Amy Karon

For children with Crohn’s disease, fecal calprotectin levels below 300 mcg indicated mucosal healing, while values below 100 mcg signified deep healing in a multicenter, 151-patient study.

Sensitivity was 80% for mucosal healing and 71% for deep healing, while specificities were 81% and 92%, respectively, said Inbar Nakar of the Hebrew University of Jerusalem, with her associates. In line with prior studies, adding C-reactive protein (CRP) to fecal calprotectin improved neither sensitivity or specificity, the researchers wrote in Clinical Gastroenterology and Hepatology.

Bowel healing is a crucial goal in Crohn’s disease (CD). Because pediatric transmural healing had not been studied, the researchers analyzed data from the ImageKids study, a multicenter effort to develop magnetic resonance enterography (MRE) measures for CD patients aged 6-18 years. Participants averaged 14 years old with a standard deviation of 2 years. Assessments included MRE, complete ileocolonoscopic evaluation, CRP, and fecal calprotectin. The researchers defined mucosal healing as a Simple Endoscopic Severity Index in Crohn’s Disease score below 3, transmural healing as an MRE visual analog score below 20 mm, and deep healing as transmural plus mucosal healing.

Nearly one-third of patients had healing only in the mucosa or the bowel wall, but not both; 6% had mucosal healing but transmural inflammation, and 25% of children had transmural healing but mucosal inflammation. In addition, 14% of children had deep healing, and 55% of children had both mucosal and transmural inflammation. Those findings highlight “the discrepancy between mucosal and transmural inflammation and the importance of evaluating the disease by both ileocolonoscopy and imaging,” the researchers wrote.

Median calprotectin levels varied significantly by healing status (P less than .001). They were lowest (10 mcg/g) for deep healing, followed by either transmural or mucosal inflammation, and were highest (median, 810 mcg/g) when children had both mucosal and transmural inflammation. Calprotectin in children with deep healing had an area under the receiver operating characteristic curve value of 0.93 (95% confidence interval, 0.89- 0.98). In contrast, CRP level identified children with deep healing with an AUROC value of only 0.81 (95% CI, 0.71-0.90).

Although “calprotectin level is driven primarily by mucosal healing, [it] is still superior to CRP,” the investigators concluded. “Although a calprotectin cutoff [less than] 300 mcg/g predicted mucosal healing, a lower cutoff of [less than] 100 mcg/g may be more suitable to predict deep healing.” However, they emphasized that fecal calprotectin level is only moderately accurate in predicting mucosal or transmural healing in children with CD. They advised physicians to “be familiar with the predictive values of each cutoff before incorporating them in clinical decision making.”

An educational grant from AbbVie funded the ImageKids study. AbbVie was not otherwise involved in the study. Two coinvestigators disclosed ties to AbbVie and other pharmaceutical companies. There were no other disclosures.

SOURCE: Nakar I et al. Clin Gastroenterol Hepatol. 2018 Mar 2. doi: 10.1016/j.cgh.2018.01.024.

For children with Crohn’s disease, fecal calprotectin levels below 300 mcg indicated mucosal healing, while values below 100 mcg signified deep healing in a multicenter, 151-patient study.

Sensitivity was 80% for mucosal healing and 71% for deep healing, while specificities were 81% and 92%, respectively, said Inbar Nakar of the Hebrew University of Jerusalem, with her associates. In line with prior studies, adding C-reactive protein (CRP) to fecal calprotectin improved neither sensitivity or specificity, the researchers wrote in Clinical Gastroenterology and Hepatology.

Bowel healing is a crucial goal in Crohn’s disease (CD). Because pediatric transmural healing had not been studied, the researchers analyzed data from the ImageKids study, a multicenter effort to develop magnetic resonance enterography (MRE) measures for CD patients aged 6-18 years. Participants averaged 14 years old with a standard deviation of 2 years. Assessments included MRE, complete ileocolonoscopic evaluation, CRP, and fecal calprotectin. The researchers defined mucosal healing as a Simple Endoscopic Severity Index in Crohn’s Disease score below 3, transmural healing as an MRE visual analog score below 20 mm, and deep healing as transmural plus mucosal healing.

Nearly one-third of patients had healing only in the mucosa or the bowel wall, but not both; 6% had mucosal healing but transmural inflammation, and 25% of children had transmural healing but mucosal inflammation. In addition, 14% of children had deep healing, and 55% of children had both mucosal and transmural inflammation. Those findings highlight “the discrepancy between mucosal and transmural inflammation and the importance of evaluating the disease by both ileocolonoscopy and imaging,” the researchers wrote.

Median calprotectin levels varied significantly by healing status (P less than .001). They were lowest (10 mcg/g) for deep healing, followed by either transmural or mucosal inflammation, and were highest (median, 810 mcg/g) when children had both mucosal and transmural inflammation. Calprotectin in children with deep healing had an area under the receiver operating characteristic curve value of 0.93 (95% confidence interval, 0.89- 0.98). In contrast, CRP level identified children with deep healing with an AUROC value of only 0.81 (95% CI, 0.71-0.90).

Although “calprotectin level is driven primarily by mucosal healing, [it] is still superior to CRP,” the investigators concluded. “Although a calprotectin cutoff [less than] 300 mcg/g predicted mucosal healing, a lower cutoff of [less than] 100 mcg/g may be more suitable to predict deep healing.” However, they emphasized that fecal calprotectin level is only moderately accurate in predicting mucosal or transmural healing in children with CD. They advised physicians to “be familiar with the predictive values of each cutoff before incorporating them in clinical decision making.”

An educational grant from AbbVie funded the ImageKids study. AbbVie was not otherwise involved in the study. Two coinvestigators disclosed ties to AbbVie and other pharmaceutical companies. There were no other disclosures.

SOURCE: Nakar I et al. Clin Gastroenterol Hepatol. 2018 Mar 2. doi: 10.1016/j.cgh.2018.01.024.

For children with Crohn’s disease, fecal calprotectin levels below 300 mcg indicated mucosal healing, while values below 100 mcg signified deep healing in a multicenter, 151-patient study.

Sensitivity was 80% for mucosal healing and 71% for deep healing, while specificities were 81% and 92%, respectively, said Inbar Nakar of the Hebrew University of Jerusalem, with her associates. In line with prior studies, adding C-reactive protein (CRP) to fecal calprotectin improved neither sensitivity or specificity, the researchers wrote in Clinical Gastroenterology and Hepatology.

Bowel healing is a crucial goal in Crohn’s disease (CD). Because pediatric transmural healing had not been studied, the researchers analyzed data from the ImageKids study, a multicenter effort to develop magnetic resonance enterography (MRE) measures for CD patients aged 6-18 years. Participants averaged 14 years old with a standard deviation of 2 years. Assessments included MRE, complete ileocolonoscopic evaluation, CRP, and fecal calprotectin. The researchers defined mucosal healing as a Simple Endoscopic Severity Index in Crohn’s Disease score below 3, transmural healing as an MRE visual analog score below 20 mm, and deep healing as transmural plus mucosal healing.

Nearly one-third of patients had healing only in the mucosa or the bowel wall, but not both; 6% had mucosal healing but transmural inflammation, and 25% of children had transmural healing but mucosal inflammation. In addition, 14% of children had deep healing, and 55% of children had both mucosal and transmural inflammation. Those findings highlight “the discrepancy between mucosal and transmural inflammation and the importance of evaluating the disease by both ileocolonoscopy and imaging,” the researchers wrote.

Median calprotectin levels varied significantly by healing status (P less than .001). They were lowest (10 mcg/g) for deep healing, followed by either transmural or mucosal inflammation, and were highest (median, 810 mcg/g) when children had both mucosal and transmural inflammation. Calprotectin in children with deep healing had an area under the receiver operating characteristic curve value of 0.93 (95% confidence interval, 0.89- 0.98). In contrast, CRP level identified children with deep healing with an AUROC value of only 0.81 (95% CI, 0.71-0.90).

Although “calprotectin level is driven primarily by mucosal healing, [it] is still superior to CRP,” the investigators concluded. “Although a calprotectin cutoff [less than] 300 mcg/g predicted mucosal healing, a lower cutoff of [less than] 100 mcg/g may be more suitable to predict deep healing.” However, they emphasized that fecal calprotectin level is only moderately accurate in predicting mucosal or transmural healing in children with CD. They advised physicians to “be familiar with the predictive values of each cutoff before incorporating them in clinical decision making.”

An educational grant from AbbVie funded the ImageKids study. AbbVie was not otherwise involved in the study. Two coinvestigators disclosed ties to AbbVie and other pharmaceutical companies. There were no other disclosures.

SOURCE: Nakar I et al. Clin Gastroenterol Hepatol. 2018 Mar 2. doi: 10.1016/j.cgh.2018.01.024.

Median progression-free survival (PFS) based on traditional RECIST criteria did not correlate with overall survival (OS) in a meta-analysis of 12 randomized controlled trials of nivolumab or pembrolizumab monotherapy.

There was no correlation in terms of medians or gains in medians, although hazard ratios for OS and PFS did correlate significantly, said Bishal Gyawali, MD, PhD, of Nagoya (Japan) University Hospital with his associates. “The protective effects of treatment were greater for OS than for PFS,” they concluded in JAMA Network Open. “Progression-free survival cannot adequately capture the benefit of PD-1 inhibitors; thus, OS should remain the gold standard end point for trials of PD-1 inhibitors.”

