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Prolia tops risedronate at 2 years in steroid-induced osteoporosis
AMSTERDAM – Greater increases in bone strength were achieved with denosumab (Prolia) than with risedronate in patients receiving glucocorticoid treatment in a phase 3 trial, suggesting it may prove to be an effective means of preventing osteoporosis in this at-risk population of patients.
At 2 years, the percentage change in bone mineral density (BMD) from baseline with denosumab compared to risedronate in patients initiating steroid treatment was significantly higher (all P values less than .001) at the lumbar spine (6% vs. 2%), total hip (3% vs. 0%), and the femoral neck (1.5% vs. –1%). Similar results were seen in patients who were continuing steroid treatment when they entered the randomized, multicenter, double blind trial.
These data build on the 1-year data that have just been published (Lancet Diabetes Endocrinol. 2018;6[6]:445-54), Willem F. Lems, MD, the presenting study investigator, said at the European Congress of Rheumatology.
“Denosumab continued to increased BMD significantly more then risedronate through 24 months,” said Dr. Lems of VU University Medical Center, Amsterdam. He added that “the treatment differences at all skeletal sites were larger at 24 months than as 12 months.”
The Food and Drug Administration approved an additional indication in May of 2018 for denosumab to treat glucocorticoid-induced osteoporosis in adults at high risk of fracture. The biologic, a monoclonal antibody that targets the RANK ligand, was already approved to treat postmenopausal women with osteoporosis at high fracture risk, to increase bone mass in men with osteoporosis at high fracture risk, and to increase bone mass in women receiving adjuvant aromatase inhibitor therapy for breast cancer and in men receiving androgen deprivation therapy for nonmetastatic prostate cancer.
Secondary osteoporosis is a well known downside of glucocorticoid treatment, and despite there being approved therapies, many patients do not receive such treatment, Dr. Lems noted.
“This 24-month study assessed the safety and efficacy of denosumab versus risedronate in glucocorticoid-treated individuals, in whom guidelines advocate treatment,” Dr. Lems said.
In all, 795 adults who were taking glucocorticoids (7.5 mg prednisone or more daily, or equivalent) were enrolled at 79 sites in Europe, North America, Latin America, and Asia. Patients were subdivided into two populations based on their duration of glucocorticoid use, with 290 designated “glucocorticoid initiating” as they had been treated for less than 3 months, and 505 as “glucocorticoid continuing” as they had been treated for 3 or more months. Within these groups, approximately half were randomized to receive denosumab at a 60-mg subcutaneous dose every 6 months and half to receive risedronate 5 mg orally every day. All participants received calcium and vitamin D supplementation.
Bone turnover markers also declined “significantly more” with denosumab than with risedronate, with the exception of procollagen type 1 N-terminal telopeptide on day 10 and at 2 years and serum C-telopeptide of type 1 collagen at 2 years.
As for safety, a similar percentage of adverse events, including serious adverse events, was seen, Dr. Lems said. So far, he added, “data seem to be reassuring” regarding the risk for serious infections in high-risk subgroups of patients, such as those also taking biologic or immunosuppressant medications. There were no infections reported in patients taking biologics (vs. 12.1% for risedronate) and fewer infections in those taking immunosuppressant or biologic medication (3.6% vs. 6.8%).
Although the study was not powered to look at the rate of fractures between the two treatments, Dr. Lems noted that there was no significant difference in the rates of either new vertebral (4.1% for denosumab; 5.8% risedronate) or clinical (5.8% vs. 6.3%) fractures at 2 years.
“Additional studies are needed to confirm if denosumab is superior to other bisphosphonates for BMD improvement and fracture reduction,” Dr. Lems said. “Denosumab may offer a useful osteoporosis treatment option for patients receiving glucocorticoids,” he concluded.
Amgen sponsored the study. Dr. Lems acknowledged ties to Amgen, Eli Lilly, and Merck: being on the speakers bureau, receiving honoraria for advisory board meetings, and acting as a consultant. All but one other author disclosed ties to Amgen.
SOURCE: Saag KG et al. Ann Rheum Dis. 2018;77(Suppl 2):218. Abstract OP0345.
AMSTERDAM – Greater increases in bone strength were achieved with denosumab (Prolia) than with risedronate in patients receiving glucocorticoid treatment in a phase 3 trial, suggesting it may prove to be an effective means of preventing osteoporosis in this at-risk population of patients.
At 2 years, the percentage change in bone mineral density (BMD) from baseline with denosumab compared to risedronate in patients initiating steroid treatment was significantly higher (all P values less than .001) at the lumbar spine (6% vs. 2%), total hip (3% vs. 0%), and the femoral neck (1.5% vs. –1%). Similar results were seen in patients who were continuing steroid treatment when they entered the randomized, multicenter, double blind trial.
These data build on the 1-year data that have just been published (Lancet Diabetes Endocrinol. 2018;6[6]:445-54), Willem F. Lems, MD, the presenting study investigator, said at the European Congress of Rheumatology.
“Denosumab continued to increased BMD significantly more then risedronate through 24 months,” said Dr. Lems of VU University Medical Center, Amsterdam. He added that “the treatment differences at all skeletal sites were larger at 24 months than as 12 months.”
The Food and Drug Administration approved an additional indication in May of 2018 for denosumab to treat glucocorticoid-induced osteoporosis in adults at high risk of fracture. The biologic, a monoclonal antibody that targets the RANK ligand, was already approved to treat postmenopausal women with osteoporosis at high fracture risk, to increase bone mass in men with osteoporosis at high fracture risk, and to increase bone mass in women receiving adjuvant aromatase inhibitor therapy for breast cancer and in men receiving androgen deprivation therapy for nonmetastatic prostate cancer.
Secondary osteoporosis is a well known downside of glucocorticoid treatment, and despite there being approved therapies, many patients do not receive such treatment, Dr. Lems noted.
“This 24-month study assessed the safety and efficacy of denosumab versus risedronate in glucocorticoid-treated individuals, in whom guidelines advocate treatment,” Dr. Lems said.
In all, 795 adults who were taking glucocorticoids (7.5 mg prednisone or more daily, or equivalent) were enrolled at 79 sites in Europe, North America, Latin America, and Asia. Patients were subdivided into two populations based on their duration of glucocorticoid use, with 290 designated “glucocorticoid initiating” as they had been treated for less than 3 months, and 505 as “glucocorticoid continuing” as they had been treated for 3 or more months. Within these groups, approximately half were randomized to receive denosumab at a 60-mg subcutaneous dose every 6 months and half to receive risedronate 5 mg orally every day. All participants received calcium and vitamin D supplementation.
Bone turnover markers also declined “significantly more” with denosumab than with risedronate, with the exception of procollagen type 1 N-terminal telopeptide on day 10 and at 2 years and serum C-telopeptide of type 1 collagen at 2 years.
As for safety, a similar percentage of adverse events, including serious adverse events, was seen, Dr. Lems said. So far, he added, “data seem to be reassuring” regarding the risk for serious infections in high-risk subgroups of patients, such as those also taking biologic or immunosuppressant medications. There were no infections reported in patients taking biologics (vs. 12.1% for risedronate) and fewer infections in those taking immunosuppressant or biologic medication (3.6% vs. 6.8%).
Although the study was not powered to look at the rate of fractures between the two treatments, Dr. Lems noted that there was no significant difference in the rates of either new vertebral (4.1% for denosumab; 5.8% risedronate) or clinical (5.8% vs. 6.3%) fractures at 2 years.
“Additional studies are needed to confirm if denosumab is superior to other bisphosphonates for BMD improvement and fracture reduction,” Dr. Lems said. “Denosumab may offer a useful osteoporosis treatment option for patients receiving glucocorticoids,” he concluded.
Amgen sponsored the study. Dr. Lems acknowledged ties to Amgen, Eli Lilly, and Merck: being on the speakers bureau, receiving honoraria for advisory board meetings, and acting as a consultant. All but one other author disclosed ties to Amgen.
SOURCE: Saag KG et al. Ann Rheum Dis. 2018;77(Suppl 2):218. Abstract OP0345.
AMSTERDAM – Greater increases in bone strength were achieved with denosumab (Prolia) than with risedronate in patients receiving glucocorticoid treatment in a phase 3 trial, suggesting it may prove to be an effective means of preventing osteoporosis in this at-risk population of patients.
At 2 years, the percentage change in bone mineral density (BMD) from baseline with denosumab compared to risedronate in patients initiating steroid treatment was significantly higher (all P values less than .001) at the lumbar spine (6% vs. 2%), total hip (3% vs. 0%), and the femoral neck (1.5% vs. –1%). Similar results were seen in patients who were continuing steroid treatment when they entered the randomized, multicenter, double blind trial.
These data build on the 1-year data that have just been published (Lancet Diabetes Endocrinol. 2018;6[6]:445-54), Willem F. Lems, MD, the presenting study investigator, said at the European Congress of Rheumatology.
“Denosumab continued to increased BMD significantly more then risedronate through 24 months,” said Dr. Lems of VU University Medical Center, Amsterdam. He added that “the treatment differences at all skeletal sites were larger at 24 months than as 12 months.”
The Food and Drug Administration approved an additional indication in May of 2018 for denosumab to treat glucocorticoid-induced osteoporosis in adults at high risk of fracture. The biologic, a monoclonal antibody that targets the RANK ligand, was already approved to treat postmenopausal women with osteoporosis at high fracture risk, to increase bone mass in men with osteoporosis at high fracture risk, and to increase bone mass in women receiving adjuvant aromatase inhibitor therapy for breast cancer and in men receiving androgen deprivation therapy for nonmetastatic prostate cancer.
Secondary osteoporosis is a well known downside of glucocorticoid treatment, and despite there being approved therapies, many patients do not receive such treatment, Dr. Lems noted.
“This 24-month study assessed the safety and efficacy of denosumab versus risedronate in glucocorticoid-treated individuals, in whom guidelines advocate treatment,” Dr. Lems said.
In all, 795 adults who were taking glucocorticoids (7.5 mg prednisone or more daily, or equivalent) were enrolled at 79 sites in Europe, North America, Latin America, and Asia. Patients were subdivided into two populations based on their duration of glucocorticoid use, with 290 designated “glucocorticoid initiating” as they had been treated for less than 3 months, and 505 as “glucocorticoid continuing” as they had been treated for 3 or more months. Within these groups, approximately half were randomized to receive denosumab at a 60-mg subcutaneous dose every 6 months and half to receive risedronate 5 mg orally every day. All participants received calcium and vitamin D supplementation.
Bone turnover markers also declined “significantly more” with denosumab than with risedronate, with the exception of procollagen type 1 N-terminal telopeptide on day 10 and at 2 years and serum C-telopeptide of type 1 collagen at 2 years.
As for safety, a similar percentage of adverse events, including serious adverse events, was seen, Dr. Lems said. So far, he added, “data seem to be reassuring” regarding the risk for serious infections in high-risk subgroups of patients, such as those also taking biologic or immunosuppressant medications. There were no infections reported in patients taking biologics (vs. 12.1% for risedronate) and fewer infections in those taking immunosuppressant or biologic medication (3.6% vs. 6.8%).
