EULAR (European League Against Rheumatism): 2011 Congress

Young adults with hyperuricemia faced a significantly increased risk for later developing hypertension, based on follow-up of more than 4,900 Americans.

This link between hyperuricemia and the later appearance of hypertension did not involve a confounding role by metabolic syndrome. And although the analysis could not establish a causal link between hyperuricemia and hypertension, the results indicated that an elevated serum level of uric acid marks people with an increased risk for later having hypertension, according to Dr. Eswar Krishnan.

In a multivariate analysis that adjusted for baseline differences in subject age, gender, race, serum creatinine clearance, and waist circumferences, people in the highest quartile of serum uric acid level at baseline had a significant, 76%-increased risk for later developing hypertension, compared with the quartile of people with the lowest baseline serum uric acid level, reported Dr. Krishnan, a rheumatologist at Stanford (Calif.) University.

The study used data from the 5,115 people enrolled in the Coronary Artery Risk Development in Young Adults (CARDIA), which entered people aged 18-33 years at four U.S. sites in 1986 and followed them for up to 20 years. Excluding people who at baseline had hypertension or any other component of metabolic syndrome (abdominal obesity, elevated triglycerides, depressed high density lipoprotein cholesterol, elevated fasting glucose) left 4,918 people for the analysis.

The researchers divided the study group into quartiles by serum uric acid level, which in men ranged from 0.4-5.3 mg/dL uric acid in the lowest quartile to 6.8 mg/dL or greater in the highest quartile, and in women ranged from 0.6-3.7 mg/dL in the lowest quartile to 5.0 mg/dL or greater in the highest quartile.

During follow-up, the incidence of new cases of hypertension ran 7% in the lowest uric acid quartile and 16% in the highest quartile, a statistically significant difference, Dr. Krishnan and his associates reported at the annual European Congress of Rheumatology in London.

When the researchers subdivided the CARDIA subjects by race and sex, elevated serum uric acid levels linked with a significantly increased risk of later developing hypertension among black men and women and among white men. The link did not reach statistical significance among white women because of the small number of incident cases of hypertension during follow-up.

The analysis was sponsored by Takeda, which markets febuxostat (Uloric), a drug approved to lower serum uric acid levels in patients with gout. Dr. Krishnan said that he has been a consultant to Takeda, Savient, and Ardea. Three coauthors on the study are Takeda employees.

Young adults with hyperuricemia faced a significantly increased risk for later developing hypertension, based on follow-up of more than 4,900 Americans.

This link between hyperuricemia and the later appearance of hypertension did not involve a confounding role by metabolic syndrome. And although the analysis could not establish a causal link between hyperuricemia and hypertension, the results indicated that an elevated serum level of uric acid marks people with an increased risk for later having hypertension, according to Dr. Eswar Krishnan.

In a multivariate analysis that adjusted for baseline differences in subject age, gender, race, serum creatinine clearance, and waist circumferences, people in the highest quartile of serum uric acid level at baseline had a significant, 76%-increased risk for later developing hypertension, compared with the quartile of people with the lowest baseline serum uric acid level, reported Dr. Krishnan, a rheumatologist at Stanford (Calif.) University.

The study used data from the 5,115 people enrolled in the Coronary Artery Risk Development in Young Adults (CARDIA), which entered people aged 18-33 years at four U.S. sites in 1986 and followed them for up to 20 years. Excluding people who at baseline had hypertension or any other component of metabolic syndrome (abdominal obesity, elevated triglycerides, depressed high density lipoprotein cholesterol, elevated fasting glucose) left 4,918 people for the analysis.

The researchers divided the study group into quartiles by serum uric acid level, which in men ranged from 0.4-5.3 mg/dL uric acid in the lowest quartile to 6.8 mg/dL or greater in the highest quartile, and in women ranged from 0.6-3.7 mg/dL in the lowest quartile to 5.0 mg/dL or greater in the highest quartile.

During follow-up, the incidence of new cases of hypertension ran 7% in the lowest uric acid quartile and 16% in the highest quartile, a statistically significant difference, Dr. Krishnan and his associates reported at the annual European Congress of Rheumatology in London.

When the researchers subdivided the CARDIA subjects by race and sex, elevated serum uric acid levels linked with a significantly increased risk of later developing hypertension among black men and women and among white men. The link did not reach statistical significance among white women because of the small number of incident cases of hypertension during follow-up.

The analysis was sponsored by Takeda, which markets febuxostat (Uloric), a drug approved to lower serum uric acid levels in patients with gout. Dr. Krishnan said that he has been a consultant to Takeda, Savient, and Ardea. Three coauthors on the study are Takeda employees.

Young adults with hyperuricemia faced a significantly increased risk for later developing hypertension, based on follow-up of more than 4,900 Americans.

This link between hyperuricemia and the later appearance of hypertension did not involve a confounding role by metabolic syndrome. And although the analysis could not establish a causal link between hyperuricemia and hypertension, the results indicated that an elevated serum level of uric acid marks people with an increased risk for later having hypertension, according to Dr. Eswar Krishnan.

In a multivariate analysis that adjusted for baseline differences in subject age, gender, race, serum creatinine clearance, and waist circumferences, people in the highest quartile of serum uric acid level at baseline had a significant, 76%-increased risk for later developing hypertension, compared with the quartile of people with the lowest baseline serum uric acid level, reported Dr. Krishnan, a rheumatologist at Stanford (Calif.) University.

The study used data from the 5,115 people enrolled in the Coronary Artery Risk Development in Young Adults (CARDIA), which entered people aged 18-33 years at four U.S. sites in 1986 and followed them for up to 20 years. Excluding people who at baseline had hypertension or any other component of metabolic syndrome (abdominal obesity, elevated triglycerides, depressed high density lipoprotein cholesterol, elevated fasting glucose) left 4,918 people for the analysis.

The researchers divided the study group into quartiles by serum uric acid level, which in men ranged from 0.4-5.3 mg/dL uric acid in the lowest quartile to 6.8 mg/dL or greater in the highest quartile, and in women ranged from 0.6-3.7 mg/dL in the lowest quartile to 5.0 mg/dL or greater in the highest quartile.

During follow-up, the incidence of new cases of hypertension ran 7% in the lowest uric acid quartile and 16% in the highest quartile, a statistically significant difference, Dr. Krishnan and his associates reported at the annual European Congress of Rheumatology in London.

When the researchers subdivided the CARDIA subjects by race and sex, elevated serum uric acid levels linked with a significantly increased risk of later developing hypertension among black men and women and among white men. The link did not reach statistical significance among white women because of the small number of incident cases of hypertension during follow-up.

The analysis was sponsored by Takeda, which markets febuxostat (Uloric), a drug approved to lower serum uric acid levels in patients with gout. Dr. Krishnan said that he has been a consultant to Takeda, Savient, and Ardea. Three coauthors on the study are Takeda employees.

Magnetic resonance imaging has an increasingly important role in the early detection and diagnosis of osteoarthritis, although for now it remains one of several diagnostic tools that also include x-rays, clinical findings, and lab results.

Physicians who treat patients with osteoarthritis (OA) need further research results to better clarify the best use of MRI in early OA detection, said Dr. Philip Conaghan, professor of musculoskeletal medicine at the University of Leeds (England).

In June, Dr. Conaghan and his colleagues on the OA Imaging Working Group for the Osteoarthritis Research Society International (OARSI) issued 11 propositions on using MRI to define OA – propositions that the group said need formal testing "regarding their diagnostic performance before they are more widely used" (Osteoarthritis Cartilage 2011;19:963-9).

The working group clearly endorsed MRI, saying that "MRI may add to the diagnosis of OA and should be incorporated into the [American College of Rheumatology] diagnostic criteria," but in the same proposition, the working group also reiterated the role of x-ray, clinical, and laboratory parameters. Other propositions caution that "no single MRI finding is diagnostic of MRI," and that "certain MRI changes in isolation ... are not diagnostic of osteoarthritis."

The working group’s propositions included two MRI-based definitions of OA, for the tibiofemoral form and for the patellofemoral type.

In a recent talk on MRI and OA, Dr. Conaghan stressed the potential that MRI holds for early OA detection.

"We need to develop an early OA culture," similar to what has emerged for rheumatoid arthritis, he said speaking in May at the annual European Congress of Rheumatology in London. "In OA, we need a culture of early intervention" that would rely on early detection, most likely using MRI.

"Clinical features may suffice at present" for early OA detection, but MRI offers the best individualized option for assessing cartilage, bone features, and possibly the meniscus, he said. Soluble biomarkers may be more feasible than MRI, but biomarkers need more development and for early detection are "not there yet."

The sheer frequency of MRI lesions in OA patients may prove limiting. OA lesions appear more often on MRI than on x-rays. In five different reported series, the prevalence of cartilage defects visible by MRI in OA patients was 85%-98%, and the prevalence of osteophytes was 70%-100%, Dr. Conaghan noted. Often the MRI changes appear with no radiographic change visible. Other MRI changes that look like promising OA markers are bone marrow lesions and bone shape.

The OARSI Working Group defined tibiofemoral OA by MRI as either both items from group A, or one group A item and at least two from group B. The group A diagnostic features are definite osteophyte formation and full-thickness cartilage loss. The group B items are a subchondral bone marrow lesion or cyst that is not associated with meniscal or ligamentous attachments; meniscal subluxation, maceration, or degenerative tear; partial-thickness cartilage loss, and bone attrition.

The working group’s definition of patellofemoral OA requires both a definitive osteophyte and partial- or full-thickness cartilage loss.

Dr. Conaghan said that he had no relevant disclosures.

Magnetic resonance imaging has an increasingly important role in the early detection and diagnosis of osteoarthritis, although for now it remains one of several diagnostic tools that also include x-rays, clinical findings, and lab results.

Physicians who treat patients with osteoarthritis (OA) need further research results to better clarify the best use of MRI in early OA detection, said Dr. Philip Conaghan, professor of musculoskeletal medicine at the University of Leeds (England).

In June, Dr. Conaghan and his colleagues on the OA Imaging Working Group for the Osteoarthritis Research Society International (OARSI) issued 11 propositions on using MRI to define OA – propositions that the group said need formal testing "regarding their diagnostic performance before they are more widely used" (Osteoarthritis Cartilage 2011;19:963-9).

The working group clearly endorsed MRI, saying that "MRI may add to the diagnosis of OA and should be incorporated into the [American College of Rheumatology] diagnostic criteria," but in the same proposition, the working group also reiterated the role of x-ray, clinical, and laboratory parameters. Other propositions caution that "no single MRI finding is diagnostic of MRI," and that "certain MRI changes in isolation ... are not diagnostic of osteoarthritis."

The working group’s propositions included two MRI-based definitions of OA, for the tibiofemoral form and for the patellofemoral type.

In a recent talk on MRI and OA, Dr. Conaghan stressed the potential that MRI holds for early OA detection.

"We need to develop an early OA culture," similar to what has emerged for rheumatoid arthritis, he said speaking in May at the annual European Congress of Rheumatology in London. "In OA, we need a culture of early intervention" that would rely on early detection, most likely using MRI.

"Clinical features may suffice at present" for early OA detection, but MRI offers the best individualized option for assessing cartilage, bone features, and possibly the meniscus, he said. Soluble biomarkers may be more feasible than MRI, but biomarkers need more development and for early detection are "not there yet."

The sheer frequency of MRI lesions in OA patients may prove limiting. OA lesions appear more often on MRI than on x-rays. In five different reported series, the prevalence of cartilage defects visible by MRI in OA patients was 85%-98%, and the prevalence of osteophytes was 70%-100%, Dr. Conaghan noted. Often the MRI changes appear with no radiographic change visible. Other MRI changes that look like promising OA markers are bone marrow lesions and bone shape.

The OARSI Working Group defined tibiofemoral OA by MRI as either both items from group A, or one group A item and at least two from group B. The group A diagnostic features are definite osteophyte formation and full-thickness cartilage loss. The group B items are a subchondral bone marrow lesion or cyst that is not associated with meniscal or ligamentous attachments; meniscal subluxation, maceration, or degenerative tear; partial-thickness cartilage loss, and bone attrition.

