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TRACTISS to Study Rituximab Effects in Sjögren's Syndrome
BRIGHTON, ENGLAND – Sjögren’s syndrome may be one of the lesser known autoimmune conditions treated by rheumatologists, but research is by no means less active in trying to find novel biologic approaches to managing the often debilitating disease.
Indeed, a new study will start patient enrollment within the next few months in the United Kingdom. The multicenter TRACTISS (Trial of Anti-B-Cell Therapy in Patients With Primary Sjögren’s Syndrome) will investigate the efficacy of rituximab versus placebo in the treatment of the autoimmune connective tissue disease. The trial is planned to run for 5 years.
"Everything is falling into place to start," Dr. Simon Bowman, a principal investigator for the trial, said in an interview at the annual meeting of the British Society for Rheumatology.
Dr. Bowman, a consultant rheumatologist and honorary clinical reader at the University of Birmingham (England), added: "We’re waiting for the final ethics approval and delivery of the study drug, but the plan is to start patient recruitment in July." The aim is to recruit up to 110 patients.
According to Arthritis Research UK, which is funding the £1 million study, around half a million people in the United Kingdom have Sjögren’s syndrome.
Sjögren’s syndrome is associated with dry eyes, dry mouth, fatigue, and arthritis, Dr. Bowman explained. It can be a very disabling condition, reducing the overall quality of life of those it affects. "It can also lead to cancer of the lymph glands," he warned.
There is no cure, and current treatments for Sjögren’s target the symptoms of dry eyes and dry mouth but not always with great effect. It is hoped that, by looking at the underlying biology of the condition, which involves inflammatory cell infiltration into the salivary and lacrimal glands, more successful treatments can be developed.
"In the era of biologic therapies we should, theoretically at least, be able to devise a therapeutic approach in the glands and to ameliorate or reverse the systemic immune abnormalities," reasoned Dr. Bowman.
"The current approach is very much focused on B-cells," he added, "principally because drugs like rituximab are already available for use."
That’s not to say that a principally B-cell focused drug such as rituximab isn’t having an effect on T-cell infiltration – a predominant feature found in the salivary glands of patients with Sjögren’s syndrome.
"It’s important to bear in mind that any drug that affects the immune system will have a ripple effect, so that a drug that is normally an anti-B-cell agent will also affect the T-cells," Dr. Bowman said.
The issue is to determine if such biologic agents, regardless of whether they target B- or T-cells, could work in Sjögren’s syndrome. Already approved for use in rheumatoid arthritis and in non-Hodgkin’s lymphoma in the U.K., rituximab is backed by clinical efficacy and safety data and is, therefore, a known entity.
Although rituximab may be the "drug of the moment," Dr. Bowman noted that there were other biologic agents that could be of interest, such as belimumab, a monoclonal antibody that inhibits B-cell activation factor of the tumor necrosis factor (BAFF) or a BLyS (B-lymphocyte simulator) inhibitor.
"The [U.S. Food and Drug Administration] is currently looking at belimumab," Dr. Bowman said, adding that the National Institute for Health and Clinical Effectiveness is also considering if this agent is going to be useful for U.K. patients.
If TRACTISS is successful, then further trials will be needed for the drug’s manufacturer, Roche, to obtain a product license for Sjögren’s syndrome in the U.K. Currently, the only way for patients with Sjögren’s syndrome to receive the drug outside of a clinical trial is on a compassionate-use basis, or if they also have non-Hodgkin’s lymphoma.
TRACTISS is being funded by Arthritis Research UK. Dr. Bowman disclosed acting as consultant for Merck-Serono, Roche, and UCB.
BRIGHTON, ENGLAND – Sjögren’s syndrome may be one of the lesser known autoimmune conditions treated by rheumatologists, but research is by no means less active in trying to find novel biologic approaches to managing the often debilitating disease.
Indeed, a new study will start patient enrollment within the next few months in the United Kingdom. The multicenter TRACTISS (Trial of Anti-B-Cell Therapy in Patients With Primary Sjögren’s Syndrome) will investigate the efficacy of rituximab versus placebo in the treatment of the autoimmune connective tissue disease. The trial is planned to run for 5 years.
"Everything is falling into place to start," Dr. Simon Bowman, a principal investigator for the trial, said in an interview at the annual meeting of the British Society for Rheumatology.
Dr. Bowman, a consultant rheumatologist and honorary clinical reader at the University of Birmingham (England), added: "We’re waiting for the final ethics approval and delivery of the study drug, but the plan is to start patient recruitment in July." The aim is to recruit up to 110 patients.
According to Arthritis Research UK, which is funding the £1 million study, around half a million people in the United Kingdom have Sjögren’s syndrome.
Sjögren’s syndrome is associated with dry eyes, dry mouth, fatigue, and arthritis, Dr. Bowman explained. It can be a very disabling condition, reducing the overall quality of life of those it affects. "It can also lead to cancer of the lymph glands," he warned.
There is no cure, and current treatments for Sjögren’s target the symptoms of dry eyes and dry mouth but not always with great effect. It is hoped that, by looking at the underlying biology of the condition, which involves inflammatory cell infiltration into the salivary and lacrimal glands, more successful treatments can be developed.
"In the era of biologic therapies we should, theoretically at least, be able to devise a therapeutic approach in the glands and to ameliorate or reverse the systemic immune abnormalities," reasoned Dr. Bowman.
"The current approach is very much focused on B-cells," he added, "principally because drugs like rituximab are already available for use."
That’s not to say that a principally B-cell focused drug such as rituximab isn’t having an effect on T-cell infiltration – a predominant feature found in the salivary glands of patients with Sjögren’s syndrome.
"It’s important to bear in mind that any drug that affects the immune system will have a ripple effect, so that a drug that is normally an anti-B-cell agent will also affect the T-cells," Dr. Bowman said.
The issue is to determine if such biologic agents, regardless of whether they target B- or T-cells, could work in Sjögren’s syndrome. Already approved for use in rheumatoid arthritis and in non-Hodgkin’s lymphoma in the U.K., rituximab is backed by clinical efficacy and safety data and is, therefore, a known entity.
Although rituximab may be the "drug of the moment," Dr. Bowman noted that there were other biologic agents that could be of interest, such as belimumab, a monoclonal antibody that inhibits B-cell activation factor of the tumor necrosis factor (BAFF) or a BLyS (B-lymphocyte simulator) inhibitor.
"The [U.S. Food and Drug Administration] is currently looking at belimumab," Dr. Bowman said, adding that the National Institute for Health and Clinical Effectiveness is also considering if this agent is going to be useful for U.K. patients.
If TRACTISS is successful, then further trials will be needed for the drug’s manufacturer, Roche, to obtain a product license for Sjögren’s syndrome in the U.K. Currently, the only way for patients with Sjögren’s syndrome to receive the drug outside of a clinical trial is on a compassionate-use basis, or if they also have non-Hodgkin’s lymphoma.
TRACTISS is being funded by Arthritis Research UK. Dr. Bowman disclosed acting as consultant for Merck-Serono, Roche, and UCB.
BRIGHTON, ENGLAND – Sjögren’s syndrome may be one of the lesser known autoimmune conditions treated by rheumatologists, but research is by no means less active in trying to find novel biologic approaches to managing the often debilitating disease.
Indeed, a new study will start patient enrollment within the next few months in the United Kingdom. The multicenter TRACTISS (Trial of Anti-B-Cell Therapy in Patients With Primary Sjögren’s Syndrome) will investigate the efficacy of rituximab versus placebo in the treatment of the autoimmune connective tissue disease. The trial is planned to run for 5 years.
"Everything is falling into place to start," Dr. Simon Bowman, a principal investigator for the trial, said in an interview at the annual meeting of the British Society for Rheumatology.
Dr. Bowman, a consultant rheumatologist and honorary clinical reader at the University of Birmingham (England), added: "We’re waiting for the final ethics approval and delivery of the study drug, but the plan is to start patient recruitment in July." The aim is to recruit up to 110 patients.
According to Arthritis Research UK, which is funding the £1 million study, around half a million people in the United Kingdom have Sjögren’s syndrome.
Sjögren’s syndrome is associated with dry eyes, dry mouth, fatigue, and arthritis, Dr. Bowman explained. It can be a very disabling condition, reducing the overall quality of life of those it affects. "It can also lead to cancer of the lymph glands," he warned.
There is no cure, and current treatments for Sjögren’s target the symptoms of dry eyes and dry mouth but not always with great effect. It is hoped that, by looking at the underlying biology of the condition, which involves inflammatory cell infiltration into the salivary and lacrimal glands, more successful treatments can be developed.
"In the era of biologic therapies we should, theoretically at least, be able to devise a therapeutic approach in the glands and to ameliorate or reverse the systemic immune abnormalities," reasoned Dr. Bowman.
"The current approach is very much focused on B-cells," he added, "principally because drugs like rituximab are already available for use."
That’s not to say that a principally B-cell focused drug such as rituximab isn’t having an effect on T-cell infiltration – a predominant feature found in the salivary glands of patients with Sjögren’s syndrome.
"It’s important to bear in mind that any drug that affects the immune system will have a ripple effect, so that a drug that is normally an anti-B-cell agent will also affect the T-cells," Dr. Bowman said.
The issue is to determine if such biologic agents, regardless of whether they target B- or T-cells, could work in Sjögren’s syndrome. Already approved for use in rheumatoid arthritis and in non-Hodgkin’s lymphoma in the U.K., rituximab is backed by clinical efficacy and safety data and is, therefore, a known entity.
Although rituximab may be the "drug of the moment," Dr. Bowman noted that there were other biologic agents that could be of interest, such as belimumab, a monoclonal antibody that inhibits B-cell activation factor of the tumor necrosis factor (BAFF) or a BLyS (B-lymphocyte simulator) inhibitor.
"The [U.S. Food and Drug Administration] is currently looking at belimumab," Dr. Bowman said, adding that the National Institute for Health and Clinical Effectiveness is also considering if this agent is going to be useful for U.K. patients.
If TRACTISS is successful, then further trials will be needed for the drug’s manufacturer, Roche, to obtain a product license for Sjögren’s syndrome in the U.K. Currently, the only way for patients with Sjögren’s syndrome to receive the drug outside of a clinical trial is on a compassionate-use basis, or if they also have non-Hodgkin’s lymphoma.
TRACTISS is being funded by Arthritis Research UK. Dr. Bowman disclosed acting as consultant for Merck-Serono, Roche, and UCB.
FROM THE ANNUAL MEETING OF THE BRITISH SOCIETY FOR RHEUMATOLOGY
Major Finding: TRACTISS is expected to start patient recruitment in July 2011 and will investigate the use of rituximab vs. placebo for the treatment of Sjögren’s syndrome.
Data Source: Interview with Dr. Simon Bowman at the annual meeting of the British Society for Rheumatology (BSR).
Disclosures: The TRACTISS study is being funded by Arthritis Research UK. Dr. Bowman disclosed acting as consultant for Roche, UCB and Merck-Serono.
TRACTISS to Study Rituximab Effects in Sjögren's Syndrome
BRIGHTON, ENGLAND – Sjögren’s syndrome may be one of the lesser known autoimmune conditions treated by rheumatologists, but research is by no means less active in trying to find novel biologic approaches to managing the often debilitating disease.
Indeed, a new study will start patient enrollment within the next few months in the United Kingdom. The multicenter TRACTISS (Trial of Anti-B-Cell Therapy in Patients With Primary Sjögren’s Syndrome) will investigate the efficacy of rituximab versus placebo in the treatment of the autoimmune connective tissue disease. The trial is planned to run for 5 years.
"Everything is falling into place to start," Dr. Simon Bowman, a principal investigator for the trial, said in an interview at the annual meeting of the British Society for Rheumatology.
Dr. Bowman, a consultant rheumatologist and honorary clinical reader at the University of Birmingham (England), added: "We’re waiting for the final ethics approval and delivery of the study drug, but the plan is to start patient recruitment in July." The aim is to recruit up to 110 patients.
According to Arthritis Research UK, which is funding the £1 million study, around half a million people in the United Kingdom have Sjögren’s syndrome.
Sjögren’s syndrome is associated with dry eyes, dry mouth, fatigue, and arthritis, Dr. Bowman explained. It can be a very disabling condition, reducing the overall quality of life of those it affects. "It can also lead to cancer of the lymph glands," he warned.
There is no cure, and current treatments for Sjögren’s target the symptoms of dry eyes and dry mouth but not always with great effect. It is hoped that, by looking at the underlying biology of the condition, which involves inflammatory cell infiltration into the salivary and lacrimal glands, more successful treatments can be developed.
"In the era of biologic therapies we should, theoretically at least, be able to devise a therapeutic approach in the glands and to ameliorate or reverse the systemic immune abnormalities," reasoned Dr. Bowman.
"The current approach is very much focused on B-cells," he added, "principally because drugs like rituximab are already available for use."
That’s not to say that a principally B-cell focused drug such as rituximab isn’t having an effect on T-cell infiltration – a predominant feature found in the salivary glands of patients with Sjögren’s syndrome.
"It’s important to bear in mind that any drug that affects the immune system will have a ripple effect, so that a drug that is normally an anti-B-cell agent will also affect the T-cells," Dr. Bowman said.
