Susan London

VICTORIA, B.C. – Physician and patient assessments of disease activity in rheumatoid arthritis show considerable disagreement that seems to be driven by subjective perceptions of pain, a study has shown.

The study involved nearly 900 patients with early rheumatoid arthritis (RA) and 100 patients with established RA in remission, all of whom had been treated only with disease-modifying antirheumatic drugs (DMARDs). Findings on physician and patient assessments of disease activity disagreed to a clinically meaningful extent roughly one-fourth to one-third of the time, based on the results of this as-yet unpublished study, reported at the annual meeting of the Canadian Rheumatology Association.

In most cases of discordance, patients rated their RA as being worse than their physicians did. Findings from additional analyses suggested that the discrepancy was largely due to subjective pain, and pain levels showed some association with cumulative RA-related joint damage.

"For a rheumatologist who is using these global assessment scores" – the patient global assessment (PtGA) and the physician global assessment (MDGA) – "75% of the time, you can expect the patient to agree with you on their disease activity level. They are going to report a pretty similar score. But for the other 25% of the time, the patient’s going to say, ‘My disease is worse than what you think it is,’ " explained presenting author May Choi, a second-year medical student at the University of Alberta, Edmonton.

"We think it’s more a reflection of their subjective pain, and that pain is probably not in their joints – it probably has something to do with soft tissue pain, like fibromyalgia," she added. In patients with established disease, the pain appears to reflect "all of the joint damage they have accumulated over the years because of the RA. So it’s not a reflection of their current disease activity, but the damage that has resulted."

Physicians who find a discrepancy between assessments for a given patient should take a closer look to determine the reason, especially as it has implications for treatment, Ms. Choi advised in an interview. "If a patient is in a lot of pain, but a physician is feeling their joints and they don’t really see [an explanation for] what’s going on, they are not going to give them a drug for their joints. They are going to look at other reasons and treat them for that – pain that’s related to their soft tissues," she explained.

The study’s findings also suggest that the two assessments are complementary, and both should be used, she maintained. "I don’t think one is more important than the other. They provide different information" and in clinical studies, "absolutely, they should get both numbers to get the big picture."

Previous research has found a difference between physician and patient global assessments of RA disease activity, but the reason remains unknown, according to Ms. Choi. "This is an important question because physicians use this tool to monitor their patients, and we think it’s important to increase awareness that there is a difference. We wanted to look at reasons why this difference exists and what are its implications for patient management," she said.

For the study, which was supported by the Canadian Rheumatology Association–Roche Summer Studentship, the researchers identified 897 patients with early RA (mean disease duration, 0.5 years) from the Canadian Early Arthritis Cohort database and 100 patients with established RA in remission from one practice (mean disease duration, 18 years).

Scores were compared from the patient-completed PtGA and physician-completed MDGA. Discrepancy between results on the two 100-mm scales was assessed by subtracting the latter from the former and was classified as clinically meaningful if it was at least 30 mm.

Study results, reported in a poster session, revealed that in the early RA group, the PtGA and MDGA scores showed no discrepancy in 64% of patients. But in 24%, patients reported worse disease than their physicians did, and in 12%, physicians reported worse disease than patients did.

Compared with their counterparts having no discrepancy, patients over-reporting disease activity had lower swollen and tender joint counts and similar C-reactive protein levels. Yet they also reported more pain. "So here is a group of patients who are reporting a lot of pain, but it’s not in their joints necessarily," commented Ms. Choi. On the other hand, compared with their counterparts having no discrepancy, patients underreporting disease activity had higher swollen joint counts and C-reactive protein levels, and yet less pain. This finding may be related to differing pain thresholds across individuals, she noted, saying, "There are some patients like that. They are just not as sensitive."

In the established RA group, the PtGA and MDGA scores showed no discrepancy in 75% of patients. But in 24%, patients reported worse disease than their physicians did, and in 1%, physicians reported worse disease than patients did.

Compared with their counterparts having no discrepancy, patients over-reporting or under-reporting disease activity were younger; had a higher damaged joint count, erythrocyte sedimentation rate, and C-reactive protein level; and reported more pain.

"So in both groups, pain is a common theme," Ms. Choi pointed out. And indeed, additional analysis showed that reported pain scores were positively correlated with the magnitude of the PtGA-MDGA discrepancy (r = 0.84). Also, among the patients with established disease, pain scores were positively correlated with the number of damaged joints (rS = 0.37).

Ms. Choi said she had no relevant financial disclosures.

VICTORIA, B.C. – Physician and patient assessments of disease activity in rheumatoid arthritis show considerable disagreement that seems to be driven by subjective perceptions of pain, a study has shown.

The study involved nearly 900 patients with early rheumatoid arthritis (RA) and 100 patients with established RA in remission, all of whom had been treated only with disease-modifying antirheumatic drugs (DMARDs). Findings on physician and patient assessments of disease activity disagreed to a clinically meaningful extent roughly one-fourth to one-third of the time, based on the results of this as-yet unpublished study, reported at the annual meeting of the Canadian Rheumatology Association.

In most cases of discordance, patients rated their RA as being worse than their physicians did. Findings from additional analyses suggested that the discrepancy was largely due to subjective pain, and pain levels showed some association with cumulative RA-related joint damage.

"For a rheumatologist who is using these global assessment scores" – the patient global assessment (PtGA) and the physician global assessment (MDGA) – "75% of the time, you can expect the patient to agree with you on their disease activity level. They are going to report a pretty similar score. But for the other 25% of the time, the patient’s going to say, ‘My disease is worse than what you think it is,’ " explained presenting author May Choi, a second-year medical student at the University of Alberta, Edmonton.

"We think it’s more a reflection of their subjective pain, and that pain is probably not in their joints – it probably has something to do with soft tissue pain, like fibromyalgia," she added. In patients with established disease, the pain appears to reflect "all of the joint damage they have accumulated over the years because of the RA. So it’s not a reflection of their current disease activity, but the damage that has resulted."

Physicians who find a discrepancy between assessments for a given patient should take a closer look to determine the reason, especially as it has implications for treatment, Ms. Choi advised in an interview. "If a patient is in a lot of pain, but a physician is feeling their joints and they don’t really see [an explanation for] what’s going on, they are not going to give them a drug for their joints. They are going to look at other reasons and treat them for that – pain that’s related to their soft tissues," she explained.

The study’s findings also suggest that the two assessments are complementary, and both should be used, she maintained. "I don’t think one is more important than the other. They provide different information" and in clinical studies, "absolutely, they should get both numbers to get the big picture."

Previous research has found a difference between physician and patient global assessments of RA disease activity, but the reason remains unknown, according to Ms. Choi. "This is an important question because physicians use this tool to monitor their patients, and we think it’s important to increase awareness that there is a difference. We wanted to look at reasons why this difference exists and what are its implications for patient management," she said.

For the study, which was supported by the Canadian Rheumatology Association–Roche Summer Studentship, the researchers identified 897 patients with early RA (mean disease duration, 0.5 years) from the Canadian Early Arthritis Cohort database and 100 patients with established RA in remission from one practice (mean disease duration, 18 years).

Scores were compared from the patient-completed PtGA and physician-completed MDGA. Discrepancy between results on the two 100-mm scales was assessed by subtracting the latter from the former and was classified as clinically meaningful if it was at least 30 mm.

Study results, reported in a poster session, revealed that in the early RA group, the PtGA and MDGA scores showed no discrepancy in 64% of patients. But in 24%, patients reported worse disease than their physicians did, and in 12%, physicians reported worse disease than patients did.

Compared with their counterparts having no discrepancy, patients over-reporting disease activity had lower swollen and tender joint counts and similar C-reactive protein levels. Yet they also reported more pain. "So here is a group of patients who are reporting a lot of pain, but it’s not in their joints necessarily," commented Ms. Choi. On the other hand, compared with their counterparts having no discrepancy, patients underreporting disease activity had higher swollen joint counts and C-reactive protein levels, and yet less pain. This finding may be related to differing pain thresholds across individuals, she noted, saying, "There are some patients like that. They are just not as sensitive."

In the established RA group, the PtGA and MDGA scores showed no discrepancy in 75% of patients. But in 24%, patients reported worse disease than their physicians did, and in 1%, physicians reported worse disease than patients did.

Compared with their counterparts having no discrepancy, patients over-reporting or under-reporting disease activity were younger; had a higher damaged joint count, erythrocyte sedimentation rate, and C-reactive protein level; and reported more pain.

"So in both groups, pain is a common theme," Ms. Choi pointed out. And indeed, additional analysis showed that reported pain scores were positively correlated with the magnitude of the PtGA-MDGA discrepancy (r = 0.84). Also, among the patients with established disease, pain scores were positively correlated with the number of damaged joints (rS = 0.37).

Ms. Choi said she had no relevant financial disclosures.

VICTORIA, B.C. – Physician and patient assessments of disease activity in rheumatoid arthritis show considerable disagreement that seems to be driven by subjective perceptions of pain, a study has shown.

The study involved nearly 900 patients with early rheumatoid arthritis (RA) and 100 patients with established RA in remission, all of whom had been treated only with disease-modifying antirheumatic drugs (DMARDs). Findings on physician and patient assessments of disease activity disagreed to a clinically meaningful extent roughly one-fourth to one-third of the time, based on the results of this as-yet unpublished study, reported at the annual meeting of the Canadian Rheumatology Association.

In most cases of discordance, patients rated their RA as being worse than their physicians did. Findings from additional analyses suggested that the discrepancy was largely due to subjective pain, and pain levels showed some association with cumulative RA-related joint damage.

"For a rheumatologist who is using these global assessment scores" – the patient global assessment (PtGA) and the physician global assessment (MDGA) – "75% of the time, you can expect the patient to agree with you on their disease activity level. They are going to report a pretty similar score. But for the other 25% of the time, the patient’s going to say, ‘My disease is worse than what you think it is,’ " explained presenting author May Choi, a second-year medical student at the University of Alberta, Edmonton.

"We think it’s more a reflection of their subjective pain, and that pain is probably not in their joints – it probably has something to do with soft tissue pain, like fibromyalgia," she added. In patients with established disease, the pain appears to reflect "all of the joint damage they have accumulated over the years because of the RA. So it’s not a reflection of their current disease activity, but the damage that has resulted."

Physicians who find a discrepancy between assessments for a given patient should take a closer look to determine the reason, especially as it has implications for treatment, Ms. Choi advised in an interview. "If a patient is in a lot of pain, but a physician is feeling their joints and they don’t really see [an explanation for] what’s going on, they are not going to give them a drug for their joints. They are going to look at other reasons and treat them for that – pain that’s related to their soft tissues," she explained.

The study’s findings also suggest that the two assessments are complementary, and both should be used, she maintained. "I don’t think one is more important than the other. They provide different information" and in clinical studies, "absolutely, they should get both numbers to get the big picture."

Previous research has found a difference between physician and patient global assessments of RA disease activity, but the reason remains unknown, according to Ms. Choi. "This is an important question because physicians use this tool to monitor their patients, and we think it’s important to increase awareness that there is a difference. We wanted to look at reasons why this difference exists and what are its implications for patient management," she said.

For the study, which was supported by the Canadian Rheumatology Association–Roche Summer Studentship, the researchers identified 897 patients with early RA (mean disease duration, 0.5 years) from the Canadian Early Arthritis Cohort database and 100 patients with established RA in remission from one practice (mean disease duration, 18 years).

Scores were compared from the patient-completed PtGA and physician-completed MDGA. Discrepancy between results on the two 100-mm scales was assessed by subtracting the latter from the former and was classified as clinically meaningful if it was at least 30 mm.

Study results, reported in a poster session, revealed that in the early RA group, the PtGA and MDGA scores showed no discrepancy in 64% of patients. But in 24%, patients reported worse disease than their physicians did, and in 12%, physicians reported worse disease than patients did.

Compared with their counterparts having no discrepancy, patients over-reporting disease activity had lower swollen and tender joint counts and similar C-reactive protein levels. Yet they also reported more pain. "So here is a group of patients who are reporting a lot of pain, but it’s not in their joints necessarily," commented Ms. Choi. On the other hand, compared with their counterparts having no discrepancy, patients underreporting disease activity had higher swollen joint counts and C-reactive protein levels, and yet less pain. This finding may be related to differing pain thresholds across individuals, she noted, saying, "There are some patients like that. They are just not as sensitive."

In the established RA group, the PtGA and MDGA scores showed no discrepancy in 75% of patients. But in 24%, patients reported worse disease than their physicians did, and in 1%, physicians reported worse disease than patients did.

Compared with their counterparts having no discrepancy, patients over-reporting or under-reporting disease activity were younger; had a higher damaged joint count, erythrocyte sedimentation rate, and C-reactive protein level; and reported more pain.

"So in both groups, pain is a common theme," Ms. Choi pointed out. And indeed, additional analysis showed that reported pain scores were positively correlated with the magnitude of the PtGA-MDGA discrepancy (r = 0.84). Also, among the patients with established disease, pain scores were positively correlated with the number of damaged joints (rS = 0.37).

Ms. Choi said she had no relevant financial disclosures.

VICTORIA, B.C. – Autoantibodies directed against homocitrullinated fibrinogen may help identify patients with rheumatoid arthritis who would currently be missed, a study has shown.

A team led by Dr. Lillian Barra and Dr. Ewa Cairns of the University of Western Ontario, London, tested 84 patients with rheumatoid arthritis (RA) and found that nearly half had antihomocitrullinated fibrinogen antibodies (AHFAs) in their serum.

Perhaps most importantly, these antibodies were present in almost a fifth of patients who did not have anticitrullinated fibrinogen antibodies (ACFAs) and would thus have otherwise been considered to be seronegative.

