Rheumatoid Arthritis

Ten recommendations for how best to investigate and follow patients with undifferentiated peripheral inflammatory arthritis were developed by an expert panel of nearly 700 rheumatologists from 17 countries.

Many patients who present to rheumatologists have recent-onset arthritis that doesn't meet clinical criteria, but they are concerned about their odds of developing a more serious disease, wrote Dr. Pedro Machado of the University of Coimbra (Portugal) Hospital and colleagues on behalf of the panel (Ann. Rheum. Dis. 2010 Aug. 19 [doi:10.1136/ard.2010.130625]).

To develop the recommendations, the panelists participating in the 3E (Evidence, Expertise, Exchange) Initiative created 10 clinical questions related to undifferentiated peripheral inflammatory arthritis (UPIA) and reviewed the evidence-based literature that addressed each one.

They agreed on 10 recommendations, and each participant indicated whether the recommendations would change their current clinical practices:

▸ Consider all alternatives. UPIA is a diagnosis of exclusion. All causes of arthritis — including trauma, malignancy, and metabolic problems, as well as autoimmune causes — should be ruled out. This recommendation applies only if arthritis persists, and not if it is self-limiting.

▸ Note red flags during the history and physical. Previous studies have shown that older age, female sex, and greater morning stiffness are predictors of an ultimate rheumatoid arthritis diagnosis.

▸ Perform erythrocyte sedimentation rate and C-reactive protein assessments. Do these at baseline, and repeat when clinically relevant.

▸ Test for rheumatoid factor and/or anticytoplasmic antibodies (ACPA) in patients with UPIA. But remember that negative results do not exclude eventual progression to RA.

▸ Perform baseline x-rays of affected joints. Be sure to review x-rays of affected hands, wrists, and feet when evaluating a patient for UPIA, as erosions in these areas can predict future RA. Repeat within a year of the first evaluation.

▸ MRI can be used, cautiously, to diagnose UPIA in the hands and wrists. Some evidence shows that MRI can be useful for predicting RA in UPIA patients, but the data are too limited to recommend the routine use of MRI or ultrasound imaging in these patients.

▸ Consider HLA-B27 genetic test in certain clinical settings. Although no genetic test is available that can be routinely recommended for UPIA, the HLA-B27 test might be helpful in patients with suspected spondyloarthritis.

▸ Synovial biopsy can help in the differential diagnosis in patients with monoarthritis. However, there is not enough evidence to recommend this as a routine procedure in UPIA patients.

▸ Document predictors of persistent inflammatory arthritis. Predictors include duration of 6 weeks or longer, over 30 minutes of morning stiffness, involvement of more than three joints, and evidence of radiographic erosion.

▸ Monitor disease activity as well as possible. In five studies that evaluated four different questionnaires, none stood out as fully validated for use in UPIA, but it is important to make an effort to record disease activity using a tool such as the WHO Disability Assessment Scale or the London Handicap Scale.

When the panelists were asked which recommendations were most likely to change the way they approach patients with suspected UPIA, 25% mentioned the recommendation on documenting predictors of persistent inflammatory arthritis. About 18% of the panelists said that the recommendation on MRI and ultrasound would change their practice.

The development of new criteria for RA from ACR/EULAR will likely make it harder to diagnose UPIA, because some of these patients meet the new criteria for RA, the researchers noted.

Disclosures: The study was supported by Abbott Laboratories.

View on The News

Guidelines Lack Definition

This is a very difficult area, and the authors are to be commended for the tremendous amount of work they did to try to make undifferentiated peripheral inflammatory arthritis a little clearer. They did a careful literature search and a grading system so they could be transparent about what data they had.

The question is how much the guidelines will be used. There are some problems because of the lack of data in some areas. This unavoidably led to several recommendations that were based on expert opinion rather than evidence.

Ultimately, what makes the guidelines difficult to use is that we do not end up with a definition. This document tells us how to try to define what is going on with a patient, but it doesn't say, “So this is what UPIA is.” Instead, it says a lot about what it is not. The guidelines lean strongly toward a diagnosis of RA, but it would help to have a table of tests the researchers recommend and why they recommend them.

A key point the recommendations make is to do a good history and physical, plus appropriate laboratory investigations. It is good to have that in writing.

These recommendations are a good effort, and more helpful in what not to do than what to do.

DANIEL E. FURST, M.D., is Carl M. Pearson Professor of Rheumatology at the University of California, Los Angeles. He reports having no conflicts relevant to this discussion.

Ten recommendations for how best to investigate and follow patients with undifferentiated peripheral inflammatory arthritis were developed by an expert panel of nearly 700 rheumatologists from 17 countries.

Many patients who present to rheumatologists have recent-onset arthritis that doesn't meet clinical criteria, but they are concerned about their odds of developing a more serious disease, wrote Dr. Pedro Machado of the University of Coimbra (Portugal) Hospital and colleagues on behalf of the panel (Ann. Rheum. Dis. 2010 Aug. 19 [doi:10.1136/ard.2010.130625]).

To develop the recommendations, the panelists participating in the 3E (Evidence, Expertise, Exchange) Initiative created 10 clinical questions related to undifferentiated peripheral inflammatory arthritis (UPIA) and reviewed the evidence-based literature that addressed each one.

They agreed on 10 recommendations, and each participant indicated whether the recommendations would change their current clinical practices:

▸ Consider all alternatives. UPIA is a diagnosis of exclusion. All causes of arthritis — including trauma, malignancy, and metabolic problems, as well as autoimmune causes — should be ruled out. This recommendation applies only if arthritis persists, and not if it is self-limiting.

▸ Note red flags during the history and physical. Previous studies have shown that older age, female sex, and greater morning stiffness are predictors of an ultimate rheumatoid arthritis diagnosis.

▸ Perform erythrocyte sedimentation rate and C-reactive protein assessments. Do these at baseline, and repeat when clinically relevant.

▸ Test for rheumatoid factor and/or anticytoplasmic antibodies (ACPA) in patients with UPIA. But remember that negative results do not exclude eventual progression to RA.

▸ Perform baseline x-rays of affected joints. Be sure to review x-rays of affected hands, wrists, and feet when evaluating a patient for UPIA, as erosions in these areas can predict future RA. Repeat within a year of the first evaluation.

▸ MRI can be used, cautiously, to diagnose UPIA in the hands and wrists. Some evidence shows that MRI can be useful for predicting RA in UPIA patients, but the data are too limited to recommend the routine use of MRI or ultrasound imaging in these patients.

▸ Consider HLA-B27 genetic test in certain clinical settings. Although no genetic test is available that can be routinely recommended for UPIA, the HLA-B27 test might be helpful in patients with suspected spondyloarthritis.

▸ Synovial biopsy can help in the differential diagnosis in patients with monoarthritis. However, there is not enough evidence to recommend this as a routine procedure in UPIA patients.

▸ Document predictors of persistent inflammatory arthritis. Predictors include duration of 6 weeks or longer, over 30 minutes of morning stiffness, involvement of more than three joints, and evidence of radiographic erosion.

▸ Monitor disease activity as well as possible. In five studies that evaluated four different questionnaires, none stood out as fully validated for use in UPIA, but it is important to make an effort to record disease activity using a tool such as the WHO Disability Assessment Scale or the London Handicap Scale.

When the panelists were asked which recommendations were most likely to change the way they approach patients with suspected UPIA, 25% mentioned the recommendation on documenting predictors of persistent inflammatory arthritis. About 18% of the panelists said that the recommendation on MRI and ultrasound would change their practice.

The development of new criteria for RA from ACR/EULAR will likely make it harder to diagnose UPIA, because some of these patients meet the new criteria for RA, the researchers noted.

Disclosures: The study was supported by Abbott Laboratories.

View on The News

Guidelines Lack Definition

This is a very difficult area, and the authors are to be commended for the tremendous amount of work they did to try to make undifferentiated peripheral inflammatory arthritis a little clearer. They did a careful literature search and a grading system so they could be transparent about what data they had.

The question is how much the guidelines will be used. There are some problems because of the lack of data in some areas. This unavoidably led to several recommendations that were based on expert opinion rather than evidence.

Ultimately, what makes the guidelines difficult to use is that we do not end up with a definition. This document tells us how to try to define what is going on with a patient, but it doesn't say, “So this is what UPIA is.” Instead, it says a lot about what it is not. The guidelines lean strongly toward a diagnosis of RA, but it would help to have a table of tests the researchers recommend and why they recommend them.

A key point the recommendations make is to do a good history and physical, plus appropriate laboratory investigations. It is good to have that in writing.

These recommendations are a good effort, and more helpful in what not to do than what to do.

DANIEL E. FURST, M.D., is Carl M. Pearson Professor of Rheumatology at the University of California, Los Angeles. He reports having no conflicts relevant to this discussion.

Ten recommendations for how best to investigate and follow patients with undifferentiated peripheral inflammatory arthritis were developed by an expert panel of nearly 700 rheumatologists from 17 countries.

Many patients who present to rheumatologists have recent-onset arthritis that doesn't meet clinical criteria, but they are concerned about their odds of developing a more serious disease, wrote Dr. Pedro Machado of the University of Coimbra (Portugal) Hospital and colleagues on behalf of the panel (Ann. Rheum. Dis. 2010 Aug. 19 [doi:10.1136/ard.2010.130625]).

To develop the recommendations, the panelists participating in the 3E (Evidence, Expertise, Exchange) Initiative created 10 clinical questions related to undifferentiated peripheral inflammatory arthritis (UPIA) and reviewed the evidence-based literature that addressed each one.

They agreed on 10 recommendations, and each participant indicated whether the recommendations would change their current clinical practices:

▸ Consider all alternatives. UPIA is a diagnosis of exclusion. All causes of arthritis — including trauma, malignancy, and metabolic problems, as well as autoimmune causes — should be ruled out. This recommendation applies only if arthritis persists, and not if it is self-limiting.

▸ Note red flags during the history and physical. Previous studies have shown that older age, female sex, and greater morning stiffness are predictors of an ultimate rheumatoid arthritis diagnosis.

▸ Perform erythrocyte sedimentation rate and C-reactive protein assessments. Do these at baseline, and repeat when clinically relevant.

▸ Test for rheumatoid factor and/or anticytoplasmic antibodies (ACPA) in patients with UPIA. But remember that negative results do not exclude eventual progression to RA.

▸ Perform baseline x-rays of affected joints. Be sure to review x-rays of affected hands, wrists, and feet when evaluating a patient for UPIA, as erosions in these areas can predict future RA. Repeat within a year of the first evaluation.

▸ MRI can be used, cautiously, to diagnose UPIA in the hands and wrists. Some evidence shows that MRI can be useful for predicting RA in UPIA patients, but the data are too limited to recommend the routine use of MRI or ultrasound imaging in these patients.

▸ Consider HLA-B27 genetic test in certain clinical settings. Although no genetic test is available that can be routinely recommended for UPIA, the HLA-B27 test might be helpful in patients with suspected spondyloarthritis.

▸ Synovial biopsy can help in the differential diagnosis in patients with monoarthritis. However, there is not enough evidence to recommend this as a routine procedure in UPIA patients.

▸ Document predictors of persistent inflammatory arthritis. Predictors include duration of 6 weeks or longer, over 30 minutes of morning stiffness, involvement of more than three joints, and evidence of radiographic erosion.

▸ Monitor disease activity as well as possible. In five studies that evaluated four different questionnaires, none stood out as fully validated for use in UPIA, but it is important to make an effort to record disease activity using a tool such as the WHO Disability Assessment Scale or the London Handicap Scale.

When the panelists were asked which recommendations were most likely to change the way they approach patients with suspected UPIA, 25% mentioned the recommendation on documenting predictors of persistent inflammatory arthritis. About 18% of the panelists said that the recommendation on MRI and ultrasound would change their practice.

