Clinical Edge Journal Scan

Key clinical point: Treatment with radiation therapy is safe and effective for men with prostate cancer and underlying inflammatory bowel disease, with no biochemical relapses during an early follow-up period. 

Major finding: With a median time of 22 months to any GI toxicity, one IBD patient experienced a high-grade toxicity (grade 3 proctitis) and 3 patients reported hemorrhoidal flares as the most common low-grade toxicity.

Study details: The data come from an institutional database of 4245 men who underwent stereotactic body radiation therapy for prostate cancer, including 31 patients with underlying inflammatory bowel disease.

Disclosures: The study was supported in part by a grant from Accuray. The researchers had no other financial conflicts to disclose.

Source: Lischalk JW et al. Radiat Oncol. 2021 Jul 9 doi: 10.1186/s13014-021-01850-1.

Key clinical point: Treatment with radiation therapy is safe and effective for men with prostate cancer and underlying inflammatory bowel disease, with no biochemical relapses during an early follow-up period. 

Major finding: With a median time of 22 months to any GI toxicity, one IBD patient experienced a high-grade toxicity (grade 3 proctitis) and 3 patients reported hemorrhoidal flares as the most common low-grade toxicity.

Study details: The data come from an institutional database of 4245 men who underwent stereotactic body radiation therapy for prostate cancer, including 31 patients with underlying inflammatory bowel disease.

Disclosures: The study was supported in part by a grant from Accuray. The researchers had no other financial conflicts to disclose.

Source: Lischalk JW et al. Radiat Oncol. 2021 Jul 9 doi: 10.1186/s13014-021-01850-1.

Key clinical point: Treatment with radiation therapy is safe and effective for men with prostate cancer and underlying inflammatory bowel disease, with no biochemical relapses during an early follow-up period. 

Major finding: With a median time of 22 months to any GI toxicity, one IBD patient experienced a high-grade toxicity (grade 3 proctitis) and 3 patients reported hemorrhoidal flares as the most common low-grade toxicity.

Study details: The data come from an institutional database of 4245 men who underwent stereotactic body radiation therapy for prostate cancer, including 31 patients with underlying inflammatory bowel disease.

Disclosures: The study was supported in part by a grant from Accuray. The researchers had no other financial conflicts to disclose.

Source: Lischalk JW et al. Radiat Oncol. 2021 Jul 9 doi: 10.1186/s13014-021-01850-1.

Varying strategies have been evaluated to diagnose and predict risk of prostate cancer more optimally. The presence of local or systemic inflammation has been postulated to be associated with increased risk of the presence and aggressiveness of prostate cancer. Complete blood counts with differential white counts are routinely obtained, and the ratio of platelets to lymphocytes (PLR), neutrophils to lymphocytes (NLR), and monocytes to lymphocytes (MLR) have been proposed as markers of inflammation. In the study by Lee et al., the authors evaluated whether the PLR was associated with benign prostate disease, clinically insignificant prostate cancer (Gleason 6 or lower), or clinically significant prostate cancer (Gleason 7 or higher) in patients undergoing prostate biopsy. In a cohort of 1652 who underwent biopsy, the only significant finding was a lower PLR in patients with clinically significant prostate cancer and a PSA < 10 ng/mL compared with patients having benign disease or clinically insignificant disease.

Rundle et al evaluated whether NLR or MLR in the setting of cancer varied by race, as African American and Black men are at higher risk for prostate cancer than White men. In this case-control study that included 822 cases of prostate cancer and 573 controls, there were no significant differences in the trajectories of NLR or MLR over time between cases or controls in the entire cohort. The NLR and MLR were higher over time for White men without prostate cancer compared with White men with prostate cancer; however, no such difference was identified when comparing Black men with or without prostate cancer. Thus, while there may be some association between inflammation and prostate cancer diagnoses or risk of aggressiveness, the use of PLR, NLR, or MLR requires much more study to fully determine the usefulness of these ratios.

A slightly different approach to improve diagnostic strategies has been to utilize prostate MRI to identify areas of the prostate suggestive of cancer. Eklund et al evaluated the use of MRI in the setting of an organized prostate screening program. The use of MRI with targeted and standard biopsy was noninferior to standard biopsy alone in detecting clinically significant prostate cancer while fewer clinically insignificant prostate cancers were identified in the MRI with targeted and standard biopsy group compared with the standard biopsy group. This study further supports the increasing utilization of MRI as part of a biopsy approach in men at risk for prostate cancer.

