Rheumatoid Arthritis

Major Finding: Opioid users had higher rates of overall adverse events, severe adverse events, cardiovascular events, fractures, and all-cause mortality than did NSAID users or coxib users.

Data Source: A propensity score–matched cohort analysis involving 12,840 elderly patients taking opioids, NSAIDs, or coxibs for rheumatoid arthritis or osteoarthritis pain.

Disclosures: The study was supported by the Agency for Healthcare Research and Quality. Dr. Solomon reported being an unpaid member of a celecoxib trial executive committee sponsored by Pfizer and an unpaid member of the data safety monitoring board for an analgesic trial sponsored by Pfizer.

Opioids were associated with more risks than were other analgesics in elderly patients taking the drugs for arthritis pain.

Although NSAIDs are known to pose certain risks, the results of the study “support the safety of [NSAIDs] compared with other analgesics,” said Dr. Daniel H. Solomon and his associates at Brigham and Women's Hospital, Boston.

Few studies have examined the relative risks of the three major analgesic groups: NSAIDs, opioids, and coxibs (selective cyclooxygenase-2 inhibitors). “Postmarketing surveillance data from usual care cohorts provide an opportunity to examine comparative safety across a wid-range of events and can complement safety data from randomized controlled trials. However, imbalance in baseline population characteristics confounds many postmarketing surveillance studies,” Dr. Solomon and his colleagues noted (Arch. Intern. Med. 2010;170:1968-78).

“Propensity score–matched analyses may provide better balance of confounders and facilitate relatively straightforward comparative safety analyses,” they added.

To compare safety, the researchers performed a propensity-matched cohort analysis using information from a Medicare database of pharmaceutical coverage for low-income elderly residents of Pennsylvania and New Jersey in 1999-2005. The study population included 12,840 adults with rheumatoid arthritis or osteoarthritis who began using one of the three types of analgesics during the study period and were followed for at least 1 year.

Overall, adverse safety event rates were high for all three groups, with the rate of adverse events leading to hospitalization being greater than 100 per 1,000 person-years for all three types of analgesics. Opioid users had the highest rates of serious adverse events. In particular, the rate of hip, pelvis, wrist, or humerus fractures was 101 per 1,000 person-years in the opioid group, compared with 19 per 1,000 person-years in the coxib group and 26 per 1,000 person-years in the NSAID group.

Even though a link between opioids and fractures has been reported previously, “the strength of the association we observed is larger than in previous reports,” Dr. Solomon and his associates said.

Compared with NSAIDs, opioids (hazard ratio, 1.77) and coxibs (HR, 1.28) were associated with elevated risk for cardiovascular events such as MI, stroke, heart failure, revascularization, and cardiac death. That “unexpected” finding regarding such severe events warrants further study, the investigators noted.

Compared with NSAIDs, risk for upper GI bleeding, lower GI bleeding, or bowel obstruction was similarly high for opioid users (HR, 1.07) but was lower for coxib users (HR, 0.60).

In general, opioid users experienced the most adverse events over time, while NSAID users experienced the fewest.

In addition, “opioid users experienced moderate risk early in treatment,” the investigators noted, while the other groups did not.

Opioid users had significantly higher all-cause mortality (75 deaths per 1,000 person-years) than did either NSAID users (48 deaths per 1,000 person-years) or coxib users (47 deaths per 1,000 person-years).

View on the news

Oversight in the Statistical Methods

The propensity matching was meticulous in this study, leading to well-balanced baseline characteristics among the three treatment groups.

This reassures readers that the observational study design is as robust as possible, and that treatment effects alone account for the observed differences among opioid, NSAID, and coxib users.

However, there is a single unmeasured confounder that calls into question the validity of some of the study findings: the use of over-the-counter NSAIDs, said Dr. William C. Becker and Dr. Patrick G. O'Connor.

It is likely that “a significant proportion” of patients in the opioid group were also taking NSAIDs, because “physicians routinely recommend antiinflammatory medication in addition to opioids to achieve therapeutic synergy in the treatment of arthritis,” they noted.

“It seems implausible that a group of 'opioid-only' elderly patients” who were actually taking supplemental NSAIDs would have a higher risk of adverse cardiovascular events, GI bleeding, and acute kidney injury than would a group taking NSAIDs alone, because these are all known effects of NSAID therapy.

Despite this limitation, “the data on falls and fracture from this … study are nonetheless compelling and carry important clinical implications,” Dr. Becker and Dr. O'Connor said.

DR. BECKER and DR. O'CONNOR are in general internal medicine at Yale University, New Haven, Conn. They reported no financial disclosures. These comments were taken from their invited commentary accompanying Dr. Solomon's report (Arch. Intern. Med. 2010;170:1986-8).

Major Finding: Opioid users had higher rates of overall adverse events, severe adverse events, cardiovascular events, fractures, and all-cause mortality than did NSAID users or coxib users.

Data Source: A propensity score–matched cohort analysis involving 12,840 elderly patients taking opioids, NSAIDs, or coxibs for rheumatoid arthritis or osteoarthritis pain.

Disclosures: The study was supported by the Agency for Healthcare Research and Quality. Dr. Solomon reported being an unpaid member of a celecoxib trial executive committee sponsored by Pfizer and an unpaid member of the data safety monitoring board for an analgesic trial sponsored by Pfizer.

Opioids were associated with more risks than were other analgesics in elderly patients taking the drugs for arthritis pain.

Although NSAIDs are known to pose certain risks, the results of the study “support the safety of [NSAIDs] compared with other analgesics,” said Dr. Daniel H. Solomon and his associates at Brigham and Women's Hospital, Boston.

Few studies have examined the relative risks of the three major analgesic groups: NSAIDs, opioids, and coxibs (selective cyclooxygenase-2 inhibitors). “Postmarketing surveillance data from usual care cohorts provide an opportunity to examine comparative safety across a wid-range of events and can complement safety data from randomized controlled trials. However, imbalance in baseline population characteristics confounds many postmarketing surveillance studies,” Dr. Solomon and his colleagues noted (Arch. Intern. Med. 2010;170:1968-78).

“Propensity score–matched analyses may provide better balance of confounders and facilitate relatively straightforward comparative safety analyses,” they added.

To compare safety, the researchers performed a propensity-matched cohort analysis using information from a Medicare database of pharmaceutical coverage for low-income elderly residents of Pennsylvania and New Jersey in 1999-2005. The study population included 12,840 adults with rheumatoid arthritis or osteoarthritis who began using one of the three types of analgesics during the study period and were followed for at least 1 year.

Overall, adverse safety event rates were high for all three groups, with the rate of adverse events leading to hospitalization being greater than 100 per 1,000 person-years for all three types of analgesics. Opioid users had the highest rates of serious adverse events. In particular, the rate of hip, pelvis, wrist, or humerus fractures was 101 per 1,000 person-years in the opioid group, compared with 19 per 1,000 person-years in the coxib group and 26 per 1,000 person-years in the NSAID group.

Even though a link between opioids and fractures has been reported previously, “the strength of the association we observed is larger than in previous reports,” Dr. Solomon and his associates said.

Compared with NSAIDs, opioids (hazard ratio, 1.77) and coxibs (HR, 1.28) were associated with elevated risk for cardiovascular events such as MI, stroke, heart failure, revascularization, and cardiac death. That “unexpected” finding regarding such severe events warrants further study, the investigators noted.

Compared with NSAIDs, risk for upper GI bleeding, lower GI bleeding, or bowel obstruction was similarly high for opioid users (HR, 1.07) but was lower for coxib users (HR, 0.60).

In general, opioid users experienced the most adverse events over time, while NSAID users experienced the fewest.

In addition, “opioid users experienced moderate risk early in treatment,” the investigators noted, while the other groups did not.

Opioid users had significantly higher all-cause mortality (75 deaths per 1,000 person-years) than did either NSAID users (48 deaths per 1,000 person-years) or coxib users (47 deaths per 1,000 person-years).

View on the news

Oversight in the Statistical Methods

The propensity matching was meticulous in this study, leading to well-balanced baseline characteristics among the three treatment groups.

This reassures readers that the observational study design is as robust as possible, and that treatment effects alone account for the observed differences among opioid, NSAID, and coxib users.

However, there is a single unmeasured confounder that calls into question the validity of some of the study findings: the use of over-the-counter NSAIDs, said Dr. William C. Becker and Dr. Patrick G. O'Connor.

It is likely that “a significant proportion” of patients in the opioid group were also taking NSAIDs, because “physicians routinely recommend antiinflammatory medication in addition to opioids to achieve therapeutic synergy in the treatment of arthritis,” they noted.

“It seems implausible that a group of 'opioid-only' elderly patients” who were actually taking supplemental NSAIDs would have a higher risk of adverse cardiovascular events, GI bleeding, and acute kidney injury than would a group taking NSAIDs alone, because these are all known effects of NSAID therapy.

Despite this limitation, “the data on falls and fracture from this … study are nonetheless compelling and carry important clinical implications,” Dr. Becker and Dr. O'Connor said.

DR. BECKER and DR. O'CONNOR are in general internal medicine at Yale University, New Haven, Conn. They reported no financial disclosures. These comments were taken from their invited commentary accompanying Dr. Solomon's report (Arch. Intern. Med. 2010;170:1986-8).

Major Finding: Opioid users had higher rates of overall adverse events, severe adverse events, cardiovascular events, fractures, and all-cause mortality than did NSAID users or coxib users.

Data Source: A propensity score–matched cohort analysis involving 12,840 elderly patients taking opioids, NSAIDs, or coxibs for rheumatoid arthritis or osteoarthritis pain.

Disclosures: The study was supported by the Agency for Healthcare Research and Quality. Dr. Solomon reported being an unpaid member of a celecoxib trial executive committee sponsored by Pfizer and an unpaid member of the data safety monitoring board for an analgesic trial sponsored by Pfizer.

Opioids were associated with more risks than were other analgesics in elderly patients taking the drugs for arthritis pain.

Although NSAIDs are known to pose certain risks, the results of the study “support the safety of [NSAIDs] compared with other analgesics,” said Dr. Daniel H. Solomon and his associates at Brigham and Women's Hospital, Boston.

Few studies have examined the relative risks of the three major analgesic groups: NSAIDs, opioids, and coxibs (selective cyclooxygenase-2 inhibitors). “Postmarketing surveillance data from usual care cohorts provide an opportunity to examine comparative safety across a wid-range of events and can complement safety data from randomized controlled trials. However, imbalance in baseline population characteristics confounds many postmarketing surveillance studies,” Dr. Solomon and his colleagues noted (Arch. Intern. Med. 2010;170:1968-78).

“Propensity score–matched analyses may provide better balance of confounders and facilitate relatively straightforward comparative safety analyses,” they added.

To compare safety, the researchers performed a propensity-matched cohort analysis using information from a Medicare database of pharmaceutical coverage for low-income elderly residents of Pennsylvania and New Jersey in 1999-2005. The study population included 12,840 adults with rheumatoid arthritis or osteoarthritis who began using one of the three types of analgesics during the study period and were followed for at least 1 year.