Progression-free survival often has been used as a surrogate for OS because the latter takes time to ascertain and can be contaminated by crossover or postprogression treatment. However, it can be problematic to assume that the two outcomes correlate. Progression “is defined as an increase in tumor size beyond an arbitrary cutoff and is prone to bias, particularly when the investigators are not blinded,” the researchers noted. Furthermore, PD-1 inhibitors show an “atypical response pattern,” including long durations of response, responses after initial progression (known as pseudoprogression), and even response after treatment cessation.

The analysis, the first to formally compare PFS and OS across PD-1 inhibitors, included 10 randomized, controlled trials comparing nivolumab or pembrolizumab with nonimmunotherapy in adults with solid tumors. Two additional trials evaluated pembrolizumab or nivolumab following treatment with ipilimumab. In all, the studies included 5,417 patients. There was no significant heterogeneity among studies, the researchers said.

Median PFS and median OS correlated poorly, with an R² value of 0.46 (P = .09). Change in PFS also did not correlate with change in OS (R² = 0.23; P = .28). In contrast, hazard ratios for PFS and OS correlated significantly (R2 = 0.41; P = .048). The protective effects of treatment were higher for OS than for PFS (pooled HR, 1.2; 95% confidence interval, 1.1-1.3; P = .002).

This might be because traditional RECIST (response evaluation criteria in solid tumors) criteria predate the era of immunotherapy and do not accurately capture disease progression when patients are on immuno-oncologics. For example, pseudoprogression (in which T-cell infiltrates cause the tumor to grow before it shrinks) could be misconstrued as progression. Also, PD-1 inhibitors can continue working even after treatment cessation, which could affect OS more than PFS, the researchers noted.

Regardless, “PD-1 inhibitors may have larger effects on OS than on PFS, which would be unprecedented in oncology therapeutics,” they concluded. “These results support the rationale of using OS as the primary end point of future phase 3 trials of PD-1 inhibitors and discourage the use of PFS as a sole primary end point as the latter may provide misleading information about the efficacy of these drugs.”

Funders included the Laura and John Arnold Foundation, the Harvard Program in Therapeutic Science, and the Engelberg Foundation. The investigators reported having no relevant conflicts of interest. One coinvestigator reported research support from the Laura and John Arnold Foundation. The other investigators had no conflicts.

SOURCE: Gyawali B et al. JAMA Network Open. 2018 June 22. doi: 10.1001/jamanetworkopen.2018.0416.

Median progression-free survival (PFS) based on traditional RECIST criteria did not correlate with overall survival (OS) in a meta-analysis of 12 randomized controlled trials of nivolumab or pembrolizumab monotherapy.

There was no correlation in terms of medians or gains in medians, although hazard ratios for OS and PFS did correlate significantly, said Bishal Gyawali, MD, PhD, of Nagoya (Japan) University Hospital with his associates. “The protective effects of treatment were greater for OS than for PFS,” they concluded in JAMA Network Open. “Progression-free survival cannot adequately capture the benefit of PD-1 inhibitors; thus, OS should remain the gold standard end point for trials of PD-1 inhibitors.”

Progression-free survival often has been used as a surrogate for OS because the latter takes time to ascertain and can be contaminated by crossover or postprogression treatment. However, it can be problematic to assume that the two outcomes correlate. Progression “is defined as an increase in tumor size beyond an arbitrary cutoff and is prone to bias, particularly when the investigators are not blinded,” the researchers noted. Furthermore, PD-1 inhibitors show an “atypical response pattern,” including long durations of response, responses after initial progression (known as pseudoprogression), and even response after treatment cessation.

The analysis, the first to formally compare PFS and OS across PD-1 inhibitors, included 10 randomized, controlled trials comparing nivolumab or pembrolizumab with nonimmunotherapy in adults with solid tumors. Two additional trials evaluated pembrolizumab or nivolumab following treatment with ipilimumab. In all, the studies included 5,417 patients. There was no significant heterogeneity among studies, the researchers said.

Median PFS and median OS correlated poorly, with an R² value of 0.46 (P = .09). Change in PFS also did not correlate with change in OS (R² = 0.23; P = .28). In contrast, hazard ratios for PFS and OS correlated significantly (R2 = 0.41; P = .048). The protective effects of treatment were higher for OS than for PFS (pooled HR, 1.2; 95% confidence interval, 1.1-1.3; P = .002).

This might be because traditional RECIST (response evaluation criteria in solid tumors) criteria predate the era of immunotherapy and do not accurately capture disease progression when patients are on immuno-oncologics. For example, pseudoprogression (in which T-cell infiltrates cause the tumor to grow before it shrinks) could be misconstrued as progression. Also, PD-1 inhibitors can continue working even after treatment cessation, which could affect OS more than PFS, the researchers noted.

Regardless, “PD-1 inhibitors may have larger effects on OS than on PFS, which would be unprecedented in oncology therapeutics,” they concluded. “These results support the rationale of using OS as the primary end point of future phase 3 trials of PD-1 inhibitors and discourage the use of PFS as a sole primary end point as the latter may provide misleading information about the efficacy of these drugs.”

Funders included the Laura and John Arnold Foundation, the Harvard Program in Therapeutic Science, and the Engelberg Foundation. The investigators reported having no relevant conflicts of interest. One coinvestigator reported research support from the Laura and John Arnold Foundation. The other investigators had no conflicts.

SOURCE: Gyawali B et al. JAMA Network Open. 2018 June 22. doi: 10.1001/jamanetworkopen.2018.0416.

Median progression-free survival (PFS) based on traditional RECIST criteria did not correlate with overall survival (OS) in a meta-analysis of 12 randomized controlled trials of nivolumab or pembrolizumab monotherapy.

There was no correlation in terms of medians or gains in medians, although hazard ratios for OS and PFS did correlate significantly, said Bishal Gyawali, MD, PhD, of Nagoya (Japan) University Hospital with his associates. “The protective effects of treatment were greater for OS than for PFS,” they concluded in JAMA Network Open. “Progression-free survival cannot adequately capture the benefit of PD-1 inhibitors; thus, OS should remain the gold standard end point for trials of PD-1 inhibitors.”

Progression-free survival often has been used as a surrogate for OS because the latter takes time to ascertain and can be contaminated by crossover or postprogression treatment. However, it can be problematic to assume that the two outcomes correlate. Progression “is defined as an increase in tumor size beyond an arbitrary cutoff and is prone to bias, particularly when the investigators are not blinded,” the researchers noted. Furthermore, PD-1 inhibitors show an “atypical response pattern,” including long durations of response, responses after initial progression (known as pseudoprogression), and even response after treatment cessation.

The analysis, the first to formally compare PFS and OS across PD-1 inhibitors, included 10 randomized, controlled trials comparing nivolumab or pembrolizumab with nonimmunotherapy in adults with solid tumors. Two additional trials evaluated pembrolizumab or nivolumab following treatment with ipilimumab. In all, the studies included 5,417 patients. There was no significant heterogeneity among studies, the researchers said.

Median PFS and median OS correlated poorly, with an R² value of 0.46 (P = .09). Change in PFS also did not correlate with change in OS (R² = 0.23; P = .28). In contrast, hazard ratios for PFS and OS correlated significantly (R2 = 0.41; P = .048). The protective effects of treatment were higher for OS than for PFS (pooled HR, 1.2; 95% confidence interval, 1.1-1.3; P = .002).

This might be because traditional RECIST (response evaluation criteria in solid tumors) criteria predate the era of immunotherapy and do not accurately capture disease progression when patients are on immuno-oncologics. For example, pseudoprogression (in which T-cell infiltrates cause the tumor to grow before it shrinks) could be misconstrued as progression. Also, PD-1 inhibitors can continue working even after treatment cessation, which could affect OS more than PFS, the researchers noted.

Regardless, “PD-1 inhibitors may have larger effects on OS than on PFS, which would be unprecedented in oncology therapeutics,” they concluded. “These results support the rationale of using OS as the primary end point of future phase 3 trials of PD-1 inhibitors and discourage the use of PFS as a sole primary end point as the latter may provide misleading information about the efficacy of these drugs.”

Funders included the Laura and John Arnold Foundation, the Harvard Program in Therapeutic Science, and the Engelberg Foundation. The investigators reported having no relevant conflicts of interest. One coinvestigator reported research support from the Laura and John Arnold Foundation. The other investigators had no conflicts.

SOURCE: Gyawali B et al. JAMA Network Open. 2018 June 22. doi: 10.1001/jamanetworkopen.2018.0416.

Although obesity increases the risk of breast cancer in postmenopausal women, a large multicenter analysis has confirmed the opposite effect in premenopausal women.

The association had “a greater magnitude than previously shown and across the entire distribution of body mass index,” wrote Minouk J. Schoemaker, PhD, of the Institute of Cancer Research in London, with his associates, on behalf of the Premenopausal Breast Cancer Collaborative Group. The protective effect of adiposity was strongest during young adulthood (ages 18-24 years), when it spanned breast cancer subtypes. “Understanding the biological mechanisms underlying these associations could have important preventive potential,” they wrote in JAMA Oncology.