The working group’s definition of patellofemoral OA requires both a definitive osteophyte and partial- or full-thickness cartilage loss.

Dr. Conaghan said that he had no relevant disclosures.

Magnetic resonance imaging has an increasingly important role in the early detection and diagnosis of osteoarthritis, although for now it remains one of several diagnostic tools that also include x-rays, clinical findings, and lab results.

Physicians who treat patients with osteoarthritis (OA) need further research results to better clarify the best use of MRI in early OA detection, said Dr. Philip Conaghan, professor of musculoskeletal medicine at the University of Leeds (England).

In June, Dr. Conaghan and his colleagues on the OA Imaging Working Group for the Osteoarthritis Research Society International (OARSI) issued 11 propositions on using MRI to define OA – propositions that the group said need formal testing "regarding their diagnostic performance before they are more widely used" (Osteoarthritis Cartilage 2011;19:963-9).

The working group clearly endorsed MRI, saying that "MRI may add to the diagnosis of OA and should be incorporated into the [American College of Rheumatology] diagnostic criteria," but in the same proposition, the working group also reiterated the role of x-ray, clinical, and laboratory parameters. Other propositions caution that "no single MRI finding is diagnostic of MRI," and that "certain MRI changes in isolation ... are not diagnostic of osteoarthritis."

The working group’s propositions included two MRI-based definitions of OA, for the tibiofemoral form and for the patellofemoral type.

In a recent talk on MRI and OA, Dr. Conaghan stressed the potential that MRI holds for early OA detection.

"We need to develop an early OA culture," similar to what has emerged for rheumatoid arthritis, he said speaking in May at the annual European Congress of Rheumatology in London. "In OA, we need a culture of early intervention" that would rely on early detection, most likely using MRI.

"Clinical features may suffice at present" for early OA detection, but MRI offers the best individualized option for assessing cartilage, bone features, and possibly the meniscus, he said. Soluble biomarkers may be more feasible than MRI, but biomarkers need more development and for early detection are "not there yet."

The sheer frequency of MRI lesions in OA patients may prove limiting. OA lesions appear more often on MRI than on x-rays. In five different reported series, the prevalence of cartilage defects visible by MRI in OA patients was 85%-98%, and the prevalence of osteophytes was 70%-100%, Dr. Conaghan noted. Often the MRI changes appear with no radiographic change visible. Other MRI changes that look like promising OA markers are bone marrow lesions and bone shape.

The OARSI Working Group defined tibiofemoral OA by MRI as either both items from group A, or one group A item and at least two from group B. The group A diagnostic features are definite osteophyte formation and full-thickness cartilage loss. The group B items are a subchondral bone marrow lesion or cyst that is not associated with meniscal or ligamentous attachments; meniscal subluxation, maceration, or degenerative tear; partial-thickness cartilage loss, and bone attrition.

The working group’s definition of patellofemoral OA requires both a definitive osteophyte and partial- or full-thickness cartilage loss.

Dr. Conaghan said that he had no relevant disclosures.

The science supporting vitamin D supplementation in lupus patients is catching up to the recommendation that all patients with the autoimmune disease increase their intake of the fat-soluble secosteroids.

Findings from a new study by Dr. Suzan Abou-Raya, professor of geriatric medicine at the University of Alexandria (Egypt), and her associates demonstrate that there is a high prevalence of vitamin-D deficiency associated with an increased inflammatory burden and thrombophilic state in patients with systemic lupus erythematosus (SLE). The findings also suggest that oral vitamin D supplementation ameliorates chronic inflammatory and hemostatic markers in this patient group.

The use of supplementary calcium and vitamin D is routinely recommended for SLE patients to help minimize the bone loss and increased risk of developing osteoporosis associated with the disease and its treatment. Beyond supporting bone and mineral hemostasis, "vitamin D is now recognized as having additional pleiotropic roles," according to Dr. Abou-Raya. "We’ve learned that it has potent immunomodulatory properties that have promoted its potential use in the treatment of autoimmune conditions, including lupus."

The study was designed to evaluate vitamin D status in lupus patients and to assess alterations in disease-related inflammatory and hemostatic markers before and after vitamin D supplementation.

To do this, Dr. Abou-Raya and her fellow researchers conducted a randomized, placebo-controlled trial comprising 148 males and premenopausal females who fulfilled the ACR (American College of Rheumatology) classification criteria for SLE. Also enrolled in the study were 75 lupus-free adults who served as controls and who matched the cases in age, sex, ethnicity, and body mass index. Individuals with other inflammatory disorders and those taking supplemental vitamin D at the time of the study were excluded from participation, she noted.

Study patients were randomized in a 1:1 fashion to receive either 2,000 IU per day of oral cholecalciferol (vitamin D₃) or placebo for 6 months together with standard SLE treatment, Dr. Abou-Raya explained. Before and after 6 months of vitamin D supplementation, the investigators evaluated disease activity using the SLE disease activity index (SLEDAI), levels of serum 25-hydroxyvitamin D (25[OH]D) via DiaSorin’s Liaison immunoassay, levels of proinflammatory cytokines interleukin-1 (IL-1), IL-6, IL-18, tumor necrosis factor (TNF)–alpha, C-reactive protein (CRP), and the hemostatic markers fibrinogen and von Willebrand factor (vWF), she explained. Individuals with 25(OH)D levels of 10-30 ng/mL were classified as having vitamin D insufficiency and those with levels lower than 10 ng/mL were considered vitamin D deficient, she noted.

With respect to baseline demographics, the mean age of the SLE patients was 38.8 years and the mean disease duration was 5.2 years. The mean baseline vitamin D level in the SLE patients was 19.8 ng/mL, which was significantly lower than the mean 28.7 ng/mL in the control group, Dr. Abou-Raya reported. The baseline levels of the inflammatory and hemostatic markers were significantly higher in the SLE patients. "The overall prevalence of vitamin D insufficiency and deficiency, respectively, was 69% and 39%," she said.

At 6 months, "there was a significant decrease in levels of inflammatory and hemostatic makers in lupus patients who were supplemented with vitamin D" compared with patients who were given placebo together with ongoing therapy, Dr. Abou-Raya reported at the annual European Congress of Rheumatology in London. After multivariate adjustment, the investigators observed a negative correlation between vitamin D levels and IL-1, IL-6, IL-18, TNF-alpha, CRP, fibrinogen, and vWF, "and lower vitamin D levels were associated with significantly higher SLEDAI scores," she said.

The results suggest that hypovitaminosis D contributes to a chronic inflammatory and thrombophilic state in SLE patients, said Dr. Abou-Raya. "The findings support the routine recommendation for oral vitamin D supplementation in these patients," she said.

Dr. Abou-Raya disclosed having no financial conflicts of interest related to her presentation.

The science supporting vitamin D supplementation in lupus patients is catching up to the recommendation that all patients with the autoimmune disease increase their intake of the fat-soluble secosteroids.

Findings from a new study by Dr. Suzan Abou-Raya, professor of geriatric medicine at the University of Alexandria (Egypt), and her associates demonstrate that there is a high prevalence of vitamin-D deficiency associated with an increased inflammatory burden and thrombophilic state in patients with systemic lupus erythematosus (SLE). The findings also suggest that oral vitamin D supplementation ameliorates chronic inflammatory and hemostatic markers in this patient group.

The use of supplementary calcium and vitamin D is routinely recommended for SLE patients to help minimize the bone loss and increased risk of developing osteoporosis associated with the disease and its treatment. Beyond supporting bone and mineral hemostasis, "vitamin D is now recognized as having additional pleiotropic roles," according to Dr. Abou-Raya. "We’ve learned that it has potent immunomodulatory properties that have promoted its potential use in the treatment of autoimmune conditions, including lupus."

The study was designed to evaluate vitamin D status in lupus patients and to assess alterations in disease-related inflammatory and hemostatic markers before and after vitamin D supplementation.

To do this, Dr. Abou-Raya and her fellow researchers conducted a randomized, placebo-controlled trial comprising 148 males and premenopausal females who fulfilled the ACR (American College of Rheumatology) classification criteria for SLE. Also enrolled in the study were 75 lupus-free adults who served as controls and who matched the cases in age, sex, ethnicity, and body mass index. Individuals with other inflammatory disorders and those taking supplemental vitamin D at the time of the study were excluded from participation, she noted.

Study patients were randomized in a 1:1 fashion to receive either 2,000 IU per day of oral cholecalciferol (vitamin D₃) or placebo for 6 months together with standard SLE treatment, Dr. Abou-Raya explained. Before and after 6 months of vitamin D supplementation, the investigators evaluated disease activity using the SLE disease activity index (SLEDAI), levels of serum 25-hydroxyvitamin D (25[OH]D) via DiaSorin’s Liaison immunoassay, levels of proinflammatory cytokines interleukin-1 (IL-1), IL-6, IL-18, tumor necrosis factor (TNF)–alpha, C-reactive protein (CRP), and the hemostatic markers fibrinogen and von Willebrand factor (vWF), she explained. Individuals with 25(OH)D levels of 10-30 ng/mL were classified as having vitamin D insufficiency and those with levels lower than 10 ng/mL were considered vitamin D deficient, she noted.

With respect to baseline demographics, the mean age of the SLE patients was 38.8 years and the mean disease duration was 5.2 years. The mean baseline vitamin D level in the SLE patients was 19.8 ng/mL, which was significantly lower than the mean 28.7 ng/mL in the control group, Dr. Abou-Raya reported. The baseline levels of the inflammatory and hemostatic markers were significantly higher in the SLE patients. "The overall prevalence of vitamin D insufficiency and deficiency, respectively, was 69% and 39%," she said.

At 6 months, "there was a significant decrease in levels of inflammatory and hemostatic makers in lupus patients who were supplemented with vitamin D" compared with patients who were given placebo together with ongoing therapy, Dr. Abou-Raya reported at the annual European Congress of Rheumatology in London. After multivariate adjustment, the investigators observed a negative correlation between vitamin D levels and IL-1, IL-6, IL-18, TNF-alpha, CRP, fibrinogen, and vWF, "and lower vitamin D levels were associated with significantly higher SLEDAI scores," she said.

The results suggest that hypovitaminosis D contributes to a chronic inflammatory and thrombophilic state in SLE patients, said Dr. Abou-Raya. "The findings support the routine recommendation for oral vitamin D supplementation in these patients," she said.

Dr. Abou-Raya disclosed having no financial conflicts of interest related to her presentation.

The science supporting vitamin D supplementation in lupus patients is catching up to the recommendation that all patients with the autoimmune disease increase their intake of the fat-soluble secosteroids.

Findings from a new study by Dr. Suzan Abou-Raya, professor of geriatric medicine at the University of Alexandria (Egypt), and her associates demonstrate that there is a high prevalence of vitamin-D deficiency associated with an increased inflammatory burden and thrombophilic state in patients with systemic lupus erythematosus (SLE). The findings also suggest that oral vitamin D supplementation ameliorates chronic inflammatory and hemostatic markers in this patient group.

The use of supplementary calcium and vitamin D is routinely recommended for SLE patients to help minimize the bone loss and increased risk of developing osteoporosis associated with the disease and its treatment. Beyond supporting bone and mineral hemostasis, "vitamin D is now recognized as having additional pleiotropic roles," according to Dr. Abou-Raya. "We’ve learned that it has potent immunomodulatory properties that have promoted its potential use in the treatment of autoimmune conditions, including lupus."

The study was designed to evaluate vitamin D status in lupus patients and to assess alterations in disease-related inflammatory and hemostatic markers before and after vitamin D supplementation.

To do this, Dr. Abou-Raya and her fellow researchers conducted a randomized, placebo-controlled trial comprising 148 males and premenopausal females who fulfilled the ACR (American College of Rheumatology) classification criteria for SLE. Also enrolled in the study were 75 lupus-free adults who served as controls and who matched the cases in age, sex, ethnicity, and body mass index. Individuals with other inflammatory disorders and those taking supplemental vitamin D at the time of the study were excluded from participation, she noted.

