoke about recent findings showing that patients with SpA were more likely to have distinct noninflammatory spinal MRI lesions (known as Fatty Romanus lesions) than were patients with degenerative arthritis or spinal malignancy (Ann. Rheum. Dis. 2010; 69:891-94).

"As MRI is becoming more important, rheumatologists should be trained to interpret MRIs," he said. "You don’t need to be a specialist in radiology."

Dr. Dougados has received grants for research projects and/or honorarium fees for participation at advisory boards/symposiums from Abbott, Bristol-Myers Squibb, Merck, Pfizer, Sanofi, and UCB.

NEW YORK – When magnetic resonance imaging is used instead of plain x-rays in patients with early inflammatory back pain, the diagnostic accuracy for spondyloarthritis jumps from 25% to 70%, according to Dr. Maxime Dougados, who spoke at a rheumatology meeting sponsored by New York University.

"Seventy-five percent of the time, you cannot make the diagnosis with plain x-rays," said Dr. Dougados, professor of rheumatology at Paris-Descartes University/Cochin Hospital in Paris and the president-elect of EULAR. He presented the Ira Goldstein Memorial Lecture at the meeting, focusing on spondyloarthritis (SpA).

Dr. Dougados presented the as yet unpublished results from the DESIR cohort, a large French national multicenter database of long-term follow-up of 708 patients presenting with early inflammatory back pain that was initiated by the French Society of Rheumatology. Patients were recruited between December 2007 and April 2010 if they had inflammatory back pain lasting more than 3 months and less than 3 years. The group will be followed for 10 years in the ongoing study. At baseline, the mean age was 35 years, 54% were female and 57% were HLA-B27 positive (Joint Bone Spine 2011 March 30 [doi: 10.1016/j.jbspin.2011.01.013]).

Looking at radiological sacroiliac changes, the diagnosis was "obvious" for 25.6% of the cohort, "doubtful" for 21.3%, and "normal" for 53.1%. "These results indicate that at the first clinical visit, the interview is very important to pick up other clinical symptoms," said Dr. Dougados. In fact, about 80% were found to have non-axial clinical manifestations, including articular peripheral involvement, enthesopathy, dactylitis, anterior chest wall pain, uveitis, or psoriasis.

Using MRI, 70% of the cohort were determined to have "obvious" sacroiliitis, about 20% had a "doubtful" diagnosis and about 10% were thought to be "normal."

"These results indicate that you can detect early abnormalities of the sacroiliac joint on MRI even if x-rays are normal," he said.

According to Dr. Dougados, these imaging findings fit well with recent results from the DECLIC study, in which 163 rheumatologists were asked to diagnose 472 patients with early inflammatory back pain, including 161 patients with spondyloarthritis, according to four different sets of criteria. The specificity of the modified New York criteria, which relies on radiographic signs of sacroiliitis (unilateral grade III or bilateral grade II), fell well below that of the modified Amor criteria, the modified ESSG (European Spondyloarthropathy Study Group) criteria, and the ASAS (Assessment of Spondyloarthritis International Society) criteria. The latter three criteria include the option of diagnosing sacroiliitis with MRI.

In the new classification criteria from the ASAS, separate criteria are listed for patients with axial SpA with and without peripheral manifestations and patients with peripheral manifestations only. For axial SpA, one diagnostic pathway requires sacroiliitis on imaging plus one or more SpA feature. Sacroiliitis on MRI is given as much weight as is sacroiliitis on radiographs (Best Pract. Res. Clin. Rheumatol. 2010;24:589-604). The other pathway requires HLA-B27 positivity plus two or more SpA features. In patients with peripheral manifestations only, the requirements include peripheral arthritis, enthesitis or dactylitis plus one or more SpA features, including sacroiliitis on imaging.

Dr. Dougados also spoke about recent findings showing that patients with SpA were more likely to have distinct noninflammatory spinal MRI lesions (known as Fatty Romanus lesions) than were patients with degenerative arthritis or spinal malignancy (Ann. Rheum. Dis. 2010; 69:891-94).