Prior studies have linked greater body fat with reduced risk of breast cancer in younger women, but the effect has not been well characterized. For this analysis, the investigators pooled data from 19 cohort studies that included a total of 758,592 premenopausal women; median age was 40.6 years (interquartile range, 35.2-45.5 years).

For each 5-unit increase in BMI, the estimated reduction in risk of breast cancer was 23% among women aged 18-24 years (hazard ratio, 0.77; 95% confidence interval, 0.73-0.80), 15% in women aged 25-34 years, 13% in women aged 35-44 years, and 12% in women aged 45-54 years. There was no BMI threshold for risk reduction: the inverse correlation existed even when women were not overweight. Risk also did vary significantly among subgroups stratified by other risk factors for breast cancer. Adiposity was more protective against estrogen receptor-positive and progesterone-receptor positive breast cancers and less protective against hormone receptor–negative breast cancers, which “implies a hormonal mechanism,” the investigators said. “Body mass index at ages 25-54 years was not consistently associated with triple-negative or hormone receptor–negative breast cancer overall.”

Funders included Breast Cancer Now, the Institute of Cancer Research, the National Institutes of Health, and many others. The researchers reported having no relevant conflicts of interest.

SOURCE: Schoemaker MJ et al. JAMA Oncol. 2018; Jun 21. doi: 10.1001/jamaoncol.2018.1771.

Although obesity increases the risk of breast cancer in postmenopausal women, a large multicenter analysis has confirmed the opposite effect in premenopausal women.

The association had “a greater magnitude than previously shown and across the entire distribution of body mass index,” wrote Minouk J. Schoemaker, PhD, of the Institute of Cancer Research in London, with his associates, on behalf of the Premenopausal Breast Cancer Collaborative Group. The protective effect of adiposity was strongest during young adulthood (ages 18-24 years), when it spanned breast cancer subtypes. “Understanding the biological mechanisms underlying these associations could have important preventive potential,” they wrote in JAMA Oncology.

Prior studies have linked greater body fat with reduced risk of breast cancer in younger women, but the effect has not been well characterized. For this analysis, the investigators pooled data from 19 cohort studies that included a total of 758,592 premenopausal women; median age was 40.6 years (interquartile range, 35.2-45.5 years).

For each 5-unit increase in BMI, the estimated reduction in risk of breast cancer was 23% among women aged 18-24 years (hazard ratio, 0.77; 95% confidence interval, 0.73-0.80), 15% in women aged 25-34 years, 13% in women aged 35-44 years, and 12% in women aged 45-54 years. There was no BMI threshold for risk reduction: the inverse correlation existed even when women were not overweight. Risk also did vary significantly among subgroups stratified by other risk factors for breast cancer. Adiposity was more protective against estrogen receptor-positive and progesterone-receptor positive breast cancers and less protective against hormone receptor–negative breast cancers, which “implies a hormonal mechanism,” the investigators said. “Body mass index at ages 25-54 years was not consistently associated with triple-negative or hormone receptor–negative breast cancer overall.”

Funders included Breast Cancer Now, the Institute of Cancer Research, the National Institutes of Health, and many others. The researchers reported having no relevant conflicts of interest.

SOURCE: Schoemaker MJ et al. JAMA Oncol. 2018; Jun 21. doi: 10.1001/jamaoncol.2018.1771.

Although obesity increases the risk of breast cancer in postmenopausal women, a large multicenter analysis has confirmed the opposite effect in premenopausal women.

The association had “a greater magnitude than previously shown and across the entire distribution of body mass index,” wrote Minouk J. Schoemaker, PhD, of the Institute of Cancer Research in London, with his associates, on behalf of the Premenopausal Breast Cancer Collaborative Group. The protective effect of adiposity was strongest during young adulthood (ages 18-24 years), when it spanned breast cancer subtypes. “Understanding the biological mechanisms underlying these associations could have important preventive potential,” they wrote in JAMA Oncology.

Prior studies have linked greater body fat with reduced risk of breast cancer in younger women, but the effect has not been well characterized. For this analysis, the investigators pooled data from 19 cohort studies that included a total of 758,592 premenopausal women; median age was 40.6 years (interquartile range, 35.2-45.5 years).

For each 5-unit increase in BMI, the estimated reduction in risk of breast cancer was 23% among women aged 18-24 years (hazard ratio, 0.77; 95% confidence interval, 0.73-0.80), 15% in women aged 25-34 years, 13% in women aged 35-44 years, and 12% in women aged 45-54 years. There was no BMI threshold for risk reduction: the inverse correlation existed even when women were not overweight. Risk also did vary significantly among subgroups stratified by other risk factors for breast cancer. Adiposity was more protective against estrogen receptor-positive and progesterone-receptor positive breast cancers and less protective against hormone receptor–negative breast cancers, which “implies a hormonal mechanism,” the investigators said. “Body mass index at ages 25-54 years was not consistently associated with triple-negative or hormone receptor–negative breast cancer overall.”

Funders included Breast Cancer Now, the Institute of Cancer Research, the National Institutes of Health, and many others. The researchers reported having no relevant conflicts of interest.

SOURCE: Schoemaker MJ et al. JAMA Oncol. 2018; Jun 21. doi: 10.1001/jamaoncol.2018.1771.

Patients with type 2 diabetes were significantly less likely to develop or die from cardiovascular disease when they followed a healthy lifestyle, according to the results of a pooled analysis of two large observational cohort studies.

Relevant criteria included following a high-quality diet, not smoking, exercising moderately to vigorously for at least 2.5 hours per week, and limiting alcohol intake to 5-15 g of alcohol per day for women or 5-30 g/day for men. After the researchers controlled for possible confounders, individuals who met at least three of these criteria had about a 52% lower risk of new-onset CVD (adjusted hazard ratio, 0.48; 95% confidence interval, 0.40-0.59) and a 68% lower risk of CVD-related mortality (HR, 0.32; 95% CI, 0.22-0.47), said Gang Liu, PhD, of Harvard T.H. Chan School of Public Health, Boston, and his associates. “Further research is needed to identify the most effective strategies to encourage patients with diabetes to adopt and maintain a healthy lifestyle,” they wrote. The report was published online June 18 in the Journal of the American College of Cardiology.

Cardiovascular disease is common in type 2 diabetes (T2DM), but few studies have examined the possible mitigating effects of healthy lifestyle. For this study, the researchers analyzed questionnaire data for 11,527 participants with T2DM diagnosed after enrollment in either the Nurses’ Health Study or the Health Professionals Follow-Up Study. Over an average follow-up time of 13.3 years, there were 2,311 incident cases of CVD, including 498 cases of stroke, and 858 deaths from CVD. The reduced risk of cardiovascular events remained significant even after the researchers controlled for factors such as body mass index, hypertension, hypercholesterolemia, use of antihypertensive agents, cholesterol lowering drugs, diabetes medication, and hemoglobin A_1c.

pojoslaw/ThinkStock

Healthy lifestyle also was associated with significant reductions in the individual risk of coronary heart disease (HR, 0.53) and stroke (HR, 0.33), the investigators said. In this population, 40% of the risk of CVD mortality could be attributed to poor adherence to a healthy lifestyle, they added. Importantly, individuals who improved their lifestyle after a T2DM diagnosis had a significantly lower risk of CVD and CVD mortality than those who did not. The findings, they concluded, “support the tremendous benefits of adopting a healthy lifestyle in reducing the subsequent burden of cardiovascular complications in patients with T2DM.”

The National Institutes of Health provided funding. The investigators reported having no relevant conflicts of interest.

SOURCE: Liu G et al. J Am Coll Cardiol. 2018;71:2867-76. doi: 10.1016/j.jacc.2018.04.027.

Patients with type 2 diabetes were significantly less likely to develop or die from cardiovascular disease when they followed a healthy lifestyle, according to the results of a pooled analysis of two large observational cohort studies.

Relevant criteria included following a high-quality diet, not smoking, exercising moderately to vigorously for at least 2.5 hours per week, and limiting alcohol intake to 5-15 g of alcohol per day for women or 5-30 g/day for men. After the researchers controlled for possible confounders, individuals who met at least three of these criteria had about a 52% lower risk of new-onset CVD (adjusted hazard ratio, 0.48; 95% confidence interval, 0.40-0.59) and a 68% lower risk of CVD-related mortality (HR, 0.32; 95% CI, 0.22-0.47), said Gang Liu, PhD, of Harvard T.H. Chan School of Public Health, Boston, and his associates. “Further research is needed to identify the most effective strategies to encourage patients with diabetes to adopt and maintain a healthy lifestyle,” they wrote. The report was published online June 18 in the Journal of the American College of Cardiology.