Study patients were randomized in a 1:1 fashion to receive either 2,000 IU per day of oral cholecalciferol (vitamin D₃) or placebo for 6 months together with standard SLE treatment, Dr. Abou-Raya explained. Before and after 6 months of vitamin D supplementation, the investigators evaluated disease activity using the SLE disease activity index (SLEDAI), levels of serum 25-hydroxyvitamin D (25[OH]D) via DiaSorin’s Liaison immunoassay, levels of proinflammatory cytokines interleukin-1 (IL-1), IL-6, IL-18, tumor necrosis factor (TNF)–alpha, C-reactive protein (CRP), and the hemostatic markers fibrinogen and von Willebrand factor (vWF), she explained. Individuals with 25(OH)D levels of 10-30 ng/mL were classified as having vitamin D insufficiency and those with levels lower than 10 ng/mL were considered vitamin D deficient, she noted.

With respect to baseline demographics, the mean age of the SLE patients was 38.8 years and the mean disease duration was 5.2 years. The mean baseline vitamin D level in the SLE patients was 19.8 ng/mL, which was significantly lower than the mean 28.7 ng/mL in the control group, Dr. Abou-Raya reported. The baseline levels of the inflammatory and hemostatic markers were significantly higher in the SLE patients. "The overall prevalence of vitamin D insufficiency and deficiency, respectively, was 69% and 39%," she said.

At 6 months, "there was a significant decrease in levels of inflammatory and hemostatic makers in lupus patients who were supplemented with vitamin D" compared with patients who were given placebo together with ongoing therapy, Dr. Abou-Raya reported at the annual European Congress of Rheumatology in London. After multivariate adjustment, the investigators observed a negative correlation between vitamin D levels and IL-1, IL-6, IL-18, TNF-alpha, CRP, fibrinogen, and vWF, "and lower vitamin D levels were associated with significantly higher SLEDAI scores," she said.

The results suggest that hypovitaminosis D contributes to a chronic inflammatory and thrombophilic state in SLE patients, said Dr. Abou-Raya. "The findings support the routine recommendation for oral vitamin D supplementation in these patients," she said.

Dr. Abou-Raya disclosed having no financial conflicts of interest related to her presentation.

Is vitamin D a neglected analgesic for chronic musculoskeletal pain? Dr. Suzan Abou-Raya, professor of geriatric medicine at the University of Alexandria in Egypt, thinks it could be and recommends that physicians should consider oral supplementation for all pain patients. Dr. Abou-Raya based her opinion on the findings of a recent study in which she and her colleagues evaluated the association between vitamin D status and chronic musculoskeletal pain in a cohort of community-dwelling older adults.

The investigators compared the vitamin D status of 265 adults aged 65 years and older who presented to their institution for musculoskeletal pain management with that of 200 other adults who were free of chronic musculoskeletal pain. These controls were matched to the cases by age, sex, and body mass index, according to Dr. Abou-Raya. Individuals with known vitamin D deficiency and calcium abnormality were excluded from the study, as were those with severe cognitive impairment or infectious, blood, hepatic, and renal disorders.

All of the participants in the study, which was conducted during the months of April through September to account for seasonal variation, underwent an initial survey about sun exposure and nutritional intake to assess daily intake of vitamin D and calcium, Dr. Abou-Raya explained. All of the participants underwent a comprehensive clinical examination, during which pain was assessed using the Brief Pain Inventory and Visual Analogue Scale. "Chronic pain was defined as pain that was present in the previous month and for at least 3 months during the previous year, and it was assessed according to the site of pain, the overall severity of the pain, and interference with daily activities," she said. Additionally, all of the patients completed a joint pain questionnaire to assess chronic musculoskeletal pain in the hands and wrists, shoulders, back, hips, knees, and feet, and they were directed to record daily pain in a diary.

Levels of pain were assessed at monthly intervals during follow-up, as was physical performance using activities of daily living, grip strength, six-minute walk distance, and the timed Get up and Go Test of mobility, Dr. Abou-Raya stated. Additionally, serum vitamin D was measured by Liaison immunoassay and levels between 10 and 30 ng/ml were classified as vitamin D insufficiency and levels lower than 10 ng/ml were classified as vitamin D deficiency, she noted.

In musculoskeletal patients, the mean 25-hydroxy vitamin D level was 18.4 ng/ml compared with 28.9 ng/ml in the control group, which represents a statistically significant difference, Dr. Abou-Raya reported. "The overall prevalence of suboptimal vitamin D levels among patients was 70% vs. 32% in the controls," she said, noting that 41% of the chronic musculoskeletal pain patients and only 1% of the controls met the criteria for vitamin D deficiency. "We also found that patients with multisite chronic pain had significantly lower levels of vitamin D compared with patients reporting sing-site chronic pain, and patients with more severe pain at baseline had significantly lower vitamin D levels than those with less severe pain."

After multivariate adjustment, "chronic, multisite, musculoskeletal pain was associated with lower levels of 25-hydroxy vitamin D, and lower levels of vitamin D correlated with pain severity and poor physical performance," Dr. Abou-Raya stated. One likely contributing factor is that sun exposure in the chronic pain group was significantly lower than that of the controls, with 40% of the pain patients reporting that they received fewer than 15 minutes of sun exposure weekly compared with 11% of the controls, likely due to limitations on physical activity associated with chronic pain, she said.

The results of this observational study should not be used to infer causation, Dr. Abou-Raya stressed. "They simply demonstrate that patients with chronic musculoskeletal pain have lower levels of vitamin D compared with individuals who are pain free, thus the possibility of inadequate vitamin D should be considered in the differential diagnosis of chronic musculoskeletal pain sufferers," she said at the annual European Congress of Rheumatology.

The implication of the findings, she continued, "is that all patients with chronic musculoskeletal pain should receive oral vitamin D supplementation, as optimal vitamin D levels appear to be associated with less pain and better physical performance."

Dr. Abou-Raya disclosed having no financial conflicts of interest related to her presentation.

Is vitamin D a neglected analgesic for chronic musculoskeletal pain? Dr. Suzan Abou-Raya, professor of geriatric medicine at the University of Alexandria in Egypt, thinks it could be and recommends that physicians should consider oral supplementation for all pain patients. Dr. Abou-Raya based her opinion on the findings of a recent study in which she and her colleagues evaluated the association between vitamin D status and chronic musculoskeletal pain in a cohort of community-dwelling older adults.

The investigators compared the vitamin D status of 265 adults aged 65 years and older who presented to their institution for musculoskeletal pain management with that of 200 other adults who were free of chronic musculoskeletal pain. These controls were matched to the cases by age, sex, and body mass index, according to Dr. Abou-Raya. Individuals with known vitamin D deficiency and calcium abnormality were excluded from the study, as were those with severe cognitive impairment or infectious, blood, hepatic, and renal disorders.

All of the participants in the study, which was conducted during the months of April through September to account for seasonal variation, underwent an initial survey about sun exposure and nutritional intake to assess daily intake of vitamin D and calcium, Dr. Abou-Raya explained. All of the participants underwent a comprehensive clinical examination, during which pain was assessed using the Brief Pain Inventory and Visual Analogue Scale. "Chronic pain was defined as pain that was present in the previous month and for at least 3 months during the previous year, and it was assessed according to the site of pain, the overall severity of the pain, and interference with daily activities," she said. Additionally, all of the patients completed a joint pain questionnaire to assess chronic musculoskeletal pain in the hands and wrists, shoulders, back, hips, knees, and feet, and they were directed to record daily pain in a diary.

Levels of pain were assessed at monthly intervals during follow-up, as was physical performance using activities of daily living, grip strength, six-minute walk distance, and the timed Get up and Go Test of mobility, Dr. Abou-Raya stated. Additionally, serum vitamin D was measured by Liaison immunoassay and levels between 10 and 30 ng/ml were classified as vitamin D insufficiency and levels lower than 10 ng/ml were classified as vitamin D deficiency, she noted.

In musculoskeletal patients, the mean 25-hydroxy vitamin D level was 18.4 ng/ml compared with 28.9 ng/ml in the control group, which represents a statistically significant difference, Dr. Abou-Raya reported. "The overall prevalence of suboptimal vitamin D levels among patients was 70% vs. 32% in the controls," she said, noting that 41% of the chronic musculoskeletal pain patients and only 1% of the controls met the criteria for vitamin D deficiency. "We also found that patients with multisite chronic pain had significantly lower levels of vitamin D compared with patients reporting sing-site chronic pain, and patients with more severe pain at baseline had significantly lower vitamin D levels than those with less severe pain."

After multivariate adjustment, "chronic, multisite, musculoskeletal pain was associated with lower levels of 25-hydroxy vitamin D, and lower levels of vitamin D correlated with pain severity and poor physical performance," Dr. Abou-Raya stated. One likely contributing factor is that sun exposure in the chronic pain group was significantly lower than that of the controls, with 40% of the pain patients reporting that they received fewer than 15 minutes of sun exposure weekly compared with 11% of the controls, likely due to limitations on physical activity associated with chronic pain, she said.

The results of this observational study should not be used to infer causation, Dr. Abou-Raya stressed. "They simply demonstrate that patients with chronic musculoskeletal pain have lower levels of vitamin D compared with individuals who are pain free, thus the possibility of inadequate vitamin D should be considered in the differential diagnosis of chronic musculoskeletal pain sufferers," she said at the annual European Congress of Rheumatology.

The implication of the findings, she continued, "is that all patients with chronic musculoskeletal pain should receive oral vitamin D supplementation, as optimal vitamin D levels appear to be associated with less pain and better physical performance."

Dr. Abou-Raya disclosed having no financial conflicts of interest related to her presentation.

Is vitamin D a neglected analgesic for chronic musculoskeletal pain? Dr. Suzan Abou-Raya, professor of geriatric medicine at the University of Alexandria in Egypt, thinks it could be and recommends that physicians should consider oral supplementation for all pain patients. Dr. Abou-Raya based her opinion on the findings of a recent study in which she and her colleagues evaluated the association between vitamin D status and chronic musculoskeletal pain in a cohort of community-dwelling older adults.

The investigators compared the vitamin D status of 265 adults aged 65 years and older who presented to their institution for musculoskeletal pain management with that of 200 other adults who were free of chronic musculoskeletal pain. These controls were matched to the cases by age, sex, and body mass index, according to Dr. Abou-Raya. Individuals with known vitamin D deficiency and calcium abnormality were excluded from the study, as were those with severe cognitive impairment or infectious, blood, hepatic, and renal disorders.

All of the participants in the study, which was conducted during the months of April through September to account for seasonal variation, underwent an initial survey about sun exposure and nutritional intake to assess daily intake of vitamin D and calcium, Dr. Abou-Raya explained. All of the participants underwent a comprehensive clinical examination, during which pain was assessed using the Brief Pain Inventory and Visual Analogue Scale. "Chronic pain was defined as pain that was present in the previous month and for at least 3 months during the previous year, and it was assessed according to the site of pain, the overall severity of the pain, and interference with daily activities," she said. Additionally, all of the patients completed a joint pain questionnaire to assess chronic musculoskeletal pain in the hands and wrists, shoulders, back, hips, knees, and feet, and they were directed to record daily pain in a diary.

Levels of pain were assessed at monthly intervals during follow-up, as was physical performance using activities of daily living, grip strength, six-minute walk distance, and the timed Get up and Go Test of mobility, Dr. Abou-Raya stated. Additionally, serum vitamin D was measured by Liaison immunoassay and levels between 10 and 30 ng/ml were classified as vitamin D insufficiency and levels lower than 10 ng/ml were classified as vitamin D deficiency, she noted.

In musculoskeletal patients, the mean 25-hydroxy vitamin D level was 18.4 ng/ml compared with 28.9 ng/ml in the control group, which represents a statistically significant difference, Dr. Abou-Raya reported. "The overall prevalence of suboptimal vitamin D levels among patients was 70% vs. 32% in the controls," she said, noting that 41% of the chronic musculoskeletal pain patients and only 1% of the controls met the criteria for vitamin D deficiency. "We also found that patients with multisite chronic pain had significantly lower levels of vitamin D compared with patients reporting sing-site chronic pain, and patients with more severe pain at baseline had significantly lower vitamin D levels than those with less severe pain."