Overall, adverse safety event rates were high for all three groups, with the rate of adverse events leading to hospitalization being greater than 100 per 1,000 person-years for all three types of analgesics. Opioid users had the highest rates of serious adverse events. In particular, the rate of hip, pelvis, wrist, or humerus fractures was 101 per 1,000 person-years in the opioid group, compared with 19 per 1,000 person-years in the coxib group and 26 per 1,000 person-years in the NSAID group.

Even though a link between opioids and fractures has been reported previously, “the strength of the association we observed is larger than in previous reports,” Dr. Solomon and his associates said.

Compared with NSAIDs, opioids (hazard ratio, 1.77) and coxibs (HR, 1.28) were associated with elevated risk for cardiovascular events such as MI, stroke, heart failure, revascularization, and cardiac death. That “unexpected” finding regarding such severe events warrants further study, the investigators noted.

Compared with NSAIDs, risk for upper GI bleeding, lower GI bleeding, or bowel obstruction was similarly high for opioid users (HR, 1.07) but was lower for coxib users (HR, 0.60).

In general, opioid users experienced the most adverse events over time, while NSAID users experienced the fewest.

In addition, “opioid users experienced moderate risk early in treatment,” the investigators noted, while the other groups did not.

Opioid users had significantly higher all-cause mortality (75 deaths per 1,000 person-years) than did either NSAID users (48 deaths per 1,000 person-years) or coxib users (47 deaths per 1,000 person-years).

View on the news

Oversight in the Statistical Methods

The propensity matching was meticulous in this study, leading to well-balanced baseline characteristics among the three treatment groups.

This reassures readers that the observational study design is as robust as possible, and that treatment effects alone account for the observed differences among opioid, NSAID, and coxib users.

However, there is a single unmeasured confounder that calls into question the validity of some of the study findings: the use of over-the-counter NSAIDs, said Dr. William C. Becker and Dr. Patrick G. O'Connor.

It is likely that “a significant proportion” of patients in the opioid group were also taking NSAIDs, because “physicians routinely recommend antiinflammatory medication in addition to opioids to achieve therapeutic synergy in the treatment of arthritis,” they noted.

“It seems implausible that a group of 'opioid-only' elderly patients” who were actually taking supplemental NSAIDs would have a higher risk of adverse cardiovascular events, GI bleeding, and acute kidney injury than would a group taking NSAIDs alone, because these are all known effects of NSAID therapy.

Despite this limitation, “the data on falls and fracture from this … study are nonetheless compelling and carry important clinical implications,” Dr. Becker and Dr. O'Connor said.

DR. BECKER and DR. O'CONNOR are in general internal medicine at Yale University, New Haven, Conn. They reported no financial disclosures. These comments were taken from their invited commentary accompanying Dr. Solomon's report (Arch. Intern. Med. 2010;170:1986-8).

Smoking is implicated in over a third of cases of the most severe and common form of rheumatoid arthritis, researchers in Sweden have found, and in one in five cases of RA overall.

Results from a population-based study strengthened the growing body of evidence that links smoking with development of anti-cyclic citrullinated peptide (anti-CCP) antibody–positive rheumatoid arthritis. In a dose-response manner, the link became stronger with heavier smoking, regardless of allele status.

The investigators, led by Henrik Källberg, Ph.D., of the Karolinska Institute in Stockholm, determined the excess fraction of RA cases attributable to smoking to be 20%, regardless of the presence of known genetic risk factors, which comprise single or dual copies of the HLA-DRB1 shared epitope. Smoking was estimated to be responsible for 35% of anti-CCP–positive cases (31% for women and 42% for men) and for each copy of the HLA-DRB1 shared epitope (SE) that was found, smoking was dose-dependently associated with an increased risk of anti-CCP–positive RA. In people with two copies of the HLA-DRB1 SE, 55% of anti-CCP–positive RA was attributable to smoking.

They also found an increased risk of developing RA (OR, 1.9; 95% confidence interval, 1.1-3.5) among heavy smokers without any genetic risk factors. “That was one really interesting finding,” Dr. Källberg said in an interview. “As a heavy smoker, you are almost two times more likely to develop RA” even without the HLA-DRB1 SE alleles.

For their research, Dr. Källberg and colleagues collected blood samples and questionnaire information from 1,205 people who were diagnosed with RA according to the American College of Rheumatology's 1987 criteria, as well as 872 healthy controls matched for age, sex, and geographic location. The cases were part of the Swedish EIRA (Epidemiological Investigation of Rheumatoid Arthritis) cohort study.

The questionnaires solicited information on past and current smoking, thereby allowing investigators to classify each subject by smoking history (current and former smokers of 0-9, 10-19, and 20 pack-years, with 1 pack-year defined as equaling 20 cigarettes per day for 1 year). The investigators tested blood samples for anti-CCP antibody status and the presence of genotyped SE alleles.

The investigators calculated the odds ratios of developing RA associated with different smoking levels and SE alleles, together with 95% confidence intervals, by using logistic regression models. The interaction between smoking and the presence of SE alleles was evaluated as a departure from additive effects, and was estimated by calculating the attributable proportion due to interaction.

For former light and moderate smokers, the risk of developing RA declined and approached never-smoker levels the longer the person had not smoked since quitting. Former heavy smokers, however, continued to see elevated risk, even decades after quitting.

The dose-dependent association with smoking was “not a total surprise. We knew from earlier studies that there was some sort of relationship with the amount,” Dr. Källberg said. “We just didn't expect it to be so clear cut.”

The fact that ex–heavy smokers continued to see elevated risk does not mean that smokers shouldn't quit, Dr. Källberg said. “To some degree, the damage may be done, but we actually find that you gain something by quitting smoking. Quitting smoking can affect how well you respond to treatment.”

Although smoking's presence in RA is smaller than in lung cancer, it is “similar to that seen for ischemic heart disease,” the investigators wrote in their analysis. Furthermore, cardiovascular disease is associated with RA and is the major cause of premature death in people with RA (Ann. Rheum. Dis. 2010 [doi:10.1136/ard.2009.120899]).

Dr. Källberg and colleagues' study was funded by grants from the Swedish government; the insurance company AFA; the European Union; the Flight Attendant Medical Research Institute; National Institutes of Health; and the COMBINE (Controlling Chronic Inflammatory Diseases With Combined Efforts) project. Neither Dr. Källberg nor any of his colleagues declared conflicts of interest.

Smoking is implicated in over a third of cases of the most severe and common form of rheumatoid arthritis, researchers in Sweden have found, and in one in five cases of RA overall.

Results from a population-based study strengthened the growing body of evidence that links smoking with development of anti-cyclic citrullinated peptide (anti-CCP) antibody–positive rheumatoid arthritis. In a dose-response manner, the link became stronger with heavier smoking, regardless of allele status.

The investigators, led by Henrik Källberg, Ph.D., of the Karolinska Institute in Stockholm, determined the excess fraction of RA cases attributable to smoking to be 20%, regardless of the presence of known genetic risk factors, which comprise single or dual copies of the HLA-DRB1 shared epitope. Smoking was estimated to be responsible for 35% of anti-CCP–positive cases (31% for women and 42% for men) and for each copy of the HLA-DRB1 shared epitope (SE) that was found, smoking was dose-dependently associated with an increased risk of anti-CCP–positive RA. In people with two copies of the HLA-DRB1 SE, 55% of anti-CCP–positive RA was attributable to smoking.

They also found an increased risk of developing RA (OR, 1.9; 95% confidence interval, 1.1-3.5) among heavy smokers without any genetic risk factors. “That was one really interesting finding,” Dr. Källberg said in an interview. “As a heavy smoker, you are almost two times more likely to develop RA” even without the HLA-DRB1 SE alleles.

For their research, Dr. Källberg and colleagues collected blood samples and questionnaire information from 1,205 people who were diagnosed with RA according to the American College of Rheumatology's 1987 criteria, as well as 872 healthy controls matched for age, sex, and geographic location. The cases were part of the Swedish EIRA (Epidemiological Investigation of Rheumatoid Arthritis) cohort study.

The questionnaires solicited information on past and current smoking, thereby allowing investigators to classify each subject by smoking history (current and former smokers of 0-9, 10-19, and 20 pack-years, with 1 pack-year defined as equaling 20 cigarettes per day for 1 year). The investigators tested blood samples for anti-CCP antibody status and the presence of genotyped SE alleles.

The investigators calculated the odds ratios of developing RA associated with different smoking levels and SE alleles, together with 95% confidence intervals, by using logistic regression models. The interaction between smoking and the presence of SE alleles was evaluated as a departure from additive effects, and was estimated by calculating the attributable proportion due to interaction.

For former light and moderate smokers, the risk of developing RA declined and approached never-smoker levels the longer the person had not smoked since quitting. Former heavy smokers, however, continued to see elevated risk, even decades after quitting.

The dose-dependent association with smoking was “not a total surprise. We knew from earlier studies that there was some sort of relationship with the amount,” Dr. Källberg said. “We just didn't expect it to be so clear cut.”

The fact that ex–heavy smokers continued to see elevated risk does not mean that smokers shouldn't quit, Dr. Källberg said. “To some degree, the damage may be done, but we actually find that you gain something by quitting smoking. Quitting smoking can affect how well you respond to treatment.”

Although smoking's presence in RA is smaller than in lung cancer, it is “similar to that seen for ischemic heart disease,” the investigators wrote in their analysis. Furthermore, cardiovascular disease is associated with RA and is the major cause of premature death in people with RA (Ann. Rheum. Dis. 2010 [doi:10.1136/ard.2009.120899]).

Dr. Källberg and colleagues' study was funded by grants from the Swedish government; the insurance company AFA; the European Union; the Flight Attendant Medical Research Institute; National Institutes of Health; and the COMBINE (Controlling Chronic Inflammatory Diseases With Combined Efforts) project. Neither Dr. Källberg nor any of his colleagues declared conflicts of interest.

Smoking is implicated in over a third of cases of the most severe and common form of rheumatoid arthritis, researchers in Sweden have found, and in one in five cases of RA overall.

Results from a population-based study strengthened the growing body of evidence that links smoking with development of anti-cyclic citrullinated peptide (anti-CCP) antibody–positive rheumatoid arthritis. In a dose-response manner, the link became stronger with heavier smoking, regardless of allele status.

The investigators, led by Henrik Källberg, Ph.D., of the Karolinska Institute in Stockholm, determined the excess fraction of RA cases attributable to smoking to be 20%, regardless of the presence of known genetic risk factors, which comprise single or dual copies of the HLA-DRB1 shared epitope. Smoking was estimated to be responsible for 35% of anti-CCP–positive cases (31% for women and 42% for men) and for each copy of the HLA-DRB1 shared epitope (SE) that was found, smoking was dose-dependently associated with an increased risk of anti-CCP–positive RA. In people with two copies of the HLA-DRB1 SE, 55% of anti-CCP–positive RA was attributable to smoking.