Varying strategies have been evaluated to diagnose and predict risk of prostate cancer more optimally. The presence of local or systemic inflammation has been postulated to be associated with increased risk of the presence and aggressiveness of prostate cancer. Complete blood counts with differential white counts are routinely obtained, and the ratio of platelets to lymphocytes (PLR), neutrophils to lymphocytes (NLR), and monocytes to lymphocytes (MLR) have been proposed as markers of inflammation. In the study by Lee et al., the authors evaluated whether the PLR was associated with benign prostate disease, clinically insignificant prostate cancer (Gleason 6 or lower), or clinically significant prostate cancer (Gleason 7 or higher) in patients undergoing prostate biopsy. In a cohort of 1652 who underwent biopsy, the only significant finding was a lower PLR in patients with clinically significant prostate cancer and a PSA < 10 ng/mL compared with patients having benign disease or clinically insignificant disease.

Rundle et al evaluated whether NLR or MLR in the setting of cancer varied by race, as African American and Black men are at higher risk for prostate cancer than White men. In this case-control study that included 822 cases of prostate cancer and 573 controls, there were no significant differences in the trajectories of NLR or MLR over time between cases or controls in the entire cohort. The NLR and MLR were higher over time for White men without prostate cancer compared with White men with prostate cancer; however, no such difference was identified when comparing Black men with or without prostate cancer. Thus, while there may be some association between inflammation and prostate cancer diagnoses or risk of aggressiveness, the use of PLR, NLR, or MLR requires much more study to fully determine the usefulness of these ratios.

A slightly different approach to improve diagnostic strategies has been to utilize prostate MRI to identify areas of the prostate suggestive of cancer. Eklund et al evaluated the use of MRI in the setting of an organized prostate screening program. The use of MRI with targeted and standard biopsy was noninferior to standard biopsy alone in detecting clinically significant prostate cancer while fewer clinically insignificant prostate cancers were identified in the MRI with targeted and standard biopsy group compared with the standard biopsy group. This study further supports the increasing utilization of MRI as part of a biopsy approach in men at risk for prostate cancer.

Varying strategies have been evaluated to diagnose and predict risk of prostate cancer more optimally. The presence of local or systemic inflammation has been postulated to be associated with increased risk of the presence and aggressiveness of prostate cancer. Complete blood counts with differential white counts are routinely obtained, and the ratio of platelets to lymphocytes (PLR), neutrophils to lymphocytes (NLR), and monocytes to lymphocytes (MLR) have been proposed as markers of inflammation. In the study by Lee et al., the authors evaluated whether the PLR was associated with benign prostate disease, clinically insignificant prostate cancer (Gleason 6 or lower), or clinically significant prostate cancer (Gleason 7 or higher) in patients undergoing prostate biopsy. In a cohort of 1652 who underwent biopsy, the only significant finding was a lower PLR in patients with clinically significant prostate cancer and a PSA < 10 ng/mL compared with patients having benign disease or clinically insignificant disease.

Rundle et al evaluated whether NLR or MLR in the setting of cancer varied by race, as African American and Black men are at higher risk for prostate cancer than White men. In this case-control study that included 822 cases of prostate cancer and 573 controls, there were no significant differences in the trajectories of NLR or MLR over time between cases or controls in the entire cohort. The NLR and MLR were higher over time for White men without prostate cancer compared with White men with prostate cancer; however, no such difference was identified when comparing Black men with or without prostate cancer. Thus, while there may be some association between inflammation and prostate cancer diagnoses or risk of aggressiveness, the use of PLR, NLR, or MLR requires much more study to fully determine the usefulness of these ratios.

A slightly different approach to improve diagnostic strategies has been to utilize prostate MRI to identify areas of the prostate suggestive of cancer. Eklund et al evaluated the use of MRI in the setting of an organized prostate screening program. The use of MRI with targeted and standard biopsy was noninferior to standard biopsy alone in detecting clinically significant prostate cancer while fewer clinically insignificant prostate cancers were identified in the MRI with targeted and standard biopsy group compared with the standard biopsy group. This study further supports the increasing utilization of MRI as part of a biopsy approach in men at risk for prostate cancer.

Key clinical point: The risk for dementia in patients with rheumatoid arthritis (RA) appears to be decreasing over time even when compared with non-RA referents.

Major finding: The 10-year cumulative incidence of ADRD for incident RA in the 1980s, 1990s and 2000s was 12.7%, 7.2% and 6.2%, respectively. Overall risk for ADRD was higher among patients with RA vs non-RA referents (HR, 1.37; 95% CI, 1.04-1.81), but this gap narrowed over time, with ADRD risk being higher in patients diagnosed with RA vs referents in the 1990s (HR, 1.72; 95% CI, 1.09-2.70) but not in the 2000s (HR, 0.86; 95% CI, 0.51-1.45).