The issue is to determine if such biologic agents, regardless of whether they target B- or T-cells, could work in Sjögren’s syndrome. Already approved for use in rheumatoid arthritis and in non-Hodgkin’s lymphoma in the U.K., rituximab is backed by clinical efficacy and safety data and is, therefore, a known entity.
Although rituximab may be the "drug of the moment," Dr. Bowman noted that there were other biologic agents that could be of interest, such as belimumab, a monoclonal antibody that inhibits B-cell activation factor of the tumor necrosis factor (BAFF) or a BLyS (B-lymphocyte simulator) inhibitor.
"The [U.S. Food and Drug Administration] is currently looking at belimumab," Dr. Bowman said, adding that the National Institute for Health and Clinical Effectiveness is also considering if this agent is going to be useful for U.K. patients.
If TRACTISS is successful, then further trials will be needed for the drug’s manufacturer, Roche, to obtain a product license for Sjögren’s syndrome in the U.K. Currently, the only way for patients with Sjögren’s syndrome to receive the drug outside of a clinical trial is on a compassionate-use basis, or if they also have non-Hodgkin’s lymphoma.
TRACTISS is being funded by Arthritis Research UK. Dr. Bowman disclosed acting as consultant for Merck-Serono, Roche, and UCB.
BRIGHTON, ENGLAND – Sjögren’s syndrome may be one of the lesser known autoimmune conditions treated by rheumatologists, but research is by no means less active in trying to find novel biologic approaches to managing the often debilitating disease.
Indeed, a new study will start patient enrollment within the next few months in the United Kingdom. The multicenter TRACTISS (Trial of Anti-B-Cell Therapy in Patients With Primary Sjögren’s Syndrome) will investigate the efficacy of rituximab versus placebo in the treatment of the autoimmune connective tissue disease. The trial is planned to run for 5 years.
"Everything is falling into place to start," Dr. Simon Bowman, a principal investigator for the trial, said in an interview at the annual meeting of the British Society for Rheumatology.
Dr. Bowman, a consultant rheumatologist and honorary clinical reader at the University of Birmingham (England), added: "We’re waiting for the final ethics approval and delivery of the study drug, but the plan is to start patient recruitment in July." The aim is to recruit up to 110 patients.
According to Arthritis Research UK, which is funding the £1 million study, around half a million people in the United Kingdom have Sjögren’s syndrome.
Sjögren’s syndrome is associated with dry eyes, dry mouth, fatigue, and arthritis, Dr. Bowman explained. It can be a very disabling condition, reducing the overall quality of life of those it affects. "It can also lead to cancer of the lymph glands," he warned.
There is no cure, and current treatments for Sjögren’s target the symptoms of dry eyes and dry mouth but not always with great effect. It is hoped that, by looking at the underlying biology of the condition, which involves inflammatory cell infiltration into the salivary and lacrimal glands, more successful treatments can be developed.
"In the era of biologic therapies we should, theoretically at least, be able to devise a therapeutic approach in the glands and to ameliorate or reverse the systemic immune abnormalities," reasoned Dr. Bowman.
"The current approach is very much focused on B-cells," he added, "principally because drugs like rituximab are already available for use."
That’s not to say that a principally B-cell focused drug such as rituximab isn’t having an effect on T-cell infiltration – a predominant feature found in the salivary glands of patients with Sjögren’s syndrome.
"It’s important to bear in mind that any drug that affects the immune system will have a ripple effect, so that a drug that is normally an anti-B-cell agent will also affect the T-cells," Dr. Bowman said.
The issue is to determine if such biologic agents, regardless of whether they target B- or T-cells, could work in Sjögren’s syndrome. Already approved for use in rheumatoid arthritis and in non-Hodgkin’s lymphoma in the U.K., rituximab is backed by clinical efficacy and safety data and is, therefore, a known entity.
Although rituximab may be the "drug of the moment," Dr. Bowman noted that there were other biologic agents that could be of interest, such as belimumab, a monoclonal antibody that inhibits B-cell activation factor of the tumor necrosis factor (BAFF) or a BLyS (B-lymphocyte simulator) inhibitor.
"The [U.S. Food and Drug Administration] is currently looking at belimumab," Dr. Bowman said, adding that the National Institute for Health and Clinical Effectiveness is also considering if this agent is going to be useful for U.K. patients.
If TRACTISS is successful, then further trials will be needed for the drug’s manufacturer, Roche, to obtain a product license for Sjögren’s syndrome in the U.K. Currently, the only way for patients with Sjögren’s syndrome to receive the drug outside of a clinical trial is on a compassionate-use basis, or if they also have non-Hodgkin’s lymphoma.
TRACTISS is being funded by Arthritis Research UK. Dr. Bowman disclosed acting as consultant for Merck-Serono, Roche, and UCB.
BRIGHTON, ENGLAND – Sjögren’s syndrome may be one of the lesser known autoimmune conditions treated by rheumatologists, but research is by no means less active in trying to find novel biologic approaches to managing the often debilitating disease.
Indeed, a new study will start patient enrollment within the next few months in the United Kingdom. The multicenter TRACTISS (Trial of Anti-B-Cell Therapy in Patients With Primary Sjögren’s Syndrome) will investigate the efficacy of rituximab versus placebo in the treatment of the autoimmune connective tissue disease. The trial is planned to run for 5 years.
"Everything is falling into place to start," Dr. Simon Bowman, a principal investigator for the trial, said in an interview at the annual meeting of the British Society for Rheumatology.
Dr. Bowman, a consultant rheumatologist and honorary clinical reader at the University of Birmingham (England), added: "We’re waiting for the final ethics approval and delivery of the study drug, but the plan is to start patient recruitment in July." The aim is to recruit up to 110 patients.
According to Arthritis Research UK, which is funding the £1 million study, around half a million people in the United Kingdom have Sjögren’s syndrome.
Sjögren’s syndrome is associated with dry eyes, dry mouth, fatigue, and arthritis, Dr. Bowman explained. It can be a very disabling condition, reducing the overall quality of life of those it affects. "It can also lead to cancer of the lymph glands," he warned.
There is no cure, and current treatments for Sjögren’s target the symptoms of dry eyes and dry mouth but not always with great effect. It is hoped that, by looking at the underlying biology of the condition, which involves inflammatory cell infiltration into the salivary and lacrimal glands, more successful treatments can be developed.
"In the era of biologic therapies we should, theoretically at least, be able to devise a therapeutic approach in the glands and to ameliorate or reverse the systemic immune abnormalities," reasoned Dr. Bowman.
"The current approach is very much focused on B-cells," he added, "principally because drugs like rituximab are already available for use."
That’s not to say that a principally B-cell focused drug such as rituximab isn’t having an effect on T-cell infiltration – a predominant feature found in the salivary glands of patients with Sjögren’s syndrome.
"It’s important to bear in mind that any drug that affects the immune system will have a ripple effect, so that a drug that is normally an anti-B-cell agent will also affect the T-cells," Dr. Bowman said.
The issue is to determine if such biologic agents, regardless of whether they target B- or T-cells, could work in Sjögren’s syndrome. Already approved for use in rheumatoid arthritis and in non-Hodgkin’s lymphoma in the U.K., rituximab is backed by clinical efficacy and safety data and is, therefore, a known entity.
Although rituximab may be the "drug of the moment," Dr. Bowman noted that there were other biologic agents that could be of interest, such as belimumab, a monoclonal antibody that inhibits B-cell activation factor of the tumor necrosis factor (BAFF) or a BLyS (B-lymphocyte simulator) inhibitor.
"The [U.S. Food and Drug Administration] is currently looking at belimumab," Dr. Bowman said, adding that the National Institute for Health and Clinical Effectiveness is also considering if this agent is going to be useful for U.K. patients.
If TRACTISS is successful, then further trials will be needed for the drug’s manufacturer, Roche, to obtain a product license for Sjögren’s syndrome in the U.K. Currently, the only way for patients with Sjögren’s syndrome to receive the drug outside of a clinical trial is on a compassionate-use basis, or if they also have non-Hodgkin’s lymphoma.
TRACTISS is being funded by Arthritis Research UK. Dr. Bowman disclosed acting as consultant for Merck-Serono, Roche, and UCB.
FROM THE ANNUAL MEETING OF THE BRITISH SOCIETY FOR RHEUMATOLOGY
Major Finding: TRACTISS is expected to start patient recruitment in July 2011 and will investigate the use of rituximab vs. placebo for the treatment of Sjögren’s syndrome.
Data Source: Interview with Dr. Simon Bowman at the annual meeting of the British Society for Rheumatology (BSR).
Disclosures: The TRACTISS study is being funded by Arthritis Research UK. Dr. Bowman disclosed acting as consultant for Roche, UCB and Merck-Serono.
Updated ACR/EULAR Criteria May Result in Early RA Overdiagnosis, Overtreatment
BRIGHTON, ENGLAND – Use of the 2010 classification criteria for rheumatoid arthritis that were developed jointly by the American College of Rheumatology and the European League Against Rheumatism could result in overdiagnosis and subsequent overtreatment of early disease.
Although the 2010 ACR/EULAR criteria for RA classification allow for the more rapid identification of patients early in the course of the disease, their widespread use could also mean that some people with an essentially self-limiting illness could be given unnecessary – and perhaps too aggressive – treatment.
Study findings that were presented April 12 at the annual meeting of the British Society for Rheumatology found that more than 30% of 265 patients with early synovitis were identified as having RA via the 2010 ACR/EULAR criteria only (Arthritis Rheum. 2010;62:2569-81). In comparison, around half the number of patients (17.7%) were identified using the 1987 ACR criteria (Arthritis Rheum. 1988;31:315-24) alone.
"When we look at the early, and often undifferentiated phase, of arthritis, this poses a potential dilemma to clinicians," study author Dr. Zaeem Cader of the Rheumatology Research Group at the University of Birmingham (England) commented.
"The disease of many patients will resolve without ever requiring treatment," he observed, "whilst others progress to a persistent arthritis. And within this category, some patients may convert to an established rheumatoid phenotype, with others developing a non-RA, but persistent, arthropathy."
It is within the latter group that the 1987 ACR classification criteria were originally developed, Dr. Cader explained; those criteria aimed to help differentiate RA from other rheumatologic joint conditions of several years’ duration.
In recent years, however, it has become clear that the earlier RA is treated, the better the outcome in terms of radiologic progression, which can be halted or prevented with the use of DMARDs (disease-modifying antirheumatic drugs) very early on in the course of the disease.
With this in mind, Dr. Cader and associates looked at whether the updated 2010 ACR/EULAR criteria could better identify patients within the first 3 months of symptom onset in their early RA cohort.
In all, 265 patients with clinically apparent synovial swelling in one or more joint were studied; they had a mean age of 49 years and median symptom duration of 42 days. The percentage of patients meeting 2010 criteria only at baseline was 17.4%, whereas 2.3% met ACR criteria only, 15.5% met both, 42.2% neither, and 22.6% had a clear, alternative diagnosis to RA.
After 18 months of treatment, however, reassessment of patients showed that only 6% and 7%, respectively, still met either the 2010 or 1987 criteria, with 28.8% fulfilling both sets of criteria, 29.9% fulfilling neither, and 27.9% not being diagnosed with RA.
Application of the new criteria vs. the old at baseline also detected significantly more patients who would later require methotrexate or another DMARD, but the use of the new criteria also detected significantly more patients whose disease spontaneously resolved (in both, P less than .01).
"Classification is not the same as diagnosis," Dr. Cader conceded. "However, two core goals of the new criteria were to identify patients who were at risk of progressing to persistent disease, and [to identify] patients who will require treatment with drugs such as methotrexate."
Although the authors of the 2010 criteria resisted a direct comparison, or even basing the new criteria on the old, Dr. Cader argued that this was an important comparison to make. Indeed, if the 2010 criteria are more widely used, it’s important to know if they do indeed meet the goal of more rapidly identifying patients. In addition, it might be hard to translate findings from epidemiologic and clinical research based on these old criteria.
"The early identification of patients at risk of developing RA will allow for the early institution of treatment and improved clinical outcomes," the senior author of the study Dr. Karim Raza said separately in a press statement.
Dr. Raza, a senior lecturer and honorary consultant rheumatologist at the University of Birmingham, cautioned however, that the use of the updated RA criteria could lead to the overdiagnosis and subsequent overtreatment of patients.
"The new 2010 ACR/EULAR criteria represent an important step in that direction. However, detailed testing of these criteria in other cohorts is needed to fully assess to what extent ‘overtreatment’ would be a problem if these were widely applied."
Dr. Cader stated that he had no conflicts of interest. Dr. Raza and other coauthors disclosed receiving research grants from Cellzome, UCB, and Wyeth.
BRIGHTON, ENGLAND – Use of the 2010 classification criteria for rheumatoid arthritis that were developed jointly by the American College of Rheumatology and the European League Against Rheumatism could result in overdiagnosis and subsequent overtreatment of early disease.
Although the 2010 ACR/EULAR criteria for RA classification allow for the more rapid identification of patients early in the course of the disease, their widespread use could also mean that some people with an essentially self-limiting illness could be given unnecessary – and perhaps too aggressive – treatment.