They also found an increased risk of developing RA (OR, 1.9; 95% confidence interval, 1.1-3.5) among heavy smokers without any genetic risk factors. “That was one really interesting finding,” Dr. Källberg said in an interview. “As a heavy smoker, you are almost two times more likely to develop RA” even without the HLA-DRB1 SE alleles.

For their research, Dr. Källberg and colleagues collected blood samples and questionnaire information from 1,205 people who were diagnosed with RA according to the American College of Rheumatology's 1987 criteria, as well as 872 healthy controls matched for age, sex, and geographic location. The cases were part of the Swedish EIRA (Epidemiological Investigation of Rheumatoid Arthritis) cohort study.

The questionnaires solicited information on past and current smoking, thereby allowing investigators to classify each subject by smoking history (current and former smokers of 0-9, 10-19, and 20 pack-years, with 1 pack-year defined as equaling 20 cigarettes per day for 1 year). The investigators tested blood samples for anti-CCP antibody status and the presence of genotyped SE alleles.

The investigators calculated the odds ratios of developing RA associated with different smoking levels and SE alleles, together with 95% confidence intervals, by using logistic regression models. The interaction between smoking and the presence of SE alleles was evaluated as a departure from additive effects, and was estimated by calculating the attributable proportion due to interaction.

For former light and moderate smokers, the risk of developing RA declined and approached never-smoker levels the longer the person had not smoked since quitting. Former heavy smokers, however, continued to see elevated risk, even decades after quitting.

The dose-dependent association with smoking was “not a total surprise. We knew from earlier studies that there was some sort of relationship with the amount,” Dr. Källberg said. “We just didn't expect it to be so clear cut.”

The fact that ex–heavy smokers continued to see elevated risk does not mean that smokers shouldn't quit, Dr. Källberg said. “To some degree, the damage may be done, but we actually find that you gain something by quitting smoking. Quitting smoking can affect how well you respond to treatment.”

Although smoking's presence in RA is smaller than in lung cancer, it is “similar to that seen for ischemic heart disease,” the investigators wrote in their analysis. Furthermore, cardiovascular disease is associated with RA and is the major cause of premature death in people with RA (Ann. Rheum. Dis. 2010 [doi:10.1136/ard.2009.120899]).

Dr. Källberg and colleagues' study was funded by grants from the Swedish government; the insurance company AFA; the European Union; the Flight Attendant Medical Research Institute; National Institutes of Health; and the COMBINE (Controlling Chronic Inflammatory Diseases With Combined Efforts) project. Neither Dr. Källberg nor any of his colleagues declared conflicts of interest.

Major Finding: TNF inhibitor use was associated with a 60% reduction in the risk of developing diabetes.

Data Source: Data from 1,287 adults with nonincident RA.

Disclosures: Dr. Antohe said that she had no financial conflicts to disclose. Several of her co-investigators have received research grants from pharmaceutical companies including Wyeth, Amgen, and Centocor.

ATLANTA — Use of tumor necrosis factor inhibitors reduced the risk of developing type 2 diabetes by 60%, based on data from 1,287 nondiabetic adults with rheumatoid arthritis.

“Interventions that treat RA and improve insulin resistance are highly desirable,” said Dr. Jana Antohe of Geisinger Health System in Danville, Penn.

To examine the impact of TNF inhibitor use in RA patients, Dr. Antohe and her colleagues followed 1,287 incident RA patients who were identified during January 2001–March 2008 at a rural tertiary health center.

Of the 1,539 RA patients identified, 252 with preexisting diabetes were excluded.

The researchers compared the 884 patients who had never used TNF inhibitors with the 403 patients who had ever used them.

Patients in the ever-use group had a higher median body mass index and C-reactive protein (CRP) level than did the never-use group, but these differences were not significant.

After a median follow-up time of 35 months for the ever users and 23 months for the never users, the researchers identified 13 new cases of diabetes in the ever-use group and 43 in the never-use group, for incidence rates of 11/1,000 person-years and 22/1,000 person-years, respectively, according to the researcher.

The median age of the patients was 61 years, the median BMI was 28.6 kg/m

The findings were adjusted for gender, age, race, hypertension, BMI, positive rheumatoid factor and anti-cyclic citrullinated peptide (anti-CCP) levels, erythrocyte sedimentation rate, CRP levels, and the use of NSAIDs, glucocorticoids, hydroxychloroquine, and methotrexate.

Additional research is needed to confirm the findings in patients at increased risk for cardiovascular disease, Dr. Antohe said.

Major Finding: TNF inhibitor use was associated with a 60% reduction in the risk of developing diabetes.

Data Source: Data from 1,287 adults with nonincident RA.

Disclosures: Dr. Antohe said that she had no financial conflicts to disclose. Several of her co-investigators have received research grants from pharmaceutical companies including Wyeth, Amgen, and Centocor.

ATLANTA — Use of tumor necrosis factor inhibitors reduced the risk of developing type 2 diabetes by 60%, based on data from 1,287 nondiabetic adults with rheumatoid arthritis.

“Interventions that treat RA and improve insulin resistance are highly desirable,” said Dr. Jana Antohe of Geisinger Health System in Danville, Penn.

To examine the impact of TNF inhibitor use in RA patients, Dr. Antohe and her colleagues followed 1,287 incident RA patients who were identified during January 2001–March 2008 at a rural tertiary health center.

Of the 1,539 RA patients identified, 252 with preexisting diabetes were excluded.

The researchers compared the 884 patients who had never used TNF inhibitors with the 403 patients who had ever used them.

Patients in the ever-use group had a higher median body mass index and C-reactive protein (CRP) level than did the never-use group, but these differences were not significant.

After a median follow-up time of 35 months for the ever users and 23 months for the never users, the researchers identified 13 new cases of diabetes in the ever-use group and 43 in the never-use group, for incidence rates of 11/1,000 person-years and 22/1,000 person-years, respectively, according to the researcher.

The median age of the patients was 61 years, the median BMI was 28.6 kg/m

The findings were adjusted for gender, age, race, hypertension, BMI, positive rheumatoid factor and anti-cyclic citrullinated peptide (anti-CCP) levels, erythrocyte sedimentation rate, CRP levels, and the use of NSAIDs, glucocorticoids, hydroxychloroquine, and methotrexate.

Additional research is needed to confirm the findings in patients at increased risk for cardiovascular disease, Dr. Antohe said.

Major Finding: TNF inhibitor use was associated with a 60% reduction in the risk of developing diabetes.

Data Source: Data from 1,287 adults with nonincident RA.

Disclosures: Dr. Antohe said that she had no financial conflicts to disclose. Several of her co-investigators have received research grants from pharmaceutical companies including Wyeth, Amgen, and Centocor.

ATLANTA — Use of tumor necrosis factor inhibitors reduced the risk of developing type 2 diabetes by 60%, based on data from 1,287 nondiabetic adults with rheumatoid arthritis.

“Interventions that treat RA and improve insulin resistance are highly desirable,” said Dr. Jana Antohe of Geisinger Health System in Danville, Penn.

To examine the impact of TNF inhibitor use in RA patients, Dr. Antohe and her colleagues followed 1,287 incident RA patients who were identified during January 2001–March 2008 at a rural tertiary health center.

Of the 1,539 RA patients identified, 252 with preexisting diabetes were excluded.

The researchers compared the 884 patients who had never used TNF inhibitors with the 403 patients who had ever used them.

Patients in the ever-use group had a higher median body mass index and C-reactive protein (CRP) level than did the never-use group, but these differences were not significant.

After a median follow-up time of 35 months for the ever users and 23 months for the never users, the researchers identified 13 new cases of diabetes in the ever-use group and 43 in the never-use group, for incidence rates of 11/1,000 person-years and 22/1,000 person-years, respectively, according to the researcher.

The median age of the patients was 61 years, the median BMI was 28.6 kg/m

The findings were adjusted for gender, age, race, hypertension, BMI, positive rheumatoid factor and anti-cyclic citrullinated peptide (anti-CCP) levels, erythrocyte sedimentation rate, CRP levels, and the use of NSAIDs, glucocorticoids, hydroxychloroquine, and methotrexate.

Additional research is needed to confirm the findings in patients at increased risk for cardiovascular disease, Dr. Antohe said.

ATLANTA — Getting to the place in rheumatoid arthritis therapy where remission is a possibility has been much like the process of conquering a treacherous mountain, according to Dr. Duncan Porter.

Early climbers struggled and failed, but lessons were learned, better equipment was developed, and those who followed in the footsteps of the pioneers achieved what was once thought to be impossible.

“In rheumatology, we have had our own mountain to climb: Twenty years ago we were still puttering around in the foothills with symptom control, through the '80s and '90s we were developing increasing evidence that confirmed that conventional disease-modifying drugs … truly did modify disease activity, but it's been only recently that we've come to focus on the possibility of achieving remission,” he said at the meeting.

Now the top of the mountain is being reached “a good deal more often and a good deal more quickly,” he said, citing findings from the Dutch Rheumatoid Arthritis Monitoring (DREAM) cohort study, which were also presented at the meeting, showing that in 64% of 534 patients with newly diagnosed RA, remission was rapidly achieved with a tight control treatment strategy (Arthritis Rheum. 2010;62[suppl.]:abstract 662).

“I think the reason we're getting there is because we've got better equipment, so we've got more drugs to employ,” Dr. Porter said, adding that although the “better equipment” includes biologics, the improvements are primarily due to the new strategies of care.

“It's how we attack the mountain, it's how we deploy the drugs that we have that has yielded the greatest improvements in outcome,” said Dr. Porter of the University of Glasgow (Scotland).

The treatment strategies he discussed included intensive management, treatment to target, combination disease-modifying anti-rheumatic drug (DMARD) strategies, and remission induction.

Although intensive management and treatment to target often overlap, they are not the same, he stressed.

Intensive management, using monthly patient visits, liberal intramuscular and intra-articular steroid injections, escalation of therapy for persistent disease, and step-up dosing, has been shown to be highly effective for inducing remission. In the TICORA (Tight Control for Rheumatoid Arthritis) study (Lancet 2004;364:263-9), for example, 65% of patients achieved remission, compared with 16% of patients who did not receive intensive management.

Treatment to target was a component of that study, but treatment to target doesn't necessarily include intensive management components, Dr. Porter explained, adding, “I think that may be significant.”

Nonetheless, a recent literature review concluded that although few studies have used a randomized approach to test the value of treatment to target strategies, there is “unanimous” and “compelling” evidence that targeted approaches have value (Ann. Rheum. Dis. 2010;69:638-43).

With a treatment to target strategy, it is important to measure progress toward the target and to adjust therapy accordingly based on clinical judgment. Targets can be based on disease activity scores, or they can be based on remission, ultrasound findings, or biomarkers.

“If nothing else, using [the] disease activity score and applying it to treat to target and intensive management strategies has simply been proven to work,” Dr. Porter said, adding that “starting [patients] on methotrexate and sending them away for 6 months is no longer acceptable.”