The results also indicated that AHFAs were specific for RA: They were seldom found in 37 patients with systemic lupus erythematosus and 37 patients with psoriatic arthritis. And they were not found at all in any of 27 healthy volunteers.

These findings add to similar results seen in a cohort of patients from Leiden, the Netherlands (Proc. Natl. Acad. Sci. USA 2011;108:17372-7), noted Dr. Barra, who presented the findings at the annual meeting of the Canadian Rheumatology Association "This is an exploratory study, and we are going to do a lot of future work looking at these antibodies in a larger cohort, hopefully the CATCH [Canadian Arthritis Cohort]," she said.

The large collective group of anticitrullinated protein antibodies (ACPAs) target citrullinated proteins, such as the collagen, fibrinogen, and vimentin found in joint synovial fluid. "They are highly specific for rheumatoid arthritis and have been included in the new [American College of Rheumatology]-EULAR criteria" for diagnosing early disease, Dr. Barra pointed out.

ACPAs associate with the shared epitope, the strongest genetic risk factor for RA, and have been found to be pathogenic in mice, she further noted. "However, nearly 50% of patients with early rheumatoid arthritis do not have ACPAs, which begs the question of whether these patients have a different type of antibody that we don’t know about."

The investigators recruited patients meeting diagnostic criteria for various rheumatologic diseases from St. Joseph’s Health Care in Southwestern Ontario, nearly all of whom were white. They also recruited age- and sex-matched healthy volunteers.

Descriptive data indicated that, on average, the patients with rheumatoid arthritis had had their disease for about 9 years and had 4.3 swollen joints, Dr. Barra reported. Fifty-six percent were in remission.

The main study results showed that 49% of patients with rheumatoid arthritis overall had AHFAs. This compared with just 5% of patients with SLE, 3% of patients with psoriatic arthritis, and none of the healthy volunteers.

A full 31% of the patients with RA were negative for ACFAs, but 19% of this subgroup were found to have AHFAs. Viewed another way, 6% of the patients with RA overall were negative for ACFAs but positive for AHFAs. "These patients were previously considered seronegative, but they do have an antibody," Dr. Barra commented.

The investigators also used a computer algorithm to assess whether the proteins and peptides that are homocitrullinated would bind to the shared epitope. The results indicated that 35 of them, only 5 of which could also be citrullinated, would bind with high affinity. "This suggests that there are unique homocitrullinated peptides, but there is also the possibility of cross-reactivity" between AHFAs and ACFAs, she explained.

"We are going to investigate cross-reactivity further, and we would like to look at the immune responses [to these proteins] in vivo in future work," Dr. Barra concluded.

Dr. Barra said she had no relevant financial disclosures.

VICTORIA, B.C. – Autoantibodies directed against homocitrullinated fibrinogen may help identify patients with rheumatoid arthritis who would currently be missed, a study has shown.

A team led by Dr. Lillian Barra and Dr. Ewa Cairns of the University of Western Ontario, London, tested 84 patients with rheumatoid arthritis (RA) and found that nearly half had antihomocitrullinated fibrinogen antibodies (AHFAs) in their serum.

Perhaps most importantly, these antibodies were present in almost a fifth of patients who did not have anticitrullinated fibrinogen antibodies (ACFAs) and would thus have otherwise been considered to be seronegative.

The results also indicated that AHFAs were specific for RA: They were seldom found in 37 patients with systemic lupus erythematosus and 37 patients with psoriatic arthritis. And they were not found at all in any of 27 healthy volunteers.

These findings add to similar results seen in a cohort of patients from Leiden, the Netherlands (Proc. Natl. Acad. Sci. USA 2011;108:17372-7), noted Dr. Barra, who presented the findings at the annual meeting of the Canadian Rheumatology Association "This is an exploratory study, and we are going to do a lot of future work looking at these antibodies in a larger cohort, hopefully the CATCH [Canadian Arthritis Cohort]," she said.

The large collective group of anticitrullinated protein antibodies (ACPAs) target citrullinated proteins, such as the collagen, fibrinogen, and vimentin found in joint synovial fluid. "They are highly specific for rheumatoid arthritis and have been included in the new [American College of Rheumatology]-EULAR criteria" for diagnosing early disease, Dr. Barra pointed out.

ACPAs associate with the shared epitope, the strongest genetic risk factor for RA, and have been found to be pathogenic in mice, she further noted. "However, nearly 50% of patients with early rheumatoid arthritis do not have ACPAs, which begs the question of whether these patients have a different type of antibody that we don’t know about."

The investigators recruited patients meeting diagnostic criteria for various rheumatologic diseases from St. Joseph’s Health Care in Southwestern Ontario, nearly all of whom were white. They also recruited age- and sex-matched healthy volunteers.

Descriptive data indicated that, on average, the patients with rheumatoid arthritis had had their disease for about 9 years and had 4.3 swollen joints, Dr. Barra reported. Fifty-six percent were in remission.

The main study results showed that 49% of patients with rheumatoid arthritis overall had AHFAs. This compared with just 5% of patients with SLE, 3% of patients with psoriatic arthritis, and none of the healthy volunteers.

A full 31% of the patients with RA were negative for ACFAs, but 19% of this subgroup were found to have AHFAs. Viewed another way, 6% of the patients with RA overall were negative for ACFAs but positive for AHFAs. "These patients were previously considered seronegative, but they do have an antibody," Dr. Barra commented.

The investigators also used a computer algorithm to assess whether the proteins and peptides that are homocitrullinated would bind to the shared epitope. The results indicated that 35 of them, only 5 of which could also be citrullinated, would bind with high affinity. "This suggests that there are unique homocitrullinated peptides, but there is also the possibility of cross-reactivity" between AHFAs and ACFAs, she explained.

"We are going to investigate cross-reactivity further, and we would like to look at the immune responses [to these proteins] in vivo in future work," Dr. Barra concluded.

Dr. Barra said she had no relevant financial disclosures.

VICTORIA, B.C. – Autoantibodies directed against homocitrullinated fibrinogen may help identify patients with rheumatoid arthritis who would currently be missed, a study has shown.

A team led by Dr. Lillian Barra and Dr. Ewa Cairns of the University of Western Ontario, London, tested 84 patients with rheumatoid arthritis (RA) and found that nearly half had antihomocitrullinated fibrinogen antibodies (AHFAs) in their serum.

Perhaps most importantly, these antibodies were present in almost a fifth of patients who did not have anticitrullinated fibrinogen antibodies (ACFAs) and would thus have otherwise been considered to be seronegative.

The results also indicated that AHFAs were specific for RA: They were seldom found in 37 patients with systemic lupus erythematosus and 37 patients with psoriatic arthritis. And they were not found at all in any of 27 healthy volunteers.

These findings add to similar results seen in a cohort of patients from Leiden, the Netherlands (Proc. Natl. Acad. Sci. USA 2011;108:17372-7), noted Dr. Barra, who presented the findings at the annual meeting of the Canadian Rheumatology Association "This is an exploratory study, and we are going to do a lot of future work looking at these antibodies in a larger cohort, hopefully the CATCH [Canadian Arthritis Cohort]," she said.

The large collective group of anticitrullinated protein antibodies (ACPAs) target citrullinated proteins, such as the collagen, fibrinogen, and vimentin found in joint synovial fluid. "They are highly specific for rheumatoid arthritis and have been included in the new [American College of Rheumatology]-EULAR criteria" for diagnosing early disease, Dr. Barra pointed out.

ACPAs associate with the shared epitope, the strongest genetic risk factor for RA, and have been found to be pathogenic in mice, she further noted. "However, nearly 50% of patients with early rheumatoid arthritis do not have ACPAs, which begs the question of whether these patients have a different type of antibody that we don’t know about."

The investigators recruited patients meeting diagnostic criteria for various rheumatologic diseases from St. Joseph’s Health Care in Southwestern Ontario, nearly all of whom were white. They also recruited age- and sex-matched healthy volunteers.

Descriptive data indicated that, on average, the patients with rheumatoid arthritis had had their disease for about 9 years and had 4.3 swollen joints, Dr. Barra reported. Fifty-six percent were in remission.

The main study results showed that 49% of patients with rheumatoid arthritis overall had AHFAs. This compared with just 5% of patients with SLE, 3% of patients with psoriatic arthritis, and none of the healthy volunteers.

A full 31% of the patients with RA were negative for ACFAs, but 19% of this subgroup were found to have AHFAs. Viewed another way, 6% of the patients with RA overall were negative for ACFAs but positive for AHFAs. "These patients were previously considered seronegative, but they do have an antibody," Dr. Barra commented.

The investigators also used a computer algorithm to assess whether the proteins and peptides that are homocitrullinated would bind to the shared epitope. The results indicated that 35 of them, only 5 of which could also be citrullinated, would bind with high affinity. "This suggests that there are unique homocitrullinated peptides, but there is also the possibility of cross-reactivity" between AHFAs and ACFAs, she explained.

"We are going to investigate cross-reactivity further, and we would like to look at the immune responses [to these proteins] in vivo in future work," Dr. Barra concluded.

Dr. Barra said she had no relevant financial disclosures.

VICTORIA, B.C. – Individuals who have physically demanding occupations are at increased risk for osteoarthritis, even in this era of protective measures and equipment, a population-based study has shown.

In this study of a random sample of 88,202 noninstitutionalized U.S. adults, almost one in five reported having physician-diagnosed osteoarthritis (OA), Dr. Chengwei Wang reported in a poster session at the annual meeting of the Canadian Rheumatology Association.

Photo ftwitty/iStockphoto.com

After adjustment for age, sex, ethnicity, and obesity, participants in physically demanding jobs such as building maintenance, health care support, and construction had significantly elevated risks of OA relative to their counterparts in computer and mathematical occupations (the group used for comparison because it had the lowest OA rate). The risk was increased to the greatest extent, essentially doubled, for those in military-specific occupations.

The risk of OA was significantly elevated for participants who were in office and administrative support occupations (relative risk, 1.24); sales and related occupations (1.28); building and grounds cleaning and maintenance (1.37); transportation and material moving (1.38); food preparation and serving (1.41); production (1.47); protective services (1.51); construction and extraction (1.51); health care support (1.54); installation, maintenance, and repair (1.54); and military-specific occupations (2.04).

These findings come from adjusted analyses of data from the U.S. National Health Interview Survey for the years 2005 through 2009 that used participants in computer and mathematical occupations as the reference group. Overall, 19.5% of the sample reported having physician-diagnosed OA.

"Doctors should know that people working in these occupations have a risk factor that plays an important role in developing osteoarthritis," Dr. Wang said in an interview. "I don’t think they need to change occupations. But doctors may want to tell patients to use some preventive measures when they work in these occupations other than to just prescribe medications" for musculoskeletal symptoms, she said.

"We need more-detailed studies to determine what kinds of factors in these occupations play a role in the development of this disease," such as various biomechanical factors, added Dr. Wang, a statistician at Nassau University Medical Center in East Meadow, N.Y. Additionally, the role of duration of exposure requires further investigation.

Such research could eventually help inform the redesign of workplaces and work practices to minimize risk, she said. For example, "occupational therapists and physical medicine and rehabilitation specialists could develop facilities to help protect workers in these occupations further," Dr. Wang suggested.

Dr. Wang said that she and her coauthors had no relevant financial disclosures.

VICTORIA, B.C. – Individuals who have physically demanding occupations are at increased risk for osteoarthritis, even in this era of protective measures and equipment, a population-based study has shown.

In this study of a random sample of 88,202 noninstitutionalized U.S. adults, almost one in five reported having physician-diagnosed osteoarthritis (OA), Dr. Chengwei Wang reported in a poster session at the annual meeting of the Canadian Rheumatology Association.

Photo ftwitty/iStockphoto.com

After adjustment for age, sex, ethnicity, and obesity, participants in physically demanding jobs such as building maintenance, health care support, and construction had significantly elevated risks of OA relative to their counterparts in computer and mathematical occupations (the group used for comparison because it had the lowest OA rate). The risk was increased to the greatest extent, essentially doubled, for those in military-specific occupations.

The risk of OA was significantly elevated for participants who were in office and administrative support occupations (relative risk, 1.24); sales and related occupations (1.28); building and grounds cleaning and maintenance (1.37); transportation and material moving (1.38); food preparation and serving (1.41); production (1.47); protective services (1.51); construction and extraction (1.51); health care support (1.54); installation, maintenance, and repair (1.54); and military-specific occupations (2.04).

These findings come from adjusted analyses of data from the U.S. National Health Interview Survey for the years 2005 through 2009 that used participants in computer and mathematical occupations as the reference group. Overall, 19.5% of the sample reported having physician-diagnosed OA.

"Doctors should know that people working in these occupations have a risk factor that plays an important role in developing osteoarthritis," Dr. Wang said in an interview. "I don’t think they need to change occupations. But doctors may want to tell patients to use some preventive measures when they work in these occupations other than to just prescribe medications" for musculoskeletal symptoms, she said.

"We need more-detailed studies to determine what kinds of factors in these occupations play a role in the development of this disease," such as various biomechanical factors, added Dr. Wang, a statistician at Nassau University Medical Center in East Meadow, N.Y. Additionally, the role of duration of exposure requires further investigation.

Such research could eventually help inform the redesign of workplaces and work practices to minimize risk, she said. For example, "occupational therapists and physical medicine and rehabilitation specialists could develop facilities to help protect workers in these occupations further," Dr. Wang suggested.

Dr. Wang said that she and her coauthors had no relevant financial disclosures.

VICTORIA, B.C. – Individuals who have physically demanding occupations are at increased risk for osteoarthritis, even in this era of protective measures and equipment, a population-based study has shown.