After multivariate adjustment, "chronic, multisite, musculoskeletal pain was associated with lower levels of 25-hydroxy vitamin D, and lower levels of vitamin D correlated with pain severity and poor physical performance," Dr. Abou-Raya stated. One likely contributing factor is that sun exposure in the chronic pain group was significantly lower than that of the controls, with 40% of the pain patients reporting that they received fewer than 15 minutes of sun exposure weekly compared with 11% of the controls, likely due to limitations on physical activity associated with chronic pain, she said.

The results of this observational study should not be used to infer causation, Dr. Abou-Raya stressed. "They simply demonstrate that patients with chronic musculoskeletal pain have lower levels of vitamin D compared with individuals who are pain free, thus the possibility of inadequate vitamin D should be considered in the differential diagnosis of chronic musculoskeletal pain sufferers," she said at the annual European Congress of Rheumatology.

The implication of the findings, she continued, "is that all patients with chronic musculoskeletal pain should receive oral vitamin D supplementation, as optimal vitamin D levels appear to be associated with less pain and better physical performance."

Dr. Abou-Raya disclosed having no financial conflicts of interest related to her presentation.

LONDON – In an everyday setting, HLA-B27 positivity is the strongest predictor of an early, good response to the first use of an anti-tumor necrosis factor agent in patients with ankylosing spondylitis, according to the results of a longitudinal, observational study.

Other "real-world" and independent predictors of a good response using the ankylosing spondylitis disease activity score (ASDAS) are younger age, male sex, a higher baseline C-reactive protein (CRP) level, and a higher baseline patient global assessment score.

"TNF [tumor necrosis factor] inhibitors are effective in reducing symptoms in ankylosing spondylitis [AS], but not all patients have a response, [they] sometimes have side effects, and the medication is expensive," said Karen Fagerli, Ph.D., of the department of rheumatology at Diakonhjemmet Hospital in Oslo.

"So we want to identify characteristics of patients who will have a response in order to potentially utilize this knowledge when selecting patients for TNF-inhibitor therapy, and [therefore] treat patients with an optimized benefit-to-risk ratio," Dr. Fagerli added. ASDAS was used as the main outcome measure, which may be the first time it has been used in an observational study setting.

Using data from the NOR-DMARD (Norway-Disease-Modifying Antirheumatic Drug) register, researchers identified a study population of 171 patients with AS who were starting a TNF-inhibitor for the first time. The aim was to identify predictors of response to this treatment using the recently developed ASDAS outcome measure.

NOR-DMARD is a large, observational register that includes all patients with inflammatory arthropathies who are starting treatment with a DMARD for the first time at five rheumatology centers in Norway. Patients are routinely assessed at baseline, then after 3, 6, and 12 months, and then annually.

ASDAS major improvement was defined as a change in score of 2 or more; this was achieved by 32.7% of patients after 3 months of anti-TNF therapy.

Several parameters that had been identified as predictors of response in univariate analysis did not hold up as being statistically significant in a multivariate analysis model; these included the number of swollen joints, physician’s global score, the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and the Bath Ankylosing Spondylitis Functional Activity Index (BASFAI).

Patients who were HLA-B27 positive had a much higher chance of achieving ASDAS major improvement at 3 months than did those who were HLA-B27 negative (odds ratio, 6.72; 95% confidence interval, 1.33-33.87; P = .02).

Baseline CRP levels higher than 10 mg/L were also significantly predictive of an early treatment response (OR, 5.31; 95% CI, 2.23-12.42; P less than .001).

The next strongest predictor was male sex, with men almost three times more likely than women to show a benefit of anti-TNF treatment at 3 months (OR, 2.69; 95% CI, 1.04-7.00; P less than .04). However, the majority of the study population (73.4%) was male.

For every 1-year increase in age, the likelihood of achieving ASDAS major improvement declined, with young patients faring the best overall (OR, 0.95; 95% CI, 0.91-1.00; P less than .03).

Furthermore, for every 10-mm increase in a 0- to 100-mm visual analog scale of patient global assessment, the chance of a good response improved (OR, 1.75; 95% CI, 1.40-2.19; P less than .0001).

Taken together, these data could help clinicians to identify patients who not only may respond to anti-TNF inhibitors but also should be prioritized for such treatment.

However, "this is on a crude level; we don’t know to what extent we can use [this information] on an individual level," Dr. Fagerli said in an interview. "We know for certain that there are patients who have none of these characteristics that I’ve talked about, who do get a response, so this is not the full truth; this is a little piece of the puzzle."

Dr. Fagerli disclosed receiving a speaker’s fee from Pfizer in the past.

LONDON – In an everyday setting, HLA-B27 positivity is the strongest predictor of an early, good response to the first use of an anti-tumor necrosis factor agent in patients with ankylosing spondylitis, according to the results of a longitudinal, observational study.

Other "real-world" and independent predictors of a good response using the ankylosing spondylitis disease activity score (ASDAS) are younger age, male sex, a higher baseline C-reactive protein (CRP) level, and a higher baseline patient global assessment score.

"TNF [tumor necrosis factor] inhibitors are effective in reducing symptoms in ankylosing spondylitis [AS], but not all patients have a response, [they] sometimes have side effects, and the medication is expensive," said Karen Fagerli, Ph.D., of the department of rheumatology at Diakonhjemmet Hospital in Oslo.

"So we want to identify characteristics of patients who will have a response in order to potentially utilize this knowledge when selecting patients for TNF-inhibitor therapy, and [therefore] treat patients with an optimized benefit-to-risk ratio," Dr. Fagerli added. ASDAS was used as the main outcome measure, which may be the first time it has been used in an observational study setting.

Using data from the NOR-DMARD (Norway-Disease-Modifying Antirheumatic Drug) register, researchers identified a study population of 171 patients with AS who were starting a TNF-inhibitor for the first time. The aim was to identify predictors of response to this treatment using the recently developed ASDAS outcome measure.

NOR-DMARD is a large, observational register that includes all patients with inflammatory arthropathies who are starting treatment with a DMARD for the first time at five rheumatology centers in Norway. Patients are routinely assessed at baseline, then after 3, 6, and 12 months, and then annually.

ASDAS major improvement was defined as a change in score of 2 or more; this was achieved by 32.7% of patients after 3 months of anti-TNF therapy.

Several parameters that had been identified as predictors of response in univariate analysis did not hold up as being statistically significant in a multivariate analysis model; these included the number of swollen joints, physician’s global score, the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and the Bath Ankylosing Spondylitis Functional Activity Index (BASFAI).

Patients who were HLA-B27 positive had a much higher chance of achieving ASDAS major improvement at 3 months than did those who were HLA-B27 negative (odds ratio, 6.72; 95% confidence interval, 1.33-33.87; P = .02).

Baseline CRP levels higher than 10 mg/L were also significantly predictive of an early treatment response (OR, 5.31; 95% CI, 2.23-12.42; P less than .001).

The next strongest predictor was male sex, with men almost three times more likely than women to show a benefit of anti-TNF treatment at 3 months (OR, 2.69; 95% CI, 1.04-7.00; P less than .04). However, the majority of the study population (73.4%) was male.

For every 1-year increase in age, the likelihood of achieving ASDAS major improvement declined, with young patients faring the best overall (OR, 0.95; 95% CI, 0.91-1.00; P less than .03).

Furthermore, for every 10-mm increase in a 0- to 100-mm visual analog scale of patient global assessment, the chance of a good response improved (OR, 1.75; 95% CI, 1.40-2.19; P less than .0001).

Taken together, these data could help clinicians to identify patients who not only may respond to anti-TNF inhibitors but also should be prioritized for such treatment.

However, "this is on a crude level; we don’t know to what extent we can use [this information] on an individual level," Dr. Fagerli said in an interview. "We know for certain that there are patients who have none of these characteristics that I’ve talked about, who do get a response, so this is not the full truth; this is a little piece of the puzzle."

Dr. Fagerli disclosed receiving a speaker’s fee from Pfizer in the past.

LONDON – In an everyday setting, HLA-B27 positivity is the strongest predictor of an early, good response to the first use of an anti-tumor necrosis factor agent in patients with ankylosing spondylitis, according to the results of a longitudinal, observational study.

Other "real-world" and independent predictors of a good response using the ankylosing spondylitis disease activity score (ASDAS) are younger age, male sex, a higher baseline C-reactive protein (CRP) level, and a higher baseline patient global assessment score.

"TNF [tumor necrosis factor] inhibitors are effective in reducing symptoms in ankylosing spondylitis [AS], but not all patients have a response, [they] sometimes have side effects, and the medication is expensive," said Karen Fagerli, Ph.D., of the department of rheumatology at Diakonhjemmet Hospital in Oslo.

"So we want to identify characteristics of patients who will have a response in order to potentially utilize this knowledge when selecting patients for TNF-inhibitor therapy, and [therefore] treat patients with an optimized benefit-to-risk ratio," Dr. Fagerli added. ASDAS was used as the main outcome measure, which may be the first time it has been used in an observational study setting.

Using data from the NOR-DMARD (Norway-Disease-Modifying Antirheumatic Drug) register, researchers identified a study population of 171 patients with AS who were starting a TNF-inhibitor for the first time. The aim was to identify predictors of response to this treatment using the recently developed ASDAS outcome measure.

NOR-DMARD is a large, observational register that includes all patients with inflammatory arthropathies who are starting treatment with a DMARD for the first time at five rheumatology centers in Norway. Patients are routinely assessed at baseline, then after 3, 6, and 12 months, and then annually.

ASDAS major improvement was defined as a change in score of 2 or more; this was achieved by 32.7% of patients after 3 months of anti-TNF therapy.

Several parameters that had been identified as predictors of response in univariate analysis did not hold up as being statistically significant in a multivariate analysis model; these included the number of swollen joints, physician’s global score, the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and the Bath Ankylosing Spondylitis Functional Activity Index (BASFAI).

Patients who were HLA-B27 positive had a much higher chance of achieving ASDAS major improvement at 3 months than did those who were HLA-B27 negative (odds ratio, 6.72; 95% confidence interval, 1.33-33.87; P = .02).

Baseline CRP levels higher than 10 mg/L were also significantly predictive of an early treatment response (OR, 5.31; 95% CI, 2.23-12.42; P less than .001).

The next strongest predictor was male sex, with men almost three times more likely than women to show a benefit of anti-TNF treatment at 3 months (OR, 2.69; 95% CI, 1.04-7.00; P less than .04). However, the majority of the study population (73.4%) was male.

For every 1-year increase in age, the likelihood of achieving ASDAS major improvement declined, with young patients faring the best overall (OR, 0.95; 95% CI, 0.91-1.00; P less than .03).

Furthermore, for every 10-mm increase in a 0- to 100-mm visual analog scale of patient global assessment, the chance of a good response improved (OR, 1.75; 95% CI, 1.40-2.19; P less than .0001).

Taken together, these data could help clinicians to identify patients who not only may respond to anti-TNF inhibitors but also should be prioritized for such treatment.

However, "this is on a crude level; we don’t know to what extent we can use [this information] on an individual level," Dr. Fagerli said in an interview. "We know for certain that there are patients who have none of these characteristics that I’ve talked about, who do get a response, so this is not the full truth; this is a little piece of the puzzle."

Dr. Fagerli disclosed receiving a speaker’s fee from Pfizer in the past.

LONDON – Patients with rheumatoid arthritis have a high risk of concomitant chronic obstructive pulmonary disease, according to data from two studies.

In one of the studies – which involved more than 15,000 patients with rheumatoid arthritis (RA) and 15,000 healthy individuals as case-matched controls – the risk of the long-term lung condition was 8.9% vs. 4.4%, respectively (P less than .001).

Other data, from the Norfolk Arthritis Register (NOAR) showed that the prevalence of chronic obstructive pulmonary disease (COPD) in patients with inflammatory polyarthritis (IP) or RA was 7.3% (n = 425) at 15 years’ follow-up. Prevalence of the respiratory disease was again doubled when compared to the general population.