Cardiovascular disease is common in type 2 diabetes (T2DM), but few studies have examined the possible mitigating effects of healthy lifestyle. For this study, the researchers analyzed questionnaire data for 11,527 participants with T2DM diagnosed after enrollment in either the Nurses’ Health Study or the Health Professionals Follow-Up Study. Over an average follow-up time of 13.3 years, there were 2,311 incident cases of CVD, including 498 cases of stroke, and 858 deaths from CVD. The reduced risk of cardiovascular events remained significant even after the researchers controlled for factors such as body mass index, hypertension, hypercholesterolemia, use of antihypertensive agents, cholesterol lowering drugs, diabetes medication, and hemoglobin A_1c.

pojoslaw/ThinkStock

Healthy lifestyle also was associated with significant reductions in the individual risk of coronary heart disease (HR, 0.53) and stroke (HR, 0.33), the investigators said. In this population, 40% of the risk of CVD mortality could be attributed to poor adherence to a healthy lifestyle, they added. Importantly, individuals who improved their lifestyle after a T2DM diagnosis had a significantly lower risk of CVD and CVD mortality than those who did not. The findings, they concluded, “support the tremendous benefits of adopting a healthy lifestyle in reducing the subsequent burden of cardiovascular complications in patients with T2DM.”

The National Institutes of Health provided funding. The investigators reported having no relevant conflicts of interest.

SOURCE: Liu G et al. J Am Coll Cardiol. 2018;71:2867-76. doi: 10.1016/j.jacc.2018.04.027.

Patients with type 2 diabetes were significantly less likely to develop or die from cardiovascular disease when they followed a healthy lifestyle, according to the results of a pooled analysis of two large observational cohort studies.

Relevant criteria included following a high-quality diet, not smoking, exercising moderately to vigorously for at least 2.5 hours per week, and limiting alcohol intake to 5-15 g of alcohol per day for women or 5-30 g/day for men. After the researchers controlled for possible confounders, individuals who met at least three of these criteria had about a 52% lower risk of new-onset CVD (adjusted hazard ratio, 0.48; 95% confidence interval, 0.40-0.59) and a 68% lower risk of CVD-related mortality (HR, 0.32; 95% CI, 0.22-0.47), said Gang Liu, PhD, of Harvard T.H. Chan School of Public Health, Boston, and his associates. “Further research is needed to identify the most effective strategies to encourage patients with diabetes to adopt and maintain a healthy lifestyle,” they wrote. The report was published online June 18 in the Journal of the American College of Cardiology.

Cardiovascular disease is common in type 2 diabetes (T2DM), but few studies have examined the possible mitigating effects of healthy lifestyle. For this study, the researchers analyzed questionnaire data for 11,527 participants with T2DM diagnosed after enrollment in either the Nurses’ Health Study or the Health Professionals Follow-Up Study. Over an average follow-up time of 13.3 years, there were 2,311 incident cases of CVD, including 498 cases of stroke, and 858 deaths from CVD. The reduced risk of cardiovascular events remained significant even after the researchers controlled for factors such as body mass index, hypertension, hypercholesterolemia, use of antihypertensive agents, cholesterol lowering drugs, diabetes medication, and hemoglobin A_1c.

pojoslaw/ThinkStock

Healthy lifestyle also was associated with significant reductions in the individual risk of coronary heart disease (HR, 0.53) and stroke (HR, 0.33), the investigators said. In this population, 40% of the risk of CVD mortality could be attributed to poor adherence to a healthy lifestyle, they added. Importantly, individuals who improved their lifestyle after a T2DM diagnosis had a significantly lower risk of CVD and CVD mortality than those who did not. The findings, they concluded, “support the tremendous benefits of adopting a healthy lifestyle in reducing the subsequent burden of cardiovascular complications in patients with T2DM.”

The National Institutes of Health provided funding. The investigators reported having no relevant conflicts of interest.

SOURCE: Liu G et al. J Am Coll Cardiol. 2018;71:2867-76. doi: 10.1016/j.jacc.2018.04.027.

The introduction of the new high-sensitivity cardiac troponin T (hs-cTnT) test was linked with an 11% decrease in reinfarctions but showed no evidence of improving survival in a large longitudinal cohort study.

Over an average of 3.9 years of follow-up, the adjusted risk of all-cause mortality was identical whether patients’ initial MI was diagnosed with the new troponin test or the conventional one, reported Maria Odqvist, MD, of South Alvsborg Hospital, Boras, Sweden, and her associates. “As hs-cTn assays become widely available and clinicians gain experience interpreting the results, more work is needed to enhance clinical reasoning and implementation to improve patient outcomes,” the researchers wrote in the Journal of the American College of Cardiology.

High-sensitivity cardiac troponin T assays detect acute coronary syndrome more rapidly than their conventional predecessors. However, hs-cTnT’s higher sensitivity comes with lost specificity and hence has raised concerns about potentially wasting health care resources. Some clinicians have asked whether the new test is worthwhile and how to maximize its benefits.

The study, which included nearly 88,000 patients with initial MI from the Swedish National Patient Registry, spanned 2009-2013, when 73% of Swedish acute care hospitals transitioned from conventional troponin tests (cTn) to hs-cTnT. After adjustment for factors such as age, sex, location, chronic kidney disease, cardiovascular history, and prescriptions, Dr. Odqvist and her associates compared each test types’ risks of death, reinfarction, coronary angiography, and revascularization among patients diagnosed.

In all, 47,133 (54%) patients’ initial MI was diagnosed with cTn while 46% were diagnosed with hs-cTnT. Overall, the rate of MI rose by 5% during the 90 days after hospitals implemented hs-cTnT, compared with the 90 days before. But hospitals used varying hs-cTnT thresholds for MI, which might explain why some hospitals initially observed a marked initial decrease in MI while others saw a relatively large increase, the investigators wrote.

There were 15,766 reinfarctions over an average of 3.1 years of follow-up. Although there was no difference in all-cause mortality, risk of reinfarction was 11% lower among patients diagnosed using hs-cTnT, compared with those diagnosed by cTn.

At the hospital level, coronary angiography and revascularization became only slightly more common during the 3 months after hospitals switched to hs-cTnT, the researchers wrote. However, patients whose MIs were diagnosed with hs-cTnT were 16% more likely to undergo coronary angiography and 13% more likely to undergo revascularization within the next 30 days, compared with patients diagnosed with cTn. Patients diagnosed with hs-cTnT also were more likely to receive statins, but trends in other prescriptions did not change.

The Swedish Heart-Lung Foundation funded one investigator. Dr. Odqvist and one coinvestigator reported having no relevant conflicts of interest. Senior author Martin J. Holzmann, MD, PhD, disclosed ties to Actelion and Pfizer. Two other coinvestigators disclosed ties to Roche, Gilead, Janssen, Abbvie, CTI Bipharma, GlaxoSmithKline, Abbott Laboratories, and AstraZeneca, and Fiomi Diagnostics.

SOURCE: Odqvist M et al. J Am Coll Cardiol. 2018 Jun 12;71(23):2616-24

The introduction of the new high-sensitivity cardiac troponin T (hs-cTnT) test was linked with an 11% decrease in reinfarctions but showed no evidence of improving survival in a large longitudinal cohort study.

Over an average of 3.9 years of follow-up, the adjusted risk of all-cause mortality was identical whether patients’ initial MI was diagnosed with the new troponin test or the conventional one, reported Maria Odqvist, MD, of South Alvsborg Hospital, Boras, Sweden, and her associates. “As hs-cTn assays become widely available and clinicians gain experience interpreting the results, more work is needed to enhance clinical reasoning and implementation to improve patient outcomes,” the researchers wrote in the Journal of the American College of Cardiology.

High-sensitivity cardiac troponin T assays detect acute coronary syndrome more rapidly than their conventional predecessors. However, hs-cTnT’s higher sensitivity comes with lost specificity and hence has raised concerns about potentially wasting health care resources. Some clinicians have asked whether the new test is worthwhile and how to maximize its benefits.

The study, which included nearly 88,000 patients with initial MI from the Swedish National Patient Registry, spanned 2009-2013, when 73% of Swedish acute care hospitals transitioned from conventional troponin tests (cTn) to hs-cTnT. After adjustment for factors such as age, sex, location, chronic kidney disease, cardiovascular history, and prescriptions, Dr. Odqvist and her associates compared each test types’ risks of death, reinfarction, coronary angiography, and revascularization among patients diagnosed.

In all, 47,133 (54%) patients’ initial MI was diagnosed with cTn while 46% were diagnosed with hs-cTnT. Overall, the rate of MI rose by 5% during the 90 days after hospitals implemented hs-cTnT, compared with the 90 days before. But hospitals used varying hs-cTnT thresholds for MI, which might explain why some hospitals initially observed a marked initial decrease in MI while others saw a relatively large increase, the investigators wrote.

There were 15,766 reinfarctions over an average of 3.1 years of follow-up. Although there was no difference in all-cause mortality, risk of reinfarction was 11% lower among patients diagnosed using hs-cTnT, compared with those diagnosed by cTn.

At the hospital level, coronary angiography and revascularization became only slightly more common during the 3 months after hospitals switched to hs-cTnT, the researchers wrote. However, patients whose MIs were diagnosed with hs-cTnT were 16% more likely to undergo coronary angiography and 13% more likely to undergo revascularization within the next 30 days, compared with patients diagnosed with cTn. Patients diagnosed with hs-cTnT also were more likely to receive statins, but trends in other prescriptions did not change.