The development of new criteria for RA from ACR/EULAR will likely make it harder to diagnose UPIA, because some of these patients meet the new criteria for RA, the researchers noted.

Disclosures: The study was supported by Abbott Laboratories.

View on The News

Guidelines Lack Definition

This is a very difficult area, and the authors are to be commended for the tremendous amount of work they did to try to make undifferentiated peripheral inflammatory arthritis a little clearer. They did a careful literature search and a grading system so they could be transparent about what data they had.

The question is how much the guidelines will be used. There are some problems because of the lack of data in some areas. This unavoidably led to several recommendations that were based on expert opinion rather than evidence.

Ultimately, what makes the guidelines difficult to use is that we do not end up with a definition. This document tells us how to try to define what is going on with a patient, but it doesn't say, “So this is what UPIA is.” Instead, it says a lot about what it is not. The guidelines lean strongly toward a diagnosis of RA, but it would help to have a table of tests the researchers recommend and why they recommend them.

A key point the recommendations make is to do a good history and physical, plus appropriate laboratory investigations. It is good to have that in writing.

These recommendations are a good effort, and more helpful in what not to do than what to do.

DANIEL E. FURST, M.D., is Carl M. Pearson Professor of Rheumatology at the University of California, Los Angeles. He reports having no conflicts relevant to this discussion.

The promised overhaul of treatment guidelines for rheumatoid arthritis has finally arrived, and with it, a “new paradigm” that focuses on early identification and treatment of the disabling disease.

The guidelines, which were developed by a joint committee from the American College of Rheumatology and the European League Against Rheumatism, are the latest update since the current guidelines were created in 1987.

Published jointly in the EULAR journal Annals of the Rheumatic Diseases (2010;69:1580-8) and the ACR's Arthritis & Rheumatism (2010;62:2569-81), the new guidelines were created in three phases over 2 years.

In the first phase, the goal was to “to identify the contributions of clinical and laboratory variables that in practice were the most predictive of the decision to initiate [disease-modifying antirheumatic drug] therapy in … patients with early undifferentiated synovitis,” wrote the authors, led by Dr. Daniel Aletaha of the Medical University of Vienna.

To do this, a working group from both societies looked at data from 3,115 patients and correlated whether or not the patients were ultimately prescribed methotrexate to an “agreed-upon list of standardized clinical and laboratory variables collected at baseline.”

The odds of eventual methotrexate initiation were calculated for each variable. For example, swelling of the metacarpophalangeal joint had an odds ratio of 1.5, as did swelling of the proximal interphalangeal joint and the wrist. Tenderness of the hand (either the MCP, PIP, or wrist) was assigned an odds ratio of 2.0.

Moderate elevation of C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) was assigned an OR of 1.0; high elevation of either assay got an OR of 2.0.

In phase II, a panel of 12 rheumatologists related the above clinical and laboratory factors to the “probability of developing 'persistent inflammatory and/or erosive arthritis that is currently considered to be RA.'”

Finally, phase III aimed to utilize the results of phases I and II “to develop a scoring system that would be applicable to newly presenting patients with undifferentiated inflammatory arthritis, to permit identification of those with a high probability of developing persistent and/or erosive RA.”

This final scale assigns points in the following manner:

▸ One swollen “large joint” (defined as shoulders, elbows, hips, knees, and ankles) gets 0 points; involvement of 2-10 large joints gets 1 point.

▸ Involvement of 1-3 “small” joints (defined as metacarpophalangeal joints, proximal interphalangeal joints, second to fifth metatarsophalangeal joints, thumb interphalangeal joints, and wrists) gets 2 points, regardless of large-joint involvement; involvement of 4-10 small joints gets 3 points.

▸ Involvement of more than 10 joints, including at least 1 small joint, gets 5 points.

▸ Both a negative rheumatoid factor (RF) test and a negative anti—citrullinated protein antibody (ACPA) testgets 0 points, whereas having a “low-positive” RF or ACPA (defined as lower than three times the upper limit of normal) gets 2 points. A “high-positive” of either test gets 3 points.

▸ A normal CRP and normal ESR get 0 points, whereas at least one abnormal test gets 1 point.

▸ Symptom duration of fewer than 6 weeks gets 0 points; duration of 6 weeks or longer gets 1 point.

Scores of 6 or more out of 10 are classified as “definite RA.”

Commenting on the new criteria in an interview, Dr. Eric L. Matteson, who is with the Mayo Clinic in Rochester, Minn., and was not involved with the new guidelines, said, “A major useful feature is that the new guidelines do not require multiple joints to be inflamed before a diagnosis can be [made] of early inflammatory rheumatoid arthritis.”

Indeed, a patient may score 6 points without multiple joint inflammation, according to the new guidelines.

When asked what was missing from the new guidelines, he pointed to a lack of awareness of extra-articular components of RA, which also can occur early in the course of the disease.

Disclosures: Several of the guideline authors disclosed financial and other relationships with multiple pharmaceutical companies; Dr. Matteson stated that he had no financial disclosures relative to his comments.

The promised overhaul of treatment guidelines for rheumatoid arthritis has finally arrived, and with it, a “new paradigm” that focuses on early identification and treatment of the disabling disease.

The guidelines, which were developed by a joint committee from the American College of Rheumatology and the European League Against Rheumatism, are the latest update since the current guidelines were created in 1987.

Published jointly in the EULAR journal Annals of the Rheumatic Diseases (2010;69:1580-8) and the ACR's Arthritis & Rheumatism (2010;62:2569-81), the new guidelines were created in three phases over 2 years.

In the first phase, the goal was to “to identify the contributions of clinical and laboratory variables that in practice were the most predictive of the decision to initiate [disease-modifying antirheumatic drug] therapy in … patients with early undifferentiated synovitis,” wrote the authors, led by Dr. Daniel Aletaha of the Medical University of Vienna.

To do this, a working group from both societies looked at data from 3,115 patients and correlated whether or not the patients were ultimately prescribed methotrexate to an “agreed-upon list of standardized clinical and laboratory variables collected at baseline.”

The odds of eventual methotrexate initiation were calculated for each variable. For example, swelling of the metacarpophalangeal joint had an odds ratio of 1.5, as did swelling of the proximal interphalangeal joint and the wrist. Tenderness of the hand (either the MCP, PIP, or wrist) was assigned an odds ratio of 2.0.

Moderate elevation of C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) was assigned an OR of 1.0; high elevation of either assay got an OR of 2.0.

In phase II, a panel of 12 rheumatologists related the above clinical and laboratory factors to the “probability of developing 'persistent inflammatory and/or erosive arthritis that is currently considered to be RA.'”

Finally, phase III aimed to utilize the results of phases I and II “to develop a scoring system that would be applicable to newly presenting patients with undifferentiated inflammatory arthritis, to permit identification of those with a high probability of developing persistent and/or erosive RA.”

This final scale assigns points in the following manner:

▸ One swollen “large joint” (defined as shoulders, elbows, hips, knees, and ankles) gets 0 points; involvement of 2-10 large joints gets 1 point.

▸ Involvement of 1-3 “small” joints (defined as metacarpophalangeal joints, proximal interphalangeal joints, second to fifth metatarsophalangeal joints, thumb interphalangeal joints, and wrists) gets 2 points, regardless of large-joint involvement; involvement of 4-10 small joints gets 3 points.

▸ Involvement of more than 10 joints, including at least 1 small joint, gets 5 points.

▸ Both a negative rheumatoid factor (RF) test and a negative anti—citrullinated protein antibody (ACPA) testgets 0 points, whereas having a “low-positive” RF or ACPA (defined as lower than three times the upper limit of normal) gets 2 points. A “high-positive” of either test gets 3 points.

▸ A normal CRP and normal ESR get 0 points, whereas at least one abnormal test gets 1 point.

▸ Symptom duration of fewer than 6 weeks gets 0 points; duration of 6 weeks or longer gets 1 point.

Scores of 6 or more out of 10 are classified as “definite RA.”

Commenting on the new criteria in an interview, Dr. Eric L. Matteson, who is with the Mayo Clinic in Rochester, Minn., and was not involved with the new guidelines, said, “A major useful feature is that the new guidelines do not require multiple joints to be inflamed before a diagnosis can be [made] of early inflammatory rheumatoid arthritis.”

Indeed, a patient may score 6 points without multiple joint inflammation, according to the new guidelines.

When asked what was missing from the new guidelines, he pointed to a lack of awareness of extra-articular components of RA, which also can occur early in the course of the disease.

Disclosures: Several of the guideline authors disclosed financial and other relationships with multiple pharmaceutical companies; Dr. Matteson stated that he had no financial disclosures relative to his comments.

The promised overhaul of treatment guidelines for rheumatoid arthritis has finally arrived, and with it, a “new paradigm” that focuses on early identification and treatment of the disabling disease.

The guidelines, which were developed by a joint committee from the American College of Rheumatology and the European League Against Rheumatism, are the latest update since the current guidelines were created in 1987.

Published jointly in the EULAR journal Annals of the Rheumatic Diseases (2010;69:1580-8) and the ACR's Arthritis & Rheumatism (2010;62:2569-81), the new guidelines were created in three phases over 2 years.

In the first phase, the goal was to “to identify the contributions of clinical and laboratory variables that in practice were the most predictive of the decision to initiate [disease-modifying antirheumatic drug] therapy in … patients with early undifferentiated synovitis,” wrote the authors, led by Dr. Daniel Aletaha of the Medical University of Vienna.

To do this, a working group from both societies looked at data from 3,115 patients and correlated whether or not the patients were ultimately prescribed methotrexate to an “agreed-upon list of standardized clinical and laboratory variables collected at baseline.”

The odds of eventual methotrexate initiation were calculated for each variable. For example, swelling of the metacarpophalangeal joint had an odds ratio of 1.5, as did swelling of the proximal interphalangeal joint and the wrist. Tenderness of the hand (either the MCP, PIP, or wrist) was assigned an odds ratio of 2.0.

Moderate elevation of C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) was assigned an OR of 1.0; high elevation of either assay got an OR of 2.0.

In phase II, a panel of 12 rheumatologists related the above clinical and laboratory factors to the “probability of developing 'persistent inflammatory and/or erosive arthritis that is currently considered to be RA.'”

Finally, phase III aimed to utilize the results of phases I and II “to develop a scoring system that would be applicable to newly presenting patients with undifferentiated inflammatory arthritis, to permit identification of those with a high probability of developing persistent and/or erosive RA.”

This final scale assigns points in the following manner:

▸ One swollen “large joint” (defined as shoulders, elbows, hips, knees, and ankles) gets 0 points; involvement of 2-10 large joints gets 1 point.

▸ Involvement of 1-3 “small” joints (defined as metacarpophalangeal joints, proximal interphalangeal joints, second to fifth metatarsophalangeal joints, thumb interphalangeal joints, and wrists) gets 2 points, regardless of large-joint involvement; involvement of 4-10 small joints gets 3 points.

▸ Involvement of more than 10 joints, including at least 1 small joint, gets 5 points.

▸ Both a negative rheumatoid factor (RF) test and a negative anti—citrullinated protein antibody (ACPA) testgets 0 points, whereas having a “low-positive” RF or ACPA (defined as lower than three times the upper limit of normal) gets 2 points. A “high-positive” of either test gets 3 points.

▸ A normal CRP and normal ESR get 0 points, whereas at least one abnormal test gets 1 point.

▸ Symptom duration of fewer than 6 weeks gets 0 points; duration of 6 weeks or longer gets 1 point.

Scores of 6 or more out of 10 are classified as “definite RA.”