Although the study was not powered to look at the rate of fractures between the two treatments, Dr. Lems noted that there was no significant difference in the rates of either new vertebral (4.1% for denosumab; 5.8% risedronate) or clinical (5.8% vs. 6.3%) fractures at 2 years.
“Additional studies are needed to confirm if denosumab is superior to other bisphosphonates for BMD improvement and fracture reduction,” Dr. Lems said. “Denosumab may offer a useful osteoporosis treatment option for patients receiving glucocorticoids,” he concluded.
Amgen sponsored the study. Dr. Lems acknowledged ties to Amgen, Eli Lilly, and Merck: being on the speakers bureau, receiving honoraria for advisory board meetings, and acting as a consultant. All but one other author disclosed ties to Amgen.
SOURCE: Saag KG et al. Ann Rheum Dis. 2018;77(Suppl 2):218. Abstract OP0345.
REPORTING FROM THE EULAR 2018 CONGRESS
Key clinical point: Denosumab may offer a useful alternative to risedronate in patients at risk for steroid-induced osteoporosis.
Major finding: Treatment differences were greater at 2 years than at 1 year at all skeletal sites assessed.
Study details: A phase 3, randomized, double-blind, active-controlled study to evaluate the efficacy and safety of denosumab versus risedronate in 795 glucocorticoid-treated individuals.
Disclosures: Amgen sponsored the study. Dr. Lems acknowledged ties to Amgen, Eli Lilly, and Merck: being on the speakers bureau, receiving honoraria for advisory board meetings, and acting as a consultant. All but one other author disclosed ties to Amgen.
Source: Saag KG et al. Ann Rheum Dis. 2018;77(Suppl 2):218. Abstract OP0345.
Bisphosphonate ‘holidays’ exceeding 2 years linked to increased fractures
AMSTERDAM – Older women on bisphosphonate treatment for at least 3 years who then stopped taking the drug showed a 40% increased risk for hip fracture after they were off the bisphosphonate for more than 2 years, compared with women who never stopped using the drug, according to an analysis of more than 150,000 women in a Medicare database.
The implication of this observational-data finding is that drug holidays from a bisphosphonate regimen “may not be appropriate for all patients,” Kenneth G. Saag, MD, said at the European Congress of Rheumatology.
The finding seems to dispute a recent recommendation from the American College of Physicians (Ann Intern Med. 2017 June 6;166[11]:818-39) that drug treatment to prevent bone fractures in osteoporotic women should stop after 5 years, noted Dr. Saag, a rheumatologist and professor of medicine at the University of Alabama, Birmingham. The median duration of bisphosphonate treatment in the studied cohort before the drug use stopped was 5.5 years.
“Drug holidays [from a bisphosphonate] have become increasingly common” because of concerns about potential adverse effects from prolonged, continuous bisphosphonate treatment, especially the risk for osteonecrosis of the jaw and atypical femoral fractures, he said. These bisphosphonate stoppages are sometimes permanent and sometimes temporary, Dr. Saag noted. Ideally, assessment of the risks and benefits from a bisphosphonate drug holiday should occur in a randomized study, but in current U.S. practice such a trial would be “impossible because there is not equipoise around the decision of whether or not to stop,” he said.
To try to gain insight into the impact of halting bisphosphonate treatment with observational data, Dr. Saag and his associates used records collected by Medicare on 153,236 women who started a new course of bisphosphonate treatment and remained on it for at least 3 years during 2006 to 2014. When selecting these women, the researchers also focused on those with at least 80% adherence to their bisphosphonate regimen, based on prescription coverage data. The analysis censored women who also received other treatments that can affect bone density, such as estrogen or denosumab (Prolia, Xgeva). The average age of the women was 79 years; two-thirds were aged 75 years or older. The median duration of follow-up information after bisphosphonate stoppage was 2.1 years. Forty percent of the women stopped their bisphosphonate treatment for at least 6 months, and 13% of the women who stopped treatment subsequently restarted a bisphosphonate drug. The most commonly used bisphosphonate was alendronate (Fosamax, Binosto), used by 72%, followed by zoledronic acid (Reclast, Zometa), used by 16%.
The analysis divided women who stopped their bisphosphonate treatment into subgroups based on the duration of stoppage, and showed that the rate of hip fracture was 40% higher among women who stopped treatment for more than 2 years but not more than 3 years, compared with the women who never interrupted their bisphosphonate treatment, a statistically significant difference, Dr. Saag said. In contrast, among women who halted bisphosphonate treatment for more than 1 year but not more than 2 years, the hip fracture risk was 20% higher than that of nonstoppers, also a statistically significant difference. These and all the other analyses the researchers ran adjusted for the possible impact from baseline differences in several demographic and clinical variables.
Dr. Saag cautioned that while the relatively increased risk for hip fracture from a prolonged halt to bisphosphonate treatment was 40%, the absolute increase in risk was “relatively modest,” representing an increased fracture rate of 0.5-1 additional fractures during every 100 patient years of follow-up.
For the endpoint of major osteoporotic fracture at any location, the risk was 10% higher among women who stopped treatment for more than 2 years but not for longer than 3 years, compared with nonstoppers.
The researchers also focused on two key subgroups. Among women who only took alendronate, a drug holiday of more than 2 years was linked with a statistically significant 20% rise in hip fractures, compared with women who never stopped the drug. And among the 4% of studied women who had a history of a bone fracture because of bone fragility, stoppage of their bisphosphonate treatment for more than 2 years doubled their hip fracture rate, compared with similar women who did not stop their treatment.
The study received no commercial funding. Dr. Saag has been a consultant to and has received research funding from Amgen, Lilly, and Radius.
SOURCE: Curtis J et al. EULAR 2018 Congress, abstract OP0017.
AMSTERDAM – Older women on bisphosphonate treatment for at least 3 years who then stopped taking the drug showed a 40% increased risk for hip fracture after they were off the bisphosphonate for more than 2 years, compared with women who never stopped using the drug, according to an analysis of more than 150,000 women in a Medicare database.
The implication of this observational-data finding is that drug holidays from a bisphosphonate regimen “may not be appropriate for all patients,” Kenneth G. Saag, MD, said at the European Congress of Rheumatology.
The finding seems to dispute a recent recommendation from the American College of Physicians (Ann Intern Med. 2017 June 6;166[11]:818-39) that drug treatment to prevent bone fractures in osteoporotic women should stop after 5 years, noted Dr. Saag, a rheumatologist and professor of medicine at the University of Alabama, Birmingham. The median duration of bisphosphonate treatment in the studied cohort before the drug use stopped was 5.5 years.
“Drug holidays [from a bisphosphonate] have become increasingly common” because of concerns about potential adverse effects from prolonged, continuous bisphosphonate treatment, especially the risk for osteonecrosis of the jaw and atypical femoral fractures, he said. These bisphosphonate stoppages are sometimes permanent and sometimes temporary, Dr. Saag noted. Ideally, assessment of the risks and benefits from a bisphosphonate drug holiday should occur in a randomized study, but in current U.S. practice such a trial would be “impossible because there is not equipoise around the decision of whether or not to stop,” he said.
To try to gain insight into the impact of halting bisphosphonate treatment with observational data, Dr. Saag and his associates used records collected by Medicare on 153,236 women who started a new course of bisphosphonate treatment and remained on it for at least 3 years during 2006 to 2014. When selecting these women, the researchers also focused on those with at least 80% adherence to their bisphosphonate regimen, based on prescription coverage data. The analysis censored women who also received other treatments that can affect bone density, such as estrogen or denosumab (Prolia, Xgeva). The average age of the women was 79 years; two-thirds were aged 75 years or older. The median duration of follow-up information after bisphosphonate stoppage was 2.1 years. Forty percent of the women stopped their bisphosphonate treatment for at least 6 months, and 13% of the women who stopped treatment subsequently restarted a bisphosphonate drug. The most commonly used bisphosphonate was alendronate (Fosamax, Binosto), used by 72%, followed by zoledronic acid (Reclast, Zometa), used by 16%.
The analysis divided women who stopped their bisphosphonate treatment into subgroups based on the duration of stoppage, and showed that the rate of hip fracture was 40% higher among women who stopped treatment for more than 2 years but not more than 3 years, compared with the women who never interrupted their bisphosphonate treatment, a statistically significant difference, Dr. Saag said. In contrast, among women who halted bisphosphonate treatment for more than 1 year but not more than 2 years, the hip fracture risk was 20% higher than that of nonstoppers, also a statistically significant difference. These and all the other analyses the researchers ran adjusted for the possible impact from baseline differences in several demographic and clinical variables.
Dr. Saag cautioned that while the relatively increased risk for hip fracture from a prolonged halt to bisphosphonate treatment was 40%, the absolute increase in risk was “relatively modest,” representing an increased fracture rate of 0.5-1 additional fractures during every 100 patient years of follow-up.
For the endpoint of major osteoporotic fracture at any location, the risk was 10% higher among women who stopped treatment for more than 2 years but not for longer than 3 years, compared with nonstoppers.
The researchers also focused on two key subgroups. Among women who only took alendronate, a drug holiday of more than 2 years was linked with a statistically significant 20% rise in hip fractures, compared with women who never stopped the drug. And among the 4% of studied women who had a history of a bone fracture because of bone fragility, stoppage of their bisphosphonate treatment for more than 2 years doubled their hip fracture rate, compared with similar women who did not stop their treatment.
The study received no commercial funding. Dr. Saag has been a consultant to and has received research funding from Amgen, Lilly, and Radius.
SOURCE: Curtis J et al. EULAR 2018 Congress, abstract OP0017.
AMSTERDAM – Older women on bisphosphonate treatment for at least 3 years who then stopped taking the drug showed a 40% increased risk for hip fracture after they were off the bisphosphonate for more than 2 years, compared with women who never stopped using the drug, according to an analysis of more than 150,000 women in a Medicare database.
The implication of this observational-data finding is that drug holidays from a bisphosphonate regimen “may not be appropriate for all patients,” Kenneth G. Saag, MD, said at the European Congress of Rheumatology.
The finding seems to dispute a recent recommendation from the American College of Physicians (Ann Intern Med. 2017 June 6;166[11]:818-39) that drug treatment to prevent bone fractures in osteoporotic women should stop after 5 years, noted Dr. Saag, a rheumatologist and professor of medicine at the University of Alabama, Birmingham. The median duration of bisphosphonate treatment in the studied cohort before the drug use stopped was 5.5 years.
“Drug holidays [from a bisphosphonate] have become increasingly common” because of concerns about potential adverse effects from prolonged, continuous bisphosphonate treatment, especially the risk for osteonecrosis of the jaw and atypical femoral fractures, he said. These bisphosphonate stoppages are sometimes permanent and sometimes temporary, Dr. Saag noted. Ideally, assessment of the risks and benefits from a bisphosphonate drug holiday should occur in a randomized study, but in current U.S. practice such a trial would be “impossible because there is not equipoise around the decision of whether or not to stop,” he said.