Study findings that were presented April 12 at the annual meeting of the British Society for Rheumatology found that more than 30% of 265 patients with early synovitis were identified as having RA via the 2010 ACR/EULAR criteria only (Arthritis Rheum. 2010;62:2569-81). In comparison, around half the number of patients (17.7%) were identified using the 1987 ACR criteria (Arthritis Rheum. 1988;31:315-24) alone.
"When we look at the early, and often undifferentiated phase, of arthritis, this poses a potential dilemma to clinicians," study author Dr. Zaeem Cader of the Rheumatology Research Group at the University of Birmingham (England) commented.
"The disease of many patients will resolve without ever requiring treatment," he observed, "whilst others progress to a persistent arthritis. And within this category, some patients may convert to an established rheumatoid phenotype, with others developing a non-RA, but persistent, arthropathy."
It is within the latter group that the 1987 ACR classification criteria were originally developed, Dr. Cader explained; those criteria aimed to help differentiate RA from other rheumatologic joint conditions of several years’ duration.
In recent years, however, it has become clear that the earlier RA is treated, the better the outcome in terms of radiologic progression, which can be halted or prevented with the use of DMARDs (disease-modifying antirheumatic drugs) very early on in the course of the disease.
With this in mind, Dr. Cader and associates looked at whether the updated 2010 ACR/EULAR criteria could better identify patients within the first 3 months of symptom onset in their early RA cohort.
In all, 265 patients with clinically apparent synovial swelling in one or more joint were studied; they had a mean age of 49 years and median symptom duration of 42 days. The percentage of patients meeting 2010 criteria only at baseline was 17.4%, whereas 2.3% met ACR criteria only, 15.5% met both, 42.2% neither, and 22.6% had a clear, alternative diagnosis to RA.
After 18 months of treatment, however, reassessment of patients showed that only 6% and 7%, respectively, still met either the 2010 or 1987 criteria, with 28.8% fulfilling both sets of criteria, 29.9% fulfilling neither, and 27.9% not being diagnosed with RA.
Application of the new criteria vs. the old at baseline also detected significantly more patients who would later require methotrexate or another DMARD, but the use of the new criteria also detected significantly more patients whose disease spontaneously resolved (in both, P less than .01).
"Classification is not the same as diagnosis," Dr. Cader conceded. "However, two core goals of the new criteria were to identify patients who were at risk of progressing to persistent disease, and [to identify] patients who will require treatment with drugs such as methotrexate."
Although the authors of the 2010 criteria resisted a direct comparison, or even basing the new criteria on the old, Dr. Cader argued that this was an important comparison to make. Indeed, if the 2010 criteria are more widely used, it’s important to know if they do indeed meet the goal of more rapidly identifying patients. In addition, it might be hard to translate findings from epidemiologic and clinical research based on these old criteria.
"The early identification of patients at risk of developing RA will allow for the early institution of treatment and improved clinical outcomes," the senior author of the study Dr. Karim Raza said separately in a press statement.
Dr. Raza, a senior lecturer and honorary consultant rheumatologist at the University of Birmingham, cautioned however, that the use of the updated RA criteria could lead to the overdiagnosis and subsequent overtreatment of patients.
"The new 2010 ACR/EULAR criteria represent an important step in that direction. However, detailed testing of these criteria in other cohorts is needed to fully assess to what extent ‘overtreatment’ would be a problem if these were widely applied."
Dr. Cader stated that he had no conflicts of interest. Dr. Raza and other coauthors disclosed receiving research grants from Cellzome, UCB, and Wyeth.
BRIGHTON, ENGLAND – Use of the 2010 classification criteria for rheumatoid arthritis that were developed jointly by the American College of Rheumatology and the European League Against Rheumatism could result in overdiagnosis and subsequent overtreatment of early disease.
Although the 2010 ACR/EULAR criteria for RA classification allow for the more rapid identification of patients early in the course of the disease, their widespread use could also mean that some people with an essentially self-limiting illness could be given unnecessary – and perhaps too aggressive – treatment.
Study findings that were presented April 12 at the annual meeting of the British Society for Rheumatology found that more than 30% of 265 patients with early synovitis were identified as having RA via the 2010 ACR/EULAR criteria only (Arthritis Rheum. 2010;62:2569-81). In comparison, around half the number of patients (17.7%) were identified using the 1987 ACR criteria (Arthritis Rheum. 1988;31:315-24) alone.
"When we look at the early, and often undifferentiated phase, of arthritis, this poses a potential dilemma to clinicians," study author Dr. Zaeem Cader of the Rheumatology Research Group at the University of Birmingham (England) commented.
"The disease of many patients will resolve without ever requiring treatment," he observed, "whilst others progress to a persistent arthritis. And within this category, some patients may convert to an established rheumatoid phenotype, with others developing a non-RA, but persistent, arthropathy."
It is within the latter group that the 1987 ACR classification criteria were originally developed, Dr. Cader explained; those criteria aimed to help differentiate RA from other rheumatologic joint conditions of several years’ duration.
In recent years, however, it has become clear that the earlier RA is treated, the better the outcome in terms of radiologic progression, which can be halted or prevented with the use of DMARDs (disease-modifying antirheumatic drugs) very early on in the course of the disease.
With this in mind, Dr. Cader and associates looked at whether the updated 2010 ACR/EULAR criteria could better identify patients within the first 3 months of symptom onset in their early RA cohort.
In all, 265 patients with clinically apparent synovial swelling in one or more joint were studied; they had a mean age of 49 years and median symptom duration of 42 days. The percentage of patients meeting 2010 criteria only at baseline was 17.4%, whereas 2.3% met ACR criteria only, 15.5% met both, 42.2% neither, and 22.6% had a clear, alternative diagnosis to RA.
After 18 months of treatment, however, reassessment of patients showed that only 6% and 7%, respectively, still met either the 2010 or 1987 criteria, with 28.8% fulfilling both sets of criteria, 29.9% fulfilling neither, and 27.9% not being diagnosed with RA.
Application of the new criteria vs. the old at baseline also detected significantly more patients who would later require methotrexate or another DMARD, but the use of the new criteria also detected significantly more patients whose disease spontaneously resolved (in both, P less than .01).
"Classification is not the same as diagnosis," Dr. Cader conceded. "However, two core goals of the new criteria were to identify patients who were at risk of progressing to persistent disease, and [to identify] patients who will require treatment with drugs such as methotrexate."
Although the authors of the 2010 criteria resisted a direct comparison, or even basing the new criteria on the old, Dr. Cader argued that this was an important comparison to make. Indeed, if the 2010 criteria are more widely used, it’s important to know if they do indeed meet the goal of more rapidly identifying patients. In addition, it might be hard to translate findings from epidemiologic and clinical research based on these old criteria.
"The early identification of patients at risk of developing RA will allow for the early institution of treatment and improved clinical outcomes," the senior author of the study Dr. Karim Raza said separately in a press statement.
Dr. Raza, a senior lecturer and honorary consultant rheumatologist at the University of Birmingham, cautioned however, that the use of the updated RA criteria could lead to the overdiagnosis and subsequent overtreatment of patients.
"The new 2010 ACR/EULAR criteria represent an important step in that direction. However, detailed testing of these criteria in other cohorts is needed to fully assess to what extent ‘overtreatment’ would be a problem if these were widely applied."
Dr. Cader stated that he had no conflicts of interest. Dr. Raza and other coauthors disclosed receiving research grants from Cellzome, UCB, and Wyeth.
FROM THE ANNUAL MEETING OF THE BRITISH SOCIETY FOR RHEUMATOLOGY
Major Finding: After 18 months of treatment, reassessment of patients showed that only 6% and 7%, respectively, still met either the 2010 or 1987 criteria, with 28.8% fulfilling both sets of criteria, 29.9% fulfilling neither, and 27.9% with an alternative diagnosis to RA.
Data Source: Analysis of 265 patients with synovitis seen within 3 months of symptom onset using the 2010 ACR/EULAR or the older 1987 ACR criteria.
Disclosures: Dr. Cader stated that he had no conflicts of interest. Dr. Raza and other coauthors disclosed receiving research grants from Cellzome, UCB, and Wyeth.
Updated ACR/EULAR Criteria May Result in Early RA Overdiagnosis, Overtreatment
BRIGHTON, ENGLAND – Use of the 2010 classification criteria for rheumatoid arthritis that were developed jointly by the American College of Rheumatology and the European League Against Rheumatism could result in overdiagnosis and subsequent overtreatment of early disease.
Although the 2010 ACR/EULAR criteria for RA classification allow for the more rapid identification of patients early in the course of the disease, their widespread use could also mean that some people with an essentially self-limiting illness could be given unnecessary – and perhaps too aggressive – treatment.
Study findings that were presented April 12 at the annual meeting of the British Society for Rheumatology found that more than 30% of 265 patients with early synovitis were identified as having RA via the 2010 ACR/EULAR criteria only (Arthritis Rheum. 2010;62:2569-81). In comparison, around half the number of patients (17.7%) were identified using the 1987 ACR criteria (Arthritis Rheum. 1988;31:315-24) alone.
"When we look at the early, and often undifferentiated phase, of arthritis, this poses a potential dilemma to clinicians," study author Dr. Zaeem Cader of the Rheumatology Research Group at the University of Birmingham (England) commented.
"The disease of many patients will resolve without ever requiring treatment," he observed, "whilst others progress to a persistent arthritis. And within this category, some patients may convert to an established rheumatoid phenotype, with others developing a non-RA, but persistent, arthropathy."
It is within the latter group that the 1987 ACR classification criteria were originally developed, Dr. Cader explained; those criteria aimed to help differentiate RA from other rheumatologic joint conditions of several years’ duration.
In recent years, however, it has become clear that the earlier RA is treated, the better the outcome in terms of radiologic progression, which can be halted or prevented with the use of DMARDs (disease-modifying antirheumatic drugs) very early on in the course of the disease.
With this in mind, Dr. Cader and associates looked at whether the updated 2010 ACR/EULAR criteria could better identify patients within the first 3 months of symptom onset in their early RA cohort.
In all, 265 patients with clinically apparent synovial swelling in one or more joint were studied; they had a mean age of 49 years and median symptom duration of 42 days. The percentage of patients meeting 2010 criteria only at baseline was 17.4%, whereas 2.3% met ACR criteria only, 15.5% met both, 42.2% neither, and 22.6% had a clear, alternative diagnosis to RA.
After 18 months of treatment, however, reassessment of patients showed that only 6% and 7%, respectively, still met either the 2010 or 1987 criteria, with 28.8% fulfilling both sets of criteria, 29.9% fulfilling neither, and 27.9% not being diagnosed with RA.
Application of the new criteria vs. the old at baseline also detected significantly more patients who would later require methotrexate or another DMARD, but the use of the new criteria also detected significantly more patients whose disease spontaneously resolved (in both, P less than .01).
"Classification is not the same as diagnosis," Dr. Cader conceded. "However, two core goals of the new criteria were to identify patients who were at risk of progressing to persistent disease, and [to identify] patients who will require treatment with drugs such as methotrexate."
Although the authors of the 2010 criteria resisted a direct comparison, or even basing the new criteria on the old, Dr. Cader argued that this was an important comparison to make. Indeed, if the 2010 criteria are more widely used, it’s important to know if they do indeed meet the goal of more rapidly identifying patients. In addition, it might be hard to translate findings from epidemiologic and clinical research based on these old criteria.
"The early identification of patients at risk of developing RA will allow for the early institution of treatment and improved clinical outcomes," the senior author of the study Dr. Karim Raza said separately in a press statement.
Dr. Raza, a senior lecturer and honorary consultant rheumatologist at the University of Birmingham, cautioned however, that the use of the updated RA criteria could lead to the overdiagnosis and subsequent overtreatment of patients.
"The new 2010 ACR/EULAR criteria represent an important step in that direction. However, detailed testing of these criteria in other cohorts is needed to fully assess to what extent ‘overtreatment’ would be a problem if these were widely applied."
Dr. Cader stated that he had no conflicts of interest. Dr. Raza and other coauthors disclosed receiving research grants from Cellzome, UCB, and Wyeth.
BRIGHTON, ENGLAND – Use of the 2010 classification criteria for rheumatoid arthritis that were developed jointly by the American College of Rheumatology and the European League Against Rheumatism could result in overdiagnosis and subsequent overtreatment of early disease.
Although the 2010 ACR/EULAR criteria for RA classification allow for the more rapid identification of patients early in the course of the disease, their widespread use could also mean that some people with an essentially self-limiting illness could be given unnecessary – and perhaps too aggressive – treatment.
Study findings that were presented April 12 at the annual meeting of the British Society for Rheumatology found that more than 30% of 265 patients with early synovitis were identified as having RA via the 2010 ACR/EULAR criteria only (Arthritis Rheum. 2010;62:2569-81). In comparison, around half the number of patients (17.7%) were identified using the 1987 ACR criteria (Arthritis Rheum. 1988;31:315-24) alone.
"When we look at the early, and often undifferentiated phase, of arthritis, this poses a potential dilemma to clinicians," study author Dr. Zaeem Cader of the Rheumatology Research Group at the University of Birmingham (England) commented.