In this study of a random sample of 88,202 noninstitutionalized U.S. adults, almost one in five reported having physician-diagnosed osteoarthritis (OA), Dr. Chengwei Wang reported in a poster session at the annual meeting of the Canadian Rheumatology Association.

Photo ftwitty/iStockphoto.com

After adjustment for age, sex, ethnicity, and obesity, participants in physically demanding jobs such as building maintenance, health care support, and construction had significantly elevated risks of OA relative to their counterparts in computer and mathematical occupations (the group used for comparison because it had the lowest OA rate). The risk was increased to the greatest extent, essentially doubled, for those in military-specific occupations.

The risk of OA was significantly elevated for participants who were in office and administrative support occupations (relative risk, 1.24); sales and related occupations (1.28); building and grounds cleaning and maintenance (1.37); transportation and material moving (1.38); food preparation and serving (1.41); production (1.47); protective services (1.51); construction and extraction (1.51); health care support (1.54); installation, maintenance, and repair (1.54); and military-specific occupations (2.04).

These findings come from adjusted analyses of data from the U.S. National Health Interview Survey for the years 2005 through 2009 that used participants in computer and mathematical occupations as the reference group. Overall, 19.5% of the sample reported having physician-diagnosed OA.

"Doctors should know that people working in these occupations have a risk factor that plays an important role in developing osteoarthritis," Dr. Wang said in an interview. "I don’t think they need to change occupations. But doctors may want to tell patients to use some preventive measures when they work in these occupations other than to just prescribe medications" for musculoskeletal symptoms, she said.

"We need more-detailed studies to determine what kinds of factors in these occupations play a role in the development of this disease," such as various biomechanical factors, added Dr. Wang, a statistician at Nassau University Medical Center in East Meadow, N.Y. Additionally, the role of duration of exposure requires further investigation.

Such research could eventually help inform the redesign of workplaces and work practices to minimize risk, she said. For example, "occupational therapists and physical medicine and rehabilitation specialists could develop facilities to help protect workers in these occupations further," Dr. Wang suggested.

Dr. Wang said that she and her coauthors had no relevant financial disclosures.

VICTORIA, B.C. – Some patients with systemic lupus erythematosus may be more likely than others to experience a prolonged remission, new data suggest.

In a study of more than 1,500 patients who had SLE, about 2% achieved a remission lasting at least 5 years on either no medication or only antimalarial drugs, Anjali Papneja reported at the annual meeting of the Canadian Rheumatology Association.

The prolonged remissions lasted on average almost 12 years. Nearly a third of the patients had had a monophasic clinical disease course, characterized by only a single flare, before their remission.

Patients achieving a prolonged remission were more likely to be white, had milder disease, and were less likely to have involvement of certain organ systems and to have received steroids or other immunosuppressive agents prior to remission onset.

"Prolonged remission is an infrequent outcome among SLE patients, but it generally lasts for over a decade, and it is preceded by an atypically monophasic clinical course in a significant minority," Ms. Papneja commented.

"We want to know what makes these patients different, how they can be treated most effectively, and how we can harness this unique and desirable outcome more generally," she added.

An attendee asked what the remission rate was if patients who achieved remission on stable immunosuppressive regimens and/or low-dose prednisone were also included.

The reason for including only those patients who had remitted off all steroids and immunosuppressive agents was to distinguish those whose SLE was in true remission (i.e., those in the cohort), from those whose disease was merely suppressed by the ongoing use of these medications, replied Ms. Papneja, a medical student at the University of Toronto. "But they do remain on antimalarials because in recent decades, it has been found that these patients have cardiovascular protective benefits from antimalarials."

The investigators studied all patients with SLE followed at the university’s Lupus Clinic from July 1970 through May 2011.

Patients were defined as having a prolonged remission if they did not have any clinical disease activity for at least 5 years, had regular clinic visits, and received no immunosuppressive medications or at most antimalarial drugs during the remission.

With a mean duration of follow-up of nearly 22 years, 2.4% of the 1,613 patients studied achieved a prolonged remission, after a mean disease duration of about 9 years. These sustained remissions lasted an average of nearly 12 years.

By type, 44% of the remissions were serologically and clinically quiescent, 28% were serologically active but clinically quiescent, and 28% fluctuated between these types.

In the years leading up to the remission, the majority of patients (71%) had a relapsing-remitting clinical course, but a sizable proportion (29%) had a monophasic course. "It’s worthwhile to study these patients further to determine at what point we can safely define a disease course as being monophasic," Ms. Papneja commented. None of the patients achieving prolonged remission had a chronic active course.

In a case-control comparison, in which each patient who achieved prolonged remission was matched with three who did not, the former were more likely to be white (82% vs. 72%), had a lower SLE Disease Activity Index (SLEDAI-2K) score at their first clinic visit (8 vs. 10.6), and had a lower adjusted mean SLEDAI-2K score in the 3 years leading up to remission (3 vs. 5.9).

The group achieving prolonged remission was also significantly less likely to have skin, pulmonary, and central nervous system involvement, but "we noted that there was no difference in renal involvement between cases and controls," she pointed out. Additionally, they were less likely to have received steroids (58% vs. 80%) and other immunosuppressive agents (24% vs. 47%) prior to remission onset, also seeming to point to milder disease.

A study limitation, Ms. Papneja acknowledged, was that only patients continuing care at the clinic were included, and the clinic’s attrition rate was about 10%. Thus, some patients achieving remission and dropping out of care, or having a flare and seeking treatment elsewhere, may have been lost to follow-up.

Ms. Papneja disclosed that she had no relevant conflicts of interest.

VICTORIA, B.C. – Some patients with systemic lupus erythematosus may be more likely than others to experience a prolonged remission, new data suggest.

In a study of more than 1,500 patients who had SLE, about 2% achieved a remission lasting at least 5 years on either no medication or only antimalarial drugs, Anjali Papneja reported at the annual meeting of the Canadian Rheumatology Association.

The prolonged remissions lasted on average almost 12 years. Nearly a third of the patients had had a monophasic clinical disease course, characterized by only a single flare, before their remission.

Patients achieving a prolonged remission were more likely to be white, had milder disease, and were less likely to have involvement of certain organ systems and to have received steroids or other immunosuppressive agents prior to remission onset.

"Prolonged remission is an infrequent outcome among SLE patients, but it generally lasts for over a decade, and it is preceded by an atypically monophasic clinical course in a significant minority," Ms. Papneja commented.

"We want to know what makes these patients different, how they can be treated most effectively, and how we can harness this unique and desirable outcome more generally," she added.

An attendee asked what the remission rate was if patients who achieved remission on stable immunosuppressive regimens and/or low-dose prednisone were also included.

The reason for including only those patients who had remitted off all steroids and immunosuppressive agents was to distinguish those whose SLE was in true remission (i.e., those in the cohort), from those whose disease was merely suppressed by the ongoing use of these medications, replied Ms. Papneja, a medical student at the University of Toronto. "But they do remain on antimalarials because in recent decades, it has been found that these patients have cardiovascular protective benefits from antimalarials."

The investigators studied all patients with SLE followed at the university’s Lupus Clinic from July 1970 through May 2011.

Patients were defined as having a prolonged remission if they did not have any clinical disease activity for at least 5 years, had regular clinic visits, and received no immunosuppressive medications or at most antimalarial drugs during the remission.

With a mean duration of follow-up of nearly 22 years, 2.4% of the 1,613 patients studied achieved a prolonged remission, after a mean disease duration of about 9 years. These sustained remissions lasted an average of nearly 12 years.

By type, 44% of the remissions were serologically and clinically quiescent, 28% were serologically active but clinically quiescent, and 28% fluctuated between these types.

In the years leading up to the remission, the majority of patients (71%) had a relapsing-remitting clinical course, but a sizable proportion (29%) had a monophasic course. "It’s worthwhile to study these patients further to determine at what point we can safely define a disease course as being monophasic," Ms. Papneja commented. None of the patients achieving prolonged remission had a chronic active course.

In a case-control comparison, in which each patient who achieved prolonged remission was matched with three who did not, the former were more likely to be white (82% vs. 72%), had a lower SLE Disease Activity Index (SLEDAI-2K) score at their first clinic visit (8 vs. 10.6), and had a lower adjusted mean SLEDAI-2K score in the 3 years leading up to remission (3 vs. 5.9).

The group achieving prolonged remission was also significantly less likely to have skin, pulmonary, and central nervous system involvement, but "we noted that there was no difference in renal involvement between cases and controls," she pointed out. Additionally, they were less likely to have received steroids (58% vs. 80%) and other immunosuppressive agents (24% vs. 47%) prior to remission onset, also seeming to point to milder disease.

A study limitation, Ms. Papneja acknowledged, was that only patients continuing care at the clinic were included, and the clinic’s attrition rate was about 10%. Thus, some patients achieving remission and dropping out of care, or having a flare and seeking treatment elsewhere, may have been lost to follow-up.

Ms. Papneja disclosed that she had no relevant conflicts of interest.

VICTORIA, B.C. – Some patients with systemic lupus erythematosus may be more likely than others to experience a prolonged remission, new data suggest.

In a study of more than 1,500 patients who had SLE, about 2% achieved a remission lasting at least 5 years on either no medication or only antimalarial drugs, Anjali Papneja reported at the annual meeting of the Canadian Rheumatology Association.

The prolonged remissions lasted on average almost 12 years. Nearly a third of the patients had had a monophasic clinical disease course, characterized by only a single flare, before their remission.

Patients achieving a prolonged remission were more likely to be white, had milder disease, and were less likely to have involvement of certain organ systems and to have received steroids or other immunosuppressive agents prior to remission onset.

"Prolonged remission is an infrequent outcome among SLE patients, but it generally lasts for over a decade, and it is preceded by an atypically monophasic clinical course in a significant minority," Ms. Papneja commented.

"We want to know what makes these patients different, how they can be treated most effectively, and how we can harness this unique and desirable outcome more generally," she added.

An attendee asked what the remission rate was if patients who achieved remission on stable immunosuppressive regimens and/or low-dose prednisone were also included.

The reason for including only those patients who had remitted off all steroids and immunosuppressive agents was to distinguish those whose SLE was in true remission (i.e., those in the cohort), from those whose disease was merely suppressed by the ongoing use of these medications, replied Ms. Papneja, a medical student at the University of Toronto. "But they do remain on antimalarials because in recent decades, it has been found that these patients have cardiovascular protective benefits from antimalarials."

The investigators studied all patients with SLE followed at the university’s Lupus Clinic from July 1970 through May 2011.

Patients were defined as having a prolonged remission if they did not have any clinical disease activity for at least 5 years, had regular clinic visits, and received no immunosuppressive medications or at most antimalarial drugs during the remission.

With a mean duration of follow-up of nearly 22 years, 2.4% of the 1,613 patients studied achieved a prolonged remission, after a mean disease duration of about 9 years. These sustained remissions lasted an average of nearly 12 years.

By type, 44% of the remissions were serologically and clinically quiescent, 28% were serologically active but clinically quiescent, and 28% fluctuated between these types.

In the years leading up to the remission, the majority of patients (71%) had a relapsing-remitting clinical course, but a sizable proportion (29%) had a monophasic course. "It’s worthwhile to study these patients further to determine at what point we can safely define a disease course as being monophasic," Ms. Papneja commented. None of the patients achieving prolonged remission had a chronic active course.

In a case-control comparison, in which each patient who achieved prolonged remission was matched with three who did not, the former were more likely to be white (82% vs. 72%), had a lower SLE Disease Activity Index (SLEDAI-2K) score at their first clinic visit (8 vs. 10.6), and had a lower adjusted mean SLEDAI-2K score in the 3 years leading up to remission (3 vs. 5.9).

The group achieving prolonged remission was also significantly less likely to have skin, pulmonary, and central nervous system involvement, but "we noted that there was no difference in renal involvement between cases and controls," she pointed out. Additionally, they were less likely to have received steroids (58% vs. 80%) and other immunosuppressive agents (24% vs. 47%) prior to remission onset, also seeming to point to milder disease.

A study limitation, Ms. Papneja acknowledged, was that only patients continuing care at the clinic were included, and the clinic’s attrition rate was about 10%. Thus, some patients achieving remission and dropping out of care, or having a flare and seeking treatment elsewhere, may have been lost to follow-up.

Ms. Papneja disclosed that she had no relevant conflicts of interest.

VICTORIA, B.C. – Patients with rheumatoid arthritis who achieve remission on an agent targeting tumor necrosis factor have improvements in a variety of measures of resource use, activities of daily living, and employment, data have shown.

Investigators led by Dr. Cheryl Barnabe, a rheumatologist at the University of Calgary (Alta.), analyzed data from the Alberta Biologics Pharmacosurveillance Program for 1,315 patients with rheumatoid arthritis (RA) treated with a monoclonal antibody to tumor necrosis factor (TNF).

"Even in this patient group with severe disease and long disease duration, 34% were able to achieve remission in their first year of anti-TNF therapy, and an additional 25% were able to achieve minimal disease activity," she reported at the annual meeting of the Canadian Rheumatology Association.

Compared with their counterparts who had continued moderate or high disease activity, these patients had roughly one-third to three-fourths reductions in rates of limitations of daily activities, hospitalization, and curtailed work hours, and in over-the-counter drug costs.

The group who improved to the point of having minimal disease activity on therapy also had comparatively better outcomes, although the differences were generally smaller.

"The patients who achieved remission had benefits over those who had only attained minimal disease activity, implicating that our treatment goal should be remission and not just minimal disease activity," Dr. Barnabe said.

The Alberta Biologics Pharmacosurveillance Program prospectively collected data on safety, efficacy, function, quality of life, and resource use among patients with RA treated with anti-TNF biologics between April 2004 and March 2011. Costs to the health care system were ascertained by linking to the provincial health care utilization database.