Study details: The data come from a retrospective, population-based cohort study involving 897 patients with RA diagnosed between 1980 and 2009 and matched with 885 non-RA referents.

Disclosures: This study was supported by grants from the National Institutes of Health, National Institute of Arthritis and Musculoskeletal and Skin Disease and National Institute of Aging. No conflicts of interest were reported.

Source: Kronzer VL et al. Semin Arthritis Rheum. 2021 Jun 15. doi: 10.1016/j.semarthrit.2021.06.003.

Key clinical point: The risk for dementia in patients with rheumatoid arthritis (RA) appears to be decreasing over time even when compared with non-RA referents.

Major finding: The 10-year cumulative incidence of ADRD for incident RA in the 1980s, 1990s and 2000s was 12.7%, 7.2% and 6.2%, respectively. Overall risk for ADRD was higher among patients with RA vs non-RA referents (HR, 1.37; 95% CI, 1.04-1.81), but this gap narrowed over time, with ADRD risk being higher in patients diagnosed with RA vs referents in the 1990s (HR, 1.72; 95% CI, 1.09-2.70) but not in the 2000s (HR, 0.86; 95% CI, 0.51-1.45).

Study details: The data come from a retrospective, population-based cohort study involving 897 patients with RA diagnosed between 1980 and 2009 and matched with 885 non-RA referents.

Disclosures: This study was supported by grants from the National Institutes of Health, National Institute of Arthritis and Musculoskeletal and Skin Disease and National Institute of Aging. No conflicts of interest were reported.

Source: Kronzer VL et al. Semin Arthritis Rheum. 2021 Jun 15. doi: 10.1016/j.semarthrit.2021.06.003.

Key clinical point: The risk for dementia in patients with rheumatoid arthritis (RA) appears to be decreasing over time even when compared with non-RA referents.

Major finding: The 10-year cumulative incidence of ADRD for incident RA in the 1980s, 1990s and 2000s was 12.7%, 7.2% and 6.2%, respectively. Overall risk for ADRD was higher among patients with RA vs non-RA referents (HR, 1.37; 95% CI, 1.04-1.81), but this gap narrowed over time, with ADRD risk being higher in patients diagnosed with RA vs referents in the 1990s (HR, 1.72; 95% CI, 1.09-2.70) but not in the 2000s (HR, 0.86; 95% CI, 0.51-1.45).

Study details: The data come from a retrospective, population-based cohort study involving 897 patients with RA diagnosed between 1980 and 2009 and matched with 885 non-RA referents.

Disclosures: This study was supported by grants from the National Institutes of Health, National Institute of Arthritis and Musculoskeletal and Skin Disease and National Institute of Aging. No conflicts of interest were reported.

Source: Kronzer VL et al. Semin Arthritis Rheum. 2021 Jun 15. doi: 10.1016/j.semarthrit.2021.06.003.

Key clinical point: Among patients with rheumatoid arthritis (RA), traditional risk factors for cardiovascular disease (CVD) mostly predicted atherosclerotic CVD (ASCVD), except for obesity, which was a risk factor for unprovoked venous thromboembolism (VTE).

Major finding: Obesity was associated with increased VTE risk (adjusted hazard ratio [aHR], 1.47; 95% confidence interval [CI], 1.14-1.89) and reduced ASCVD risk (aHR, 0.56; 95% CI, 0.48-0.66). Other traditional CVD risk factors such as diabetes (aHR, 1.39; 95% CI, 1.20-1.62), hypertension (aHR, 1.21; 95% CI, 1.07-1.39), and chronic kidney disease (aHR, 1.31; 95% CI, 1.10-1.66) predicted higher ASCVD risk.

Study details: The data come from an analysis of 31,366 patients with RA from a US-wide longitudinal observational registry, who did not have any prior CVD at baseline and active cancer throughout follow-up.

Disclosures: No sources of funding were reported. K Michaud reported receiving grant support from the Rheumatology Research Foundation. No competing interests were declared.

Source: Ozen G et al. RMD Open. 2021 Jun 30. doi: 10.1136/rmdopen-2021-001618.

Key clinical point: Among patients with rheumatoid arthritis (RA), traditional risk factors for cardiovascular disease (CVD) mostly predicted atherosclerotic CVD (ASCVD), except for obesity, which was a risk factor for unprovoked venous thromboembolism (VTE).

Major finding: Obesity was associated with increased VTE risk (adjusted hazard ratio [aHR], 1.47; 95% confidence interval [CI], 1.14-1.89) and reduced ASCVD risk (aHR, 0.56; 95% CI, 0.48-0.66). Other traditional CVD risk factors such as diabetes (aHR, 1.39; 95% CI, 1.20-1.62), hypertension (aHR, 1.21; 95% CI, 1.07-1.39), and chronic kidney disease (aHR, 1.31; 95% CI, 1.10-1.66) predicted higher ASCVD risk.

