Rheumatoid Arthritis

Are rheumatoid arthritis patients who are told that they meet criteria for clinical remission getting the full story?

“Despite clinical remission, histology and imaging studies documented a persistently active disease state that may benefit from more aggressive therapy.” That’s the conclusion of Dr. Allen P. Anandarajah, an immunology and rheumatology researcher at the University of Rochester (N.Y.), and his colleagues, who documented persistently active rheumatoid arthritis (RA) in more than three-quarters of 14 patients in clinical remission (J. Rheumatol. 2014 [doi:10.3899/jrheum.140411]).

The study is the latest addition to the literature demonstrating that the sensitivity of current criteria for measuring diminished disease activity in persons with RA is too low (Arthritis Rheum. 2005;52:3381-90; Ann. Rheum. Dis. 2010;69:631-7; and Semin. Arthritis Rheum. 2005;35:185-96).

“The current outcome measures fall short,” Dr. Anandarajah and his coauthors wrote. “A major gap to be addressed is accurate and reliable methods to detect active synovitis in patients deemed to be in clinical remission.”

Dr. Anandarajah and his colleagues retrospectively analyzed 15 synovial specimens from 14 patients who met 1996 revised American College of Rheumatology criteria for clinical remission from RA who had undergone orthopedic surgery. The investigators also scored histologic specimens for hyperplasia of synovial lining and stroma, as well as inflammation, lymphoid follicles, and vascularity.

The disease-modifying antirheumatic drug regimens for the patients included four on anti–tumor necrosis factor therapy (two monotherapy and two with methotrexate); four were receiving methotrexate alone; four were on combined methotrexate and hydroxychloroquine therapy; one on methotrexate and low-dose prednisone; and one on hydroxychloroquine, sulfasalazine, and low-dose prednisone.

On histology, the investigators rated disease activity as severe in four specimens, moderate in six, mild in three, and minimal in two. Three of the four specimens with minimal and mild histology were from those receiving anti-tumor necrosis factor therapy.

The investigators detected synovitis on ultrasound grayscale in 8 of 10 joints in nine patients and power Doppler signal in 6 of 10 joints. Synovitis and bone marrow edema was shown on MRI scans in six of seven patients. The authors also calculated positive, although not significant, correlations between synovitis scores on ultrasonography and histology.

Although the study was limited in that the evaluations were scored retrospectively, and the images had been obtained for reasons other than future scoring of synovitis, the authors wrote that their findings were evidence that additional prospective studies could help determine whether incorporating histologic and imaging studies into remission criteria would be beneficial.

No disclosures were reported with the study.

wmcknight@frontlinemedcom.com

On Twitter @whitneymcknight

Are rheumatoid arthritis patients who are told that they meet criteria for clinical remission getting the full story?

“Despite clinical remission, histology and imaging studies documented a persistently active disease state that may benefit from more aggressive therapy.” That’s the conclusion of Dr. Allen P. Anandarajah, an immunology and rheumatology researcher at the University of Rochester (N.Y.), and his colleagues, who documented persistently active rheumatoid arthritis (RA) in more than three-quarters of 14 patients in clinical remission (J. Rheumatol. 2014 [doi:10.3899/jrheum.140411]).

The study is the latest addition to the literature demonstrating that the sensitivity of current criteria for measuring diminished disease activity in persons with RA is too low (Arthritis Rheum. 2005;52:3381-90; Ann. Rheum. Dis. 2010;69:631-7; and Semin. Arthritis Rheum. 2005;35:185-96).

“The current outcome measures fall short,” Dr. Anandarajah and his coauthors wrote. “A major gap to be addressed is accurate and reliable methods to detect active synovitis in patients deemed to be in clinical remission.”

Dr. Anandarajah and his colleagues retrospectively analyzed 15 synovial specimens from 14 patients who met 1996 revised American College of Rheumatology criteria for clinical remission from RA who had undergone orthopedic surgery. The investigators also scored histologic specimens for hyperplasia of synovial lining and stroma, as well as inflammation, lymphoid follicles, and vascularity.

The disease-modifying antirheumatic drug regimens for the patients included four on anti–tumor necrosis factor therapy (two monotherapy and two with methotrexate); four were receiving methotrexate alone; four were on combined methotrexate and hydroxychloroquine therapy; one on methotrexate and low-dose prednisone; and one on hydroxychloroquine, sulfasalazine, and low-dose prednisone.

On histology, the investigators rated disease activity as severe in four specimens, moderate in six, mild in three, and minimal in two. Three of the four specimens with minimal and mild histology were from those receiving anti-tumor necrosis factor therapy.

The investigators detected synovitis on ultrasound grayscale in 8 of 10 joints in nine patients and power Doppler signal in 6 of 10 joints. Synovitis and bone marrow edema was shown on MRI scans in six of seven patients. The authors also calculated positive, although not significant, correlations between synovitis scores on ultrasonography and histology.

Although the study was limited in that the evaluations were scored retrospectively, and the images had been obtained for reasons other than future scoring of synovitis, the authors wrote that their findings were evidence that additional prospective studies could help determine whether incorporating histologic and imaging studies into remission criteria would be beneficial.

No disclosures were reported with the study.

wmcknight@frontlinemedcom.com

On Twitter @whitneymcknight

Are rheumatoid arthritis patients who are told that they meet criteria for clinical remission getting the full story?

“Despite clinical remission, histology and imaging studies documented a persistently active disease state that may benefit from more aggressive therapy.” That’s the conclusion of Dr. Allen P. Anandarajah, an immunology and rheumatology researcher at the University of Rochester (N.Y.), and his colleagues, who documented persistently active rheumatoid arthritis (RA) in more than three-quarters of 14 patients in clinical remission (J. Rheumatol. 2014 [doi:10.3899/jrheum.140411]).

The study is the latest addition to the literature demonstrating that the sensitivity of current criteria for measuring diminished disease activity in persons with RA is too low (Arthritis Rheum. 2005;52:3381-90; Ann. Rheum. Dis. 2010;69:631-7; and Semin. Arthritis Rheum. 2005;35:185-96).

“The current outcome measures fall short,” Dr. Anandarajah and his coauthors wrote. “A major gap to be addressed is accurate and reliable methods to detect active synovitis in patients deemed to be in clinical remission.”

Dr. Anandarajah and his colleagues retrospectively analyzed 15 synovial specimens from 14 patients who met 1996 revised American College of Rheumatology criteria for clinical remission from RA who had undergone orthopedic surgery. The investigators also scored histologic specimens for hyperplasia of synovial lining and stroma, as well as inflammation, lymphoid follicles, and vascularity.

The disease-modifying antirheumatic drug regimens for the patients included four on anti–tumor necrosis factor therapy (two monotherapy and two with methotrexate); four were receiving methotrexate alone; four were on combined methotrexate and hydroxychloroquine therapy; one on methotrexate and low-dose prednisone; and one on hydroxychloroquine, sulfasalazine, and low-dose prednisone.

On histology, the investigators rated disease activity as severe in four specimens, moderate in six, mild in three, and minimal in two. Three of the four specimens with minimal and mild histology were from those receiving anti-tumor necrosis factor therapy.