"Lung involvement is a common extra-articular manifestation in rheumatoid arthritis," said Dr. Suzanne Verstappen, who presented the findings from the NOAR at the annual European Congress of Rheumatology.

"As could be expected, age and gender were associated with obstructive and restrictive lung disease," said Dr. Verstappen, a research fellow at the Arthritis Research UK Epidemiology Unit at the University of Manchester, England, where the NOAR is coordinated.

Validated spirometry parameters and the Medical Research Council respiratory symptoms questionnaire were used to identify patients with IP or RA who also had COPD. The latter was distinguished from restrictive lung disease whereby the lungs are restricted by the extent that they can inflate. The prevalence of restrictive lung disease was 9.7%.

COPD was observed in 7.3% of the population at 15 years, with higher prevalence rates found in men versus women over the age of 45 years (12.7% vs. 6%, respectively) in a crude comparison. Published rates for the U.K. general population without IP or RA are 6.8% and 3.9% (Popul. Health Metr. 2007;5:8).

Like RA, COPD is a chronic and often debilitating disease. The disease manifests later in life and treatment is symptomatic rather than curative, as the obstruction in the airways is permanent and not usually reversible with bronchodilator therapy. Unlike RA, however, which has multiple etiologic factors and autoimmunity at its root, COPD is almost always caused by smoking. In the NOAR analysis, 53% of the 425 patients were ex-smokers and 13% were current smokers; 34% had never smoked.

Data from the first study, presented during a poster session by Dr. Howard Amital of Sheba Medical Centre in Tel Hashomer, Israel, showed, however, that even with smoking out of the equation, the risk of COPD in patients with RA was higher than in the general population.

Indeed, multivariate analysis showed that RA was associated with COPD after the researchers controlled for confounding factors such as age, gender, smoking, obesity and socioeconomic status.

"The strength of the association increased," Dr. Amital and colleagues reported, with an adjusted odds ratio (OR) of 2.015 (95% confidence interval 1.83-2.22; P less than .001) and an unadjusted OR of 1.89 (95% CI 1.74-2.05, P less than .0001).

The case-control study involved 15,766 patients with RA and 15,240 age- and sex-matched healthy individuals without RA. The study also found higher rates of other chronic disease in patients versus controls, including diabetes (23.9% vs. 19.8%, P less than .0001), ischemic heart disease (19.5% vs. 15.4%, P less than .0001), and heart failure (6.3% vs. 4.3%, P less than .0001).

"This study corroborates the hypothesis that COPD and RA are closely interrelated," Dr. Amital and his team concluded.

NOAR is funded by Arthritis Research UK. Dr. Verstappen and Dr. Amital and colleagues had no conflicts of interest to declare.

LONDON – Patients with rheumatoid arthritis have a high risk of concomitant chronic obstructive pulmonary disease, according to data from two studies.

In one of the studies – which involved more than 15,000 patients with rheumatoid arthritis (RA) and 15,000 healthy individuals as case-matched controls – the risk of the long-term lung condition was 8.9% vs. 4.4%, respectively (P less than .001).

Other data, from the Norfolk Arthritis Register (NOAR) showed that the prevalence of chronic obstructive pulmonary disease (COPD) in patients with inflammatory polyarthritis (IP) or RA was 7.3% (n = 425) at 15 years’ follow-up. Prevalence of the respiratory disease was again doubled when compared to the general population.

"Lung involvement is a common extra-articular manifestation in rheumatoid arthritis," said Dr. Suzanne Verstappen, who presented the findings from the NOAR at the annual European Congress of Rheumatology.

"As could be expected, age and gender were associated with obstructive and restrictive lung disease," said Dr. Verstappen, a research fellow at the Arthritis Research UK Epidemiology Unit at the University of Manchester, England, where the NOAR is coordinated.

Validated spirometry parameters and the Medical Research Council respiratory symptoms questionnaire were used to identify patients with IP or RA who also had COPD. The latter was distinguished from restrictive lung disease whereby the lungs are restricted by the extent that they can inflate. The prevalence of restrictive lung disease was 9.7%.

COPD was observed in 7.3% of the population at 15 years, with higher prevalence rates found in men versus women over the age of 45 years (12.7% vs. 6%, respectively) in a crude comparison. Published rates for the U.K. general population without IP or RA are 6.8% and 3.9% (Popul. Health Metr. 2007;5:8).

Like RA, COPD is a chronic and often debilitating disease. The disease manifests later in life and treatment is symptomatic rather than curative, as the obstruction in the airways is permanent and not usually reversible with bronchodilator therapy. Unlike RA, however, which has multiple etiologic factors and autoimmunity at its root, COPD is almost always caused by smoking. In the NOAR analysis, 53% of the 425 patients were ex-smokers and 13% were current smokers; 34% had never smoked.

Data from the first study, presented during a poster session by Dr. Howard Amital of Sheba Medical Centre in Tel Hashomer, Israel, showed, however, that even with smoking out of the equation, the risk of COPD in patients with RA was higher than in the general population.

Indeed, multivariate analysis showed that RA was associated with COPD after the researchers controlled for confounding factors such as age, gender, smoking, obesity and socioeconomic status.

"The strength of the association increased," Dr. Amital and colleagues reported, with an adjusted odds ratio (OR) of 2.015 (95% confidence interval 1.83-2.22; P less than .001) and an unadjusted OR of 1.89 (95% CI 1.74-2.05, P less than .0001).

The case-control study involved 15,766 patients with RA and 15,240 age- and sex-matched healthy individuals without RA. The study also found higher rates of other chronic disease in patients versus controls, including diabetes (23.9% vs. 19.8%, P less than .0001), ischemic heart disease (19.5% vs. 15.4%, P less than .0001), and heart failure (6.3% vs. 4.3%, P less than .0001).

"This study corroborates the hypothesis that COPD and RA are closely interrelated," Dr. Amital and his team concluded.

NOAR is funded by Arthritis Research UK. Dr. Verstappen and Dr. Amital and colleagues had no conflicts of interest to declare.

LONDON – Patients with rheumatoid arthritis have a high risk of concomitant chronic obstructive pulmonary disease, according to data from two studies.

In one of the studies – which involved more than 15,000 patients with rheumatoid arthritis (RA) and 15,000 healthy individuals as case-matched controls – the risk of the long-term lung condition was 8.9% vs. 4.4%, respectively (P less than .001).

Other data, from the Norfolk Arthritis Register (NOAR) showed that the prevalence of chronic obstructive pulmonary disease (COPD) in patients with inflammatory polyarthritis (IP) or RA was 7.3% (n = 425) at 15 years’ follow-up. Prevalence of the respiratory disease was again doubled when compared to the general population.

"Lung involvement is a common extra-articular manifestation in rheumatoid arthritis," said Dr. Suzanne Verstappen, who presented the findings from the NOAR at the annual European Congress of Rheumatology.

"As could be expected, age and gender were associated with obstructive and restrictive lung disease," said Dr. Verstappen, a research fellow at the Arthritis Research UK Epidemiology Unit at the University of Manchester, England, where the NOAR is coordinated.

Validated spirometry parameters and the Medical Research Council respiratory symptoms questionnaire were used to identify patients with IP or RA who also had COPD. The latter was distinguished from restrictive lung disease whereby the lungs are restricted by the extent that they can inflate. The prevalence of restrictive lung disease was 9.7%.

COPD was observed in 7.3% of the population at 15 years, with higher prevalence rates found in men versus women over the age of 45 years (12.7% vs. 6%, respectively) in a crude comparison. Published rates for the U.K. general population without IP or RA are 6.8% and 3.9% (Popul. Health Metr. 2007;5:8).

Like RA, COPD is a chronic and often debilitating disease. The disease manifests later in life and treatment is symptomatic rather than curative, as the obstruction in the airways is permanent and not usually reversible with bronchodilator therapy. Unlike RA, however, which has multiple etiologic factors and autoimmunity at its root, COPD is almost always caused by smoking. In the NOAR analysis, 53% of the 425 patients were ex-smokers and 13% were current smokers; 34% had never smoked.

Data from the first study, presented during a poster session by Dr. Howard Amital of Sheba Medical Centre in Tel Hashomer, Israel, showed, however, that even with smoking out of the equation, the risk of COPD in patients with RA was higher than in the general population.

Indeed, multivariate analysis showed that RA was associated with COPD after the researchers controlled for confounding factors such as age, gender, smoking, obesity and socioeconomic status.

"The strength of the association increased," Dr. Amital and colleagues reported, with an adjusted odds ratio (OR) of 2.015 (95% confidence interval 1.83-2.22; P less than .001) and an unadjusted OR of 1.89 (95% CI 1.74-2.05, P less than .0001).

The case-control study involved 15,766 patients with RA and 15,240 age- and sex-matched healthy individuals without RA. The study also found higher rates of other chronic disease in patients versus controls, including diabetes (23.9% vs. 19.8%, P less than .0001), ischemic heart disease (19.5% vs. 15.4%, P less than .0001), and heart failure (6.3% vs. 4.3%, P less than .0001).

"This study corroborates the hypothesis that COPD and RA are closely interrelated," Dr. Amital and his team concluded.

NOAR is funded by Arthritis Research UK. Dr. Verstappen and Dr. Amital and colleagues had no conflicts of interest to declare.

LONDON – Patients with rheumatoid arthritis who have had a heart attack for the first time do not appear to be getting medications recommended to prevent a further cardiovascular event, according to the findings of a large Danish study.

Aspirin, statins, and beta-blockers – cardioprotective medications that are given as the standard of care to most patients immediately following a myocardial infarction – were all less frequently prescribed to patients with rheumatoid arthritis (RA) than to members of the general patient population.

Indeed, 1 month after an MI, the odds ratios for the prescription of these drugs were 0.75 (95% confidence interval, 0.63-0.90) for aspirin, 0.68 (95% CI, 0.57-0.82) for a statin, and 0.76 (95% CI, 0.63-0.91) for beta-blockers. These results did not change greatly at follow-ups of 3 months, 6 months, or 1 year.

The increased risk of cardiovascular disease in RA patients is well known and could result from a number of causes, including the presence of classical risk factors such as dyslipidemia and hypertension, possible adverse effects of RA treatment, and an accelerated atherosclerotic process driven by the high levels of inflammation characteristic of the rheumatic disease.

"What’s not been considered, [however,] and perhaps the simplest explanation, is whether or not there is undertreatment of [RA] patients," Dr. Jesper Lindhardsen, of the cardiology department at Gentofte University Hospital, Copenhagen, said at a press briefing during the annual European Congress of Rheumatology.

To determine whether patients with RA were being given standard cardioprotective medications after a first MI, he and his colleagues analyzed data from several Danish patient registries, including those giving prescription records, details of comorbidities, and income.

The study population consisted of 66,389 patients who had had a first heart attack between 2002 and 2009. Of these, 875 (1.3%) had RA. The median age was 72.6 years for RA patients and 69.4 years for patients without RA.

At baseline, the use of cardioprotective medications by patients with and without RA were relatively similar or the same, at 27% and 25.1%, respectively, for aspirin; 19.1% and 19.1% for a statin; 23.9% and 22.5% for a beta-blocker; and 3.3% and 2.2% for clopidogrel.

Although aspirin, statin, and beta-blocker use was later found to be lower in the RA patients than in the non-RA patients throughout the early post-MI period, there was no significant difference in the prescription of clopidogrel at 1, 3, or 6 months or at 1 year.

Commenting on the findings in an interview, Dr. Lindhardsen conceded that this data raises more questions than it answers. For one thing, it’s not known what medications patients were taking before they had their heart attack, which could influence the findings.

Dr. Georg Schett, who is chief of rheumatology at the University of Erlangen-Nuremberg, Germany, but was not involved in the study, said the findings illustrate that the high cardiovascular risk in patients with RA is still not being taken seriously enough.

Speaking at a press conference, Dr. Schett said that "the risk of cardiovascular disease in RA is similar to diabetes, but people sometimes forget this."

Indeed, Dr. Lindhardsen and his colleagues recently published data showing that RA is associated with the same risk of MI as diabetes (Ann. Rheum. Dis. 2011;70:929-34).