"As MRI is becoming more important, rheumatologists should be trained to interpret MRIs," he said. "You don’t need to be a specialist in radiology."

Dr. Dougados has received grants for research projects and/or honorarium fees for participation at advisory boards/symposiums from Abbott, Bristol-Myers Squibb, Merck, Pfizer, Sanofi, and UCB.

NEW YORK – When magnetic resonance imaging is used instead of plain x-rays in patients with early inflammatory back pain, the diagnostic accuracy for spondyloarthritis jumps from 25% to 70%, according to Dr. Maxime Dougados, who spoke at a rheumatology meeting sponsored by New York University.

"Seventy-five percent of the time, you cannot make the diagnosis with plain x-rays," said Dr. Dougados, professor of rheumatology at Paris-Descartes University/Cochin Hospital in Paris and the president-elect of EULAR. He presented the Ira Goldstein Memorial Lecture at the meeting, focusing on spondyloarthritis (SpA).

Dr. Dougados presented the as yet unpublished results from the DESIR cohort, a large French national multicenter database of long-term follow-up of 708 patients presenting with early inflammatory back pain that was initiated by the French Society of Rheumatology. Patients were recruited between December 2007 and April 2010 if they had inflammatory back pain lasting more than 3 months and less than 3 years. The group will be followed for 10 years in the ongoing study. At baseline, the mean age was 35 years, 54% were female and 57% were HLA-B27 positive (Joint Bone Spine 2011 March 30 [doi: 10.1016/j.jbspin.2011.01.013]).

Looking at radiological sacroiliac changes, the diagnosis was "obvious" for 25.6% of the cohort, "doubtful" for 21.3%, and "normal" for 53.1%. "These results indicate that at the first clinical visit, the interview is very important to pick up other clinical symptoms," said Dr. Dougados. In fact, about 80% were found to have non-axial clinical manifestations, including articular peripheral involvement, enthesopathy, dactylitis, anterior chest wall pain, uveitis, or psoriasis.

Using MRI, 70% of the cohort were determined to have "obvious" sacroiliitis, about 20% had a "doubtful" diagnosis and about 10% were thought to be "normal."

"These results indicate that you can detect early abnormalities of the sacroiliac joint on MRI even if x-rays are normal," he said.

According to Dr. Dougados, these imaging findings fit well with recent results from the DECLIC study, in which 163 rheumatologists were asked to diagnose 472 patients with early inflammatory back pain, including 161 patients with spondyloarthritis, according to four different sets of criteria. The specificity of the modified New York criteria, which relies on radiographic signs of sacroiliitis (unilateral grade III or bilateral grade II), fell well below that of the modified Amor criteria, the modified ESSG (European Spondyloarthropathy Study Group) criteria, and the ASAS (Assessment of Spondyloarthritis International Society) criteria. The latter three criteria include the option of diagnosing sacroiliitis with MRI.

In the new classification criteria from the ASAS, separate criteria are listed for patients with axial SpA with and without peripheral manifestations and patients with peripheral manifestations only. For axial SpA, one diagnostic pathway requires sacroiliitis on imaging plus one or more SpA feature. Sacroiliitis on MRI is given as much weight as is sacroiliitis on radiographs (Best Pract. Res. Clin. Rheumatol. 2010;24:589-604). The other pathway requires HLA-B27 positivity plus two or more SpA features. In patients with peripheral manifestations only, the requirements include peripheral arthritis, enthesitis or dactylitis plus one or more SpA features, including sacroiliitis on imaging.

Dr. Dougados also spoke about recent findings showing that patients with SpA were more likely to have distinct noninflammatory spinal MRI lesions (known as Fatty Romanus lesions) than were patients with degenerative arthritis or spinal malignancy (Ann. Rheum. Dis. 2010; 69:891-94).