Commenting on the new criteria in an interview, Dr. Eric L. Matteson, who is with the Mayo Clinic in Rochester, Minn., and was not involved with the new guidelines, said, “A major useful feature is that the new guidelines do not require multiple joints to be inflamed before a diagnosis can be [made] of early inflammatory rheumatoid arthritis.”

Indeed, a patient may score 6 points without multiple joint inflammation, according to the new guidelines.

When asked what was missing from the new guidelines, he pointed to a lack of awareness of extra-articular components of RA, which also can occur early in the course of the disease.

Disclosures: Several of the guideline authors disclosed financial and other relationships with multiple pharmaceutical companies; Dr. Matteson stated that he had no financial disclosures relative to his comments.

ROME — Cardiovascular risk profiles in osteoarthritis patients are, on average, comparable to those in patients with rheumatoid arthritis, according to a Dutch study.

In recent years, much attention has been focused on the elevated risk of cardiovascular events in patients with rheumatoid arthritis, as a consequence of their increased prevalence of the standard cardiovascular risk factors coupled with a further boost in risk resulting from the chronic systemic inflammatory disease process. The cardiovascular risk associated with osteoarthritis has received far less attention, Dr. Inger Meek said.

She determined the cardiovascular risk profiles of 285 consecutive rheumatoid arthritis patients and 112 consecutive osteoarthritis patients using the SCORE (Systematic Coronary Risk Evaluation) system, which is routinely employed in Europe in lieu of the Framingham risk score. The two groups were similar in terms of mean age and sex. The mean disease duration of the rheumatoid arthritis patients was 6.8 years.

In all, 18% of the osteoarthritis patients had a greater-than-10% estimated 10-year risk of a fatal cardiovascular event by SCORE, as did 15% of rheumatoid arthritis patients, according to Dr. Meek of the University of Twente in Enschede, the Netherlands.

Hypercholesterolemia was significantly more prevalent in the osteoarthritis patients (45%) than in the rheumatoid arthritis patients (29%).

The two groups did not differ significantly in terms of the other elements of SCORE (smoking status, systolic blood pressure, age, and sex).

The SCORE system, developed by the European Society of Cardiology, is based upon 3 million person-years of observation, and doesn't factor in body mass index, Dr. Meek noted. The prevalence of obesity is greatly increased in osteoarthritis patients. Thus, SCORE likely underestimates their cardiovascular mortality risk.

Recent evidence-based recommendations by the European League Against Rheumatism advise physicians to apply a 1.5 multiplication factor to the conventional cardiovascular mortality risk SCORE in rheumatoid arthritis patients who meet two of three criteria: disease duration greater than 10 years, rheumatoid factor or anti–cyclic citrullinated peptide positivity, or extra-articular disease manifestations (Ann. Rheum. Dis. 2010;69:325-31). This is designed to account for the heightened cardiovascular risk imposed by a high degree of systemic inflammation.

The high percentage of osteoarthritis patients in this study with a greater-than-10% estimated likelihood of cardiovascular death within 10 years is of concern, Dr. Meek stressed, because the prevalence of osteoarthritis is expected to mushroom as a result of the graying of the baby boom generation.

Dr. Johannes W.J. Bijlsma of the University Medical Center Utrecht (the Netherlands) commented that the take-home message of Dr. Meek's study is that physicians need to be aware that not only rheumatoid arthritis patients but also osteoarthritis patients are at increased cardiovascular risk.

Disclosures: Dr. Meek declared that she had no financial conflicts.

ROME — Cardiovascular risk profiles in osteoarthritis patients are, on average, comparable to those in patients with rheumatoid arthritis, according to a Dutch study.

In recent years, much attention has been focused on the elevated risk of cardiovascular events in patients with rheumatoid arthritis, as a consequence of their increased prevalence of the standard cardiovascular risk factors coupled with a further boost in risk resulting from the chronic systemic inflammatory disease process. The cardiovascular risk associated with osteoarthritis has received far less attention, Dr. Inger Meek said.

She determined the cardiovascular risk profiles of 285 consecutive rheumatoid arthritis patients and 112 consecutive osteoarthritis patients using the SCORE (Systematic Coronary Risk Evaluation) system, which is routinely employed in Europe in lieu of the Framingham risk score. The two groups were similar in terms of mean age and sex. The mean disease duration of the rheumatoid arthritis patients was 6.8 years.

In all, 18% of the osteoarthritis patients had a greater-than-10% estimated 10-year risk of a fatal cardiovascular event by SCORE, as did 15% of rheumatoid arthritis patients, according to Dr. Meek of the University of Twente in Enschede, the Netherlands.

Hypercholesterolemia was significantly more prevalent in the osteoarthritis patients (45%) than in the rheumatoid arthritis patients (29%).

The two groups did not differ significantly in terms of the other elements of SCORE (smoking status, systolic blood pressure, age, and sex).

The SCORE system, developed by the European Society of Cardiology, is based upon 3 million person-years of observation, and doesn't factor in body mass index, Dr. Meek noted. The prevalence of obesity is greatly increased in osteoarthritis patients. Thus, SCORE likely underestimates their cardiovascular mortality risk.

Recent evidence-based recommendations by the European League Against Rheumatism advise physicians to apply a 1.5 multiplication factor to the conventional cardiovascular mortality risk SCORE in rheumatoid arthritis patients who meet two of three criteria: disease duration greater than 10 years, rheumatoid factor or anti–cyclic citrullinated peptide positivity, or extra-articular disease manifestations (Ann. Rheum. Dis. 2010;69:325-31). This is designed to account for the heightened cardiovascular risk imposed by a high degree of systemic inflammation.

The high percentage of osteoarthritis patients in this study with a greater-than-10% estimated likelihood of cardiovascular death within 10 years is of concern, Dr. Meek stressed, because the prevalence of osteoarthritis is expected to mushroom as a result of the graying of the baby boom generation.

Dr. Johannes W.J. Bijlsma of the University Medical Center Utrecht (the Netherlands) commented that the take-home message of Dr. Meek's study is that physicians need to be aware that not only rheumatoid arthritis patients but also osteoarthritis patients are at increased cardiovascular risk.

Disclosures: Dr. Meek declared that she had no financial conflicts.

ROME — Cardiovascular risk profiles in osteoarthritis patients are, on average, comparable to those in patients with rheumatoid arthritis, according to a Dutch study.

In recent years, much attention has been focused on the elevated risk of cardiovascular events in patients with rheumatoid arthritis, as a consequence of their increased prevalence of the standard cardiovascular risk factors coupled with a further boost in risk resulting from the chronic systemic inflammatory disease process. The cardiovascular risk associated with osteoarthritis has received far less attention, Dr. Inger Meek said.

She determined the cardiovascular risk profiles of 285 consecutive rheumatoid arthritis patients and 112 consecutive osteoarthritis patients using the SCORE (Systematic Coronary Risk Evaluation) system, which is routinely employed in Europe in lieu of the Framingham risk score. The two groups were similar in terms of mean age and sex. The mean disease duration of the rheumatoid arthritis patients was 6.8 years.

In all, 18% of the osteoarthritis patients had a greater-than-10% estimated 10-year risk of a fatal cardiovascular event by SCORE, as did 15% of rheumatoid arthritis patients, according to Dr. Meek of the University of Twente in Enschede, the Netherlands.

Hypercholesterolemia was significantly more prevalent in the osteoarthritis patients (45%) than in the rheumatoid arthritis patients (29%).

The two groups did not differ significantly in terms of the other elements of SCORE (smoking status, systolic blood pressure, age, and sex).

The SCORE system, developed by the European Society of Cardiology, is based upon 3 million person-years of observation, and doesn't factor in body mass index, Dr. Meek noted. The prevalence of obesity is greatly increased in osteoarthritis patients. Thus, SCORE likely underestimates their cardiovascular mortality risk.

Recent evidence-based recommendations by the European League Against Rheumatism advise physicians to apply a 1.5 multiplication factor to the conventional cardiovascular mortality risk SCORE in rheumatoid arthritis patients who meet two of three criteria: disease duration greater than 10 years, rheumatoid factor or anti–cyclic citrullinated peptide positivity, or extra-articular disease manifestations (Ann. Rheum. Dis. 2010;69:325-31). This is designed to account for the heightened cardiovascular risk imposed by a high degree of systemic inflammation.

The high percentage of osteoarthritis patients in this study with a greater-than-10% estimated likelihood of cardiovascular death within 10 years is of concern, Dr. Meek stressed, because the prevalence of osteoarthritis is expected to mushroom as a result of the graying of the baby boom generation.

Dr. Johannes W.J. Bijlsma of the University Medical Center Utrecht (the Netherlands) commented that the take-home message of Dr. Meek's study is that physicians need to be aware that not only rheumatoid arthritis patients but also osteoarthritis patients are at increased cardiovascular risk.

Disclosures: Dr. Meek declared that she had no financial conflicts.

ROME — The investigational oral Janus kinase 3 inhibitor tasocitinib, in combination with methotrexate, showed impressive dose-dependent efficacy for rheumatoid arthritis in a phase II study.

If the results of the ongoing phase III trials are positive, tasocitinib could become the first JAK3 inhibitor licensed for a nononcology indication, and the first new oral disease-modifying antirheumatic drug for RA in more than a decade.

In the phase II RA study presented by Dr. Yoshiya Tanaka, 136 patients with active disease (defined as six or more tender and swollen joints and a C-reactive protein level greater than 7 mg/dL) despite standard-dose methotrexate were randomized to add-on oral tasocitinib at 1, 3, 5, or 10 mg b.i.d. in double-blind fashion for 12 weeks.

Tasocitinib demonstrated a rapid, strong effect; significant benefit was seen within the first week, noted Dr. Tanaka, chair of internal medicine at the University of Occupational and Environmental Health in Kitakyushu, Japan.

In patients with a lower baseline DAS (Disease Activity Score) of 5.1 or less, the tasocitinib 1- and 3-mg b.i.d. arms showed a mean 1.5-point drop from baseline, whereas the 5- and 10-mg b.i.d. groups had decreases of 2.2 and 2.3 points, respectively, compared with a 0.7-point reduction with placebo.

In patients with a high baseline DAS (greater than 5.1), the mean reductions over 12 weeks of treatment with 1, 3, 5, and 10 mg b.i.d. were 2.3, 2.4, 2.8, and 3.4 points, respectively. But only the 10-mg b.i.d. dose was significantly better than placebo in achieving the key end points of DAS remission (a score lower than 2.6) and low disease activity state (a DAS of 3.2 or less). By week 12, roughly 70% of patients with a high baseline DAS and 90% of those with a lower baseline DAS had achieved LDAS on 10 mg b.i.d. of tasocitinib, compared with 10% and 20% of those on placebo.

Disclosures: The study was funded by Pfizer Inc. Dr. Tanaka disclosed that he serves as a consultant to Pfizer and is on the speakers bureaus for Mitsubishi Tanabe Pharma Corp. and several other Japanese pharmaceutical companies.

ROME — The investigational oral Janus kinase 3 inhibitor tasocitinib, in combination with methotrexate, showed impressive dose-dependent efficacy for rheumatoid arthritis in a phase II study.

If the results of the ongoing phase III trials are positive, tasocitinib could become the first JAK3 inhibitor licensed for a nononcology indication, and the first new oral disease-modifying antirheumatic drug for RA in more than a decade.

In the phase II RA study presented by Dr. Yoshiya Tanaka, 136 patients with active disease (defined as six or more tender and swollen joints and a C-reactive protein level greater than 7 mg/dL) despite standard-dose methotrexate were randomized to add-on oral tasocitinib at 1, 3, 5, or 10 mg b.i.d. in double-blind fashion for 12 weeks.