Study details: The data come from an analysis of 31,366 patients with RA from a US-wide longitudinal observational registry, who did not have any prior CVD at baseline and active cancer throughout follow-up.

Disclosures: No sources of funding were reported. K Michaud reported receiving grant support from the Rheumatology Research Foundation. No competing interests were declared.

Source: Ozen G et al. RMD Open. 2021 Jun 30. doi: 10.1136/rmdopen-2021-001618.

Key clinical point: Among patients with rheumatoid arthritis (RA), traditional risk factors for cardiovascular disease (CVD) mostly predicted atherosclerotic CVD (ASCVD), except for obesity, which was a risk factor for unprovoked venous thromboembolism (VTE).

Major finding: Obesity was associated with increased VTE risk (adjusted hazard ratio [aHR], 1.47; 95% confidence interval [CI], 1.14-1.89) and reduced ASCVD risk (aHR, 0.56; 95% CI, 0.48-0.66). Other traditional CVD risk factors such as diabetes (aHR, 1.39; 95% CI, 1.20-1.62), hypertension (aHR, 1.21; 95% CI, 1.07-1.39), and chronic kidney disease (aHR, 1.31; 95% CI, 1.10-1.66) predicted higher ASCVD risk.

Study details: The data come from an analysis of 31,366 patients with RA from a US-wide longitudinal observational registry, who did not have any prior CVD at baseline and active cancer throughout follow-up.

Disclosures: No sources of funding were reported. K Michaud reported receiving grant support from the Rheumatology Research Foundation. No competing interests were declared.

Source: Ozen G et al. RMD Open. 2021 Jun 30. doi: 10.1136/rmdopen-2021-001618.

Key clinical point: Patients with rheumatoid arthritis (RA) receiving interleukin-6 inhibition (IL-6i) therapy with or without T-cell inhibitors had a significantly lower risk for type 2 diabetes mellitus (T2DM) vs those receiving tumor necrosis factor inhibitors (TNFi) or not receiving any biological disease-modifying antirheumatic drugs (bDMARDs).

Major finding: Compared with patients not receiving bDMARDs, those who received IL-6i and IL-6i+T-cell inhibitors had a significant 37% (hazard ratio [HR], 0.63; P = .021) and 34% (HR, 0.66; P = .019) lower risk for T2DM, respectively, whereas no significant difference was observed among patients receiving TNFi (HR, 0.99; P = .26) and T-cell inhibitors (HR, 0.96; P = .37).

Study details: This was a retrospective cohort study of 283,756 patients with RA categorized as bDMARD recipients (TNFi, n=34,873; IL-6i, n=1,884; T-cell inhibitors, n=5,935; and IL-6i+T-cell inhibitor abatacept, n=1,213) and non-bDMARD recipients (n=125,337).

Disclosures: This study was supported by Roche/Genentech. The principal author reported receiving grants, consultancy, and/or speaker fees from various sources. JH Best, S Gale, and K Sarsour reported being employees of Genentech.

Source: Paul SK et al. BMJ Open. 2021 Jun 16. doi: 10.1136/bmjopen-2020-042246.

Key clinical point: Patients with rheumatoid arthritis (RA) receiving interleukin-6 inhibition (IL-6i) therapy with or without T-cell inhibitors had a significantly lower risk for type 2 diabetes mellitus (T2DM) vs those receiving tumor necrosis factor inhibitors (TNFi) or not receiving any biological disease-modifying antirheumatic drugs (bDMARDs).

Major finding: Compared with patients not receiving bDMARDs, those who received IL-6i and IL-6i+T-cell inhibitors had a significant 37% (hazard ratio [HR], 0.63; P = .021) and 34% (HR, 0.66; P = .019) lower risk for T2DM, respectively, whereas no significant difference was observed among patients receiving TNFi (HR, 0.99; P = .26) and T-cell inhibitors (HR, 0.96; P = .37).

Study details: This was a retrospective cohort study of 283,756 patients with RA categorized as bDMARD recipients (TNFi, n=34,873; IL-6i, n=1,884; T-cell inhibitors, n=5,935; and IL-6i+T-cell inhibitor abatacept, n=1,213) and non-bDMARD recipients (n=125,337).

Disclosures: This study was supported by Roche/Genentech. The principal author reported receiving grants, consultancy, and/or speaker fees from various sources. JH Best, S Gale, and K Sarsour reported being employees of Genentech.

Source: Paul SK et al. BMJ Open. 2021 Jun 16. doi: 10.1136/bmjopen-2020-042246.