To try to gain insight into the impact of halting bisphosphonate treatment with observational data, Dr. Saag and his associates used records collected by Medicare on 153,236 women who started a new course of bisphosphonate treatment and remained on it for at least 3 years during 2006 to 2014. When selecting these women, the researchers also focused on those with at least 80% adherence to their bisphosphonate regimen, based on prescription coverage data. The analysis censored women who also received other treatments that can affect bone density, such as estrogen or denosumab (Prolia, Xgeva). The average age of the women was 79 years; two-thirds were aged 75 years or older. The median duration of follow-up information after bisphosphonate stoppage was 2.1 years. Forty percent of the women stopped their bisphosphonate treatment for at least 6 months, and 13% of the women who stopped treatment subsequently restarted a bisphosphonate drug. The most commonly used bisphosphonate was alendronate (Fosamax, Binosto), used by 72%, followed by zoledronic acid (Reclast, Zometa), used by 16%.
The analysis divided women who stopped their bisphosphonate treatment into subgroups based on the duration of stoppage, and showed that the rate of hip fracture was 40% higher among women who stopped treatment for more than 2 years but not more than 3 years, compared with the women who never interrupted their bisphosphonate treatment, a statistically significant difference, Dr. Saag said. In contrast, among women who halted bisphosphonate treatment for more than 1 year but not more than 2 years, the hip fracture risk was 20% higher than that of nonstoppers, also a statistically significant difference. These and all the other analyses the researchers ran adjusted for the possible impact from baseline differences in several demographic and clinical variables.
Dr. Saag cautioned that while the relatively increased risk for hip fracture from a prolonged halt to bisphosphonate treatment was 40%, the absolute increase in risk was “relatively modest,” representing an increased fracture rate of 0.5-1 additional fractures during every 100 patient years of follow-up.
For the endpoint of major osteoporotic fracture at any location, the risk was 10% higher among women who stopped treatment for more than 2 years but not for longer than 3 years, compared with nonstoppers.
The researchers also focused on two key subgroups. Among women who only took alendronate, a drug holiday of more than 2 years was linked with a statistically significant 20% rise in hip fractures, compared with women who never stopped the drug. And among the 4% of studied women who had a history of a bone fracture because of bone fragility, stoppage of their bisphosphonate treatment for more than 2 years doubled their hip fracture rate, compared with similar women who did not stop their treatment.
The study received no commercial funding. Dr. Saag has been a consultant to and has received research funding from Amgen, Lilly, and Radius.
SOURCE: Curtis J et al. EULAR 2018 Congress, abstract OP0017.
REPORTING FROM THE EULAR 2018 CONGRESS
Key clinical point: Stopping a bisphosphonate for more than 2 years boosts hip fracture risk.
Major finding: Women stopping bisphosphonate use for more than 2 years had a 40% higher rate of hip fractures compared with women who didn’t stop the drug.
Study details: Review of data collected by Medicare for 153,236 women treated with a bisphosphonate drug.
Disclosures: The study received no commercial funding. Dr. Saag has been a consultant to and has received research funding from Amgen, Lilly, and Radius.
Source: Curtis J et al. EULAR 2018 Congress, abstract OP0017.
What underlies post–bariatric surgery bone fragility?
BOSTON – Charting a healthy path for patients after bariatric surgery can be complicated and addressing bone health is an important part of the endocrinologist’s role in keeping patients safe from postsurgical fractures, according to John Bilezikian, MD.
said Dr. Bilezikian, speaking during a bariatric surgery–focused session at the annual scientific & clinical congress of the American Academy of Clinical Endocrinologists.
It’s not easy to assess bone health, even before surgery, said Dr. Bilezikian. Even objective measures of bone density, such as dual-energy x-ray absorptiometry (DXA), may be skewed: very high fat mass causes artifact that interferes with accurate measurement of bone density, and DXA can’t distinguish between cortical and trabecular bone. The latter is a particular issue in high body mass index patients, since obesity is known to be associated with a more fragile bone microarchitecture, said Dr. Bilezikian, the Dorothy L. and Daniel H. Silberberg Professor of Medicine and director of the metabolic bone diseases unit at Columbia University, New York.
With these caveats in mind, Dr. Bilezikian said, there are some lessons to be learned from existing research to better manage bone health in bariatric patients.
After Roux-en-Y gastric bypass surgery (RYGB), bone turnover soon increases, with bone resorption markers increasing by up to 200% in the first 12-18 months after surgery. Bone formation markers also are elevated but to a lesser extent, said Dr. Bilezikian. Over time, the weight loss from RYGB is associated with a significant drop in bone mineral density (BMD) at weight-bearing sites. Weight loss was associated with bone loss at the total hip (r = 0.70; P less than .0003) and femoral neck (r = 0.47; P = .03 (J Clin Endocrinol Metab. 2013 Feb;98[2] 541-9).
A newer-technology, high-resolution peripheral quantitative CT (HR-pQCT) offers a noninvasive look not just at bone size and density but also at microarchitecture, including cortical thickness and details of trabecular structure. This technology “can help elucidate the structural basis for fragility,” said Dr. Bilezikian.
HR-pQCT was used in a recent study (J Bone Min Res. 2017 Dec. 27. doi: 10.1002/jbmr.3371) that followed 48 patients for 1 year after RYGB. Using HR-pQCT, DXA, and serum markers of bone turnover, the researchers found significant decrease in BMD and estimated decrease in bone strength after RYGB. Bone cortex became increasingly porous as well. Taken together, these changes may indicate an increased fracture risk, concluded the investigators.
A longer study that followed RYGB recipients for 2 years and used similar imaging and serum parameters also found that participants had decreased BMD. Tellingly, these investigators saw more marked increase in cortical porosity in the second year after bypass. Estimated bone strength continued to decline during the study period, even after weight loss had stopped.
All of these findings, said Dr. Bilezikian, point to a pathogenetic process other than weight loss that promotes the deteriorating bone microarchitecture seen years after RYGB. “Loss of bone mass and skeletal deterioration after gastric bypass surgery cannot be explained by weight loss alone,” said Dr. Bilezikian.
Another recent study was able to follow a small cohort of patients for a full 5 years, using DXA, lumbar CT, and Hr-pQCT. Though weight loss stabilized after 2 years and 25-OH D and calcium levels were unchanged from presurgical baseline, bone density continued to drop, and bone microarchitecture further deteriorated, said Dr. Bilezikian (Greenblatt L et al. ASBMR 2017, Abstract 1125).
Initially, post–bariatric surgery weight loss may induce bone changes because of skeletal unloading; further down the road, estrogen production by adipose tissue is decreased with ongoing fat loss, and sarcopenia may have an adverse effect on bone microarchitecture. Postsurgical malabsorption may also be an early mechanism of bone loss.
Other hormonal changes can include secondary hyperparathyroidism. Leptin, adiponectin, and peptide YY levels also may be altered.
Do these changes in BMD and bone architecture result in increased fracture risk? This question is difficult to answer, for the same reasons that other bariatric surgery research can be challenging, said Dr. Bilezikian. There is heterogeneity of procedures and supplement regimens, sample sizes can be small, follow-up times short, and adherence often is not tracked.
However, there are some clues that RYGB may be associated with an increased risk of all fractures and of fragility fractures, with appendicular fractures seen most frequently (Osteoporos Int. 2014 Jan; 25[1]:151-8). A larger study that tracked 12,676 patients receiving bariatric surgery, 38,028 patients with obesity, and 126,760 nonobese participants found that the bariatric patients had a 4.1% risk of fracture at 4 years post surgery, compared with 2.7% and 2.4% fracture rates in the participants with and without obesity, respectively (BMJ. 2016;354:i3794).
Other retrospective studies have found “a time-dependent increase in nonvertebral fractures with Roux-en-Y gastric bypass compared to gastric banding,” said Dr. Bilezikian.
How can these risks be managed after gastric bypass surgery? “Strive for nutritional adequacy” as the first step, said Dr. Bilezikian, meaning that calcium and vitamin D should be prescribed – and adherence encouraged – as indicated. Levels of 25-OH D should be checked regularly, with supplementation managed to keep levels over 30 ng/mL, he said.
All patients should be encouraged to develop and maintain an appropriate exercise regimen, and BMD should be followed over time. Those caring for post–gastric bypass patients can still use a bisphosphonate or other bone-health medication, if indicated using standard parameters. However, “You probably shouldn’t use an oral bisphosphonate in this population,” said Dr. Bilezikian.
Dr. Bilezikian reported that he has consulting or advisory relationships with Amgen, Radius Pharmaceuticals, Shire Pharmaceuticals, and Ultragenyx, and serves on a data safety monitoring board for Regeneron.
BOSTON – Charting a healthy path for patients after bariatric surgery can be complicated and addressing bone health is an important part of the endocrinologist’s role in keeping patients safe from postsurgical fractures, according to John Bilezikian, MD.
said Dr. Bilezikian, speaking during a bariatric surgery–focused session at the annual scientific & clinical congress of the American Academy of Clinical Endocrinologists.
It’s not easy to assess bone health, even before surgery, said Dr. Bilezikian. Even objective measures of bone density, such as dual-energy x-ray absorptiometry (DXA), may be skewed: very high fat mass causes artifact that interferes with accurate measurement of bone density, and DXA can’t distinguish between cortical and trabecular bone. The latter is a particular issue in high body mass index patients, since obesity is known to be associated with a more fragile bone microarchitecture, said Dr. Bilezikian, the Dorothy L. and Daniel H. Silberberg Professor of Medicine and director of the metabolic bone diseases unit at Columbia University, New York.
With these caveats in mind, Dr. Bilezikian said, there are some lessons to be learned from existing research to better manage bone health in bariatric patients.
After Roux-en-Y gastric bypass surgery (RYGB), bone turnover soon increases, with bone resorption markers increasing by up to 200% in the first 12-18 months after surgery. Bone formation markers also are elevated but to a lesser extent, said Dr. Bilezikian. Over time, the weight loss from RYGB is associated with a significant drop in bone mineral density (BMD) at weight-bearing sites. Weight loss was associated with bone loss at the total hip (r = 0.70; P less than .0003) and femoral neck (r = 0.47; P = .03 (J Clin Endocrinol Metab. 2013 Feb;98[2] 541-9).
A newer-technology, high-resolution peripheral quantitative CT (HR-pQCT) offers a noninvasive look not just at bone size and density but also at microarchitecture, including cortical thickness and details of trabecular structure. This technology “can help elucidate the structural basis for fragility,” said Dr. Bilezikian.
HR-pQCT was used in a recent study (J Bone Min Res. 2017 Dec. 27. doi: 10.1002/jbmr.3371) that followed 48 patients for 1 year after RYGB. Using HR-pQCT, DXA, and serum markers of bone turnover, the researchers found significant decrease in BMD and estimated decrease in bone strength after RYGB. Bone cortex became increasingly porous as well. Taken together, these changes may indicate an increased fracture risk, concluded the investigators.
