Lupus & Connective Tissue Diseases

The baseline physical component score of the Medical Outcomes Short Form 36 (SF-36) was an independent predictor of mortality for patients with systemic lupus erythematosus (SLE), according to recent analysis of data from the University of California, San Francisco, (UCSF) Lupus Outcomes Study.

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Desiree R. Azizoddin, PsyD, of Stanford Health Care in Palo Alto, Calif., and her colleagues analyzed patient-reported outcomes (PROs) of 728 patients with SLE from the UCSF study, which included measures such as self-rated health, the Center for Epidemiologic Studies Depression scale (CESD), and SF-36 mental and physical component scores between 2007 and 2015. Patients had a mean age of 50.6 years and consisted of mostly whites (68.5%) and women (92.2%), with a mean SLE disease duration of 16.7 years.

“As PROs can be measured easily, quickly, reliably in a systematic manner, without use of many resources (including cost) and experts, PROs can serve as an important tool in community settings that provide care for individuals with SLE,” Dr. Azizoddin and her colleagues wrote in Arthritis Care & Research. “Implementation and integration of PROs may potentially help decrease mortality among patients with SLE in the long run.”

The researchers reported 71 deaths (9.8%) in the study. A univariate analysis showed that self-rated health as fair or poor and all SF-36 subscale scores, except for mental health and role emotional subscales, were predictors of mortality. After the investigators performed a multivariate analysis, they found that baseline SF-36 physical component scores alone were associated with an increased mortality risk (hazard ratio, 0.97; 95% confidence interval, 0.94-0.99; P less than .01), with a 3.5% lower risk for each point-rating increase in the score.

“Insight to predictors of mortality, above and beyond those that require physician resources such as assessments of renal involvement and traditional physician-completed measures of disease activity and damage in this complex disease, affords rheumatologists and SLE providers with additional tools to assess potential patient health trajectories,” Dr. Azizoddin and her colleagues wrote in their study. “Identification of such predictors will expand opportunities for early interventions aimed at the reduction of such risk, including allocation of appropriate medical resources in areas with large numbers of patients with compromised health.”

The researchers noted that bias in self-reporting, a lack of prospective evaluations at each visit, and clinical applicability to only similar cohorts were limitations in the study.

This study was funded by the Robert Wood Johnson Foundation Investigator Awards in Health Policy Research and individually was awarded grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases.

SOURCE: Azizoddin DR et al. Arthritis Care Res. 2018 Aug 24. doi: 10.1002/acr.23734.

The baseline physical component score of the Medical Outcomes Short Form 36 (SF-36) was an independent predictor of mortality for patients with systemic lupus erythematosus (SLE), according to recent analysis of data from the University of California, San Francisco, (UCSF) Lupus Outcomes Study.

wildpixel/Thinkstock

Desiree R. Azizoddin, PsyD, of Stanford Health Care in Palo Alto, Calif., and her colleagues analyzed patient-reported outcomes (PROs) of 728 patients with SLE from the UCSF study, which included measures such as self-rated health, the Center for Epidemiologic Studies Depression scale (CESD), and SF-36 mental and physical component scores between 2007 and 2015. Patients had a mean age of 50.6 years and consisted of mostly whites (68.5%) and women (92.2%), with a mean SLE disease duration of 16.7 years.

“As PROs can be measured easily, quickly, reliably in a systematic manner, without use of many resources (including cost) and experts, PROs can serve as an important tool in community settings that provide care for individuals with SLE,” Dr. Azizoddin and her colleagues wrote in Arthritis Care & Research. “Implementation and integration of PROs may potentially help decrease mortality among patients with SLE in the long run.”

The researchers reported 71 deaths (9.8%) in the study. A univariate analysis showed that self-rated health as fair or poor and all SF-36 subscale scores, except for mental health and role emotional subscales, were predictors of mortality. After the investigators performed a multivariate analysis, they found that baseline SF-36 physical component scores alone were associated with an increased mortality risk (hazard ratio, 0.97; 95% confidence interval, 0.94-0.99; P less than .01), with a 3.5% lower risk for each point-rating increase in the score.

“Insight to predictors of mortality, above and beyond those that require physician resources such as assessments of renal involvement and traditional physician-completed measures of disease activity and damage in this complex disease, affords rheumatologists and SLE providers with additional tools to assess potential patient health trajectories,” Dr. Azizoddin and her colleagues wrote in their study. “Identification of such predictors will expand opportunities for early interventions aimed at the reduction of such risk, including allocation of appropriate medical resources in areas with large numbers of patients with compromised health.”

The researchers noted that bias in self-reporting, a lack of prospective evaluations at each visit, and clinical applicability to only similar cohorts were limitations in the study.

This study was funded by the Robert Wood Johnson Foundation Investigator Awards in Health Policy Research and individually was awarded grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases.

SOURCE: Azizoddin DR et al. Arthritis Care Res. 2018 Aug 24. doi: 10.1002/acr.23734.

The baseline physical component score of the Medical Outcomes Short Form 36 (SF-36) was an independent predictor of mortality for patients with systemic lupus erythematosus (SLE), according to recent analysis of data from the University of California, San Francisco, (UCSF) Lupus Outcomes Study.

wildpixel/Thinkstock

Desiree R. Azizoddin, PsyD, of Stanford Health Care in Palo Alto, Calif., and her colleagues analyzed patient-reported outcomes (PROs) of 728 patients with SLE from the UCSF study, which included measures such as self-rated health, the Center for Epidemiologic Studies Depression scale (CESD), and SF-36 mental and physical component scores between 2007 and 2015. Patients had a mean age of 50.6 years and consisted of mostly whites (68.5%) and women (92.2%), with a mean SLE disease duration of 16.7 years.

“As PROs can be measured easily, quickly, reliably in a systematic manner, without use of many resources (including cost) and experts, PROs can serve as an important tool in community settings that provide care for individuals with SLE,” Dr. Azizoddin and her colleagues wrote in Arthritis Care & Research. “Implementation and integration of PROs may potentially help decrease mortality among patients with SLE in the long run.”

The researchers reported 71 deaths (9.8%) in the study. A univariate analysis showed that self-rated health as fair or poor and all SF-36 subscale scores, except for mental health and role emotional subscales, were predictors of mortality. After the investigators performed a multivariate analysis, they found that baseline SF-36 physical component scores alone were associated with an increased mortality risk (hazard ratio, 0.97; 95% confidence interval, 0.94-0.99; P less than .01), with a 3.5% lower risk for each point-rating increase in the score.

“Insight to predictors of mortality, above and beyond those that require physician resources such as assessments of renal involvement and traditional physician-completed measures of disease activity and damage in this complex disease, affords rheumatologists and SLE providers with additional tools to assess potential patient health trajectories,” Dr. Azizoddin and her colleagues wrote in their study. “Identification of such predictors will expand opportunities for early interventions aimed at the reduction of such risk, including allocation of appropriate medical resources in areas with large numbers of patients with compromised health.”

The researchers noted that bias in self-reporting, a lack of prospective evaluations at each visit, and clinical applicability to only similar cohorts were limitations in the study.

This study was funded by the Robert Wood Johnson Foundation Investigator Awards in Health Policy Research and individually was awarded grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases.

SOURCE: Azizoddin DR et al. Arthritis Care Res. 2018 Aug 24. doi: 10.1002/acr.23734.

The majority of adults with childhood-onset systemic lupus erythematosus in a longitudinal Dutch study developed significant damage at a young age, remain on corticosteroids in adulthood, and have an impaired health-related quality of life.

Courtesy Wikimedia Commons/doktorinternet/Creative Commons License

The findings in the study, dubbed Childhood-Onset SLE in the Netherlands (CHILL-NL), highlighted the need for preventive screening measures to be put in place before the age of 30 to facilitate a better outcome for patients, who still face high morbidity from childhood-onset systemic lupus erythematosus (cSLE) despite improved survival. Such information is helpful to “answer questions from children and parents regarding the future course of the disease,” wrote Noortje Groot, PhD, of the department of pediatric rheumatology at Erasmus Medical Center–Sophia Children’s Hospital in Rotterdam, the Netherlands, and her colleagues. The report is in Arthritis & Rheumatology.

The current study included all adult SLE patients treated in any Dutch public hospital during the period of November 2013 to April 2016 who were diagnosed with the autoimmune disease prior to their 18th birthday.

All 111 patients involved in the study were seen for a 1.5-hour visit at Erasmus University Medical Center or a local hospital of their choice. During the appointment, a medical history was taken, a physical examination was performed, and the patients completed questionnaires on health-related quality of life (HRQOL).

The average age of patients at the study visit was 33 years, 91% were female, and 72% were white. Median disease duration was 20 years and disease activity was low (median SLE Disease Activity Index 2000 [SLEDAI-2k] = 4). Low complement (32%), skin rashes (14%), and proteinuria (13%) were the most common SLEDAI items reported.

Overall, 68% of the cohort (n = 76) were taking hydroxychloroquine (HCQ), 29% of whom (n = 22) were taking it as monotherapy.