Key clinical point: Patients with rheumatoid arthritis (RA) receiving interleukin-6 inhibition (IL-6i) therapy with or without T-cell inhibitors had a significantly lower risk for type 2 diabetes mellitus (T2DM) vs those receiving tumor necrosis factor inhibitors (TNFi) or not receiving any biological disease-modifying antirheumatic drugs (bDMARDs).

Major finding: Compared with patients not receiving bDMARDs, those who received IL-6i and IL-6i+T-cell inhibitors had a significant 37% (hazard ratio [HR], 0.63; P = .021) and 34% (HR, 0.66; P = .019) lower risk for T2DM, respectively, whereas no significant difference was observed among patients receiving TNFi (HR, 0.99; P = .26) and T-cell inhibitors (HR, 0.96; P = .37).

Study details: This was a retrospective cohort study of 283,756 patients with RA categorized as bDMARD recipients (TNFi, n=34,873; IL-6i, n=1,884; T-cell inhibitors, n=5,935; and IL-6i+T-cell inhibitor abatacept, n=1,213) and non-bDMARD recipients (n=125,337).

Disclosures: This study was supported by Roche/Genentech. The principal author reported receiving grants, consultancy, and/or speaker fees from various sources. JH Best, S Gale, and K Sarsour reported being employees of Genentech.

Source: Paul SK et al. BMJ Open. 2021 Jun 16. doi: 10.1136/bmjopen-2020-042246.

Key clinical point: Despite limited radiological damage, rapid radiological progression (RRP) still occurred in about 1 of 5 patients in a real-world cohort of patients with rheumatoid arthritis (RA) treated to the target of remission. RRP was most strongly predicted by baseline erosive disease.

Major finding: Most radiological damage occurred in the first year of treatment vs subsequent 5 years of follow-up (median Sharp/van der Heijde score, 2.0 vs 3.0). Despite achieving low disease activity, almost 18.8% of the patients developed RRP within 6 months, and the number of patients with erosive disease increased from 16% at baseline to 58% at 6 years. The erosive disease was the strongest predictor of RRP (odds ratio, 8.8; P less than .001).

Study details: Findings are from the observational DREAM remission induction cohort involving 219 patients diagnosed with RA who had at least 1 radiograph of hands and feet at baseline and at least 1 additional pair of radiographs during 6 years of follow-up and were treated to the target of remission.

Disclosures: No external funding and/or potential conflicts of interest were reported.

Source: Versteeg GA et al. Scand J Rheumatol. 2021 Jun 21. doi: 10.1080/03009742.2021.1917161.

Key clinical point: Despite limited radiological damage, rapid radiological progression (RRP) still occurred in about 1 of 5 patients in a real-world cohort of patients with rheumatoid arthritis (RA) treated to the target of remission. RRP was most strongly predicted by baseline erosive disease.

Major finding: Most radiological damage occurred in the first year of treatment vs subsequent 5 years of follow-up (median Sharp/van der Heijde score, 2.0 vs 3.0). Despite achieving low disease activity, almost 18.8% of the patients developed RRP within 6 months, and the number of patients with erosive disease increased from 16% at baseline to 58% at 6 years. The erosive disease was the strongest predictor of RRP (odds ratio, 8.8; P less than .001).

Study details: Findings are from the observational DREAM remission induction cohort involving 219 patients diagnosed with RA who had at least 1 radiograph of hands and feet at baseline and at least 1 additional pair of radiographs during 6 years of follow-up and were treated to the target of remission.

Disclosures: No external funding and/or potential conflicts of interest were reported.

Source: Versteeg GA et al. Scand J Rheumatol. 2021 Jun 21. doi: 10.1080/03009742.2021.1917161.

Key clinical point: Despite limited radiological damage, rapid radiological progression (RRP) still occurred in about 1 of 5 patients in a real-world cohort of patients with rheumatoid arthritis (RA) treated to the target of remission. RRP was most strongly predicted by baseline erosive disease.

Major finding: Most radiological damage occurred in the first year of treatment vs subsequent 5 years of follow-up (median Sharp/van der Heijde score, 2.0 vs 3.0). Despite achieving low disease activity, almost 18.8% of the patients developed RRP within 6 months, and the number of patients with erosive disease increased from 16% at baseline to 58% at 6 years. The erosive disease was the strongest predictor of RRP (odds ratio, 8.8; P less than .001).

Study details: Findings are from the observational DREAM remission induction cohort involving 219 patients diagnosed with RA who had at least 1 radiograph of hands and feet at baseline and at least 1 additional pair of radiographs during 6 years of follow-up and were treated to the target of remission.

Disclosures: No external funding and/or potential conflicts of interest were reported.