With regard to this post-MI data, Dr. Lindhardsen stressed the importance of communication between the cardiologist discharging a patient and the rheumatologist responsible for the patient’s long-term care to ensure that standard cardioprotective medications are being used.

"We have quantitative data. Now we need more qualitative data," Dr. Lindhardsen observed in an interview. The next steps are to try to determine the reasons RA patients get fewer prescriptions for these standard post-MI drugs, he said.

Dr. Lindhardsen and Dr. Schett had no conflicts of interest to declare.

LONDON – Patients with rheumatoid arthritis who have had a heart attack for the first time do not appear to be getting medications recommended to prevent a further cardiovascular event, according to the findings of a large Danish study.

Aspirin, statins, and beta-blockers – cardioprotective medications that are given as the standard of care to most patients immediately following a myocardial infarction – were all less frequently prescribed to patients with rheumatoid arthritis (RA) than to members of the general patient population.

Indeed, 1 month after an MI, the odds ratios for the prescription of these drugs were 0.75 (95% confidence interval, 0.63-0.90) for aspirin, 0.68 (95% CI, 0.57-0.82) for a statin, and 0.76 (95% CI, 0.63-0.91) for beta-blockers. These results did not change greatly at follow-ups of 3 months, 6 months, or 1 year.

The increased risk of cardiovascular disease in RA patients is well known and could result from a number of causes, including the presence of classical risk factors such as dyslipidemia and hypertension, possible adverse effects of RA treatment, and an accelerated atherosclerotic process driven by the high levels of inflammation characteristic of the rheumatic disease.

"What’s not been considered, [however,] and perhaps the simplest explanation, is whether or not there is undertreatment of [RA] patients," Dr. Jesper Lindhardsen, of the cardiology department at Gentofte University Hospital, Copenhagen, said at a press briefing during the annual European Congress of Rheumatology.

To determine whether patients with RA were being given standard cardioprotective medications after a first MI, he and his colleagues analyzed data from several Danish patient registries, including those giving prescription records, details of comorbidities, and income.

The study population consisted of 66,389 patients who had had a first heart attack between 2002 and 2009. Of these, 875 (1.3%) had RA. The median age was 72.6 years for RA patients and 69.4 years for patients without RA.

At baseline, the use of cardioprotective medications by patients with and without RA were relatively similar or the same, at 27% and 25.1%, respectively, for aspirin; 19.1% and 19.1% for a statin; 23.9% and 22.5% for a beta-blocker; and 3.3% and 2.2% for clopidogrel.

Although aspirin, statin, and beta-blocker use was later found to be lower in the RA patients than in the non-RA patients throughout the early post-MI period, there was no significant difference in the prescription of clopidogrel at 1, 3, or 6 months or at 1 year.

Commenting on the findings in an interview, Dr. Lindhardsen conceded that this data raises more questions than it answers. For one thing, it’s not known what medications patients were taking before they had their heart attack, which could influence the findings.

Dr. Georg Schett, who is chief of rheumatology at the University of Erlangen-Nuremberg, Germany, but was not involved in the study, said the findings illustrate that the high cardiovascular risk in patients with RA is still not being taken seriously enough.

Speaking at a press conference, Dr. Schett said that "the risk of cardiovascular disease in RA is similar to diabetes, but people sometimes forget this."

Indeed, Dr. Lindhardsen and his colleagues recently published data showing that RA is associated with the same risk of MI as diabetes (Ann. Rheum. Dis. 2011;70:929-34).

With regard to this post-MI data, Dr. Lindhardsen stressed the importance of communication between the cardiologist discharging a patient and the rheumatologist responsible for the patient’s long-term care to ensure that standard cardioprotective medications are being used.

"We have quantitative data. Now we need more qualitative data," Dr. Lindhardsen observed in an interview. The next steps are to try to determine the reasons RA patients get fewer prescriptions for these standard post-MI drugs, he said.

Dr. Lindhardsen and Dr. Schett had no conflicts of interest to declare.

LONDON – Patients with rheumatoid arthritis who have had a heart attack for the first time do not appear to be getting medications recommended to prevent a further cardiovascular event, according to the findings of a large Danish study.

Aspirin, statins, and beta-blockers – cardioprotective medications that are given as the standard of care to most patients immediately following a myocardial infarction – were all less frequently prescribed to patients with rheumatoid arthritis (RA) than to members of the general patient population.

Indeed, 1 month after an MI, the odds ratios for the prescription of these drugs were 0.75 (95% confidence interval, 0.63-0.90) for aspirin, 0.68 (95% CI, 0.57-0.82) for a statin, and 0.76 (95% CI, 0.63-0.91) for beta-blockers. These results did not change greatly at follow-ups of 3 months, 6 months, or 1 year.

The increased risk of cardiovascular disease in RA patients is well known and could result from a number of causes, including the presence of classical risk factors such as dyslipidemia and hypertension, possible adverse effects of RA treatment, and an accelerated atherosclerotic process driven by the high levels of inflammation characteristic of the rheumatic disease.

"What’s not been considered, [however,] and perhaps the simplest explanation, is whether or not there is undertreatment of [RA] patients," Dr. Jesper Lindhardsen, of the cardiology department at Gentofte University Hospital, Copenhagen, said at a press briefing during the annual European Congress of Rheumatology.

To determine whether patients with RA were being given standard cardioprotective medications after a first MI, he and his colleagues analyzed data from several Danish patient registries, including those giving prescription records, details of comorbidities, and income.

The study population consisted of 66,389 patients who had had a first heart attack between 2002 and 2009. Of these, 875 (1.3%) had RA. The median age was 72.6 years for RA patients and 69.4 years for patients without RA.

At baseline, the use of cardioprotective medications by patients with and without RA were relatively similar or the same, at 27% and 25.1%, respectively, for aspirin; 19.1% and 19.1% for a statin; 23.9% and 22.5% for a beta-blocker; and 3.3% and 2.2% for clopidogrel.

Although aspirin, statin, and beta-blocker use was later found to be lower in the RA patients than in the non-RA patients throughout the early post-MI period, there was no significant difference in the prescription of clopidogrel at 1, 3, or 6 months or at 1 year.

Commenting on the findings in an interview, Dr. Lindhardsen conceded that this data raises more questions than it answers. For one thing, it’s not known what medications patients were taking before they had their heart attack, which could influence the findings.

Dr. Georg Schett, who is chief of rheumatology at the University of Erlangen-Nuremberg, Germany, but was not involved in the study, said the findings illustrate that the high cardiovascular risk in patients with RA is still not being taken seriously enough.

Speaking at a press conference, Dr. Schett said that "the risk of cardiovascular disease in RA is similar to diabetes, but people sometimes forget this."

Indeed, Dr. Lindhardsen and his colleagues recently published data showing that RA is associated with the same risk of MI as diabetes (Ann. Rheum. Dis. 2011;70:929-34).

With regard to this post-MI data, Dr. Lindhardsen stressed the importance of communication between the cardiologist discharging a patient and the rheumatologist responsible for the patient’s long-term care to ensure that standard cardioprotective medications are being used.

"We have quantitative data. Now we need more qualitative data," Dr. Lindhardsen observed in an interview. The next steps are to try to determine the reasons RA patients get fewer prescriptions for these standard post-MI drugs, he said.

Dr. Lindhardsen and Dr. Schett had no conflicts of interest to declare.

LONDON – The incidence of rheumatoid arthritis rises with age in both men and women and shows the biggest jump during the sixth decade of life, when the incidence among adults in their 50s nearly doubles compared with those in their 40s, based on findings from an analysis of about 10,000 Swedish patients diagnosed for the first time during 2006-2008.

The nationwide data also showed that peak rheumatoid arthritis (RA) incidence occurs among men and women in their 70s, with a new onset rate of at least 73 cases per 100,000 population annually, Jonas Eriksson said at the Annual European Congress of Rheumatology.

The nationwide Swedish data that allowed analysis of about 10,000 cases far exceeded the scope of previous incidence estimates, enabling Mr. Eriksson and his associates in the clinical epidemiology unit at the Karolinska Institute, Stockholm, to estimate incidence rates by age and sex. They used data collected by the Swedish Rheumatology Quality Register, the National Patient Register, and the Prescribed Drug Register.

To assess incident RA cases they used three different definitions of new-onset disease. The most restrictive definition involved patients who met all of five separate defining criteria: a first-ever inpatient visit, a specialist outpatient visit, or inclusion in the Swedish Rheumatology Quality Register with a RA diagnosis during 2006-2008; at least one visit to a rheumatology or internal medicine department; at least two visits with a diagnosis of RA during 2006-2008; a second visit with a RA diagnosis within 1 year after a first visit; and exclusion of patients treated with a disease-modifying antirheumatic drug more than 6 months before the first visit with a RA diagnosis, pain in joints, or an unspecified diagnosis.

Applying these criteria to the databases for 2006-2008 identified 7,953 patients with a presumed first-time diagnosis of RA, which resulted in a calculated incidence rate of 35 cases/100,000 population per year. Broken down by gender, the rates were 22 cases/100,000 in men and 48 cases/100,000 in women. Mr. Eriksson also reported incidence rates among men and women broken down by age. The peak new-onset rates occurred in people aged 70-79 years, with rates of 60 cases/100,000 per year among men and 86 cases/100,000 per year in women.

To further broaden the analysis, the researchers calculated incidence rates using two less stringent definitions. They applied a "medium" definition that eliminated the exclusion portion of their initial, strict definition. This identified 9,133 new-onset cases during the 3 years studied, with an overall incidence rate of 41 cases/100,000 per year and rates of 25 cases/100,000 per year in men and 55 cases/100,000 per year in women.

A third, "liberal" definition of RA limited the identifying criteria to the first two elements from the original list of five: a first-ever inpatient visit, a specialist outpatient visit, or inclusion in the Swedish Rheumatology Quality Register during 2006-2008; and at least one visit to a rheumatology or internal medicine department. This identified 11,715 new-onset cases in 2006-2008, an overall rate of 52/100,000 per year, with rates of 33/100,000 per year in men and 71/100,000 per year in women, Mr. Eriksson said.

The range of overall annual incidence rates they calculated – 35/100,000, 41/100,000, and 52/100,00 – collectively matched the annual incidence rates in previously reported studies of much smaller numbers of patients in Sweden, the United States, and Finland with newly diagnosed RA, he noted.

Mr. Eriksson said that he had no disclosures.

LONDON – The incidence of rheumatoid arthritis rises with age in both men and women and shows the biggest jump during the sixth decade of life, when the incidence among adults in their 50s nearly doubles compared with those in their 40s, based on findings from an analysis of about 10,000 Swedish patients diagnosed for the first time during 2006-2008.

The nationwide data also showed that peak rheumatoid arthritis (RA) incidence occurs among men and women in their 70s, with a new onset rate of at least 73 cases per 100,000 population annually, Jonas Eriksson said at the Annual European Congress of Rheumatology.

The nationwide Swedish data that allowed analysis of about 10,000 cases far exceeded the scope of previous incidence estimates, enabling Mr. Eriksson and his associates in the clinical epidemiology unit at the Karolinska Institute, Stockholm, to estimate incidence rates by age and sex. They used data collected by the Swedish Rheumatology Quality Register, the National Patient Register, and the Prescribed Drug Register.

To assess incident RA cases they used three different definitions of new-onset disease. The most restrictive definition involved patients who met all of five separate defining criteria: a first-ever inpatient visit, a specialist outpatient visit, or inclusion in the Swedish Rheumatology Quality Register with a RA diagnosis during 2006-2008; at least one visit to a rheumatology or internal medicine department; at least two visits with a diagnosis of RA during 2006-2008; a second visit with a RA diagnosis within 1 year after a first visit; and exclusion of patients treated with a disease-modifying antirheumatic drug more than 6 months before the first visit with a RA diagnosis, pain in joints, or an unspecified diagnosis.