Furthermore, 68% of patients at the study visit were taking corticosteroids and/or non-HCQ disease-modifying antirheumatic drugs (DMARDs), and just over half (51%) of patients (n = 56) were taking corticosteroids either alone or with a non-HCQ DMARD.

“This [finding] is worrying as corticosteroids are associated with the development of damage. Patients are certainly eager to limit corticosteroid use, as almost all patients in the CHILL-NL cohort reported to have negative experiences with prednisone regarding their physical appearance and or mental well-being,” the study authors wrote.

Results also showed that 62% of the patients had damage, predominantly in the musculoskeletal, neuropsychiatric, and renal systems.

Most organ systems became involved within the first 2 years of diagnosis, but after 5 years of disease the nature of disease manifestations tended to shift to damage such as myocardial infarctions.

Notably, after 10-20 years, when cSLE patients were in their early 20s and 30s, significant damage had occurred in more than half of the patients, the authors noted.

“This shift to damage has also been observed in adult-onset SLE patients and urges for preventative screening measures of such (cardiovascular) damage and healthy lifestyle advice (healthy diet, regular exercise, abstinence from smoking),” they wrote.

Multivariate logistic regression showed that damage accrual was associated with disease duration (odds ratio, 1.15; P less than .001), antiphospholipid‐antibody positivity (OR, 3.56; P = .026), and hypertension (OR, 3.21; P = .043). On the other hand, current HCQ monotherapy was associated with an SLICC-Damage Index score of 0 (OR, 0.16; P = .009).

The HRQOL of the cohort, assessed via the Short Form–36, was also impaired compared with the general population, the researchers discovered. For example, the presence of damage reduced HRQOL in one domain, and high disease activity, defined as SLEDAI-2k of 8 or more, strongly reduced HRQOL in four of eight domains. Changes in physical appearance lowered HRQOL in seven of eight domains.

“HRQOL of adults with cSLE is impaired and affected by other factors than disease activity or damage alone. By identifying and addressing these factors, like physical appearance and potentially coping styles, HRQOL may be improved,” they advised.

The study was supported financially by the Dutch Arthritis Foundation and the Dutch national patient association for lupus, antiphospholipid syndrome, scleroderma, and mixed connective tissue diseases.

SOURCE: Groot N et al. Arthritis Rheumatol. 2018 Aug 27. doi: 10.1002/art.40697

The majority of adults with childhood-onset systemic lupus erythematosus in a longitudinal Dutch study developed significant damage at a young age, remain on corticosteroids in adulthood, and have an impaired health-related quality of life.

Courtesy Wikimedia Commons/doktorinternet/Creative Commons License

The findings in the study, dubbed Childhood-Onset SLE in the Netherlands (CHILL-NL), highlighted the need for preventive screening measures to be put in place before the age of 30 to facilitate a better outcome for patients, who still face high morbidity from childhood-onset systemic lupus erythematosus (cSLE) despite improved survival. Such information is helpful to “answer questions from children and parents regarding the future course of the disease,” wrote Noortje Groot, PhD, of the department of pediatric rheumatology at Erasmus Medical Center–Sophia Children’s Hospital in Rotterdam, the Netherlands, and her colleagues. The report is in Arthritis & Rheumatology.

The current study included all adult SLE patients treated in any Dutch public hospital during the period of November 2013 to April 2016 who were diagnosed with the autoimmune disease prior to their 18th birthday.

All 111 patients involved in the study were seen for a 1.5-hour visit at Erasmus University Medical Center or a local hospital of their choice. During the appointment, a medical history was taken, a physical examination was performed, and the patients completed questionnaires on health-related quality of life (HRQOL).

The average age of patients at the study visit was 33 years, 91% were female, and 72% were white. Median disease duration was 20 years and disease activity was low (median SLE Disease Activity Index 2000 [SLEDAI-2k] = 4). Low complement (32%), skin rashes (14%), and proteinuria (13%) were the most common SLEDAI items reported.

Overall, 68% of the cohort (n = 76) were taking hydroxychloroquine (HCQ), 29% of whom (n = 22) were taking it as monotherapy.

Furthermore, 68% of patients at the study visit were taking corticosteroids and/or non-HCQ disease-modifying antirheumatic drugs (DMARDs), and just over half (51%) of patients (n = 56) were taking corticosteroids either alone or with a non-HCQ DMARD.

“This [finding] is worrying as corticosteroids are associated with the development of damage. Patients are certainly eager to limit corticosteroid use, as almost all patients in the CHILL-NL cohort reported to have negative experiences with prednisone regarding their physical appearance and or mental well-being,” the study authors wrote.

Results also showed that 62% of the patients had damage, predominantly in the musculoskeletal, neuropsychiatric, and renal systems.

Most organ systems became involved within the first 2 years of diagnosis, but after 5 years of disease the nature of disease manifestations tended to shift to damage such as myocardial infarctions.

Notably, after 10-20 years, when cSLE patients were in their early 20s and 30s, significant damage had occurred in more than half of the patients, the authors noted.

“This shift to damage has also been observed in adult-onset SLE patients and urges for preventative screening measures of such (cardiovascular) damage and healthy lifestyle advice (healthy diet, regular exercise, abstinence from smoking),” they wrote.

Multivariate logistic regression showed that damage accrual was associated with disease duration (odds ratio, 1.15; P less than .001), antiphospholipid‐antibody positivity (OR, 3.56; P = .026), and hypertension (OR, 3.21; P = .043). On the other hand, current HCQ monotherapy was associated with an SLICC-Damage Index score of 0 (OR, 0.16; P = .009).

The HRQOL of the cohort, assessed via the Short Form–36, was also impaired compared with the general population, the researchers discovered. For example, the presence of damage reduced HRQOL in one domain, and high disease activity, defined as SLEDAI-2k of 8 or more, strongly reduced HRQOL in four of eight domains. Changes in physical appearance lowered HRQOL in seven of eight domains.

“HRQOL of adults with cSLE is impaired and affected by other factors than disease activity or damage alone. By identifying and addressing these factors, like physical appearance and potentially coping styles, HRQOL may be improved,” they advised.

The study was supported financially by the Dutch Arthritis Foundation and the Dutch national patient association for lupus, antiphospholipid syndrome, scleroderma, and mixed connective tissue diseases.

SOURCE: Groot N et al. Arthritis Rheumatol. 2018 Aug 27. doi: 10.1002/art.40697

The majority of adults with childhood-onset systemic lupus erythematosus in a longitudinal Dutch study developed significant damage at a young age, remain on corticosteroids in adulthood, and have an impaired health-related quality of life.

Courtesy Wikimedia Commons/doktorinternet/Creative Commons License

The findings in the study, dubbed Childhood-Onset SLE in the Netherlands (CHILL-NL), highlighted the need for preventive screening measures to be put in place before the age of 30 to facilitate a better outcome for patients, who still face high morbidity from childhood-onset systemic lupus erythematosus (cSLE) despite improved survival. Such information is helpful to “answer questions from children and parents regarding the future course of the disease,” wrote Noortje Groot, PhD, of the department of pediatric rheumatology at Erasmus Medical Center–Sophia Children’s Hospital in Rotterdam, the Netherlands, and her colleagues. The report is in Arthritis & Rheumatology.

The current study included all adult SLE patients treated in any Dutch public hospital during the period of November 2013 to April 2016 who were diagnosed with the autoimmune disease prior to their 18th birthday.

All 111 patients involved in the study were seen for a 1.5-hour visit at Erasmus University Medical Center or a local hospital of their choice. During the appointment, a medical history was taken, a physical examination was performed, and the patients completed questionnaires on health-related quality of life (HRQOL).

The average age of patients at the study visit was 33 years, 91% were female, and 72% were white. Median disease duration was 20 years and disease activity was low (median SLE Disease Activity Index 2000 [SLEDAI-2k] = 4). Low complement (32%), skin rashes (14%), and proteinuria (13%) were the most common SLEDAI items reported.

Overall, 68% of the cohort (n = 76) were taking hydroxychloroquine (HCQ), 29% of whom (n = 22) were taking it as monotherapy.

Furthermore, 68% of patients at the study visit were taking corticosteroids and/or non-HCQ disease-modifying antirheumatic drugs (DMARDs), and just over half (51%) of patients (n = 56) were taking corticosteroids either alone or with a non-HCQ DMARD.

“This [finding] is worrying as corticosteroids are associated with the development of damage. Patients are certainly eager to limit corticosteroid use, as almost all patients in the CHILL-NL cohort reported to have negative experiences with prednisone regarding their physical appearance and or mental well-being,” the study authors wrote.

Results also showed that 62% of the patients had damage, predominantly in the musculoskeletal, neuropsychiatric, and renal systems.

Most organ systems became involved within the first 2 years of diagnosis, but after 5 years of disease the nature of disease manifestations tended to shift to damage such as myocardial infarctions.

Notably, after 10-20 years, when cSLE patients were in their early 20s and 30s, significant damage had occurred in more than half of the patients, the authors noted.

“This shift to damage has also been observed in adult-onset SLE patients and urges for preventative screening measures of such (cardiovascular) damage and healthy lifestyle advice (healthy diet, regular exercise, abstinence from smoking),” they wrote.