A longer study that followed RYGB recipients for 2 years and used similar imaging and serum parameters also found that participants had decreased BMD. Tellingly, these investigators saw more marked increase in cortical porosity in the second year after bypass. Estimated bone strength continued to decline during the study period, even after weight loss had stopped.
All of these findings, said Dr. Bilezikian, point to a pathogenetic process other than weight loss that promotes the deteriorating bone microarchitecture seen years after RYGB. “Loss of bone mass and skeletal deterioration after gastric bypass surgery cannot be explained by weight loss alone,” said Dr. Bilezikian.
Another recent study was able to follow a small cohort of patients for a full 5 years, using DXA, lumbar CT, and Hr-pQCT. Though weight loss stabilized after 2 years and 25-OH D and calcium levels were unchanged from presurgical baseline, bone density continued to drop, and bone microarchitecture further deteriorated, said Dr. Bilezikian (Greenblatt L et al. ASBMR 2017, Abstract 1125).
Initially, post–bariatric surgery weight loss may induce bone changes because of skeletal unloading; further down the road, estrogen production by adipose tissue is decreased with ongoing fat loss, and sarcopenia may have an adverse effect on bone microarchitecture. Postsurgical malabsorption may also be an early mechanism of bone loss.
Other hormonal changes can include secondary hyperparathyroidism. Leptin, adiponectin, and peptide YY levels also may be altered.
Do these changes in BMD and bone architecture result in increased fracture risk? This question is difficult to answer, for the same reasons that other bariatric surgery research can be challenging, said Dr. Bilezikian. There is heterogeneity of procedures and supplement regimens, sample sizes can be small, follow-up times short, and adherence often is not tracked.
However, there are some clues that RYGB may be associated with an increased risk of all fractures and of fragility fractures, with appendicular fractures seen most frequently (Osteoporos Int. 2014 Jan; 25[1]:151-8). A larger study that tracked 12,676 patients receiving bariatric surgery, 38,028 patients with obesity, and 126,760 nonobese participants found that the bariatric patients had a 4.1% risk of fracture at 4 years post surgery, compared with 2.7% and 2.4% fracture rates in the participants with and without obesity, respectively (BMJ. 2016;354:i3794).
Other retrospective studies have found “a time-dependent increase in nonvertebral fractures with Roux-en-Y gastric bypass compared to gastric banding,” said Dr. Bilezikian.
How can these risks be managed after gastric bypass surgery? “Strive for nutritional adequacy” as the first step, said Dr. Bilezikian, meaning that calcium and vitamin D should be prescribed – and adherence encouraged – as indicated. Levels of 25-OH D should be checked regularly, with supplementation managed to keep levels over 30 ng/mL, he said.
All patients should be encouraged to develop and maintain an appropriate exercise regimen, and BMD should be followed over time. Those caring for post–gastric bypass patients can still use a bisphosphonate or other bone-health medication, if indicated using standard parameters. However, “You probably shouldn’t use an oral bisphosphonate in this population,” said Dr. Bilezikian.
Dr. Bilezikian reported that he has consulting or advisory relationships with Amgen, Radius Pharmaceuticals, Shire Pharmaceuticals, and Ultragenyx, and serves on a data safety monitoring board for Regeneron.
BOSTON – Charting a healthy path for patients after bariatric surgery can be complicated and addressing bone health is an important part of the endocrinologist’s role in keeping patients safe from postsurgical fractures, according to John Bilezikian, MD.
said Dr. Bilezikian, speaking during a bariatric surgery–focused session at the annual scientific & clinical congress of the American Academy of Clinical Endocrinologists.
It’s not easy to assess bone health, even before surgery, said Dr. Bilezikian. Even objective measures of bone density, such as dual-energy x-ray absorptiometry (DXA), may be skewed: very high fat mass causes artifact that interferes with accurate measurement of bone density, and DXA can’t distinguish between cortical and trabecular bone. The latter is a particular issue in high body mass index patients, since obesity is known to be associated with a more fragile bone microarchitecture, said Dr. Bilezikian, the Dorothy L. and Daniel H. Silberberg Professor of Medicine and director of the metabolic bone diseases unit at Columbia University, New York.
With these caveats in mind, Dr. Bilezikian said, there are some lessons to be learned from existing research to better manage bone health in bariatric patients.
After Roux-en-Y gastric bypass surgery (RYGB), bone turnover soon increases, with bone resorption markers increasing by up to 200% in the first 12-18 months after surgery. Bone formation markers also are elevated but to a lesser extent, said Dr. Bilezikian. Over time, the weight loss from RYGB is associated with a significant drop in bone mineral density (BMD) at weight-bearing sites. Weight loss was associated with bone loss at the total hip (r = 0.70; P less than .0003) and femoral neck (r = 0.47; P = .03 (J Clin Endocrinol Metab. 2013 Feb;98[2] 541-9).
A newer-technology, high-resolution peripheral quantitative CT (HR-pQCT) offers a noninvasive look not just at bone size and density but also at microarchitecture, including cortical thickness and details of trabecular structure. This technology “can help elucidate the structural basis for fragility,” said Dr. Bilezikian.
HR-pQCT was used in a recent study (J Bone Min Res. 2017 Dec. 27. doi: 10.1002/jbmr.3371) that followed 48 patients for 1 year after RYGB. Using HR-pQCT, DXA, and serum markers of bone turnover, the researchers found significant decrease in BMD and estimated decrease in bone strength after RYGB. Bone cortex became increasingly porous as well. Taken together, these changes may indicate an increased fracture risk, concluded the investigators.
A longer study that followed RYGB recipients for 2 years and used similar imaging and serum parameters also found that participants had decreased BMD. Tellingly, these investigators saw more marked increase in cortical porosity in the second year after bypass. Estimated bone strength continued to decline during the study period, even after weight loss had stopped.
All of these findings, said Dr. Bilezikian, point to a pathogenetic process other than weight loss that promotes the deteriorating bone microarchitecture seen years after RYGB. “Loss of bone mass and skeletal deterioration after gastric bypass surgery cannot be explained by weight loss alone,” said Dr. Bilezikian.
Another recent study was able to follow a small cohort of patients for a full 5 years, using DXA, lumbar CT, and Hr-pQCT. Though weight loss stabilized after 2 years and 25-OH D and calcium levels were unchanged from presurgical baseline, bone density continued to drop, and bone microarchitecture further deteriorated, said Dr. Bilezikian (Greenblatt L et al. ASBMR 2017, Abstract 1125).
Initially, post–bariatric surgery weight loss may induce bone changes because of skeletal unloading; further down the road, estrogen production by adipose tissue is decreased with ongoing fat loss, and sarcopenia may have an adverse effect on bone microarchitecture. Postsurgical malabsorption may also be an early mechanism of bone loss.
Other hormonal changes can include secondary hyperparathyroidism. Leptin, adiponectin, and peptide YY levels also may be altered.
Do these changes in BMD and bone architecture result in increased fracture risk? This question is difficult to answer, for the same reasons that other bariatric surgery research can be challenging, said Dr. Bilezikian. There is heterogeneity of procedures and supplement regimens, sample sizes can be small, follow-up times short, and adherence often is not tracked.
However, there are some clues that RYGB may be associated with an increased risk of all fractures and of fragility fractures, with appendicular fractures seen most frequently (Osteoporos Int. 2014 Jan; 25[1]:151-8). A larger study that tracked 12,676 patients receiving bariatric surgery, 38,028 patients with obesity, and 126,760 nonobese participants found that the bariatric patients had a 4.1% risk of fracture at 4 years post surgery, compared with 2.7% and 2.4% fracture rates in the participants with and without obesity, respectively (BMJ. 2016;354:i3794).
Other retrospective studies have found “a time-dependent increase in nonvertebral fractures with Roux-en-Y gastric bypass compared to gastric banding,” said Dr. Bilezikian.
How can these risks be managed after gastric bypass surgery? “Strive for nutritional adequacy” as the first step, said Dr. Bilezikian, meaning that calcium and vitamin D should be prescribed – and adherence encouraged – as indicated. Levels of 25-OH D should be checked regularly, with supplementation managed to keep levels over 30 ng/mL, he said.
All patients should be encouraged to develop and maintain an appropriate exercise regimen, and BMD should be followed over time. Those caring for post–gastric bypass patients can still use a bisphosphonate or other bone-health medication, if indicated using standard parameters. However, “You probably shouldn’t use an oral bisphosphonate in this population,” said Dr. Bilezikian.
Dr. Bilezikian reported that he has consulting or advisory relationships with Amgen, Radius Pharmaceuticals, Shire Pharmaceuticals, and Ultragenyx, and serves on a data safety monitoring board for Regeneron.
REPORTING FROM AACE 2018
EULAR scientific program highlights spectrum of translational research
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.
Also on Wednesday, a session will tackle the relationship between psychological distress and pain in immune-mediated disease. “Pain is the major symptom of rheumatic diseases, and the role of the psyche remains poorly understood,” Dr. Landewé said. “But we know one thing for sure: There is an association, and speakers from outside the field of rheumatology will help explain.”
Attendees at this bench-to-bedside session will learn how distress appears to exacerbate arthritis pain and how managing psychological stress can help optimize outcomes in arthritis pain. Experts also will describe research on integrated brain pathways in pain and distress, as well as risk factors for cognitive impairment in 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.
Another clinical science session scheduled for Thursday afternoon will delve into structural damage progression in patients with axial spondyloarthritis, Dr. Landewé said. “Can we inhibit this structural progression? Can we show it? Does it make sense? And which drug company will win the battle to have the precedent?”
He hopes that Dr. Désirée van der Heijde of the Netherlands and Dr. Xenofon Baraliakos of Germany will help answer these questions when they discuss the latest evidence on identifying and treating clinically relevant structural progression. Also in this session, researchers will describe the combined effects of tumor necrosis factor inhibitors and NSAIDs on radiographic progression in ankylosing spondylitis, and MRI evidence supporting treating early axial spondyloarthritis to target with the goal of achieving sustained remission of inflammation.
Also on Thursday afternoon, a case-based session will take a deep dive into giant cell arteritis (GCA), Dr. Landewé noted. Attendees will learn about diagnosing and managing vision loss and stroke and the latest on corticosteroid therapy in GCA. The session also will cover biologics. “Giant cell arteritis has entered the field of biologicals!” said Dr. Landewé. “This has major implications for this disease and the clinical choices to be made.”
The past 5 decades have seen marked progress in the diagnosis and treatment of SLE, with corresponding improvements in survival and quality of life. “Still, lupus is awfully difficult,” Dr. Landewé said. “Therefore, we have planned a classical bench-to-bedside symposium to provide an all-inclusive look at current thinking and future developments.”
Talks during this Thursday afternoon session will cover the latest findings on the pathogenesis of SLE, the clinical significance of autoantibodies, distinguishing early SLE from mimics, and the role of blood-brain barrier permeability and neuropsychiatric manifestations of SLE and progressive systemic sclerosis.
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.
Also on Wednesday, a session will tackle the relationship between psychological distress and pain in immune-mediated disease. “Pain is the major symptom of rheumatic diseases, and the role of the psyche remains poorly understood,” Dr. Landewé said. “But we know one thing for sure: There is an association, and speakers from outside the field of rheumatology will help explain.”