Patients’ clinical response was defined as remission, minimal disease activity, or moderate-to-high disease activity using established assessment tools. The investigators compared outcomes for patients in their first year of a first anti-TNF therapy.

On average, the patients were 42 years old at diagnosis and had had RA for 14 years, Dr. Barnabe reported. The median number of disease-modifying antirheumatic drugs they had received was three. Their mean 28-joint Disease Activity Score at treatment start was 5.93.

The anti-TNF agent administered was etanercept (Enbrel) in 55% of patients, infliximab (Remicade) in 22%, adalimumab (Humira) in 18%, golimumab (Simponi) in 4%, and certolizumab (Cimzia) in 1%.

Compared with other patients, those who achieved remission in the first year of therapy had lower measures of inflammation, disease activity, and pain at baseline, according to Dr. Barnabe. However, they were similar with respect to measures of resource use, activities of daily living, and employment.

The main results showed that relative to their counterparts who had continued moderate-to-high disease activity, patients achieving remission were significantly less likely to have had a recent hospitalization (5% vs. 8%), had lower monthly costs for over-the-counter drugs ($15 vs. $59), and were less likely to have been unable to do usual activities in the past month (28% vs. 52%), to have needed help from others with activities of daily living in the past month (18% vs. 39%), and to have had to reduce their work hours in the past 6 months because of poor health (2% vs. 7%).

Patients achieving minimal disease activity also fared better than those with continued moderate-to-high disease activity, although benefits were smaller, according to Dr. Barnabe.

The disease response groups were statistically indistinguishable with respect to some other outcomes, such as outpatient visits, diagnostic tests, the use of community services, missed days of work, and the need to stop work or retire early because of arthritis.

Dr. Barnabe disclosed financial relationships with Abbott, Amgen/Pfizer, Bristol-Myers Squibb, and UCB. The program had independent multisource industry funding between 2009 and 2012.

VICTORIA, B.C. – Patients with rheumatoid arthritis who achieve remission on an agent targeting tumor necrosis factor have improvements in a variety of measures of resource use, activities of daily living, and employment, data have shown.

Investigators led by Dr. Cheryl Barnabe, a rheumatologist at the University of Calgary (Alta.), analyzed data from the Alberta Biologics Pharmacosurveillance Program for 1,315 patients with rheumatoid arthritis (RA) treated with a monoclonal antibody to tumor necrosis factor (TNF).

"Even in this patient group with severe disease and long disease duration, 34% were able to achieve remission in their first year of anti-TNF therapy, and an additional 25% were able to achieve minimal disease activity," she reported at the annual meeting of the Canadian Rheumatology Association.

Compared with their counterparts who had continued moderate or high disease activity, these patients had roughly one-third to three-fourths reductions in rates of limitations of daily activities, hospitalization, and curtailed work hours, and in over-the-counter drug costs.

The group who improved to the point of having minimal disease activity on therapy also had comparatively better outcomes, although the differences were generally smaller.

"The patients who achieved remission had benefits over those who had only attained minimal disease activity, implicating that our treatment goal should be remission and not just minimal disease activity," Dr. Barnabe said.

The Alberta Biologics Pharmacosurveillance Program prospectively collected data on safety, efficacy, function, quality of life, and resource use among patients with RA treated with anti-TNF biologics between April 2004 and March 2011. Costs to the health care system were ascertained by linking to the provincial health care utilization database.

Patients’ clinical response was defined as remission, minimal disease activity, or moderate-to-high disease activity using established assessment tools. The investigators compared outcomes for patients in their first year of a first anti-TNF therapy.

On average, the patients were 42 years old at diagnosis and had had RA for 14 years, Dr. Barnabe reported. The median number of disease-modifying antirheumatic drugs they had received was three. Their mean 28-joint Disease Activity Score at treatment start was 5.93.

The anti-TNF agent administered was etanercept (Enbrel) in 55% of patients, infliximab (Remicade) in 22%, adalimumab (Humira) in 18%, golimumab (Simponi) in 4%, and certolizumab (Cimzia) in 1%.

Compared with other patients, those who achieved remission in the first year of therapy had lower measures of inflammation, disease activity, and pain at baseline, according to Dr. Barnabe. However, they were similar with respect to measures of resource use, activities of daily living, and employment.

The main results showed that relative to their counterparts who had continued moderate-to-high disease activity, patients achieving remission were significantly less likely to have had a recent hospitalization (5% vs. 8%), had lower monthly costs for over-the-counter drugs ($15 vs. $59), and were less likely to have been unable to do usual activities in the past month (28% vs. 52%), to have needed help from others with activities of daily living in the past month (18% vs. 39%), and to have had to reduce their work hours in the past 6 months because of poor health (2% vs. 7%).

Patients achieving minimal disease activity also fared better than those with continued moderate-to-high disease activity, although benefits were smaller, according to Dr. Barnabe.

The disease response groups were statistically indistinguishable with respect to some other outcomes, such as outpatient visits, diagnostic tests, the use of community services, missed days of work, and the need to stop work or retire early because of arthritis.

Dr. Barnabe disclosed financial relationships with Abbott, Amgen/Pfizer, Bristol-Myers Squibb, and UCB. The program had independent multisource industry funding between 2009 and 2012.

VICTORIA, B.C. – Patients with rheumatoid arthritis who achieve remission on an agent targeting tumor necrosis factor have improvements in a variety of measures of resource use, activities of daily living, and employment, data have shown.

Investigators led by Dr. Cheryl Barnabe, a rheumatologist at the University of Calgary (Alta.), analyzed data from the Alberta Biologics Pharmacosurveillance Program for 1,315 patients with rheumatoid arthritis (RA) treated with a monoclonal antibody to tumor necrosis factor (TNF).

"Even in this patient group with severe disease and long disease duration, 34% were able to achieve remission in their first year of anti-TNF therapy, and an additional 25% were able to achieve minimal disease activity," she reported at the annual meeting of the Canadian Rheumatology Association.

Compared with their counterparts who had continued moderate or high disease activity, these patients had roughly one-third to three-fourths reductions in rates of limitations of daily activities, hospitalization, and curtailed work hours, and in over-the-counter drug costs.

The group who improved to the point of having minimal disease activity on therapy also had comparatively better outcomes, although the differences were generally smaller.

"The patients who achieved remission had benefits over those who had only attained minimal disease activity, implicating that our treatment goal should be remission and not just minimal disease activity," Dr. Barnabe said.

The Alberta Biologics Pharmacosurveillance Program prospectively collected data on safety, efficacy, function, quality of life, and resource use among patients with RA treated with anti-TNF biologics between April 2004 and March 2011. Costs to the health care system were ascertained by linking to the provincial health care utilization database.

Patients’ clinical response was defined as remission, minimal disease activity, or moderate-to-high disease activity using established assessment tools. The investigators compared outcomes for patients in their first year of a first anti-TNF therapy.

On average, the patients were 42 years old at diagnosis and had had RA for 14 years, Dr. Barnabe reported. The median number of disease-modifying antirheumatic drugs they had received was three. Their mean 28-joint Disease Activity Score at treatment start was 5.93.

The anti-TNF agent administered was etanercept (Enbrel) in 55% of patients, infliximab (Remicade) in 22%, adalimumab (Humira) in 18%, golimumab (Simponi) in 4%, and certolizumab (Cimzia) in 1%.

Compared with other patients, those who achieved remission in the first year of therapy had lower measures of inflammation, disease activity, and pain at baseline, according to Dr. Barnabe. However, they were similar with respect to measures of resource use, activities of daily living, and employment.

The main results showed that relative to their counterparts who had continued moderate-to-high disease activity, patients achieving remission were significantly less likely to have had a recent hospitalization (5% vs. 8%), had lower monthly costs for over-the-counter drugs ($15 vs. $59), and were less likely to have been unable to do usual activities in the past month (28% vs. 52%), to have needed help from others with activities of daily living in the past month (18% vs. 39%), and to have had to reduce their work hours in the past 6 months because of poor health (2% vs. 7%).

Patients achieving minimal disease activity also fared better than those with continued moderate-to-high disease activity, although benefits were smaller, according to Dr. Barnabe.

The disease response groups were statistically indistinguishable with respect to some other outcomes, such as outpatient visits, diagnostic tests, the use of community services, missed days of work, and the need to stop work or retire early because of arthritis.

Dr. Barnabe disclosed financial relationships with Abbott, Amgen/Pfizer, Bristol-Myers Squibb, and UCB. The program had independent multisource industry funding between 2009 and 2012.

VICTORIA, B.C. – The risk for cardiovascular disease is greater in people with osteoarthritis, but the reason why remains unclear, researchers reported at the annual meeting of the Canadian Rheumatology Association.

Using diagnosis codes, a team led by M. Mushfiqur Rahman, a biostatistician at the Arthritis Research Center of the University of British Columbia, Vancouver and a doctoral student with the School of Population and Public Health there, compared risk by osteoarthritis (OA) in a random sample of adults from the province’s general population who were free of cardiovascular disease (CVD) at baseline.

In all, 12,624 people with prevalent or incident OA were matched with 61,131 unaffected people. With a mean follow-up of 13 years, there were 1.3 new cases of CVD per 100 person-years in the study sample, according to results reported in a poster session.

Analyses showed a statistically significant 19% increase in the risk of CVD in people who had OA vs. those without, after multivariate adjustment for a variety of potential confounders, such as hypertension, diabetes, and comorbidity burden.

In sex-stratified analyses, the elevation of risk was below average for men, whether they were younger than 65 years of age (12% increase in risk) or older than this age (13%). But it was notably above average for both women younger than age 65 years (41%) and women over this age (27%).

The mechanisms underlying the observed association are unknown, according to Mr. Rahman. Inflammation is one possibility, although there is no evidence to support this relationship at present.

"We cannot explain this relationship biologically," he commented in an interview. "Maybe reduced physical activity is a major factor here: After a diagnosis of OA, people are not as physically active as they were before."

"Prescription medication could also be a big factor," Mr. Rahman continued. "We didn’t adjust for any prescription drugs here," although patients with [OA] are more likely to be using acetaminophen, nonsteroidal anti-inflammatory drugs, and opioids. "Those medications may have an effect [in elevating CVD risk]. We will see in the future."

The investigators are obtaining linked self-reported data that may shed further light on mechanisms. They will also be cross-checking the findings by assessing CVD mortality in patients with OA. If patients with OA prove to have higher CVD mortality, "that will be a good validation study."

In the meantime, physicians who see patients with OA may want to counsel them, "do more physical activity and take care of your heart," said Mr. Rahman.

Study participants were a random sample of individuals drawn from Population Data British Columbia for the years 1991 to 2009.

They were defined as having OA if the OA diagnostic code was used on either two or more visits to a health professional in 2 years or at least one discharge from the hospital. Similarly, they were defined as having CVD if they had a hospital record having a diagnosis code for ischemic heart disease, congestive heart failure, or stroke.

The mean age was about 58 years, and 59% of participants were women. About 16% had hypertension, 5% had hyperlipidemia, and 2% were obese. The mean Charlson comorbidity index was 0.41 in the OA group and 0.32 in the control group.

In addition to the elevated risk of CVD associated with OA (relative risk, 1.19), study results showed that participants were more likely to receive a CVD diagnosis if they had chronic obstructive pulmonary disease (1.18), had hypertension (1.38), were obese (1.21), or were in the lowest quintile of socioeconomic status (1.05). Also, risk increased with Charlson comorbidity index (1.11).

"There are some unmeasured confounders, for sure," Mr. Rahman acknowledged, noting that some variables, prescription drug use among them, were not available in the database used. Obesity was assessed from physician diagnoses instead of from body mass index; thus, the prevalence may have been underestimated. Also, "although we adjusted for [chronic obstructive pulmonary disease], smoking is an unmeasured confounder. And the physical activity level of the patients could be an unmeasured confounder, too."

Mr. Rahman disclosed that he had no relevant conflicts of interest.

VICTORIA, B.C. – The risk for cardiovascular disease is greater in people with osteoarthritis, but the reason why remains unclear, researchers reported at the annual meeting of the Canadian Rheumatology Association.

Using diagnosis codes, a team led by M. Mushfiqur Rahman, a biostatistician at the Arthritis Research Center of the University of British Columbia, Vancouver and a doctoral student with the School of Population and Public Health there, compared risk by osteoarthritis (OA) in a random sample of adults from the province’s general population who were free of cardiovascular disease (CVD) at baseline.

In all, 12,624 people with prevalent or incident OA were matched with 61,131 unaffected people. With a mean follow-up of 13 years, there were 1.3 new cases of CVD per 100 person-years in the study sample, according to results reported in a poster session.

Analyses showed a statistically significant 19% increase in the risk of CVD in people who had OA vs. those without, after multivariate adjustment for a variety of potential confounders, such as hypertension, diabetes, and comorbidity burden.

In sex-stratified analyses, the elevation of risk was below average for men, whether they were younger than 65 years of age (12% increase in risk) or older than this age (13%). But it was notably above average for both women younger than age 65 years (41%) and women over this age (27%).

The mechanisms underlying the observed association are unknown, according to Mr. Rahman. Inflammation is one possibility, although there is no evidence to support this relationship at present.

"We cannot explain this relationship biologically," he commented in an interview. "Maybe reduced physical activity is a major factor here: After a diagnosis of OA, people are not as physically active as they were before."

"Prescription medication could also be a big factor," Mr. Rahman continued. "We didn’t adjust for any prescription drugs here," although patients with [OA] are more likely to be using acetaminophen, nonsteroidal anti-inflammatory drugs, and opioids. "Those medications may have an effect [in elevating CVD risk]. We will see in the future."