Multivariate logistic regression showed that damage accrual was associated with disease duration (odds ratio, 1.15; P less than .001), antiphospholipid‐antibody positivity (OR, 3.56; P = .026), and hypertension (OR, 3.21; P = .043). On the other hand, current HCQ monotherapy was associated with an SLICC-Damage Index score of 0 (OR, 0.16; P = .009).

The HRQOL of the cohort, assessed via the Short Form–36, was also impaired compared with the general population, the researchers discovered. For example, the presence of damage reduced HRQOL in one domain, and high disease activity, defined as SLEDAI-2k of 8 or more, strongly reduced HRQOL in four of eight domains. Changes in physical appearance lowered HRQOL in seven of eight domains.

“HRQOL of adults with cSLE is impaired and affected by other factors than disease activity or damage alone. By identifying and addressing these factors, like physical appearance and potentially coping styles, HRQOL may be improved,” they advised.

The study was supported financially by the Dutch Arthritis Foundation and the Dutch national patient association for lupus, antiphospholipid syndrome, scleroderma, and mixed connective tissue diseases.

SOURCE: Groot N et al. Arthritis Rheumatol. 2018 Aug 27. doi: 10.1002/art.40697

Black women who smoke cigarettes are at increased risk of systemic lupus erythematosus (SLE), while those who drink alcohol in moderation have a decreased risk, data from the prospective Black Women’s Health Study suggests.

The current findings among black women, who are the demographic group at the highest risk of SLE in the U.S. population, are consistent with the previously reported positive association of cigarette smoking with risk of SLE and inverse association of alcohol consumption with SLE,” lead researchers Yvette Cozier, DSc, and Medha Barbhaiya, MD, and their colleagues wrote in a study published in Arthritis Care & Research.

“The role of environmental factors in the pathogenesis of SLE is of great interest, as genetic factors do not explain a major portion of the incidence. Cigarette smoking has been associated with SLE risk in several, but not all, past studies,” wrote Dr. Cozier of the Slone Epidemiology Center at Boston University and Dr. Barbhaiya of the Hospital for Special Surgery, New York, and their coauthors.

Their analysis of data from the Black Women’s Health Study, a prospective study following 59,000 black women in the United States since 1995, identified 127 new cases of SLE between 1995 and 2015 that were confirmed by medical records.

At baseline, 8,851 women (16%) were current smokers, and 10,447 (18%) were past smokers. A total of 14,001 (25%) were current drinkers, and 10,255 (18%) were past drinkers.

The researchers reported that, compared with never smokers, women who had ever smoked had a 45% higher risk for SLE than did never smokers (hazard ratio, 1.45; 95% confidence interval, 0.97-2.18), but the finding was not statistically significant.

The risk of SLE was greater among current smokers (52% higher risk) than among past smokers (41% higher risk), and greater for 20 or more pack-years of smoking (60% higher risk) than for less than 20 pack-years of smoking (37% higher risk), although the authors noted that none of these differences were statistically significant.

Current and past alcohol consumption were associated with nonsignificant reductions in risk for SLE, 29% and 21%, respectively. However, “moderate” current alcohol consumption, measured as four or more drinks per week, was associated with a 57% reduction in risk for SLE (HR, 0.43; 95% CI, 0.19-0.96).

The researchers said that the associations between cigarette smoking and alcohol intake with SLE risk were biologically plausible and may lead to insights into SLE pathogenesis. For example, exposure to toxic components from cigarette smoke was associated with increased oxidative stress and stimulation of autoantibody production, and such exposure can directly damage endogenous proteins and DNA. Alcohol suppresses the synthesis of proinflammatory cytokines and may inhibit DNA synthesis.

The small number of lupus cases in the Black Women’s Health Study cohort limited the statistical power of the analysis. Smoking and alcohol use were also relatively uncommon among women in the Black Women’s Health Study cohort, the investigators said.

“Future studies are needed to confirm these findings and establish the biologic mechanisms by which cigarette smoking and alcohol consumption influence the risk of SLE in this population and others,“ they wrote.

The study was supported by individual investigators’ grant awards from the National Cancer Institute, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Rheumatology Research Foundation, and the Lupus Foundation of America. The authors declared no relevant conflicts of interest.

SOURCE: Cozier Y et al. Arthritis Care Res. 2018 Aug 9. doi: 10.1002/acr.23703.

Black women who smoke cigarettes are at increased risk of systemic lupus erythematosus (SLE), while those who drink alcohol in moderation have a decreased risk, data from the prospective Black Women’s Health Study suggests.

The current findings among black women, who are the demographic group at the highest risk of SLE in the U.S. population, are consistent with the previously reported positive association of cigarette smoking with risk of SLE and inverse association of alcohol consumption with SLE,” lead researchers Yvette Cozier, DSc, and Medha Barbhaiya, MD, and their colleagues wrote in a study published in Arthritis Care & Research.

“The role of environmental factors in the pathogenesis of SLE is of great interest, as genetic factors do not explain a major portion of the incidence. Cigarette smoking has been associated with SLE risk in several, but not all, past studies,” wrote Dr. Cozier of the Slone Epidemiology Center at Boston University and Dr. Barbhaiya of the Hospital for Special Surgery, New York, and their coauthors.

Their analysis of data from the Black Women’s Health Study, a prospective study following 59,000 black women in the United States since 1995, identified 127 new cases of SLE between 1995 and 2015 that were confirmed by medical records.

At baseline, 8,851 women (16%) were current smokers, and 10,447 (18%) were past smokers. A total of 14,001 (25%) were current drinkers, and 10,255 (18%) were past drinkers.

The researchers reported that, compared with never smokers, women who had ever smoked had a 45% higher risk for SLE than did never smokers (hazard ratio, 1.45; 95% confidence interval, 0.97-2.18), but the finding was not statistically significant.

The risk of SLE was greater among current smokers (52% higher risk) than among past smokers (41% higher risk), and greater for 20 or more pack-years of smoking (60% higher risk) than for less than 20 pack-years of smoking (37% higher risk), although the authors noted that none of these differences were statistically significant.

Current and past alcohol consumption were associated with nonsignificant reductions in risk for SLE, 29% and 21%, respectively. However, “moderate” current alcohol consumption, measured as four or more drinks per week, was associated with a 57% reduction in risk for SLE (HR, 0.43; 95% CI, 0.19-0.96).

The researchers said that the associations between cigarette smoking and alcohol intake with SLE risk were biologically plausible and may lead to insights into SLE pathogenesis. For example, exposure to toxic components from cigarette smoke was associated with increased oxidative stress and stimulation of autoantibody production, and such exposure can directly damage endogenous proteins and DNA. Alcohol suppresses the synthesis of proinflammatory cytokines and may inhibit DNA synthesis.

The small number of lupus cases in the Black Women’s Health Study cohort limited the statistical power of the analysis. Smoking and alcohol use were also relatively uncommon among women in the Black Women’s Health Study cohort, the investigators said.

“Future studies are needed to confirm these findings and establish the biologic mechanisms by which cigarette smoking and alcohol consumption influence the risk of SLE in this population and others,“ they wrote.

The study was supported by individual investigators’ grant awards from the National Cancer Institute, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Rheumatology Research Foundation, and the Lupus Foundation of America. The authors declared no relevant conflicts of interest.

SOURCE: Cozier Y et al. Arthritis Care Res. 2018 Aug 9. doi: 10.1002/acr.23703.

Black women who smoke cigarettes are at increased risk of systemic lupus erythematosus (SLE), while those who drink alcohol in moderation have a decreased risk, data from the prospective Black Women’s Health Study suggests.

The current findings among black women, who are the demographic group at the highest risk of SLE in the U.S. population, are consistent with the previously reported positive association of cigarette smoking with risk of SLE and inverse association of alcohol consumption with SLE,” lead researchers Yvette Cozier, DSc, and Medha Barbhaiya, MD, and their colleagues wrote in a study published in Arthritis Care & Research.

“The role of environmental factors in the pathogenesis of SLE is of great interest, as genetic factors do not explain a major portion of the incidence. Cigarette smoking has been associated with SLE risk in several, but not all, past studies,” wrote Dr. Cozier of the Slone Epidemiology Center at Boston University and Dr. Barbhaiya of the Hospital for Special Surgery, New York, and their coauthors.

Their analysis of data from the Black Women’s Health Study, a prospective study following 59,000 black women in the United States since 1995, identified 127 new cases of SLE between 1995 and 2015 that were confirmed by medical records.

At baseline, 8,851 women (16%) were current smokers, and 10,447 (18%) were past smokers. A total of 14,001 (25%) were current drinkers, and 10,255 (18%) were past drinkers.

The researchers reported that, compared with never smokers, women who had ever smoked had a 45% higher risk for SLE than did never smokers (hazard ratio, 1.45; 95% confidence interval, 0.97-2.18), but the finding was not statistically significant.

The risk of SLE was greater among current smokers (52% higher risk) than among past smokers (41% higher risk), and greater for 20 or more pack-years of smoking (60% higher risk) than for less than 20 pack-years of smoking (37% higher risk), although the authors noted that none of these differences were statistically significant.