Attendees at this bench-to-bedside session will learn how distress appears to exacerbate arthritis pain and how managing psychological stress can help optimize outcomes in arthritis pain. Experts also will describe research on integrated brain pathways in pain and distress, as well as risk factors for cognitive impairment in 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.
Another clinical science session scheduled for Thursday afternoon will delve into structural damage progression in patients with axial spondyloarthritis, Dr. Landewé said. “Can we inhibit this structural progression? Can we show it? Does it make sense? And which drug company will win the battle to have the precedent?”
He hopes that Dr. Désirée van der Heijde of the Netherlands and Dr. Xenofon Baraliakos of Germany will help answer these questions when they discuss the latest evidence on identifying and treating clinically relevant structural progression. Also in this session, researchers will describe the combined effects of tumor necrosis factor inhibitors and NSAIDs on radiographic progression in ankylosing spondylitis, and MRI evidence supporting treating early axial spondyloarthritis to target with the goal of achieving sustained remission of inflammation.
Also on Thursday afternoon, a case-based session will take a deep dive into giant cell arteritis (GCA), Dr. Landewé noted. Attendees will learn about diagnosing and managing vision loss and stroke and the latest on corticosteroid therapy in GCA. The session also will cover biologics. “Giant cell arteritis has entered the field of biologicals!” said Dr. Landewé. “This has major implications for this disease and the clinical choices to be made.”
The past 5 decades have seen marked progress in the diagnosis and treatment of SLE, with corresponding improvements in survival and quality of life. “Still, lupus is awfully difficult,” Dr. Landewé said. “Therefore, we have planned a classical bench-to-bedside symposium to provide an all-inclusive look at current thinking and future developments.”
Talks during this Thursday afternoon session will cover the latest findings on the pathogenesis of SLE, the clinical significance of autoantibodies, distinguishing early SLE from mimics, and the role of blood-brain barrier permeability and neuropsychiatric manifestations of SLE and progressive systemic sclerosis.
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.
Also on Wednesday, a session will tackle the relationship between psychological distress and pain in immune-mediated disease. “Pain is the major symptom of rheumatic diseases, and the role of the psyche remains poorly understood,” Dr. Landewé said. “But we know one thing for sure: There is an association, and speakers from outside the field of rheumatology will help explain.”
Attendees at this bench-to-bedside session will learn how distress appears to exacerbate arthritis pain and how managing psychological stress can help optimize outcomes in arthritis pain. Experts also will describe research on integrated brain pathways in pain and distress, as well as risk factors for cognitive impairment in 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.
Another clinical science session scheduled for Thursday afternoon will delve into structural damage progression in patients with axial spondyloarthritis, Dr. Landewé said. “Can we inhibit this structural progression? Can we show it? Does it make sense? And which drug company will win the battle to have the precedent?”
He hopes that Dr. Désirée van der Heijde of the Netherlands and Dr. Xenofon Baraliakos of Germany will help answer these questions when they discuss the latest evidence on identifying and treating clinically relevant structural progression. Also in this session, researchers will describe the combined effects of tumor necrosis factor inhibitors and NSAIDs on radiographic progression in ankylosing spondylitis, and MRI evidence supporting treating early axial spondyloarthritis to target with the goal of achieving sustained remission of inflammation.
Also on Thursday afternoon, a case-based session will take a deep dive into giant cell arteritis (GCA), Dr. Landewé noted. Attendees will learn about diagnosing and managing vision loss and stroke and the latest on corticosteroid therapy in GCA. The session also will cover biologics. “Giant cell arteritis has entered the field of biologicals!” said Dr. Landewé. “This has major implications for this disease and the clinical choices to be made.”
The past 5 decades have seen marked progress in the diagnosis and treatment of SLE, with corresponding improvements in survival and quality of life. “Still, lupus is awfully difficult,” Dr. Landewé said. “Therefore, we have planned a classical bench-to-bedside symposium to provide an all-inclusive look at current thinking and future developments.”
Talks during this Thursday afternoon session will cover the latest findings on the pathogenesis of SLE, the clinical significance of autoantibodies, distinguishing early SLE from mimics, and the role of blood-brain barrier permeability and neuropsychiatric manifestations of SLE and progressive systemic sclerosis.
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.”
FDA approves Prolia for glucocorticoid-induced osteoporosis
at high risk of fracture, the drug’s manufacturer Amgen announced May 21.
FDA approval was based on 12-month primary analysis results from a randomized, double-blind, phase 3 trial. Patients who received a 60-mg dose of Prolia subcutaneously every 6 months had greater lumbar spine bone mineral density at 1 year than did those who received a 5-mg dose of risedronate daily in all study subpopulations. These results were maintained after researchers controlled for gender, race, geographic region, and menopausal status, as well as baseline age, lumbar spine bone mineral density T score, and glucocorticoid dose within each subpopulation.
The most common adverse events associated with Prolia during the phase 3 study were back pain, hypertension, bronchitis, and headache, which are in line with previously reported safety data.
“Patients on long-term systemic glucocorticoid medications can experience a rapid reduction in bone mineral density within a few months of beginning treatment. With this approval, patients who receive treatment with glucocorticoids now have a new option to help improve their bone mineral density,” lead study author Kenneth F. Saag, MD, professor of medicine at the University of Alabama, Birmingham, said in Amgen’s news release.
at high risk of fracture, the drug’s manufacturer Amgen announced May 21.
FDA approval was based on 12-month primary analysis results from a randomized, double-blind, phase 3 trial. Patients who received a 60-mg dose of Prolia subcutaneously every 6 months had greater lumbar spine bone mineral density at 1 year than did those who received a 5-mg dose of risedronate daily in all study subpopulations. These results were maintained after researchers controlled for gender, race, geographic region, and menopausal status, as well as baseline age, lumbar spine bone mineral density T score, and glucocorticoid dose within each subpopulation.
The most common adverse events associated with Prolia during the phase 3 study were back pain, hypertension, bronchitis, and headache, which are in line with previously reported safety data.
“Patients on long-term systemic glucocorticoid medications can experience a rapid reduction in bone mineral density within a few months of beginning treatment. With this approval, patients who receive treatment with glucocorticoids now have a new option to help improve their bone mineral density,” lead study author Kenneth F. Saag, MD, professor of medicine at the University of Alabama, Birmingham, said in Amgen’s news release.
at high risk of fracture, the drug’s manufacturer Amgen announced May 21.
FDA approval was based on 12-month primary analysis results from a randomized, double-blind, phase 3 trial. Patients who received a 60-mg dose of Prolia subcutaneously every 6 months had greater lumbar spine bone mineral density at 1 year than did those who received a 5-mg dose of risedronate daily in all study subpopulations. These results were maintained after researchers controlled for gender, race, geographic region, and menopausal status, as well as baseline age, lumbar spine bone mineral density T score, and glucocorticoid dose within each subpopulation.
The most common adverse events associated with Prolia during the phase 3 study were back pain, hypertension, bronchitis, and headache, which are in line with previously reported safety data.
“Patients on long-term systemic glucocorticoid medications can experience a rapid reduction in bone mineral density within a few months of beginning treatment. With this approval, patients who receive treatment with glucocorticoids now have a new option to help improve their bone mineral density,” lead study author Kenneth F. Saag, MD, professor of medicine at the University of Alabama, Birmingham, said in Amgen’s news release.
VIDEO: BMI helps predict bone fragility in obese patients
BOSTON – An index that takes into account the ratio between body mass index (BMI) and bone mineral density (BMD) correlated well with trabecular bone scores, a newer assessment of bone fragility. The index may help predict risk for fragility fractures in individuals with obesity when trabecular bone scores are not available.
“Obesity is traditionally thought to be protective against bone fractures,” said Mikiko Watanabe, MD, an endocrinologist at Sapienza University of Rome. “But recent evidence suggests that this is not entirely true, especially in morbidly obese patients.”
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Lumbar spine BMD alone may not accurately capture bone fragility in patients with obesity, said Dr. Watanabe in an interview at the annual meeting of the American Association of Clinical Endocrinologists.
Adding the trabecular bone score (TBS) to BMD gives additional information about bone microarchitecture, refining risk assessment for fragility fractures. This newer technology, however, may not be readily available and may be associated with extra cost.
Accordingly, said Dr. Watanabe, the study’s senior investigator, Sapienza University’s Carla Lubrano, MD, had the idea to index bone density to BMI, and then see how well the ratio correlated to TBS; obesity is known to be associated with lower TBS scores, indicating increased bone fragility.
Living in Italy, with relatively fewer medical resources available, “We were trying to find some readily available index that could predict the risk of fracture as well as the indexes that are around right now,” said Dr. Watanabe.
“We did find some very interesting data in our population of over 2,000 obese patients living in Rome,” she said. “We do confirm something from the literature, where BMD tends to go high with increasing BMI.” Further, the relatively weak correlation between TBS and BMI was confirmed in the investigators’ work (r = 0.3).
“If you correct the BMD by BMI – so if you use our index – then the correlation becomes more stringent, and definitely so much better,” she said (r = 0.54).
Dr. Watanabe and her colleagues also conducted an analysis to see if there were differences between participants with and without metabolic syndrome. The 45.7% of participants who had metabolic syndrome had similar lumbar spine BMD scores to the rest of the cohort (1.067 versus 1.063 g/cm2, P = .50754).
However, both the TBS and BMD/BMI ratio were significantly lower for those with metabolic syndrome than for the metabolically healthy participants. The TBS, as expected, was 1.21 in patients with metabolic syndrome, and 1.31 in patients without metabolic syndrome; the BMD/BMI ratio followed the same pattern, with ratios of 0.28 for those with, and 0.30 for those without, metabolic syndrome (P less than .00001 for both).
Dr. Watanabe said that she and her associates are continuing research “to see whether our ratio is actually able to predict the risk of fractures." The hope, she said, is to use the BMD/BMI index together with or instead of TBS to better assess bone strength in patients with obesity.
Dr. Watanabe reported that she had no relevant conflicts of interest.
BOSTON – An index that takes into account the ratio between body mass index (BMI) and bone mineral density (BMD) correlated well with trabecular bone scores, a newer assessment of bone fragility. The index may help predict risk for fragility fractures in individuals with obesity when trabecular bone scores are not available.
“Obesity is traditionally thought to be protective against bone fractures,” said Mikiko Watanabe, MD, an endocrinologist at Sapienza University of Rome. “But recent evidence suggests that this is not entirely true, especially in morbidly obese patients.”
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Lumbar spine BMD alone may not accurately capture bone fragility in patients with obesity, said Dr. Watanabe in an interview at the annual meeting of the American Association of Clinical Endocrinologists.
Adding the trabecular bone score (TBS) to BMD gives additional information about bone microarchitecture, refining risk assessment for fragility fractures. This newer technology, however, may not be readily available and may be associated with extra cost.
Accordingly, said Dr. Watanabe, the study’s senior investigator, Sapienza University’s Carla Lubrano, MD, had the idea to index bone density to BMI, and then see how well the ratio correlated to TBS; obesity is known to be associated with lower TBS scores, indicating increased bone fragility.