Because most studies use a constant dose of the study drug, interpretation in terms of treatment to target strategies can be difficult, as that's not the way treatment to target works, and it's not the way most physicians practice, he said.

“Keeping that in mind is critical if we're to … come to the best strategy,” he added.

One area where it is important to make a distinction between intensive management and treatment to target is with the third strategy Dr. Porter discussed: the combined use of DMARDs. These can include step-up, step-down, and parallel therapy.

In the Bone Estrogen Strength Training (BEST) study, for example, treatment to target, but not intensive management, was used. Four strategies were evaluated, including sequential monotherapy, step-up combination therapy, initial combination therapy plus steroids, and initial biologic therapy.

At 2 years, the groups were identical, and importantly, 39% of patients had sustained low disease activity on monotherapy (Arthritis Rheum. 2005;52:3381-90).

“I think that's quite important if we're to avoid overtreating patients with multiple drugs when they will just do fine on one drug alone,” he said.

Other studies have compared various combinations, and showed that nothing is lost in waiting to see whether combination therapy versus monotherapy is needed. As for the use of biologics, the decision must be based on the complex synthesis of knowledge about efficacy, toxicity, and cost.

A key factor – and a challenge – is knowing the clinical significance of small numbers of Sharp score changes, particularly when you recognize that there is no evidence at all of a window of opportunity when it comes to biologic therapy and halting radiographic progression, Dr. Porter said.

The final strategy – remission induction – remains largely uncharacterized, he said, noting that there are few good studies, and more definitive research is needed to clarify its role.

“By and large we need to maintain the therapies we've started that get our patients into remission, and by and large we cannot plan to withdraw therapies large scale. … There's little compelling evidence, as far as I can see, of early aggressive therapy of any form that can substantially and permanently modify disease processes such that therapy can be withdrawn,” Dr. Porter said.

That suggests rheumatologists are doing much better than 20 years ago in terms of climbing the RA therapy mountain but that the summit has not been reached. And if the RA therapy goals of drug-free remission, cure, and prevention are added to that mountain – which currently has symptom control at its base, followed by disease modification and remission, then half of the mountain remains to be conquered.

In conclusion, Dr. Porter quoted a recent editorial that accompanied another DMARD combination trial (Lancet 2009;374:430-2):

“The most important information to be gathered from clinical trials in RA is not necessarily comparison of agents, but rather the strategy of tight control aiming for remission.”

Dr. Porter said that he has received research funding, served as a consultant, and/or served on the speakers bureau for Abbott, Pfizer, Roche, Schering Plough, and UCB.

ATLANTA — Getting to the place in rheumatoid arthritis therapy where remission is a possibility has been much like the process of conquering a treacherous mountain, according to Dr. Duncan Porter.

Early climbers struggled and failed, but lessons were learned, better equipment was developed, and those who followed in the footsteps of the pioneers achieved what was once thought to be impossible.

“In rheumatology, we have had our own mountain to climb: Twenty years ago we were still puttering around in the foothills with symptom control, through the '80s and '90s we were developing increasing evidence that confirmed that conventional disease-modifying drugs … truly did modify disease activity, but it's been only recently that we've come to focus on the possibility of achieving remission,” he said at the meeting.

Now the top of the mountain is being reached “a good deal more often and a good deal more quickly,” he said, citing findings from the Dutch Rheumatoid Arthritis Monitoring (DREAM) cohort study, which were also presented at the meeting, showing that in 64% of 534 patients with newly diagnosed RA, remission was rapidly achieved with a tight control treatment strategy (Arthritis Rheum. 2010;62[suppl.]:abstract 662).

“I think the reason we're getting there is because we've got better equipment, so we've got more drugs to employ,” Dr. Porter said, adding that although the “better equipment” includes biologics, the improvements are primarily due to the new strategies of care.

“It's how we attack the mountain, it's how we deploy the drugs that we have that has yielded the greatest improvements in outcome,” said Dr. Porter of the University of Glasgow (Scotland).

The treatment strategies he discussed included intensive management, treatment to target, combination disease-modifying anti-rheumatic drug (DMARD) strategies, and remission induction.

Although intensive management and treatment to target often overlap, they are not the same, he stressed.

Intensive management, using monthly patient visits, liberal intramuscular and intra-articular steroid injections, escalation of therapy for persistent disease, and step-up dosing, has been shown to be highly effective for inducing remission. In the TICORA (Tight Control for Rheumatoid Arthritis) study (Lancet 2004;364:263-9), for example, 65% of patients achieved remission, compared with 16% of patients who did not receive intensive management.

Treatment to target was a component of that study, but treatment to target doesn't necessarily include intensive management components, Dr. Porter explained, adding, “I think that may be significant.”

Nonetheless, a recent literature review concluded that although few studies have used a randomized approach to test the value of treatment to target strategies, there is “unanimous” and “compelling” evidence that targeted approaches have value (Ann. Rheum. Dis. 2010;69:638-43).

With a treatment to target strategy, it is important to measure progress toward the target and to adjust therapy accordingly based on clinical judgment. Targets can be based on disease activity scores, or they can be based on remission, ultrasound findings, or biomarkers.

“If nothing else, using [the] disease activity score and applying it to treat to target and intensive management strategies has simply been proven to work,” Dr. Porter said, adding that “starting [patients] on methotrexate and sending them away for 6 months is no longer acceptable.”

Because most studies use a constant dose of the study drug, interpretation in terms of treatment to target strategies can be difficult, as that's not the way treatment to target works, and it's not the way most physicians practice, he said.

“Keeping that in mind is critical if we're to … come to the best strategy,” he added.

One area where it is important to make a distinction between intensive management and treatment to target is with the third strategy Dr. Porter discussed: the combined use of DMARDs. These can include step-up, step-down, and parallel therapy.

In the Bone Estrogen Strength Training (BEST) study, for example, treatment to target, but not intensive management, was used. Four strategies were evaluated, including sequential monotherapy, step-up combination therapy, initial combination therapy plus steroids, and initial biologic therapy.

At 2 years, the groups were identical, and importantly, 39% of patients had sustained low disease activity on monotherapy (Arthritis Rheum. 2005;52:3381-90).

“I think that's quite important if we're to avoid overtreating patients with multiple drugs when they will just do fine on one drug alone,” he said.

Other studies have compared various combinations, and showed that nothing is lost in waiting to see whether combination therapy versus monotherapy is needed. As for the use of biologics, the decision must be based on the complex synthesis of knowledge about efficacy, toxicity, and cost.

A key factor – and a challenge – is knowing the clinical significance of small numbers of Sharp score changes, particularly when you recognize that there is no evidence at all of a window of opportunity when it comes to biologic therapy and halting radiographic progression, Dr. Porter said.

The final strategy – remission induction – remains largely uncharacterized, he said, noting that there are few good studies, and more definitive research is needed to clarify its role.

“By and large we need to maintain the therapies we've started that get our patients into remission, and by and large we cannot plan to withdraw therapies large scale. … There's little compelling evidence, as far as I can see, of early aggressive therapy of any form that can substantially and permanently modify disease processes such that therapy can be withdrawn,” Dr. Porter said.

That suggests rheumatologists are doing much better than 20 years ago in terms of climbing the RA therapy mountain but that the summit has not been reached. And if the RA therapy goals of drug-free remission, cure, and prevention are added to that mountain – which currently has symptom control at its base, followed by disease modification and remission, then half of the mountain remains to be conquered.

In conclusion, Dr. Porter quoted a recent editorial that accompanied another DMARD combination trial (Lancet 2009;374:430-2):

“The most important information to be gathered from clinical trials in RA is not necessarily comparison of agents, but rather the strategy of tight control aiming for remission.”

Dr. Porter said that he has received research funding, served as a consultant, and/or served on the speakers bureau for Abbott, Pfizer, Roche, Schering Plough, and UCB.

ATLANTA — Getting to the place in rheumatoid arthritis therapy where remission is a possibility has been much like the process of conquering a treacherous mountain, according to Dr. Duncan Porter.

Early climbers struggled and failed, but lessons were learned, better equipment was developed, and those who followed in the footsteps of the pioneers achieved what was once thought to be impossible.

“In rheumatology, we have had our own mountain to climb: Twenty years ago we were still puttering around in the foothills with symptom control, through the '80s and '90s we were developing increasing evidence that confirmed that conventional disease-modifying drugs … truly did modify disease activity, but it's been only recently that we've come to focus on the possibility of achieving remission,” he said at the meeting.

Now the top of the mountain is being reached “a good deal more often and a good deal more quickly,” he said, citing findings from the Dutch Rheumatoid Arthritis Monitoring (DREAM) cohort study, which were also presented at the meeting, showing that in 64% of 534 patients with newly diagnosed RA, remission was rapidly achieved with a tight control treatment strategy (Arthritis Rheum. 2010;62[suppl.]:abstract 662).

“I think the reason we're getting there is because we've got better equipment, so we've got more drugs to employ,” Dr. Porter said, adding that although the “better equipment” includes biologics, the improvements are primarily due to the new strategies of care.

“It's how we attack the mountain, it's how we deploy the drugs that we have that has yielded the greatest improvements in outcome,” said Dr. Porter of the University of Glasgow (Scotland).

The treatment strategies he discussed included intensive management, treatment to target, combination disease-modifying anti-rheumatic drug (DMARD) strategies, and remission induction.

Although intensive management and treatment to target often overlap, they are not the same, he stressed.

Intensive management, using monthly patient visits, liberal intramuscular and intra-articular steroid injections, escalation of therapy for persistent disease, and step-up dosing, has been shown to be highly effective for inducing remission. In the TICORA (Tight Control for Rheumatoid Arthritis) study (Lancet 2004;364:263-9), for example, 65% of patients achieved remission, compared with 16% of patients who did not receive intensive management.

Treatment to target was a component of that study, but treatment to target doesn't necessarily include intensive management components, Dr. Porter explained, adding, “I think that may be significant.”

Nonetheless, a recent literature review concluded that although few studies have used a randomized approach to test the value of treatment to target strategies, there is “unanimous” and “compelling” evidence that targeted approaches have value (Ann. Rheum. Dis. 2010;69:638-43).

With a treatment to target strategy, it is important to measure progress toward the target and to adjust therapy accordingly based on clinical judgment. Targets can be based on disease activity scores, or they can be based on remission, ultrasound findings, or biomarkers.

“If nothing else, using [the] disease activity score and applying it to treat to target and intensive management strategies has simply been proven to work,” Dr. Porter said, adding that “starting [patients] on methotrexate and sending them away for 6 months is no longer acceptable.”

Because most studies use a constant dose of the study drug, interpretation in terms of treatment to target strategies can be difficult, as that's not the way treatment to target works, and it's not the way most physicians practice, he said.

“Keeping that in mind is critical if we're to … come to the best strategy,” he added.

One area where it is important to make a distinction between intensive management and treatment to target is with the third strategy Dr. Porter discussed: the combined use of DMARDs. These can include step-up, step-down, and parallel therapy.