Current and past alcohol consumption were associated with nonsignificant reductions in risk for SLE, 29% and 21%, respectively. However, “moderate” current alcohol consumption, measured as four or more drinks per week, was associated with a 57% reduction in risk for SLE (HR, 0.43; 95% CI, 0.19-0.96).

The researchers said that the associations between cigarette smoking and alcohol intake with SLE risk were biologically plausible and may lead to insights into SLE pathogenesis. For example, exposure to toxic components from cigarette smoke was associated with increased oxidative stress and stimulation of autoantibody production, and such exposure can directly damage endogenous proteins and DNA. Alcohol suppresses the synthesis of proinflammatory cytokines and may inhibit DNA synthesis.

The small number of lupus cases in the Black Women’s Health Study cohort limited the statistical power of the analysis. Smoking and alcohol use were also relatively uncommon among women in the Black Women’s Health Study cohort, the investigators said.

“Future studies are needed to confirm these findings and establish the biologic mechanisms by which cigarette smoking and alcohol consumption influence the risk of SLE in this population and others,“ they wrote.

The study was supported by individual investigators’ grant awards from the National Cancer Institute, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Rheumatology Research Foundation, and the Lupus Foundation of America. The authors declared no relevant conflicts of interest.

SOURCE: Cozier Y et al. Arthritis Care Res. 2018 Aug 9. doi: 10.1002/acr.23703.

People with systemic lupus erythematosus (SLE) taking antimalarials, particularly for prolonged periods, could be at risk for cardiomyopathy, and measuring specific myocardial biomarkers could help identify patients at particularly high risk, researchers have suggested.

Writing in the Journal of Rheumatology, the research team led by Konstantinos Tselios, MD, PhD, of the University of Toronto Lupus Clinic at the Centre for Prognosis Studies in the Rheumatic Diseases, noted that antimalarial-induced cardiomyopathy (AMIC) had been reported in 47 patients to date, 19 of whom had SLE, with duration and cumulative use of antimalarials thought to be the cause.

The authors suggested that AMIC could be underrecognized because antimalarials were currently recommended for all patients with SLE (without known contraindications) for prolonged periods. It was speculated that the mechanism by which AMIC occurred involved the deposition of antimalarials in the myocardial fibers and that this could lead to chronic, subclinical tissue necrosis, a process which, if not reversed, could lead to heart failure.

“Heart-specific biomarkers, such as cardiac troponin (for the assessment of myocardial necrosis) and brain natriuretic peptide (BNP; for the assessment of volume and/or pressure overload), may be of value in identifying subclinical heart damage,” the research team suggested.

The current study involved 151 consecutive patients with SLE who had no prior cardiac disease and were attending the University of Toronto Lupus Clinic from March to May 2016.

During the course of the disease, 28 of the patients had been taking chloroquine, and 137 had been taking hydroxychloroquine (14 patients had been treated with both drugs at different time periods). In the study, normal range was less than 26 ng/mL for high-sensitivity cardiac troponin I (cTnI) and less than 100 pg/mL for BNP.

Overall, 16 patients (10.6%) had abnormal BNP, of whom 9 (6%) also had abnormal cTnI. Prolonged antimalarial use (greater than 5.6 yrs) was associated with increased risk for these elevated biomarkers, regardless of age and SLE disease duration.

“Because duration of AM [antimalarial] treatment is the critical predictor of AMIC, the majority of patients with SLE should be considered at risk because most of them receive long-term maintenance therapy,” the researchers wrote.

They said that elevations of the biomarkers implicated possible active myocardial necrosis (elevated cTnI) and/or increased intracardiac ventricular pressure (elevated BNP).

“In this context, AM deposition in the myocardium, leading over time to overt cardiomyopathy, may be an important contributing factor. Indeed, 6 out of 16 of these patients were ultimately diagnosed with definite or possible AMIC, while 3 of them were completely asymptomatic, and their investigation was initiated because of the abnormal biomarkers,” they wrote.

The researchers also found that persistent creatine phosphokinase (CPK) elevation was also an important predictor for elevated cardiac biomarkers.

“We showed that chronic AM use is associated with a more than threefold increased risk for elevated CPK (after excluding patients with active myositis and statin therapy). ... It is not known whether elevated CPK may predict patients at risk for development of AMIC or whether certain patients are predisposed to AM-related muscle damage,” they said.

“Prolonged AM therapy and persistent CPK elevation conferred an increased risk for abnormal BNP and cTnI, which might predict AMIC,” they concluded.

Nevertheless, the authors acknowledged that expensive and invasive investigation was unjustified in asymptomatic individuals. They therefore suggested that identifying heart-specific biomarkers for the detection of subclinical heart damage could allow patients to be stratified according to their risk.

“Cardiac biomarkers could become a screening test for patients with SLE using AM for longer than 5.6 years and/or who have persistently elevated CPK levels. Further research is needed to delineate the differential toxicity of CQ [chloroquine] and HCQ [hydroxychloroquine],” they suggested.

The University of Toronto Lupus Research Program is supported by the University Health Network, Lou and Marissa Rocca, and the Lupus Foundation of Ontario. Dr. Tselios is financially supported by Lupus Ontario.

SOURCE: Tselios K et al. J Rheumatol. 2018. doi: 10.3899/jrheum.171436.

People with systemic lupus erythematosus (SLE) taking antimalarials, particularly for prolonged periods, could be at risk for cardiomyopathy, and measuring specific myocardial biomarkers could help identify patients at particularly high risk, researchers have suggested.

Writing in the Journal of Rheumatology, the research team led by Konstantinos Tselios, MD, PhD, of the University of Toronto Lupus Clinic at the Centre for Prognosis Studies in the Rheumatic Diseases, noted that antimalarial-induced cardiomyopathy (AMIC) had been reported in 47 patients to date, 19 of whom had SLE, with duration and cumulative use of antimalarials thought to be the cause.

The authors suggested that AMIC could be underrecognized because antimalarials were currently recommended for all patients with SLE (without known contraindications) for prolonged periods. It was speculated that the mechanism by which AMIC occurred involved the deposition of antimalarials in the myocardial fibers and that this could lead to chronic, subclinical tissue necrosis, a process which, if not reversed, could lead to heart failure.

“Heart-specific biomarkers, such as cardiac troponin (for the assessment of myocardial necrosis) and brain natriuretic peptide (BNP; for the assessment of volume and/or pressure overload), may be of value in identifying subclinical heart damage,” the research team suggested.

The current study involved 151 consecutive patients with SLE who had no prior cardiac disease and were attending the University of Toronto Lupus Clinic from March to May 2016.

During the course of the disease, 28 of the patients had been taking chloroquine, and 137 had been taking hydroxychloroquine (14 patients had been treated with both drugs at different time periods). In the study, normal range was less than 26 ng/mL for high-sensitivity cardiac troponin I (cTnI) and less than 100 pg/mL for BNP.

Overall, 16 patients (10.6%) had abnormal BNP, of whom 9 (6%) also had abnormal cTnI. Prolonged antimalarial use (greater than 5.6 yrs) was associated with increased risk for these elevated biomarkers, regardless of age and SLE disease duration.

“Because duration of AM [antimalarial] treatment is the critical predictor of AMIC, the majority of patients with SLE should be considered at risk because most of them receive long-term maintenance therapy,” the researchers wrote.

They said that elevations of the biomarkers implicated possible active myocardial necrosis (elevated cTnI) and/or increased intracardiac ventricular pressure (elevated BNP).

“In this context, AM deposition in the myocardium, leading over time to overt cardiomyopathy, may be an important contributing factor. Indeed, 6 out of 16 of these patients were ultimately diagnosed with definite or possible AMIC, while 3 of them were completely asymptomatic, and their investigation was initiated because of the abnormal biomarkers,” they wrote.

The researchers also found that persistent creatine phosphokinase (CPK) elevation was also an important predictor for elevated cardiac biomarkers.

“We showed that chronic AM use is associated with a more than threefold increased risk for elevated CPK (after excluding patients with active myositis and statin therapy). ... It is not known whether elevated CPK may predict patients at risk for development of AMIC or whether certain patients are predisposed to AM-related muscle damage,” they said.

“Prolonged AM therapy and persistent CPK elevation conferred an increased risk for abnormal BNP and cTnI, which might predict AMIC,” they concluded.

Nevertheless, the authors acknowledged that expensive and invasive investigation was unjustified in asymptomatic individuals. They therefore suggested that identifying heart-specific biomarkers for the detection of subclinical heart damage could allow patients to be stratified according to their risk.

“Cardiac biomarkers could become a screening test for patients with SLE using AM for longer than 5.6 years and/or who have persistently elevated CPK levels. Further research is needed to delineate the differential toxicity of CQ [chloroquine] and HCQ [hydroxychloroquine],” they suggested.

The University of Toronto Lupus Research Program is supported by the University Health Network, Lou and Marissa Rocca, and the Lupus Foundation of Ontario. Dr. Tselios is financially supported by Lupus Ontario.

SOURCE: Tselios K et al. J Rheumatol. 2018. doi: 10.3899/jrheum.171436.

People with systemic lupus erythematosus (SLE) taking antimalarials, particularly for prolonged periods, could be at risk for cardiomyopathy, and measuring specific myocardial biomarkers could help identify patients at particularly high risk, researchers have suggested.