Living in Italy, with relatively fewer medical resources available, “We were trying to find some readily available index that could predict the risk of fracture as well as the indexes that are around right now,” said Dr. Watanabe.
“We did find some very interesting data in our population of over 2,000 obese patients living in Rome,” she said. “We do confirm something from the literature, where BMD tends to go high with increasing BMI.” Further, the relatively weak correlation between TBS and BMI was confirmed in the investigators’ work (r = 0.3).
“If you correct the BMD by BMI – so if you use our index – then the correlation becomes more stringent, and definitely so much better,” she said (r = 0.54).
Dr. Watanabe and her colleagues also conducted an analysis to see if there were differences between participants with and without metabolic syndrome. The 45.7% of participants who had metabolic syndrome had similar lumbar spine BMD scores to the rest of the cohort (1.067 versus 1.063 g/cm2, P = .50754).
However, both the TBS and BMD/BMI ratio were significantly lower for those with metabolic syndrome than for the metabolically healthy participants. The TBS, as expected, was 1.21 in patients with metabolic syndrome, and 1.31 in patients without metabolic syndrome; the BMD/BMI ratio followed the same pattern, with ratios of 0.28 for those with, and 0.30 for those without, metabolic syndrome (P less than .00001 for both).
Dr. Watanabe said that she and her associates are continuing research “to see whether our ratio is actually able to predict the risk of fractures." The hope, she said, is to use the BMD/BMI index together with or instead of TBS to better assess bone strength in patients with obesity.
Dr. Watanabe reported that she had no relevant conflicts of interest.
BOSTON – An index that takes into account the ratio between body mass index (BMI) and bone mineral density (BMD) correlated well with trabecular bone scores, a newer assessment of bone fragility. The index may help predict risk for fragility fractures in individuals with obesity when trabecular bone scores are not available.
“Obesity is traditionally thought to be protective against bone fractures,” said Mikiko Watanabe, MD, an endocrinologist at Sapienza University of Rome. “But recent evidence suggests that this is not entirely true, especially in morbidly obese patients.”
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Lumbar spine BMD alone may not accurately capture bone fragility in patients with obesity, said Dr. Watanabe in an interview at the annual meeting of the American Association of Clinical Endocrinologists.
Adding the trabecular bone score (TBS) to BMD gives additional information about bone microarchitecture, refining risk assessment for fragility fractures. This newer technology, however, may not be readily available and may be associated with extra cost.
Accordingly, said Dr. Watanabe, the study’s senior investigator, Sapienza University’s Carla Lubrano, MD, had the idea to index bone density to BMI, and then see how well the ratio correlated to TBS; obesity is known to be associated with lower TBS scores, indicating increased bone fragility.
Living in Italy, with relatively fewer medical resources available, “We were trying to find some readily available index that could predict the risk of fracture as well as the indexes that are around right now,” said Dr. Watanabe.
“We did find some very interesting data in our population of over 2,000 obese patients living in Rome,” she said. “We do confirm something from the literature, where BMD tends to go high with increasing BMI.” Further, the relatively weak correlation between TBS and BMI was confirmed in the investigators’ work (r = 0.3).
“If you correct the BMD by BMI – so if you use our index – then the correlation becomes more stringent, and definitely so much better,” she said (r = 0.54).
Dr. Watanabe and her colleagues also conducted an analysis to see if there were differences between participants with and without metabolic syndrome. The 45.7% of participants who had metabolic syndrome had similar lumbar spine BMD scores to the rest of the cohort (1.067 versus 1.063 g/cm2, P = .50754).
However, both the TBS and BMD/BMI ratio were significantly lower for those with metabolic syndrome than for the metabolically healthy participants. The TBS, as expected, was 1.21 in patients with metabolic syndrome, and 1.31 in patients without metabolic syndrome; the BMD/BMI ratio followed the same pattern, with ratios of 0.28 for those with, and 0.30 for those without, metabolic syndrome (P less than .00001 for both).
Dr. Watanabe said that she and her associates are continuing research “to see whether our ratio is actually able to predict the risk of fractures." The hope, she said, is to use the BMD/BMI index together with or instead of TBS to better assess bone strength in patients with obesity.
Dr. Watanabe reported that she had no relevant conflicts of interest.
REPORTING FROM AACE 2018
AACE 2018: A dream team of presenters
Boston is the location and inspiration for the featured presentations at the annual meeting of the American Association of Clinical Endocrinologists, program chair Vin Tangpricha, MD, PhD, said in an interview.
The program agenda for the congress, held May 16-20, boasts 143 speakers, 66 distinct clinical endocrinology educational sessions, and an opening plenary presentation featuring one of modern medicine’s most renowned diabetes and obesity researchers, according to a statement from the AACE.
New Dimensions in Insulin Action and Why They Are Important to Know
C. Ronald Kahn, MD, chief academic officer and head of Integrative Physiology and Metabolism at Joslin Diabetes Center in Boston, pioneered revolutionary work with insulin receptors and insulin resistance in diabetes and obesity. What makes his presentation on Thursday from 8:30 a.m. to 9:15 a.m. a must-see is its focus on the future: “Many new drugs are being developed based on the research on how insulin works. This lecture will be exciting to hear what is in the pipeline for drugs that manipulate insulin action,” Dr. Tangpricha said.
Cushing’s Syndrome
Beta-Cell Regeneration
The work of Andrew F. Stewart, MD, scientific director of the Mount Sinai Diabetes, Obesity and Metabolism Institute in New York, leads research into the basic mechanisms, prevention, and treatment of metabolic diseases. “In the past, we thought that there was a fixed number of beta cells in the body. However, recent research by Dr. Stewart’s group suggests that beta cells can be stimulated to grow. This is very exciting and can shape the future of how we take care of diabetes,” noted Dr. Tangpricha. The session is on Friday from 8:20 a.m. to 9:05 a.m.
New Insights Into Thyroid Hormone Action
On Thursday from 11:15 a.m. to 12:00 p.m., Anthony N. Hollenberg, MD, will present “an outstanding review on thyroid hormone and action and how this impacts patient care of those with thyroid disease,” Dr. Tangpricha said. Dr. Hollenberg is chief of the thyroid unit and the division of endocrinology, diabetes, and metabolism at Beth Israel Deaconess Medical Center in Boston.
Current and Evolving Approaches for Osteoporosis Treatment
Sundeep Khosla, MD, an expert on bone loss, will distill the myriad osteoporosis treatments into useful information that can inform your practice now. “There have been a number of drugs that have been released for the treatment of osteoporosis. We are now in an era where we can consider using drugs targeted for specific populations or specific combinations,” Dr. Tangpricha commented. This session is on Saturday at 8:15 a.m. to 9:00 a.m.
Boston is the location and inspiration for the featured presentations at the annual meeting of the American Association of Clinical Endocrinologists, program chair Vin Tangpricha, MD, PhD, said in an interview.
The program agenda for the congress, held May 16-20, boasts 143 speakers, 66 distinct clinical endocrinology educational sessions, and an opening plenary presentation featuring one of modern medicine’s most renowned diabetes and obesity researchers, according to a statement from the AACE.
New Dimensions in Insulin Action and Why They Are Important to Know
C. Ronald Kahn, MD, chief academic officer and head of Integrative Physiology and Metabolism at Joslin Diabetes Center in Boston, pioneered revolutionary work with insulin receptors and insulin resistance in diabetes and obesity. What makes his presentation on Thursday from 8:30 a.m. to 9:15 a.m. a must-see is its focus on the future: “Many new drugs are being developed based on the research on how insulin works. This lecture will be exciting to hear what is in the pipeline for drugs that manipulate insulin action,” Dr. Tangpricha said.
Cushing’s Syndrome
Beta-Cell Regeneration
The work of Andrew F. Stewart, MD, scientific director of the Mount Sinai Diabetes, Obesity and Metabolism Institute in New York, leads research into the basic mechanisms, prevention, and treatment of metabolic diseases. “In the past, we thought that there was a fixed number of beta cells in the body. However, recent research by Dr. Stewart’s group suggests that beta cells can be stimulated to grow. This is very exciting and can shape the future of how we take care of diabetes,” noted Dr. Tangpricha. The session is on Friday from 8:20 a.m. to 9:05 a.m.
New Insights Into Thyroid Hormone Action
On Thursday from 11:15 a.m. to 12:00 p.m., Anthony N. Hollenberg, MD, will present “an outstanding review on thyroid hormone and action and how this impacts patient care of those with thyroid disease,” Dr. Tangpricha said. Dr. Hollenberg is chief of the thyroid unit and the division of endocrinology, diabetes, and metabolism at Beth Israel Deaconess Medical Center in Boston.
Current and Evolving Approaches for Osteoporosis Treatment
Sundeep Khosla, MD, an expert on bone loss, will distill the myriad osteoporosis treatments into useful information that can inform your practice now. “There have been a number of drugs that have been released for the treatment of osteoporosis. We are now in an era where we can consider using drugs targeted for specific populations or specific combinations,” Dr. Tangpricha commented. This session is on Saturday at 8:15 a.m. to 9:00 a.m.
Boston is the location and inspiration for the featured presentations at the annual meeting of the American Association of Clinical Endocrinologists, program chair Vin Tangpricha, MD, PhD, said in an interview.
The program agenda for the congress, held May 16-20, boasts 143 speakers, 66 distinct clinical endocrinology educational sessions, and an opening plenary presentation featuring one of modern medicine’s most renowned diabetes and obesity researchers, according to a statement from the AACE.
New Dimensions in Insulin Action and Why They Are Important to Know
C. Ronald Kahn, MD, chief academic officer and head of Integrative Physiology and Metabolism at Joslin Diabetes Center in Boston, pioneered revolutionary work with insulin receptors and insulin resistance in diabetes and obesity. What makes his presentation on Thursday from 8:30 a.m. to 9:15 a.m. a must-see is its focus on the future: “Many new drugs are being developed based on the research on how insulin works. This lecture will be exciting to hear what is in the pipeline for drugs that manipulate insulin action,” Dr. Tangpricha said.
Cushing’s Syndrome
Beta-Cell Regeneration
The work of Andrew F. Stewart, MD, scientific director of the Mount Sinai Diabetes, Obesity and Metabolism Institute in New York, leads research into the basic mechanisms, prevention, and treatment of metabolic diseases. “In the past, we thought that there was a fixed number of beta cells in the body. However, recent research by Dr. Stewart’s group suggests that beta cells can be stimulated to grow. This is very exciting and can shape the future of how we take care of diabetes,” noted Dr. Tangpricha. The session is on Friday from 8:20 a.m. to 9:05 a.m.
New Insights Into Thyroid Hormone Action
On Thursday from 11:15 a.m. to 12:00 p.m., Anthony N. Hollenberg, MD, will present “an outstanding review on thyroid hormone and action and how this impacts patient care of those with thyroid disease,” Dr. Tangpricha said. Dr. Hollenberg is chief of the thyroid unit and the division of endocrinology, diabetes, and metabolism at Beth Israel Deaconess Medical Center in Boston.