Applying these criteria to the databases for 2006-2008 identified 7,953 patients with a presumed first-time diagnosis of RA, which resulted in a calculated incidence rate of 35 cases/100,000 population per year. Broken down by gender, the rates were 22 cases/100,000 in men and 48 cases/100,000 in women. Mr. Eriksson also reported incidence rates among men and women broken down by age. The peak new-onset rates occurred in people aged 70-79 years, with rates of 60 cases/100,000 per year among men and 86 cases/100,000 per year in women.

To further broaden the analysis, the researchers calculated incidence rates using two less stringent definitions. They applied a "medium" definition that eliminated the exclusion portion of their initial, strict definition. This identified 9,133 new-onset cases during the 3 years studied, with an overall incidence rate of 41 cases/100,000 per year and rates of 25 cases/100,000 per year in men and 55 cases/100,000 per year in women.

A third, "liberal" definition of RA limited the identifying criteria to the first two elements from the original list of five: a first-ever inpatient visit, a specialist outpatient visit, or inclusion in the Swedish Rheumatology Quality Register during 2006-2008; and at least one visit to a rheumatology or internal medicine department. This identified 11,715 new-onset cases in 2006-2008, an overall rate of 52/100,000 per year, with rates of 33/100,000 per year in men and 71/100,000 per year in women, Mr. Eriksson said.

The range of overall annual incidence rates they calculated – 35/100,000, 41/100,000, and 52/100,00 – collectively matched the annual incidence rates in previously reported studies of much smaller numbers of patients in Sweden, the United States, and Finland with newly diagnosed RA, he noted.

Mr. Eriksson said that he had no disclosures.

LONDON – The incidence of rheumatoid arthritis rises with age in both men and women and shows the biggest jump during the sixth decade of life, when the incidence among adults in their 50s nearly doubles compared with those in their 40s, based on findings from an analysis of about 10,000 Swedish patients diagnosed for the first time during 2006-2008.

The nationwide data also showed that peak rheumatoid arthritis (RA) incidence occurs among men and women in their 70s, with a new onset rate of at least 73 cases per 100,000 population annually, Jonas Eriksson said at the Annual European Congress of Rheumatology.

The nationwide Swedish data that allowed analysis of about 10,000 cases far exceeded the scope of previous incidence estimates, enabling Mr. Eriksson and his associates in the clinical epidemiology unit at the Karolinska Institute, Stockholm, to estimate incidence rates by age and sex. They used data collected by the Swedish Rheumatology Quality Register, the National Patient Register, and the Prescribed Drug Register.

To assess incident RA cases they used three different definitions of new-onset disease. The most restrictive definition involved patients who met all of five separate defining criteria: a first-ever inpatient visit, a specialist outpatient visit, or inclusion in the Swedish Rheumatology Quality Register with a RA diagnosis during 2006-2008; at least one visit to a rheumatology or internal medicine department; at least two visits with a diagnosis of RA during 2006-2008; a second visit with a RA diagnosis within 1 year after a first visit; and exclusion of patients treated with a disease-modifying antirheumatic drug more than 6 months before the first visit with a RA diagnosis, pain in joints, or an unspecified diagnosis.

Applying these criteria to the databases for 2006-2008 identified 7,953 patients with a presumed first-time diagnosis of RA, which resulted in a calculated incidence rate of 35 cases/100,000 population per year. Broken down by gender, the rates were 22 cases/100,000 in men and 48 cases/100,000 in women. Mr. Eriksson also reported incidence rates among men and women broken down by age. The peak new-onset rates occurred in people aged 70-79 years, with rates of 60 cases/100,000 per year among men and 86 cases/100,000 per year in women.

To further broaden the analysis, the researchers calculated incidence rates using two less stringent definitions. They applied a "medium" definition that eliminated the exclusion portion of their initial, strict definition. This identified 9,133 new-onset cases during the 3 years studied, with an overall incidence rate of 41 cases/100,000 per year and rates of 25 cases/100,000 per year in men and 55 cases/100,000 per year in women.

A third, "liberal" definition of RA limited the identifying criteria to the first two elements from the original list of five: a first-ever inpatient visit, a specialist outpatient visit, or inclusion in the Swedish Rheumatology Quality Register during 2006-2008; and at least one visit to a rheumatology or internal medicine department. This identified 11,715 new-onset cases in 2006-2008, an overall rate of 52/100,000 per year, with rates of 33/100,000 per year in men and 71/100,000 per year in women, Mr. Eriksson said.

The range of overall annual incidence rates they calculated – 35/100,000, 41/100,000, and 52/100,00 – collectively matched the annual incidence rates in previously reported studies of much smaller numbers of patients in Sweden, the United States, and Finland with newly diagnosed RA, he noted.

Mr. Eriksson said that he had no disclosures.

LONDON – Many recently performed rheumatology drug trials ran into the ethical trap of treating control patients with an ineffective regimen, with the result that some patients experienced ongoing pain and joint dysfunction and continued disease progression.

"I would propose that we change the trial design for the placebo control to use an active comparator against the [investigational] drug," Dr. Aaron Juche said while presenting a poster at the annual European Congress of Rheumatology.

In most cases for current studies testing a new drug aimed at controlling rheumatoid arthritis pain, dysfunction, and progression, "the standard of care would be a tumor necrosis factor [TNF] inhibitor as the active comparator," said Dr. Juche, a rheumatologist at Johanniter Hospital in Treuenbrietzen, Germany. Because TNF inhibitors are so effective, a study that uses this treatment in the comparator arm would likely have to be a noninferiority study and would also probably have to involve a relatively large number of patients, he said in an interview.

Dr. Juche said he first became interested in this issue because he "wondered whether placebo-treated patients [in recent drug trials] were being treated as I would treat a patient in standard practice." The standard approach for drug-trial design in patients with rheumatoid arthritis (RA) in recent years has been to follow a model that’s more than a decade old, dating back to the first studies on TNF inhibitors during the 1990s: "Patients who did not adequately respond to immunosuppressive drugs were randomly assigned to either an experimental condition under which they received the new substance, or to a control condition under which they continued their formerly inefficient treatment and received a placebo."

To more systematically assess the scope of the problem, he and his associate reviewed 17 recent, published clinical trials that drug companies used to document the safety and efficacy of three new drugs, abatacept, golimumab, and tocilizumab, to the European Medicines Agency. Dr. Juche said these studies fairly represented most recently performed drug efficacy trials for patients with RA.

Of the seven studies he reviewed that tested abatacept, none used a control therapy that effectively treated the patients’ disease. In all seven studies, patients remained on treatment with a disease-modifying antirheumatic drug (DMARD) that they had already failed on, most commonly methotrexate. During these studies, "patients experienced a persistent, high disease activity," Dr. Juche reported in his poster.

Among four pivotal studies involving golimumab, one enrolled methotrexate-naive patients and then used methotrexate as the control drug. The other three used control groups that either received placebo and nothing else, or placebo plus methotrexate for enrolled patients who had already failed methotrexate.

A similar pattern existed for the six studies of tocilizumab that Dr. Juche reviewed. One of the six studies used methotrexate as the comparator in a trial that enrolled methotrexate-naive patients. The other five studies used comparator groups on either placebo alone or placebo plus a DMARD to which the patient had already not responded.

Dr. Juche added that he did not believe that rheumatology was a unique medical specialty in having so many of its trials involve ineffective regimens in the control groups, but he did not systematically assess efficacy trials done in other specialties. As a rheumatologist, he focused his attention only on those studies from his specialty.

These designs run counter to the stipulations of the 2008 Declaration of Helsinki of the World Medical Association, Dr. Juche noted. The Declaration said: "The benefits, risks, burdens, and effectiveness of a new intervention must be tested against those of the best current proven intervention, except ... where no current proven intervention exists or where, for compelling and scientifically sound methodological reasons, the use of placebo is necessary to determine the efficacy of an intervention and the patients who receive placebo or no treatment will not be subject to any risk or serious or irreversible harm."

Dr. Juche said that he has received travel expense support from Actelion.

LONDON – Many recently performed rheumatology drug trials ran into the ethical trap of treating control patients with an ineffective regimen, with the result that some patients experienced ongoing pain and joint dysfunction and continued disease progression.

"I would propose that we change the trial design for the placebo control to use an active comparator against the [investigational] drug," Dr. Aaron Juche said while presenting a poster at the annual European Congress of Rheumatology.

In most cases for current studies testing a new drug aimed at controlling rheumatoid arthritis pain, dysfunction, and progression, "the standard of care would be a tumor necrosis factor [TNF] inhibitor as the active comparator," said Dr. Juche, a rheumatologist at Johanniter Hospital in Treuenbrietzen, Germany. Because TNF inhibitors are so effective, a study that uses this treatment in the comparator arm would likely have to be a noninferiority study and would also probably have to involve a relatively large number of patients, he said in an interview.

Dr. Juche said he first became interested in this issue because he "wondered whether placebo-treated patients [in recent drug trials] were being treated as I would treat a patient in standard practice." The standard approach for drug-trial design in patients with rheumatoid arthritis (RA) in recent years has been to follow a model that’s more than a decade old, dating back to the first studies on TNF inhibitors during the 1990s: "Patients who did not adequately respond to immunosuppressive drugs were randomly assigned to either an experimental condition under which they received the new substance, or to a control condition under which they continued their formerly inefficient treatment and received a placebo."

To more systematically assess the scope of the problem, he and his associate reviewed 17 recent, published clinical trials that drug companies used to document the safety and efficacy of three new drugs, abatacept, golimumab, and tocilizumab, to the European Medicines Agency. Dr. Juche said these studies fairly represented most recently performed drug efficacy trials for patients with RA.

Of the seven studies he reviewed that tested abatacept, none used a control therapy that effectively treated the patients’ disease. In all seven studies, patients remained on treatment with a disease-modifying antirheumatic drug (DMARD) that they had already failed on, most commonly methotrexate. During these studies, "patients experienced a persistent, high disease activity," Dr. Juche reported in his poster.

Among four pivotal studies involving golimumab, one enrolled methotrexate-naive patients and then used methotrexate as the control drug. The other three used control groups that either received placebo and nothing else, or placebo plus methotrexate for enrolled patients who had already failed methotrexate.

A similar pattern existed for the six studies of tocilizumab that Dr. Juche reviewed. One of the six studies used methotrexate as the comparator in a trial that enrolled methotrexate-naive patients. The other five studies used comparator groups on either placebo alone or placebo plus a DMARD to which the patient had already not responded.

Dr. Juche added that he did not believe that rheumatology was a unique medical specialty in having so many of its trials involve ineffective regimens in the control groups, but he did not systematically assess efficacy trials done in other specialties. As a rheumatologist, he focused his attention only on those studies from his specialty.

These designs run counter to the stipulations of the 2008 Declaration of Helsinki of the World Medical Association, Dr. Juche noted. The Declaration said: "The benefits, risks, burdens, and effectiveness of a new intervention must be tested against those of the best current proven intervention, except ... where no current proven intervention exists or where, for compelling and scientifically sound methodological reasons, the use of placebo is necessary to determine the efficacy of an intervention and the patients who receive placebo or no treatment will not be subject to any risk or serious or irreversible harm."

Dr. Juche said that he has received travel expense support from Actelion.

LONDON – Many recently performed rheumatology drug trials ran into the ethical trap of treating control patients with an ineffective regimen, with the result that some patients experienced ongoing pain and joint dysfunction and continued disease progression.

"I would propose that we change the trial design for the placebo control to use an active comparator against the [investigational] drug," Dr. Aaron Juche said while presenting a poster at the annual European Congress of Rheumatology.

In most cases for current studies testing a new drug aimed at controlling rheumatoid arthritis pain, dysfunction, and progression, "the standard of care would be a tumor necrosis factor [TNF] inhibitor as the active comparator," said Dr. Juche, a rheumatologist at Johanniter Hospital in Treuenbrietzen, Germany. Because TNF inhibitors are so effective, a study that uses this treatment in the comparator arm would likely have to be a noninferiority study and would also probably have to involve a relatively large number of patients, he said in an interview.