Writing in the Journal of Rheumatology, the research team led by Konstantinos Tselios, MD, PhD, of the University of Toronto Lupus Clinic at the Centre for Prognosis Studies in the Rheumatic Diseases, noted that antimalarial-induced cardiomyopathy (AMIC) had been reported in 47 patients to date, 19 of whom had SLE, with duration and cumulative use of antimalarials thought to be the cause.

The authors suggested that AMIC could be underrecognized because antimalarials were currently recommended for all patients with SLE (without known contraindications) for prolonged periods. It was speculated that the mechanism by which AMIC occurred involved the deposition of antimalarials in the myocardial fibers and that this could lead to chronic, subclinical tissue necrosis, a process which, if not reversed, could lead to heart failure.

“Heart-specific biomarkers, such as cardiac troponin (for the assessment of myocardial necrosis) and brain natriuretic peptide (BNP; for the assessment of volume and/or pressure overload), may be of value in identifying subclinical heart damage,” the research team suggested.

The current study involved 151 consecutive patients with SLE who had no prior cardiac disease and were attending the University of Toronto Lupus Clinic from March to May 2016.

During the course of the disease, 28 of the patients had been taking chloroquine, and 137 had been taking hydroxychloroquine (14 patients had been treated with both drugs at different time periods). In the study, normal range was less than 26 ng/mL for high-sensitivity cardiac troponin I (cTnI) and less than 100 pg/mL for BNP.

Overall, 16 patients (10.6%) had abnormal BNP, of whom 9 (6%) also had abnormal cTnI. Prolonged antimalarial use (greater than 5.6 yrs) was associated with increased risk for these elevated biomarkers, regardless of age and SLE disease duration.

“Because duration of AM [antimalarial] treatment is the critical predictor of AMIC, the majority of patients with SLE should be considered at risk because most of them receive long-term maintenance therapy,” the researchers wrote.

They said that elevations of the biomarkers implicated possible active myocardial necrosis (elevated cTnI) and/or increased intracardiac ventricular pressure (elevated BNP).

“In this context, AM deposition in the myocardium, leading over time to overt cardiomyopathy, may be an important contributing factor. Indeed, 6 out of 16 of these patients were ultimately diagnosed with definite or possible AMIC, while 3 of them were completely asymptomatic, and their investigation was initiated because of the abnormal biomarkers,” they wrote.

The researchers also found that persistent creatine phosphokinase (CPK) elevation was also an important predictor for elevated cardiac biomarkers.

“We showed that chronic AM use is associated with a more than threefold increased risk for elevated CPK (after excluding patients with active myositis and statin therapy). ... It is not known whether elevated CPK may predict patients at risk for development of AMIC or whether certain patients are predisposed to AM-related muscle damage,” they said.

“Prolonged AM therapy and persistent CPK elevation conferred an increased risk for abnormal BNP and cTnI, which might predict AMIC,” they concluded.

Nevertheless, the authors acknowledged that expensive and invasive investigation was unjustified in asymptomatic individuals. They therefore suggested that identifying heart-specific biomarkers for the detection of subclinical heart damage could allow patients to be stratified according to their risk.

“Cardiac biomarkers could become a screening test for patients with SLE using AM for longer than 5.6 years and/or who have persistently elevated CPK levels. Further research is needed to delineate the differential toxicity of CQ [chloroquine] and HCQ [hydroxychloroquine],” they suggested.

The University of Toronto Lupus Research Program is supported by the University Health Network, Lou and Marissa Rocca, and the Lupus Foundation of Ontario. Dr. Tselios is financially supported by Lupus Ontario.

SOURCE: Tselios K et al. J Rheumatol. 2018. doi: 10.3899/jrheum.171436.

Systemic lupus erythematosus (SLE) patients who achieve prolonged low disease activity have damage accrual over 10 years similar to patients in sustained clinical remission, Canadian researchers report.

The findings endorse the endpoint used to define low disease activity in the study – Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) of 2 or less – as a meaningful treat-to-target outcome in SLE and also help to fill in missing information about the long-term longitudinal status of patients with recent-onset disease who enter either low disease activity or clinical remission status, first author Konstantinos Tselios, MD, PhD, and coauthors at the Centre for Prognosis Studies in the Rheumatic Diseases at the University Health Network’s Toronto Lupus Clinic, wrote in Arthritis Care & Research.

The concept of low disease activity (LDA) has emerged because it is rare for SLE patients to achieve sustained complete remission, the authors said. Existing studies on the outcomes of LDA and clinical remission have demonstrated comparable outcomes between the two in terms of damage accrual after 2 years, but they enrolled patients with prevalent disease, many of whom were in late stages.

“Given that disease duration has a significant impact on disease activity, the prevalence and characteristics of complete remission and LDA might have been affected,” they wrote.

The investigators therefore conducted the current study to assess damage accrual, medications used, flare rate, and mortality in inception patients who sustained complete remission and LDA status for 10 years.

The study involved 267 patients attending the University of Toronto Lupus Clinic who had at least 10 years of follow-up and no time interval between clinic visits exceeding 18 months. All patients fulfilled the revised American College of Rheumatology criteria for SLE classification or had three criteria and a supportive biopsy. The patients all had either LDA or clinical remission (SLEDAI-2K = 0, excluding serology) within the first 5 years since enrollment and maintained that status for 10 consecutive years, regardless of therapy.

A total of 10.1% of patients (n = 27) achieved prolonged clinical remission. Clinical manifestations at baseline included mucocutaneous disease in 70.4%, arthritis in 59.3%, cytopenias in 55.6%, nephritis in 25.9%, and central nervous involvement in 25.9%. Nephritis was class II in three patients, class III in one, and class IV in three.

For the 18% of patients (n = 48) who achieved sustained LDA, clinical manifestations included mucocutaneous disease in 81.3%, cytopenias in 66.7%, arthritis in 60.4%, serositis in 29.2%, nephritis in 22.9%, and central nervous system disease in 8.3%. The nephritis was class II in two patients, class III in four, class IV in two, and class VI in one. Patients in both groups were similar at baseline, but mean prednisone dose was higher in the remission group and more patients in the LDA group were taking antimalarials.

Time to remission and time to LDA were 1.2 years in both groups. After 10 years of follow-up, the mean SLEDAI was 1.2 in the remission group and 1.6 in the LDA group (P = .31) and 3.7 among patients not achieving either goal (n = 192; P less than .001).

Moreover, serology (complement C3/C4 and anti-double stranded DNA positivity) and antiextractable nuclear antigen antibody profile were similar in both groups.

No differences in flare rate or mortality emerged. Disease flares were observed in 25.9% of the remission group and 31.2% of the LDA group (P = .63) and flare rates were 0.038/patient-year and 0.065/patient-year, respectively (P = .23). Mortality after 10 years was 11.1% in the remission group and 10.4% in the LDA group (P = .93).

“Maintenance of this state could be an acceptable target for the long-term management of SLE. The concept of LDA is relatively new in SLE. Since complete remission has not been strictly defined yet and is rare, a more realistic target, such as LDA, may be of value in daily clinical practice as well as in clinical trials,” the investigators wrote.

The authors noted that the study was limited by the relatively low number of patients.

The University of Toronto Lupus Research Program is supported by the University Health Network, Lou & Marissa Rocca, and the Lupus Foundation of Ontario. The authors declared no potential conflicts of interests.

SOURCE: Tselios K et al. Arthritis Care Res. 2018 Jul 28. doi: 10.1002/acr.23720

Systemic lupus erythematosus (SLE) patients who achieve prolonged low disease activity have damage accrual over 10 years similar to patients in sustained clinical remission, Canadian researchers report.

The findings endorse the endpoint used to define low disease activity in the study – Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) of 2 or less – as a meaningful treat-to-target outcome in SLE and also help to fill in missing information about the long-term longitudinal status of patients with recent-onset disease who enter either low disease activity or clinical remission status, first author Konstantinos Tselios, MD, PhD, and coauthors at the Centre for Prognosis Studies in the Rheumatic Diseases at the University Health Network’s Toronto Lupus Clinic, wrote in Arthritis Care & Research.

The concept of low disease activity (LDA) has emerged because it is rare for SLE patients to achieve sustained complete remission, the authors said. Existing studies on the outcomes of LDA and clinical remission have demonstrated comparable outcomes between the two in terms of damage accrual after 2 years, but they enrolled patients with prevalent disease, many of whom were in late stages.

“Given that disease duration has a significant impact on disease activity, the prevalence and characteristics of complete remission and LDA might have been affected,” they wrote.

The investigators therefore conducted the current study to assess damage accrual, medications used, flare rate, and mortality in inception patients who sustained complete remission and LDA status for 10 years.

The study involved 267 patients attending the University of Toronto Lupus Clinic who had at least 10 years of follow-up and no time interval between clinic visits exceeding 18 months. All patients fulfilled the revised American College of Rheumatology criteria for SLE classification or had three criteria and a supportive biopsy. The patients all had either LDA or clinical remission (SLEDAI-2K = 0, excluding serology) within the first 5 years since enrollment and maintained that status for 10 consecutive years, regardless of therapy.