The Swedish Heart-Lung Foundation funded one investigator. Dr. Odqvist and one coinvestigator reported having no relevant conflicts of interest. Senior author Martin J. Holzmann, MD, PhD, disclosed ties to Actelion and Pfizer. Two other coinvestigators disclosed ties to Roche, Gilead, Janssen, Abbvie, CTI Bipharma, GlaxoSmithKline, Abbott Laboratories, and AstraZeneca, and Fiomi Diagnostics.

SOURCE: Odqvist M et al. J Am Coll Cardiol. 2018 Jun 12;71(23):2616-24

The introduction of the new high-sensitivity cardiac troponin T (hs-cTnT) test was linked with an 11% decrease in reinfarctions but showed no evidence of improving survival in a large longitudinal cohort study.

Over an average of 3.9 years of follow-up, the adjusted risk of all-cause mortality was identical whether patients’ initial MI was diagnosed with the new troponin test or the conventional one, reported Maria Odqvist, MD, of South Alvsborg Hospital, Boras, Sweden, and her associates. “As hs-cTn assays become widely available and clinicians gain experience interpreting the results, more work is needed to enhance clinical reasoning and implementation to improve patient outcomes,” the researchers wrote in the Journal of the American College of Cardiology.

High-sensitivity cardiac troponin T assays detect acute coronary syndrome more rapidly than their conventional predecessors. However, hs-cTnT’s higher sensitivity comes with lost specificity and hence has raised concerns about potentially wasting health care resources. Some clinicians have asked whether the new test is worthwhile and how to maximize its benefits.

The study, which included nearly 88,000 patients with initial MI from the Swedish National Patient Registry, spanned 2009-2013, when 73% of Swedish acute care hospitals transitioned from conventional troponin tests (cTn) to hs-cTnT. After adjustment for factors such as age, sex, location, chronic kidney disease, cardiovascular history, and prescriptions, Dr. Odqvist and her associates compared each test types’ risks of death, reinfarction, coronary angiography, and revascularization among patients diagnosed.

In all, 47,133 (54%) patients’ initial MI was diagnosed with cTn while 46% were diagnosed with hs-cTnT. Overall, the rate of MI rose by 5% during the 90 days after hospitals implemented hs-cTnT, compared with the 90 days before. But hospitals used varying hs-cTnT thresholds for MI, which might explain why some hospitals initially observed a marked initial decrease in MI while others saw a relatively large increase, the investigators wrote.

There were 15,766 reinfarctions over an average of 3.1 years of follow-up. Although there was no difference in all-cause mortality, risk of reinfarction was 11% lower among patients diagnosed using hs-cTnT, compared with those diagnosed by cTn.

At the hospital level, coronary angiography and revascularization became only slightly more common during the 3 months after hospitals switched to hs-cTnT, the researchers wrote. However, patients whose MIs were diagnosed with hs-cTnT were 16% more likely to undergo coronary angiography and 13% more likely to undergo revascularization within the next 30 days, compared with patients diagnosed with cTn. Patients diagnosed with hs-cTnT also were more likely to receive statins, but trends in other prescriptions did not change.

The Swedish Heart-Lung Foundation funded one investigator. Dr. Odqvist and one coinvestigator reported having no relevant conflicts of interest. Senior author Martin J. Holzmann, MD, PhD, disclosed ties to Actelion and Pfizer. Two other coinvestigators disclosed ties to Roche, Gilead, Janssen, Abbvie, CTI Bipharma, GlaxoSmithKline, Abbott Laboratories, and AstraZeneca, and Fiomi Diagnostics.

SOURCE: Odqvist M et al. J Am Coll Cardiol. 2018 Jun 12;71(23):2616-24

EULAR 2018’s scientific program in Amsterdam is packed with lectures, clinical and basic science symposia, workshops, and special interest sessions covering the full spectrum of rheumatic diseases, said Dr. Robert Landewé, chair of the Scientific Program Committee.

“More than 5,000 scientific abstracts were submitted, which is an absolute, all-time record,” Dr. Landewé said. Four experts scored each abstract, and only the top 7% were invited for oral presentation during abstract sessions or symposia, he explained in an interview.

Wednesday, June 13

A high point of the 2018 scientific program is Wednesday’s opening plenary session, which will feature abstracts that were handpicked by Dr. Landewé and Dr. Thomas Dörner, professor of rheumatology at Charite Universitätsmedizin, Berlin. “This session includes highly scored abstracts, including late-breakers, on current advances in therapeutics and disease classification,” said Dr. Dörner, who chaired this year’s Abstract Selection Committee.

The plenary abstract session will cover new findings on gout and cardiovascular disease from CANTOS (Canakinumab Anti-inflammatory Thrombosis Outcome Study), long-term mortality in patients with early RA from the COBRA (Combinatietherapie Bij Reumatoide Artritis) study, the use of zoledronic acid to treat knee osteoarthritis with bone lesions, and the relationship between bisphosphonate drug holidays and hip fracture risk. Researchers also will discuss baricitinib in systemic lupus erythematosus (SLE), the value of MRI when treating remitted RA to target, the validation of SLE classification criteria, and draft classification criteria for ANCA-associated vasculitides.

A notable clinical science session on Wednesday will cover cancer and inflammation, Dr. Landewé said. “This is a topic of increasing interest because cancer and inflammation share mutual pathways.”

Novel cancer therapies such as immune checkpoint inhibitors have improved outcomes across a range of tumor types, but also can induce rheumatic disease, he added. Accordingly, presenters will discuss inflammation as “friend” versus “foe” in cancer treatment, the role of tumor necrosis factor in cancer, and risk of malignancy among patients with RA.

Thursday, June 14

Topics in this session will include the use of estrogens and other hormonal therapies in patients with rheumatic disease, registry studies of rheumatologic conditions during pregnancy, and how clinicians can best discuss sexual concerns with their rheumatology patients.

Friday, June 15

For the first time, the scientific program also will include a clinical science session held jointly with the European Society of Musculoskeletal Radiology (ESSR). Dr. Joachim Sieper of Germany and ESSR President Dr. Monique Reijnierse of the Netherlands will cochair the Friday afternoon session on the role of MRI in rheumatology. Attendees from both organizations will learn when to use MRI in early and established RA and spondyloarthritis, and how to interpret the results, with abundant time built in for questions and answers. Dr. Landewé called the joint session “a test case” for exciting web-based interactions between EULAR and ESSR.

Another clinical science session on Friday afternoon will dive into the diagnosis of spondyloarthritis, which Dr. Landewé called “a matter of recognizing patterns, not ticking boxes on a list of criteria. This symposium leads you through the art of pattern recognition.”

Later on Friday afternoon, a session will explore advances in biologic therapy of small-vessel vasculitis, he added. “Biologic disease-modifying antirheumatic drugs [bDMARDs] are becoming more and more important in this area of expanding interest.” Experts will address complement inhibition in ANCA-associated vasculitis (AAV), the use of induction and maintenance rituximab in AAV, the evolving role of mepolizumab in eosinophilic granulomatosis with polyangiitis, survival in AAV, and the use of rituximab for treating children with granulomatosis with polyangiitis and microscopic polyangiitis.

Saturday, June 16

On Saturday, a bench-to-bedside session will cover gout and kidney function. “This is an area with important new insights,” Dr. Dörner said. Presenters will discuss the genetics of hyperuricemia, renal urate transporters, and the pros and cons of using xanthine oxidase inhibitors to treat chronic kidney disease. Researchers will also cover studies of impaired neutrophil chemotaxis in patients with chronic kidney disease and hyperuricemia, and the relationship between renal medullar hyperechogenicity and gout severity.

Also on Saturday, a clinical science session titled, “Rheumatoid arthritis: Is it all in your head?” will explore emerging data on the relationship between inflammation and depression. Patients with RA often face both clinical depression and social isolation, and these complex psychosocial conditions can worsen one another. “In addition to proper drug choice, treating RA effectively depends on how concomitant problems, such as nonspecific pain, depression, and social isolation, are coped with in a broad context,” Dr. Landewé said. “When it comes to optimal management, rheumatologists need to communicate and prescribe, not just prescribe.”

Christian Apfelbacher, PhD, of Germany will discuss prevention and treatment strategies and Dr. Jonathan Cavanagh of the United Kingdom will cover neuroimaging in RA. Researchers also will discuss new findings on pain, depression, and anxiety in patients recently diagnosed with RA.

Also on Saturday, a special session will cover EULAR’s initiatives to improve clinical approaches (ESSCA), Dr. Dörner noted. This effort has produced new or updated recommendations on topics such as vaccination, Sjögren’s syndrome, glucocorticoid therapy, and management of hand osteoarthritis, he said. “These recommendations follow a number of others and are expected to impact clinical science as well as clinical practice.”

EULAR 2018’s scientific program in Amsterdam is packed with lectures, clinical and basic science symposia, workshops, and special interest sessions covering the full spectrum of rheumatic diseases, said Dr. Robert Landewé, chair of the Scientific Program Committee.

“More than 5,000 scientific abstracts were submitted, which is an absolute, all-time record,” Dr. Landewé said. Four experts scored each abstract, and only the top 7% were invited for oral presentation during abstract sessions or symposia, he explained in an interview.