Source: Versteeg GA et al. Scand J Rheumatol. 2021 Jun 21. doi: 10.1080/03009742.2021.1917161.

Key clinical point: Sarcopenia and low muscle mass are common comorbidities among middle-aged and elderly patients with rheumatoid arthritis (RA). Corticosteroid therapy was positively and conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) were inversely associated with sarcopenia.

Major finding: Overall, the prevalence of low muscle mass and sarcopenia was 30.2% (95% confidence interval [CI], 24.2%-36.2%). The use of csDMARDs was inversely (odds ratio [OR], 0.70; P = .019) and corticosteroid was positively (OR, 1.46; 95% CI, 0.94-2.29) associated with sarcopenia. No association was observed between biological/targeted DMARDs and sarcopenia (OR, 0.83; P = .420).

Study details: Findings are from a meta-analysis of 16 observational studies involving 2,240 middle-aged and older adults with RA.

Disclosures: No specific funding was received for this study. All the authors declared no conflicts of interest.

Source: Dao T et al. Calcif Tissue Int. 2021 Jun 16. doi: 10.1007/s00223-021-00873-w.

Key clinical point: Sarcopenia and low muscle mass are common comorbidities among middle-aged and elderly patients with rheumatoid arthritis (RA). Corticosteroid therapy was positively and conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) were inversely associated with sarcopenia.

Major finding: Overall, the prevalence of low muscle mass and sarcopenia was 30.2% (95% confidence interval [CI], 24.2%-36.2%). The use of csDMARDs was inversely (odds ratio [OR], 0.70; P = .019) and corticosteroid was positively (OR, 1.46; 95% CI, 0.94-2.29) associated with sarcopenia. No association was observed between biological/targeted DMARDs and sarcopenia (OR, 0.83; P = .420).

Study details: Findings are from a meta-analysis of 16 observational studies involving 2,240 middle-aged and older adults with RA.

Disclosures: No specific funding was received for this study. All the authors declared no conflicts of interest.

Source: Dao T et al. Calcif Tissue Int. 2021 Jun 16. doi: 10.1007/s00223-021-00873-w.

Key clinical point: Sarcopenia and low muscle mass are common comorbidities among middle-aged and elderly patients with rheumatoid arthritis (RA). Corticosteroid therapy was positively and conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) were inversely associated with sarcopenia.

Major finding: Overall, the prevalence of low muscle mass and sarcopenia was 30.2% (95% confidence interval [CI], 24.2%-36.2%). The use of csDMARDs was inversely (odds ratio [OR], 0.70; P = .019) and corticosteroid was positively (OR, 1.46; 95% CI, 0.94-2.29) associated with sarcopenia. No association was observed between biological/targeted DMARDs and sarcopenia (OR, 0.83; P = .420).

Study details: Findings are from a meta-analysis of 16 observational studies involving 2,240 middle-aged and older adults with RA.

Disclosures: No specific funding was received for this study. All the authors declared no conflicts of interest.

Source: Dao T et al. Calcif Tissue Int. 2021 Jun 16. doi: 10.1007/s00223-021-00873-w.

Key clinical point: Almost one-third of patients with new-onset rheumatoid arthritis (RA) had long-lasting unacceptable pain. Patients with a less inflammatory disease at baseline, in the form of lower swollen joint count (SJC), were at an increased risk for unacceptable pain at 5 years.

Major finding: Almost 49.1% of patients had unacceptable pain at inclusion, which decreased to 30.1% during the first year and remained unchanged thereafter. At 5 years, lower SJC (adjusted odds ratio [aOR] per standard deviation, 0.61; P = .01) was a significant predictor of unacceptable pain.

Study details: The data come from an inception cohort of 232 patients with early RA with symptom duration of at least 12 months.

Disclosures: This work was supported by the Swedish Research Council, the Swedish Rheumatism Association, and Lund University. Some of the authors declared receiving grants, personal fees, and lecture/consulting fees from and/or being an employee of or working as a medical advisor for various sources.

Source: Eberhard A et al. Arthritis Res Ther. 2021 Jun 14. doi: 10.1186/s13075-021-02550-7.

Key clinical point: Almost one-third of patients with new-onset rheumatoid arthritis (RA) had long-lasting unacceptable pain. Patients with a less inflammatory disease at baseline, in the form of lower swollen joint count (SJC), were at an increased risk for unacceptable pain at 5 years.

Major finding: Almost 49.1% of patients had unacceptable pain at inclusion, which decreased to 30.1% during the first year and remained unchanged thereafter. At 5 years, lower SJC (adjusted odds ratio [aOR] per standard deviation, 0.61; P = .01) was a significant predictor of unacceptable pain.