Current and Evolving Approaches for Osteoporosis Treatment
Sundeep Khosla, MD, an expert on bone loss, will distill the myriad osteoporosis treatments into useful information that can inform your practice now. “There have been a number of drugs that have been released for the treatment of osteoporosis. We are now in an era where we can consider using drugs targeted for specific populations or specific combinations,” Dr. Tangpricha commented. This session is on Saturday at 8:15 a.m. to 9:00 a.m.
FROM AACE 2018
Original research expands at AACE 2018
This year’s meeting, in Boston May 16-20, has brought in a record number of accepted abstracts – 1,126 – in all areas of endocrinology. The lion’s share focuses on diabetes, thyroid disease, and bone disease. Most will be presented in Poster Viewing and Judging sessions at 10:00 a.m on Thursday for young investigators and during a poster viewing and wine and cheese reception from 4:30 p.m. to 6:30 p.m. on Friday for senior investigators.
Of note, the mother lode of clinical trials, retrospective analyses, and registry studies will be shown at the senior investigator competition on Friday evening.
That viewing session will include two post hoc analyses of data from the global SUSTAIN trial program in the investigational GLP-1 receptor agonist semaglutide. The first, Abstract 245, examines whether reductions in body weight and HbA1c differed between elderly and younger patients in SUSTAIN 7. The second, Abstract 298, is an analysis of SUSTAIN 1-5 and 7, looking at semaglutide’s effectiveness across racial and ethnic subgroups.
Another large trial, CANVAS, will be represented in two abstracts in this Friday session. In CANVAS, canagliflozin for primary prevention didn’t significantly reduce cardiovascular events in patients with at-risk type 2 diabetes, but it did so convincingly in a secondary prevention population. Outcomes by age group will be presented in Abstract 233, while those by changes in HbA1c and use of antihyperglycemic drugs will be presented in Abstract 262.
Other studies of interest in this viewing session include but are not limited to a comparison of the effects of hypnosis and certified diabetes educators on weight loss and changes in HbA1c levels (Abstract 602) and an investigation into whether the anabolic agent teriparatide can aid in foot bone remodeling in patients with Charcot neuroarthropathy (Abstract 225).
This year’s meeting, in Boston May 16-20, has brought in a record number of accepted abstracts – 1,126 – in all areas of endocrinology. The lion’s share focuses on diabetes, thyroid disease, and bone disease. Most will be presented in Poster Viewing and Judging sessions at 10:00 a.m on Thursday for young investigators and during a poster viewing and wine and cheese reception from 4:30 p.m. to 6:30 p.m. on Friday for senior investigators.
Of note, the mother lode of clinical trials, retrospective analyses, and registry studies will be shown at the senior investigator competition on Friday evening.
That viewing session will include two post hoc analyses of data from the global SUSTAIN trial program in the investigational GLP-1 receptor agonist semaglutide. The first, Abstract 245, examines whether reductions in body weight and HbA1c differed between elderly and younger patients in SUSTAIN 7. The second, Abstract 298, is an analysis of SUSTAIN 1-5 and 7, looking at semaglutide’s effectiveness across racial and ethnic subgroups.
Another large trial, CANVAS, will be represented in two abstracts in this Friday session. In CANVAS, canagliflozin for primary prevention didn’t significantly reduce cardiovascular events in patients with at-risk type 2 diabetes, but it did so convincingly in a secondary prevention population. Outcomes by age group will be presented in Abstract 233, while those by changes in HbA1c and use of antihyperglycemic drugs will be presented in Abstract 262.
Other studies of interest in this viewing session include but are not limited to a comparison of the effects of hypnosis and certified diabetes educators on weight loss and changes in HbA1c levels (Abstract 602) and an investigation into whether the anabolic agent teriparatide can aid in foot bone remodeling in patients with Charcot neuroarthropathy (Abstract 225).
This year’s meeting, in Boston May 16-20, has brought in a record number of accepted abstracts – 1,126 – in all areas of endocrinology. The lion’s share focuses on diabetes, thyroid disease, and bone disease. Most will be presented in Poster Viewing and Judging sessions at 10:00 a.m on Thursday for young investigators and during a poster viewing and wine and cheese reception from 4:30 p.m. to 6:30 p.m. on Friday for senior investigators.
Of note, the mother lode of clinical trials, retrospective analyses, and registry studies will be shown at the senior investigator competition on Friday evening.
That viewing session will include two post hoc analyses of data from the global SUSTAIN trial program in the investigational GLP-1 receptor agonist semaglutide. The first, Abstract 245, examines whether reductions in body weight and HbA1c differed between elderly and younger patients in SUSTAIN 7. The second, Abstract 298, is an analysis of SUSTAIN 1-5 and 7, looking at semaglutide’s effectiveness across racial and ethnic subgroups.
Another large trial, CANVAS, will be represented in two abstracts in this Friday session. In CANVAS, canagliflozin for primary prevention didn’t significantly reduce cardiovascular events in patients with at-risk type 2 diabetes, but it did so convincingly in a secondary prevention population. Outcomes by age group will be presented in Abstract 233, while those by changes in HbA1c and use of antihyperglycemic drugs will be presented in Abstract 262.
Other studies of interest in this viewing session include but are not limited to a comparison of the effects of hypnosis and certified diabetes educators on weight loss and changes in HbA1c levels (Abstract 602) and an investigation into whether the anabolic agent teriparatide can aid in foot bone remodeling in patients with Charcot neuroarthropathy (Abstract 225).
FROM AACE 2018
Spine fracture risk may be increased in IBD patients
Moreover, fracture risk appears to be higher among IBD patients using steroids, according to a report published in the Journal of Clinical Gastroenterology by Yuga Komaki, MD, of the Inflammatory Bowel Disease Center, University of Chicago, and coauthors.
“Further studies addressing the differential risk among Crohn’s disease and ulcerative colitis are needed, but strict surveillance and prevention of spine fractures are indicated in IBD,” wrote Dr. Komaki and associates.
The systematic review and meta-analysis by Dr. Komaki and colleagues was based on 10 studies comprising 470,541 patients with IBD for whom the risk of fracture was reported.
“It is of importance to identify the risk of fractures, as it will increase patient morbidity, disability, and mortality,” the authors wrote. “However, it is often overlooked in the management of IBD.”
Results of the analysis by this group of researchers showed that there was no significant difference in fracture risk overall between IBD patients and controls (odds ratio, 1.08; 95% confidence interval, 0.72-1.62; P = .70).
By contrast, the OR for spine fractures was significantly elevated (OR, 2.21; 95% CI, 1.39-3.50; P less than .0001), while risk of hip, rib, and wrist fractures were not, Dr. Komaki and coauthors said in their report.
Steroids were more often being used in the treatment of IBD patients who had fractures than in patients with no fractures, though the finding did not quite reach statistical significance (OR, 1.47; 95% CI, 0.99-2.20; P = .057).
Prior studies of fracture risk in IBD have shown “controversial results,” according to Dr. Komaki and colleagues. Some of those studies suggest an increased risk of fractures, whereas others suggest the risk is not different from what is seen in the general population.
“Individual studies may be underpowered to detect any risk,” they said in the report.
Steroids have been shown to increase risk of spine and rib fracture, but whether those earlier studies apply in IBD is unclear, they noted.
While the present meta-analysis sheds light on fracture risk in IBD patients, further meta-analyses may be needed to specifically look at cohorts of patients with Crohn’s disease and ulcerative colitis.
In this study, the investigators did find that spine fracture risk was significantly elevated in patients with Crohn’s disease, and was trending toward significance for ulcerative colitis patients. They cautioned that those results were based on a limited amount of patient data.
Dr. Komaki reported that he had no disclosures related to the reported study. One study coauthor reported disclosures related to AbbVie and Celltrion.
SOURCE: Komaki Y et al. J Clin Gastroenterol. 2018 Apr 18. 2018 Apr 18. doi: 10.1097/MCG.0000000000001031.
Moreover, fracture risk appears to be higher among IBD patients using steroids, according to a report published in the Journal of Clinical Gastroenterology by Yuga Komaki, MD, of the Inflammatory Bowel Disease Center, University of Chicago, and coauthors.
“Further studies addressing the differential risk among Crohn’s disease and ulcerative colitis are needed, but strict surveillance and prevention of spine fractures are indicated in IBD,” wrote Dr. Komaki and associates.
The systematic review and meta-analysis by Dr. Komaki and colleagues was based on 10 studies comprising 470,541 patients with IBD for whom the risk of fracture was reported.
“It is of importance to identify the risk of fractures, as it will increase patient morbidity, disability, and mortality,” the authors wrote. “However, it is often overlooked in the management of IBD.”
Results of the analysis by this group of researchers showed that there was no significant difference in fracture risk overall between IBD patients and controls (odds ratio, 1.08; 95% confidence interval, 0.72-1.62; P = .70).
By contrast, the OR for spine fractures was significantly elevated (OR, 2.21; 95% CI, 1.39-3.50; P less than .0001), while risk of hip, rib, and wrist fractures were not, Dr. Komaki and coauthors said in their report.
Steroids were more often being used in the treatment of IBD patients who had fractures than in patients with no fractures, though the finding did not quite reach statistical significance (OR, 1.47; 95% CI, 0.99-2.20; P = .057).
Prior studies of fracture risk in IBD have shown “controversial results,” according to Dr. Komaki and colleagues. Some of those studies suggest an increased risk of fractures, whereas others suggest the risk is not different from what is seen in the general population.
“Individual studies may be underpowered to detect any risk,” they said in the report.
Steroids have been shown to increase risk of spine and rib fracture, but whether those earlier studies apply in IBD is unclear, they noted.
While the present meta-analysis sheds light on fracture risk in IBD patients, further meta-analyses may be needed to specifically look at cohorts of patients with Crohn’s disease and ulcerative colitis.
In this study, the investigators did find that spine fracture risk was significantly elevated in patients with Crohn’s disease, and was trending toward significance for ulcerative colitis patients. They cautioned that those results were based on a limited amount of patient data.
Dr. Komaki reported that he had no disclosures related to the reported study. One study coauthor reported disclosures related to AbbVie and Celltrion.
SOURCE: Komaki Y et al. J Clin Gastroenterol. 2018 Apr 18. 2018 Apr 18. doi: 10.1097/MCG.0000000000001031.
Moreover, fracture risk appears to be higher among IBD patients using steroids, according to a report published in the Journal of Clinical Gastroenterology by Yuga Komaki, MD, of the Inflammatory Bowel Disease Center, University of Chicago, and coauthors.
“Further studies addressing the differential risk among Crohn’s disease and ulcerative colitis are needed, but strict surveillance and prevention of spine fractures are indicated in IBD,” wrote Dr. Komaki and associates.
The systematic review and meta-analysis by Dr. Komaki and colleagues was based on 10 studies comprising 470,541 patients with IBD for whom the risk of fracture was reported.
“It is of importance to identify the risk of fractures, as it will increase patient morbidity, disability, and mortality,” the authors wrote. “However, it is often overlooked in the management of IBD.”