Wednesday, June 13

A high point of the 2018 scientific program is Wednesday’s opening plenary session, which will feature abstracts that were handpicked by Dr. Landewé and Dr. Thomas Dörner, professor of rheumatology at Charite Universitätsmedizin, Berlin. “This session includes highly scored abstracts, including late-breakers, on current advances in therapeutics and disease classification,” said Dr. Dörner, who chaired this year’s Abstract Selection Committee.

The plenary abstract session will cover new findings on gout and cardiovascular disease from CANTOS (Canakinumab Anti-inflammatory Thrombosis Outcome Study), long-term mortality in patients with early RA from the COBRA (Combinatietherapie Bij Reumatoide Artritis) study, the use of zoledronic acid to treat knee osteoarthritis with bone lesions, and the relationship between bisphosphonate drug holidays and hip fracture risk. Researchers also will discuss baricitinib in systemic lupus erythematosus (SLE), the value of MRI when treating remitted RA to target, the validation of SLE classification criteria, and draft classification criteria for ANCA-associated vasculitides.

A notable clinical science session on Wednesday will cover cancer and inflammation, Dr. Landewé said. “This is a topic of increasing interest because cancer and inflammation share mutual pathways.”

Novel cancer therapies such as immune checkpoint inhibitors have improved outcomes across a range of tumor types, but also can induce rheumatic disease, he added. Accordingly, presenters will discuss inflammation as “friend” versus “foe” in cancer treatment, the role of tumor necrosis factor in cancer, and risk of malignancy among patients with RA.

Thursday, June 14

Topics in this session will include the use of estrogens and other hormonal therapies in patients with rheumatic disease, registry studies of rheumatologic conditions during pregnancy, and how clinicians can best discuss sexual concerns with their rheumatology patients.

Friday, June 15

For the first time, the scientific program also will include a clinical science session held jointly with the European Society of Musculoskeletal Radiology (ESSR). Dr. Joachim Sieper of Germany and ESSR President Dr. Monique Reijnierse of the Netherlands will cochair the Friday afternoon session on the role of MRI in rheumatology. Attendees from both organizations will learn when to use MRI in early and established RA and spondyloarthritis, and how to interpret the results, with abundant time built in for questions and answers. Dr. Landewé called the joint session “a test case” for exciting web-based interactions between EULAR and ESSR.

Another clinical science session on Friday afternoon will dive into the diagnosis of spondyloarthritis, which Dr. Landewé called “a matter of recognizing patterns, not ticking boxes on a list of criteria. This symposium leads you through the art of pattern recognition.”

Later on Friday afternoon, a session will explore advances in biologic therapy of small-vessel vasculitis, he added. “Biologic disease-modifying antirheumatic drugs [bDMARDs] are becoming more and more important in this area of expanding interest.” Experts will address complement inhibition in ANCA-associated vasculitis (AAV), the use of induction and maintenance rituximab in AAV, the evolving role of mepolizumab in eosinophilic granulomatosis with polyangiitis, survival in AAV, and the use of rituximab for treating children with granulomatosis with polyangiitis and microscopic polyangiitis.

Saturday, June 16

On Saturday, a bench-to-bedside session will cover gout and kidney function. “This is an area with important new insights,” Dr. Dörner said. Presenters will discuss the genetics of hyperuricemia, renal urate transporters, and the pros and cons of using xanthine oxidase inhibitors to treat chronic kidney disease. Researchers will also cover studies of impaired neutrophil chemotaxis in patients with chronic kidney disease and hyperuricemia, and the relationship between renal medullar hyperechogenicity and gout severity.

Also on Saturday, a clinical science session titled, “Rheumatoid arthritis: Is it all in your head?” will explore emerging data on the relationship between inflammation and depression. Patients with RA often face both clinical depression and social isolation, and these complex psychosocial conditions can worsen one another. “In addition to proper drug choice, treating RA effectively depends on how concomitant problems, such as nonspecific pain, depression, and social isolation, are coped with in a broad context,” Dr. Landewé said. “When it comes to optimal management, rheumatologists need to communicate and prescribe, not just prescribe.”

Christian Apfelbacher, PhD, of Germany will discuss prevention and treatment strategies and Dr. Jonathan Cavanagh of the United Kingdom will cover neuroimaging in RA. Researchers also will discuss new findings on pain, depression, and anxiety in patients recently diagnosed with RA.

Also on Saturday, a special session will cover EULAR’s initiatives to improve clinical approaches (ESSCA), Dr. Dörner noted. This effort has produced new or updated recommendations on topics such as vaccination, Sjögren’s syndrome, glucocorticoid therapy, and management of hand osteoarthritis, he said. “These recommendations follow a number of others and are expected to impact clinical science as well as clinical practice.”

EULAR 2018’s scientific program in Amsterdam is packed with lectures, clinical and basic science symposia, workshops, and special interest sessions covering the full spectrum of rheumatic diseases, said Dr. Robert Landewé, chair of the Scientific Program Committee.

“More than 5,000 scientific abstracts were submitted, which is an absolute, all-time record,” Dr. Landewé said. Four experts scored each abstract, and only the top 7% were invited for oral presentation during abstract sessions or symposia, he explained in an interview.

Wednesday, June 13

A high point of the 2018 scientific program is Wednesday’s opening plenary session, which will feature abstracts that were handpicked by Dr. Landewé and Dr. Thomas Dörner, professor of rheumatology at Charite Universitätsmedizin, Berlin. “This session includes highly scored abstracts, including late-breakers, on current advances in therapeutics and disease classification,” said Dr. Dörner, who chaired this year’s Abstract Selection Committee.

The plenary abstract session will cover new findings on gout and cardiovascular disease from CANTOS (Canakinumab Anti-inflammatory Thrombosis Outcome Study), long-term mortality in patients with early RA from the COBRA (Combinatietherapie Bij Reumatoide Artritis) study, the use of zoledronic acid to treat knee osteoarthritis with bone lesions, and the relationship between bisphosphonate drug holidays and hip fracture risk. Researchers also will discuss baricitinib in systemic lupus erythematosus (SLE), the value of MRI when treating remitted RA to target, the validation of SLE classification criteria, and draft classification criteria for ANCA-associated vasculitides.

A notable clinical science session on Wednesday will cover cancer and inflammation, Dr. Landewé said. “This is a topic of increasing interest because cancer and inflammation share mutual pathways.”

Novel cancer therapies such as immune checkpoint inhibitors have improved outcomes across a range of tumor types, but also can induce rheumatic disease, he added. Accordingly, presenters will discuss inflammation as “friend” versus “foe” in cancer treatment, the role of tumor necrosis factor in cancer, and risk of malignancy among patients with RA.

Thursday, June 14

Topics in this session will include the use of estrogens and other hormonal therapies in patients with rheumatic disease, registry studies of rheumatologic conditions during pregnancy, and how clinicians can best discuss sexual concerns with their rheumatology patients.

Friday, June 15

For the first time, the scientific program also will include a clinical science session held jointly with the European Society of Musculoskeletal Radiology (ESSR). Dr. Joachim Sieper of Germany and ESSR President Dr. Monique Reijnierse of the Netherlands will cochair the Friday afternoon session on the role of MRI in rheumatology. Attendees from both organizations will learn when to use MRI in early and established RA and spondyloarthritis, and how to interpret the results, with abundant time built in for questions and answers. Dr. Landewé called the joint session “a test case” for exciting web-based interactions between EULAR and ESSR.

Another clinical science session on Friday afternoon will dive into the diagnosis of spondyloarthritis, which Dr. Landewé called “a matter of recognizing patterns, not ticking boxes on a list of criteria. This symposium leads you through the art of pattern recognition.”

Later on Friday afternoon, a session will explore advances in biologic therapy of small-vessel vasculitis, he added. “Biologic disease-modifying antirheumatic drugs [bDMARDs] are becoming more and more important in this area of expanding interest.” Experts will address complement inhibition in ANCA-associated vasculitis (AAV), the use of induction and maintenance rituximab in AAV, the evolving role of mepolizumab in eosinophilic granulomatosis with polyangiitis, survival in AAV, and the use of rituximab for treating children with granulomatosis with polyangiitis and microscopic polyangiitis.

Saturday, June 16

On Saturday, a bench-to-bedside session will cover gout and kidney function. “This is an area with important new insights,” Dr. Dörner said. Presenters will discuss the genetics of hyperuricemia, renal urate transporters, and the pros and cons of using xanthine oxidase inhibitors to treat chronic kidney disease. Researchers will also cover studies of impaired neutrophil chemotaxis in patients with chronic kidney disease and hyperuricemia, and the relationship between renal medullar hyperechogenicity and gout severity.

Also on Saturday, a clinical science session titled, “Rheumatoid arthritis: Is it all in your head?” will explore emerging data on the relationship between inflammation and depression. Patients with RA often face both clinical depression and social isolation, and these complex psychosocial conditions can worsen one another. “In addition to proper drug choice, treating RA effectively depends on how concomitant problems, such as nonspecific pain, depression, and social isolation, are coped with in a broad context,” Dr. Landewé said. “When it comes to optimal management, rheumatologists need to communicate and prescribe, not just prescribe.”

Christian Apfelbacher, PhD, of Germany will discuss prevention and treatment strategies and Dr. Jonathan Cavanagh of the United Kingdom will cover neuroimaging in RA. Researchers also will discuss new findings on pain, depression, and anxiety in patients recently diagnosed with RA.