Study details: The data come from an inception cohort of 232 patients with early RA with symptom duration of at least 12 months.

Disclosures: This work was supported by the Swedish Research Council, the Swedish Rheumatism Association, and Lund University. Some of the authors declared receiving grants, personal fees, and lecture/consulting fees from and/or being an employee of or working as a medical advisor for various sources.

Source: Eberhard A et al. Arthritis Res Ther. 2021 Jun 14. doi: 10.1186/s13075-021-02550-7.

Key clinical point: Almost one-third of patients with new-onset rheumatoid arthritis (RA) had long-lasting unacceptable pain. Patients with a less inflammatory disease at baseline, in the form of lower swollen joint count (SJC), were at an increased risk for unacceptable pain at 5 years.

Major finding: Almost 49.1% of patients had unacceptable pain at inclusion, which decreased to 30.1% during the first year and remained unchanged thereafter. At 5 years, lower SJC (adjusted odds ratio [aOR] per standard deviation, 0.61; P = .01) was a significant predictor of unacceptable pain.

Study details: The data come from an inception cohort of 232 patients with early RA with symptom duration of at least 12 months.

Disclosures: This work was supported by the Swedish Research Council, the Swedish Rheumatism Association, and Lund University. Some of the authors declared receiving grants, personal fees, and lecture/consulting fees from and/or being an employee of or working as a medical advisor for various sources.

Source: Eberhard A et al. Arthritis Res Ther. 2021 Jun 14. doi: 10.1186/s13075-021-02550-7.

Key clinical point: The long-term safety profile of sarilumab was consistent with prior clinical studies and postmarketing reports in patients with rheumatoid arthritis (RA) refractory to tumor necrosis factor inhibitors (TNFi).

Major finding: Incidence rates of adverse events (AEs) and serious AEs were 160.4 and 10.2 per 100 patient-years (PY), respectively, with 132 discontinuations (8.1/100 PY). The rate of serious infections was 3.9 per 100 PY. Grade 3/4 neutropenia was observed in 14% of patients and normalized on treatment in 65% of patients. Clinical efficacy was sustained throughout the 5-year follow-up.

Study details: Findings are from the open-label extension (OLE), EXTEND study, which included 454 patients with TNFi-refractory RA who completed the phase 3 TARGET study. In the OLE, patients received sarilumab 200 mg twice per week plus conventional synthetic disease-modifying antirheumatic drugs.

Disclosures: This work was supported by Sanofi (Cambridge, MA, USA) and Regeneron Pharmaceuticals, Inc. (Tarrytown, NY, USA). Some of the authors reported receiving research grants and/or consulting fees from various sources. Some authors declared being an employee of and/or holding stocks/stock options at Sanofi or Regeneron Pharmaceuticals, Inc.

Source: Fleischmann R et al. Rheumatology (Oxford). 2021 Jun 24. doi: 10.1093/rheumatology/keab355.

Key clinical point: The long-term safety profile of sarilumab was consistent with prior clinical studies and postmarketing reports in patients with rheumatoid arthritis (RA) refractory to tumor necrosis factor inhibitors (TNFi).

Major finding: Incidence rates of adverse events (AEs) and serious AEs were 160.4 and 10.2 per 100 patient-years (PY), respectively, with 132 discontinuations (8.1/100 PY). The rate of serious infections was 3.9 per 100 PY. Grade 3/4 neutropenia was observed in 14% of patients and normalized on treatment in 65% of patients. Clinical efficacy was sustained throughout the 5-year follow-up.

Study details: Findings are from the open-label extension (OLE), EXTEND study, which included 454 patients with TNFi-refractory RA who completed the phase 3 TARGET study. In the OLE, patients received sarilumab 200 mg twice per week plus conventional synthetic disease-modifying antirheumatic drugs.

Disclosures: This work was supported by Sanofi (Cambridge, MA, USA) and Regeneron Pharmaceuticals, Inc. (Tarrytown, NY, USA). Some of the authors reported receiving research grants and/or consulting fees from various sources. Some authors declared being an employee of and/or holding stocks/stock options at Sanofi or Regeneron Pharmaceuticals, Inc.

Source: Fleischmann R et al. Rheumatology (Oxford). 2021 Jun 24. doi: 10.1093/rheumatology/keab355.

Key clinical point: The long-term safety profile of sarilumab was consistent with prior clinical studies and postmarketing reports in patients with rheumatoid arthritis (RA) refractory to tumor necrosis factor inhibitors (TNFi).

Major finding: Incidence rates of adverse events (AEs) and serious AEs were 160.4 and 10.2 per 100 patient-years (PY), respectively, with 132 discontinuations (8.1/100 PY). The rate of serious infections was 3.9 per 100 PY. Grade 3/4 neutropenia was observed in 14% of patients and normalized on treatment in 65% of patients. Clinical efficacy was sustained throughout the 5-year follow-up.