The investigators are obtaining linked self-reported data that may shed further light on mechanisms. They will also be cross-checking the findings by assessing CVD mortality in patients with OA. If patients with OA prove to have higher CVD mortality, "that will be a good validation study."

In the meantime, physicians who see patients with OA may want to counsel them, "do more physical activity and take care of your heart," said Mr. Rahman.

Study participants were a random sample of individuals drawn from Population Data British Columbia for the years 1991 to 2009.

They were defined as having OA if the OA diagnostic code was used on either two or more visits to a health professional in 2 years or at least one discharge from the hospital. Similarly, they were defined as having CVD if they had a hospital record having a diagnosis code for ischemic heart disease, congestive heart failure, or stroke.

The mean age was about 58 years, and 59% of participants were women. About 16% had hypertension, 5% had hyperlipidemia, and 2% were obese. The mean Charlson comorbidity index was 0.41 in the OA group and 0.32 in the control group.

In addition to the elevated risk of CVD associated with OA (relative risk, 1.19), study results showed that participants were more likely to receive a CVD diagnosis if they had chronic obstructive pulmonary disease (1.18), had hypertension (1.38), were obese (1.21), or were in the lowest quintile of socioeconomic status (1.05). Also, risk increased with Charlson comorbidity index (1.11).

"There are some unmeasured confounders, for sure," Mr. Rahman acknowledged, noting that some variables, prescription drug use among them, were not available in the database used. Obesity was assessed from physician diagnoses instead of from body mass index; thus, the prevalence may have been underestimated. Also, "although we adjusted for [chronic obstructive pulmonary disease], smoking is an unmeasured confounder. And the physical activity level of the patients could be an unmeasured confounder, too."

Mr. Rahman disclosed that he had no relevant conflicts of interest.

VICTORIA, B.C. – The risk for cardiovascular disease is greater in people with osteoarthritis, but the reason why remains unclear, researchers reported at the annual meeting of the Canadian Rheumatology Association.

Using diagnosis codes, a team led by M. Mushfiqur Rahman, a biostatistician at the Arthritis Research Center of the University of British Columbia, Vancouver and a doctoral student with the School of Population and Public Health there, compared risk by osteoarthritis (OA) in a random sample of adults from the province’s general population who were free of cardiovascular disease (CVD) at baseline.

In all, 12,624 people with prevalent or incident OA were matched with 61,131 unaffected people. With a mean follow-up of 13 years, there were 1.3 new cases of CVD per 100 person-years in the study sample, according to results reported in a poster session.

Analyses showed a statistically significant 19% increase in the risk of CVD in people who had OA vs. those without, after multivariate adjustment for a variety of potential confounders, such as hypertension, diabetes, and comorbidity burden.

In sex-stratified analyses, the elevation of risk was below average for men, whether they were younger than 65 years of age (12% increase in risk) or older than this age (13%). But it was notably above average for both women younger than age 65 years (41%) and women over this age (27%).

The mechanisms underlying the observed association are unknown, according to Mr. Rahman. Inflammation is one possibility, although there is no evidence to support this relationship at present.

"We cannot explain this relationship biologically," he commented in an interview. "Maybe reduced physical activity is a major factor here: After a diagnosis of OA, people are not as physically active as they were before."

"Prescription medication could also be a big factor," Mr. Rahman continued. "We didn’t adjust for any prescription drugs here," although patients with [OA] are more likely to be using acetaminophen, nonsteroidal anti-inflammatory drugs, and opioids. "Those medications may have an effect [in elevating CVD risk]. We will see in the future."

The investigators are obtaining linked self-reported data that may shed further light on mechanisms. They will also be cross-checking the findings by assessing CVD mortality in patients with OA. If patients with OA prove to have higher CVD mortality, "that will be a good validation study."

In the meantime, physicians who see patients with OA may want to counsel them, "do more physical activity and take care of your heart," said Mr. Rahman.

Study participants were a random sample of individuals drawn from Population Data British Columbia for the years 1991 to 2009.

They were defined as having OA if the OA diagnostic code was used on either two or more visits to a health professional in 2 years or at least one discharge from the hospital. Similarly, they were defined as having CVD if they had a hospital record having a diagnosis code for ischemic heart disease, congestive heart failure, or stroke.

The mean age was about 58 years, and 59% of participants were women. About 16% had hypertension, 5% had hyperlipidemia, and 2% were obese. The mean Charlson comorbidity index was 0.41 in the OA group and 0.32 in the control group.

In addition to the elevated risk of CVD associated with OA (relative risk, 1.19), study results showed that participants were more likely to receive a CVD diagnosis if they had chronic obstructive pulmonary disease (1.18), had hypertension (1.38), were obese (1.21), or were in the lowest quintile of socioeconomic status (1.05). Also, risk increased with Charlson comorbidity index (1.11).

"There are some unmeasured confounders, for sure," Mr. Rahman acknowledged, noting that some variables, prescription drug use among them, were not available in the database used. Obesity was assessed from physician diagnoses instead of from body mass index; thus, the prevalence may have been underestimated. Also, "although we adjusted for [chronic obstructive pulmonary disease], smoking is an unmeasured confounder. And the physical activity level of the patients could be an unmeasured confounder, too."

Mr. Rahman disclosed that he had no relevant conflicts of interest.

SEATTLE – Patients with poorly controlled HIV infection have a more rapid decline of lung function over time than their uninfected counterparts, researchers reported at the Conference on Retroviruses and Opportunistic Infections.

The findings "suggest that, potentially, optimal antiretroviral therapy (ART) with HIV virological suppression may diminish the accelerated lung function decline that we are seeing," said Dr. M. Bradley Drummond, a pulmonologist at the Johns Hopkins University in Baltimore.

"Certainly, all individuals should quit smoking, but these data suggest that those with HIV should be specifically counseled about the importance of smoking cessation," he further noted in a related press briefing.

Dr. Drummond and colleagues assessed lung function over a period of 3 years in 1,064 injection drug users, about a third of whom were HIV positive.

Results showed that the rate of decline in forced expiratory volume in 1 second (FEV₁) was about 50% greater in HIV-positive individuals than in their HIV-negative counterparts overall even after taking into account potential confounders such as bacterial and Pneumocystis lung infections, pack-years of smoking, and current smoking status.

In stratified analyses, the decline was especially high – three to four times that in the HIV-negative group – for HIV-positive individuals who had poorly controlled HIV infection as indicated by high HIV viral loads or low CD4 counts.

"We conclude that markers of advanced and uncontrolled HIV disease are associated with more rapid decline in lung function. We also feel that the FEV₁ decline associated with uncontrolled HIV exceeds the effect of smoking in the general population," Dr. Drummond commented.

For the study, the investigators analyzed data from a subset of individuals enrolled in AIDS-Linked to the Intravenous Experience (ALIVE), a community-based cohort of current or former injection drug users who had semiannual clinical exams, blood tests, and spirometry measurements.

The individuals were 49 years old, on average, and predominantly male (65%), black (91%), and current or former smokers (94%). In all, 30% were HIV positive, of whom slightly more than half were on ART. The median duration of follow-up was 2.8 years.

Modeling results suggested that for typical individuals in the cohort, FEV₁ at baseline was 139 mL lower in HIV-positive individuals, compared with their HIV-negative counterparts after adjustment for potential confounders. This is statistically significant and clinically significant, Dr. Drummond commented.

In addition, over time, FEV₁ declined by 36 mL/yr in HIV-positive individuals (P = .06), or 50% faster than the 24 mL/yr decline seen in HIV-negative individuals. "That is probably not clinically significant; however, the reality about the ALIVE cohort is there is a relatively heterogeneous group of individuals with different degrees of HIV severity," he noted.

Analyses looking at the impact of viral load showed that HIV-positive individuals having a load of more than 75,000 copies/mL had a rate of FEV₁ decline of 99 mL/yr – more than four times that of HIV-negative individuals (P less than .01). But HIV-positive individuals with a lower viral load had a similar rate of decline as those who were HIV-negative.

Likewise, in analyses looking at the impact of CD4 count, the rate of FEV₁ decline steadily increased as CD4 count decreased. HIV-positive individuals having fewer than 100 CD4 cells/mm3 had a rate of 81 mL/yr – more than three times the rate among the HIV-negative group (P less than .01).

The investigators also conducted doubly stratified analyses looking at both viral load and CD4 count. "It really does look like actually the viral load effect is what’s driving most of the FEV₁ decline. So our money is on the viral load," Dr. Drummond said.

One session attendee asked whether the decline in pulmonary function was reversible when patients started ART. Dr. Drummond replied that most of the HIV-positive group did not have any changes to their therapy during observation, making it difficult to assess this. "We are doing a separate study where we are actually looking at pre- and post-ART initiation ... Hopefully, we would see some stabilization of breathing tests."

Regarding the nature of the obstructive lung disease being observed – asthma, chronic obstructive pulmonary disease, or something else – "we have done some bronchodilator reversibility testing, and it does look like it is a mix of diseases," he said.

Another attendee asked how these new data could be reconciled with those of the 1990s, when such declines in lung function were not observed in HIV-positive patients. Dr. Drummond replied that possibly clinicians weren’t looking for them much at that time or any declines observed were attributed to opportunistic lung infections.

"I think that what we are seeing is a real effect. Now whether it’s generalizable to other cohorts is going to be an important question, and our work with the Lung HIV Consortium, which is a multicenter site, will hopefully answer that question," he said. "But I think that what we are seeing is individuals who are living longer with controlled HIV, so we may be seeing much like we see accelerated cardiovascular disease [and] accelerated nephrotoxicity – that maybe the lungs are now implicated as another end organ of chronic HIV infection even when controlled."

He acknowledged that it was hard in this study to tease apart the effects of smoking and HIV on lung function, given that most of the cohort smoked. But on the flip side, "it makes it nice because it’s a homogenous population, to get rid of the effect of smoking."

Dr. Drummond disclosed that he had no relevant conflicts of interest.

SEATTLE – Patients with poorly controlled HIV infection have a more rapid decline of lung function over time than their uninfected counterparts, researchers reported at the Conference on Retroviruses and Opportunistic Infections.

The findings "suggest that, potentially, optimal antiretroviral therapy (ART) with HIV virological suppression may diminish the accelerated lung function decline that we are seeing," said Dr. M. Bradley Drummond, a pulmonologist at the Johns Hopkins University in Baltimore.

"Certainly, all individuals should quit smoking, but these data suggest that those with HIV should be specifically counseled about the importance of smoking cessation," he further noted in a related press briefing.

Dr. Drummond and colleagues assessed lung function over a period of 3 years in 1,064 injection drug users, about a third of whom were HIV positive.

Results showed that the rate of decline in forced expiratory volume in 1 second (FEV₁) was about 50% greater in HIV-positive individuals than in their HIV-negative counterparts overall even after taking into account potential confounders such as bacterial and Pneumocystis lung infections, pack-years of smoking, and current smoking status.

In stratified analyses, the decline was especially high – three to four times that in the HIV-negative group – for HIV-positive individuals who had poorly controlled HIV infection as indicated by high HIV viral loads or low CD4 counts.

"We conclude that markers of advanced and uncontrolled HIV disease are associated with more rapid decline in lung function. We also feel that the FEV₁ decline associated with uncontrolled HIV exceeds the effect of smoking in the general population," Dr. Drummond commented.

For the study, the investigators analyzed data from a subset of individuals enrolled in AIDS-Linked to the Intravenous Experience (ALIVE), a community-based cohort of current or former injection drug users who had semiannual clinical exams, blood tests, and spirometry measurements.

The individuals were 49 years old, on average, and predominantly male (65%), black (91%), and current or former smokers (94%). In all, 30% were HIV positive, of whom slightly more than half were on ART. The median duration of follow-up was 2.8 years.

Modeling results suggested that for typical individuals in the cohort, FEV₁ at baseline was 139 mL lower in HIV-positive individuals, compared with their HIV-negative counterparts after adjustment for potential confounders. This is statistically significant and clinically significant, Dr. Drummond commented.

In addition, over time, FEV₁ declined by 36 mL/yr in HIV-positive individuals (P = .06), or 50% faster than the 24 mL/yr decline seen in HIV-negative individuals. "That is probably not clinically significant; however, the reality about the ALIVE cohort is there is a relatively heterogeneous group of individuals with different degrees of HIV severity," he noted.

Analyses looking at the impact of viral load showed that HIV-positive individuals having a load of more than 75,000 copies/mL had a rate of FEV₁ decline of 99 mL/yr – more than four times that of HIV-negative individuals (P less than .01). But HIV-positive individuals with a lower viral load had a similar rate of decline as those who were HIV-negative.

Likewise, in analyses looking at the impact of CD4 count, the rate of FEV₁ decline steadily increased as CD4 count decreased. HIV-positive individuals having fewer than 100 CD4 cells/mm3 had a rate of 81 mL/yr – more than three times the rate among the HIV-negative group (P less than .01).

The investigators also conducted doubly stratified analyses looking at both viral load and CD4 count. "It really does look like actually the viral load effect is what’s driving most of the FEV₁ decline. So our money is on the viral load," Dr. Drummond said.

One session attendee asked whether the decline in pulmonary function was reversible when patients started ART. Dr. Drummond replied that most of the HIV-positive group did not have any changes to their therapy during observation, making it difficult to assess this. "We are doing a separate study where we are actually looking at pre- and post-ART initiation ... Hopefully, we would see some stabilization of breathing tests."

Regarding the nature of the obstructive lung disease being observed – asthma, chronic obstructive pulmonary disease, or something else – "we have done some bronchodilator reversibility testing, and it does look like it is a mix of diseases," he said.