Tasocitinib demonstrated a rapid, strong effect; significant benefit was seen within the first week, noted Dr. Tanaka, chair of internal medicine at the University of Occupational and Environmental Health in Kitakyushu, Japan.

In patients with a lower baseline DAS (Disease Activity Score) of 5.1 or less, the tasocitinib 1- and 3-mg b.i.d. arms showed a mean 1.5-point drop from baseline, whereas the 5- and 10-mg b.i.d. groups had decreases of 2.2 and 2.3 points, respectively, compared with a 0.7-point reduction with placebo.

In patients with a high baseline DAS (greater than 5.1), the mean reductions over 12 weeks of treatment with 1, 3, 5, and 10 mg b.i.d. were 2.3, 2.4, 2.8, and 3.4 points, respectively. But only the 10-mg b.i.d. dose was significantly better than placebo in achieving the key end points of DAS remission (a score lower than 2.6) and low disease activity state (a DAS of 3.2 or less). By week 12, roughly 70% of patients with a high baseline DAS and 90% of those with a lower baseline DAS had achieved LDAS on 10 mg b.i.d. of tasocitinib, compared with 10% and 20% of those on placebo.

Disclosures: The study was funded by Pfizer Inc. Dr. Tanaka disclosed that he serves as a consultant to Pfizer and is on the speakers bureaus for Mitsubishi Tanabe Pharma Corp. and several other Japanese pharmaceutical companies.

ROME — The investigational oral Janus kinase 3 inhibitor tasocitinib, in combination with methotrexate, showed impressive dose-dependent efficacy for rheumatoid arthritis in a phase II study.

If the results of the ongoing phase III trials are positive, tasocitinib could become the first JAK3 inhibitor licensed for a nononcology indication, and the first new oral disease-modifying antirheumatic drug for RA in more than a decade.

In the phase II RA study presented by Dr. Yoshiya Tanaka, 136 patients with active disease (defined as six or more tender and swollen joints and a C-reactive protein level greater than 7 mg/dL) despite standard-dose methotrexate were randomized to add-on oral tasocitinib at 1, 3, 5, or 10 mg b.i.d. in double-blind fashion for 12 weeks.

Tasocitinib demonstrated a rapid, strong effect; significant benefit was seen within the first week, noted Dr. Tanaka, chair of internal medicine at the University of Occupational and Environmental Health in Kitakyushu, Japan.

In patients with a lower baseline DAS (Disease Activity Score) of 5.1 or less, the tasocitinib 1- and 3-mg b.i.d. arms showed a mean 1.5-point drop from baseline, whereas the 5- and 10-mg b.i.d. groups had decreases of 2.2 and 2.3 points, respectively, compared with a 0.7-point reduction with placebo.

In patients with a high baseline DAS (greater than 5.1), the mean reductions over 12 weeks of treatment with 1, 3, 5, and 10 mg b.i.d. were 2.3, 2.4, 2.8, and 3.4 points, respectively. But only the 10-mg b.i.d. dose was significantly better than placebo in achieving the key end points of DAS remission (a score lower than 2.6) and low disease activity state (a DAS of 3.2 or less). By week 12, roughly 70% of patients with a high baseline DAS and 90% of those with a lower baseline DAS had achieved LDAS on 10 mg b.i.d. of tasocitinib, compared with 10% and 20% of those on placebo.

Disclosures: The study was funded by Pfizer Inc. Dr. Tanaka disclosed that he serves as a consultant to Pfizer and is on the speakers bureaus for Mitsubishi Tanabe Pharma Corp. and several other Japanese pharmaceutical companies.

ROME — Weight loss in obese patients with knee osteoarthritis has been shown for the first time in a prospective study to have beneficial structure-modifying effects upon knee cartilage.

This finding has major public health implications. Weight loss now becomes the only therapy ever shown to have salutary structural effects on knee articular cartilage. No drug has yet been shown to have such a benefit, said presenter Dr. Ana Ananda, a rheumatologist at the University of Sydney.

“We found that with a mean weight loss of 9%, which is fairly achievable… we can make meaningful, clinically important differences in terms of cartilage structure,” she said in an interview. Focusing on weight loss might “prevent or delay the need for knee replacement down the line.”

She presented the results of MRI studies conducted before and 12 months after a weight-loss intervention in a group of patients with knee OA and a body mass index greater than 35 kg/m

Patients who achieved at least a 9% reduction in body weight at the 1-year mark had a significantly lower rate of loss in cartilage thickness in the medial compartment, vs. those who had weight gain or lesser weight loss at follow-up.

Moreover, patients with significant weight loss also showed improvement in cartilage quality, as reflected in increased proteoglycan content seen on delayed gadolinium-enhanced MRI. Evidence from other studies suggests that loss in proteoglycan is perhaps the earliest OA-induced change in cartilage, and might be potentially reversible with early intervention, she said.

In all, 78 patients had baseline and follow-up measurements of knee cartilage thickness as a proxy for cartilage volume. Of these, 28 underwent bariatric surgery involving laparoscopic adjustable gastric banding with a mean 1-year weight loss of 17.5%, vs. the mean 2.5% weight loss in patients who participated in a dietary weight-loss program.

The MRIs showed a graded inverse relationship between the percent weight loss and the rate of loss in cartilage thickness in the medial compartment, through which most of the load on the knee joint is transmitted. This relationship remained significant in a multivariate analysis adjusted for age, sex, baseline BMI, and knee range of motion.

The MRI studies were done in 54 patients. The 24 with surgical weight loss had a mean 56-msec increase in delayed gadolinium-enhanced MRI index in the medial compartment during 1 year of follow-up, reflecting a substantial increase in cartilage proteoglycan content. In contrast, the 30 patients with lesser, nonsurgical weight loss had a mean 23-msec decrease in the index. In a multivariate analysis, the correlation between percentage of body weight loss and increase in the index remained significant. For every 10% loss in body weight, a patient's cartilage proteoglycan index improved by about 40 msec.

A second study presented at the congress concluded that substantial weight loss has a chondroprotective effect. The study assessed changes in pain scores, joint biomarkers, and markers of systemic inflammation as outcomes.

Dr. Pascal Richette of Lariboisière Hospital, Paris, reported on 44 obese patients with knee osteoarthritis who underwent bariatric surgery, with a resultant 20% decrease in BMI.

At 6 months post surgery, the group's mean osteoarthritis pain scores had dropped from a baseline of 50 out of a possible 100 points to 24.5 points. This was accompanied by significant functional improvement as measured on the WOMAC (Western Ontario and McMaster Universities) osteoarthritis index subscales.

Serum levels of N-propeptide of type IIA procollagen, a biomarker of cartilage type II collagen synthesis, increased by 32%. Serum levels of cartilage oligomeric matrix protein, a biomarker for cartilage degradation, were down by 36%. Serum levels of interleukin-6 decreased by 26% from baseline, high-sensitivity C-reactive protein was down by 46%, and fibrinogen decreased by 5%, all indicative of reduced systemic inflammation. In addition, serum lipids and insulin resistance were significantly reduced.

Disclosures: Dr. Richette and Dr. Ananda reported having no conflicts of interest.

ROME — Weight loss in obese patients with knee osteoarthritis has been shown for the first time in a prospective study to have beneficial structure-modifying effects upon knee cartilage.

This finding has major public health implications. Weight loss now becomes the only therapy ever shown to have salutary structural effects on knee articular cartilage. No drug has yet been shown to have such a benefit, said presenter Dr. Ana Ananda, a rheumatologist at the University of Sydney.

“We found that with a mean weight loss of 9%, which is fairly achievable… we can make meaningful, clinically important differences in terms of cartilage structure,” she said in an interview. Focusing on weight loss might “prevent or delay the need for knee replacement down the line.”

She presented the results of MRI studies conducted before and 12 months after a weight-loss intervention in a group of patients with knee OA and a body mass index greater than 35 kg/m

Patients who achieved at least a 9% reduction in body weight at the 1-year mark had a significantly lower rate of loss in cartilage thickness in the medial compartment, vs. those who had weight gain or lesser weight loss at follow-up.

Moreover, patients with significant weight loss also showed improvement in cartilage quality, as reflected in increased proteoglycan content seen on delayed gadolinium-enhanced MRI. Evidence from other studies suggests that loss in proteoglycan is perhaps the earliest OA-induced change in cartilage, and might be potentially reversible with early intervention, she said.

In all, 78 patients had baseline and follow-up measurements of knee cartilage thickness as a proxy for cartilage volume. Of these, 28 underwent bariatric surgery involving laparoscopic adjustable gastric banding with a mean 1-year weight loss of 17.5%, vs. the mean 2.5% weight loss in patients who participated in a dietary weight-loss program.

The MRIs showed a graded inverse relationship between the percent weight loss and the rate of loss in cartilage thickness in the medial compartment, through which most of the load on the knee joint is transmitted. This relationship remained significant in a multivariate analysis adjusted for age, sex, baseline BMI, and knee range of motion.

The MRI studies were done in 54 patients. The 24 with surgical weight loss had a mean 56-msec increase in delayed gadolinium-enhanced MRI index in the medial compartment during 1 year of follow-up, reflecting a substantial increase in cartilage proteoglycan content. In contrast, the 30 patients with lesser, nonsurgical weight loss had a mean 23-msec decrease in the index. In a multivariate analysis, the correlation between percentage of body weight loss and increase in the index remained significant. For every 10% loss in body weight, a patient's cartilage proteoglycan index improved by about 40 msec.

A second study presented at the congress concluded that substantial weight loss has a chondroprotective effect. The study assessed changes in pain scores, joint biomarkers, and markers of systemic inflammation as outcomes.

Dr. Pascal Richette of Lariboisière Hospital, Paris, reported on 44 obese patients with knee osteoarthritis who underwent bariatric surgery, with a resultant 20% decrease in BMI.

At 6 months post surgery, the group's mean osteoarthritis pain scores had dropped from a baseline of 50 out of a possible 100 points to 24.5 points. This was accompanied by significant functional improvement as measured on the WOMAC (Western Ontario and McMaster Universities) osteoarthritis index subscales.

Serum levels of N-propeptide of type IIA procollagen, a biomarker of cartilage type II collagen synthesis, increased by 32%. Serum levels of cartilage oligomeric matrix protein, a biomarker for cartilage degradation, were down by 36%. Serum levels of interleukin-6 decreased by 26% from baseline, high-sensitivity C-reactive protein was down by 46%, and fibrinogen decreased by 5%, all indicative of reduced systemic inflammation. In addition, serum lipids and insulin resistance were significantly reduced.

Disclosures: Dr. Richette and Dr. Ananda reported having no conflicts of interest.

ROME — Weight loss in obese patients with knee osteoarthritis has been shown for the first time in a prospective study to have beneficial structure-modifying effects upon knee cartilage.

This finding has major public health implications. Weight loss now becomes the only therapy ever shown to have salutary structural effects on knee articular cartilage. No drug has yet been shown to have such a benefit, said presenter Dr. Ana Ananda, a rheumatologist at the University of Sydney.

“We found that with a mean weight loss of 9%, which is fairly achievable… we can make meaningful, clinically important differences in terms of cartilage structure,” she said in an interview. Focusing on weight loss might “prevent or delay the need for knee replacement down the line.”

She presented the results of MRI studies conducted before and 12 months after a weight-loss intervention in a group of patients with knee OA and a body mass index greater than 35 kg/m

Patients who achieved at least a 9% reduction in body weight at the 1-year mark had a significantly lower rate of loss in cartilage thickness in the medial compartment, vs. those who had weight gain or lesser weight loss at follow-up.

Moreover, patients with significant weight loss also showed improvement in cartilage quality, as reflected in increased proteoglycan content seen on delayed gadolinium-enhanced MRI. Evidence from other studies suggests that loss in proteoglycan is perhaps the earliest OA-induced change in cartilage, and might be potentially reversible with early intervention, she said.