"As MRI is becoming more important, rheumatologists should be trained to interpret MRIs," he said. "You don’t need to be a specialist in radiology."

Dr. Dougados has received grants for research projects and/or honorarium fees for participation at advisory boards/symposiums from Abbott, Bristol-Myers Squibb, Merck, Pfizer, Sanofi, and UCB.

NEW YORK – When magnetic resonance imaging is used instead of plain x-rays in patients with early inflammatory back pain, the diagnostic accuracy for spondyloarthritis jumps from 25% to 70%, according to Dr. Maxime Dougados, who spoke at a rheumatology meeting sponsored by New York University.

"Seventy-five percent of the time, you cannot make the diagnosis with plain x-rays," said Dr. Dougados, professor of rheumatology at Paris-Descartes University/Cochin Hospital in Paris and the president-elect of EULAR. He presented the Ira Goldstein Memorial Lecture at the meeting, focusing on spondyloarthritis (SpA).

Dr. Dougados presented the as yet unpublished results from the DESIR cohort, a large French national multicenter database of long-term follow-up of 708 patients presenting with early inflammatory back pain that was initiated by the French Society of Rheumatology. Patients were recruited between December 2007 and April 2010 if they had inflammatory back pain lasting more than 3 months and less than 3 years. The group will be followed for 10 years in the ongoing study. At baseline, the mean age was 35 years, 54% were female and 57% were HLA-B27 positive (Joint Bone Spine 2011 March 30 [doi: 10.1016/j.jbspin.2011.01.013]).

Looking at radiological sacroiliac changes, the diagnosis was "obvious" for 25.6% of the cohort, "doubtful" for 21.3%, and "normal" for 53.1%. "These results indicate that at the first clinical visit, the interview is very important to pick up other clinical symptoms," said Dr. Dougados. In fact, about 80% were found to have non-axial clinical manifestations, including articular peripheral involvement, enthesopathy, dactylitis, anterior chest wall pain, uveitis, or psoriasis.

Using MRI, 70% of the cohort were determined to have "obvious" sacroiliitis, about 20% had a "doubtful" diagnosis and about 10% were thought to be "normal."

"These results indicate that you can detect early abnormalities of the sacroiliac joint on MRI even if x-rays are normal," he said.

According to Dr. Dougados, these imaging findings fit well with recent results from the DECLIC study, in which 163 rheumatologists were asked to diagnose 472 patients with early inflammatory back pain, including 161 patients with spondyloarthritis, according to four different sets of criteria. The specificity of the modified New York criteria, which relies on radiographic signs of sacroiliitis (unilateral grade III or bilateral grade II), fell well below that of the modified Amor criteria, the modified ESSG (European Spondyloarthropathy Study Group) criteria, and the ASAS (Assessment of Spondyloarthritis International Society) criteria. The latter three criteria include the option of diagnosing sacroiliitis with MRI.

In the new classification criteria from the ASAS, separate criteria are listed for patients with axial SpA with and without peripheral manifestations and patients with peripheral manifestations only. For axial SpA, one diagnostic pathway requires sacroiliitis on imaging plus one or more SpA feature. Sacroiliitis on MRI is given as much weight as is sacroiliitis on radiographs (Best Pract. Res. Clin. Rheumatol. 2010;24:589-604). The other pathway requires HLA-B27 positivity plus two or more SpA features. In patients with peripheral manifestations only, the requirements include peripheral arthritis, enthesitis or dactylitis plus one or more SpA features, including sacroiliitis on imaging.

Dr. Dougados also spoke about recent findings showing that patients with SpA were more likely to have distinct noninflammatory spinal MRI lesions (known as Fatty Romanus lesions) than were patients with degenerative arthritis or spinal malignancy (Ann. Rheum. Dis. 2010; 69:891-94).

"As MRI is becoming more important, rheumatologists should be trained to interpret MRIs," he said. "You don’t need to be a specialist in radiology."