Dr. Juche said he first became interested in this issue because he "wondered whether placebo-treated patients [in recent drug trials] were being treated as I would treat a patient in standard practice." The standard approach for drug-trial design in patients with rheumatoid arthritis (RA) in recent years has been to follow a model that’s more than a decade old, dating back to the first studies on TNF inhibitors during the 1990s: "Patients who did not adequately respond to immunosuppressive drugs were randomly assigned to either an experimental condition under which they received the new substance, or to a control condition under which they continued their formerly inefficient treatment and received a placebo."

To more systematically assess the scope of the problem, he and his associate reviewed 17 recent, published clinical trials that drug companies used to document the safety and efficacy of three new drugs, abatacept, golimumab, and tocilizumab, to the European Medicines Agency. Dr. Juche said these studies fairly represented most recently performed drug efficacy trials for patients with RA.

Of the seven studies he reviewed that tested abatacept, none used a control therapy that effectively treated the patients’ disease. In all seven studies, patients remained on treatment with a disease-modifying antirheumatic drug (DMARD) that they had already failed on, most commonly methotrexate. During these studies, "patients experienced a persistent, high disease activity," Dr. Juche reported in his poster.

Among four pivotal studies involving golimumab, one enrolled methotrexate-naive patients and then used methotrexate as the control drug. The other three used control groups that either received placebo and nothing else, or placebo plus methotrexate for enrolled patients who had already failed methotrexate.

A similar pattern existed for the six studies of tocilizumab that Dr. Juche reviewed. One of the six studies used methotrexate as the comparator in a trial that enrolled methotrexate-naive patients. The other five studies used comparator groups on either placebo alone or placebo plus a DMARD to which the patient had already not responded.

Dr. Juche added that he did not believe that rheumatology was a unique medical specialty in having so many of its trials involve ineffective regimens in the control groups, but he did not systematically assess efficacy trials done in other specialties. As a rheumatologist, he focused his attention only on those studies from his specialty.

These designs run counter to the stipulations of the 2008 Declaration of Helsinki of the World Medical Association, Dr. Juche noted. The Declaration said: "The benefits, risks, burdens, and effectiveness of a new intervention must be tested against those of the best current proven intervention, except ... where no current proven intervention exists or where, for compelling and scientifically sound methodological reasons, the use of placebo is necessary to determine the efficacy of an intervention and the patients who receive placebo or no treatment will not be subject to any risk or serious or irreversible harm."

Dr. Juche said that he has received travel expense support from Actelion.

LONDON – Many recently performed rheumatology drug trials ran into the ethical trap of treating control patients with an ineffective regimen, with the result that some patients experienced ongoing pain and joint dysfunction and continued disease progression.

"I would propose that we change the trial design for the placebo control to use an active comparator against the [investigational] drug," Dr. Aaron Juche said while presenting a poster at the annual European Congress of Rheumatology.

In most cases for current studies testing a new drug aimed at controlling rheumatoid arthritis pain, dysfunction, and progression, "the standard of care would be a tumor necrosis factor [TNF] inhibitor as the active comparator," said Dr. Juche, a rheumatologist at Johanniter Hospital in Treuenbrietzen, Germany. Because TNF inhibitors are so effective, a study that uses this treatment in the comparator arm would likely have to be a noninferiority study and would also probably have to involve a relatively large number of patients, he said in an interview.

Dr. Juche said he first became interested in this issue because he "wondered whether placebo-treated patients [in recent drug trials] were being treated as I would treat a patient in standard practice." The standard approach for drug-trial design in patients with rheumatoid arthritis (RA) in recent years has been to follow a model that’s more than a decade old, dating back to the first studies on TNF inhibitors during the 1990s: "Patients who did not adequately respond to immunosuppressive drugs were randomly assigned to either an experimental condition under which they received the new substance, or to a control condition under which they continued their formerly inefficient treatment and received a placebo."

To more systematically assess the scope of the problem, he and his associate reviewed 17 recent, published clinical trials that drug companies used to document the safety and efficacy of three new drugs, abatacept, golimumab, and tocilizumab, to the European Medicines Agency. Dr. Juche said these studies fairly represented most recently performed drug efficacy trials for patients with RA.

Of the seven studies he reviewed that tested abatacept, none used a control therapy that effectively treated the patients’ disease. In all seven studies, patients remained on treatment with a disease-modifying antirheumatic drug (DMARD) that they had already failed on, most commonly methotrexate. During these studies, "patients experienced a persistent, high disease activity," Dr. Juche reported in his poster.

Among four pivotal studies involving golimumab, one enrolled methotrexate-naive patients and then used methotrexate as the control drug. The other three used control groups that either received placebo and nothing else, or placebo plus methotrexate for enrolled patients who had already failed methotrexate.

A similar pattern existed for the six studies of tocilizumab that Dr. Juche reviewed. One of the six studies used methotrexate as the comparator in a trial that enrolled methotrexate-naive patients. The other five studies used comparator groups on either placebo alone or placebo plus a DMARD to which the patient had already not responded.

Dr. Juche added that he did not believe that rheumatology was a unique medical specialty in having so many of its trials involve ineffective regimens in the control groups, but he did not systematically assess efficacy trials done in other specialties. As a rheumatologist, he focused his attention only on those studies from his specialty.

These designs run counter to the stipulations of the 2008 Declaration of Helsinki of the World Medical Association, Dr. Juche noted. The Declaration said: "The benefits, risks, burdens, and effectiveness of a new intervention must be tested against those of the best current proven intervention, except ... where no current proven intervention exists or where, for compelling and scientifically sound methodological reasons, the use of placebo is necessary to determine the efficacy of an intervention and the patients who receive placebo or no treatment will not be subject to any risk or serious or irreversible harm."

Dr. Juche said that he has received travel expense support from Actelion.

LONDON – Many recently performed rheumatology drug trials ran into the ethical trap of treating control patients with an ineffective regimen, with the result that some patients experienced ongoing pain and joint dysfunction and continued disease progression.

"I would propose that we change the trial design for the placebo control to use an active comparator against the [investigational] drug," Dr. Aaron Juche said while presenting a poster at the annual European Congress of Rheumatology.

In most cases for current studies testing a new drug aimed at controlling rheumatoid arthritis pain, dysfunction, and progression, "the standard of care would be a tumor necrosis factor [TNF] inhibitor as the active comparator," said Dr. Juche, a rheumatologist at Johanniter Hospital in Treuenbrietzen, Germany. Because TNF inhibitors are so effective, a study that uses this treatment in the comparator arm would likely have to be a noninferiority study and would also probably have to involve a relatively large number of patients, he said in an interview.

Dr. Juche said he first became interested in this issue because he "wondered whether placebo-treated patients [in recent drug trials] were being treated as I would treat a patient in standard practice." The standard approach for drug-trial design in patients with rheumatoid arthritis (RA) in recent years has been to follow a model that’s more than a decade old, dating back to the first studies on TNF inhibitors during the 1990s: "Patients who did not adequately respond to immunosuppressive drugs were randomly assigned to either an experimental condition under which they received the new substance, or to a control condition under which they continued their formerly inefficient treatment and received a placebo."

To more systematically assess the scope of the problem, he and his associate reviewed 17 recent, published clinical trials that drug companies used to document the safety and efficacy of three new drugs, abatacept, golimumab, and tocilizumab, to the European Medicines Agency. Dr. Juche said these studies fairly represented most recently performed drug efficacy trials for patients with RA.

Of the seven studies he reviewed that tested abatacept, none used a control therapy that effectively treated the patients’ disease. In all seven studies, patients remained on treatment with a disease-modifying antirheumatic drug (DMARD) that they had already failed on, most commonly methotrexate. During these studies, "patients experienced a persistent, high disease activity," Dr. Juche reported in his poster.

Among four pivotal studies involving golimumab, one enrolled methotrexate-naive patients and then used methotrexate as the control drug. The other three used control groups that either received placebo and nothing else, or placebo plus methotrexate for enrolled patients who had already failed methotrexate.

A similar pattern existed for the six studies of tocilizumab that Dr. Juche reviewed. One of the six studies used methotrexate as the comparator in a trial that enrolled methotrexate-naive patients. The other five studies used comparator groups on either placebo alone or placebo plus a DMARD to which the patient had already not responded.

Dr. Juche added that he did not believe that rheumatology was a unique medical specialty in having so many of its trials involve ineffective regimens in the control groups, but he did not systematically assess efficacy trials done in other specialties. As a rheumatologist, he focused his attention only on those studies from his specialty.

These designs run counter to the stipulations of the 2008 Declaration of Helsinki of the World Medical Association, Dr. Juche noted. The Declaration said: "The benefits, risks, burdens, and effectiveness of a new intervention must be tested against those of the best current proven intervention, except ... where no current proven intervention exists or where, for compelling and scientifically sound methodological reasons, the use of placebo is necessary to determine the efficacy of an intervention and the patients who receive placebo or no treatment will not be subject to any risk or serious or irreversible harm."

Dr. Juche said that he has received travel expense support from Actelion.

LONDON – Many recently performed rheumatology drug trials ran into the ethical trap of treating control patients with an ineffective regimen, with the result that some patients experienced ongoing pain and joint dysfunction and continued disease progression.

"I would propose that we change the trial design for the placebo control to use an active comparator against the [investigational] drug," Dr. Aaron Juche said while presenting a poster at the annual European Congress of Rheumatology.

In most cases for current studies testing a new drug aimed at controlling rheumatoid arthritis pain, dysfunction, and progression, "the standard of care would be a tumor necrosis factor [TNF] inhibitor as the active comparator," said Dr. Juche, a rheumatologist at Johanniter Hospital in Treuenbrietzen, Germany. Because TNF inhibitors are so effective, a study that uses this treatment in the comparator arm would likely have to be a noninferiority study and would also probably have to involve a relatively large number of patients, he said in an interview.

Dr. Juche said he first became interested in this issue because he "wondered whether placebo-treated patients [in recent drug trials] were being treated as I would treat a patient in standard practice." The standard approach for drug-trial design in patients with rheumatoid arthritis (RA) in recent years has been to follow a model that’s more than a decade old, dating back to the first studies on TNF inhibitors during the 1990s: "Patients who did not adequately respond to immunosuppressive drugs were randomly assigned to either an experimental condition under which they received the new substance, or to a control condition under which they continued their formerly inefficient treatment and received a placebo."

To more systematically assess the scope of the problem, he and his associate reviewed 17 recent, published clinical trials that drug companies used to document the safety and efficacy of three new drugs, abatacept, golimumab, and tocilizumab, to the European Medicines Agency. Dr. Juche said these studies fairly represented most recently performed drug efficacy trials for patients with RA.

Of the seven studies he reviewed that tested abatacept, none used a control therapy that effectively treated the patients’ disease. In all seven studies, patients remained on treatment with a disease-modifying antirheumatic drug (DMARD) that they had already failed on, most commonly methotrexate. During these studies, "patients experienced a persistent, high disease activity," Dr. Juche reported in his poster.

Among four pivotal studies involving golimumab, one enrolled methotrexate-naive patients and then used methotrexate as the control drug. The other three used control groups that either received placebo and nothing else, or placebo plus methotrexate for enrolled patients who had already failed methotrexate.

A similar pattern existed for the six studies of tocilizumab that Dr. Juche reviewed. One of the six studies used methotrexate as the comparator in a trial that enrolled methotrexate-naive patients. The other five studies used comparator groups on either placebo alone or placebo plus a DMARD to which the patient had already not responded.

Dr. Juche added that he did not believe that rheumatology was a unique medical specialty in having so many of its trials involve ineffective regimens in the control groups, but he did not systematically assess efficacy trials done in other specialties. As a rheumatologist, he focused his attention only on those studies from his specialty.

These designs run counter to the stipulations of the 2008 Declaration of Helsinki of the World Medical Association, Dr. Juche noted. The Declaration said: "The benefits, risks, burdens, and effectiveness of a new intervention must be tested against those of the best current proven intervention, except ... where no current proven intervention exists or where, for compelling and scientifically sound methodological reasons, the use of placebo is necessary to determine the efficacy of an intervention and the patients who receive placebo or no treatment will not be subject to any risk or serious or irreversible harm."

Dr. Juche said that he has received travel expense support from Actelion.