The investigators detected synovitis on ultrasound grayscale in 8 of 10 joints in nine patients and power Doppler signal in 6 of 10 joints. Synovitis and bone marrow edema was shown on MRI scans in six of seven patients. The authors also calculated positive, although not significant, correlations between synovitis scores on ultrasonography and histology.

Although the study was limited in that the evaluations were scored retrospectively, and the images had been obtained for reasons other than future scoring of synovitis, the authors wrote that their findings were evidence that additional prospective studies could help determine whether incorporating histologic and imaging studies into remission criteria would be beneficial.

No disclosures were reported with the study.

wmcknight@frontlinemedcom.com

On Twitter @whitneymcknight

Rheumatoid arthritis patients with differing prognoses achieved similar improvements in clinical outcomes and functional improvements with initial combination therapy but fared differently when given initial monotherapy, according to the results of a post-hoc analysis of a randomized controlled trial.

The results challenge a recent push to tailor treatment strategy to risk stratification, argued Dr. Iris Markusse of the department of rheumatology at Leiden (the Netherlands) University Medical Center and her coauthors.

The researchers examined the treatment outcomes of 508 patients with rheumatoid arthritis in a post-hoc analysis of the BEST study in which patients were randomized to one of four treatment groups: sequential monotherapy starting with methotrexate, step-up combination therapy, initial combination therapy with prednisone, or initial combination with infliximab. For this post-hoc analysis of 1-year results, the investigators combined the first two groups that both started with methotrexate monotherapy because they had very similar disease outcomes during the first year of follow-up. The third and fourth groups that received initial combination therapy were combined as well.

The results were analyzed according to whether the patients were classified by disease characteristics and radiographic progression as having a poor or nonpoor prognosis. The researchers defined poor prognosis – 417 of the 508 patients – by the presence of at least three of four poor prognostic factors: Disease Activity Score of 3.7 or greater, swollen joint count of 10 or higher, four or more erosions, and positive results for both rheumatoid factor and anti-citrullinated peptide autoantibodies.

They found little difference between the two prognostic groups, with both showing significantly higher rates of remission and functional improvements with combination therapy than monotherapy, and the differences were preserved at 1 year. Among poor-prognosis patients, 93% achieved an American College of Rheumatology 20 (ACR 20) response at 1 year, compared with 80% of those on initial monotherapy. In the non–poor prognosis patients, initial combination therapy proved significantly better than initial monotherapy at achieving ACR20 response (85% vs. 72%).

Both poor- and non–poor prognosis groups had similar improvements in Health Assessment Questionnaire scores, and there was no significant differences in the toxicity of the treatment approaches in the different prognosis groups based on the numbers of reported adverse events (Arthritis Res. Ther. 2014 Sept. 25 [doi:10.1186/s13075-014-0430-3]).

“These results suggest that prognostic factors associated with future radiographic damage progression contribute little to predict early clinical response to initial treatment, and therefore in our opinion tailored treatment based on prognosis as suggested by the EULAR [European League Against Rheumatism] guidelines is currently not feasible,” Dr. Markusse and her associates wrote.

The study was supported by grants from the Dutch Insurance Companies, Schering-Plough, and Janssen. The authors declared having no other conflicts of interest.

Rheumatoid arthritis patients with differing prognoses achieved similar improvements in clinical outcomes and functional improvements with initial combination therapy but fared differently when given initial monotherapy, according to the results of a post-hoc analysis of a randomized controlled trial.

The results challenge a recent push to tailor treatment strategy to risk stratification, argued Dr. Iris Markusse of the department of rheumatology at Leiden (the Netherlands) University Medical Center and her coauthors.

The researchers examined the treatment outcomes of 508 patients with rheumatoid arthritis in a post-hoc analysis of the BEST study in which patients were randomized to one of four treatment groups: sequential monotherapy starting with methotrexate, step-up combination therapy, initial combination therapy with prednisone, or initial combination with infliximab. For this post-hoc analysis of 1-year results, the investigators combined the first two groups that both started with methotrexate monotherapy because they had very similar disease outcomes during the first year of follow-up. The third and fourth groups that received initial combination therapy were combined as well.

The results were analyzed according to whether the patients were classified by disease characteristics and radiographic progression as having a poor or nonpoor prognosis. The researchers defined poor prognosis – 417 of the 508 patients – by the presence of at least three of four poor prognostic factors: Disease Activity Score of 3.7 or greater, swollen joint count of 10 or higher, four or more erosions, and positive results for both rheumatoid factor and anti-citrullinated peptide autoantibodies.

They found little difference between the two prognostic groups, with both showing significantly higher rates of remission and functional improvements with combination therapy than monotherapy, and the differences were preserved at 1 year. Among poor-prognosis patients, 93% achieved an American College of Rheumatology 20 (ACR 20) response at 1 year, compared with 80% of those on initial monotherapy. In the non–poor prognosis patients, initial combination therapy proved significantly better than initial monotherapy at achieving ACR20 response (85% vs. 72%).

Both poor- and non–poor prognosis groups had similar improvements in Health Assessment Questionnaire scores, and there was no significant differences in the toxicity of the treatment approaches in the different prognosis groups based on the numbers of reported adverse events (Arthritis Res. Ther. 2014 Sept. 25 [doi:10.1186/s13075-014-0430-3]).

“These results suggest that prognostic factors associated with future radiographic damage progression contribute little to predict early clinical response to initial treatment, and therefore in our opinion tailored treatment based on prognosis as suggested by the EULAR [European League Against Rheumatism] guidelines is currently not feasible,” Dr. Markusse and her associates wrote.

The study was supported by grants from the Dutch Insurance Companies, Schering-Plough, and Janssen. The authors declared having no other conflicts of interest.

Rheumatoid arthritis patients with differing prognoses achieved similar improvements in clinical outcomes and functional improvements with initial combination therapy but fared differently when given initial monotherapy, according to the results of a post-hoc analysis of a randomized controlled trial.

The results challenge a recent push to tailor treatment strategy to risk stratification, argued Dr. Iris Markusse of the department of rheumatology at Leiden (the Netherlands) University Medical Center and her coauthors.

The researchers examined the treatment outcomes of 508 patients with rheumatoid arthritis in a post-hoc analysis of the BEST study in which patients were randomized to one of four treatment groups: sequential monotherapy starting with methotrexate, step-up combination therapy, initial combination therapy with prednisone, or initial combination with infliximab. For this post-hoc analysis of 1-year results, the investigators combined the first two groups that both started with methotrexate monotherapy because they had very similar disease outcomes during the first year of follow-up. The third and fourth groups that received initial combination therapy were combined as well.

The results were analyzed according to whether the patients were classified by disease characteristics and radiographic progression as having a poor or nonpoor prognosis. The researchers defined poor prognosis – 417 of the 508 patients – by the presence of at least three of four poor prognostic factors: Disease Activity Score of 3.7 or greater, swollen joint count of 10 or higher, four or more erosions, and positive results for both rheumatoid factor and anti-citrullinated peptide autoantibodies.

They found little difference between the two prognostic groups, with both showing significantly higher rates of remission and functional improvements with combination therapy than monotherapy, and the differences were preserved at 1 year. Among poor-prognosis patients, 93% achieved an American College of Rheumatology 20 (ACR 20) response at 1 year, compared with 80% of those on initial monotherapy. In the non–poor prognosis patients, initial combination therapy proved significantly better than initial monotherapy at achieving ACR20 response (85% vs. 72%).