A total of 10.1% of patients (n = 27) achieved prolonged clinical remission. Clinical manifestations at baseline included mucocutaneous disease in 70.4%, arthritis in 59.3%, cytopenias in 55.6%, nephritis in 25.9%, and central nervous involvement in 25.9%. Nephritis was class II in three patients, class III in one, and class IV in three.

For the 18% of patients (n = 48) who achieved sustained LDA, clinical manifestations included mucocutaneous disease in 81.3%, cytopenias in 66.7%, arthritis in 60.4%, serositis in 29.2%, nephritis in 22.9%, and central nervous system disease in 8.3%. The nephritis was class II in two patients, class III in four, class IV in two, and class VI in one. Patients in both groups were similar at baseline, but mean prednisone dose was higher in the remission group and more patients in the LDA group were taking antimalarials.

Time to remission and time to LDA were 1.2 years in both groups. After 10 years of follow-up, the mean SLEDAI was 1.2 in the remission group and 1.6 in the LDA group (P = .31) and 3.7 among patients not achieving either goal (n = 192; P less than .001).

Moreover, serology (complement C3/C4 and anti-double stranded DNA positivity) and antiextractable nuclear antigen antibody profile were similar in both groups.

No differences in flare rate or mortality emerged. Disease flares were observed in 25.9% of the remission group and 31.2% of the LDA group (P = .63) and flare rates were 0.038/patient-year and 0.065/patient-year, respectively (P = .23). Mortality after 10 years was 11.1% in the remission group and 10.4% in the LDA group (P = .93).

“Maintenance of this state could be an acceptable target for the long-term management of SLE. The concept of LDA is relatively new in SLE. Since complete remission has not been strictly defined yet and is rare, a more realistic target, such as LDA, may be of value in daily clinical practice as well as in clinical trials,” the investigators wrote.

The authors noted that the study was limited by the relatively low number of patients.

The University of Toronto Lupus Research Program is supported by the University Health Network, Lou & Marissa Rocca, and the Lupus Foundation of Ontario. The authors declared no potential conflicts of interests.

SOURCE: Tselios K et al. Arthritis Care Res. 2018 Jul 28. doi: 10.1002/acr.23720

Systemic lupus erythematosus (SLE) patients who achieve prolonged low disease activity have damage accrual over 10 years similar to patients in sustained clinical remission, Canadian researchers report.

The findings endorse the endpoint used to define low disease activity in the study – Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) of 2 or less – as a meaningful treat-to-target outcome in SLE and also help to fill in missing information about the long-term longitudinal status of patients with recent-onset disease who enter either low disease activity or clinical remission status, first author Konstantinos Tselios, MD, PhD, and coauthors at the Centre for Prognosis Studies in the Rheumatic Diseases at the University Health Network’s Toronto Lupus Clinic, wrote in Arthritis Care & Research.

The concept of low disease activity (LDA) has emerged because it is rare for SLE patients to achieve sustained complete remission, the authors said. Existing studies on the outcomes of LDA and clinical remission have demonstrated comparable outcomes between the two in terms of damage accrual after 2 years, but they enrolled patients with prevalent disease, many of whom were in late stages.

“Given that disease duration has a significant impact on disease activity, the prevalence and characteristics of complete remission and LDA might have been affected,” they wrote.

The investigators therefore conducted the current study to assess damage accrual, medications used, flare rate, and mortality in inception patients who sustained complete remission and LDA status for 10 years.

The study involved 267 patients attending the University of Toronto Lupus Clinic who had at least 10 years of follow-up and no time interval between clinic visits exceeding 18 months. All patients fulfilled the revised American College of Rheumatology criteria for SLE classification or had three criteria and a supportive biopsy. The patients all had either LDA or clinical remission (SLEDAI-2K = 0, excluding serology) within the first 5 years since enrollment and maintained that status for 10 consecutive years, regardless of therapy.

A total of 10.1% of patients (n = 27) achieved prolonged clinical remission. Clinical manifestations at baseline included mucocutaneous disease in 70.4%, arthritis in 59.3%, cytopenias in 55.6%, nephritis in 25.9%, and central nervous involvement in 25.9%. Nephritis was class II in three patients, class III in one, and class IV in three.

For the 18% of patients (n = 48) who achieved sustained LDA, clinical manifestations included mucocutaneous disease in 81.3%, cytopenias in 66.7%, arthritis in 60.4%, serositis in 29.2%, nephritis in 22.9%, and central nervous system disease in 8.3%. The nephritis was class II in two patients, class III in four, class IV in two, and class VI in one. Patients in both groups were similar at baseline, but mean prednisone dose was higher in the remission group and more patients in the LDA group were taking antimalarials.

Time to remission and time to LDA were 1.2 years in both groups. After 10 years of follow-up, the mean SLEDAI was 1.2 in the remission group and 1.6 in the LDA group (P = .31) and 3.7 among patients not achieving either goal (n = 192; P less than .001).

Moreover, serology (complement C3/C4 and anti-double stranded DNA positivity) and antiextractable nuclear antigen antibody profile were similar in both groups.

No differences in flare rate or mortality emerged. Disease flares were observed in 25.9% of the remission group and 31.2% of the LDA group (P = .63) and flare rates were 0.038/patient-year and 0.065/patient-year, respectively (P = .23). Mortality after 10 years was 11.1% in the remission group and 10.4% in the LDA group (P = .93).

“Maintenance of this state could be an acceptable target for the long-term management of SLE. The concept of LDA is relatively new in SLE. Since complete remission has not been strictly defined yet and is rare, a more realistic target, such as LDA, may be of value in daily clinical practice as well as in clinical trials,” the investigators wrote.

The authors noted that the study was limited by the relatively low number of patients.

The University of Toronto Lupus Research Program is supported by the University Health Network, Lou & Marissa Rocca, and the Lupus Foundation of Ontario. The authors declared no potential conflicts of interests.

SOURCE: Tselios K et al. Arthritis Care Res. 2018 Jul 28. doi: 10.1002/acr.23720

Patients at risk of autoimmune connective tissue disease who progressed to actual disease had elevated interferon scores and a family history of autoimmune rheumatic disease, suggesting the interferon scores could be used to predict disease progression, according to results from a prospective, observational study published in Annals of the Rheumatic Diseases.

SOURCE: Yusof MYM et al. Ann Rheum Dis. 21 Jun 2018. doi: 10.1136/annrheumdis-2018-213386.

Patients at risk of autoimmune connective tissue disease who progressed to actual disease had elevated interferon scores and a family history of autoimmune rheumatic disease, suggesting the interferon scores could be used to predict disease progression, according to results from a prospective, observational study published in Annals of the Rheumatic Diseases.

SOURCE: Yusof MYM et al. Ann Rheum Dis. 21 Jun 2018. doi: 10.1136/annrheumdis-2018-213386.

Patients at risk of autoimmune connective tissue disease who progressed to actual disease had elevated interferon scores and a family history of autoimmune rheumatic disease, suggesting the interferon scores could be used to predict disease progression, according to results from a prospective, observational study published in Annals of the Rheumatic Diseases.

SOURCE: Yusof MYM et al. Ann Rheum Dis. 21 Jun 2018. doi: 10.1136/annrheumdis-2018-213386.

AMSTERDAM – Abatacept used on top of the standard of care did not improve the primary endpoint of a complete renal response versus placebo in the ALLURE phase 3 study.

Criteria for a complete renal response (CRR) at 1 year was met by 35.1% of abatacept-treated and 33.5% of placebo-treated patients (P = .73). CRR criteria included having a urine protein to creatinine ratio (UPCR) of less than 0.5, a normal estimated glomerular filtration rate (eGFR) or an eGFR of 85% or more of baseline values, no cellular casts, and a daily corticosteroid dose of 10 mg or less.

Sara Freeman/MDedge News

SOURCE: Furie RA et al. EULAR 2018. Abstract OP0253.

AMSTERDAM – Abatacept used on top of the standard of care did not improve the primary endpoint of a complete renal response versus placebo in the ALLURE phase 3 study.

Criteria for a complete renal response (CRR) at 1 year was met by 35.1% of abatacept-treated and 33.5% of placebo-treated patients (P = .73). CRR criteria included having a urine protein to creatinine ratio (UPCR) of less than 0.5, a normal estimated glomerular filtration rate (eGFR) or an eGFR of 85% or more of baseline values, no cellular casts, and a daily corticosteroid dose of 10 mg or less.

Sara Freeman/MDedge News

SOURCE: Furie RA et al. EULAR 2018. Abstract OP0253.

AMSTERDAM – Abatacept used on top of the standard of care did not improve the primary endpoint of a complete renal response versus placebo in the ALLURE phase 3 study.

Criteria for a complete renal response (CRR) at 1 year was met by 35.1% of abatacept-treated and 33.5% of placebo-treated patients (P = .73). CRR criteria included having a urine protein to creatinine ratio (UPCR) of less than 0.5, a normal estimated glomerular filtration rate (eGFR) or an eGFR of 85% or more of baseline values, no cellular casts, and a daily corticosteroid dose of 10 mg or less.