"The disease of many patients will resolve without ever requiring treatment," he observed, "whilst others progress to a persistent arthritis. And within this category, some patients may convert to an established rheumatoid phenotype, with others developing a non-RA, but persistent, arthropathy."
It is within the latter group that the 1987 ACR classification criteria were originally developed, Dr. Cader explained; those criteria aimed to help differentiate RA from other rheumatologic joint conditions of several years’ duration.
In recent years, however, it has become clear that the earlier RA is treated, the better the outcome in terms of radiologic progression, which can be halted or prevented with the use of DMARDs (disease-modifying antirheumatic drugs) very early on in the course of the disease.
With this in mind, Dr. Cader and associates looked at whether the updated 2010 ACR/EULAR criteria could better identify patients within the first 3 months of symptom onset in their early RA cohort.
In all, 265 patients with clinically apparent synovial swelling in one or more joint were studied; they had a mean age of 49 years and median symptom duration of 42 days. The percentage of patients meeting 2010 criteria only at baseline was 17.4%, whereas 2.3% met ACR criteria only, 15.5% met both, 42.2% neither, and 22.6% had a clear, alternative diagnosis to RA.
After 18 months of treatment, however, reassessment of patients showed that only 6% and 7%, respectively, still met either the 2010 or 1987 criteria, with 28.8% fulfilling both sets of criteria, 29.9% fulfilling neither, and 27.9% not being diagnosed with RA.
Application of the new criteria vs. the old at baseline also detected significantly more patients who would later require methotrexate or another DMARD, but the use of the new criteria also detected significantly more patients whose disease spontaneously resolved (in both, P less than .01).
"Classification is not the same as diagnosis," Dr. Cader conceded. "However, two core goals of the new criteria were to identify patients who were at risk of progressing to persistent disease, and [to identify] patients who will require treatment with drugs such as methotrexate."
Although the authors of the 2010 criteria resisted a direct comparison, or even basing the new criteria on the old, Dr. Cader argued that this was an important comparison to make. Indeed, if the 2010 criteria are more widely used, it’s important to know if they do indeed meet the goal of more rapidly identifying patients. In addition, it might be hard to translate findings from epidemiologic and clinical research based on these old criteria.
"The early identification of patients at risk of developing RA will allow for the early institution of treatment and improved clinical outcomes," the senior author of the study Dr. Karim Raza said separately in a press statement.
Dr. Raza, a senior lecturer and honorary consultant rheumatologist at the University of Birmingham, cautioned however, that the use of the updated RA criteria could lead to the overdiagnosis and subsequent overtreatment of patients.
"The new 2010 ACR/EULAR criteria represent an important step in that direction. However, detailed testing of these criteria in other cohorts is needed to fully assess to what extent ‘overtreatment’ would be a problem if these were widely applied."
Dr. Cader stated that he had no conflicts of interest. Dr. Raza and other coauthors disclosed receiving research grants from Cellzome, UCB, and Wyeth.
BRIGHTON, ENGLAND – Use of the 2010 classification criteria for rheumatoid arthritis that were developed jointly by the American College of Rheumatology and the European League Against Rheumatism could result in overdiagnosis and subsequent overtreatment of early disease.
Although the 2010 ACR/EULAR criteria for RA classification allow for the more rapid identification of patients early in the course of the disease, their widespread use could also mean that some people with an essentially self-limiting illness could be given unnecessary – and perhaps too aggressive – treatment.
Study findings that were presented April 12 at the annual meeting of the British Society for Rheumatology found that more than 30% of 265 patients with early synovitis were identified as having RA via the 2010 ACR/EULAR criteria only (Arthritis Rheum. 2010;62:2569-81). In comparison, around half the number of patients (17.7%) were identified using the 1987 ACR criteria (Arthritis Rheum. 1988;31:315-24) alone.
"When we look at the early, and often undifferentiated phase, of arthritis, this poses a potential dilemma to clinicians," study author Dr. Zaeem Cader of the Rheumatology Research Group at the University of Birmingham (England) commented.
"The disease of many patients will resolve without ever requiring treatment," he observed, "whilst others progress to a persistent arthritis. And within this category, some patients may convert to an established rheumatoid phenotype, with others developing a non-RA, but persistent, arthropathy."
It is within the latter group that the 1987 ACR classification criteria were originally developed, Dr. Cader explained; those criteria aimed to help differentiate RA from other rheumatologic joint conditions of several years’ duration.
In recent years, however, it has become clear that the earlier RA is treated, the better the outcome in terms of radiologic progression, which can be halted or prevented with the use of DMARDs (disease-modifying antirheumatic drugs) very early on in the course of the disease.
With this in mind, Dr. Cader and associates looked at whether the updated 2010 ACR/EULAR criteria could better identify patients within the first 3 months of symptom onset in their early RA cohort.
In all, 265 patients with clinically apparent synovial swelling in one or more joint were studied; they had a mean age of 49 years and median symptom duration of 42 days. The percentage of patients meeting 2010 criteria only at baseline was 17.4%, whereas 2.3% met ACR criteria only, 15.5% met both, 42.2% neither, and 22.6% had a clear, alternative diagnosis to RA.
After 18 months of treatment, however, reassessment of patients showed that only 6% and 7%, respectively, still met either the 2010 or 1987 criteria, with 28.8% fulfilling both sets of criteria, 29.9% fulfilling neither, and 27.9% not being diagnosed with RA.
Application of the new criteria vs. the old at baseline also detected significantly more patients who would later require methotrexate or another DMARD, but the use of the new criteria also detected significantly more patients whose disease spontaneously resolved (in both, P less than .01).
"Classification is not the same as diagnosis," Dr. Cader conceded. "However, two core goals of the new criteria were to identify patients who were at risk of progressing to persistent disease, and [to identify] patients who will require treatment with drugs such as methotrexate."
Although the authors of the 2010 criteria resisted a direct comparison, or even basing the new criteria on the old, Dr. Cader argued that this was an important comparison to make. Indeed, if the 2010 criteria are more widely used, it’s important to know if they do indeed meet the goal of more rapidly identifying patients. In addition, it might be hard to translate findings from epidemiologic and clinical research based on these old criteria.
"The early identification of patients at risk of developing RA will allow for the early institution of treatment and improved clinical outcomes," the senior author of the study Dr. Karim Raza said separately in a press statement.
Dr. Raza, a senior lecturer and honorary consultant rheumatologist at the University of Birmingham, cautioned however, that the use of the updated RA criteria could lead to the overdiagnosis and subsequent overtreatment of patients.
"The new 2010 ACR/EULAR criteria represent an important step in that direction. However, detailed testing of these criteria in other cohorts is needed to fully assess to what extent ‘overtreatment’ would be a problem if these were widely applied."
Dr. Cader stated that he had no conflicts of interest. Dr. Raza and other coauthors disclosed receiving research grants from Cellzome, UCB, and Wyeth.
FROM THE ANNUAL MEETING OF THE BRITISH SOCIETY FOR RHEUMATOLOGY
Major Finding: After 18 months of treatment, reassessment of patients showed that only 6% and 7%, respectively, still met either the 2010 or 1987 criteria, with 28.8% fulfilling both sets of criteria, 29.9% fulfilling neither, and 27.9% with an alternative diagnosis to RA.
Data Source: Analysis of 265 patients with synovitis seen within 3 months of symptom onset using the 2010 ACR/EULAR or the older 1987 ACR criteria.
Disclosures: Dr. Cader stated that he had no conflicts of interest. Dr. Raza and other coauthors disclosed receiving research grants from Cellzome, UCB, and Wyeth.
Disease Activity Higher in Obese RA Patients
BRIGHTON, ENGLAND – Very obese patients with early rheumatoid arthritis appear to have higher disease activity at presentation, according to recent data presented at the annual meeting of the British Society for Rheumatology.
In a study of 216 individuals with early, clinically diagnosed rheumatoid arthritis (RA), those with a body mass index (BMI) of 35 kg/m2 or higher were more likely than those with lower BMIs to have higher 28-joint count disease activity scores (DAS28), mainly because of higher erythrocyte sedimentation rates (ESRs).
As a result, use of the DAS28 to guide clinical decision-making could result in disease-modifying antirheumatic drug (DMARD) therapy being given early on, suggested Stephanie Ling, who presented the findings.
Ms. Ling, a fifth-year medical student at the University of Liverpool, England, noted that earlier, more aggressive treatment of obese RA patients might explain why some studies have suggested that obesity, somewhat paradoxically, is actually beneficial in some patients with RA.
Indeed, studies have linked obesity with reduced mortality (Arch. Intern. Med. 2005;165:1624-9; Ann. Rheum. Dis. 2010;69:i61-4) and protection against radiographic joint damage (Ann. Rheum. Dis. 2008;67:769-74), although high levels of adiponectin – secreted from the fat tissue – are associated with increased joint inflammation (Arthritis Rheum. 2009;61:1248-56).
"Physiologically, obesity is characterized by the expansion of white adipose tissue, which is not a benign tissue," Ms. Ling explained. White adipose tissue secretes fatty acids, and its constituent cells, the adipocytes, also secrete proinflammatory proteins, or adipokines.
"Obesity can be thought of as a chronic inflammatory state," said Ms. Ling, adding that studies also indicate that "obesity could have adverse effect on RA disease activity."
In the current study, patients’ baseline disease characteristics, including DAS28 scores, rheumatoid factor status, and anti-cyclic citrullinated protein antibody status, were assessed according to BMI at presentation. All patients had early RA diagnosed by a consultant rheumatologist and had symptoms lasting for less than 1 year. The mean age of participants was 57 years and 57% of the cohort was female.
Patients were grouped according to their BMI category, as defined by World Health Organization (WHO) criteria. One-third fulfilled criteria for obesity, with approximately 22% in the obese I category (BMI more than 30 kg/m2 but less than 35 kg/m2) and just over 11% in the obese II–III category (BMI of more than 35 kg/m2). One-third of patients were overweight and the remaining third were either normal weight or underweight.
Results showed that obese II–III patients were more likely to present with elevated (5.1 or higher) DAS28 scores than their lighter counterparts. Odds ratios (OR) adjusted for age, gender, and smoking status were 4.1 for DAS28 and 3.67 for ESR when comparing the very obese patients with the other BMI groups.
Considering each component of the DAS28 separately, a high ESR (32 mm/h or more) was the main factor that appeared to be significantly higher as body weight increased. There was no association with tender or swollen joint counts, global visual analog scale, symptom duration, or rheumatoid factor/anti-cyclic citrullinated protein antibody status, Ms. Ling said.
"There is a need for well-designed longitudinal studies to examine the effect of obesity on the extent of RA disease progression," she suggested.
Ms. Ling reported no conflicts of interest.
disease-modifying antirheumatic drug, DMARD,
BRIGHTON, ENGLAND – Very obese patients with early rheumatoid arthritis appear to have higher disease activity at presentation, according to recent data presented at the annual meeting of the British Society for Rheumatology.
In a study of 216 individuals with early, clinically diagnosed rheumatoid arthritis (RA), those with a body mass index (BMI) of 35 kg/m2 or higher were more likely than those with lower BMIs to have higher 28-joint count disease activity scores (DAS28), mainly because of higher erythrocyte sedimentation rates (ESRs).
As a result, use of the DAS28 to guide clinical decision-making could result in disease-modifying antirheumatic drug (DMARD) therapy being given early on, suggested Stephanie Ling, who presented the findings.
Ms. Ling, a fifth-year medical student at the University of Liverpool, England, noted that earlier, more aggressive treatment of obese RA patients might explain why some studies have suggested that obesity, somewhat paradoxically, is actually beneficial in some patients with RA.
Indeed, studies have linked obesity with reduced mortality (Arch. Intern. Med. 2005;165:1624-9; Ann. Rheum. Dis. 2010;69:i61-4) and protection against radiographic joint damage (Ann. Rheum. Dis. 2008;67:769-74), although high levels of adiponectin – secreted from the fat tissue – are associated with increased joint inflammation (Arthritis Rheum. 2009;61:1248-56).
"Physiologically, obesity is characterized by the expansion of white adipose tissue, which is not a benign tissue," Ms. Ling explained. White adipose tissue secretes fatty acids, and its constituent cells, the adipocytes, also secrete proinflammatory proteins, or adipokines.
"Obesity can be thought of as a chronic inflammatory state," said Ms. Ling, adding that studies also indicate that "obesity could have adverse effect on RA disease activity."
In the current study, patients’ baseline disease characteristics, including DAS28 scores, rheumatoid factor status, and anti-cyclic citrullinated protein antibody status, were assessed according to BMI at presentation. All patients had early RA diagnosed by a consultant rheumatologist and had symptoms lasting for less than 1 year. The mean age of participants was 57 years and 57% of the cohort was female.
Patients were grouped according to their BMI category, as defined by World Health Organization (WHO) criteria. One-third fulfilled criteria for obesity, with approximately 22% in the obese I category (BMI more than 30 kg/m2 but less than 35 kg/m2) and just over 11% in the obese II–III category (BMI of more than 35 kg/m2). One-third of patients were overweight and the remaining third were either normal weight or underweight.