Both poor- and non–poor prognosis groups had similar improvements in Health Assessment Questionnaire scores, and there was no significant differences in the toxicity of the treatment approaches in the different prognosis groups based on the numbers of reported adverse events (Arthritis Res. Ther. 2014 Sept. 25 [doi:10.1186/s13075-014-0430-3]).

“These results suggest that prognostic factors associated with future radiographic damage progression contribute little to predict early clinical response to initial treatment, and therefore in our opinion tailored treatment based on prognosis as suggested by the EULAR [European League Against Rheumatism] guidelines is currently not feasible,” Dr. Markusse and her associates wrote.

The study was supported by grants from the Dutch Insurance Companies, Schering-Plough, and Janssen. The authors declared having no other conflicts of interest.

Randomized, controlled trials of patients with rheumatoid arthritis are published sooner and more likely to be published if the outcome is positive, indicating publication bias, a recent study found.

The study surveyed ClinicalTrials.gov for randomized, controlled trials (RCTs) of patients with rheumatoid arthritis (RA), finding 143 eligible studies registered before 2012 and completed before 2010. The outcome of 16 trials could not be ascertained. Among the 127 RCTs whose outcomes were known, 74 had a positive result, and 53 were negative, according to Dr. Nasim A. Khan of the University of Arkansas, Little Rock, and his associates (Arthritis Rheumatol. 2014;66:2664-74). The researchers also found that trial registration at ClinicalTrials.gov increased dramatically after July 2005, when the International Committee of Medical Journal Editors made trial registration in a public registry a requirement for publication, with 37 trials being registered before 2006, and 106 registered during 2006-2009.

Of the 143 trials, 95 studies had been published, with 64 of these having positive results and 31 having negative results. Only 10 trials with positive outcomes had not been published, compared with 22 RCTs with negative outcomes, Dr. Khan and his associates reported. The median time to publication for studies with a positive outcome was 30 months, while studies with a negative outcome had a median time to publication of 49 months.

The rate of publication was slightly higher for studies completed after 2005, with 65% of studies completed before 2006 being published, 78% of studies completed from 2006-2007 being published, and 59% of studies completed from 2008-2009 being published. Some of those later trials may still be published, Dr. Khan and his fellow investigators conceded. The time to publication was much slower for studies completed before 2006, taking a median time of 55 months. Studies completed from 2006-2007 took 30 months to publication, and studies completed from 2008-2009 took 34 months.

The authors noted that while progress has been made to increase transparency, there are still issues within the system, and that “efforts must be made to increase awareness of the existence and drawbacks of publication bias among current and future physicians, scientists, individuals working in the pharmaceutical industry and insurances companies, and patients.”

The authors had no disclosures to report.

lfranki@frontlinemedcom.com

Randomized, controlled trials of patients with rheumatoid arthritis are published sooner and more likely to be published if the outcome is positive, indicating publication bias, a recent study found.

The study surveyed ClinicalTrials.gov for randomized, controlled trials (RCTs) of patients with rheumatoid arthritis (RA), finding 143 eligible studies registered before 2012 and completed before 2010. The outcome of 16 trials could not be ascertained. Among the 127 RCTs whose outcomes were known, 74 had a positive result, and 53 were negative, according to Dr. Nasim A. Khan of the University of Arkansas, Little Rock, and his associates (Arthritis Rheumatol. 2014;66:2664-74). The researchers also found that trial registration at ClinicalTrials.gov increased dramatically after July 2005, when the International Committee of Medical Journal Editors made trial registration in a public registry a requirement for publication, with 37 trials being registered before 2006, and 106 registered during 2006-2009.

Of the 143 trials, 95 studies had been published, with 64 of these having positive results and 31 having negative results. Only 10 trials with positive outcomes had not been published, compared with 22 RCTs with negative outcomes, Dr. Khan and his associates reported. The median time to publication for studies with a positive outcome was 30 months, while studies with a negative outcome had a median time to publication of 49 months.

The rate of publication was slightly higher for studies completed after 2005, with 65% of studies completed before 2006 being published, 78% of studies completed from 2006-2007 being published, and 59% of studies completed from 2008-2009 being published. Some of those later trials may still be published, Dr. Khan and his fellow investigators conceded. The time to publication was much slower for studies completed before 2006, taking a median time of 55 months. Studies completed from 2006-2007 took 30 months to publication, and studies completed from 2008-2009 took 34 months.

The authors noted that while progress has been made to increase transparency, there are still issues within the system, and that “efforts must be made to increase awareness of the existence and drawbacks of publication bias among current and future physicians, scientists, individuals working in the pharmaceutical industry and insurances companies, and patients.”

The authors had no disclosures to report.

lfranki@frontlinemedcom.com

Randomized, controlled trials of patients with rheumatoid arthritis are published sooner and more likely to be published if the outcome is positive, indicating publication bias, a recent study found.

The study surveyed ClinicalTrials.gov for randomized, controlled trials (RCTs) of patients with rheumatoid arthritis (RA), finding 143 eligible studies registered before 2012 and completed before 2010. The outcome of 16 trials could not be ascertained. Among the 127 RCTs whose outcomes were known, 74 had a positive result, and 53 were negative, according to Dr. Nasim A. Khan of the University of Arkansas, Little Rock, and his associates (Arthritis Rheumatol. 2014;66:2664-74). The researchers also found that trial registration at ClinicalTrials.gov increased dramatically after July 2005, when the International Committee of Medical Journal Editors made trial registration in a public registry a requirement for publication, with 37 trials being registered before 2006, and 106 registered during 2006-2009.

Of the 143 trials, 95 studies had been published, with 64 of these having positive results and 31 having negative results. Only 10 trials with positive outcomes had not been published, compared with 22 RCTs with negative outcomes, Dr. Khan and his associates reported. The median time to publication for studies with a positive outcome was 30 months, while studies with a negative outcome had a median time to publication of 49 months.

The rate of publication was slightly higher for studies completed after 2005, with 65% of studies completed before 2006 being published, 78% of studies completed from 2006-2007 being published, and 59% of studies completed from 2008-2009 being published. Some of those later trials may still be published, Dr. Khan and his fellow investigators conceded. The time to publication was much slower for studies completed before 2006, taking a median time of 55 months. Studies completed from 2006-2007 took 30 months to publication, and studies completed from 2008-2009 took 34 months.

The authors noted that while progress has been made to increase transparency, there are still issues within the system, and that “efforts must be made to increase awareness of the existence and drawbacks of publication bias among current and future physicians, scientists, individuals working in the pharmaceutical industry and insurances companies, and patients.”

The authors had no disclosures to report.

lfranki@frontlinemedcom.com

LAS VEGAS – When methotrexate doesn’t work in rheumatoid arthritis and patients are still suffering after their first tumor necrosis factor inhibitor, it’s worthwhile to try a second TNF inhibitor, according to Dr. Daniel Furst, the Carl M Pearson Professor in Rheumatology at University of California, Los Angeles.

Even just side effects from the first TNF inhibitor indicate that the second one might work, he said at the conference held by Global Academy for Medical Education.

Dr. Furst also explains in the video how to safely use steroids in RA patients, and when to move them to non–TNF inhibitor biologics.