In the Bone Estrogen Strength Training (BEST) study, for example, treatment to target, but not intensive management, was used. Four strategies were evaluated, including sequential monotherapy, step-up combination therapy, initial combination therapy plus steroids, and initial biologic therapy.

At 2 years, the groups were identical, and importantly, 39% of patients had sustained low disease activity on monotherapy (Arthritis Rheum. 2005;52:3381-90).

“I think that's quite important if we're to avoid overtreating patients with multiple drugs when they will just do fine on one drug alone,” he said.

Other studies have compared various combinations, and showed that nothing is lost in waiting to see whether combination therapy versus monotherapy is needed. As for the use of biologics, the decision must be based on the complex synthesis of knowledge about efficacy, toxicity, and cost.

A key factor – and a challenge – is knowing the clinical significance of small numbers of Sharp score changes, particularly when you recognize that there is no evidence at all of a window of opportunity when it comes to biologic therapy and halting radiographic progression, Dr. Porter said.

The final strategy – remission induction – remains largely uncharacterized, he said, noting that there are few good studies, and more definitive research is needed to clarify its role.

“By and large we need to maintain the therapies we've started that get our patients into remission, and by and large we cannot plan to withdraw therapies large scale. … There's little compelling evidence, as far as I can see, of early aggressive therapy of any form that can substantially and permanently modify disease processes such that therapy can be withdrawn,” Dr. Porter said.

That suggests rheumatologists are doing much better than 20 years ago in terms of climbing the RA therapy mountain but that the summit has not been reached. And if the RA therapy goals of drug-free remission, cure, and prevention are added to that mountain – which currently has symptom control at its base, followed by disease modification and remission, then half of the mountain remains to be conquered.

In conclusion, Dr. Porter quoted a recent editorial that accompanied another DMARD combination trial (Lancet 2009;374:430-2):

“The most important information to be gathered from clinical trials in RA is not necessarily comparison of agents, but rather the strategy of tight control aiming for remission.”

Dr. Porter said that he has received research funding, served as a consultant, and/or served on the speakers bureau for Abbott, Pfizer, Roche, Schering Plough, and UCB.

Major Finding: TNF-inhibitor users reduced the average sick leave time from 9.8 days per month at the start of treatment to 6.5 days after 6 months of treatment.

Data Source: A study of 365 Swedish adults aged 18-58 years with rheumatoid arthritis

Disclosures: The researchers said that they had no relevant financial disclosures.

A significant 30% reduction in the number of sick leave days per month was seen in adults with rheumatoid arthritis after using TNF antagonists for 6 months.

The finding was observed in a population-based study of 365 RA patients aged 18-85 years.

The study is among the first to address the quantitative impact of TNF inhibitors on sick leave and disability pension, said Dr. Tor Olofsson of Lund (Sweden) University, and colleagues, whose study was published in the December issue of Annals of the Rheumatic Diseases.

They reviewed insurance database information on RA patients enrolled in the South Swedish Arthritis Treatment Group registry.

Each patient was matched with four controls from the general population.

The study population averaged 9 sick days per month in the first month of anti-TNF treatment. The monthly rate dropped to an average of 6.5 days after 6 months and remained steady at an average of 6.6 days per month for months 6-12 (Ann. Rheum. Dis. 2010;69:2131-6).

Compared with the controls in the general population, the relative risk of being on sick leave in the RA group was 6.6 at the start of treatment, but dropped to 5.1 after 6 months, and remained at an average of 5.2 for the rest of the year. The relative risk of being on disability pension was 3.4 at the start of treatment and 3.2 after one year of treatment.

Approximately 98% of the patients had tried at least one disease-modifying antirheumatic drug (DMARD) before starting anti-TNF therapy.

The average age of the patients was 46 years, and 82% were women. A total of 92 patients (25%) discontinued treatment, including 34 for adverse events, 32 for treatment failure, and 26 for other reasons.

Major Finding: TNF-inhibitor users reduced the average sick leave time from 9.8 days per month at the start of treatment to 6.5 days after 6 months of treatment.

Data Source: A study of 365 Swedish adults aged 18-58 years with rheumatoid arthritis

Disclosures: The researchers said that they had no relevant financial disclosures.

A significant 30% reduction in the number of sick leave days per month was seen in adults with rheumatoid arthritis after using TNF antagonists for 6 months.

The finding was observed in a population-based study of 365 RA patients aged 18-85 years.

The study is among the first to address the quantitative impact of TNF inhibitors on sick leave and disability pension, said Dr. Tor Olofsson of Lund (Sweden) University, and colleagues, whose study was published in the December issue of Annals of the Rheumatic Diseases.

They reviewed insurance database information on RA patients enrolled in the South Swedish Arthritis Treatment Group registry.

Each patient was matched with four controls from the general population.

The study population averaged 9 sick days per month in the first month of anti-TNF treatment. The monthly rate dropped to an average of 6.5 days after 6 months and remained steady at an average of 6.6 days per month for months 6-12 (Ann. Rheum. Dis. 2010;69:2131-6).

Compared with the controls in the general population, the relative risk of being on sick leave in the RA group was 6.6 at the start of treatment, but dropped to 5.1 after 6 months, and remained at an average of 5.2 for the rest of the year. The relative risk of being on disability pension was 3.4 at the start of treatment and 3.2 after one year of treatment.

Approximately 98% of the patients had tried at least one disease-modifying antirheumatic drug (DMARD) before starting anti-TNF therapy.

The average age of the patients was 46 years, and 82% were women. A total of 92 patients (25%) discontinued treatment, including 34 for adverse events, 32 for treatment failure, and 26 for other reasons.

Major Finding: TNF-inhibitor users reduced the average sick leave time from 9.8 days per month at the start of treatment to 6.5 days after 6 months of treatment.

Data Source: A study of 365 Swedish adults aged 18-58 years with rheumatoid arthritis

Disclosures: The researchers said that they had no relevant financial disclosures.

A significant 30% reduction in the number of sick leave days per month was seen in adults with rheumatoid arthritis after using TNF antagonists for 6 months.

The finding was observed in a population-based study of 365 RA patients aged 18-85 years.

The study is among the first to address the quantitative impact of TNF inhibitors on sick leave and disability pension, said Dr. Tor Olofsson of Lund (Sweden) University, and colleagues, whose study was published in the December issue of Annals of the Rheumatic Diseases.

They reviewed insurance database information on RA patients enrolled in the South Swedish Arthritis Treatment Group registry.

Each patient was matched with four controls from the general population.

The study population averaged 9 sick days per month in the first month of anti-TNF treatment. The monthly rate dropped to an average of 6.5 days after 6 months and remained steady at an average of 6.6 days per month for months 6-12 (Ann. Rheum. Dis. 2010;69:2131-6).

Compared with the controls in the general population, the relative risk of being on sick leave in the RA group was 6.6 at the start of treatment, but dropped to 5.1 after 6 months, and remained at an average of 5.2 for the rest of the year. The relative risk of being on disability pension was 3.4 at the start of treatment and 3.2 after one year of treatment.

Approximately 98% of the patients had tried at least one disease-modifying antirheumatic drug (DMARD) before starting anti-TNF therapy.

The average age of the patients was 46 years, and 82% were women. A total of 92 patients (25%) discontinued treatment, including 34 for adverse events, 32 for treatment failure, and 26 for other reasons.

Major Finding: After taking into consideration the propensity for prescribing methotrexate, prednisone, and anti–tumor necrosis factor agents over time, and after adjusting for potential confounding factors such as disease severity, a strong protective effect on mortality in RA patients was shown for methotrexate (adjusted hazard ratio 0.23) but not for prednisone (adjusted hazard ratio 1.80).

Data Source: An analysis of data – using a novel propensity scoring method – from a longitudinal multicenter observational database of 5,629 RA patients.

Disclosures: Dr. Wasko disclosed that she has received research grants from Amgen, has served as the principle investigator for clinical trials for Centocor, and has served as a consultant for Centocor and UCB.

ATLANTA — Methotrexate use is strongly associated with longer survival in rheumatoid arthritis patients.

After taking into consideration the propensity for prescribing methotrexate, prednisone, and anti–tumor necrosis factor (TNF) agents over time, and after adjusting for potential confounding factors such as disease severity, a strong protective effect on mortality was shown for methotrexate (adjusted hazard ratio 0.23) but not for prednisone (adjusted hazard ratio 1.80), said Dr. Mary Chester Wasko.

Combined treatment with methotrexate and prednisone also had a significant protective effect (hazard ratio 0.34).

“Since methotrexate appeared to be strongly protective with respect to survival in these analyses, and because methotrexate and prednisone are often prescribed together in practice, we questioned whether there might be an interaction between the two drugs with respect to survival,” said Dr. Wasko of the University of Pittsburgh.

Indeed, the strength of the association between methotrexate and improved mortality was only modestly reduced when methotrexate was used in combination with prednisone, she added.

Anti-TNF agents were associated with a slightly decreased risk of mortality. Although the result was not statistically significant (adjusted hazard ratio 0.15), follow-up was limited, as the analyses were based on only 10 deaths out of 598 treated patients with only 5 years of follow-up after these drugs were approved. Additional follow-up is needed to strengthen the results.

Dr. Wasko and her colleagues used the Arthritis, Rheumatism, and Aging Medical Information Systems (ARAMIS) database of patients from 10 U.S. rheumatology practices for their study. The median age of the 5,629 participants was 58 years, 75% were female, 90% were white, and follow-up was a median of 4 years and 3 months. A total of 1,027 patients died during 36,612 patient years of observation.

Patients were evaluated biannually from 1981 to 2003 using the Health Assessment Questionnaire (HAQ).

They reported on demographics, health status (including comorbidities), and medication use.

The outcome of interest was all-cause mortality as confirmed by next of kin.

Major Finding: After taking into consideration the propensity for prescribing methotrexate, prednisone, and anti–tumor necrosis factor agents over time, and after adjusting for potential confounding factors such as disease severity, a strong protective effect on mortality in RA patients was shown for methotrexate (adjusted hazard ratio 0.23) but not for prednisone (adjusted hazard ratio 1.80).

Data Source: An analysis of data – using a novel propensity scoring method – from a longitudinal multicenter observational database of 5,629 RA patients.

Disclosures: Dr. Wasko disclosed that she has received research grants from Amgen, has served as the principle investigator for clinical trials for Centocor, and has served as a consultant for Centocor and UCB.

ATLANTA — Methotrexate use is strongly associated with longer survival in rheumatoid arthritis patients.

After taking into consideration the propensity for prescribing methotrexate, prednisone, and anti–tumor necrosis factor (TNF) agents over time, and after adjusting for potential confounding factors such as disease severity, a strong protective effect on mortality was shown for methotrexate (adjusted hazard ratio 0.23) but not for prednisone (adjusted hazard ratio 1.80), said Dr. Mary Chester Wasko.

Combined treatment with methotrexate and prednisone also had a significant protective effect (hazard ratio 0.34).