In all, 78 patients had baseline and follow-up measurements of knee cartilage thickness as a proxy for cartilage volume. Of these, 28 underwent bariatric surgery involving laparoscopic adjustable gastric banding with a mean 1-year weight loss of 17.5%, vs. the mean 2.5% weight loss in patients who participated in a dietary weight-loss program.

The MRIs showed a graded inverse relationship between the percent weight loss and the rate of loss in cartilage thickness in the medial compartment, through which most of the load on the knee joint is transmitted. This relationship remained significant in a multivariate analysis adjusted for age, sex, baseline BMI, and knee range of motion.

The MRI studies were done in 54 patients. The 24 with surgical weight loss had a mean 56-msec increase in delayed gadolinium-enhanced MRI index in the medial compartment during 1 year of follow-up, reflecting a substantial increase in cartilage proteoglycan content. In contrast, the 30 patients with lesser, nonsurgical weight loss had a mean 23-msec decrease in the index. In a multivariate analysis, the correlation between percentage of body weight loss and increase in the index remained significant. For every 10% loss in body weight, a patient's cartilage proteoglycan index improved by about 40 msec.

A second study presented at the congress concluded that substantial weight loss has a chondroprotective effect. The study assessed changes in pain scores, joint biomarkers, and markers of systemic inflammation as outcomes.

Dr. Pascal Richette of Lariboisière Hospital, Paris, reported on 44 obese patients with knee osteoarthritis who underwent bariatric surgery, with a resultant 20% decrease in BMI.

At 6 months post surgery, the group's mean osteoarthritis pain scores had dropped from a baseline of 50 out of a possible 100 points to 24.5 points. This was accompanied by significant functional improvement as measured on the WOMAC (Western Ontario and McMaster Universities) osteoarthritis index subscales.

Serum levels of N-propeptide of type IIA procollagen, a biomarker of cartilage type II collagen synthesis, increased by 32%. Serum levels of cartilage oligomeric matrix protein, a biomarker for cartilage degradation, were down by 36%. Serum levels of interleukin-6 decreased by 26% from baseline, high-sensitivity C-reactive protein was down by 46%, and fibrinogen decreased by 5%, all indicative of reduced systemic inflammation. In addition, serum lipids and insulin resistance were significantly reduced.

Disclosures: Dr. Richette and Dr. Ananda reported having no conflicts of interest.

NATIONAL HARBOR, MD. — Hybrid plating for midfoot arthrodesis offers a high union rate, according to a review.

About three-fourths of patients (76%) had radiographic union by 9 weeks. An additional 15% had union by 12 weeks, and 4% had union by 16 weeks. Only four patients did not achieve union, Dr. Jorge Filippi Nussbaum reported. Most patients (82%) had no complications. In all, 5% of patients had wound dehiscence, 5% had neuropraxia, 2.5% had hardware irritation, 4% had screw breakage, and 2.5% had tendon adhesion, said Dr. Nussbaum.

The researchers conducted a retrospective, multicenter study of patients who had undergone multijoint tarsometatarsal fusion. This technique was used in 78 patients: 60% with primary osteoarthritis, 21% with posttraumatic osteoarthritis, and the remainder with instability and OA, nonunion, Paget's disease, or metatarsus adductus. A plate—flat or curved, depending on the dorsal surface—was aligned, and locking and compression screws were placed, said Dr. Nussbaum, an orthopedic surgeon at Pontifical Catholic University of Chile in Santiago.

Disclosures: Dr. Nussbaum reported that he has no relevant financial relationships.

NATIONAL HARBOR, MD. — Hybrid plating for midfoot arthrodesis offers a high union rate, according to a review.

About three-fourths of patients (76%) had radiographic union by 9 weeks. An additional 15% had union by 12 weeks, and 4% had union by 16 weeks. Only four patients did not achieve union, Dr. Jorge Filippi Nussbaum reported. Most patients (82%) had no complications. In all, 5% of patients had wound dehiscence, 5% had neuropraxia, 2.5% had hardware irritation, 4% had screw breakage, and 2.5% had tendon adhesion, said Dr. Nussbaum.

The researchers conducted a retrospective, multicenter study of patients who had undergone multijoint tarsometatarsal fusion. This technique was used in 78 patients: 60% with primary osteoarthritis, 21% with posttraumatic osteoarthritis, and the remainder with instability and OA, nonunion, Paget's disease, or metatarsus adductus. A plate—flat or curved, depending on the dorsal surface—was aligned, and locking and compression screws were placed, said Dr. Nussbaum, an orthopedic surgeon at Pontifical Catholic University of Chile in Santiago.

Disclosures: Dr. Nussbaum reported that he has no relevant financial relationships.

NATIONAL HARBOR, MD. — Hybrid plating for midfoot arthrodesis offers a high union rate, according to a review.

About three-fourths of patients (76%) had radiographic union by 9 weeks. An additional 15% had union by 12 weeks, and 4% had union by 16 weeks. Only four patients did not achieve union, Dr. Jorge Filippi Nussbaum reported. Most patients (82%) had no complications. In all, 5% of patients had wound dehiscence, 5% had neuropraxia, 2.5% had hardware irritation, 4% had screw breakage, and 2.5% had tendon adhesion, said Dr. Nussbaum.

The researchers conducted a retrospective, multicenter study of patients who had undergone multijoint tarsometatarsal fusion. This technique was used in 78 patients: 60% with primary osteoarthritis, 21% with posttraumatic osteoarthritis, and the remainder with instability and OA, nonunion, Paget's disease, or metatarsus adductus. A plate—flat or curved, depending on the dorsal surface—was aligned, and locking and compression screws were placed, said Dr. Nussbaum, an orthopedic surgeon at Pontifical Catholic University of Chile in Santiago.

Disclosures: Dr. Nussbaum reported that he has no relevant financial relationships.

ROME — Treatment of patients with the dietary supplement avocado-soybean unsaponifiables over 3 years led to a modest but statistically significant reduction in radiographic disease progression in a placebo-controlled study with 345 people with symptomatic hip osteoarthritis.

“The results indicate a potential structure-modifying effect of ASU [avocado-soybean unsaponifiables] over 3 years,” Dr. Emmanuel Maheu said at the annual meeting of the European Congress of Rheumatology.

The finding follows earlier reports that treatment of osteoarthritis with ASU led to “moderate clinical effects on pain and function,” said Dr. Maheu, a rheumatologist at St. Antoine Hospital in Paris.

The new findings “indicate modest structural efficacy from ASU in hip osteoarthritis,” commented Dr. Laure Gossec, a rheumatologist at Cochin Hospital in Paris, who was not involved in the study.

Based on results from pre-clinical studies, ASU is believed to counter the effects of interleukin-1, a cytokine active in the degradation processes of osteoarthritis. ASU might also affect the catabolic-anabolic balance in patients with osteoarthritis, Dr. Maheu said.

The study enrolled patients aged 45 years or older with painful osteoarthritis of the hip that met the clinical and radiologic diagnostic criteria of the American College of Rheumatology. A total of 399 patients met the enrollment criteria and began the study, with 345 undergoing at least two follow-up radiographs that made them eligible for the primary outcome assessment, including 179 in the placebo group and 166 patients who received 300 mg ASU daily.

A total of 237 patients completed all 3 years of treatment, with an equal number of patients withdrawing from the study in each of the two treatment arms. The most common reason for withdrawal from the study was hip replacement surgery. The average age of the patients was 62 years, and slightly more than half were women. Their average joint space width in the affected hip joint at baseline was about 2.8 mm.

The investigators defined progressive structural disease during the study as further loss of at least 0.5 mm of joint space width. This occurred in 50% of the placebo patients and 40% of the patients on ASU, a 10% absolute difference and a 20% relative reduction with ASU that was statistically significant.

Patients treated with ASU had no improvement in their symptom and pain scores compared with the placebo patients, but the study was not designed to assess changes in these end points, Dr. Maheu noted.

The safety profile of patients treated with ASU closely matched the placebo group. Treatment-related adverse events occurred in 4% of placebo patients and 8% of those on ASU. Adverse events leading to withdrawal from the study occurred in 6% of patients in each group.

The supplement is an extract made from avocado and soybean oils that is taken in a 300-mg softgel preparation.

Disclosures: ASU is marketed as a drug in France and several other countries by Expanscience Labs, a French company. The study was sponsored by Expanscience, and Dr. Maheu has received consulting fees and research support from Expanscience; several coauthors on the study are employees of the Expanscience. ASU is marketed as a supplement in the United States.

Source ©subjug/iStockphoto.com

ROME — Treatment of patients with the dietary supplement avocado-soybean unsaponifiables over 3 years led to a modest but statistically significant reduction in radiographic disease progression in a placebo-controlled study with 345 people with symptomatic hip osteoarthritis.

“The results indicate a potential structure-modifying effect of ASU [avocado-soybean unsaponifiables] over 3 years,” Dr. Emmanuel Maheu said at the annual meeting of the European Congress of Rheumatology.

The finding follows earlier reports that treatment of osteoarthritis with ASU led to “moderate clinical effects on pain and function,” said Dr. Maheu, a rheumatologist at St. Antoine Hospital in Paris.

The new findings “indicate modest structural efficacy from ASU in hip osteoarthritis,” commented Dr. Laure Gossec, a rheumatologist at Cochin Hospital in Paris, who was not involved in the study.

Based on results from pre-clinical studies, ASU is believed to counter the effects of interleukin-1, a cytokine active in the degradation processes of osteoarthritis. ASU might also affect the catabolic-anabolic balance in patients with osteoarthritis, Dr. Maheu said.

The study enrolled patients aged 45 years or older with painful osteoarthritis of the hip that met the clinical and radiologic diagnostic criteria of the American College of Rheumatology. A total of 399 patients met the enrollment criteria and began the study, with 345 undergoing at least two follow-up radiographs that made them eligible for the primary outcome assessment, including 179 in the placebo group and 166 patients who received 300 mg ASU daily.

A total of 237 patients completed all 3 years of treatment, with an equal number of patients withdrawing from the study in each of the two treatment arms. The most common reason for withdrawal from the study was hip replacement surgery. The average age of the patients was 62 years, and slightly more than half were women. Their average joint space width in the affected hip joint at baseline was about 2.8 mm.

The investigators defined progressive structural disease during the study as further loss of at least 0.5 mm of joint space width. This occurred in 50% of the placebo patients and 40% of the patients on ASU, a 10% absolute difference and a 20% relative reduction with ASU that was statistically significant.

Patients treated with ASU had no improvement in their symptom and pain scores compared with the placebo patients, but the study was not designed to assess changes in these end points, Dr. Maheu noted.

The safety profile of patients treated with ASU closely matched the placebo group. Treatment-related adverse events occurred in 4% of placebo patients and 8% of those on ASU. Adverse events leading to withdrawal from the study occurred in 6% of patients in each group.

The supplement is an extract made from avocado and soybean oils that is taken in a 300-mg softgel preparation.

Disclosures: ASU is marketed as a drug in France and several other countries by Expanscience Labs, a French company. The study was sponsored by Expanscience, and Dr. Maheu has received consulting fees and research support from Expanscience; several coauthors on the study are employees of the Expanscience. ASU is marketed as a supplement in the United States.

Source ©subjug/iStockphoto.com

ROME — Treatment of patients with the dietary supplement avocado-soybean unsaponifiables over 3 years led to a modest but statistically significant reduction in radiographic disease progression in a placebo-controlled study with 345 people with symptomatic hip osteoarthritis.

“The results indicate a potential structure-modifying effect of ASU [avocado-soybean unsaponifiables] over 3 years,” Dr. Emmanuel Maheu said at the annual meeting of the European Congress of Rheumatology.