Global Academy for Medical Education and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

LAS VEGAS – When methotrexate doesn’t work in rheumatoid arthritis and patients are still suffering after their first tumor necrosis factor inhibitor, it’s worthwhile to try a second TNF inhibitor, according to Dr. Daniel Furst, the Carl M Pearson Professor in Rheumatology at University of California, Los Angeles.

Even just side effects from the first TNF inhibitor indicate that the second one might work, he said at the conference held by Global Academy for Medical Education.

Dr. Furst also explains in the video how to safely use steroids in RA patients, and when to move them to non–TNF inhibitor biologics.

Global Academy for Medical Education and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

LAS VEGAS – When methotrexate doesn’t work in rheumatoid arthritis and patients are still suffering after their first tumor necrosis factor inhibitor, it’s worthwhile to try a second TNF inhibitor, according to Dr. Daniel Furst, the Carl M Pearson Professor in Rheumatology at University of California, Los Angeles.

Even just side effects from the first TNF inhibitor indicate that the second one might work, he said at the conference held by Global Academy for Medical Education.

Dr. Furst also explains in the video how to safely use steroids in RA patients, and when to move them to non–TNF inhibitor biologics.

Global Academy for Medical Education and this news organization are owned by Frontline Medical Communications.

aotto@frontlinemedcom.com

Smokers with high sodium intake were more than twice as likely to develop rheumatoid arthritis as were those with low sodium intake in a nested case-control study.

The study, which lends support to the possibility that an interaction between smoking and a diet heavy in sodium can increase RA risk, involved records from 386 individuals who had provided information on their dietary habits for a long-term, population-based study a median 7.7 years before going on to develop RA. Researchers from Umeå (Sweden) University, led by Björn Sundström, Ph.D., compared these with records for 1,886 age- and sex-matched controls who did not have RA and had taken part in the same population-based study (Rheumatology 2014 Sept. 10 [doi:10.1093/rheumatology/keu330]).

© Jupiterimages/Thinkstockphotos.com

Smokers in the highest tertile of sodium intake in the cohort (median intake was 2.15 g/day, equivalent to 5.46 g NaCl) had an odds ratio of 2.26 (95% confidence interval, 1.06-4.81; P = .036) for developing RA, compared with smokers in the lowest tertile, who had a median intake of 1.51 g/day (equivalent to 3.84 g NaCl). The significant association between high sodium intake and the development of RA was found only for smokers, not for the total study population, although smokers with low-sodium diets saw no added likelihood of developing RA, compared with nonsmokers.

Smoking is an established risk factor for RA, but in this study, “additive interaction analyses suggested that approximately half of the amount of risk from smoking in the development of RA is due to interaction with sodium intake,” Dr. Sundström and his associates wrote, with an attributable proportion of 0.54 (95% CI, 0.26-0.82). Although the researchers did not identify the possible pathways by which an interaction between smoking and high sodium intake might increase risk of RA, “these findings will provide new insights into the etiopathogenic process leading to the development of RA among smokers,” they wrote.

Their study was funded by the Swedish Research Council, the Swedish Rheumatism Association, the Swedish Controlling Chronic Inflammatory Diseases with Combined Efforts (COMBINE) program, and the Swedish royal family. None of the coauthors declared conflicts of interest.

Smokers with high sodium intake were more than twice as likely to develop rheumatoid arthritis as were those with low sodium intake in a nested case-control study.

The study, which lends support to the possibility that an interaction between smoking and a diet heavy in sodium can increase RA risk, involved records from 386 individuals who had provided information on their dietary habits for a long-term, population-based study a median 7.7 years before going on to develop RA. Researchers from Umeå (Sweden) University, led by Björn Sundström, Ph.D., compared these with records for 1,886 age- and sex-matched controls who did not have RA and had taken part in the same population-based study (Rheumatology 2014 Sept. 10 [doi:10.1093/rheumatology/keu330]).

© Jupiterimages/Thinkstockphotos.com

Smokers in the highest tertile of sodium intake in the cohort (median intake was 2.15 g/day, equivalent to 5.46 g NaCl) had an odds ratio of 2.26 (95% confidence interval, 1.06-4.81; P = .036) for developing RA, compared with smokers in the lowest tertile, who had a median intake of 1.51 g/day (equivalent to 3.84 g NaCl). The significant association between high sodium intake and the development of RA was found only for smokers, not for the total study population, although smokers with low-sodium diets saw no added likelihood of developing RA, compared with nonsmokers.

Smoking is an established risk factor for RA, but in this study, “additive interaction analyses suggested that approximately half of the amount of risk from smoking in the development of RA is due to interaction with sodium intake,” Dr. Sundström and his associates wrote, with an attributable proportion of 0.54 (95% CI, 0.26-0.82). Although the researchers did not identify the possible pathways by which an interaction between smoking and high sodium intake might increase risk of RA, “these findings will provide new insights into the etiopathogenic process leading to the development of RA among smokers,” they wrote.

Their study was funded by the Swedish Research Council, the Swedish Rheumatism Association, the Swedish Controlling Chronic Inflammatory Diseases with Combined Efforts (COMBINE) program, and the Swedish royal family. None of the coauthors declared conflicts of interest.

Smokers with high sodium intake were more than twice as likely to develop rheumatoid arthritis as were those with low sodium intake in a nested case-control study.

The study, which lends support to the possibility that an interaction between smoking and a diet heavy in sodium can increase RA risk, involved records from 386 individuals who had provided information on their dietary habits for a long-term, population-based study a median 7.7 years before going on to develop RA. Researchers from Umeå (Sweden) University, led by Björn Sundström, Ph.D., compared these with records for 1,886 age- and sex-matched controls who did not have RA and had taken part in the same population-based study (Rheumatology 2014 Sept. 10 [doi:10.1093/rheumatology/keu330]).

© Jupiterimages/Thinkstockphotos.com

Smokers in the highest tertile of sodium intake in the cohort (median intake was 2.15 g/day, equivalent to 5.46 g NaCl) had an odds ratio of 2.26 (95% confidence interval, 1.06-4.81; P = .036) for developing RA, compared with smokers in the lowest tertile, who had a median intake of 1.51 g/day (equivalent to 3.84 g NaCl). The significant association between high sodium intake and the development of RA was found only for smokers, not for the total study population, although smokers with low-sodium diets saw no added likelihood of developing RA, compared with nonsmokers.

Smoking is an established risk factor for RA, but in this study, “additive interaction analyses suggested that approximately half of the amount of risk from smoking in the development of RA is due to interaction with sodium intake,” Dr. Sundström and his associates wrote, with an attributable proportion of 0.54 (95% CI, 0.26-0.82). Although the researchers did not identify the possible pathways by which an interaction between smoking and high sodium intake might increase risk of RA, “these findings will provide new insights into the etiopathogenic process leading to the development of RA among smokers,” they wrote.

Their study was funded by the Swedish Research Council, the Swedish Rheumatism Association, the Swedish Controlling Chronic Inflammatory Diseases with Combined Efforts (COMBINE) program, and the Swedish royal family. None of the coauthors declared conflicts of interest.

Women who follow a Mediterranean-style diet – high in whole grains, nuts, fish, and legumes while low in red meats, processed meats, and saturated fats – showed no significant reduction in the risk of developing rheumatoid arthritis in a large, prospective cohort study.