Results showed that obese II–III patients were more likely to present with elevated (5.1 or higher) DAS28 scores than their lighter counterparts. Odds ratios (OR) adjusted for age, gender, and smoking status were 4.1 for DAS28 and 3.67 for ESR when comparing the very obese patients with the other BMI groups.
Considering each component of the DAS28 separately, a high ESR (32 mm/h or more) was the main factor that appeared to be significantly higher as body weight increased. There was no association with tender or swollen joint counts, global visual analog scale, symptom duration, or rheumatoid factor/anti-cyclic citrullinated protein antibody status, Ms. Ling said.
"There is a need for well-designed longitudinal studies to examine the effect of obesity on the extent of RA disease progression," she suggested.
Ms. Ling reported no conflicts of interest.
BRIGHTON, ENGLAND – Very obese patients with early rheumatoid arthritis appear to have higher disease activity at presentation, according to recent data presented at the annual meeting of the British Society for Rheumatology.
In a study of 216 individuals with early, clinically diagnosed rheumatoid arthritis (RA), those with a body mass index (BMI) of 35 kg/m2 or higher were more likely than those with lower BMIs to have higher 28-joint count disease activity scores (DAS28), mainly because of higher erythrocyte sedimentation rates (ESRs).
As a result, use of the DAS28 to guide clinical decision-making could result in disease-modifying antirheumatic drug (DMARD) therapy being given early on, suggested Stephanie Ling, who presented the findings.
Ms. Ling, a fifth-year medical student at the University of Liverpool, England, noted that earlier, more aggressive treatment of obese RA patients might explain why some studies have suggested that obesity, somewhat paradoxically, is actually beneficial in some patients with RA.
Indeed, studies have linked obesity with reduced mortality (Arch. Intern. Med. 2005;165:1624-9; Ann. Rheum. Dis. 2010;69:i61-4) and protection against radiographic joint damage (Ann. Rheum. Dis. 2008;67:769-74), although high levels of adiponectin – secreted from the fat tissue – are associated with increased joint inflammation (Arthritis Rheum. 2009;61:1248-56).
"Physiologically, obesity is characterized by the expansion of white adipose tissue, which is not a benign tissue," Ms. Ling explained. White adipose tissue secretes fatty acids, and its constituent cells, the adipocytes, also secrete proinflammatory proteins, or adipokines.
"Obesity can be thought of as a chronic inflammatory state," said Ms. Ling, adding that studies also indicate that "obesity could have adverse effect on RA disease activity."
In the current study, patients’ baseline disease characteristics, including DAS28 scores, rheumatoid factor status, and anti-cyclic citrullinated protein antibody status, were assessed according to BMI at presentation. All patients had early RA diagnosed by a consultant rheumatologist and had symptoms lasting for less than 1 year. The mean age of participants was 57 years and 57% of the cohort was female.
Patients were grouped according to their BMI category, as defined by World Health Organization (WHO) criteria. One-third fulfilled criteria for obesity, with approximately 22% in the obese I category (BMI more than 30 kg/m2 but less than 35 kg/m2) and just over 11% in the obese II–III category (BMI of more than 35 kg/m2). One-third of patients were overweight and the remaining third were either normal weight or underweight.
Results showed that obese II–III patients were more likely to present with elevated (5.1 or higher) DAS28 scores than their lighter counterparts. Odds ratios (OR) adjusted for age, gender, and smoking status were 4.1 for DAS28 and 3.67 for ESR when comparing the very obese patients with the other BMI groups.
Considering each component of the DAS28 separately, a high ESR (32 mm/h or more) was the main factor that appeared to be significantly higher as body weight increased. There was no association with tender or swollen joint counts, global visual analog scale, symptom duration, or rheumatoid factor/anti-cyclic citrullinated protein antibody status, Ms. Ling said.
"There is a need for well-designed longitudinal studies to examine the effect of obesity on the extent of RA disease progression," she suggested.
Ms. Ling reported no conflicts of interest.
disease-modifying antirheumatic drug, DMARD,
disease-modifying antirheumatic drug, DMARD,
FROM THE ANNUAL MEETING OF THE BRITISH SOCIETY FOR RHEUMATOLOGY
Major Finding: Odds ratios (OR), adjusted for age, gender, and smoking status, were 4.1 for DAS28 and 3.67 for ESR comparing the baseline values very obese patients with the other BMI groups.
Data Source: Study of 216 patients with clinically diagnosed early rheumatoid arthritis, with symptom duration of less than 1 year.
Disclosures: Ms. Ling had no conflicts of interest.
Disease Activity Higher in Obese RA Patients
BRIGHTON, ENGLAND – Very obese patients with early rheumatoid arthritis appear to have higher disease activity at presentation, according to recent data presented at the annual meeting of the British Society for Rheumatology.
In a study of 216 individuals with early, clinically diagnosed rheumatoid arthritis (RA), those with a body mass index (BMI) of 35 kg/m2 or higher were more likely than those with lower BMIs to have higher 28-joint count disease activity scores (DAS28), mainly because of higher erythrocyte sedimentation rates (ESRs).
As a result, use of the DAS28 to guide clinical decision-making could result in disease-modifying antirheumatic drug (DMARD) therapy being given early on, suggested Stephanie Ling, who presented the findings.
Ms. Ling, a fifth-year medical student at the University of Liverpool, England, noted that earlier, more aggressive treatment of obese RA patients might explain why some studies have suggested that obesity, somewhat paradoxically, is actually beneficial in some patients with RA.
Indeed, studies have linked obesity with reduced mortality (Arch. Intern. Med. 2005;165:1624-9; Ann. Rheum. Dis. 2010;69:i61-4) and protection against radiographic joint damage (Ann. Rheum. Dis. 2008;67:769-74), although high levels of adiponectin – secreted from the fat tissue – are associated with increased joint inflammation (Arthritis Rheum. 2009;61:1248-56).
"Physiologically, obesity is characterized by the expansion of white adipose tissue, which is not a benign tissue," Ms. Ling explained. White adipose tissue secretes fatty acids, and its constituent cells, the adipocytes, also secrete proinflammatory proteins, or adipokines.
"Obesity can be thought of as a chronic inflammatory state," said Ms. Ling, adding that studies also indicate that "obesity could have adverse effect on RA disease activity."
In the current study, patients’ baseline disease characteristics, including DAS28 scores, rheumatoid factor status, and anti-cyclic citrullinated protein antibody status, were assessed according to BMI at presentation. All patients had early RA diagnosed by a consultant rheumatologist and had symptoms lasting for less than 1 year. The mean age of participants was 57 years and 57% of the cohort was female.
Patients were grouped according to their BMI category, as defined by World Health Organization (WHO) criteria. One-third fulfilled criteria for obesity, with approximately 22% in the obese I category (BMI more than 30 kg/m2 but less than 35 kg/m2) and just over 11% in the obese II–III category (BMI of more than 35 kg/m2). One-third of patients were overweight and the remaining third were either normal weight or underweight.
Results showed that obese II–III patients were more likely to present with elevated (5.1 or higher) DAS28 scores than their lighter counterparts. Odds ratios (OR) adjusted for age, gender, and smoking status were 4.1 for DAS28 and 3.67 for ESR when comparing the very obese patients with the other BMI groups.
Considering each component of the DAS28 separately, a high ESR (32 mm/h or more) was the main factor that appeared to be significantly higher as body weight increased. There was no association with tender or swollen joint counts, global visual analog scale, symptom duration, or rheumatoid factor/anti-cyclic citrullinated protein antibody status, Ms. Ling said.
"There is a need for well-designed longitudinal studies to examine the effect of obesity on the extent of RA disease progression," she suggested.
Ms. Ling reported no conflicts of interest.
disease-modifying antirheumatic drug, DMARD,
BRIGHTON, ENGLAND – Very obese patients with early rheumatoid arthritis appear to have higher disease activity at presentation, according to recent data presented at the annual meeting of the British Society for Rheumatology.
In a study of 216 individuals with early, clinically diagnosed rheumatoid arthritis (RA), those with a body mass index (BMI) of 35 kg/m2 or higher were more likely than those with lower BMIs to have higher 28-joint count disease activity scores (DAS28), mainly because of higher erythrocyte sedimentation rates (ESRs).
As a result, use of the DAS28 to guide clinical decision-making could result in disease-modifying antirheumatic drug (DMARD) therapy being given early on, suggested Stephanie Ling, who presented the findings.
Ms. Ling, a fifth-year medical student at the University of Liverpool, England, noted that earlier, more aggressive treatment of obese RA patients might explain why some studies have suggested that obesity, somewhat paradoxically, is actually beneficial in some patients with RA.
Indeed, studies have linked obesity with reduced mortality (Arch. Intern. Med. 2005;165:1624-9; Ann. Rheum. Dis. 2010;69:i61-4) and protection against radiographic joint damage (Ann. Rheum. Dis. 2008;67:769-74), although high levels of adiponectin – secreted from the fat tissue – are associated with increased joint inflammation (Arthritis Rheum. 2009;61:1248-56).
"Physiologically, obesity is characterized by the expansion of white adipose tissue, which is not a benign tissue," Ms. Ling explained. White adipose tissue secretes fatty acids, and its constituent cells, the adipocytes, also secrete proinflammatory proteins, or adipokines.
"Obesity can be thought of as a chronic inflammatory state," said Ms. Ling, adding that studies also indicate that "obesity could have adverse effect on RA disease activity."
In the current study, patients’ baseline disease characteristics, including DAS28 scores, rheumatoid factor status, and anti-cyclic citrullinated protein antibody status, were assessed according to BMI at presentation. All patients had early RA diagnosed by a consultant rheumatologist and had symptoms lasting for less than 1 year. The mean age of participants was 57 years and 57% of the cohort was female.
Patients were grouped according to their BMI category, as defined by World Health Organization (WHO) criteria. One-third fulfilled criteria for obesity, with approximately 22% in the obese I category (BMI more than 30 kg/m2 but less than 35 kg/m2) and just over 11% in the obese II–III category (BMI of more than 35 kg/m2). One-third of patients were overweight and the remaining third were either normal weight or underweight.
Results showed that obese II–III patients were more likely to present with elevated (5.1 or higher) DAS28 scores than their lighter counterparts. Odds ratios (OR) adjusted for age, gender, and smoking status were 4.1 for DAS28 and 3.67 for ESR when comparing the very obese patients with the other BMI groups.
Considering each component of the DAS28 separately, a high ESR (32 mm/h or more) was the main factor that appeared to be significantly higher as body weight increased. There was no association with tender or swollen joint counts, global visual analog scale, symptom duration, or rheumatoid factor/anti-cyclic citrullinated protein antibody status, Ms. Ling said.
"There is a need for well-designed longitudinal studies to examine the effect of obesity on the extent of RA disease progression," she suggested.
Ms. Ling reported no conflicts of interest.
BRIGHTON, ENGLAND – Very obese patients with early rheumatoid arthritis appear to have higher disease activity at presentation, according to recent data presented at the annual meeting of the British Society for Rheumatology.
In a study of 216 individuals with early, clinically diagnosed rheumatoid arthritis (RA), those with a body mass index (BMI) of 35 kg/m2 or higher were more likely than those with lower BMIs to have higher 28-joint count disease activity scores (DAS28), mainly because of higher erythrocyte sedimentation rates (ESRs).
As a result, use of the DAS28 to guide clinical decision-making could result in disease-modifying antirheumatic drug (DMARD) therapy being given early on, suggested Stephanie Ling, who presented the findings.
Ms. Ling, a fifth-year medical student at the University of Liverpool, England, noted that earlier, more aggressive treatment of obese RA patients might explain why some studies have suggested that obesity, somewhat paradoxically, is actually beneficial in some patients with RA.
Indeed, studies have linked obesity with reduced mortality (Arch. Intern. Med. 2005;165:1624-9; Ann. Rheum. Dis. 2010;69:i61-4) and protection against radiographic joint damage (Ann. Rheum. Dis. 2008;67:769-74), although high levels of adiponectin – secreted from the fat tissue – are associated with increased joint inflammation (Arthritis Rheum. 2009;61:1248-56).
"Physiologically, obesity is characterized by the expansion of white adipose tissue, which is not a benign tissue," Ms. Ling explained. White adipose tissue secretes fatty acids, and its constituent cells, the adipocytes, also secrete proinflammatory proteins, or adipokines.
"Obesity can be thought of as a chronic inflammatory state," said Ms. Ling, adding that studies also indicate that "obesity could have adverse effect on RA disease activity."
In the current study, patients’ baseline disease characteristics, including DAS28 scores, rheumatoid factor status, and anti-cyclic citrullinated protein antibody status, were assessed according to BMI at presentation. All patients had early RA diagnosed by a consultant rheumatologist and had symptoms lasting for less than 1 year. The mean age of participants was 57 years and 57% of the cohort was female.
Patients were grouped according to their BMI category, as defined by World Health Organization (WHO) criteria. One-third fulfilled criteria for obesity, with approximately 22% in the obese I category (BMI more than 30 kg/m2 but less than 35 kg/m2) and just over 11% in the obese II–III category (BMI of more than 35 kg/m2). One-third of patients were overweight and the remaining third were either normal weight or underweight.