The finding follows earlier reports that treatment of osteoarthritis with ASU led to “moderate clinical effects on pain and function,” said Dr. Maheu, a rheumatologist at St. Antoine Hospital in Paris.

The new findings “indicate modest structural efficacy from ASU in hip osteoarthritis,” commented Dr. Laure Gossec, a rheumatologist at Cochin Hospital in Paris, who was not involved in the study.

Based on results from pre-clinical studies, ASU is believed to counter the effects of interleukin-1, a cytokine active in the degradation processes of osteoarthritis. ASU might also affect the catabolic-anabolic balance in patients with osteoarthritis, Dr. Maheu said.

The study enrolled patients aged 45 years or older with painful osteoarthritis of the hip that met the clinical and radiologic diagnostic criteria of the American College of Rheumatology. A total of 399 patients met the enrollment criteria and began the study, with 345 undergoing at least two follow-up radiographs that made them eligible for the primary outcome assessment, including 179 in the placebo group and 166 patients who received 300 mg ASU daily.

A total of 237 patients completed all 3 years of treatment, with an equal number of patients withdrawing from the study in each of the two treatment arms. The most common reason for withdrawal from the study was hip replacement surgery. The average age of the patients was 62 years, and slightly more than half were women. Their average joint space width in the affected hip joint at baseline was about 2.8 mm.

The investigators defined progressive structural disease during the study as further loss of at least 0.5 mm of joint space width. This occurred in 50% of the placebo patients and 40% of the patients on ASU, a 10% absolute difference and a 20% relative reduction with ASU that was statistically significant.

Patients treated with ASU had no improvement in their symptom and pain scores compared with the placebo patients, but the study was not designed to assess changes in these end points, Dr. Maheu noted.

The safety profile of patients treated with ASU closely matched the placebo group. Treatment-related adverse events occurred in 4% of placebo patients and 8% of those on ASU. Adverse events leading to withdrawal from the study occurred in 6% of patients in each group.

The supplement is an extract made from avocado and soybean oils that is taken in a 300-mg softgel preparation.

Disclosures: ASU is marketed as a drug in France and several other countries by Expanscience Labs, a French company. The study was sponsored by Expanscience, and Dr. Maheu has received consulting fees and research support from Expanscience; several coauthors on the study are employees of the Expanscience. ASU is marketed as a supplement in the United States.

Source ©subjug/iStockphoto.com

CHICAGO — The patient on biologic therapy who must travel and requires immunization with a live attenuated virus or bacteria should be immunized before beginning biologic therapy, according to a case report presented to a symposium that was sponsored by the American College of Rheumatology.

“Think hard about the patient's life before you put them on biologic therapy, and immunize before you give the medications,” advised Dr. Clifton O. Bingham, who is director of the rheumatology clinics at Johns Hopkins University, Baltimore. However, he acknowledged that this would not always be possible.

The case was a 35-year-old woman with psoriatic arthritis whose work required her to travel to Burkina Faso, a small, landlocked country in West Africa, where yellow fever is endemic. The patient's skin and articular disease was well controlled with etanercept and methotrexate.

As a practical matter, Dr. Bingham said that the immunomodulators etanercept and methotrexate could be withheld for at least a period of 1 month, and then the patient could be administered yellow fever vaccine. He advised waiting 2-3 weeks before restarting the medication.

“The disease may flare during that period of time, so that's the risk you take,” he said.

If the patient was required to travel to the infected area with only 2 weeks' notice, Dr. Bingham advised providing a letter of medical contraindication to yellow fever vaccination.

“That should allow her to enter the country, but you tell her to be really careful.” When a patient is on biological therapy, he said it is important to understand which live vaccinations could potentially reactivate in the setting of immunosuppression.

Vaccines that contain live attenuated viruses or bacteria include varicella; intranasal influenza/H1N1; measles, mumps, and rubella; yellow fever; oral polio; oral typhoid; vaccinia (smallpox); BCG; and rotavirus.

Disseminated disease has been reported in immunocompromised patients who were immunized with live-virus vaccines. Live viral dissemination has occurred in patients during chemotherapy, and there have been cases of infection in patients receiving immunosuppression for organ transplantation. Live virus dissemination has also been reported in patients with HIV infection. (J. Infect. Dis. 2008;197 [Suppl 2]; Clin. Infect. Dis. 2009;49:1550-6; AIDS Rev. 2007;9:173-87). “So, the recommendation is, with people who are on biologics and people who are immunosuppressed, they should not receive these live vaccinations,” Dr. Bingham said.

Up-to-date vaccine information is available online from the Centers for Disease Control and Prevention (www.cdc.gov/vaccines/pubs/vis/default.htm

An audience member asked, “Do you think that in some cases it may be a better choice to subject somebody to the risk of an attenuated organism, as opposed to the risk of wild-type disease in an area where the disease may be highly endemic?”

Dr. Bingham said, “The risk of developing yellow fever is about 50 per 100,000 in western Africa, and about 10 per 100,000 in Central and South America. So it is a low risk.

“But if you delve a little deeper into that information, you find out that many of those patients die. It's potentially a fatal disease. So you do have to balance the risk.”

Disclosures: Dr. Bingham disclosed financial relationships with Abbott, Amgen, Bristol-Myers Squibb, Centocor, Cypress Bioscience, Genentech, Merck, Novartis, Osiris Therapeutics, Procter & Gamble, Roche, Sonosite, Targeted Genetics, UCB, and Wyeth.

CHICAGO — The patient on biologic therapy who must travel and requires immunization with a live attenuated virus or bacteria should be immunized before beginning biologic therapy, according to a case report presented to a symposium that was sponsored by the American College of Rheumatology.

“Think hard about the patient's life before you put them on biologic therapy, and immunize before you give the medications,” advised Dr. Clifton O. Bingham, who is director of the rheumatology clinics at Johns Hopkins University, Baltimore. However, he acknowledged that this would not always be possible.

The case was a 35-year-old woman with psoriatic arthritis whose work required her to travel to Burkina Faso, a small, landlocked country in West Africa, where yellow fever is endemic. The patient's skin and articular disease was well controlled with etanercept and methotrexate.

As a practical matter, Dr. Bingham said that the immunomodulators etanercept and methotrexate could be withheld for at least a period of 1 month, and then the patient could be administered yellow fever vaccine. He advised waiting 2-3 weeks before restarting the medication.

“The disease may flare during that period of time, so that's the risk you take,” he said.

If the patient was required to travel to the infected area with only 2 weeks' notice, Dr. Bingham advised providing a letter of medical contraindication to yellow fever vaccination.

“That should allow her to enter the country, but you tell her to be really careful.” When a patient is on biological therapy, he said it is important to understand which live vaccinations could potentially reactivate in the setting of immunosuppression.

Vaccines that contain live attenuated viruses or bacteria include varicella; intranasal influenza/H1N1; measles, mumps, and rubella; yellow fever; oral polio; oral typhoid; vaccinia (smallpox); BCG; and rotavirus.

Disseminated disease has been reported in immunocompromised patients who were immunized with live-virus vaccines. Live viral dissemination has occurred in patients during chemotherapy, and there have been cases of infection in patients receiving immunosuppression for organ transplantation. Live virus dissemination has also been reported in patients with HIV infection. (J. Infect. Dis. 2008;197 [Suppl 2]; Clin. Infect. Dis. 2009;49:1550-6; AIDS Rev. 2007;9:173-87). “So, the recommendation is, with people who are on biologics and people who are immunosuppressed, they should not receive these live vaccinations,” Dr. Bingham said.

Up-to-date vaccine information is available online from the Centers for Disease Control and Prevention (www.cdc.gov/vaccines/pubs/vis/default.htm

An audience member asked, “Do you think that in some cases it may be a better choice to subject somebody to the risk of an attenuated organism, as opposed to the risk of wild-type disease in an area where the disease may be highly endemic?”

Dr. Bingham said, “The risk of developing yellow fever is about 50 per 100,000 in western Africa, and about 10 per 100,000 in Central and South America. So it is a low risk.

“But if you delve a little deeper into that information, you find out that many of those patients die. It's potentially a fatal disease. So you do have to balance the risk.”

Disclosures: Dr. Bingham disclosed financial relationships with Abbott, Amgen, Bristol-Myers Squibb, Centocor, Cypress Bioscience, Genentech, Merck, Novartis, Osiris Therapeutics, Procter & Gamble, Roche, Sonosite, Targeted Genetics, UCB, and Wyeth.

CHICAGO — The patient on biologic therapy who must travel and requires immunization with a live attenuated virus or bacteria should be immunized before beginning biologic therapy, according to a case report presented to a symposium that was sponsored by the American College of Rheumatology.

“Think hard about the patient's life before you put them on biologic therapy, and immunize before you give the medications,” advised Dr. Clifton O. Bingham, who is director of the rheumatology clinics at Johns Hopkins University, Baltimore. However, he acknowledged that this would not always be possible.

The case was a 35-year-old woman with psoriatic arthritis whose work required her to travel to Burkina Faso, a small, landlocked country in West Africa, where yellow fever is endemic. The patient's skin and articular disease was well controlled with etanercept and methotrexate.

As a practical matter, Dr. Bingham said that the immunomodulators etanercept and methotrexate could be withheld for at least a period of 1 month, and then the patient could be administered yellow fever vaccine. He advised waiting 2-3 weeks before restarting the medication.

“The disease may flare during that period of time, so that's the risk you take,” he said.

If the patient was required to travel to the infected area with only 2 weeks' notice, Dr. Bingham advised providing a letter of medical contraindication to yellow fever vaccination.

“That should allow her to enter the country, but you tell her to be really careful.” When a patient is on biological therapy, he said it is important to understand which live vaccinations could potentially reactivate in the setting of immunosuppression.

Vaccines that contain live attenuated viruses or bacteria include varicella; intranasal influenza/H1N1; measles, mumps, and rubella; yellow fever; oral polio; oral typhoid; vaccinia (smallpox); BCG; and rotavirus.

Disseminated disease has been reported in immunocompromised patients who were immunized with live-virus vaccines. Live viral dissemination has occurred in patients during chemotherapy, and there have been cases of infection in patients receiving immunosuppression for organ transplantation. Live virus dissemination has also been reported in patients with HIV infection. (J. Infect. Dis. 2008;197 [Suppl 2]; Clin. Infect. Dis. 2009;49:1550-6; AIDS Rev. 2007;9:173-87). “So, the recommendation is, with people who are on biologics and people who are immunosuppressed, they should not receive these live vaccinations,” Dr. Bingham said.

Up-to-date vaccine information is available online from the Centers for Disease Control and Prevention (www.cdc.gov/vaccines/pubs/vis/default.htm

An audience member asked, “Do you think that in some cases it may be a better choice to subject somebody to the risk of an attenuated organism, as opposed to the risk of wild-type disease in an area where the disease may be highly endemic?”

Dr. Bingham said, “The risk of developing yellow fever is about 50 per 100,000 in western Africa, and about 10 per 100,000 in Central and South America. So it is a low risk.

“But if you delve a little deeper into that information, you find out that many of those patients die. It's potentially a fatal disease. So you do have to balance the risk.”

Disclosures: Dr. Bingham disclosed financial relationships with Abbott, Amgen, Bristol-Myers Squibb, Centocor, Cypress Bioscience, Genentech, Merck, Novartis, Osiris Therapeutics, Procter & Gamble, Roche, Sonosite, Targeted Genetics, UCB, and Wyeth.

ROME — Polymyalgia rheumatica may be the presenting manifestation of silent giant cell arteritis, and therein lies a diagnostic dilemma: Which patients need a temporal artery biopsy?