Dr. Dougados has received grants for research projects and/or honorarium fees for participation at advisory boards/symposiums from Abbott, Bristol-Myers Squibb, Merck, Pfizer, Sanofi, and UCB.

NEW YORK – When magnetic resonance imaging is used instead of plain x-rays in patients with early inflammatory back pain, the diagnostic accuracy for spondyloarthritis jumps from 25% to 70%, according to Dr. Maxime Dougados, who spoke at a rheumatology meeting sponsored by New York University.

"Seventy-five percent of the time, you cannot make the diagnosis with plain x-rays," said Dr. Dougados, professor of rheumatology at Paris-Descartes University/Cochin Hospital in Paris and the president-elect of EULAR. He presented the Ira Goldstein Memorial Lecture at the meeting, focusing on spondyloarthritis (SpA).

Dr. Dougados presented the as yet unpublished results from the DESIR cohort, a large French national multicenter database of long-term follow-up of 708 patients presenting with early inflammatory back pain that was initiated by the French Society of Rheumatology. Patients were recruited between December 2007 and April 2010 if they had inflammatory back pain lasting more than 3 months and less than 3 years. The group will be followed for 10 years in the ongoing study. At baseline, the mean age was 35 years, 54% were female and 57% were HLA-B27 positive (Joint Bone Spine 2011 March 30 [doi: 10.1016/j.jbspin.2011.01.013]).

Looking at radiological sacroiliac changes, the diagnosis was "obvious" for 25.6% of the cohort, "doubtful" for 21.3%, and "normal" for 53.1%. "These results indicate that at the first clinical visit, the interview is very important to pick up other clinical symptoms," said Dr. Dougados. In fact, about 80% were found to have non-axial clinical manifestations, including articular peripheral involvement, enthesopathy, dactylitis, anterior chest wall pain, uveitis, or psoriasis.

Using MRI, 70% of the cohort were determined to have "obvious" sacroiliitis, about 20% had a "doubtful" diagnosis and about 10% were thought to be "normal."

"These results indicate that you can detect early abnormalities of the sacroiliac joint on MRI even if x-rays are normal," he said.

According to Dr. Dougados, these imaging findings fit well with recent results from the DECLIC study, in which 163 rheumatologists were asked to diagnose 472 patients with early inflammatory back pain, including 161 patients with spondyloarthritis, according to four different sets of criteria. The specificity of the modified New York criteria, which relies on radiographic signs of sacroiliitis (unilateral grade III or bilateral grade II), fell well below that of the modified Amor criteria, the modified ESSG (European Spondyloarthropathy Study Group) criteria, and the ASAS (Assessment of Spondyloarthritis International Society) criteria. The latter three criteria include the option of diagnosing sacroiliitis with MRI.

In the new classification criteria from the ASAS, separate criteria are listed for patients with axial SpA with and without peripheral manifestations and patients with peripheral manifestations only. For axial SpA, one diagnostic pathway requires sacroiliitis on imaging plus one or more SpA feature. Sacroiliitis on MRI is given as much weight as is sacroiliitis on radiographs (Best Pract. Res. Clin. Rheumatol. 2010;24:589-604). The other pathway requires HLA-B27 positivity plus two or more SpA features. In patients with peripheral manifestations only, the requirements include peripheral arthritis, enthesitis or dactylitis plus one or more SpA features, including sacroiliitis on imaging.

Dr. Dougados also spoke about recent findings showing that patients with SpA were more likely to have distinct noninflammatory spinal MRI lesions (known as Fatty Romanus lesions) than were patients with degenerative arthritis or spinal malignancy (Ann. Rheum. Dis. 2010; 69:891-94).

"As MRI is becoming more important, rheumatologists should be trained to interpret MRIs," he said. "You don’t need to be a specialist in radiology."