Another attendee asked how these new data could be reconciled with those of the 1990s, when such declines in lung function were not observed in HIV-positive patients. Dr. Drummond replied that possibly clinicians weren’t looking for them much at that time or any declines observed were attributed to opportunistic lung infections.

"I think that what we are seeing is a real effect. Now whether it’s generalizable to other cohorts is going to be an important question, and our work with the Lung HIV Consortium, which is a multicenter site, will hopefully answer that question," he said. "But I think that what we are seeing is individuals who are living longer with controlled HIV, so we may be seeing much like we see accelerated cardiovascular disease [and] accelerated nephrotoxicity – that maybe the lungs are now implicated as another end organ of chronic HIV infection even when controlled."

He acknowledged that it was hard in this study to tease apart the effects of smoking and HIV on lung function, given that most of the cohort smoked. But on the flip side, "it makes it nice because it’s a homogenous population, to get rid of the effect of smoking."

Dr. Drummond disclosed that he had no relevant conflicts of interest.

SEATTLE – Patients with poorly controlled HIV infection have a more rapid decline of lung function over time than their uninfected counterparts, researchers reported at the Conference on Retroviruses and Opportunistic Infections.

The findings "suggest that, potentially, optimal antiretroviral therapy (ART) with HIV virological suppression may diminish the accelerated lung function decline that we are seeing," said Dr. M. Bradley Drummond, a pulmonologist at the Johns Hopkins University in Baltimore.

"Certainly, all individuals should quit smoking, but these data suggest that those with HIV should be specifically counseled about the importance of smoking cessation," he further noted in a related press briefing.

Dr. Drummond and colleagues assessed lung function over a period of 3 years in 1,064 injection drug users, about a third of whom were HIV positive.

Results showed that the rate of decline in forced expiratory volume in 1 second (FEV₁) was about 50% greater in HIV-positive individuals than in their HIV-negative counterparts overall even after taking into account potential confounders such as bacterial and Pneumocystis lung infections, pack-years of smoking, and current smoking status.

In stratified analyses, the decline was especially high – three to four times that in the HIV-negative group – for HIV-positive individuals who had poorly controlled HIV infection as indicated by high HIV viral loads or low CD4 counts.

"We conclude that markers of advanced and uncontrolled HIV disease are associated with more rapid decline in lung function. We also feel that the FEV₁ decline associated with uncontrolled HIV exceeds the effect of smoking in the general population," Dr. Drummond commented.

For the study, the investigators analyzed data from a subset of individuals enrolled in AIDS-Linked to the Intravenous Experience (ALIVE), a community-based cohort of current or former injection drug users who had semiannual clinical exams, blood tests, and spirometry measurements.

The individuals were 49 years old, on average, and predominantly male (65%), black (91%), and current or former smokers (94%). In all, 30% were HIV positive, of whom slightly more than half were on ART. The median duration of follow-up was 2.8 years.

Modeling results suggested that for typical individuals in the cohort, FEV₁ at baseline was 139 mL lower in HIV-positive individuals, compared with their HIV-negative counterparts after adjustment for potential confounders. This is statistically significant and clinically significant, Dr. Drummond commented.

In addition, over time, FEV₁ declined by 36 mL/yr in HIV-positive individuals (P = .06), or 50% faster than the 24 mL/yr decline seen in HIV-negative individuals. "That is probably not clinically significant; however, the reality about the ALIVE cohort is there is a relatively heterogeneous group of individuals with different degrees of HIV severity," he noted.

Analyses looking at the impact of viral load showed that HIV-positive individuals having a load of more than 75,000 copies/mL had a rate of FEV₁ decline of 99 mL/yr – more than four times that of HIV-negative individuals (P less than .01). But HIV-positive individuals with a lower viral load had a similar rate of decline as those who were HIV-negative.

Likewise, in analyses looking at the impact of CD4 count, the rate of FEV₁ decline steadily increased as CD4 count decreased. HIV-positive individuals having fewer than 100 CD4 cells/mm3 had a rate of 81 mL/yr – more than three times the rate among the HIV-negative group (P less than .01).

The investigators also conducted doubly stratified analyses looking at both viral load and CD4 count. "It really does look like actually the viral load effect is what’s driving most of the FEV₁ decline. So our money is on the viral load," Dr. Drummond said.

One session attendee asked whether the decline in pulmonary function was reversible when patients started ART. Dr. Drummond replied that most of the HIV-positive group did not have any changes to their therapy during observation, making it difficult to assess this. "We are doing a separate study where we are actually looking at pre- and post-ART initiation ... Hopefully, we would see some stabilization of breathing tests."

Regarding the nature of the obstructive lung disease being observed – asthma, chronic obstructive pulmonary disease, or something else – "we have done some bronchodilator reversibility testing, and it does look like it is a mix of diseases," he said.

Another attendee asked how these new data could be reconciled with those of the 1990s, when such declines in lung function were not observed in HIV-positive patients. Dr. Drummond replied that possibly clinicians weren’t looking for them much at that time or any declines observed were attributed to opportunistic lung infections.

"I think that what we are seeing is a real effect. Now whether it’s generalizable to other cohorts is going to be an important question, and our work with the Lung HIV Consortium, which is a multicenter site, will hopefully answer that question," he said. "But I think that what we are seeing is individuals who are living longer with controlled HIV, so we may be seeing much like we see accelerated cardiovascular disease [and] accelerated nephrotoxicity – that maybe the lungs are now implicated as another end organ of chronic HIV infection even when controlled."

He acknowledged that it was hard in this study to tease apart the effects of smoking and HIV on lung function, given that most of the cohort smoked. But on the flip side, "it makes it nice because it’s a homogenous population, to get rid of the effect of smoking."

Dr. Drummond disclosed that he had no relevant conflicts of interest.

VICTORIA, B.C. – The results of a cluster analysis may help streamline the diagnostic work-up in children with inflammatory brain diseases, sparing some of them invasive tests such as lumbar puncture or brain biopsy.

Investigators led by Dr. Tania Cellucci, a pediatric rheumatologist at the Hospital for Sick Children, University of Toronto, retrospectively analyzed presenting clinical, laboratory, and magnetic resonance imaging features in 147 pediatric patients having one of these diseases in an as-yet unpublished study.

The results, reported in a poster session at the annual meeting of the Canadian Rheumatology Association, identified three clusters of children who had different groups of diseases and who differed significantly with respect to the prevalence of various presenting features.

The investigators studied consecutive children seen at the hospital for inflammatory brain disease between December 1998 and June 2010, reviewing medical records to identify presenting clinical, laboratory, and imaging findings, and biopsy histology. The median age was about 9 years, and half the children were girls.

The most common disease was primary CNS vasculitis (seen in 71% of the children), Dr. Cellucci reported. That was followed by CNS vasculitis secondary to a systemic condition, such as lupus (7%), the neuronal antibody syndromes (6%), and postinfectious inflammatory brain disease (4%). The rest fell into a collective category of other diseases, such as neurosarcoidosis and inflammatory channelopathy (12%).

A k-means cluster analysis identified three distinct clusters:

• Patients in cluster 1 had angiography-negative primary CNS vasculitis and neuronal antibody syndromes that were due to antibodies against NMDA (N-methyl-d-aspartate).

• Patients in cluster 2 had angiography-negative primary CNS vasculitis and neuronal antibody syndromes that were due to antibodies against some other antigen.

• Patients in cluster 3 had angiography-positive primary CNS vasculitis and secondary CNS vasculitis.

The clusters differed significantly with respect to 14 presenting features. In terms of clinical features, patients in cluster 1 were more likely than their counterparts in the other clusters to have behavioral, cognitive, and mood changes, and seizures. Patients in cluster 2 were more likely to have ataxia, fatigue, and vision abnormalities. And patients in cluster 3 were more likely to be male and to have paresis and speech deficits.

Generally, laboratory features were not helpful in differentiating among clusters, Dr. Cellucci noted. For example, the proportions of patients having an elevated erythrocyte sedimentation rate and C-reactive protein level were essentially the same across clusters. The exception was that patients in cluster 3 were less likely to have an elevated cerebrospinal fluid white blood cell count.

In contrast, presenting MRI features were helpful (but not sufficient to confirm a diagnosis). Although the majority of patients in each cluster had some abnormalities on this imaging, the specific findings differed. Patients in cluster 3 were more likely than those in the other clusters to have unilateral lesions and ischemic lesions.

"The spectrum of childhood inflammatory brain diseases has really rapidly expanded over the past decade. A lot of new diseases have been described in the literature," Dr. Cellucci explained in an interview. Furthermore, these diseases have overlapping presenting features, leading to diagnostic uncertainty.

"So this is a new field with which a lot of people feel uncomfortable," she said. "This study is the first step in which we compare the different diseases and figure out whether can we use these findings to come up with a diagnostic algorithm."

If validated in an independent cohort, the findings may help clinicians "figure out which patient needs one test, which patient needs another test, and whether we can cut down on invasive tests, like a brain biopsy or a lumbar puncture, in patients who don’t actually need it," she said.

The study’s findings, while requiring validation, could help tailor the work-up to a child’s presenting features, according to Dr. Cellucci. "All patients will need an MRI, which is reasonable since this is not invasive. But patients in cluster 1 and 2 are those who may need a lumbar puncture, testing for neuronal antibodies, and possibly a biopsy. Patients who present with the findings typical for cluster 3 may require only an angiogram in addition to the MRI," she explained.

In addition, the findings may go a long way toward identifying children in the community whose inflammatory brain disease is misdiagnosed as some other condition, such as depression, psychosis, or seizure disorder.

"It would be a really important study to find out how many of these kids we are missing in the community," Dr. Cellucci commented. "One of the critical things is that we have treatment that works well for these patients: You treat them, and they get back to normal or almost normal, most of them. So that makes it even more critical to identify them."

She described the case of a girl who had seizures as her only symptom, but they did not improve with antiseizure medications. "As part of her work-up for more aggressive antiseizure therapy – which would be surgery – she had a brain biopsy that showed inflammation. We treated the inflammation and she is now seizure free," Dr. Cellucci said. "So I think that’s where it maybe becomes important to really figure out, how do we identify these kids and get them on the right therapy, because it is reversible for them."

Dr. Cellucci said that she had no relevant financial disclosures.

VICTORIA, B.C. – The results of a cluster analysis may help streamline the diagnostic work-up in children with inflammatory brain diseases, sparing some of them invasive tests such as lumbar puncture or brain biopsy.

Investigators led by Dr. Tania Cellucci, a pediatric rheumatologist at the Hospital for Sick Children, University of Toronto, retrospectively analyzed presenting clinical, laboratory, and magnetic resonance imaging features in 147 pediatric patients having one of these diseases in an as-yet unpublished study.

The results, reported in a poster session at the annual meeting of the Canadian Rheumatology Association, identified three clusters of children who had different groups of diseases and who differed significantly with respect to the prevalence of various presenting features.

The investigators studied consecutive children seen at the hospital for inflammatory brain disease between December 1998 and June 2010, reviewing medical records to identify presenting clinical, laboratory, and imaging findings, and biopsy histology. The median age was about 9 years, and half the children were girls.

The most common disease was primary CNS vasculitis (seen in 71% of the children), Dr. Cellucci reported. That was followed by CNS vasculitis secondary to a systemic condition, such as lupus (7%), the neuronal antibody syndromes (6%), and postinfectious inflammatory brain disease (4%). The rest fell into a collective category of other diseases, such as neurosarcoidosis and inflammatory channelopathy (12%).

A k-means cluster analysis identified three distinct clusters:

• Patients in cluster 1 had angiography-negative primary CNS vasculitis and neuronal antibody syndromes that were due to antibodies against NMDA (N-methyl-d-aspartate).

• Patients in cluster 2 had angiography-negative primary CNS vasculitis and neuronal antibody syndromes that were due to antibodies against some other antigen.

• Patients in cluster 3 had angiography-positive primary CNS vasculitis and secondary CNS vasculitis.

The clusters differed significantly with respect to 14 presenting features. In terms of clinical features, patients in cluster 1 were more likely than their counterparts in the other clusters to have behavioral, cognitive, and mood changes, and seizures. Patients in cluster 2 were more likely to have ataxia, fatigue, and vision abnormalities. And patients in cluster 3 were more likely to be male and to have paresis and speech deficits.

Generally, laboratory features were not helpful in differentiating among clusters, Dr. Cellucci noted. For example, the proportions of patients having an elevated erythrocyte sedimentation rate and C-reactive protein level were essentially the same across clusters. The exception was that patients in cluster 3 were less likely to have an elevated cerebrospinal fluid white blood cell count.

In contrast, presenting MRI features were helpful (but not sufficient to confirm a diagnosis). Although the majority of patients in each cluster had some abnormalities on this imaging, the specific findings differed. Patients in cluster 3 were more likely than those in the other clusters to have unilateral lesions and ischemic lesions.

"The spectrum of childhood inflammatory brain diseases has really rapidly expanded over the past decade. A lot of new diseases have been described in the literature," Dr. Cellucci explained in an interview. Furthermore, these diseases have overlapping presenting features, leading to diagnostic uncertainty.

"So this is a new field with which a lot of people feel uncomfortable," she said. "This study is the first step in which we compare the different diseases and figure out whether can we use these findings to come up with a diagnostic algorithm."

If validated in an independent cohort, the findings may help clinicians "figure out which patient needs one test, which patient needs another test, and whether we can cut down on invasive tests, like a brain biopsy or a lumbar puncture, in patients who don’t actually need it," she said.

The study’s findings, while requiring validation, could help tailor the work-up to a child’s presenting features, according to Dr. Cellucci. "All patients will need an MRI, which is reasonable since this is not invasive. But patients in cluster 1 and 2 are those who may need a lumbar puncture, testing for neuronal antibodies, and possibly a biopsy. Patients who present with the findings typical for cluster 3 may require only an angiogram in addition to the MRI," she explained.