Results showed that obese II–III patients were more likely to present with elevated (5.1 or higher) DAS28 scores than their lighter counterparts. Odds ratios (OR) adjusted for age, gender, and smoking status were 4.1 for DAS28 and 3.67 for ESR when comparing the very obese patients with the other BMI groups.
Considering each component of the DAS28 separately, a high ESR (32 mm/h or more) was the main factor that appeared to be significantly higher as body weight increased. There was no association with tender or swollen joint counts, global visual analog scale, symptom duration, or rheumatoid factor/anti-cyclic citrullinated protein antibody status, Ms. Ling said.
"There is a need for well-designed longitudinal studies to examine the effect of obesity on the extent of RA disease progression," she suggested.
Ms. Ling reported no conflicts of interest.
disease-modifying antirheumatic drug, DMARD,
disease-modifying antirheumatic drug, DMARD,
FROM THE ANNUAL MEETING OF THE BRITISH SOCIETY FOR RHEUMATOLOGY
Major Finding: Odds ratios (OR), adjusted for age, gender, and smoking status, were 4.1 for DAS28 and 3.67 for ESR comparing the baseline values very obese patients with the other BMI groups.
Data Source: Study of 216 patients with clinically diagnosed early rheumatoid arthritis, with symptom duration of less than 1 year.
Disclosures: Ms. Ling had no conflicts of interest.
Adults With JIA Fail to Get Needed Biologics
BRIGHTON, ENGLAND – The use of biologic agents in adults with juvenile idiopathic arthritis needs guidance, a situation that the British Society for Rheumatology and British Society for Pediatric and Adolescent Rheumatology are set to address.
The two British Societies will publish a statement on the use of biologics in adults with juvenile idiopathic arthritis (JIA) very soon, said Dr. Helen Foster at the annual meeting of the British Society for Rheumatology (BSR).
Dr. Foster, professor of pediatric rheumatology at Newcastle University, England, commented that the current use of biologics in adult JIA patients is based on a paucity of data, with only one biologic agent, etanercept, currently approved for use by the National Institute for Health and Clinical Excellence (NICE).
"Clearly adults with JIA are receiving biologic treatments, and data so far, albeit from registries, are actually quite encouraging of a good response," Dr. Foster said.
Indeed, data from the BSR Biologics Register (BSRBR) show that of 495 patients registered in adulthood one third had disease onset reported before the age of 16 years, with one fifth (21%) officially diagnosed with JIA. Importantly, Dr. Foster noted that these data showed that disease flares were still possible after many years of remission, at a median of 20 years for de novo biologic use.
Last year, NICE issued guidance link to on how to improve commissioning of biologic drugs to treat inflammatory diseases in the United Kingdom. In the report, the estimated need for biologic agents in adults who had JIA was just 15% – a likely underestimate, Dr. Foster suggested.
"Undoubtedly, the proportion of patients with JIA who reach adulthood and who will require either ongoing treatment with a biologic agent or de novo treatment for disease flares is going to increase," she observed.
However, despite the need for continued or first-time biologic use in adults with JIA, these patients often fall into a gap between pediatric and adult care. Anecdotal evidence suggests that funding for treatment might be withdrawn when a JIA patient reaches 18 years of age and that if continued treatment is needed, a new application for funding must be made to adult services.
With this in mind, better links between juvenile and adult rheumatology services are sorely needed. The new BSR/British Society for Paediatric and Adolescent Rheumatology (BSPAR) statement will note that patients transferring to adult care are likely to need continued treatment with a biologic agent and that treatment should not be stopped solely on the basis of age. The process of ongoing funding needs to be in place before transfer, Dr. Foster said.
The BSR/BSPAR statement will also comment on eligibility for biologic agents, noting that appropriate tools for adults with JIA are specifically needed. Currently, the only guidance on use of biologics in JIA is for etanercept in the pediatric population and, clearly, adults with JIA are a distinct patient population.
"The management of JIA has changed dramatically in the last decade, and it’s going to change again towards a more individualized approach in the future," Dr. Foster said. She added that the choice of biologic is very much down to a variety of factors – clinician’s experience, patient choice, and clinical scenario, but that there is an obvious need for consensus on which agent or agents to use.
There is also a need for improved surveillance, and existing juvenile and adult biologics registries provide important information about the long-term safety of these agents, and these need to be linked up, both in the United Kingdom and in Europe.
"Optimal care requires adult rheumatologists who have experience or training in adolescent rheumatology," Dr. Foster further advised. Adults with JIA have multiple and often complex issues, she added, and these need to be addressed by appropriately trained staff.
Dr. Foster has received honoraria from Abbott, Pfizer, and Schering-Plough.
BRIGHTON, ENGLAND – The use of biologic agents in adults with juvenile idiopathic arthritis needs guidance, a situation that the British Society for Rheumatology and British Society for Pediatric and Adolescent Rheumatology are set to address.
The two British Societies will publish a statement on the use of biologics in adults with juvenile idiopathic arthritis (JIA) very soon, said Dr. Helen Foster at the annual meeting of the British Society for Rheumatology (BSR).
Dr. Foster, professor of pediatric rheumatology at Newcastle University, England, commented that the current use of biologics in adult JIA patients is based on a paucity of data, with only one biologic agent, etanercept, currently approved for use by the National Institute for Health and Clinical Excellence (NICE).
"Clearly adults with JIA are receiving biologic treatments, and data so far, albeit from registries, are actually quite encouraging of a good response," Dr. Foster said.
Indeed, data from the BSR Biologics Register (BSRBR) show that of 495 patients registered in adulthood one third had disease onset reported before the age of 16 years, with one fifth (21%) officially diagnosed with JIA. Importantly, Dr. Foster noted that these data showed that disease flares were still possible after many years of remission, at a median of 20 years for de novo biologic use.
Last year, NICE issued guidance link to on how to improve commissioning of biologic drugs to treat inflammatory diseases in the United Kingdom. In the report, the estimated need for biologic agents in adults who had JIA was just 15% – a likely underestimate, Dr. Foster suggested.
"Undoubtedly, the proportion of patients with JIA who reach adulthood and who will require either ongoing treatment with a biologic agent or de novo treatment for disease flares is going to increase," she observed.
However, despite the need for continued or first-time biologic use in adults with JIA, these patients often fall into a gap between pediatric and adult care. Anecdotal evidence suggests that funding for treatment might be withdrawn when a JIA patient reaches 18 years of age and that if continued treatment is needed, a new application for funding must be made to adult services.
With this in mind, better links between juvenile and adult rheumatology services are sorely needed. The new BSR/British Society for Paediatric and Adolescent Rheumatology (BSPAR) statement will note that patients transferring to adult care are likely to need continued treatment with a biologic agent and that treatment should not be stopped solely on the basis of age. The process of ongoing funding needs to be in place before transfer, Dr. Foster said.
The BSR/BSPAR statement will also comment on eligibility for biologic agents, noting that appropriate tools for adults with JIA are specifically needed. Currently, the only guidance on use of biologics in JIA is for etanercept in the pediatric population and, clearly, adults with JIA are a distinct patient population.
"The management of JIA has changed dramatically in the last decade, and it’s going to change again towards a more individualized approach in the future," Dr. Foster said. She added that the choice of biologic is very much down to a variety of factors – clinician’s experience, patient choice, and clinical scenario, but that there is an obvious need for consensus on which agent or agents to use.
There is also a need for improved surveillance, and existing juvenile and adult biologics registries provide important information about the long-term safety of these agents, and these need to be linked up, both in the United Kingdom and in Europe.
"Optimal care requires adult rheumatologists who have experience or training in adolescent rheumatology," Dr. Foster further advised. Adults with JIA have multiple and often complex issues, she added, and these need to be addressed by appropriately trained staff.
Dr. Foster has received honoraria from Abbott, Pfizer, and Schering-Plough.
BRIGHTON, ENGLAND – The use of biologic agents in adults with juvenile idiopathic arthritis needs guidance, a situation that the British Society for Rheumatology and British Society for Pediatric and Adolescent Rheumatology are set to address.
The two British Societies will publish a statement on the use of biologics in adults with juvenile idiopathic arthritis (JIA) very soon, said Dr. Helen Foster at the annual meeting of the British Society for Rheumatology (BSR).
Dr. Foster, professor of pediatric rheumatology at Newcastle University, England, commented that the current use of biologics in adult JIA patients is based on a paucity of data, with only one biologic agent, etanercept, currently approved for use by the National Institute for Health and Clinical Excellence (NICE).
"Clearly adults with JIA are receiving biologic treatments, and data so far, albeit from registries, are actually quite encouraging of a good response," Dr. Foster said.
Indeed, data from the BSR Biologics Register (BSRBR) show that of 495 patients registered in adulthood one third had disease onset reported before the age of 16 years, with one fifth (21%) officially diagnosed with JIA. Importantly, Dr. Foster noted that these data showed that disease flares were still possible after many years of remission, at a median of 20 years for de novo biologic use.
Last year, NICE issued guidance link to on how to improve commissioning of biologic drugs to treat inflammatory diseases in the United Kingdom. In the report, the estimated need for biologic agents in adults who had JIA was just 15% – a likely underestimate, Dr. Foster suggested.
"Undoubtedly, the proportion of patients with JIA who reach adulthood and who will require either ongoing treatment with a biologic agent or de novo treatment for disease flares is going to increase," she observed.
However, despite the need for continued or first-time biologic use in adults with JIA, these patients often fall into a gap between pediatric and adult care. Anecdotal evidence suggests that funding for treatment might be withdrawn when a JIA patient reaches 18 years of age and that if continued treatment is needed, a new application for funding must be made to adult services.
With this in mind, better links between juvenile and adult rheumatology services are sorely needed. The new BSR/British Society for Paediatric and Adolescent Rheumatology (BSPAR) statement will note that patients transferring to adult care are likely to need continued treatment with a biologic agent and that treatment should not be stopped solely on the basis of age. The process of ongoing funding needs to be in place before transfer, Dr. Foster said.
The BSR/BSPAR statement will also comment on eligibility for biologic agents, noting that appropriate tools for adults with JIA are specifically needed. Currently, the only guidance on use of biologics in JIA is for etanercept in the pediatric population and, clearly, adults with JIA are a distinct patient population.
"The management of JIA has changed dramatically in the last decade, and it’s going to change again towards a more individualized approach in the future," Dr. Foster said. She added that the choice of biologic is very much down to a variety of factors – clinician’s experience, patient choice, and clinical scenario, but that there is an obvious need for consensus on which agent or agents to use.
There is also a need for improved surveillance, and existing juvenile and adult biologics registries provide important information about the long-term safety of these agents, and these need to be linked up, both in the United Kingdom and in Europe.
"Optimal care requires adult rheumatologists who have experience or training in adolescent rheumatology," Dr. Foster further advised. Adults with JIA have multiple and often complex issues, she added, and these need to be addressed by appropriately trained staff.
Dr. Foster has received honoraria from Abbott, Pfizer, and Schering-Plough.
FROM THE ANNUAL MEETING OF THE BRITISH SOCIETY FOR RHEUMATOLOGY
Adults With JIA Fail to Get Needed Biologics
BRIGHTON, ENGLAND – The use of biologic agents in adults with juvenile idiopathic arthritis needs guidance, a situation that the British Society for Rheumatology and British Society for Pediatric and Adolescent Rheumatology are set to address.
The two British Societies will publish a statement on the use of biologics in adults with juvenile idiopathic arthritis (JIA) very soon, said Dr. Helen Foster at the annual meeting of the British Society for Rheumatology (BSR).
Dr. Foster, professor of pediatric rheumatology at Newcastle University, England, commented that the current use of biologics in adult JIA patients is based on a paucity of data, with only one biologic agent, etanercept, currently approved for use by the National Institute for Health and Clinical Excellence (NICE).
"Clearly adults with JIA are receiving biologic treatments, and data so far, albeit from registries, are actually quite encouraging of a good response," Dr. Foster said.
Indeed, data from the BSR Biologics Register (BSRBR) show that of 495 patients registered in adulthood one third had disease onset reported before the age of 16 years, with one fifth (21%) officially diagnosed with JIA. Importantly, Dr. Foster noted that these data showed that disease flares were still possible after many years of remission, at a median of 20 years for de novo biologic use.
Last year, NICE issued guidance link to on how to improve commissioning of biologic drugs to treat inflammatory diseases in the United Kingdom. In the report, the estimated need for biologic agents in adults who had JIA was just 15% – a likely underestimate, Dr. Foster suggested.
"Undoubtedly, the proportion of patients with JIA who reach adulthood and who will require either ongoing treatment with a biologic agent or de novo treatment for disease flares is going to increase," she observed.
However, despite the need for continued or first-time biologic use in adults with JIA, these patients often fall into a gap between pediatric and adult care. Anecdotal evidence suggests that funding for treatment might be withdrawn when a JIA patient reaches 18 years of age and that if continued treatment is needed, a new application for funding must be made to adult services.
With this in mind, better links between juvenile and adult rheumatology services are sorely needed. The new BSR/British Society for Paediatric and Adolescent Rheumatology (BSPAR) statement will note that patients transferring to adult care are likely to need continued treatment with a biologic agent and that treatment should not be stopped solely on the basis of age. The process of ongoing funding needs to be in place before transfer, Dr. Foster said.