Dr. Dougados has received grants for research projects and/or honorarium fees for participation at advisory boards/symposiums from Abbott, Bristol-Myers Squibb, Merck, Pfizer, Sanofi, and UCB.

NEW YORK – When magnetic resonance imaging is used instead of plain x-rays in patients with early inflammatory back pain, the diagnostic accuracy for spondyloarthritis jumps from 25% to 70%, according to Dr. Maxime Dougados, who spoke at a rheumatology meeting sponsored by New York University.

"Seventy-five percent of the time, you cannot make the diagnosis with plain x-rays," said Dr. Dougados, professor of rheumatology at Paris-Descartes University/Cochin Hospital in Paris and the president-elect of EULAR. He presented the Ira Goldstein Memorial Lecture at the meeting, focusing on spondyloarthritis (SpA).

Dr. Dougados presented the as yet unpublished results from the DESIR cohort, a large French national multicenter database of long-term follow-up of 708 patients presenting with early inflammatory back pain that was initiated by the French Society of Rheumatology. Patients were recruited between December 2007 and April 2010 if they had inflammatory back pain lasting more than 3 months and less than 3 years. The group will be followed for 10 years in the ongoing study. At baseline, the mean age was 35 years, 54% were female and 57% were HLA-B27 positive (Joint Bone Spine 2011 March 30 [doi: 10.1016/j.jbspin.2011.01.013]).

Looking at radiological sacroiliac changes, the diagnosis was "obvious" for 25.6% of the cohort, "doubtful" for 21.3%, and "normal" for 53.1%. "These results indicate that at the first clinical visit, the interview is very important to pick up other clinical symptoms," said Dr. Dougados. In fact, about 80% were found to have non-axial clinical manifestations, including articular peripheral involvement, enthesopathy, dactylitis, anterior chest wall pain, uveitis, or psoriasis.

Using MRI, 70% of the cohort were determined to have "obvious" sacroiliitis, about 20% had a "doubtful" diagnosis and about 10% were thought to be "normal."

"These results indicate that you can detect early abnormalities of the sacroiliac joint on MRI even if x-rays are normal," he said.

According to Dr. Dougados, these imaging findings fit well with recent results from the DECLIC study, in which 163 rheumatologists were asked to diagnose 472 patients with early inflammatory back pain, including 161 patients with spondyloarthritis, according to four different sets of criteria. The specificity of the modified New York criteria, which relies on radiographic signs of sacroiliitis (unilateral grade III or bilateral grade II), fell well below that of the modified Amor criteria, the modified ESSG (European Spondyloarthropathy Study Group) criteria, and the ASAS (Assessment of Spondyloarthritis International Society) criteria. The latter three criteria include the option of diagnosing sacroiliitis with MRI.

In the new classification criteria from the ASAS, separate criteria are listed for patients with axial SpA with and without peripheral manifestations and patients with peripheral manifestations only. For axial SpA, one diagnostic pathway requires sacroiliitis on imaging plus one or more SpA feature. Sacroiliitis on MRI is given as much weight as is sacroiliitis on radiographs (Best Pract. Res. Clin. Rheumatol. 2010;24:589-604). The other pathway requires HLA-B27 positivity plus two or more SpA features. In patients with peripheral manifestations only, the requirements include peripheral arthritis, enthesitis or dactylitis plus one or more SpA features, including sacroiliitis on imaging.

Dr. Dougados also spoke about recent findings showing that patients with SpA were more likely to have distinct noninflammatory spinal MRI lesions (known as Fatty Romanus lesions) than were patients with degenerative arthritis or spinal malignancy (Ann. Rheum. Dis. 2010; 69:891-94).

"As MRI is becoming more important, rheumatologists should be trained to interpret MRIs," he said. "You don’t need to be a specialist in radiology."

Dr. Dougados has received grants for research projects and/or honorarium fees for participation at advisory boards/symposiums from Abbott, Bristol-Myers Squibb, Merck, Pfizer, Sanofi, and UCB.