In addition, the findings may go a long way toward identifying children in the community whose inflammatory brain disease is misdiagnosed as some other condition, such as depression, psychosis, or seizure disorder.

"It would be a really important study to find out how many of these kids we are missing in the community," Dr. Cellucci commented. "One of the critical things is that we have treatment that works well for these patients: You treat them, and they get back to normal or almost normal, most of them. So that makes it even more critical to identify them."

She described the case of a girl who had seizures as her only symptom, but they did not improve with antiseizure medications. "As part of her work-up for more aggressive antiseizure therapy – which would be surgery – she had a brain biopsy that showed inflammation. We treated the inflammation and she is now seizure free," Dr. Cellucci said. "So I think that’s where it maybe becomes important to really figure out, how do we identify these kids and get them on the right therapy, because it is reversible for them."

Dr. Cellucci said that she had no relevant financial disclosures.

VICTORIA, B.C. – The results of a cluster analysis may help streamline the diagnostic work-up in children with inflammatory brain diseases, sparing some of them invasive tests such as lumbar puncture or brain biopsy.

Investigators led by Dr. Tania Cellucci, a pediatric rheumatologist at the Hospital for Sick Children, University of Toronto, retrospectively analyzed presenting clinical, laboratory, and magnetic resonance imaging features in 147 pediatric patients having one of these diseases in an as-yet unpublished study.

The results, reported in a poster session at the annual meeting of the Canadian Rheumatology Association, identified three clusters of children who had different groups of diseases and who differed significantly with respect to the prevalence of various presenting features.

The investigators studied consecutive children seen at the hospital for inflammatory brain disease between December 1998 and June 2010, reviewing medical records to identify presenting clinical, laboratory, and imaging findings, and biopsy histology. The median age was about 9 years, and half the children were girls.

The most common disease was primary CNS vasculitis (seen in 71% of the children), Dr. Cellucci reported. That was followed by CNS vasculitis secondary to a systemic condition, such as lupus (7%), the neuronal antibody syndromes (6%), and postinfectious inflammatory brain disease (4%). The rest fell into a collective category of other diseases, such as neurosarcoidosis and inflammatory channelopathy (12%).

A k-means cluster analysis identified three distinct clusters:

• Patients in cluster 1 had angiography-negative primary CNS vasculitis and neuronal antibody syndromes that were due to antibodies against NMDA (N-methyl-d-aspartate).

• Patients in cluster 2 had angiography-negative primary CNS vasculitis and neuronal antibody syndromes that were due to antibodies against some other antigen.

• Patients in cluster 3 had angiography-positive primary CNS vasculitis and secondary CNS vasculitis.

The clusters differed significantly with respect to 14 presenting features. In terms of clinical features, patients in cluster 1 were more likely than their counterparts in the other clusters to have behavioral, cognitive, and mood changes, and seizures. Patients in cluster 2 were more likely to have ataxia, fatigue, and vision abnormalities. And patients in cluster 3 were more likely to be male and to have paresis and speech deficits.

Generally, laboratory features were not helpful in differentiating among clusters, Dr. Cellucci noted. For example, the proportions of patients having an elevated erythrocyte sedimentation rate and C-reactive protein level were essentially the same across clusters. The exception was that patients in cluster 3 were less likely to have an elevated cerebrospinal fluid white blood cell count.

In contrast, presenting MRI features were helpful (but not sufficient to confirm a diagnosis). Although the majority of patients in each cluster had some abnormalities on this imaging, the specific findings differed. Patients in cluster 3 were more likely than those in the other clusters to have unilateral lesions and ischemic lesions.

"The spectrum of childhood inflammatory brain diseases has really rapidly expanded over the past decade. A lot of new diseases have been described in the literature," Dr. Cellucci explained in an interview. Furthermore, these diseases have overlapping presenting features, leading to diagnostic uncertainty.

"So this is a new field with which a lot of people feel uncomfortable," she said. "This study is the first step in which we compare the different diseases and figure out whether can we use these findings to come up with a diagnostic algorithm."

If validated in an independent cohort, the findings may help clinicians "figure out which patient needs one test, which patient needs another test, and whether we can cut down on invasive tests, like a brain biopsy or a lumbar puncture, in patients who don’t actually need it," she said.

The study’s findings, while requiring validation, could help tailor the work-up to a child’s presenting features, according to Dr. Cellucci. "All patients will need an MRI, which is reasonable since this is not invasive. But patients in cluster 1 and 2 are those who may need a lumbar puncture, testing for neuronal antibodies, and possibly a biopsy. Patients who present with the findings typical for cluster 3 may require only an angiogram in addition to the MRI," she explained.

In addition, the findings may go a long way toward identifying children in the community whose inflammatory brain disease is misdiagnosed as some other condition, such as depression, psychosis, or seizure disorder.

"It would be a really important study to find out how many of these kids we are missing in the community," Dr. Cellucci commented. "One of the critical things is that we have treatment that works well for these patients: You treat them, and they get back to normal or almost normal, most of them. So that makes it even more critical to identify them."

She described the case of a girl who had seizures as her only symptom, but they did not improve with antiseizure medications. "As part of her work-up for more aggressive antiseizure therapy – which would be surgery – she had a brain biopsy that showed inflammation. We treated the inflammation and she is now seizure free," Dr. Cellucci said. "So I think that’s where it maybe becomes important to really figure out, how do we identify these kids and get them on the right therapy, because it is reversible for them."

Dr. Cellucci said that she had no relevant financial disclosures.

VICTORIA, B.C. – Patients with rheumatoid arthritis who also have common comorbidities are at increased risk for infection when starting treatment with at least one class of biologic agents, based on the findings of a cohort study.

Investigators led by Dr. Joanne Homik, director of the division of rheumatology at the University of Alberta in Edmonton, studied 1,086 patients with rheumatoid arthritis (RA) who were initiating treatment, in most cases with a biologic agent targeting tumor necrosis factor (TNF).

In adjusted analyses, patients had more than triple the risk of a serious infection, defined as one requiring hospitalization, if they had anemia, according to data from the as-yet unpublished study. In other findings, patients were 97% more likely to develop an infection if they had lung disease and 39% more likely if they had heart disease.

"The anemia variable has an unclear relationship, but we are looking into that further. Our theory is that with lung disease, that has some biologic plausibility since bronchitis and pneumonia have prominence in our list of infections seen in this cohort," Dr. Homik commented at the annual meeting of the Canadian Rheumatology Association.

The incidence density of serious infection was 1.67 cases per 100 patient-years, about half that found in some other cohorts. "One of the things we thought of when trying to explain why our serious infection risk is so low is that health care restructuring in Alberta in the mid-90s resulted in bed closures," she explained. "So hospitalizations were reduced overall, and many patients who ... could be considered seriously ill are not admitted any longer, and it can be a bit more challenging to [identify] those serious infections."

The study occurred shortly after anti-TNF agents first became available, so the patients receiving them usually had the most severe, long-standing RA, Dr. Homik noted. Over time, as the demographic of the database changes to include more patients within the first 5 years of their RA, outcomes may differ and predictors may differ as well.

The risk of any infection among patients starting anti-TNF agents did not differ from that among patients starting the disease-modifying antirheumatic drug (DMARD) leflunomide instead. However, leflunomide confers a higher infection risk than some other DMARDs, she noted.

The investigators used registry data to study a cohort of all 943 patients with RA in Alberta who started a first anti-TNF agent between January 2004 and March 2009, and also studied a comparison cohort of 143 patients who started leflunomide (Arava). The patients completed the self-administered comorbidity questionnaire at baseline and were monitored prospectively for outcomes and adverse events. Their average age was 54 years, and 70% were female.

With a mean follow-up of 2.3 years, 70% of patients developed an infection as ascertained from physician claims data or self-report; the most common were bronchitis, cellulitis, and sinusitis. Nearly 4% of patients developed a serious infection; the most common were pneumonia, cellulitis, septicemia, and septic arthritis.

In the first multivariate analysis, patients had an elevated risk of infection if they had heart disease (hazard ratio, 1.39) or lung disease (1.97), used steroids (1.2), or currently smoked (1.24). Their risk was decreased risk if they were male (HR, 0.78). When analysis was restricted to the subset who started an anti-TNF agent, infection risk was increased for those with lung disease (2.02) and decreased for men (0.80).

In the second multivariate analysis, patients had an elevated risk of serious infection if they had anemia (HR, 3.26) or used steroids (3.21), and a decreased risk if they had more than a secondary education (0.33). In the subset who started an anti-TNF agent, risk was increased for patients who had anemia (HR, 3.7) or used steroids (3.5), and decreased for those having more than a secondary education (0.3).

The risks of infection and serious infection did not differ across subgroups when patients were stratified according to whether they stayed on their first treatment or switched from one kind of DMARD to their first anti-TNF agent (or from one anti-TNF agent to another), Dr. Homik reported.

"In the cohort of patients on their first anti-TNF agent, the specific anti-TNF agent used did not predict risk of infection," she noted.

Dr. Homik disclosed that she serves as a consultant to Abbott, Amgen, Pfizer, and Roche. The Alberta Biologics Registry has received unrestricted grant support from Abbott, Amgen, Bristol-Myers Squibb, Merck/Jansson, and Pfizer.

VICTORIA, B.C. – Patients with rheumatoid arthritis who also have common comorbidities are at increased risk for infection when starting treatment with at least one class of biologic agents, based on the findings of a cohort study.

Investigators led by Dr. Joanne Homik, director of the division of rheumatology at the University of Alberta in Edmonton, studied 1,086 patients with rheumatoid arthritis (RA) who were initiating treatment, in most cases with a biologic agent targeting tumor necrosis factor (TNF).

In adjusted analyses, patients had more than triple the risk of a serious infection, defined as one requiring hospitalization, if they had anemia, according to data from the as-yet unpublished study. In other findings, patients were 97% more likely to develop an infection if they had lung disease and 39% more likely if they had heart disease.

"The anemia variable has an unclear relationship, but we are looking into that further. Our theory is that with lung disease, that has some biologic plausibility since bronchitis and pneumonia have prominence in our list of infections seen in this cohort," Dr. Homik commented at the annual meeting of the Canadian Rheumatology Association.

The incidence density of serious infection was 1.67 cases per 100 patient-years, about half that found in some other cohorts. "One of the things we thought of when trying to explain why our serious infection risk is so low is that health care restructuring in Alberta in the mid-90s resulted in bed closures," she explained. "So hospitalizations were reduced overall, and many patients who ... could be considered seriously ill are not admitted any longer, and it can be a bit more challenging to [identify] those serious infections."

The study occurred shortly after anti-TNF agents first became available, so the patients receiving them usually had the most severe, long-standing RA, Dr. Homik noted. Over time, as the demographic of the database changes to include more patients within the first 5 years of their RA, outcomes may differ and predictors may differ as well.

The risk of any infection among patients starting anti-TNF agents did not differ from that among patients starting the disease-modifying antirheumatic drug (DMARD) leflunomide instead. However, leflunomide confers a higher infection risk than some other DMARDs, she noted.

The investigators used registry data to study a cohort of all 943 patients with RA in Alberta who started a first anti-TNF agent between January 2004 and March 2009, and also studied a comparison cohort of 143 patients who started leflunomide (Arava). The patients completed the self-administered comorbidity questionnaire at baseline and were monitored prospectively for outcomes and adverse events. Their average age was 54 years, and 70% were female.

With a mean follow-up of 2.3 years, 70% of patients developed an infection as ascertained from physician claims data or self-report; the most common were bronchitis, cellulitis, and sinusitis. Nearly 4% of patients developed a serious infection; the most common were pneumonia, cellulitis, septicemia, and septic arthritis.

In the first multivariate analysis, patients had an elevated risk of infection if they had heart disease (hazard ratio, 1.39) or lung disease (1.97), used steroids (1.2), or currently smoked (1.24). Their risk was decreased risk if they were male (HR, 0.78). When analysis was restricted to the subset who started an anti-TNF agent, infection risk was increased for those with lung disease (2.02) and decreased for men (0.80).

In the second multivariate analysis, patients had an elevated risk of serious infection if they had anemia (HR, 3.26) or used steroids (3.21), and a decreased risk if they had more than a secondary education (0.33). In the subset who started an anti-TNF agent, risk was increased for patients who had anemia (HR, 3.7) or used steroids (3.5), and decreased for those having more than a secondary education (0.3).

The risks of infection and serious infection did not differ across subgroups when patients were stratified according to whether they stayed on their first treatment or switched from one kind of DMARD to their first anti-TNF agent (or from one anti-TNF agent to another), Dr. Homik reported.

"In the cohort of patients on their first anti-TNF agent, the specific anti-TNF agent used did not predict risk of infection," she noted.

Dr. Homik disclosed that she serves as a consultant to Abbott, Amgen, Pfizer, and Roche. The Alberta Biologics Registry has received unrestricted grant support from Abbott, Amgen, Bristol-Myers Squibb, Merck/Jansson, and Pfizer.

VICTORIA, B.C. – Patients with rheumatoid arthritis who also have common comorbidities are at increased risk for infection when starting treatment with at least one class of biologic agents, based on the findings of a cohort study.

Investigators led by Dr. Joanne Homik, director of the division of rheumatology at the University of Alberta in Edmonton, studied 1,086 patients with rheumatoid arthritis (RA) who were initiating treatment, in most cases with a biologic agent targeting tumor necrosis factor (TNF).