“Since methotrexate appeared to be strongly protective with respect to survival in these analyses, and because methotrexate and prednisone are often prescribed together in practice, we questioned whether there might be an interaction between the two drugs with respect to survival,” said Dr. Wasko of the University of Pittsburgh.

Indeed, the strength of the association between methotrexate and improved mortality was only modestly reduced when methotrexate was used in combination with prednisone, she added.

Anti-TNF agents were associated with a slightly decreased risk of mortality. Although the result was not statistically significant (adjusted hazard ratio 0.15), follow-up was limited, as the analyses were based on only 10 deaths out of 598 treated patients with only 5 years of follow-up after these drugs were approved. Additional follow-up is needed to strengthen the results.

Dr. Wasko and her colleagues used the Arthritis, Rheumatism, and Aging Medical Information Systems (ARAMIS) database of patients from 10 U.S. rheumatology practices for their study. The median age of the 5,629 participants was 58 years, 75% were female, 90% were white, and follow-up was a median of 4 years and 3 months. A total of 1,027 patients died during 36,612 patient years of observation.

Patients were evaluated biannually from 1981 to 2003 using the Health Assessment Questionnaire (HAQ).

They reported on demographics, health status (including comorbidities), and medication use.

The outcome of interest was all-cause mortality as confirmed by next of kin.

Major Finding: After taking into consideration the propensity for prescribing methotrexate, prednisone, and anti–tumor necrosis factor agents over time, and after adjusting for potential confounding factors such as disease severity, a strong protective effect on mortality in RA patients was shown for methotrexate (adjusted hazard ratio 0.23) but not for prednisone (adjusted hazard ratio 1.80).

Data Source: An analysis of data – using a novel propensity scoring method – from a longitudinal multicenter observational database of 5,629 RA patients.

Disclosures: Dr. Wasko disclosed that she has received research grants from Amgen, has served as the principle investigator for clinical trials for Centocor, and has served as a consultant for Centocor and UCB.

ATLANTA — Methotrexate use is strongly associated with longer survival in rheumatoid arthritis patients.

After taking into consideration the propensity for prescribing methotrexate, prednisone, and anti–tumor necrosis factor (TNF) agents over time, and after adjusting for potential confounding factors such as disease severity, a strong protective effect on mortality was shown for methotrexate (adjusted hazard ratio 0.23) but not for prednisone (adjusted hazard ratio 1.80), said Dr. Mary Chester Wasko.

Combined treatment with methotrexate and prednisone also had a significant protective effect (hazard ratio 0.34).

“Since methotrexate appeared to be strongly protective with respect to survival in these analyses, and because methotrexate and prednisone are often prescribed together in practice, we questioned whether there might be an interaction between the two drugs with respect to survival,” said Dr. Wasko of the University of Pittsburgh.

Indeed, the strength of the association between methotrexate and improved mortality was only modestly reduced when methotrexate was used in combination with prednisone, she added.

Anti-TNF agents were associated with a slightly decreased risk of mortality. Although the result was not statistically significant (adjusted hazard ratio 0.15), follow-up was limited, as the analyses were based on only 10 deaths out of 598 treated patients with only 5 years of follow-up after these drugs were approved. Additional follow-up is needed to strengthen the results.

Dr. Wasko and her colleagues used the Arthritis, Rheumatism, and Aging Medical Information Systems (ARAMIS) database of patients from 10 U.S. rheumatology practices for their study. The median age of the 5,629 participants was 58 years, 75% were female, 90% were white, and follow-up was a median of 4 years and 3 months. A total of 1,027 patients died during 36,612 patient years of observation.

Patients were evaluated biannually from 1981 to 2003 using the Health Assessment Questionnaire (HAQ).

They reported on demographics, health status (including comorbidities), and medication use.

The outcome of interest was all-cause mortality as confirmed by next of kin.

When it comes to heart disease in rheumatoid arthritis, the classic risk factors like body mass index and abnormal lipid profiles play a role, but a very different one than among the general population, according to Dr. George D. Kitas and Dr. Sherine E. Gabriel.

Moreover, systemic inflammation is likely just as important for the development of cardiovascular disease in this cohort. Therefore, “effective, even optimal control of traditional risk factors is imperative, but may be insufficient to reduce CV risk for people with RA,” the investigators wrote (Ann. Rheum. Dis. 2010 Nov. 24 [doi:10.1136/ard.2010.142133]). Rather, “tight control of systemic inflammation is likely to be required for optimal results.”

According to Dr. Kitas of the Arthritis Research U.K. Epidemiology Unit at Manchester (England) University, and Dr. Gabriel of the division of rheumatology at the Mayo Clinic, Rochester, Minn., one of the commonest and simplest risk factors for heart disease among the general population – increased body mass index – may, paradoxically, be associated with increased survival among RA patients.

They point to one study showing that even after the presence of diabetes mellitus, cardiac history, smoking, and hypertension were controlled for, lower BMI carried a threefold risk of death, compared with patients without RA (Arthritis Rheum. 2004;50:3450-7).

“RA appears to be associated with profound alterations in body composition, which are not reflected in the BMI thresholds used in the general population,” the authors wrote.

These alterations include what the authors call “rheumatoid cachexia,” characterized by low muscle mass combined with a high fat mass, which may represent “from the CV perspective, the 'worst of both worlds.'”

A similar paradoxical relationship appears to exist concerning lipids in RA. “Serum levels of total cholesterol and LDL cholesterol decline precipitously during the 3- to 5-year period before RA incidence,” they wrote, citing a study by other investigators (Ann. Rheum. Dis. 2009;68[suppl. 3]:78).

On the other hand, dyslipidemia has been documented to affect “up to half” of hospitalized RA patients (Ann. Rheum. Dis. 2010;69:683-8).

Meanwhile, the landmark JUPITER study (Justification for the Use of Statins in Primary Prevention: An Intervention Trial Evaluating Rosuvastatin) excluded RA patients, because of C-reactive protein levels in excess of the “arbitrarily chosen threshold of 2 mg/L used in that trial, as well as a significant classical CV risk factor load, unlike the participants in JUPITER, who had no other risk factors.” They reported that a trial of statins specifically in RA, enrolling 4,000 patients, is underway in the United Kingdom, but will not report results until 2016 (www.dgoh.nhs.uk/tracera

Another area where research is lacking is concerning the effects of inflammation on CV risk. The authors pointed, for example, to the theory of “accelerated atherosclerosis,” first postulated in the 1990s.

“The cell types, cytokine signaling, adhesion interactions, and tissue-damaging processes involved in the generation, progression, instability, and rupture of atheromatous plaques are reminiscent of those seen in chronic rheumatoid synovitis,” they wrote.

Moreover, “effective RA treatment appears to be associated with some, often transient, improvements in vascular function,” they added, although “there are no clear, consistent relationships between this and contemporary disease activity.”

Another theory, that “high-grade systemic inflammation in RA does not necessarily imply accelerated atherosclerosis but rather an increased propensity to plaque instability and rupture,” was confirmed in an autopsy analysis in one study (J. Rheumatol. 2007;34:937-42).

The work was funded by Arthritis Research U.K., the British Heart Foundation, the Medical Research Council, and the U.S. National Institute of Arthritis and Musculoskeletal Diseases. Dr. Kitas and Dr. Gabriel said they had no relevant financial disclosures.

When it comes to heart disease in rheumatoid arthritis, the classic risk factors like body mass index and abnormal lipid profiles play a role, but a very different one than among the general population, according to Dr. George D. Kitas and Dr. Sherine E. Gabriel.

Moreover, systemic inflammation is likely just as important for the development of cardiovascular disease in this cohort. Therefore, “effective, even optimal control of traditional risk factors is imperative, but may be insufficient to reduce CV risk for people with RA,” the investigators wrote (Ann. Rheum. Dis. 2010 Nov. 24 [doi:10.1136/ard.2010.142133]). Rather, “tight control of systemic inflammation is likely to be required for optimal results.”

According to Dr. Kitas of the Arthritis Research U.K. Epidemiology Unit at Manchester (England) University, and Dr. Gabriel of the division of rheumatology at the Mayo Clinic, Rochester, Minn., one of the commonest and simplest risk factors for heart disease among the general population – increased body mass index – may, paradoxically, be associated with increased survival among RA patients.

They point to one study showing that even after the presence of diabetes mellitus, cardiac history, smoking, and hypertension were controlled for, lower BMI carried a threefold risk of death, compared with patients without RA (Arthritis Rheum. 2004;50:3450-7).

“RA appears to be associated with profound alterations in body composition, which are not reflected in the BMI thresholds used in the general population,” the authors wrote.

These alterations include what the authors call “rheumatoid cachexia,” characterized by low muscle mass combined with a high fat mass, which may represent “from the CV perspective, the 'worst of both worlds.'”

A similar paradoxical relationship appears to exist concerning lipids in RA. “Serum levels of total cholesterol and LDL cholesterol decline precipitously during the 3- to 5-year period before RA incidence,” they wrote, citing a study by other investigators (Ann. Rheum. Dis. 2009;68[suppl. 3]:78).

On the other hand, dyslipidemia has been documented to affect “up to half” of hospitalized RA patients (Ann. Rheum. Dis. 2010;69:683-8).

Meanwhile, the landmark JUPITER study (Justification for the Use of Statins in Primary Prevention: An Intervention Trial Evaluating Rosuvastatin) excluded RA patients, because of C-reactive protein levels in excess of the “arbitrarily chosen threshold of 2 mg/L used in that trial, as well as a significant classical CV risk factor load, unlike the participants in JUPITER, who had no other risk factors.” They reported that a trial of statins specifically in RA, enrolling 4,000 patients, is underway in the United Kingdom, but will not report results until 2016 (www.dgoh.nhs.uk/tracera

Another area where research is lacking is concerning the effects of inflammation on CV risk. The authors pointed, for example, to the theory of “accelerated atherosclerosis,” first postulated in the 1990s.

“The cell types, cytokine signaling, adhesion interactions, and tissue-damaging processes involved in the generation, progression, instability, and rupture of atheromatous plaques are reminiscent of those seen in chronic rheumatoid synovitis,” they wrote.

Moreover, “effective RA treatment appears to be associated with some, often transient, improvements in vascular function,” they added, although “there are no clear, consistent relationships between this and contemporary disease activity.”

Another theory, that “high-grade systemic inflammation in RA does not necessarily imply accelerated atherosclerosis but rather an increased propensity to plaque instability and rupture,” was confirmed in an autopsy analysis in one study (J. Rheumatol. 2007;34:937-42).

The work was funded by Arthritis Research U.K., the British Heart Foundation, the Medical Research Council, and the U.S. National Institute of Arthritis and Musculoskeletal Diseases. Dr. Kitas and Dr. Gabriel said they had no relevant financial disclosures.

When it comes to heart disease in rheumatoid arthritis, the classic risk factors like body mass index and abnormal lipid profiles play a role, but a very different one than among the general population, according to Dr. George D. Kitas and Dr. Sherine E. Gabriel.