Sara Freeman/MDedge News

SOURCE: Furie RA et al. EULAR 2018. Abstract OP0253.

AMSTERDAM – Both air temperature and air pollution levels affected the likelihood of experiencing a flare in systemic lupus erythematosus (SLE) organ-specific disease activity in a study presented at the European Congress of Rheumatology.

For every 1° F increase in temperature, there was an increase in the odds of experiencing a skin flare (odds ratio, 1.0075), joint flare (OR, 1.0110), or neurologic flare (OR, 1.0096), reported George Stojan, MD, and associates during one of the poster sessions. Conversely, renal flares were less likely to occur with rising temperature (OR, 0.9960). The latter is something previously reported, Dr. Stojan said in an interview, “as we found most renal flares occur in the winter, not in the summer months.”

Sara Freeman/MDedge News

Furthermore, for every 1 mcg per cubic meter increase in fine particulate matter pollution (PM2.5), there were increases in serositis (OR, 1.0240) and hematologic flares (OR, 1.011).

There were two reasons for looking at the role of these environmental factors in relation to SLE flares, said Dr. Stojan, an assistant professor of medicine at Johns Hopkins University, Baltimore. “The first was a clinical observation – I was getting clusters of patients with certain disease manifestations, for example with serositis or joint flares, and there wasn’t a random distribution.”

The second was a patient observation, added Dr. Stojan, who is also codirector of the Johns Hopkins Lupus Center. Every year, patients treated at the Center have the opportunity to meet each other and hear about the research being done by the team, and it was at this meeting that patients said they felt they were experiencing similar disease flares.

To look at the underlying role of environmental exposures in the development of SLE and possible associations with disease activity, Dr. Stojan and associates used a method known as cluster detection, which is commonly used in public health studies.

The investigators used a 350-km radial zone around the Johns Hopkins Lupus Center for the analysis as this was an area where a uniform number of patients treated by the center were living. They obtained data on 1,261 patients in the Hopkins Lupus Cohort, spanning a 10-year period from 1999 to 2009, and used SaTScan software to identify clusters of disease activity occurring during 3 separate monthly time intervals in different counties. The researchers then linked these clusters to average temperature and PM2.5 data obtained from the Environmental Protection Agency for the 10 days prior to patients’ visits.

“The SaTScan system predicts how many flares per organ system you would expect in a county based on the number of patients and based on the total flares we have in our cohort,” Dr. Stojan explained. Previously, the system helped to identify areas that had a higher flare incidence for each organ system that lasted for about 2-3 years, did not overlap, and could not be explained. So, the next step was to look for potential environmental triggers.

“Basically, the SaTScan adjusts the data that’s inputted for temperature and small particulate pollution. If the cluster moves in space and time then these did affect it,” Dr. Stojan said. “It seems that these do affect certain types of organ flares,” even after adjustment for other variables such as patients’ age, gender, income, ethnicity, and living situation (rural or urban).

Flares in skin symptoms during the summer have been identified before, he acknowledged, but the link to joint flares or neurologic flares have not. The latter includes things like seizures, neuropathy, or abnormal brain imaging rather than mood changes or mild cognitive dysfunction.

These data could have an impact on how clinical trials are designed, Dr. Stojan added, suggesting that factoring in where patients live and how close they are to areas of pollution could ensure a uniform population of patients is studied.

From a more practical perspective, these data might help to develop predictive models to help understand when patients are likely to experience a flare and if any action can be taken to ameliorate the effects of exposure.

The next step is a collaboration with patients to develop software or a mobile application where patients could input information about any disease flares. This would enable a finer view of what could be happening, Dr. Stojan said, as while daily readings are available for the environmental factors studied, disease activity data is only available during 3 separate monthly intervals. It would also allow other environmental factors to be considered.

“I think this is an important step in figuring out environmental factors and their influence on lupus,” he said. “There has been an extensive amount of research into viral causes and potential infectious triggers, but spatial-temporal analysis of environmental variables have never been done before in lupus.”

The study received no commercial funding, and Dr. Stojan reported having no disclosures.

SOURCE: Stojan G et al. Ann Rheum Dis. 2018;77(Suppl 2):1191. Abstract SAT0685.

AMSTERDAM – Both air temperature and air pollution levels affected the likelihood of experiencing a flare in systemic lupus erythematosus (SLE) organ-specific disease activity in a study presented at the European Congress of Rheumatology.

For every 1° F increase in temperature, there was an increase in the odds of experiencing a skin flare (odds ratio, 1.0075), joint flare (OR, 1.0110), or neurologic flare (OR, 1.0096), reported George Stojan, MD, and associates during one of the poster sessions. Conversely, renal flares were less likely to occur with rising temperature (OR, 0.9960). The latter is something previously reported, Dr. Stojan said in an interview, “as we found most renal flares occur in the winter, not in the summer months.”

Sara Freeman/MDedge News

Furthermore, for every 1 mcg per cubic meter increase in fine particulate matter pollution (PM2.5), there were increases in serositis (OR, 1.0240) and hematologic flares (OR, 1.011).

There were two reasons for looking at the role of these environmental factors in relation to SLE flares, said Dr. Stojan, an assistant professor of medicine at Johns Hopkins University, Baltimore. “The first was a clinical observation – I was getting clusters of patients with certain disease manifestations, for example with serositis or joint flares, and there wasn’t a random distribution.”

The second was a patient observation, added Dr. Stojan, who is also codirector of the Johns Hopkins Lupus Center. Every year, patients treated at the Center have the opportunity to meet each other and hear about the research being done by the team, and it was at this meeting that patients said they felt they were experiencing similar disease flares.

To look at the underlying role of environmental exposures in the development of SLE and possible associations with disease activity, Dr. Stojan and associates used a method known as cluster detection, which is commonly used in public health studies.

The investigators used a 350-km radial zone around the Johns Hopkins Lupus Center for the analysis as this was an area where a uniform number of patients treated by the center were living. They obtained data on 1,261 patients in the Hopkins Lupus Cohort, spanning a 10-year period from 1999 to 2009, and used SaTScan software to identify clusters of disease activity occurring during 3 separate monthly time intervals in different counties. The researchers then linked these clusters to average temperature and PM2.5 data obtained from the Environmental Protection Agency for the 10 days prior to patients’ visits.

“The SaTScan system predicts how many flares per organ system you would expect in a county based on the number of patients and based on the total flares we have in our cohort,” Dr. Stojan explained. Previously, the system helped to identify areas that had a higher flare incidence for each organ system that lasted for about 2-3 years, did not overlap, and could not be explained. So, the next step was to look for potential environmental triggers.

“Basically, the SaTScan adjusts the data that’s inputted for temperature and small particulate pollution. If the cluster moves in space and time then these did affect it,” Dr. Stojan said. “It seems that these do affect certain types of organ flares,” even after adjustment for other variables such as patients’ age, gender, income, ethnicity, and living situation (rural or urban).

Flares in skin symptoms during the summer have been identified before, he acknowledged, but the link to joint flares or neurologic flares have not. The latter includes things like seizures, neuropathy, or abnormal brain imaging rather than mood changes or mild cognitive dysfunction.

These data could have an impact on how clinical trials are designed, Dr. Stojan added, suggesting that factoring in where patients live and how close they are to areas of pollution could ensure a uniform population of patients is studied.

From a more practical perspective, these data might help to develop predictive models to help understand when patients are likely to experience a flare and if any action can be taken to ameliorate the effects of exposure.

The next step is a collaboration with patients to develop software or a mobile application where patients could input information about any disease flares. This would enable a finer view of what could be happening, Dr. Stojan said, as while daily readings are available for the environmental factors studied, disease activity data is only available during 3 separate monthly intervals. It would also allow other environmental factors to be considered.

“I think this is an important step in figuring out environmental factors and their influence on lupus,” he said. “There has been an extensive amount of research into viral causes and potential infectious triggers, but spatial-temporal analysis of environmental variables have never been done before in lupus.”

The study received no commercial funding, and Dr. Stojan reported having no disclosures.

SOURCE: Stojan G et al. Ann Rheum Dis. 2018;77(Suppl 2):1191. Abstract SAT0685.

AMSTERDAM – Both air temperature and air pollution levels affected the likelihood of experiencing a flare in systemic lupus erythematosus (SLE) organ-specific disease activity in a study presented at the European Congress of Rheumatology.

For every 1° F increase in temperature, there was an increase in the odds of experiencing a skin flare (odds ratio, 1.0075), joint flare (OR, 1.0110), or neurologic flare (OR, 1.0096), reported George Stojan, MD, and associates during one of the poster sessions. Conversely, renal flares were less likely to occur with rising temperature (OR, 0.9960). The latter is something previously reported, Dr. Stojan said in an interview, “as we found most renal flares occur in the winter, not in the summer months.”

Sara Freeman/MDedge News

Furthermore, for every 1 mcg per cubic meter increase in fine particulate matter pollution (PM2.5), there were increases in serositis (OR, 1.0240) and hematologic flares (OR, 1.011).

There were two reasons for looking at the role of these environmental factors in relation to SLE flares, said Dr. Stojan, an assistant professor of medicine at Johns Hopkins University, Baltimore. “The first was a clinical observation – I was getting clusters of patients with certain disease manifestations, for example with serositis or joint flares, and there wasn’t a random distribution.”