Polymyalgia rheumatica (PMR) is the most common inflammatory rheumatologic disease among the elderly. It would be inappropriate to subject everyone who has symptoms consistent with PMR to temporal artery biopsy. Yet giant cell arteritis is a diagnosis that physicians cannot afford to miss because of the risk of irreversible blindness when the vasculitis isn't promptly recognized and treated with high-dose steroids.

One scenario warranting a temporal artery biopsy involves the patient with typical PMR symptoms—including bilateral shoulder pain with or without bilateral pelvic girdle pain, and morning stiffness lasting more than 45 minutes—plus headache, tinnitus, visual abnormalities, or other potential manifestations of intracranial ischemia, Dr. Miguel A. Gonzalez-Gay said.

Temporal artery biopsy is also a must in patients who don't show marked clinical improvement in response to 15-20 mg/day of oral prednisone within 7 days. This lack of response to low-dose steroids is a strong indicator that one of PMR's plethora of mimicking conditions is at work. Giant cell arteritis belongs at the top of the list of candidates because of its catastrophic consequences if untreated, noted Dr. Gonzalez-Gay of the rheumatology division of the Hospital Universitario Marques de Valdecilla, Santander, Spain.

Another situation warranting temporal artery biopsy involves a patient with typical PMR symptoms plus high fever or other severe constitutional symptoms. Dr. Gonzalez-Gay routinely gets a temporal artery biopsy in patients with PMR symptoms and an erythrocyte sedimentation rate in excess of 80 mm/hr. In studies he has conducted, that's roughly 9% of all patients with typical PMR symptoms.

Among the other main conditions that may present initially as PMR are rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, fibromyalgia, amyloidosis, hypothyroidism, hematologic malignancies, bacterial endocarditis and other infections, and solid cancers, particularly metastases to musculoskeletal sites.

Dr. Gonzalez-Gay said features that should alert physicians to the possibility of a diagnosis other than PMR fall into two broad categories: atypical symptoms, or lack of a marked therapeutic response to prednisone at 15-20 mg/day within 7 days. In reply to an audience question, the rheumatologist said he utilizes 15 mg/day of prednisone except in the most obese patients.

Red flags in the clinical interview include little or no worsening of symptoms with movement, minimal morning stiffness, and diffuse aching. Findings on physical examination that suggest a diagnosis other than PMR include fever with or without a heart murmur, visceral enlargement, painless adenopathies, and synovitis involving the small joints of the hands and feet, the rheumatologist continued.

Laboratory findings that are discordant with PMR include a positive high-titer antinuclear antibody, hematuria, elevated muscle or liver enzymes, severe anemia, and hematologic cytopenias.

Disclosures: Dr. Gonzalez-Gay declared having no conflicts of interest regarding his presentation.

Temporal artery biopsy is a must for patients not responding to 15-20 mg/day of oral prednisone within 7 days.

Source DR. GONZALES-GAY

ROME — Polymyalgia rheumatica may be the presenting manifestation of silent giant cell arteritis, and therein lies a diagnostic dilemma: Which patients need a temporal artery biopsy?

Polymyalgia rheumatica (PMR) is the most common inflammatory rheumatologic disease among the elderly. It would be inappropriate to subject everyone who has symptoms consistent with PMR to temporal artery biopsy. Yet giant cell arteritis is a diagnosis that physicians cannot afford to miss because of the risk of irreversible blindness when the vasculitis isn't promptly recognized and treated with high-dose steroids.

One scenario warranting a temporal artery biopsy involves the patient with typical PMR symptoms—including bilateral shoulder pain with or without bilateral pelvic girdle pain, and morning stiffness lasting more than 45 minutes—plus headache, tinnitus, visual abnormalities, or other potential manifestations of intracranial ischemia, Dr. Miguel A. Gonzalez-Gay said.

Temporal artery biopsy is also a must in patients who don't show marked clinical improvement in response to 15-20 mg/day of oral prednisone within 7 days. This lack of response to low-dose steroids is a strong indicator that one of PMR's plethora of mimicking conditions is at work. Giant cell arteritis belongs at the top of the list of candidates because of its catastrophic consequences if untreated, noted Dr. Gonzalez-Gay of the rheumatology division of the Hospital Universitario Marques de Valdecilla, Santander, Spain.

Another situation warranting temporal artery biopsy involves a patient with typical PMR symptoms plus high fever or other severe constitutional symptoms. Dr. Gonzalez-Gay routinely gets a temporal artery biopsy in patients with PMR symptoms and an erythrocyte sedimentation rate in excess of 80 mm/hr. In studies he has conducted, that's roughly 9% of all patients with typical PMR symptoms.

Among the other main conditions that may present initially as PMR are rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, fibromyalgia, amyloidosis, hypothyroidism, hematologic malignancies, bacterial endocarditis and other infections, and solid cancers, particularly metastases to musculoskeletal sites.

Dr. Gonzalez-Gay said features that should alert physicians to the possibility of a diagnosis other than PMR fall into two broad categories: atypical symptoms, or lack of a marked therapeutic response to prednisone at 15-20 mg/day within 7 days. In reply to an audience question, the rheumatologist said he utilizes 15 mg/day of prednisone except in the most obese patients.

Red flags in the clinical interview include little or no worsening of symptoms with movement, minimal morning stiffness, and diffuse aching. Findings on physical examination that suggest a diagnosis other than PMR include fever with or without a heart murmur, visceral enlargement, painless adenopathies, and synovitis involving the small joints of the hands and feet, the rheumatologist continued.

Laboratory findings that are discordant with PMR include a positive high-titer antinuclear antibody, hematuria, elevated muscle or liver enzymes, severe anemia, and hematologic cytopenias.

Disclosures: Dr. Gonzalez-Gay declared having no conflicts of interest regarding his presentation.

Temporal artery biopsy is a must for patients not responding to 15-20 mg/day of oral prednisone within 7 days.

Source DR. GONZALES-GAY

ROME — Polymyalgia rheumatica may be the presenting manifestation of silent giant cell arteritis, and therein lies a diagnostic dilemma: Which patients need a temporal artery biopsy?

Polymyalgia rheumatica (PMR) is the most common inflammatory rheumatologic disease among the elderly. It would be inappropriate to subject everyone who has symptoms consistent with PMR to temporal artery biopsy. Yet giant cell arteritis is a diagnosis that physicians cannot afford to miss because of the risk of irreversible blindness when the vasculitis isn't promptly recognized and treated with high-dose steroids.

One scenario warranting a temporal artery biopsy involves the patient with typical PMR symptoms—including bilateral shoulder pain with or without bilateral pelvic girdle pain, and morning stiffness lasting more than 45 minutes—plus headache, tinnitus, visual abnormalities, or other potential manifestations of intracranial ischemia, Dr. Miguel A. Gonzalez-Gay said.

Temporal artery biopsy is also a must in patients who don't show marked clinical improvement in response to 15-20 mg/day of oral prednisone within 7 days. This lack of response to low-dose steroids is a strong indicator that one of PMR's plethora of mimicking conditions is at work. Giant cell arteritis belongs at the top of the list of candidates because of its catastrophic consequences if untreated, noted Dr. Gonzalez-Gay of the rheumatology division of the Hospital Universitario Marques de Valdecilla, Santander, Spain.

Another situation warranting temporal artery biopsy involves a patient with typical PMR symptoms plus high fever or other severe constitutional symptoms. Dr. Gonzalez-Gay routinely gets a temporal artery biopsy in patients with PMR symptoms and an erythrocyte sedimentation rate in excess of 80 mm/hr. In studies he has conducted, that's roughly 9% of all patients with typical PMR symptoms.

Among the other main conditions that may present initially as PMR are rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, fibromyalgia, amyloidosis, hypothyroidism, hematologic malignancies, bacterial endocarditis and other infections, and solid cancers, particularly metastases to musculoskeletal sites.

Dr. Gonzalez-Gay said features that should alert physicians to the possibility of a diagnosis other than PMR fall into two broad categories: atypical symptoms, or lack of a marked therapeutic response to prednisone at 15-20 mg/day within 7 days. In reply to an audience question, the rheumatologist said he utilizes 15 mg/day of prednisone except in the most obese patients.

Red flags in the clinical interview include little or no worsening of symptoms with movement, minimal morning stiffness, and diffuse aching. Findings on physical examination that suggest a diagnosis other than PMR include fever with or without a heart murmur, visceral enlargement, painless adenopathies, and synovitis involving the small joints of the hands and feet, the rheumatologist continued.

Laboratory findings that are discordant with PMR include a positive high-titer antinuclear antibody, hematuria, elevated muscle or liver enzymes, severe anemia, and hematologic cytopenias.

Disclosures: Dr. Gonzalez-Gay declared having no conflicts of interest regarding his presentation.

Temporal artery biopsy is a must for patients not responding to 15-20 mg/day of oral prednisone within 7 days.

Source DR. GONZALES-GAY

ROME — A newly launched clinical trial is examining whether adrenal insufficiency contributes to the pathology of polymyalgia rheumatica.

If the study yields data to support the adrenal insufficiency hypothesis, it's quite possible that doses lower than the currently recommended 15-20 mg/day would achieve equal disease control with fewer steroid side effects, according to Dr. Marco A. Cimmino, one of the investigators.

That's why he and other Italian rheumatologists are about to start a multicenter clinical trial in which 200 newly diagnosed polymyalgia rheumatica (PMR) patients will be randomized to 10 or 20 mg/day of prednisone, with a total dose of either 900 mg or 1,800 mg.

The rationale for the study lies in what Dr. Cimmino calls the adrenal insufficiency theory of PMR, which holds that a viral antigen or other exogenous trigger stimulates host defenses in genetically predisposed aging individuals. This results in a proinflammatory state with increased interleukin-6 levels.

If the patient cannot produce sufficient endogenous glucocorticoids to curb this systemic inflammation as a consequence of impaired hypothalamic-pituitary-adrenal axis function, the result is PMR.

If the adrenal insufficiency theory is correct, then 10 mg/day or even less might well be sufficient to abolish the chronic proinflammatory state which defines PMR while avoiding some steroid side effects, said Dr. Cimmino, professor of medicine at the University of Genova (Italy).

“PMR is still very much an open field for research, including treatment studies,” the rheumatologist observed.

Long-term prednisone is considered the standard therapy for PMR. Yet this practice is surprisingly lacking in supporting evidence from controlled trials.

Nonetheless, PMR is generally well controlled by steroid therapy, albeit with a high incidence of side effects.

Because of the lack of controlled studies, the optimal dose of prednisone for PMR is unclear. Most experts recommend using 15-20 mg/day, although studies show that in clinical practice many physicians use considerably higher doses, with a corresponding increase in side effects and no evidence of added benefit.

Another unsettled issue involves treatment duration. Most physicians keep their PMR patients on prednisone for a period of 6-18 months. Dr. Cimmino recommended tapering the medication with the goal of stopping it at the 6-month mark in order to minimize side effects. He noted, however, that he and his colleagues found in a long-term follow-up study that 30%-39% of PMR patients needed to stay on prednisone for more than 6 years.

The take-home message is that PMR is often a less benign disease over the long term than generally supposed (Clin. Exp. Rheumatol. 2008;26:395-400).

With regard to combination therapy with methotrexate and prednisone, Dr. Cimmino was coauthor of a multicenter double-blind clinical trial in which 72 newly diagnosed PMR patients were randomized to prednisone plus either oral methotrexate at 10 mg once weekly or placebo. Prednisone was started at the relatively high dose of 25 mg/day and tapered to zero within 6 months, with dosing adjustments for flares.

At 76 weeks of follow-up, significantly more patients in the methotrexate arm were off prednisone. Indeed, the mean duration on prednisone was 30 weeks in the combination treatment arm, compared to 59 months with prednisone monotherapy. The combined therapy group also had significantly fewer relapses (Ann. Intern. Med. 2004;141:493-500).