However, the findings do not jibe with the results of other studies in which the diet was associated with a reduced risk of certain other inflammatory diseases or observations of clinical improvement in people with existing rheumatoid arthritis (RA).

©snyferok/thinkstockphoto.com

The study, published Sept. 23 in Arthritis Care and Research (doi:10.1002/acr.22481), evaluated data from nearly 175,000 women in two U.S. cohorts: the 1980-2008 Nurses Health Study (n = 83,245) and the 1991-2009 Nurses Health Study II (n = 91,393). Data from both cohorts were obtained through validated diet questionnaires at baseline and every 4 years during follow-up. Investigator Yang Hu of Brigham & Women’s Hospital, Boston, and his colleagues, identified 913 incident cases of RA in 3.5 million person-years of follow-up and found the pooled hazard ratio for women in the quartile most adherent to the Mediterranean diet to be 0.98 (95% confidence interval, 0.80-1.20; P for trend = .85), compared with women in the quartile representing the lowest level of adherence.

The investigators described nine measures they used to assess the Mediterranean dietary pattern, including consumption of vegetables (not potatoes), fruits, nuts, whole grains, legumes, fish ratio of monounsaturated to saturated fats, red and processed meats, and alcohol. When components of the Mediterranean diet were evaluated as separate contributors to risk, only alcohol consumption was seen significantly associated with RA risk, with moderate consumption linked to lower risk.

Two coauthors of Mr. Hu and his colleagues’ study detailed the alcohol-related findings from the same cohort in a paper earlier this year (Arthritis Rheumatol. 2014;66:1998-2005). Mr. Hu and his colleagues hypothesized that the null findings related to the Mediterranean diet could have been influenced by the fact that within the food categories used in the study (fats, vegetables, fish), certain preparations or types of food might contribute to risk while others might help lower it.

The study was supported by grants from the National Institutes of Health. None of the authors declared conflicts of interest.

Women who follow a Mediterranean-style diet – high in whole grains, nuts, fish, and legumes while low in red meats, processed meats, and saturated fats – showed no significant reduction in the risk of developing rheumatoid arthritis in a large, prospective cohort study.

However, the findings do not jibe with the results of other studies in which the diet was associated with a reduced risk of certain other inflammatory diseases or observations of clinical improvement in people with existing rheumatoid arthritis (RA).

©snyferok/thinkstockphoto.com

The study, published Sept. 23 in Arthritis Care and Research (doi:10.1002/acr.22481), evaluated data from nearly 175,000 women in two U.S. cohorts: the 1980-2008 Nurses Health Study (n = 83,245) and the 1991-2009 Nurses Health Study II (n = 91,393). Data from both cohorts were obtained through validated diet questionnaires at baseline and every 4 years during follow-up. Investigator Yang Hu of Brigham & Women’s Hospital, Boston, and his colleagues, identified 913 incident cases of RA in 3.5 million person-years of follow-up and found the pooled hazard ratio for women in the quartile most adherent to the Mediterranean diet to be 0.98 (95% confidence interval, 0.80-1.20; P for trend = .85), compared with women in the quartile representing the lowest level of adherence.

The investigators described nine measures they used to assess the Mediterranean dietary pattern, including consumption of vegetables (not potatoes), fruits, nuts, whole grains, legumes, fish ratio of monounsaturated to saturated fats, red and processed meats, and alcohol. When components of the Mediterranean diet were evaluated as separate contributors to risk, only alcohol consumption was seen significantly associated with RA risk, with moderate consumption linked to lower risk.

Two coauthors of Mr. Hu and his colleagues’ study detailed the alcohol-related findings from the same cohort in a paper earlier this year (Arthritis Rheumatol. 2014;66:1998-2005). Mr. Hu and his colleagues hypothesized that the null findings related to the Mediterranean diet could have been influenced by the fact that within the food categories used in the study (fats, vegetables, fish), certain preparations or types of food might contribute to risk while others might help lower it.

The study was supported by grants from the National Institutes of Health. None of the authors declared conflicts of interest.

Women who follow a Mediterranean-style diet – high in whole grains, nuts, fish, and legumes while low in red meats, processed meats, and saturated fats – showed no significant reduction in the risk of developing rheumatoid arthritis in a large, prospective cohort study.

However, the findings do not jibe with the results of other studies in which the diet was associated with a reduced risk of certain other inflammatory diseases or observations of clinical improvement in people with existing rheumatoid arthritis (RA).

©snyferok/thinkstockphoto.com

The study, published Sept. 23 in Arthritis Care and Research (doi:10.1002/acr.22481), evaluated data from nearly 175,000 women in two U.S. cohorts: the 1980-2008 Nurses Health Study (n = 83,245) and the 1991-2009 Nurses Health Study II (n = 91,393). Data from both cohorts were obtained through validated diet questionnaires at baseline and every 4 years during follow-up. Investigator Yang Hu of Brigham & Women’s Hospital, Boston, and his colleagues, identified 913 incident cases of RA in 3.5 million person-years of follow-up and found the pooled hazard ratio for women in the quartile most adherent to the Mediterranean diet to be 0.98 (95% confidence interval, 0.80-1.20; P for trend = .85), compared with women in the quartile representing the lowest level of adherence.

The investigators described nine measures they used to assess the Mediterranean dietary pattern, including consumption of vegetables (not potatoes), fruits, nuts, whole grains, legumes, fish ratio of monounsaturated to saturated fats, red and processed meats, and alcohol. When components of the Mediterranean diet were evaluated as separate contributors to risk, only alcohol consumption was seen significantly associated with RA risk, with moderate consumption linked to lower risk.

Two coauthors of Mr. Hu and his colleagues’ study detailed the alcohol-related findings from the same cohort in a paper earlier this year (Arthritis Rheumatol. 2014;66:1998-2005). Mr. Hu and his colleagues hypothesized that the null findings related to the Mediterranean diet could have been influenced by the fact that within the food categories used in the study (fats, vegetables, fish), certain preparations or types of food might contribute to risk while others might help lower it.

The study was supported by grants from the National Institutes of Health. None of the authors declared conflicts of interest.

A total of 11 new research grants have been awarded by the National Institutes of Health as part of the first year of funding for the Accelerating Medicines Partnership in Rheumatoid Arthritis and Lupus.

The $6 million in first-year funding, part of $41.6 million slated for the two autoimmune diseases over a 5-year period as part of the broader Accelerating Medicines Partnership in Rheumatoid Arthritis and Systemic Lupus Erythematosus (AMP RA/SLE) Program was announced Sept. 24.

Over 5 years, the AMP RA/Lupus Network will analyze the interplay among biologic pathways, including at the single cell level, in tissues of patients with RA and lupus. The goal is to integrate data from multiple genome-wide analytic approaches to generate a comprehensive understanding of the mechanisms of tissue damage in RA and lupus.

The AMP RA/SLE Program is funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and National Institute of Allergy and Infectious Diseases (NIAID), and the following members of the AMP: AbbVie, Bristol-Myers Squibb, Merck, Pfizer, Sanofi, Takeda, the Arthritis Foundation, the Lupus Foundation of America, the Lupus Research Institute/Alliance for Lupus Research, and the Rheumatology Research Foundation.