Study details: Findings are from the open-label extension (OLE), EXTEND study, which included 454 patients with TNFi-refractory RA who completed the phase 3 TARGET study. In the OLE, patients received sarilumab 200 mg twice per week plus conventional synthetic disease-modifying antirheumatic drugs.

Disclosures: This work was supported by Sanofi (Cambridge, MA, USA) and Regeneron Pharmaceuticals, Inc. (Tarrytown, NY, USA). Some of the authors reported receiving research grants and/or consulting fees from various sources. Some authors declared being an employee of and/or holding stocks/stock options at Sanofi or Regeneron Pharmaceuticals, Inc.

Source: Fleischmann R et al. Rheumatology (Oxford). 2021 Jun 24. doi: 10.1093/rheumatology/keab355.

Key clinical point: Systemic glucocorticoids (GCs) were effective at reducing pain in patients with active rheumatoid arthritis (RA), with the effect being greatest within 3 months of initiation, whereas it appeared to be less effective beyond 6 months.

Major finding: Treatment with systemic GCs significantly decreased spontaneous pain (standardized mean differences [MD], −0.67; 95% confidence interval [CI], −0.84 to −0.50), with the effect being greatest at 3 months or lesser (MD, −14.55 mm; 95% CI, −20.40 to −8.69) and appeared to be less effective at more than 3 to 6 months (MD, −7.82 mm; 95% CI, −12.27 to -3.38) and beyond 6 months (MD, −6.52 mm; 95% CI, −13.28 to 0.24).

Study details: Findings are from a systematic review and meta-analysis of 33 randomized controlled trials including 2,658 patients with RA.

Disclosures: The study received no specific funding. D McWilliams, DA Walsh, and NG Shanker reported receiving grant support and consultancy fees from various sources like Pfizer Ltd., Eli Lilly, UCB, AbbVie, GSK, and Cambridge Nutraceuticals.

Source: McWilliams DF et al. Rheumatology (Oxford). 2021 Jul 2. doi: 10.1093/rheumatology/keab503.

Key clinical point: Systemic glucocorticoids (GCs) were effective at reducing pain in patients with active rheumatoid arthritis (RA), with the effect being greatest within 3 months of initiation, whereas it appeared to be less effective beyond 6 months.

Major finding: Treatment with systemic GCs significantly decreased spontaneous pain (standardized mean differences [MD], −0.67; 95% confidence interval [CI], −0.84 to −0.50), with the effect being greatest at 3 months or lesser (MD, −14.55 mm; 95% CI, −20.40 to −8.69) and appeared to be less effective at more than 3 to 6 months (MD, −7.82 mm; 95% CI, −12.27 to -3.38) and beyond 6 months (MD, −6.52 mm; 95% CI, −13.28 to 0.24).

Study details: Findings are from a systematic review and meta-analysis of 33 randomized controlled trials including 2,658 patients with RA.

Disclosures: The study received no specific funding. D McWilliams, DA Walsh, and NG Shanker reported receiving grant support and consultancy fees from various sources like Pfizer Ltd., Eli Lilly, UCB, AbbVie, GSK, and Cambridge Nutraceuticals.

Source: McWilliams DF et al. Rheumatology (Oxford). 2021 Jul 2. doi: 10.1093/rheumatology/keab503.

Key clinical point: Systemic glucocorticoids (GCs) were effective at reducing pain in patients with active rheumatoid arthritis (RA), with the effect being greatest within 3 months of initiation, whereas it appeared to be less effective beyond 6 months.

Major finding: Treatment with systemic GCs significantly decreased spontaneous pain (standardized mean differences [MD], −0.67; 95% confidence interval [CI], −0.84 to −0.50), with the effect being greatest at 3 months or lesser (MD, −14.55 mm; 95% CI, −20.40 to −8.69) and appeared to be less effective at more than 3 to 6 months (MD, −7.82 mm; 95% CI, −12.27 to -3.38) and beyond 6 months (MD, −6.52 mm; 95% CI, −13.28 to 0.24).

Study details: Findings are from a systematic review and meta-analysis of 33 randomized controlled trials including 2,658 patients with RA.

Disclosures: The study received no specific funding. D McWilliams, DA Walsh, and NG Shanker reported receiving grant support and consultancy fees from various sources like Pfizer Ltd., Eli Lilly, UCB, AbbVie, GSK, and Cambridge Nutraceuticals.

Source: McWilliams DF et al. Rheumatology (Oxford). 2021 Jul 2. doi: 10.1093/rheumatology/keab503.