Also on Saturday, a special session will cover EULAR’s initiatives to improve clinical approaches (ESSCA), Dr. Dörner noted. This effort has produced new or updated recommendations on topics such as vaccination, Sjögren’s syndrome, glucocorticoid therapy, and management of hand osteoarthritis, he said. “These recommendations follow a number of others and are expected to impact clinical science as well as clinical practice.”

Personalized medicine, big data, and monogenic inflammatory diseases are just a few of the high points of pediatric rheumatology sessions at this year’s EULAR Congress.

EULAR Standing Committee Chairperson for Paediatric Rheumatology Berent J. Prakken, MD, PhD, said that a bench-to-bedside session on Wednesday afternoon would highlight how EULAR projects are driving advances in pediatric rheumatology.

Attendees will learn from Vicki Seyfert-Margolis, PhD, an internationally recognized expert in personalized medicine, about how digital tools can facilitate cross-border partnerships in pediatric rheumatology, Dr. Prakken said in an interview.

“This talk will be groundbreaking because it’s not just about another useful app,” said Dr. Prakken, professor of pediatric rheumatology and vice dean of education at University Medical Center Utrecht (the Netherlands). “Dr. Seyfert-Margolis will show how the digital revolution will change the way we communicate with patients, monitor disease, and develop novel models for clinical trials.”

The session will also cover work by the Understanding Childhood Arthritis Network (UCAN), created to facilitate international translational research in pediatric rheumatology. Speakers will describe how UCAN is helping to spur personalized medicine and working with the Pediatric Rheumatology International Trials Organization (PRINTO) to align bench and bedside perspectives.

Another program highlight is a Thursday afternoon session on connections between monogenic autoinflammatory and pediatric rheumatic diseases. “Groundbreaking studies of these rare genetic inflammatory diseases have provided important new insights that, in turn, have led to new therapeutic options,” said Dr. Prakken.

Personalized medicine, big data, and monogenic inflammatory diseases are just a few of the high points of pediatric rheumatology sessions at this year’s EULAR Congress.

EULAR Standing Committee Chairperson for Paediatric Rheumatology Berent J. Prakken, MD, PhD, said that a bench-to-bedside session on Wednesday afternoon would highlight how EULAR projects are driving advances in pediatric rheumatology.

Attendees will learn from Vicki Seyfert-Margolis, PhD, an internationally recognized expert in personalized medicine, about how digital tools can facilitate cross-border partnerships in pediatric rheumatology, Dr. Prakken said in an interview.

“This talk will be groundbreaking because it’s not just about another useful app,” said Dr. Prakken, professor of pediatric rheumatology and vice dean of education at University Medical Center Utrecht (the Netherlands). “Dr. Seyfert-Margolis will show how the digital revolution will change the way we communicate with patients, monitor disease, and develop novel models for clinical trials.”

The session will also cover work by the Understanding Childhood Arthritis Network (UCAN), created to facilitate international translational research in pediatric rheumatology. Speakers will describe how UCAN is helping to spur personalized medicine and working with the Pediatric Rheumatology International Trials Organization (PRINTO) to align bench and bedside perspectives.

Another program highlight is a Thursday afternoon session on connections between monogenic autoinflammatory and pediatric rheumatic diseases. “Groundbreaking studies of these rare genetic inflammatory diseases have provided important new insights that, in turn, have led to new therapeutic options,” said Dr. Prakken.

Personalized medicine, big data, and monogenic inflammatory diseases are just a few of the high points of pediatric rheumatology sessions at this year’s EULAR Congress.

EULAR Standing Committee Chairperson for Paediatric Rheumatology Berent J. Prakken, MD, PhD, said that a bench-to-bedside session on Wednesday afternoon would highlight how EULAR projects are driving advances in pediatric rheumatology.

Attendees will learn from Vicki Seyfert-Margolis, PhD, an internationally recognized expert in personalized medicine, about how digital tools can facilitate cross-border partnerships in pediatric rheumatology, Dr. Prakken said in an interview.

“This talk will be groundbreaking because it’s not just about another useful app,” said Dr. Prakken, professor of pediatric rheumatology and vice dean of education at University Medical Center Utrecht (the Netherlands). “Dr. Seyfert-Margolis will show how the digital revolution will change the way we communicate with patients, monitor disease, and develop novel models for clinical trials.”

The session will also cover work by the Understanding Childhood Arthritis Network (UCAN), created to facilitate international translational research in pediatric rheumatology. Speakers will describe how UCAN is helping to spur personalized medicine and working with the Pediatric Rheumatology International Trials Organization (PRINTO) to align bench and bedside perspectives.

Another program highlight is a Thursday afternoon session on connections between monogenic autoinflammatory and pediatric rheumatic diseases. “Groundbreaking studies of these rare genetic inflammatory diseases have provided important new insights that, in turn, have led to new therapeutic options,” said Dr. Prakken.

As the largest network of young rheumatologists in the world, the Emerging EULAR Network (EMEUNET) is looking forward to this year’s European Congress of Rheumatology to continue to build on what it set out to do as part of its mission – to give young rheumatologists and researchers an active say in education and research.

The rationale for the birth of EMEUNET in 2009 was to provide a network where European young rheumatologists and researchers, no matter where they were based, could access mentoring programs, research funding, and education initiatives, Alessia Alunno, MD, PhD, chair-elect and EMEUNET steering committee member, said in an interview.

As the largest network of young rheumatologists in the world, the Emerging EULAR Network (EMEUNET) is looking forward to this year’s European Congress of Rheumatology to continue to build on what it set out to do as part of its mission – to give young rheumatologists and researchers an active say in education and research.

The rationale for the birth of EMEUNET in 2009 was to provide a network where European young rheumatologists and researchers, no matter where they were based, could access mentoring programs, research funding, and education initiatives, Alessia Alunno, MD, PhD, chair-elect and EMEUNET steering committee member, said in an interview.

As the largest network of young rheumatologists in the world, the Emerging EULAR Network (EMEUNET) is looking forward to this year’s European Congress of Rheumatology to continue to build on what it set out to do as part of its mission – to give young rheumatologists and researchers an active say in education and research.

The rationale for the birth of EMEUNET in 2009 was to provide a network where European young rheumatologists and researchers, no matter where they were based, could access mentoring programs, research funding, and education initiatives, Alessia Alunno, MD, PhD, chair-elect and EMEUNET steering committee member, said in an interview.

Middle-aged and older adults who closely followed a Mediterranean-style diet for 6 years were at significantly lower risk of developing fatty liver disease than others in a large prospective study.

Each 1-standard-deviation rise in Mediterranean-style Diet Score (MDS) correlated with significantly decreased hepatic fat accumulation and a 26% lower odds of new onset fatty liver disease (P = .002). “To our knowledge, ours is the first prospective study to examine the relations of long-term habitual diet to fatty liver,” Jiantao Ma, MBBS, PhD, and his associates wrote in Gastroenterology. “Our findings indicate that improved diet quality may be particularly important for those with high genetic risk for NAFLD.”

Lisovskaya/ThinkStock

SOURCE: Ma J, et al. Gastroenterology. 2018 Mar 28. doi: 10.1053/j.gastro.2018.03.038

Middle-aged and older adults who closely followed a Mediterranean-style diet for 6 years were at significantly lower risk of developing fatty liver disease than others in a large prospective study.

Each 1-standard-deviation rise in Mediterranean-style Diet Score (MDS) correlated with significantly decreased hepatic fat accumulation and a 26% lower odds of new onset fatty liver disease (P = .002). “To our knowledge, ours is the first prospective study to examine the relations of long-term habitual diet to fatty liver,” Jiantao Ma, MBBS, PhD, and his associates wrote in Gastroenterology. “Our findings indicate that improved diet quality may be particularly important for those with high genetic risk for NAFLD.”

Lisovskaya/ThinkStock

SOURCE: Ma J, et al. Gastroenterology. 2018 Mar 28. doi: 10.1053/j.gastro.2018.03.038

Middle-aged and older adults who closely followed a Mediterranean-style diet for 6 years were at significantly lower risk of developing fatty liver disease than others in a large prospective study.

Each 1-standard-deviation rise in Mediterranean-style Diet Score (MDS) correlated with significantly decreased hepatic fat accumulation and a 26% lower odds of new onset fatty liver disease (P = .002). “To our knowledge, ours is the first prospective study to examine the relations of long-term habitual diet to fatty liver,” Jiantao Ma, MBBS, PhD, and his associates wrote in Gastroenterology. “Our findings indicate that improved diet quality may be particularly important for those with high genetic risk for NAFLD.”

Lisovskaya/ThinkStock

SOURCE: Ma J, et al. Gastroenterology. 2018 Mar 28. doi: 10.1053/j.gastro.2018.03.038

A new scoring system predicted which patients with decompensated cirrhosis caused by hepatitis C virus (HCV) infection were most likely to experience meaningful benefits from direct-acting antiviral (DAA) therapy.