The second was a patient observation, added Dr. Stojan, who is also codirector of the Johns Hopkins Lupus Center. Every year, patients treated at the Center have the opportunity to meet each other and hear about the research being done by the team, and it was at this meeting that patients said they felt they were experiencing similar disease flares.

To look at the underlying role of environmental exposures in the development of SLE and possible associations with disease activity, Dr. Stojan and associates used a method known as cluster detection, which is commonly used in public health studies.

The investigators used a 350-km radial zone around the Johns Hopkins Lupus Center for the analysis as this was an area where a uniform number of patients treated by the center were living. They obtained data on 1,261 patients in the Hopkins Lupus Cohort, spanning a 10-year period from 1999 to 2009, and used SaTScan software to identify clusters of disease activity occurring during 3 separate monthly time intervals in different counties. The researchers then linked these clusters to average temperature and PM2.5 data obtained from the Environmental Protection Agency for the 10 days prior to patients’ visits.

“The SaTScan system predicts how many flares per organ system you would expect in a county based on the number of patients and based on the total flares we have in our cohort,” Dr. Stojan explained. Previously, the system helped to identify areas that had a higher flare incidence for each organ system that lasted for about 2-3 years, did not overlap, and could not be explained. So, the next step was to look for potential environmental triggers.

“Basically, the SaTScan adjusts the data that’s inputted for temperature and small particulate pollution. If the cluster moves in space and time then these did affect it,” Dr. Stojan said. “It seems that these do affect certain types of organ flares,” even after adjustment for other variables such as patients’ age, gender, income, ethnicity, and living situation (rural or urban).

Flares in skin symptoms during the summer have been identified before, he acknowledged, but the link to joint flares or neurologic flares have not. The latter includes things like seizures, neuropathy, or abnormal brain imaging rather than mood changes or mild cognitive dysfunction.

These data could have an impact on how clinical trials are designed, Dr. Stojan added, suggesting that factoring in where patients live and how close they are to areas of pollution could ensure a uniform population of patients is studied.

From a more practical perspective, these data might help to develop predictive models to help understand when patients are likely to experience a flare and if any action can be taken to ameliorate the effects of exposure.

The next step is a collaboration with patients to develop software or a mobile application where patients could input information about any disease flares. This would enable a finer view of what could be happening, Dr. Stojan said, as while daily readings are available for the environmental factors studied, disease activity data is only available during 3 separate monthly intervals. It would also allow other environmental factors to be considered.

“I think this is an important step in figuring out environmental factors and their influence on lupus,” he said. “There has been an extensive amount of research into viral causes and potential infectious triggers, but spatial-temporal analysis of environmental variables have never been done before in lupus.”

The study received no commercial funding, and Dr. Stojan reported having no disclosures.

SOURCE: Stojan G et al. Ann Rheum Dis. 2018;77(Suppl 2):1191. Abstract SAT0685.

AMSTERDAM – A new way to assess clinically meaningful, multiorgan changes in patients receiving treatment for systemic sclerosis has transformed the way new drugs for this disease are judged.

The Combined Response Index for Systemic Sclerosis (CRISS) “will change how we look at drugs” for systemic sclerosis, Daniel E. Furst, MD, said at the European Congress of Rheumatology.

Mitchel L. Zoler/MDedge News

• A new scleroderma renal crisis.
• A decline in forced vital capacity of 15% or more of predicted.
• A new decline of left ventricular ejection fraction to 45% or less.
• New onset of pulmonary arterial hypertension that requires treatment.

If none of these apply, the next step is to assess treatment response by measuring changes in five parameters and then integrating them into a single number using a mathematical formula. The five elements in the equation are:

• Modified Rodnan skin score.
• Percent of predicted forced vital capacity.
• Health Assessment Questionnaire-Disability Index.
• Patient’s global assessment.
• Physician’s global assessment.

When factored together, changes in these five measures determine the probability that the patient responded to the intervention.

One limitation of the CRISS is that it only measures change from baseline, which makes it similar to the ACR 20, Dr. Furst noted. Another useful score would be one that reflects the status of a patient with systemic sclerosis at a specific point in time, a type of disease activity score. Dr. Furst said that he and others active in the systemic sclerosis field would like to develop a method that provides this type of patient assessment. Another addition would be to develop a “minimally clinically important change” in the score, which would make the CRISS more intuitive to understand.

Dr. Furst has received research support from Amgen, Bristol-Myers Squibb, Celgene, Corbus, Genentech-Roche, GlaxoSmithKline, Pfizer, and Novartis.

[email protected]

SOURCE: Furst DE. EULAR 2018. Abstract SP0012.

AMSTERDAM – A new way to assess clinically meaningful, multiorgan changes in patients receiving treatment for systemic sclerosis has transformed the way new drugs for this disease are judged.

The Combined Response Index for Systemic Sclerosis (CRISS) “will change how we look at drugs” for systemic sclerosis, Daniel E. Furst, MD, said at the European Congress of Rheumatology.

Mitchel L. Zoler/MDedge News

• A new scleroderma renal crisis.
• A decline in forced vital capacity of 15% or more of predicted.
• A new decline of left ventricular ejection fraction to 45% or less.
• New onset of pulmonary arterial hypertension that requires treatment.

If none of these apply, the next step is to assess treatment response by measuring changes in five parameters and then integrating them into a single number using a mathematical formula. The five elements in the equation are:

• Modified Rodnan skin score.
• Percent of predicted forced vital capacity.
• Health Assessment Questionnaire-Disability Index.
• Patient’s global assessment.
• Physician’s global assessment.

When factored together, changes in these five measures determine the probability that the patient responded to the intervention.

One limitation of the CRISS is that it only measures change from baseline, which makes it similar to the ACR 20, Dr. Furst noted. Another useful score would be one that reflects the status of a patient with systemic sclerosis at a specific point in time, a type of disease activity score. Dr. Furst said that he and others active in the systemic sclerosis field would like to develop a method that provides this type of patient assessment. Another addition would be to develop a “minimally clinically important change” in the score, which would make the CRISS more intuitive to understand.

Dr. Furst has received research support from Amgen, Bristol-Myers Squibb, Celgene, Corbus, Genentech-Roche, GlaxoSmithKline, Pfizer, and Novartis.

[email protected]

SOURCE: Furst DE. EULAR 2018. Abstract SP0012.

AMSTERDAM – A new way to assess clinically meaningful, multiorgan changes in patients receiving treatment for systemic sclerosis has transformed the way new drugs for this disease are judged.

The Combined Response Index for Systemic Sclerosis (CRISS) “will change how we look at drugs” for systemic sclerosis, Daniel E. Furst, MD, said at the European Congress of Rheumatology.

Mitchel L. Zoler/MDedge News

• A new scleroderma renal crisis.
• A decline in forced vital capacity of 15% or more of predicted.
• A new decline of left ventricular ejection fraction to 45% or less.
• New onset of pulmonary arterial hypertension that requires treatment.

If none of these apply, the next step is to assess treatment response by measuring changes in five parameters and then integrating them into a single number using a mathematical formula. The five elements in the equation are:

• Modified Rodnan skin score.
• Percent of predicted forced vital capacity.
• Health Assessment Questionnaire-Disability Index.
• Patient’s global assessment.
• Physician’s global assessment.

When factored together, changes in these five measures determine the probability that the patient responded to the intervention.

One limitation of the CRISS is that it only measures change from baseline, which makes it similar to the ACR 20, Dr. Furst noted. Another useful score would be one that reflects the status of a patient with systemic sclerosis at a specific point in time, a type of disease activity score. Dr. Furst said that he and others active in the systemic sclerosis field would like to develop a method that provides this type of patient assessment. Another addition would be to develop a “minimally clinically important change” in the score, which would make the CRISS more intuitive to understand.

Dr. Furst has received research support from Amgen, Bristol-Myers Squibb, Celgene, Corbus, Genentech-Roche, GlaxoSmithKline, Pfizer, and Novartis.

[email protected]

SOURCE: Furst DE. EULAR 2018. Abstract SP0012.

AMSTERDAM – New classification criteria for antineutrophil cytoplasmic antibody (ANCA)–associated vasculitides have been drafted and now need formal review by the American College of Rheumatology and the European League Against Rheumatism before they can be put into practice.

Sara Freeman/MDedge News

SOURCE: Robson JC et al. EULAR 2018. Abstract OP0021.

AMSTERDAM – New classification criteria for antineutrophil cytoplasmic antibody (ANCA)–associated vasculitides have been drafted and now need formal review by the American College of Rheumatology and the European League Against Rheumatism before they can be put into practice.

Sara Freeman/MDedge News

SOURCE: Robson JC et al. EULAR 2018. Abstract OP0021.

AMSTERDAM – New classification criteria for antineutrophil cytoplasmic antibody (ANCA)–associated vasculitides have been drafted and now need formal review by the American College of Rheumatology and the European League Against Rheumatism before they can be put into practice.

Sara Freeman/MDedge News

SOURCE: Robson JC et al. EULAR 2018. Abstract OP0021.