“To date, treatments for RA and lupus have been aimed at decreasing inflammation and pain,” Dr. Stephen I. Katz, director of NIAMS, said in a written statement. “For the first time, we are bringing together multidisciplinary research teams to achieve a broad, systems-level understanding of these diseases, setting the stage for the development of more effective diagnostic and treatment approaches.”

Dr. Anthony S. Fauci, director of NIAID, added: “This program promises to lead to more diagnosis and treatment options for rheumatoid arthritis and lupus. We also anticipate that the flexibility of the program will enable investigators to advance research on related diseases, thus improving our overall understanding of autoimmunity.”

In addition to the AMP RA/Lupus Network’s leadership center, led by Dr. Paul J. Utz of Stanford (Calif.) University and Dr. V. Michael Holers of the University of Colorado, Denver, the 11 grants were awarded to research teams at sites that perform clinical research, technology research, or both. For a list of the research sites and descriptions of the proposed research, click here.

jevans@frontlinemedcom.com

A total of 11 new research grants have been awarded by the National Institutes of Health as part of the first year of funding for the Accelerating Medicines Partnership in Rheumatoid Arthritis and Lupus.

The $6 million in first-year funding, part of $41.6 million slated for the two autoimmune diseases over a 5-year period as part of the broader Accelerating Medicines Partnership in Rheumatoid Arthritis and Systemic Lupus Erythematosus (AMP RA/SLE) Program was announced Sept. 24.

Over 5 years, the AMP RA/Lupus Network will analyze the interplay among biologic pathways, including at the single cell level, in tissues of patients with RA and lupus. The goal is to integrate data from multiple genome-wide analytic approaches to generate a comprehensive understanding of the mechanisms of tissue damage in RA and lupus.

The AMP RA/SLE Program is funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and National Institute of Allergy and Infectious Diseases (NIAID), and the following members of the AMP: AbbVie, Bristol-Myers Squibb, Merck, Pfizer, Sanofi, Takeda, the Arthritis Foundation, the Lupus Foundation of America, the Lupus Research Institute/Alliance for Lupus Research, and the Rheumatology Research Foundation.

“To date, treatments for RA and lupus have been aimed at decreasing inflammation and pain,” Dr. Stephen I. Katz, director of NIAMS, said in a written statement. “For the first time, we are bringing together multidisciplinary research teams to achieve a broad, systems-level understanding of these diseases, setting the stage for the development of more effective diagnostic and treatment approaches.”

Dr. Anthony S. Fauci, director of NIAID, added: “This program promises to lead to more diagnosis and treatment options for rheumatoid arthritis and lupus. We also anticipate that the flexibility of the program will enable investigators to advance research on related diseases, thus improving our overall understanding of autoimmunity.”

In addition to the AMP RA/Lupus Network’s leadership center, led by Dr. Paul J. Utz of Stanford (Calif.) University and Dr. V. Michael Holers of the University of Colorado, Denver, the 11 grants were awarded to research teams at sites that perform clinical research, technology research, or both. For a list of the research sites and descriptions of the proposed research, click here.

jevans@frontlinemedcom.com

A total of 11 new research grants have been awarded by the National Institutes of Health as part of the first year of funding for the Accelerating Medicines Partnership in Rheumatoid Arthritis and Lupus.

The $6 million in first-year funding, part of $41.6 million slated for the two autoimmune diseases over a 5-year period as part of the broader Accelerating Medicines Partnership in Rheumatoid Arthritis and Systemic Lupus Erythematosus (AMP RA/SLE) Program was announced Sept. 24.

Over 5 years, the AMP RA/Lupus Network will analyze the interplay among biologic pathways, including at the single cell level, in tissues of patients with RA and lupus. The goal is to integrate data from multiple genome-wide analytic approaches to generate a comprehensive understanding of the mechanisms of tissue damage in RA and lupus.

The AMP RA/SLE Program is funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and National Institute of Allergy and Infectious Diseases (NIAID), and the following members of the AMP: AbbVie, Bristol-Myers Squibb, Merck, Pfizer, Sanofi, Takeda, the Arthritis Foundation, the Lupus Foundation of America, the Lupus Research Institute/Alliance for Lupus Research, and the Rheumatology Research Foundation.

“To date, treatments for RA and lupus have been aimed at decreasing inflammation and pain,” Dr. Stephen I. Katz, director of NIAMS, said in a written statement. “For the first time, we are bringing together multidisciplinary research teams to achieve a broad, systems-level understanding of these diseases, setting the stage for the development of more effective diagnostic and treatment approaches.”

Dr. Anthony S. Fauci, director of NIAID, added: “This program promises to lead to more diagnosis and treatment options for rheumatoid arthritis and lupus. We also anticipate that the flexibility of the program will enable investigators to advance research on related diseases, thus improving our overall understanding of autoimmunity.”

In addition to the AMP RA/Lupus Network’s leadership center, led by Dr. Paul J. Utz of Stanford (Calif.) University and Dr. V. Michael Holers of the University of Colorado, Denver, the 11 grants were awarded to research teams at sites that perform clinical research, technology research, or both. For a list of the research sites and descriptions of the proposed research, click here.

jevans@frontlinemedcom.com

In patients with early rheumatoid arthritis, combining the 2010 RA classification criteria with bone marrow edema as seen on MRI was a more sensitive and accurate diagnostic approach than using the 2010 criteria alone, researchers reported in Annals of the Rheumatic Diseases.

"The present findings are the first evidence that the diagnostic probability of early RA using the 2010 RA classification criteria is improved by combining these criteria with MRI-detected bone marrow edema of the wrist and finger joints," said Dr. Mami Tamai at Nagasaki University in Japan and associates.

The investigators studied 166 patients with early arthritis and a median disease duration of 2 months. They defined RA as using disease-modifying antirheumatic drugs (DMARDs) within the first year or as fulfilling the 1987 RA criteria at 1 year, they said (Ann. Rheum. Dis. 2014 [doi:10.1136/annrheumdis-2013-205074]).

Combining the 2010 criteria with bone marrow edema of the wrists or finger joints on MRI yielded a higher sensitivity (76.3%), negative predictive value (69.3%), and accuracy (75.9%) than did using the 2010 criteria alone with the DMARD-based definition as the reference standard. Applied alone, the 2010 RA classification had a sensitivity of only 61.9%, a negative predictive value of 60.6%, and an accuracy of 70.5%. Results were similar when they used the 1987 definition as the reference standard, the investigators said.

Bone marrow edema had a higher positive predictive value than did MRI-detected bone erosion or symmetrical synovitis when added to the 2010 RA classification criteria. "Our study may strengthen the statements of the European League Against Rheumatism recommendations for the use of imaging," they added.

Funding information for the study was not available. The authors reported no conflicts of interest.

In patients with early rheumatoid arthritis, combining the 2010 RA classification criteria with bone marrow edema as seen on MRI was a more sensitive and accurate diagnostic approach than using the 2010 criteria alone, researchers reported in Annals of the Rheumatic Diseases.

"The present findings are the first evidence that the diagnostic probability of early RA using the 2010 RA classification criteria is improved by combining these criteria with MRI-detected bone marrow edema of the wrist and finger joints," said Dr. Mami Tamai at Nagasaki University in Japan and associates.

The investigators studied 166 patients with early arthritis and a median disease duration of 2 months. They defined RA as using disease-modifying antirheumatic drugs (DMARDs) within the first year or as fulfilling the 1987 RA criteria at 1 year, they said (Ann. Rheum. Dis. 2014 [doi:10.1136/annrheumdis-2013-205074]).