Dubbed BEA3, their scoring system assigns one point each for body mass index under 25 kg/m², absence of encephalopathy, absence of ascites, ALT more than 1.5 times the upper limit of normal, and albumin above 3.5 g/dL. Patients who scored 4 or 5 were more than 50 times more likely to improve to Child-Pugh Turcotte (CPT) class A (compensated) cirrhosis with DAA therapy than were patients who scored 0 (hazard ratio, 52.3; 95% confidence interval, 15.2-179.7; P less than .001), wrote Omar El-Sherif, MB, BCh, of St. James’s Hospital, Dublin, together with his associates in the June issue of Gastroenterology.

Eradicating HCV does not necessarily improve the odds of transplant-free survival in the setting of decompensated cirrhosis, the researchers noted. Patients can end up in “MELD [Model for End-Stage Liver Disease] purgatory,” meaning they are still decompensated despite achieving sustained virologic response and improved MELD scores. Such patients can face longer waits for liver transplantation than if they had foregone DAA therapy. “There is an urgent need for data to refine our understanding of the reversibility of hepatic decompensation with viral eradication, and, ultimately, define the “point of no return,” the degree of liver dysfunction at which HCV therapy does not yield any meaningful clinical benefit, the researchers wrote.

Their study included 622 patients from the SOLAR-1, SOLAR-2, ASTRAL-4, and GS-US-334-0125 trials, which evaluated interferon-free sofosbuvir-based DAA therapy in patients with chronic hepatitis C virus infection and advanced liver disease. Patients received 12 or 24 weeks of therapy with ledipasvir, sofosbuvir, and ribavirin or velpatasvir, sofosbuvir, and/or ribavirin, or 48 weeks of treatment with sofosbuvir and ribavirin.

A total of 32% of patients with CPT class B cirrhosis improved to class A, as did 12% of patients with class C cirrhosis. Each factor in the scoring system independently affected the chances of reaching CPT class A cirrhosis, even after accounting for SVR.

Notably, patients with intermediate BEA3 scores of 1, 2, or 3 were significantly more likely to reach CPT class A cirrhosis than were patients with scores of 0, with hazard ratios ranging from 4.2 (for a score of 1) to 21.2 (for a score of 3). Most patients had scores of 0 (106 individuals), 1 (219 individuals), or 2 (180 individuals), and only 23 patients scored a 4 or a 5.

CPT score reflects prothrombin time, serum albumin and bilirubin, and the presence or severity of ascites. The investigators called the new scoring system “a tool that can enhance shared decision making at the point of care, quantifying the potential benefits of DAA therapy for patients with decompensated cirrhosis in the pretransplant setting.”Dr. El-Sherif disclosed ties to Gilead Sciences, Bristol-Myers Squibb, and the Health Research Board of Ireland. Four coinvestigators disclosed employment with Gilead, and several other coinvestigators disclosed ties to Gilead, BMS, AbbVie, and other companies.
 

SOURCE: El-Sherif O et al. Gastroenterology. 2018 Mar 10. doi: 10.1053/j.gastro.2018.03.022.

A new scoring system predicted which patients with decompensated cirrhosis caused by hepatitis C virus (HCV) infection were most likely to experience meaningful benefits from direct-acting antiviral (DAA) therapy.

Dubbed BEA3, their scoring system assigns one point each for body mass index under 25 kg/m², absence of encephalopathy, absence of ascites, ALT more than 1.5 times the upper limit of normal, and albumin above 3.5 g/dL. Patients who scored 4 or 5 were more than 50 times more likely to improve to Child-Pugh Turcotte (CPT) class A (compensated) cirrhosis with DAA therapy than were patients who scored 0 (hazard ratio, 52.3; 95% confidence interval, 15.2-179.7; P less than .001), wrote Omar El-Sherif, MB, BCh, of St. James’s Hospital, Dublin, together with his associates in the June issue of Gastroenterology.

Eradicating HCV does not necessarily improve the odds of transplant-free survival in the setting of decompensated cirrhosis, the researchers noted. Patients can end up in “MELD [Model for End-Stage Liver Disease] purgatory,” meaning they are still decompensated despite achieving sustained virologic response and improved MELD scores. Such patients can face longer waits for liver transplantation than if they had foregone DAA therapy. “There is an urgent need for data to refine our understanding of the reversibility of hepatic decompensation with viral eradication, and, ultimately, define the “point of no return,” the degree of liver dysfunction at which HCV therapy does not yield any meaningful clinical benefit, the researchers wrote.

Their study included 622 patients from the SOLAR-1, SOLAR-2, ASTRAL-4, and GS-US-334-0125 trials, which evaluated interferon-free sofosbuvir-based DAA therapy in patients with chronic hepatitis C virus infection and advanced liver disease. Patients received 12 or 24 weeks of therapy with ledipasvir, sofosbuvir, and ribavirin or velpatasvir, sofosbuvir, and/or ribavirin, or 48 weeks of treatment with sofosbuvir and ribavirin.

A total of 32% of patients with CPT class B cirrhosis improved to class A, as did 12% of patients with class C cirrhosis. Each factor in the scoring system independently affected the chances of reaching CPT class A cirrhosis, even after accounting for SVR.

Notably, patients with intermediate BEA3 scores of 1, 2, or 3 were significantly more likely to reach CPT class A cirrhosis than were patients with scores of 0, with hazard ratios ranging from 4.2 (for a score of 1) to 21.2 (for a score of 3). Most patients had scores of 0 (106 individuals), 1 (219 individuals), or 2 (180 individuals), and only 23 patients scored a 4 or a 5.

CPT score reflects prothrombin time, serum albumin and bilirubin, and the presence or severity of ascites. The investigators called the new scoring system “a tool that can enhance shared decision making at the point of care, quantifying the potential benefits of DAA therapy for patients with decompensated cirrhosis in the pretransplant setting.”Dr. El-Sherif disclosed ties to Gilead Sciences, Bristol-Myers Squibb, and the Health Research Board of Ireland. Four coinvestigators disclosed employment with Gilead, and several other coinvestigators disclosed ties to Gilead, BMS, AbbVie, and other companies.
 

SOURCE: El-Sherif O et al. Gastroenterology. 2018 Mar 10. doi: 10.1053/j.gastro.2018.03.022.

A new scoring system predicted which patients with decompensated cirrhosis caused by hepatitis C virus (HCV) infection were most likely to experience meaningful benefits from direct-acting antiviral (DAA) therapy.

Dubbed BEA3, their scoring system assigns one point each for body mass index under 25 kg/m², absence of encephalopathy, absence of ascites, ALT more than 1.5 times the upper limit of normal, and albumin above 3.5 g/dL. Patients who scored 4 or 5 were more than 50 times more likely to improve to Child-Pugh Turcotte (CPT) class A (compensated) cirrhosis with DAA therapy than were patients who scored 0 (hazard ratio, 52.3; 95% confidence interval, 15.2-179.7; P less than .001), wrote Omar El-Sherif, MB, BCh, of St. James’s Hospital, Dublin, together with his associates in the June issue of Gastroenterology.

Eradicating HCV does not necessarily improve the odds of transplant-free survival in the setting of decompensated cirrhosis, the researchers noted. Patients can end up in “MELD [Model for End-Stage Liver Disease] purgatory,” meaning they are still decompensated despite achieving sustained virologic response and improved MELD scores. Such patients can face longer waits for liver transplantation than if they had foregone DAA therapy. “There is an urgent need for data to refine our understanding of the reversibility of hepatic decompensation with viral eradication, and, ultimately, define the “point of no return,” the degree of liver dysfunction at which HCV therapy does not yield any meaningful clinical benefit, the researchers wrote.

Their study included 622 patients from the SOLAR-1, SOLAR-2, ASTRAL-4, and GS-US-334-0125 trials, which evaluated interferon-free sofosbuvir-based DAA therapy in patients with chronic hepatitis C virus infection and advanced liver disease. Patients received 12 or 24 weeks of therapy with ledipasvir, sofosbuvir, and ribavirin or velpatasvir, sofosbuvir, and/or ribavirin, or 48 weeks of treatment with sofosbuvir and ribavirin.

A total of 32% of patients with CPT class B cirrhosis improved to class A, as did 12% of patients with class C cirrhosis. Each factor in the scoring system independently affected the chances of reaching CPT class A cirrhosis, even after accounting for SVR.

Notably, patients with intermediate BEA3 scores of 1, 2, or 3 were significantly more likely to reach CPT class A cirrhosis than were patients with scores of 0, with hazard ratios ranging from 4.2 (for a score of 1) to 21.2 (for a score of 3). Most patients had scores of 0 (106 individuals), 1 (219 individuals), or 2 (180 individuals), and only 23 patients scored a 4 or a 5.

CPT score reflects prothrombin time, serum albumin and bilirubin, and the presence or severity of ascites. The investigators called the new scoring system “a tool that can enhance shared decision making at the point of care, quantifying the potential benefits of DAA therapy for patients with decompensated cirrhosis in the pretransplant setting.”Dr. El-Sherif disclosed ties to Gilead Sciences, Bristol-Myers Squibb, and the Health Research Board of Ireland. Four coinvestigators disclosed employment with Gilead, and several other coinvestigators disclosed ties to Gilead, BMS, AbbVie, and other companies.
 

SOURCE: El-Sherif O et al. Gastroenterology. 2018 Mar 10. doi: 10.1053/j.gastro.2018.03.022.