The BSR/BSPAR statement will also comment on eligibility for biologic agents, noting that appropriate tools for adults with JIA are specifically needed. Currently, the only guidance on use of biologics in JIA is for etanercept in the pediatric population and, clearly, adults with JIA are a distinct patient population.
"The management of JIA has changed dramatically in the last decade, and it’s going to change again towards a more individualized approach in the future," Dr. Foster said. She added that the choice of biologic is very much down to a variety of factors – clinician’s experience, patient choice, and clinical scenario, but that there is an obvious need for consensus on which agent or agents to use.
There is also a need for improved surveillance, and existing juvenile and adult biologics registries provide important information about the long-term safety of these agents, and these need to be linked up, both in the United Kingdom and in Europe.
"Optimal care requires adult rheumatologists who have experience or training in adolescent rheumatology," Dr. Foster further advised. Adults with JIA have multiple and often complex issues, she added, and these need to be addressed by appropriately trained staff.
Dr. Foster has received honoraria from Abbott, Pfizer, and Schering-Plough.
BRIGHTON, ENGLAND – The use of biologic agents in adults with juvenile idiopathic arthritis needs guidance, a situation that the British Society for Rheumatology and British Society for Pediatric and Adolescent Rheumatology are set to address.
The two British Societies will publish a statement on the use of biologics in adults with juvenile idiopathic arthritis (JIA) very soon, said Dr. Helen Foster at the annual meeting of the British Society for Rheumatology (BSR).
Dr. Foster, professor of pediatric rheumatology at Newcastle University, England, commented that the current use of biologics in adult JIA patients is based on a paucity of data, with only one biologic agent, etanercept, currently approved for use by the National Institute for Health and Clinical Excellence (NICE).
"Clearly adults with JIA are receiving biologic treatments, and data so far, albeit from registries, are actually quite encouraging of a good response," Dr. Foster said.
Indeed, data from the BSR Biologics Register (BSRBR) show that of 495 patients registered in adulthood one third had disease onset reported before the age of 16 years, with one fifth (21%) officially diagnosed with JIA. Importantly, Dr. Foster noted that these data showed that disease flares were still possible after many years of remission, at a median of 20 years for de novo biologic use.
Last year, NICE issued guidance link to on how to improve commissioning of biologic drugs to treat inflammatory diseases in the United Kingdom. In the report, the estimated need for biologic agents in adults who had JIA was just 15% – a likely underestimate, Dr. Foster suggested.
"Undoubtedly, the proportion of patients with JIA who reach adulthood and who will require either ongoing treatment with a biologic agent or de novo treatment for disease flares is going to increase," she observed.
However, despite the need for continued or first-time biologic use in adults with JIA, these patients often fall into a gap between pediatric and adult care. Anecdotal evidence suggests that funding for treatment might be withdrawn when a JIA patient reaches 18 years of age and that if continued treatment is needed, a new application for funding must be made to adult services.
With this in mind, better links between juvenile and adult rheumatology services are sorely needed. The new BSR/British Society for Paediatric and Adolescent Rheumatology (BSPAR) statement will note that patients transferring to adult care are likely to need continued treatment with a biologic agent and that treatment should not be stopped solely on the basis of age. The process of ongoing funding needs to be in place before transfer, Dr. Foster said.
The BSR/BSPAR statement will also comment on eligibility for biologic agents, noting that appropriate tools for adults with JIA are specifically needed. Currently, the only guidance on use of biologics in JIA is for etanercept in the pediatric population and, clearly, adults with JIA are a distinct patient population.
"The management of JIA has changed dramatically in the last decade, and it’s going to change again towards a more individualized approach in the future," Dr. Foster said. She added that the choice of biologic is very much down to a variety of factors – clinician’s experience, patient choice, and clinical scenario, but that there is an obvious need for consensus on which agent or agents to use.
There is also a need for improved surveillance, and existing juvenile and adult biologics registries provide important information about the long-term safety of these agents, and these need to be linked up, both in the United Kingdom and in Europe.
"Optimal care requires adult rheumatologists who have experience or training in adolescent rheumatology," Dr. Foster further advised. Adults with JIA have multiple and often complex issues, she added, and these need to be addressed by appropriately trained staff.
Dr. Foster has received honoraria from Abbott, Pfizer, and Schering-Plough.
BRIGHTON, ENGLAND – The use of biologic agents in adults with juvenile idiopathic arthritis needs guidance, a situation that the British Society for Rheumatology and British Society for Pediatric and Adolescent Rheumatology are set to address.
The two British Societies will publish a statement on the use of biologics in adults with juvenile idiopathic arthritis (JIA) very soon, said Dr. Helen Foster at the annual meeting of the British Society for Rheumatology (BSR).
Dr. Foster, professor of pediatric rheumatology at Newcastle University, England, commented that the current use of biologics in adult JIA patients is based on a paucity of data, with only one biologic agent, etanercept, currently approved for use by the National Institute for Health and Clinical Excellence (NICE).
"Clearly adults with JIA are receiving biologic treatments, and data so far, albeit from registries, are actually quite encouraging of a good response," Dr. Foster said.
Indeed, data from the BSR Biologics Register (BSRBR) show that of 495 patients registered in adulthood one third had disease onset reported before the age of 16 years, with one fifth (21%) officially diagnosed with JIA. Importantly, Dr. Foster noted that these data showed that disease flares were still possible after many years of remission, at a median of 20 years for de novo biologic use.
Last year, NICE issued guidance link to on how to improve commissioning of biologic drugs to treat inflammatory diseases in the United Kingdom. In the report, the estimated need for biologic agents in adults who had JIA was just 15% – a likely underestimate, Dr. Foster suggested.
"Undoubtedly, the proportion of patients with JIA who reach adulthood and who will require either ongoing treatment with a biologic agent or de novo treatment for disease flares is going to increase," she observed.
However, despite the need for continued or first-time biologic use in adults with JIA, these patients often fall into a gap between pediatric and adult care. Anecdotal evidence suggests that funding for treatment might be withdrawn when a JIA patient reaches 18 years of age and that if continued treatment is needed, a new application for funding must be made to adult services.
With this in mind, better links between juvenile and adult rheumatology services are sorely needed. The new BSR/British Society for Paediatric and Adolescent Rheumatology (BSPAR) statement will note that patients transferring to adult care are likely to need continued treatment with a biologic agent and that treatment should not be stopped solely on the basis of age. The process of ongoing funding needs to be in place before transfer, Dr. Foster said.
The BSR/BSPAR statement will also comment on eligibility for biologic agents, noting that appropriate tools for adults with JIA are specifically needed. Currently, the only guidance on use of biologics in JIA is for etanercept in the pediatric population and, clearly, adults with JIA are a distinct patient population.
"The management of JIA has changed dramatically in the last decade, and it’s going to change again towards a more individualized approach in the future," Dr. Foster said. She added that the choice of biologic is very much down to a variety of factors – clinician’s experience, patient choice, and clinical scenario, but that there is an obvious need for consensus on which agent or agents to use.
There is also a need for improved surveillance, and existing juvenile and adult biologics registries provide important information about the long-term safety of these agents, and these need to be linked up, both in the United Kingdom and in Europe.
"Optimal care requires adult rheumatologists who have experience or training in adolescent rheumatology," Dr. Foster further advised. Adults with JIA have multiple and often complex issues, she added, and these need to be addressed by appropriately trained staff.
Dr. Foster has received honoraria from Abbott, Pfizer, and Schering-Plough.
FROM THE ANNUAL MEETING OF THE BRITISH SOCIETY FOR RHEUMATOLOGY
Disease Activity Higher in Obese RA Patients
Major Finding: Odds ratios (OR), adjusted for age, gender, and smoking status, were 4.1 for DAS28 and 3.67 for ESR comparing the baseline values of very obese patients with the other BMI groups.
Data Source: Study of 216 patients with clinically diagnosed early rheumatoid arthritis, with symptom duration of less than 1 year.
Disclosures: Ms. Ling had no conflicts of interest.
BRIGHTON, ENGLAND – Very obese patients with early rheumatoid arthritis appear to have higher disease activity at presentation, according to recent data.
In a study of 216 individuals with early, clinically diagnosed rheumatoid arthritis (RA), those with a body mass index (BMI) of 35 kg/m
As a result, use of the DAS28 to guide clinical decision making could result in disease-modifying antirheumatic drug (DMARD) therapy being given early on, suggested Stephanie Ling, who presented the findings.
Ms. Ling, a fifth-year medical student at the University of Liverpool, England, noted that earlier, more aggressive treatment of obese RA patients might explain why some studies have suggested that obesity, somewhat paradoxically, is actually beneficial in some patients with RA.
Indeed, studies have linked obesity with reduced mortality (Arch. Intern. Med. 2005;165:1624-9; Ann. Rheum. Dis. 2010;69:i61-4) and protection against radiographic joint damage (Ann. Rheum. Dis. 2008;67:769-74), although high levels of adiponectin – secreted from the fat tissue – are associated with increased joint inflammation (Arthritis Rheum. 2009;61:1248-56).
“Physiologically, obesity is characterized by the expansion of white adipose tissue, which is not a benign tissue,” Ms. Ling explained. White adipose tissue secretes fatty acids, and its constituent cells, the adipocytes, also secrete proinflammatory proteins, or adipokines.
“Obesity can be thought of as a chronic inflammatory state,” said Ms. Ling, adding that studies also indicate that “obesity could have adverse effect on RA disease activity.”
In the current study, patients' baseline disease characteristics, including DAS28 scores, rheumatoid factor status, and anti-cyclic citrullinated protein antibody status, were assessed according to BMI at presentation. All patients had early RA diagnosed by a consultant rheumatologist and had symptoms lasting for less than 1 year. The mean age of participants was 57 years and 57% of the cohort was female.
Patients were grouped according to their BMI category, as defined by World Health Organization (WHO) criteria. One-third fulfilled criteria for obesity, with approximately 22% in the obese I category (BMI more than 30 kg/m
Results showed that obese II–III patients were more likely to present with elevated (5.1 or higher) DAS28 scores than their lighter counterparts. Odds ratios (OR) adjusted for age, gender, and smoking status were 4.1 for DAS28 and 3.67 for ESR when comparing the very obese patients with the other BMI groups.
Considering each component of the DAS28 separately, a high ESR (32 mm/h or more) was the main factor that appeared to be significantly higher as body weight increased. There was no association with tender or swollen joint counts, global visual analog scale, symptom duration, or rheumatoid factor/anti-cyclic citrullinated protein antibody status, Ms. Ling said.
“There is a need for well-designed longitudinal studies to examine the effect of obesity on the extent of RA disease progression,” she suggested.
Because obesity increases the erythrocyte sedimentation rate, overweight rheumatoid arthritis patients may have a higher disease activity score than their arthritis merits.
Source ©Geronimo/Fotolia.Com
Major Finding: Odds ratios (OR), adjusted for age, gender, and smoking status, were 4.1 for DAS28 and 3.67 for ESR comparing the baseline values of very obese patients with the other BMI groups.
Data Source: Study of 216 patients with clinically diagnosed early rheumatoid arthritis, with symptom duration of less than 1 year.
Disclosures: Ms. Ling had no conflicts of interest.
BRIGHTON, ENGLAND – Very obese patients with early rheumatoid arthritis appear to have higher disease activity at presentation, according to recent data.
In a study of 216 individuals with early, clinically diagnosed rheumatoid arthritis (RA), those with a body mass index (BMI) of 35 kg/m
As a result, use of the DAS28 to guide clinical decision making could result in disease-modifying antirheumatic drug (DMARD) therapy being given early on, suggested Stephanie Ling, who presented the findings.
Ms. Ling, a fifth-year medical student at the University of Liverpool, England, noted that earlier, more aggressive treatment of obese RA patients might explain why some studies have suggested that obesity, somewhat paradoxically, is actually beneficial in some patients with RA.
Indeed, studies have linked obesity with reduced mortality (Arch. Intern. Med. 2005;165:1624-9; Ann. Rheum. Dis. 2010;69:i61-4) and protection against radiographic joint damage (Ann. Rheum. Dis. 2008;67:769-74), although high levels of adiponectin – secreted from the fat tissue – are associated with increased joint inflammation (Arthritis Rheum. 2009;61:1248-56).
“Physiologically, obesity is characterized by the expansion of white adipose tissue, which is not a benign tissue,” Ms. Ling explained. White adipose tissue secretes fatty acids, and its constituent cells, the adipocytes, also secrete proinflammatory proteins, or adipokines.
“Obesity can be thought of as a chronic inflammatory state,” said Ms. Ling, adding that studies also indicate that “obesity could have adverse effect on RA disease activity.”
In the current study, patients' baseline disease characteristics, including DAS28 scores, rheumatoid factor status, and anti-cyclic citrullinated protein antibody status, were assessed according to BMI at presentation. All patients had early RA diagnosed by a consultant rheumatologist and had symptoms lasting for less than 1 year. The mean age of participants was 57 years and 57% of the cohort was female.