Combining the 2010 criteria with bone marrow edema of the wrists or finger joints on MRI yielded a higher sensitivity (76.3%), negative predictive value (69.3%), and accuracy (75.9%) than did using the 2010 criteria alone with the DMARD-based definition as the reference standard. Applied alone, the 2010 RA classification had a sensitivity of only 61.9%, a negative predictive value of 60.6%, and an accuracy of 70.5%. Results were similar when they used the 1987 definition as the reference standard, the investigators said.

Bone marrow edema had a higher positive predictive value than did MRI-detected bone erosion or symmetrical synovitis when added to the 2010 RA classification criteria. "Our study may strengthen the statements of the European League Against Rheumatism recommendations for the use of imaging," they added.

Funding information for the study was not available. The authors reported no conflicts of interest.

In patients with early rheumatoid arthritis, combining the 2010 RA classification criteria with bone marrow edema as seen on MRI was a more sensitive and accurate diagnostic approach than using the 2010 criteria alone, researchers reported in Annals of the Rheumatic Diseases.

"The present findings are the first evidence that the diagnostic probability of early RA using the 2010 RA classification criteria is improved by combining these criteria with MRI-detected bone marrow edema of the wrist and finger joints," said Dr. Mami Tamai at Nagasaki University in Japan and associates.

The investigators studied 166 patients with early arthritis and a median disease duration of 2 months. They defined RA as using disease-modifying antirheumatic drugs (DMARDs) within the first year or as fulfilling the 1987 RA criteria at 1 year, they said (Ann. Rheum. Dis. 2014 [doi:10.1136/annrheumdis-2013-205074]).

Combining the 2010 criteria with bone marrow edema of the wrists or finger joints on MRI yielded a higher sensitivity (76.3%), negative predictive value (69.3%), and accuracy (75.9%) than did using the 2010 criteria alone with the DMARD-based definition as the reference standard. Applied alone, the 2010 RA classification had a sensitivity of only 61.9%, a negative predictive value of 60.6%, and an accuracy of 70.5%. Results were similar when they used the 1987 definition as the reference standard, the investigators said.

Bone marrow edema had a higher positive predictive value than did MRI-detected bone erosion or symmetrical synovitis when added to the 2010 RA classification criteria. "Our study may strengthen the statements of the European League Against Rheumatism recommendations for the use of imaging," they added.

Funding information for the study was not available. The authors reported no conflicts of interest.

CHICAGO – The “much anticipated” guideline to help primary-care and emergency clinicians improve the management of sickle cell disease includes a consensus treatment protocol for implementing hydroxyurea therapy and more detailed guidance regarding long-term transfusion therapy, according to a summary report published online September 9 in JAMA.

Sickle cell disease (SCD), a life-threatening genetically transmitted disorder affecting 70,000-100,000 Americans, is associated with a wide array of complex acute and chronic complications that require immediate medical attention. But high-quality data on which to base management decisions are sorely lacking, and clinicians get little in the way of guidance from existing recommendations. One result is that “the 2 most widely available disease-modifying therapies, hydroxyurea and long-term transfusions, are underused, and hematopoietic stem cell transplantation, the only curative approach, has been used in only a small proportion of affected individuals,” said Dr. Barbara P. Yawn and her associates on the National Heart, Lung, and Blood Institute expert panel that issued the summary report.

Even this guideline is somewhat rudimentary (Advil) due to the dearth of good data “in virtually every area related to SCD management,” and cannot help but leave “many uncertainties for health professionals caring for individuals with SCD.” But it is hoped that this guideline will furnish a critical foundation for future research will now begin “to facilitate improved and more accessible care for all affected individuals,” said Dr. Yawn, of the department of research and education, Olmsted Medical Center, Rochester MN, and her associates.

The guideline is based on an extensive literature review of more than 13,000 abstracts and articles, which was winnowed to 1,583 original studies regarding SCD. From this, a team of health care professionals in family medicine, internal medicine, pediatric and adult hematology, psychiatry and mental health, transfusion medicine, obstetrics and gynecology, maternal/fetal medicine, and emergency department nursing compiled the guideline as well as the summary, entitled Evidence-Based Management of Sickle Cell Disease: Expert Panel Report 2014 (JAMA 2014 September 9 [doi:10.1001/jama.2014.10517]).

In addition to establishing a protocol for implementing hydroxyurea therapy, the guideline addresses changes in pneumococcal vaccination recommendations for adults and children; annual transcranial Doppler screening coupled with long-term transfusion therapy when necessary, to prevent stroke in children aged 2-16 years; rapid initiation of opioids for severe pain during vasoocclusive crises; analgesics and physical therapy for avascular necrosis; ACE inhibitor treatment for adults with microalbuminuria; referral to specialists for screening and treatment of proliferative retinopathy; echocardiography to assess signs of pulmonary hypertension; and monitoring for iron overload in patients receiving transfusion therapy.

CHICAGO – The “much anticipated” guideline to help primary-care and emergency clinicians improve the management of sickle cell disease includes a consensus treatment protocol for implementing hydroxyurea therapy and more detailed guidance regarding long-term transfusion therapy, according to a summary report published online September 9 in JAMA.

Sickle cell disease (SCD), a life-threatening genetically transmitted disorder affecting 70,000-100,000 Americans, is associated with a wide array of complex acute and chronic complications that require immediate medical attention. But high-quality data on which to base management decisions are sorely lacking, and clinicians get little in the way of guidance from existing recommendations. One result is that “the 2 most widely available disease-modifying therapies, hydroxyurea and long-term transfusions, are underused, and hematopoietic stem cell transplantation, the only curative approach, has been used in only a small proportion of affected individuals,” said Dr. Barbara P. Yawn and her associates on the National Heart, Lung, and Blood Institute expert panel that issued the summary report.

Even this guideline is somewhat rudimentary (Advil) due to the dearth of good data “in virtually every area related to SCD management,” and cannot help but leave “many uncertainties for health professionals caring for individuals with SCD.” But it is hoped that this guideline will furnish a critical foundation for future research will now begin “to facilitate improved and more accessible care for all affected individuals,” said Dr. Yawn, of the department of research and education, Olmsted Medical Center, Rochester MN, and her associates.

The guideline is based on an extensive literature review of more than 13,000 abstracts and articles, which was winnowed to 1,583 original studies regarding SCD. From this, a team of health care professionals in family medicine, internal medicine, pediatric and adult hematology, psychiatry and mental health, transfusion medicine, obstetrics and gynecology, maternal/fetal medicine, and emergency department nursing compiled the guideline as well as the summary, entitled Evidence-Based Management of Sickle Cell Disease: Expert Panel Report 2014 (JAMA 2014 September 9 [doi:10.1001/jama.2014.10517]).

In addition to establishing a protocol for implementing hydroxyurea therapy, the guideline addresses changes in pneumococcal vaccination recommendations for adults and children; annual transcranial Doppler screening coupled with long-term transfusion therapy when necessary, to prevent stroke in children aged 2-16 years; rapid initiation of opioids for severe pain during vasoocclusive crises; analgesics and physical therapy for avascular necrosis; ACE inhibitor treatment for adults with microalbuminuria; referral to specialists for screening and treatment of proliferative retinopathy; echocardiography to assess signs of pulmonary hypertension; and monitoring for iron overload in patients receiving transfusion therapy.