In adjusted analyses, patients had more than triple the risk of a serious infection, defined as one requiring hospitalization, if they had anemia, according to data from the as-yet unpublished study. In other findings, patients were 97% more likely to develop an infection if they had lung disease and 39% more likely if they had heart disease.

"The anemia variable has an unclear relationship, but we are looking into that further. Our theory is that with lung disease, that has some biologic plausibility since bronchitis and pneumonia have prominence in our list of infections seen in this cohort," Dr. Homik commented at the annual meeting of the Canadian Rheumatology Association.

The incidence density of serious infection was 1.67 cases per 100 patient-years, about half that found in some other cohorts. "One of the things we thought of when trying to explain why our serious infection risk is so low is that health care restructuring in Alberta in the mid-90s resulted in bed closures," she explained. "So hospitalizations were reduced overall, and many patients who ... could be considered seriously ill are not admitted any longer, and it can be a bit more challenging to [identify] those serious infections."

The study occurred shortly after anti-TNF agents first became available, so the patients receiving them usually had the most severe, long-standing RA, Dr. Homik noted. Over time, as the demographic of the database changes to include more patients within the first 5 years of their RA, outcomes may differ and predictors may differ as well.

The risk of any infection among patients starting anti-TNF agents did not differ from that among patients starting the disease-modifying antirheumatic drug (DMARD) leflunomide instead. However, leflunomide confers a higher infection risk than some other DMARDs, she noted.

The investigators used registry data to study a cohort of all 943 patients with RA in Alberta who started a first anti-TNF agent between January 2004 and March 2009, and also studied a comparison cohort of 143 patients who started leflunomide (Arava). The patients completed the self-administered comorbidity questionnaire at baseline and were monitored prospectively for outcomes and adverse events. Their average age was 54 years, and 70% were female.

With a mean follow-up of 2.3 years, 70% of patients developed an infection as ascertained from physician claims data or self-report; the most common were bronchitis, cellulitis, and sinusitis. Nearly 4% of patients developed a serious infection; the most common were pneumonia, cellulitis, septicemia, and septic arthritis.

In the first multivariate analysis, patients had an elevated risk of infection if they had heart disease (hazard ratio, 1.39) or lung disease (1.97), used steroids (1.2), or currently smoked (1.24). Their risk was decreased risk if they were male (HR, 0.78). When analysis was restricted to the subset who started an anti-TNF agent, infection risk was increased for those with lung disease (2.02) and decreased for men (0.80).

In the second multivariate analysis, patients had an elevated risk of serious infection if they had anemia (HR, 3.26) or used steroids (3.21), and a decreased risk if they had more than a secondary education (0.33). In the subset who started an anti-TNF agent, risk was increased for patients who had anemia (HR, 3.7) or used steroids (3.5), and decreased for those having more than a secondary education (0.3).

The risks of infection and serious infection did not differ across subgroups when patients were stratified according to whether they stayed on their first treatment or switched from one kind of DMARD to their first anti-TNF agent (or from one anti-TNF agent to another), Dr. Homik reported.

"In the cohort of patients on their first anti-TNF agent, the specific anti-TNF agent used did not predict risk of infection," she noted.

Dr. Homik disclosed that she serves as a consultant to Abbott, Amgen, Pfizer, and Roche. The Alberta Biologics Registry has received unrestricted grant support from Abbott, Amgen, Bristol-Myers Squibb, Merck/Jansson, and Pfizer.

VICTORIA, B.C. – Suboptimal vitamin D levels may play a role in the pathogenesis of inflammatory arthritis but not in its subsequent clinical course, judging from the findings of a study involving 264 adult patients with early disease.

Fully 77% of patients had vitamin D deficiency or insufficiency at baseline, reported lead investigator Dr. Carol A. Hitchon at the annual meeting of Canadian Rheumatology Association. But in findings that contrasted those of some earlier studies, levels were not significantly associated with disease activity at that time or with achievement of remission 1 year later.

The study also found that vitamin D levels did not correlate with levels of immunoglobulin directed against common pathogens implicated in the development of rheumatoid arthritis.

"It’s possible that vitamin D levels may not be that important in terms of clinical activity and that vitamin D status may be more important in predisposing to rheumatoid arthritis," Dr. Hitchon commented. "I don’t think vitamin D is the only answer. And I think it’s not just the level, it is probably other elements of the vitamin D pathway that might be important, in terms of how they may regulate autoimmune processes."

A session attendee wondered whether patients with inflammatory arthritis may simply have lower levels of this vitamin because they go out in the sun less.

That is a possible explanation, acknowledged Dr. Hitchon of the arthritis center at the University of Manitoba in Winnipeg. "We are hoping to measure vitamin D levels in a population that generally has more sun exposure based on where they reside, and that may give us some correlation," she added.

Accumulating data suggest that vitamin D plays a role in maintaining both tolerance and immunity to pathogens. Thus, the investigators hypothesized, "if you are deficient in vitamin D, it may lead to a break of self-tolerance and the development of autoimmunity. Similarly, deficient vitamin D can impair or alter the initial response to pathogens, leading to increased microbial load, which can also increase or affect autoimmunity," Dr. Hitchon said.

She and her colleagues studied patients from the Manitoba Early Arthritis Cohort. All of the patients had had symptoms of inflammatory arthritis for no more than 1 year, and had at least one swollen joint.

The severity of their arthritis was assessed with the DAS28-CRP (28-joint count Disease Activity Score, C-reactive protein). Circulating levels of 25-hydroxyvitamin D and antibodies to Escherichia coli and Proteus mirabilis – both of which have been implicated in rheumatoid arthritis – were measured in serum collected before the start of treatment.

The average age of the patients studied was 48 years, and 76% were women. Overall, 60% were rheumatoid factor–positive, and 49% were positive for CCP2 (cyclic citrullinated peptide, second-generation assay). Their mean DAS28-CRP score was 3.99.

Results showed that 16% of patients had vitamin D deficiency and 61% had vitamin D insufficiency, while just 23% had optimal levels. Smokers had significantly lower levels than did nonsmokers.

There was no association at baseline between vitamin D levels and rheumatoid factor or CCP2 levels, DAS28-CRP score, or several other measures of disease activity, reported Dr. Hitchon, who disclosed no relevant conflicts of interest.

In adjusted analyses, vitamin D levels were not significantly associated with DAS28-CRP score at baseline or with achievement of remission 1 year later. "As has been previously shown, the major predictor of 1-year outcome was the baseline DAS score," she noted.

During the study, 20% of patients had an improvement in their vitamin D levels, moving to a higher category, whereas 12% of patients had a worsening, moving to a lower category. "This is without any formal protocol or plan to supplement vitamin D," Dr. Hitchon pointed out.

There was also no significant correlation between vitamin D levels and levels of immunoglobulins –whether IgA, IgM, or IgG – to E. coli or P. mirabilis.

Dr. Hitchon disclosed no relevant conflicts of interest.

VICTORIA, B.C. – Suboptimal vitamin D levels may play a role in the pathogenesis of inflammatory arthritis but not in its subsequent clinical course, judging from the findings of a study involving 264 adult patients with early disease.

Fully 77% of patients had vitamin D deficiency or insufficiency at baseline, reported lead investigator Dr. Carol A. Hitchon at the annual meeting of Canadian Rheumatology Association. But in findings that contrasted those of some earlier studies, levels were not significantly associated with disease activity at that time or with achievement of remission 1 year later.

The study also found that vitamin D levels did not correlate with levels of immunoglobulin directed against common pathogens implicated in the development of rheumatoid arthritis.

"It’s possible that vitamin D levels may not be that important in terms of clinical activity and that vitamin D status may be more important in predisposing to rheumatoid arthritis," Dr. Hitchon commented. "I don’t think vitamin D is the only answer. And I think it’s not just the level, it is probably other elements of the vitamin D pathway that might be important, in terms of how they may regulate autoimmune processes."

A session attendee wondered whether patients with inflammatory arthritis may simply have lower levels of this vitamin because they go out in the sun less.

That is a possible explanation, acknowledged Dr. Hitchon of the arthritis center at the University of Manitoba in Winnipeg. "We are hoping to measure vitamin D levels in a population that generally has more sun exposure based on where they reside, and that may give us some correlation," she added.

Accumulating data suggest that vitamin D plays a role in maintaining both tolerance and immunity to pathogens. Thus, the investigators hypothesized, "if you are deficient in vitamin D, it may lead to a break of self-tolerance and the development of autoimmunity. Similarly, deficient vitamin D can impair or alter the initial response to pathogens, leading to increased microbial load, which can also increase or affect autoimmunity," Dr. Hitchon said.

She and her colleagues studied patients from the Manitoba Early Arthritis Cohort. All of the patients had had symptoms of inflammatory arthritis for no more than 1 year, and had at least one swollen joint.

The severity of their arthritis was assessed with the DAS28-CRP (28-joint count Disease Activity Score, C-reactive protein). Circulating levels of 25-hydroxyvitamin D and antibodies to Escherichia coli and Proteus mirabilis – both of which have been implicated in rheumatoid arthritis – were measured in serum collected before the start of treatment.

The average age of the patients studied was 48 years, and 76% were women. Overall, 60% were rheumatoid factor–positive, and 49% were positive for CCP2 (cyclic citrullinated peptide, second-generation assay). Their mean DAS28-CRP score was 3.99.

Results showed that 16% of patients had vitamin D deficiency and 61% had vitamin D insufficiency, while just 23% had optimal levels. Smokers had significantly lower levels than did nonsmokers.

There was no association at baseline between vitamin D levels and rheumatoid factor or CCP2 levels, DAS28-CRP score, or several other measures of disease activity, reported Dr. Hitchon, who disclosed no relevant conflicts of interest.

In adjusted analyses, vitamin D levels were not significantly associated with DAS28-CRP score at baseline or with achievement of remission 1 year later. "As has been previously shown, the major predictor of 1-year outcome was the baseline DAS score," she noted.

During the study, 20% of patients had an improvement in their vitamin D levels, moving to a higher category, whereas 12% of patients had a worsening, moving to a lower category. "This is without any formal protocol or plan to supplement vitamin D," Dr. Hitchon pointed out.

There was also no significant correlation between vitamin D levels and levels of immunoglobulins –whether IgA, IgM, or IgG – to E. coli or P. mirabilis.

Dr. Hitchon disclosed no relevant conflicts of interest.

VICTORIA, B.C. – Suboptimal vitamin D levels may play a role in the pathogenesis of inflammatory arthritis but not in its subsequent clinical course, judging from the findings of a study involving 264 adult patients with early disease.

Fully 77% of patients had vitamin D deficiency or insufficiency at baseline, reported lead investigator Dr. Carol A. Hitchon at the annual meeting of Canadian Rheumatology Association. But in findings that contrasted those of some earlier studies, levels were not significantly associated with disease activity at that time or with achievement of remission 1 year later.

The study also found that vitamin D levels did not correlate with levels of immunoglobulin directed against common pathogens implicated in the development of rheumatoid arthritis.

"It’s possible that vitamin D levels may not be that important in terms of clinical activity and that vitamin D status may be more important in predisposing to rheumatoid arthritis," Dr. Hitchon commented. "I don’t think vitamin D is the only answer. And I think it’s not just the level, it is probably other elements of the vitamin D pathway that might be important, in terms of how they may regulate autoimmune processes."

A session attendee wondered whether patients with inflammatory arthritis may simply have lower levels of this vitamin because they go out in the sun less.

That is a possible explanation, acknowledged Dr. Hitchon of the arthritis center at the University of Manitoba in Winnipeg. "We are hoping to measure vitamin D levels in a population that generally has more sun exposure based on where they reside, and that may give us some correlation," she added.

Accumulating data suggest that vitamin D plays a role in maintaining both tolerance and immunity to pathogens. Thus, the investigators hypothesized, "if you are deficient in vitamin D, it may lead to a break of self-tolerance and the development of autoimmunity. Similarly, deficient vitamin D can impair or alter the initial response to pathogens, leading to increased microbial load, which can also increase or affect autoimmunity," Dr. Hitchon said.

She and her colleagues studied patients from the Manitoba Early Arthritis Cohort. All of the patients had had symptoms of inflammatory arthritis for no more than 1 year, and had at least one swollen joint.

The severity of their arthritis was assessed with the DAS28-CRP (28-joint count Disease Activity Score, C-reactive protein). Circulating levels of 25-hydroxyvitamin D and antibodies to Escherichia coli and Proteus mirabilis – both of which have been implicated in rheumatoid arthritis – were measured in serum collected before the start of treatment.

The average age of the patients studied was 48 years, and 76% were women. Overall, 60% were rheumatoid factor–positive, and 49% were positive for CCP2 (cyclic citrullinated peptide, second-generation assay). Their mean DAS28-CRP score was 3.99.

Results showed that 16% of patients had vitamin D deficiency and 61% had vitamin D insufficiency, while just 23% had optimal levels. Smokers had significantly lower levels than did nonsmokers.

There was no association at baseline between vitamin D levels and rheumatoid factor or CCP2 levels, DAS28-CRP score, or several other measures of disease activity, reported Dr. Hitchon, who disclosed no relevant conflicts of interest.

In adjusted analyses, vitamin D levels were not significantly associated with DAS28-CRP score at baseline or with achievement of remission 1 year later. "As has been previously shown, the major predictor of 1-year outcome was the baseline DAS score," she noted.

During the study, 20% of patients had an improvement in their vitamin D levels, moving to a higher category, whereas 12% of patients had a worsening, moving to a lower category. "This is without any formal protocol or plan to supplement vitamin D," Dr. Hitchon pointed out.

There was also no significant correlation between vitamin D levels and levels of immunoglobulins –whether IgA, IgM, or IgG – to E. coli or P. mirabilis.

Dr. Hitchon disclosed no relevant conflicts of interest.