Patients were grouped according to their BMI category, as defined by World Health Organization (WHO) criteria. One-third fulfilled criteria for obesity, with approximately 22% in the obese I category (BMI more than 30 kg/m
Results showed that obese II–III patients were more likely to present with elevated (5.1 or higher) DAS28 scores than their lighter counterparts. Odds ratios (OR) adjusted for age, gender, and smoking status were 4.1 for DAS28 and 3.67 for ESR when comparing the very obese patients with the other BMI groups.
Considering each component of the DAS28 separately, a high ESR (32 mm/h or more) was the main factor that appeared to be significantly higher as body weight increased. There was no association with tender or swollen joint counts, global visual analog scale, symptom duration, or rheumatoid factor/anti-cyclic citrullinated protein antibody status, Ms. Ling said.
“There is a need for well-designed longitudinal studies to examine the effect of obesity on the extent of RA disease progression,” she suggested.
Because obesity increases the erythrocyte sedimentation rate, overweight rheumatoid arthritis patients may have a higher disease activity score than their arthritis merits.
Source ©Geronimo/Fotolia.Com
Major Finding: Odds ratios (OR), adjusted for age, gender, and smoking status, were 4.1 for DAS28 and 3.67 for ESR comparing the baseline values of very obese patients with the other BMI groups.
Data Source: Study of 216 patients with clinically diagnosed early rheumatoid arthritis, with symptom duration of less than 1 year.
Disclosures: Ms. Ling had no conflicts of interest.
BRIGHTON, ENGLAND – Very obese patients with early rheumatoid arthritis appear to have higher disease activity at presentation, according to recent data.
In a study of 216 individuals with early, clinically diagnosed rheumatoid arthritis (RA), those with a body mass index (BMI) of 35 kg/m
As a result, use of the DAS28 to guide clinical decision making could result in disease-modifying antirheumatic drug (DMARD) therapy being given early on, suggested Stephanie Ling, who presented the findings.
Ms. Ling, a fifth-year medical student at the University of Liverpool, England, noted that earlier, more aggressive treatment of obese RA patients might explain why some studies have suggested that obesity, somewhat paradoxically, is actually beneficial in some patients with RA.
Indeed, studies have linked obesity with reduced mortality (Arch. Intern. Med. 2005;165:1624-9; Ann. Rheum. Dis. 2010;69:i61-4) and protection against radiographic joint damage (Ann. Rheum. Dis. 2008;67:769-74), although high levels of adiponectin – secreted from the fat tissue – are associated with increased joint inflammation (Arthritis Rheum. 2009;61:1248-56).
“Physiologically, obesity is characterized by the expansion of white adipose tissue, which is not a benign tissue,” Ms. Ling explained. White adipose tissue secretes fatty acids, and its constituent cells, the adipocytes, also secrete proinflammatory proteins, or adipokines.
“Obesity can be thought of as a chronic inflammatory state,” said Ms. Ling, adding that studies also indicate that “obesity could have adverse effect on RA disease activity.”
In the current study, patients' baseline disease characteristics, including DAS28 scores, rheumatoid factor status, and anti-cyclic citrullinated protein antibody status, were assessed according to BMI at presentation. All patients had early RA diagnosed by a consultant rheumatologist and had symptoms lasting for less than 1 year. The mean age of participants was 57 years and 57% of the cohort was female.
Patients were grouped according to their BMI category, as defined by World Health Organization (WHO) criteria. One-third fulfilled criteria for obesity, with approximately 22% in the obese I category (BMI more than 30 kg/m
Results showed that obese II–III patients were more likely to present with elevated (5.1 or higher) DAS28 scores than their lighter counterparts. Odds ratios (OR) adjusted for age, gender, and smoking status were 4.1 for DAS28 and 3.67 for ESR when comparing the very obese patients with the other BMI groups.
Considering each component of the DAS28 separately, a high ESR (32 mm/h or more) was the main factor that appeared to be significantly higher as body weight increased. There was no association with tender or swollen joint counts, global visual analog scale, symptom duration, or rheumatoid factor/anti-cyclic citrullinated protein antibody status, Ms. Ling said.
“There is a need for well-designed longitudinal studies to examine the effect of obesity on the extent of RA disease progression,” she suggested.
Because obesity increases the erythrocyte sedimentation rate, overweight rheumatoid arthritis patients may have a higher disease activity score than their arthritis merits.
Source ©Geronimo/Fotolia.Com
From the Annual Meeting of the British Society for Rheumatology
Disease Activity Higher in Obese RA Patients : With obesity being a chronic inflammatory state, it affects RA adversely.
BRIGHTON, ENGLAND – Very obese patients with early rheumatoid arthritis appear to have higher disease activity at presentation, according to recent data.
In a study of 216 individuals with early, clinically diagnosed rheumatoid arthritis (RA), those with a body mass index (BMI) of 35 kg/m
As a result, by using the DAS28 to guide their clinical decision making, physicians may give disease-modifying antirheumatic drug (DMARD) therapy too early in the course of the disease, suggested Stephanie Ling, who presented the findings.
Ms. Ling, a fifth-year medical student at the University of Liverpool, England, noted that earlier, more aggressive treatment of obese RA patients might explain why some studies have suggested that obesity, somewhat paradoxically, is actually beneficial in some patients with RA.
Indeed, studies have linked obesity with reduced mortality (Arch. Intern. Med. 2005; 165:1624–9; Ann. Rheum. Dis. 2010;69:i61–4) and protection against radiographic joint damage (Ann. Rheum. Dis. 2008;67:769–74), although high levels of adiponectin – secreted from the fat tissue – are associated with increased joint inflammation (Arthritis Rheum. 2009;61:1248–56).
“Physiologically, obesity is characterized by the expansion of white adipose tissue, which is not a benign tissue,” Ms. Ling explained.
White adipose tissue secretes fatty acids, and its constituent cells, the adipocytes, also secrete proinflammatory proteins, or adipokines.
“Obesity can be thought of as a chronic inflammatory state,” said Ms. Ling, adding that studies also indicate that “obesity could have adverse effect on RA disease activity.”
In the current study, patients' baseline disease characteristics, including DAS28 scores, rheumatoid factor status, and anti-cyclic citrullinated protein antibody status, were assessed according to BMI at presentation. All patients had early RA diagnosed by a consultant rheumatologist and had symptoms lasting for less than 1 year. The mean age of participants was 57 years and 57% of the cohort was female.
Patients were grouped according to their BMI category, as defined by World Health Organization (WHO) criteria. One-third fulfilled criteria for obesity, with approximately 22% in the obese I category (BMI more than 30 kg/m
Results showed that obese II–III patients were more likely to present with elevated (5.1 or higher) DAS28 scores than their lighter counterparts. Odds ratios (OR) adjusted for age, gender, and smoking status were 4.1 for DAS28 and 3.67 for ESR when comparing the very obese patients with the other BMI groups.
Considering each component of the DAS28 separately, Ms. Ling said, a high ESR (32 mm/h or more) was the main factor that appeared to be significantly higher as body weight increased. There was no association with tender or swollen joint counts, global visual analog scale, symptom duration, or rheumatoid factor/anti-cyclic citrullinated protein antibody status, she said.
“There is a need for well-designed longitudinal studies to examine the effect of obesity on the extent of RA disease progression,” she suggested.
Ms. Ling reported no conflicts of interest.
Because obesity increases the ESR, overweight RA patients may have a higher DAS28 score than their disease merits.
Source ©geronimo/Fotolia.com
BRIGHTON, ENGLAND – Very obese patients with early rheumatoid arthritis appear to have higher disease activity at presentation, according to recent data.
In a study of 216 individuals with early, clinically diagnosed rheumatoid arthritis (RA), those with a body mass index (BMI) of 35 kg/m
As a result, by using the DAS28 to guide their clinical decision making, physicians may give disease-modifying antirheumatic drug (DMARD) therapy too early in the course of the disease, suggested Stephanie Ling, who presented the findings.
Ms. Ling, a fifth-year medical student at the University of Liverpool, England, noted that earlier, more aggressive treatment of obese RA patients might explain why some studies have suggested that obesity, somewhat paradoxically, is actually beneficial in some patients with RA.
Indeed, studies have linked obesity with reduced mortality (Arch. Intern. Med. 2005; 165:1624–9; Ann. Rheum. Dis. 2010;69:i61–4) and protection against radiographic joint damage (Ann. Rheum. Dis. 2008;67:769–74), although high levels of adiponectin – secreted from the fat tissue – are associated with increased joint inflammation (Arthritis Rheum. 2009;61:1248–56).
“Physiologically, obesity is characterized by the expansion of white adipose tissue, which is not a benign tissue,” Ms. Ling explained.
White adipose tissue secretes fatty acids, and its constituent cells, the adipocytes, also secrete proinflammatory proteins, or adipokines.
“Obesity can be thought of as a chronic inflammatory state,” said Ms. Ling, adding that studies also indicate that “obesity could have adverse effect on RA disease activity.”
In the current study, patients' baseline disease characteristics, including DAS28 scores, rheumatoid factor status, and anti-cyclic citrullinated protein antibody status, were assessed according to BMI at presentation. All patients had early RA diagnosed by a consultant rheumatologist and had symptoms lasting for less than 1 year. The mean age of participants was 57 years and 57% of the cohort was female.
Patients were grouped according to their BMI category, as defined by World Health Organization (WHO) criteria. One-third fulfilled criteria for obesity, with approximately 22% in the obese I category (BMI more than 30 kg/m
Results showed that obese II–III patients were more likely to present with elevated (5.1 or higher) DAS28 scores than their lighter counterparts. Odds ratios (OR) adjusted for age, gender, and smoking status were 4.1 for DAS28 and 3.67 for ESR when comparing the very obese patients with the other BMI groups.
Considering each component of the DAS28 separately, Ms. Ling said, a high ESR (32 mm/h or more) was the main factor that appeared to be significantly higher as body weight increased. There was no association with tender or swollen joint counts, global visual analog scale, symptom duration, or rheumatoid factor/anti-cyclic citrullinated protein antibody status, she said.
“There is a need for well-designed longitudinal studies to examine the effect of obesity on the extent of RA disease progression,” she suggested.
Ms. Ling reported no conflicts of interest.
Because obesity increases the ESR, overweight RA patients may have a higher DAS28 score than their disease merits.
Source ©geronimo/Fotolia.com
BRIGHTON, ENGLAND – Very obese patients with early rheumatoid arthritis appear to have higher disease activity at presentation, according to recent data.
In a study of 216 individuals with early, clinically diagnosed rheumatoid arthritis (RA), those with a body mass index (BMI) of 35 kg/m
As a result, by using the DAS28 to guide their clinical decision making, physicians may give disease-modifying antirheumatic drug (DMARD) therapy too early in the course of the disease, suggested Stephanie Ling, who presented the findings.
Ms. Ling, a fifth-year medical student at the University of Liverpool, England, noted that earlier, more aggressive treatment of obese RA patients might explain why some studies have suggested that obesity, somewhat paradoxically, is actually beneficial in some patients with RA.
Indeed, studies have linked obesity with reduced mortality (Arch. Intern. Med. 2005; 165:1624–9; Ann. Rheum. Dis. 2010;69:i61–4) and protection against radiographic joint damage (Ann. Rheum. Dis. 2008;67:769–74), although high levels of adiponectin – secreted from the fat tissue – are associated with increased joint inflammation (Arthritis Rheum. 2009;61:1248–56).
“Physiologically, obesity is characterized by the expansion of white adipose tissue, which is not a benign tissue,” Ms. Ling explained.
White adipose tissue secretes fatty acids, and its constituent cells, the adipocytes, also secrete proinflammatory proteins, or adipokines.
“Obesity can be thought of as a chronic inflammatory state,” said Ms. Ling, adding that studies also indicate that “obesity could have adverse effect on RA disease activity.”
In the current study, patients' baseline disease characteristics, including DAS28 scores, rheumatoid factor status, and anti-cyclic citrullinated protein antibody status, were assessed according to BMI at presentation. All patients had early RA diagnosed by a consultant rheumatologist and had symptoms lasting for less than 1 year. The mean age of participants was 57 years and 57% of the cohort was female.
Patients were grouped according to their BMI category, as defined by World Health Organization (WHO) criteria. One-third fulfilled criteria for obesity, with approximately 22% in the obese I category (BMI more than 30 kg/m
Results showed that obese II–III patients were more likely to present with elevated (5.1 or higher) DAS28 scores than their lighter counterparts. Odds ratios (OR) adjusted for age, gender, and smoking status were 4.1 for DAS28 and 3.67 for ESR when comparing the very obese patients with the other BMI groups.
Considering each component of the DAS28 separately, Ms. Ling said, a high ESR (32 mm/h or more) was the main factor that appeared to be significantly higher as body weight increased. There was no association with tender or swollen joint counts, global visual analog scale, symptom duration, or rheumatoid factor/anti-cyclic citrullinated protein antibody status, she said.
“There is a need for well-designed longitudinal studies to examine the effect of obesity on the extent of RA disease progression,” she suggested.
Ms. Ling reported no conflicts of interest.
Because obesity increases the ESR, overweight RA patients may have a higher DAS28 score than their disease merits.
Source ©geronimo/Fotolia.com