CHICAGO – The “much anticipated” guideline to help primary-care and emergency clinicians improve the management of sickle cell disease includes a consensus treatment protocol for implementing hydroxyurea therapy and more detailed guidance regarding long-term transfusion therapy, according to a summary report published online September 9 in JAMA.

Sickle cell disease (SCD), a life-threatening genetically transmitted disorder affecting 70,000-100,000 Americans, is associated with a wide array of complex acute and chronic complications that require immediate medical attention. But high-quality data on which to base management decisions are sorely lacking, and clinicians get little in the way of guidance from existing recommendations. One result is that “the 2 most widely available disease-modifying therapies, hydroxyurea and long-term transfusions, are underused, and hematopoietic stem cell transplantation, the only curative approach, has been used in only a small proportion of affected individuals,” said Dr. Barbara P. Yawn and her associates on the National Heart, Lung, and Blood Institute expert panel that issued the summary report.

Even this guideline is somewhat rudimentary (Advil) due to the dearth of good data “in virtually every area related to SCD management,” and cannot help but leave “many uncertainties for health professionals caring for individuals with SCD.” But it is hoped that this guideline will furnish a critical foundation for future research will now begin “to facilitate improved and more accessible care for all affected individuals,” said Dr. Yawn, of the department of research and education, Olmsted Medical Center, Rochester MN, and her associates.

The guideline is based on an extensive literature review of more than 13,000 abstracts and articles, which was winnowed to 1,583 original studies regarding SCD. From this, a team of health care professionals in family medicine, internal medicine, pediatric and adult hematology, psychiatry and mental health, transfusion medicine, obstetrics and gynecology, maternal/fetal medicine, and emergency department nursing compiled the guideline as well as the summary, entitled Evidence-Based Management of Sickle Cell Disease: Expert Panel Report 2014 (JAMA 2014 September 9 [doi:10.1001/jama.2014.10517]).

In addition to establishing a protocol for implementing hydroxyurea therapy, the guideline addresses changes in pneumococcal vaccination recommendations for adults and children; annual transcranial Doppler screening coupled with long-term transfusion therapy when necessary, to prevent stroke in children aged 2-16 years; rapid initiation of opioids for severe pain during vasoocclusive crises; analgesics and physical therapy for avascular necrosis; ACE inhibitor treatment for adults with microalbuminuria; referral to specialists for screening and treatment of proliferative retinopathy; echocardiography to assess signs of pulmonary hypertension; and monitoring for iron overload in patients receiving transfusion therapy.

Aggressive anti-inflammatory treatment correlated with slowed bone loss in patients with early rheumatoid arthritis, according to findings from a prospective cohort study.

The results show that "modern aggressive treatment" can reduce osteoporosis in patients with RA, said Dr. Glenn Haugeberg of the rheumatology department at the Hospital of Southern Norway Trust in Kristiansand and his associates.

Photo by Anette Stromsbo Gjorv

In all, 18.5% of patients with RA used biologic disease-modifying antirheumatic drugs during the first 2 years of the study, while 62.6% used these drugs during the next 8 years, at the same time that average bone mineral density loss slowed substantially, the researchers said.

The average yearly rate of bone loss at 2 years and 10 years slowed from –1.00% to –0.56% for the femoral neck, from –0.96% to –0.41% for total spine, and from –0.42% to 0.00% for the L1-L4 vertebrae, the researchers reported (BMC Musculoskelet. Disord. 2014 Sept. 2 [doi: 10.1186/1471-2474-15-289]).

The study included 92 patients (mean age, 50.9 years) with RA, of whom about two-thirds were women, and 80% had their bone mineral densities assessed at 10 years. Patients had experienced symptoms for a mean of 12.4 months.

Contrary to findings from some prior studies, glucocorticoid use was linked to bone loss during only the first 2 years of the study period and only for total hip measurements, the researchers said.

Almost half the patients had missing baseline data on bone mineral density. The study also lacked matched controls and did not assess the prevalence or incidence of vertebral fractures, the authors added.

Funding information for the study was not available. The authors reported having no conflicts of interest.

Aggressive anti-inflammatory treatment correlated with slowed bone loss in patients with early rheumatoid arthritis, according to findings from a prospective cohort study.

The results show that "modern aggressive treatment" can reduce osteoporosis in patients with RA, said Dr. Glenn Haugeberg of the rheumatology department at the Hospital of Southern Norway Trust in Kristiansand and his associates.

Photo by Anette Stromsbo Gjorv

In all, 18.5% of patients with RA used biologic disease-modifying antirheumatic drugs during the first 2 years of the study, while 62.6% used these drugs during the next 8 years, at the same time that average bone mineral density loss slowed substantially, the researchers said.

The average yearly rate of bone loss at 2 years and 10 years slowed from –1.00% to –0.56% for the femoral neck, from –0.96% to –0.41% for total spine, and from –0.42% to 0.00% for the L1-L4 vertebrae, the researchers reported (BMC Musculoskelet. Disord. 2014 Sept. 2 [doi: 10.1186/1471-2474-15-289]).

The study included 92 patients (mean age, 50.9 years) with RA, of whom about two-thirds were women, and 80% had their bone mineral densities assessed at 10 years. Patients had experienced symptoms for a mean of 12.4 months.

Contrary to findings from some prior studies, glucocorticoid use was linked to bone loss during only the first 2 years of the study period and only for total hip measurements, the researchers said.

Almost half the patients had missing baseline data on bone mineral density. The study also lacked matched controls and did not assess the prevalence or incidence of vertebral fractures, the authors added.

Funding information for the study was not available. The authors reported having no conflicts of interest.

Aggressive anti-inflammatory treatment correlated with slowed bone loss in patients with early rheumatoid arthritis, according to findings from a prospective cohort study.

The results show that "modern aggressive treatment" can reduce osteoporosis in patients with RA, said Dr. Glenn Haugeberg of the rheumatology department at the Hospital of Southern Norway Trust in Kristiansand and his associates.

Photo by Anette Stromsbo Gjorv

In all, 18.5% of patients with RA used biologic disease-modifying antirheumatic drugs during the first 2 years of the study, while 62.6% used these drugs during the next 8 years, at the same time that average bone mineral density loss slowed substantially, the researchers said.

The average yearly rate of bone loss at 2 years and 10 years slowed from –1.00% to –0.56% for the femoral neck, from –0.96% to –0.41% for total spine, and from –0.42% to 0.00% for the L1-L4 vertebrae, the researchers reported (BMC Musculoskelet. Disord. 2014 Sept. 2 [doi: 10.1186/1471-2474-15-289]).

The study included 92 patients (mean age, 50.9 years) with RA, of whom about two-thirds were women, and 80% had their bone mineral densities assessed at 10 years. Patients had experienced symptoms for a mean of 12.4 months.

Contrary to findings from some prior studies, glucocorticoid use was linked to bone loss during only the first 2 years of the study period and only for total hip measurements, the researchers said.

Almost half the patients had missing baseline data on bone mineral density. The study also lacked matched controls and did not assess the prevalence or incidence of vertebral fractures, the authors added.

Funding information for the study was not available. The authors reported having no conflicts of interest.