The one ray of hope that biologic therapy might be beneficial in PMR comes from a recent case report by rheumatologists at Osaka (Japan) University detailing a dramatic response to tocilizumab (Actemra) in a 65-year-old woman with long-standing steroid-refractory PMR complicated by diabetes, osteoporosis, and hypertension. After her first injection of tocilizumab her C-reactive protein and serum amyloid A levels normalized and the pain in her shoulders and pelvic girdle improved, but her morning stiffness continued. After her fifth injection at a dose of 8 mg/kg every 4 weeks, her morning stiffness was gone and she was in remission (J. Rheumatol. 2010;37:1075-6).

While this is merely a first case report, it's particularly exciting because interleukin-6 levels are consistently high in patients with PMR, and tocilizumab is a humanized monoclonal antibody directed against the IL-6 receptor. Thus, this initial report opens the door to IL-6 inhibition as a novel potential treatment strategy in PMR. “Tocilizumab for PMR is a rheumatologist's dream,” Dr. Cimmino declared.

For now, methotrexate is the only medication of proven efficacy as a steroid-sparing agent in patients with PMR—and it's considerably underutilized for this purpose.

Randomized trial data show that combining methotrexate with prednisone not only is steroid sparing, it also reduces the relapse rate, compared with steroids alone in patients with PMR, he said.

Combining methotrexate and prednisone “makes a lot of sense” in patients with PMR who are at high risk for steroid side effects or who are resistant to oral prednisone at up to 20 mg/day, he said.

In contrast, antitumor necrosis factor therapy using etanercept or infliximab has compiled an unimpressive record overall for PMR in case reports and pilot studies.

“At present, I think there is no role for antitumor necrosis factor therapy in PMR,” he said.

Disclosures: Dr. Cimmino disclosed having received research grants from numerous pharmaceutical companies, including Roche, Schering Plough, Abbott, and Pfizer.

ROME — A newly launched clinical trial is examining whether adrenal insufficiency contributes to the pathology of polymyalgia rheumatica.

If the study yields data to support the adrenal insufficiency hypothesis, it's quite possible that doses lower than the currently recommended 15-20 mg/day would achieve equal disease control with fewer steroid side effects, according to Dr. Marco A. Cimmino, one of the investigators.

That's why he and other Italian rheumatologists are about to start a multicenter clinical trial in which 200 newly diagnosed polymyalgia rheumatica (PMR) patients will be randomized to 10 or 20 mg/day of prednisone, with a total dose of either 900 mg or 1,800 mg.

The rationale for the study lies in what Dr. Cimmino calls the adrenal insufficiency theory of PMR, which holds that a viral antigen or other exogenous trigger stimulates host defenses in genetically predisposed aging individuals. This results in a proinflammatory state with increased interleukin-6 levels.

If the patient cannot produce sufficient endogenous glucocorticoids to curb this systemic inflammation as a consequence of impaired hypothalamic-pituitary-adrenal axis function, the result is PMR.

If the adrenal insufficiency theory is correct, then 10 mg/day or even less might well be sufficient to abolish the chronic proinflammatory state which defines PMR while avoiding some steroid side effects, said Dr. Cimmino, professor of medicine at the University of Genova (Italy).

“PMR is still very much an open field for research, including treatment studies,” the rheumatologist observed.

Long-term prednisone is considered the standard therapy for PMR. Yet this practice is surprisingly lacking in supporting evidence from controlled trials.

Nonetheless, PMR is generally well controlled by steroid therapy, albeit with a high incidence of side effects.

Because of the lack of controlled studies, the optimal dose of prednisone for PMR is unclear. Most experts recommend using 15-20 mg/day, although studies show that in clinical practice many physicians use considerably higher doses, with a corresponding increase in side effects and no evidence of added benefit.

Another unsettled issue involves treatment duration. Most physicians keep their PMR patients on prednisone for a period of 6-18 months. Dr. Cimmino recommended tapering the medication with the goal of stopping it at the 6-month mark in order to minimize side effects. He noted, however, that he and his colleagues found in a long-term follow-up study that 30%-39% of PMR patients needed to stay on prednisone for more than 6 years.

The take-home message is that PMR is often a less benign disease over the long term than generally supposed (Clin. Exp. Rheumatol. 2008;26:395-400).

With regard to combination therapy with methotrexate and prednisone, Dr. Cimmino was coauthor of a multicenter double-blind clinical trial in which 72 newly diagnosed PMR patients were randomized to prednisone plus either oral methotrexate at 10 mg once weekly or placebo. Prednisone was started at the relatively high dose of 25 mg/day and tapered to zero within 6 months, with dosing adjustments for flares.

At 76 weeks of follow-up, significantly more patients in the methotrexate arm were off prednisone. Indeed, the mean duration on prednisone was 30 weeks in the combination treatment arm, compared to 59 months with prednisone monotherapy. The combined therapy group also had significantly fewer relapses (Ann. Intern. Med. 2004;141:493-500).

The one ray of hope that biologic therapy might be beneficial in PMR comes from a recent case report by rheumatologists at Osaka (Japan) University detailing a dramatic response to tocilizumab (Actemra) in a 65-year-old woman with long-standing steroid-refractory PMR complicated by diabetes, osteoporosis, and hypertension. After her first injection of tocilizumab her C-reactive protein and serum amyloid A levels normalized and the pain in her shoulders and pelvic girdle improved, but her morning stiffness continued. After her fifth injection at a dose of 8 mg/kg every 4 weeks, her morning stiffness was gone and she was in remission (J. Rheumatol. 2010;37:1075-6).

While this is merely a first case report, it's particularly exciting because interleukin-6 levels are consistently high in patients with PMR, and tocilizumab is a humanized monoclonal antibody directed against the IL-6 receptor. Thus, this initial report opens the door to IL-6 inhibition as a novel potential treatment strategy in PMR. “Tocilizumab for PMR is a rheumatologist's dream,” Dr. Cimmino declared.

For now, methotrexate is the only medication of proven efficacy as a steroid-sparing agent in patients with PMR—and it's considerably underutilized for this purpose.

Randomized trial data show that combining methotrexate with prednisone not only is steroid sparing, it also reduces the relapse rate, compared with steroids alone in patients with PMR, he said.

Combining methotrexate and prednisone “makes a lot of sense” in patients with PMR who are at high risk for steroid side effects or who are resistant to oral prednisone at up to 20 mg/day, he said.

In contrast, antitumor necrosis factor therapy using etanercept or infliximab has compiled an unimpressive record overall for PMR in case reports and pilot studies.

“At present, I think there is no role for antitumor necrosis factor therapy in PMR,” he said.

Disclosures: Dr. Cimmino disclosed having received research grants from numerous pharmaceutical companies, including Roche, Schering Plough, Abbott, and Pfizer.

ROME — A newly launched clinical trial is examining whether adrenal insufficiency contributes to the pathology of polymyalgia rheumatica.

If the study yields data to support the adrenal insufficiency hypothesis, it's quite possible that doses lower than the currently recommended 15-20 mg/day would achieve equal disease control with fewer steroid side effects, according to Dr. Marco A. Cimmino, one of the investigators.

That's why he and other Italian rheumatologists are about to start a multicenter clinical trial in which 200 newly diagnosed polymyalgia rheumatica (PMR) patients will be randomized to 10 or 20 mg/day of prednisone, with a total dose of either 900 mg or 1,800 mg.

The rationale for the study lies in what Dr. Cimmino calls the adrenal insufficiency theory of PMR, which holds that a viral antigen or other exogenous trigger stimulates host defenses in genetically predisposed aging individuals. This results in a proinflammatory state with increased interleukin-6 levels.

If the patient cannot produce sufficient endogenous glucocorticoids to curb this systemic inflammation as a consequence of impaired hypothalamic-pituitary-adrenal axis function, the result is PMR.

If the adrenal insufficiency theory is correct, then 10 mg/day or even less might well be sufficient to abolish the chronic proinflammatory state which defines PMR while avoiding some steroid side effects, said Dr. Cimmino, professor of medicine at the University of Genova (Italy).

“PMR is still very much an open field for research, including treatment studies,” the rheumatologist observed.

Long-term prednisone is considered the standard therapy for PMR. Yet this practice is surprisingly lacking in supporting evidence from controlled trials.

Nonetheless, PMR is generally well controlled by steroid therapy, albeit with a high incidence of side effects.

Because of the lack of controlled studies, the optimal dose of prednisone for PMR is unclear. Most experts recommend using 15-20 mg/day, although studies show that in clinical practice many physicians use considerably higher doses, with a corresponding increase in side effects and no evidence of added benefit.

Another unsettled issue involves treatment duration. Most physicians keep their PMR patients on prednisone for a period of 6-18 months. Dr. Cimmino recommended tapering the medication with the goal of stopping it at the 6-month mark in order to minimize side effects. He noted, however, that he and his colleagues found in a long-term follow-up study that 30%-39% of PMR patients needed to stay on prednisone for more than 6 years.

The take-home message is that PMR is often a less benign disease over the long term than generally supposed (Clin. Exp. Rheumatol. 2008;26:395-400).

With regard to combination therapy with methotrexate and prednisone, Dr. Cimmino was coauthor of a multicenter double-blind clinical trial in which 72 newly diagnosed PMR patients were randomized to prednisone plus either oral methotrexate at 10 mg once weekly or placebo. Prednisone was started at the relatively high dose of 25 mg/day and tapered to zero within 6 months, with dosing adjustments for flares.

At 76 weeks of follow-up, significantly more patients in the methotrexate arm were off prednisone. Indeed, the mean duration on prednisone was 30 weeks in the combination treatment arm, compared to 59 months with prednisone monotherapy. The combined therapy group also had significantly fewer relapses (Ann. Intern. Med. 2004;141:493-500).

The one ray of hope that biologic therapy might be beneficial in PMR comes from a recent case report by rheumatologists at Osaka (Japan) University detailing a dramatic response to tocilizumab (Actemra) in a 65-year-old woman with long-standing steroid-refractory PMR complicated by diabetes, osteoporosis, and hypertension. After her first injection of tocilizumab her C-reactive protein and serum amyloid A levels normalized and the pain in her shoulders and pelvic girdle improved, but her morning stiffness continued. After her fifth injection at a dose of 8 mg/kg every 4 weeks, her morning stiffness was gone and she was in remission (J. Rheumatol. 2010;37:1075-6).

While this is merely a first case report, it's particularly exciting because interleukin-6 levels are consistently high in patients with PMR, and tocilizumab is a humanized monoclonal antibody directed against the IL-6 receptor. Thus, this initial report opens the door to IL-6 inhibition as a novel potential treatment strategy in PMR. “Tocilizumab for PMR is a rheumatologist's dream,” Dr. Cimmino declared.

For now, methotrexate is the only medication of proven efficacy as a steroid-sparing agent in patients with PMR—and it's considerably underutilized for this purpose.

Randomized trial data show that combining methotrexate with prednisone not only is steroid sparing, it also reduces the relapse rate, compared with steroids alone in patients with PMR, he said.

Combining methotrexate and prednisone “makes a lot of sense” in patients with PMR who are at high risk for steroid side effects or who are resistant to oral prednisone at up to 20 mg/day, he said.

In contrast, antitumor necrosis factor therapy using etanercept or infliximab has compiled an unimpressive record overall for PMR in case reports and pilot studies.

“At present, I think there is no role for antitumor necrosis factor therapy in PMR,” he said.

Disclosures: Dr. Cimmino disclosed having received research grants from numerous pharmaceutical companies, including Roche, Schering Plough, Abbott, and Pfizer.