Moreover, systemic inflammation is likely just as important for the development of cardiovascular disease in this cohort. Therefore, “effective, even optimal control of traditional risk factors is imperative, but may be insufficient to reduce CV risk for people with RA,” the investigators wrote (Ann. Rheum. Dis. 2010 Nov. 24 [doi:10.1136/ard.2010.142133]). Rather, “tight control of systemic inflammation is likely to be required for optimal results.”

According to Dr. Kitas of the Arthritis Research U.K. Epidemiology Unit at Manchester (England) University, and Dr. Gabriel of the division of rheumatology at the Mayo Clinic, Rochester, Minn., one of the commonest and simplest risk factors for heart disease among the general population – increased body mass index – may, paradoxically, be associated with increased survival among RA patients.

They point to one study showing that even after the presence of diabetes mellitus, cardiac history, smoking, and hypertension were controlled for, lower BMI carried a threefold risk of death, compared with patients without RA (Arthritis Rheum. 2004;50:3450-7).

“RA appears to be associated with profound alterations in body composition, which are not reflected in the BMI thresholds used in the general population,” the authors wrote.

These alterations include what the authors call “rheumatoid cachexia,” characterized by low muscle mass combined with a high fat mass, which may represent “from the CV perspective, the 'worst of both worlds.'”

A similar paradoxical relationship appears to exist concerning lipids in RA. “Serum levels of total cholesterol and LDL cholesterol decline precipitously during the 3- to 5-year period before RA incidence,” they wrote, citing a study by other investigators (Ann. Rheum. Dis. 2009;68[suppl. 3]:78).

On the other hand, dyslipidemia has been documented to affect “up to half” of hospitalized RA patients (Ann. Rheum. Dis. 2010;69:683-8).

Meanwhile, the landmark JUPITER study (Justification for the Use of Statins in Primary Prevention: An Intervention Trial Evaluating Rosuvastatin) excluded RA patients, because of C-reactive protein levels in excess of the “arbitrarily chosen threshold of 2 mg/L used in that trial, as well as a significant classical CV risk factor load, unlike the participants in JUPITER, who had no other risk factors.” They reported that a trial of statins specifically in RA, enrolling 4,000 patients, is underway in the United Kingdom, but will not report results until 2016 (www.dgoh.nhs.uk/tracera

Another area where research is lacking is concerning the effects of inflammation on CV risk. The authors pointed, for example, to the theory of “accelerated atherosclerosis,” first postulated in the 1990s.

“The cell types, cytokine signaling, adhesion interactions, and tissue-damaging processes involved in the generation, progression, instability, and rupture of atheromatous plaques are reminiscent of those seen in chronic rheumatoid synovitis,” they wrote.

Moreover, “effective RA treatment appears to be associated with some, often transient, improvements in vascular function,” they added, although “there are no clear, consistent relationships between this and contemporary disease activity.”

Another theory, that “high-grade systemic inflammation in RA does not necessarily imply accelerated atherosclerosis but rather an increased propensity to plaque instability and rupture,” was confirmed in an autopsy analysis in one study (J. Rheumatol. 2007;34:937-42).

The work was funded by Arthritis Research U.K., the British Heart Foundation, the Medical Research Council, and the U.S. National Institute of Arthritis and Musculoskeletal Diseases. Dr. Kitas and Dr. Gabriel said they had no relevant financial disclosures.

Major Finding: Of adults younger than age 60 years who have bunions, 89% inherited the condition.

Data Source: A genetic analysis and foot examination of 2,179 adults.

Disclosures: Dr. Hannan had no financial conflicts to disclose.

ATLANTA — Got bunions? Thank your parents. Bunions were inherited in 89% of adults younger than 60 years, according to genetic data from more than 2,000 adults.

Bunions and other foot disorders can limit mobility and exacerbate other musculoskeletal weaknesses, but interventions are available, and they are most effective if foot deformities are identified early, said Marian Hannan, D.Sc., of Harvard Medicalxd

School, Boston.

Foot disorders occur in 20%-60% of adults, and researchers have long suspected genetic involvement, but this study is the first to examine specific associations between genes and foot deformities, Dr. Hannan said.

Dr. Hannan and her colleagues reviewed data from 959 men and 1,220 women in the Framingham Foot Study of 2002-2005. A trained examiner evaluated the study participants for any of 20 different foot disorders. In this study, Dr. Hannan reported data about the most common and least common of the disorders: hallux valgus (bunions) and pes cavus (high arches).

Overall, 675 individuals (31%) had bunions and 154 (7%) had high arches. A bunion was defined as a big toe angled at least 15 degrees toward the first metatarsal. High arches were identified by calculating weight-bearing arch width.

The researchers used statistical genetics software to determine the heritability of the two conditions. Across all ages, 39% of women and 38% of men inherited their bunions, and 68% of women and 20% of men inherited their high arches. Among individuals younger than 60 years, 99% of women and 63% of men inherited their high arches. The heritability estimates were statistically significant for both conditions. Participants' average age was 66 years, and 57% were women.

Major Finding: Of adults younger than age 60 years who have bunions, 89% inherited the condition.

Data Source: A genetic analysis and foot examination of 2,179 adults.

Disclosures: Dr. Hannan had no financial conflicts to disclose.

ATLANTA — Got bunions? Thank your parents. Bunions were inherited in 89% of adults younger than 60 years, according to genetic data from more than 2,000 adults.

Bunions and other foot disorders can limit mobility and exacerbate other musculoskeletal weaknesses, but interventions are available, and they are most effective if foot deformities are identified early, said Marian Hannan, D.Sc., of Harvard Medicalxd

School, Boston.

Foot disorders occur in 20%-60% of adults, and researchers have long suspected genetic involvement, but this study is the first to examine specific associations between genes and foot deformities, Dr. Hannan said.

Dr. Hannan and her colleagues reviewed data from 959 men and 1,220 women in the Framingham Foot Study of 2002-2005. A trained examiner evaluated the study participants for any of 20 different foot disorders. In this study, Dr. Hannan reported data about the most common and least common of the disorders: hallux valgus (bunions) and pes cavus (high arches).

Overall, 675 individuals (31%) had bunions and 154 (7%) had high arches. A bunion was defined as a big toe angled at least 15 degrees toward the first metatarsal. High arches were identified by calculating weight-bearing arch width.

The researchers used statistical genetics software to determine the heritability of the two conditions. Across all ages, 39% of women and 38% of men inherited their bunions, and 68% of women and 20% of men inherited their high arches. Among individuals younger than 60 years, 99% of women and 63% of men inherited their high arches. The heritability estimates were statistically significant for both conditions. Participants' average age was 66 years, and 57% were women.

Major Finding: Of adults younger than age 60 years who have bunions, 89% inherited the condition.

Data Source: A genetic analysis and foot examination of 2,179 adults.

Disclosures: Dr. Hannan had no financial conflicts to disclose.

ATLANTA — Got bunions? Thank your parents. Bunions were inherited in 89% of adults younger than 60 years, according to genetic data from more than 2,000 adults.

Bunions and other foot disorders can limit mobility and exacerbate other musculoskeletal weaknesses, but interventions are available, and they are most effective if foot deformities are identified early, said Marian Hannan, D.Sc., of Harvard Medicalxd

School, Boston.

Foot disorders occur in 20%-60% of adults, and researchers have long suspected genetic involvement, but this study is the first to examine specific associations between genes and foot deformities, Dr. Hannan said.

Dr. Hannan and her colleagues reviewed data from 959 men and 1,220 women in the Framingham Foot Study of 2002-2005. A trained examiner evaluated the study participants for any of 20 different foot disorders. In this study, Dr. Hannan reported data about the most common and least common of the disorders: hallux valgus (bunions) and pes cavus (high arches).

Overall, 675 individuals (31%) had bunions and 154 (7%) had high arches. A bunion was defined as a big toe angled at least 15 degrees toward the first metatarsal. High arches were identified by calculating weight-bearing arch width.

The researchers used statistical genetics software to determine the heritability of the two conditions. Across all ages, 39% of women and 38% of men inherited their bunions, and 68% of women and 20% of men inherited their high arches. Among individuals younger than 60 years, 99% of women and 63% of men inherited their high arches. The heritability estimates were statistically significant for both conditions. Participants' average age was 66 years, and 57% were women.

Major Finding: Union occurred in 92% of 104 feet after the primary operation, and fusion after revision occurred in 99%. Most of the patients (90%) were satisfied with the results.

Data Source: Retrospective study of 95 patients with midfoot arthritis.

Disclosures: Dr. Nemec and his coinvestigators reported that they have no relevant financial relationships.

NATIONAL HARBOR, MD. ' Arthrodesis is a safe procedure for midfoot arthritis, with an excellent union rate and high patient satisfaction, according to findings in a small, retrospective study.

Union was achieved in 92% of 104 feet after the primary operation, and fusion after revision was achieved in 99%. In addition, most of the patients (90%) were satisfied with the results of their procedures, reported Dr. Scott A. Nemec.

Patients included in the study had primary midfoot arthritis with or without radiologic or clinical arch collapse. The researchers identified 95 patients (104 feet) who had undergone arthrodesis. Most were women and their mean age was 61 years. The primary indication for surgery was disabling foot pain that was not relieved by other measures. On radiograph, pre-and postoperative measurements were made of the anteroposterior talus and first metatarsal angle, the lateral talus and first metatarsal angle, the medial cuneiform height, and the talonavicular uncoverage.

Other outcomes included complications and reoperations, the AOFAS midfoot score, the visual analog scale pain score (0-10), and patient satisfaction.

In all, 297 joints were fused – roughly 3 per patient. Gastrocnemius recession was performed in 80% of the feet, and 56% had a forefoot procedure. In terms of bone grafts used, autograft was used in 91% of the feet, allograft in 4%, and no grafts were used for 5%. The most commonly fused joints were the first, second, and third tarsometatarsals and the naviculocuneiform. No further surgery was required for one asymptomatic third TMT nonunion. One delayed union was consolidated with immobilization. Radiographically, improvement was seen in all parameters.

Major complications included three deep infections and one instance of chronic pain. The infections were treated with debridement. The patient with chronic pain was referred to a pain clinic.

There were 11 reoperations—7 for refusion, 3 for debridement, and 1 gastrocnemius recession. Four of the refusion patients and one debridement patient were not satisfied with their results. Hardware removal was required for a quarter of the feet at an average of 20 months, said Dr. Nemec, who is an orthopedic specialist in private practice in Petoskey, Mich.

Patient-reported outcome data were available for 68 patients (74 feet), with a mean follow-up of 56 months. The visual analog scale pain score dropped by a significant average of 4.6 points after surgery. The AOFAS score increased by a significant 47 points (maximum 100).

Major Finding: Union occurred in 92% of 104 feet after the primary operation, and fusion after revision occurred in 99%. Most of the patients (90%) were satisfied with the results.

Data Source: Retrospective study of 95 patients with midfoot arthritis.

Disclosures: Dr. Nemec and his coinvestigators reported that they have no relevant financial relationships.

NATIONAL HARBOR, MD. ' Arthrodesis is a safe procedure for midfoot arthritis, with an excellent union rate and high patient satisfaction, according to findings in a small, retrospective study.

Union was achieved in 92% of 104 feet after the primary operation, and fusion after revision was achieved in 99%. In addition, most of the patients (90%) were satisfied with the results of their procedures, reported Dr. Scott A. Nemec.

Patients included in the study had primary midfoot arthritis with or without radiologic or clinical arch collapse. The researchers identified 95 patients (104 feet) who had undergone arthrodesis. Most were women and their mean age was 61 years. The primary indication for surgery was disabling foot pain that was not relieved by other measures. On radiograph, pre-and postoperative measurements were made of the anteroposterior talus and first metatarsal angle, the lateral talus and first metatarsal angle, the medial cuneiform height, and the talonavicular uncoverage.

Other outcomes included complications and reoperations, the AOFAS midfoot score, the visual analog scale pain score (0-10), and patient satisfaction.

In all, 297 joints were fused – roughly 3 per patient. Gastrocnemius recession was performed in 80% of the feet, and 56% had a forefoot procedure. In terms of bone grafts used, autograft was used in 91% of the feet, allograft in 4%, and no grafts were used for 5%. The most commonly fused joints were the first, second, and third tarsometatarsals and the naviculocuneiform. No further surgery was required for one asymptomatic third TMT nonunion. One delayed union was consolidated with immobilization. Radiographically, improvement was seen in all parameters.

Major complications included three deep infections and one instance of chronic pain. The infections were treated with debridement. The patient with chronic pain was referred to a pain clinic.

There were 11 reoperations—7 for refusion, 3 for debridement, and 1 gastrocnemius recession. Four of the refusion patients and one debridement patient were not satisfied with their results. Hardware removal was required for a quarter of the feet at an average of 20 months, said Dr. Nemec, who is an orthopedic specialist in private practice in Petoskey, Mich.

Patient-reported outcome data were available for 68 patients (74 feet), with a mean follow-up of 56 months. The visual analog scale pain score dropped by a significant average of 4.6 points after surgery. The AOFAS score increased by a significant 47 points (maximum 100).

Major Finding: Union occurred in 92% of 104 feet after the primary operation, and fusion after revision occurred in 99%. Most of the patients (90%) were satisfied with the results.

Data Source: Retrospective study of 95 patients with midfoot arthritis.

Disclosures: Dr. Nemec and his coinvestigators reported that they have no relevant financial relationships.

NATIONAL HARBOR, MD. ' Arthrodesis is a safe procedure for midfoot arthritis, with an excellent union rate and high patient satisfaction, according to findings in a small, retrospective study.

Union was achieved in 92% of 104 feet after the primary operation, and fusion after revision was achieved in 99%. In addition, most of the patients (90%) were satisfied with the results of their procedures, reported Dr. Scott A. Nemec.

Patients included in the study had primary midfoot arthritis with or without radiologic or clinical arch collapse. The researchers identified 95 patients (104 feet) who had undergone arthrodesis. Most were women and their mean age was 61 years. The primary indication for surgery was disabling foot pain that was not relieved by other measures. On radiograph, pre-and postoperative measurements were made of the anteroposterior talus and first metatarsal angle, the lateral talus and first metatarsal angle, the medial cuneiform height, and the talonavicular uncoverage.

Other outcomes included complications and reoperations, the AOFAS midfoot score, the visual analog scale pain score (0-10), and patient satisfaction.

In all, 297 joints were fused – roughly 3 per patient. Gastrocnemius recession was performed in 80% of the feet, and 56% had a forefoot procedure. In terms of bone grafts used, autograft was used in 91% of the feet, allograft in 4%, and no grafts were used for 5%. The most commonly fused joints were the first, second, and third tarsometatarsals and the naviculocuneiform. No further surgery was required for one asymptomatic third TMT nonunion. One delayed union was consolidated with immobilization. Radiographically, improvement was seen in all parameters.

Major complications included three deep infections and one instance of chronic pain. The infections were treated with debridement. The patient with chronic pain was referred to a pain clinic.

There were 11 reoperations—7 for refusion, 3 for debridement, and 1 gastrocnemius recession. Four of the refusion patients and one debridement patient were not satisfied with their results. Hardware removal was required for a quarter of the feet at an average of 20 months, said Dr. Nemec, who is an orthopedic specialist in private practice in Petoskey, Mich.

Patient-reported outcome data were available for 68 patients (74 feet), with a mean follow-up of 56 months. The visual analog scale pain score dropped by a significant average of 4.6 points after surgery. The AOFAS score increased by a significant 47 points (maximum 100).

Major Finding: In 20% of patients first seen in primary care settings, axial spondyloarthritis was the cause of chronic low back pain.

Data Source: A cross-sectional study of 364 adults aged 19-45 years with chronic back pain.

Disclosures: Dr. Weel said that she had no financial conflicts.

ATLANTA — Approximately 20% of cases of chronic low back pain in younger adults seen in primary care settings might be caused by spondyloarthritis, based on data from 364 patients aged 19-45 years.

In the cross-sectional study, 77 of 364 patients (22%) met the diagnosis of axial spondyloarthritis on examination by a rheumatologist. The average age of the patients was 36 years, 43% were male, and the average duration of chronic low back pain was 9 years.

The diagnostic techniques included a detailed patient questionnaire about inflammatory back pain, physical examination, and patient history; blood tests to assess C-reactive protein levels and the presence of HLA-B27 (a gene that has been linked to spondyloarthritis); and conventional and MRI images of sacroiliac joints. Two radiologists reviewed the images for the signs of inflammation and bone lesions that might indicate axial spondyloarthritis.

Fifty-two patients were diagnosed according to MRI criteria plus one additional spondyloarthritis feature. The other 12 patients were diagnosed according to a positive HLA-B27 test plus two additional spondyloarthritis features, said Dr. Angelique Weel of Maasstad Ziekenhuis, Rotterdam, the Netherlands. In addition, 24 patients (6.6%) met the criteria for ankylosing spondylitis.

The results suggest that spondyloarthritis is underdiagnosed as a cause of chronic back pain in the general population. Dr. Weel recommended that primary care physicians suspect spondyloarthritis when they see younger adults with chronic back pain, and refer these patients to a rheumatologist if they suspect an inflammatory basis for the pain.

“We also tried to make a simple questionnaire for general practitioners, so they can determine which patient with chronic low back pain should be sent to a rheumatologist to investigate possible spondyloarthritis,” she noted. Possible red flags on the questionnaire include the response to NSAIDs and a family history of spondyloarthritis, Dr. Weel said.

Dr. Weel speaks about spondyloarthritis in a video interview posted at

Source Heidi Spleet/Elsevier Global Medical Newswww.rheumatologynews.com

Major Finding: In 20% of patients first seen in primary care settings, axial spondyloarthritis was the cause of chronic low back pain.

Data Source: A cross-sectional study of 364 adults aged 19-45 years with chronic back pain.

Disclosures: Dr. Weel said that she had no financial conflicts.

ATLANTA — Approximately 20% of cases of chronic low back pain in younger adults seen in primary care settings might be caused by spondyloarthritis, based on data from 364 patients aged 19-45 years.

In the cross-sectional study, 77 of 364 patients (22%) met the diagnosis of axial spondyloarthritis on examination by a rheumatologist. The average age of the patients was 36 years, 43% were male, and the average duration of chronic low back pain was 9 years.

The diagnostic techniques included a detailed patient questionnaire about inflammatory back pain, physical examination, and patient history; blood tests to assess C-reactive protein levels and the presence of HLA-B27 (a gene that has been linked to spondyloarthritis); and conventional and MRI images of sacroiliac joints. Two radiologists reviewed the images for the signs of inflammation and bone lesions that might indicate axial spondyloarthritis.

Fifty-two patients were diagnosed according to MRI criteria plus one additional spondyloarthritis feature. The other 12 patients were diagnosed according to a positive HLA-B27 test plus two additional spondyloarthritis features, said Dr. Angelique Weel of Maasstad Ziekenhuis, Rotterdam, the Netherlands. In addition, 24 patients (6.6%) met the criteria for ankylosing spondylitis.

The results suggest that spondyloarthritis is underdiagnosed as a cause of chronic back pain in the general population. Dr. Weel recommended that primary care physicians suspect spondyloarthritis when they see younger adults with chronic back pain, and refer these patients to a rheumatologist if they suspect an inflammatory basis for the pain.

“We also tried to make a simple questionnaire for general practitioners, so they can determine which patient with chronic low back pain should be sent to a rheumatologist to investigate possible spondyloarthritis,” she noted. Possible red flags on the questionnaire include the response to NSAIDs and a family history of spondyloarthritis, Dr. Weel said.

Dr. Weel speaks about spondyloarthritis in a video interview posted at

Source Heidi Spleet/Elsevier Global Medical Newswww.rheumatologynews.com

Major Finding: In 20% of patients first seen in primary care settings, axial spondyloarthritis was the cause of chronic low back pain.

Data Source: A cross-sectional study of 364 adults aged 19-45 years with chronic back pain.

Disclosures: Dr. Weel said that she had no financial conflicts.

ATLANTA — Approximately 20% of cases of chronic low back pain in younger adults seen in primary care settings might be caused by spondyloarthritis, based on data from 364 patients aged 19-45 years.

In the cross-sectional study, 77 of 364 patients (22%) met the diagnosis of axial spondyloarthritis on examination by a rheumatologist. The average age of the patients was 36 years, 43% were male, and the average duration of chronic low back pain was 9 years.

The diagnostic techniques included a detailed patient questionnaire about inflammatory back pain, physical examination, and patient history; blood tests to assess C-reactive protein levels and the presence of HLA-B27 (a gene that has been linked to spondyloarthritis); and conventional and MRI images of sacroiliac joints. Two radiologists reviewed the images for the signs of inflammation and bone lesions that might indicate axial spondyloarthritis.

Fifty-two patients were diagnosed according to MRI criteria plus one additional spondyloarthritis feature. The other 12 patients were diagnosed according to a positive HLA-B27 test plus two additional spondyloarthritis features, said Dr. Angelique Weel of Maasstad Ziekenhuis, Rotterdam, the Netherlands. In addition, 24 patients (6.6%) met the criteria for ankylosing spondylitis.

The results suggest that spondyloarthritis is underdiagnosed as a cause of chronic back pain in the general population. Dr. Weel recommended that primary care physicians suspect spondyloarthritis when they see younger adults with chronic back pain, and refer these patients to a rheumatologist if they suspect an inflammatory basis for the pain.

“We also tried to make a simple questionnaire for general practitioners, so they can determine which patient with chronic low back pain should be sent to a rheumatologist to investigate possible spondyloarthritis,” she noted. Possible red flags on the questionnaire include the response to NSAIDs and a family history of spondyloarthritis, Dr. Weel said.

Dr. Weel speaks about spondyloarthritis in a video interview posted at

Source Heidi Spleet/Elsevier Global Medical Newswww.rheumatologynews.com