Results of the analysis by this group of researchers showed that there was no significant difference in fracture risk overall between IBD patients and controls (odds ratio, 1.08; 95% confidence interval, 0.72-1.62; P = .70).
By contrast, the OR for spine fractures was significantly elevated (OR, 2.21; 95% CI, 1.39-3.50; P less than .0001), while risk of hip, rib, and wrist fractures were not, Dr. Komaki and coauthors said in their report.
Steroids were more often being used in the treatment of IBD patients who had fractures than in patients with no fractures, though the finding did not quite reach statistical significance (OR, 1.47; 95% CI, 0.99-2.20; P = .057).
Prior studies of fracture risk in IBD have shown “controversial results,” according to Dr. Komaki and colleagues. Some of those studies suggest an increased risk of fractures, whereas others suggest the risk is not different from what is seen in the general population.
“Individual studies may be underpowered to detect any risk,” they said in the report.
Steroids have been shown to increase risk of spine and rib fracture, but whether those earlier studies apply in IBD is unclear, they noted.
While the present meta-analysis sheds light on fracture risk in IBD patients, further meta-analyses may be needed to specifically look at cohorts of patients with Crohn’s disease and ulcerative colitis.
In this study, the investigators did find that spine fracture risk was significantly elevated in patients with Crohn’s disease, and was trending toward significance for ulcerative colitis patients. They cautioned that those results were based on a limited amount of patient data.
Dr. Komaki reported that he had no disclosures related to the reported study. One study coauthor reported disclosures related to AbbVie and Celltrion.
SOURCE: Komaki Y et al. J Clin Gastroenterol. 2018 Apr 18. 2018 Apr 18. doi: 10.1097/MCG.0000000000001031.
FROM THE JOURNAL OF CLINICAL GASTROENTEROLOGY
Key clinical point: Patients with inflammatory bowel disease may be at increased risk of fractures in the spine.
Major finding: The odds ratio for spine fractures was 2.21 (95% CI, 1.39-3.50; P less than .0001).
Study details: A systematic review and meta-analysis of 10 studies including 470,541 patients.
Disclosures: One study author reported disclosures related to AbbVie and Celltrion.
Source: Komaki Y et al. J Clin Gastroenterol. 2018 Apr 18. doi: 10.1097/MCG.0000000000001031.
Transgender women on HT have lower bone density, more fat mass than men
CHICAGO – according to findings from a recent Brazilian study.
“Lumbar spine density was lower than in reference men but similar to that of reference women,” said Tayane Muniz Fighera, MD, speaking at the annual meeting of the Endocrine Society.
Lower lumbar spine density in transgender women was associated with lower appendicular lean mass and higher total fat mass, with correlation coefficients of 0.327 and 0.334, respectively (P = .0001 for both).
Dr. Fighera and her colleagues looked at the independent contribution of age, estradiol level, appendicular lean mass, and fat mass to bone mineral density (BMD) in the transgender patients, using linear regression analysis. Total fat mass and appendicular lean mass were both independent predictors of bone mineral density (P = .001 and P = .022, respectively). For femur BMD, age, and total fat mass were predictors (P = .001 and P = .000, respectively).
The study aimed to assess bone mineral density as well as other aspects of body composition within a cohort of transgender women initiating hormone therapy in order to determine how estrogen therapy affected BMD and assess the prevalence of low bone mass among this population.
The hypothesis, said Dr. Fighera, was that hormone therapy for transgender women might decrease muscle mass and increase fat mass, “leading to less bone surface strain and smaller bone size over time,” said Dr. Fighera, of the Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Previous work has shown conflicting results, she said. “While some studies report that estrogen therapy is able to increase bone mass, others have observed no difference in BMD” despite the use of hormone therapy. The studies showing an association between estrogen therapy and decreased bone mass were those that followed patients for longer periods of time – 2 years or longer, she said.
Dr. Fighera explained that in Brazil, individuals with gender dysphoria have free access to hormone therapy and gender-affirming surgery through the public health service.
A total of 142 transgender women enrolled in the study, conducted at outpatient endocrine clinics for transgender people in Porto Alegre, Brazil. The clinics’ standardized hormone therapy protocol used daily estradiol valerate 1-4 mg, daily conjugated equine estrogen 0.625-2.5 mg, or daily transdermal 17 beta estradiol 0.5-2 mg. The estrogen therapy was accompanied by either spironolactone 50-150 mg per day, or cyproterone acetate 50-100 mg per day.
For comparison, the investigators enrolled 22 men and 17 women aged 18-40 years. All participants received a dual-energy x-ray absorptiometry (DXA) scan 3 months after those in the transgender arm began hormone therapy, and a second scan at 12 months. For the first year, participants were seen for clinical evaluation and lab studies every 3 months; they were seen every 6 months thereafter.
Although ranges were wide, estradiol levels in transgender women were, on average, approximately intermediate between the female and male control values. Total testosterone for transgender women was an average 1.17 nmol/L, closer to female (0.79 nmol/L) than male (16.39 nmol/L) values.
In a subgroup of 46 participants, Dr. Fighera and her colleagues also examined change over time for transgender women who remained on hormone therapy. Though they did find that appendicular lean mass declined and total fat mass increased from baseline, these changes in body composition were not associated with significant decreases in any BMD measurement when the DXA scan was repeated at 31 months.
Participants’ mean age was 33.7 years, and the mean BMI was 25.4 kg/m2. One-third of participants had already undergone gender-affirming surgery , and most (86.6%) had some previous exposure to hormone therapy. Almost all (96%) of study participants were white.
At 18%, “the prevalence of low bone mass for age was fairly high in this sample of [transgender women] from southern Brazil,” said Dr. Fighera. She called for more work to track change over time in hormone therapy–related bone loss for transgender women. “Until then, monitoring of bone mass should be considered in this population; nonpharmacological lifestyle-related strategies for preventing bone loss may benefit transgender women” who receive long-term hormone therapy, she said.
None of the study authors had disclosures to report.
SOURCE: Fighera T et al. ENDO 2018, Abstract OR 25-5.
CHICAGO – according to findings from a recent Brazilian study.
“Lumbar spine density was lower than in reference men but similar to that of reference women,” said Tayane Muniz Fighera, MD, speaking at the annual meeting of the Endocrine Society.
Lower lumbar spine density in transgender women was associated with lower appendicular lean mass and higher total fat mass, with correlation coefficients of 0.327 and 0.334, respectively (P = .0001 for both).
Dr. Fighera and her colleagues looked at the independent contribution of age, estradiol level, appendicular lean mass, and fat mass to bone mineral density (BMD) in the transgender patients, using linear regression analysis. Total fat mass and appendicular lean mass were both independent predictors of bone mineral density (P = .001 and P = .022, respectively). For femur BMD, age, and total fat mass were predictors (P = .001 and P = .000, respectively).
The study aimed to assess bone mineral density as well as other aspects of body composition within a cohort of transgender women initiating hormone therapy in order to determine how estrogen therapy affected BMD and assess the prevalence of low bone mass among this population.
The hypothesis, said Dr. Fighera, was that hormone therapy for transgender women might decrease muscle mass and increase fat mass, “leading to less bone surface strain and smaller bone size over time,” said Dr. Fighera, of the Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Previous work has shown conflicting results, she said. “While some studies report that estrogen therapy is able to increase bone mass, others have observed no difference in BMD” despite the use of hormone therapy. The studies showing an association between estrogen therapy and decreased bone mass were those that followed patients for longer periods of time – 2 years or longer, she said.
Dr. Fighera explained that in Brazil, individuals with gender dysphoria have free access to hormone therapy and gender-affirming surgery through the public health service.
A total of 142 transgender women enrolled in the study, conducted at outpatient endocrine clinics for transgender people in Porto Alegre, Brazil. The clinics’ standardized hormone therapy protocol used daily estradiol valerate 1-4 mg, daily conjugated equine estrogen 0.625-2.5 mg, or daily transdermal 17 beta estradiol 0.5-2 mg. The estrogen therapy was accompanied by either spironolactone 50-150 mg per day, or cyproterone acetate 50-100 mg per day.
For comparison, the investigators enrolled 22 men and 17 women aged 18-40 years. All participants received a dual-energy x-ray absorptiometry (DXA) scan 3 months after those in the transgender arm began hormone therapy, and a second scan at 12 months. For the first year, participants were seen for clinical evaluation and lab studies every 3 months; they were seen every 6 months thereafter.
Although ranges were wide, estradiol levels in transgender women were, on average, approximately intermediate between the female and male control values. Total testosterone for transgender women was an average 1.17 nmol/L, closer to female (0.79 nmol/L) than male (16.39 nmol/L) values.
In a subgroup of 46 participants, Dr. Fighera and her colleagues also examined change over time for transgender women who remained on hormone therapy. Though they did find that appendicular lean mass declined and total fat mass increased from baseline, these changes in body composition were not associated with significant decreases in any BMD measurement when the DXA scan was repeated at 31 months.
Participants’ mean age was 33.7 years, and the mean BMI was 25.4 kg/m2. One-third of participants had already undergone gender-affirming surgery , and most (86.6%) had some previous exposure to hormone therapy. Almost all (96%) of study participants were white.
At 18%, “the prevalence of low bone mass for age was fairly high in this sample of [transgender women] from southern Brazil,” said Dr. Fighera. She called for more work to track change over time in hormone therapy–related bone loss for transgender women. “Until then, monitoring of bone mass should be considered in this population; nonpharmacological lifestyle-related strategies for preventing bone loss may benefit transgender women” who receive long-term hormone therapy, she said.
None of the study authors had disclosures to report.
SOURCE: Fighera T et al. ENDO 2018, Abstract OR 25-5.
CHICAGO – according to findings from a recent Brazilian study.
“Lumbar spine density was lower than in reference men but similar to that of reference women,” said Tayane Muniz Fighera, MD, speaking at the annual meeting of the Endocrine Society.
Lower lumbar spine density in transgender women was associated with lower appendicular lean mass and higher total fat mass, with correlation coefficients of 0.327 and 0.334, respectively (P = .0001 for both).
Dr. Fighera and her colleagues looked at the independent contribution of age, estradiol level, appendicular lean mass, and fat mass to bone mineral density (BMD) in the transgender patients, using linear regression analysis. Total fat mass and appendicular lean mass were both independent predictors of bone mineral density (P = .001 and P = .022, respectively). For femur BMD, age, and total fat mass were predictors (P = .001 and P = .000, respectively).
The study aimed to assess bone mineral density as well as other aspects of body composition within a cohort of transgender women initiating hormone therapy in order to determine how estrogen therapy affected BMD and assess the prevalence of low bone mass among this population.
The hypothesis, said Dr. Fighera, was that hormone therapy for transgender women might decrease muscle mass and increase fat mass, “leading to less bone surface strain and smaller bone size over time,” said Dr. Fighera, of the Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Previous work has shown conflicting results, she said. “While some studies report that estrogen therapy is able to increase bone mass, others have observed no difference in BMD” despite the use of hormone therapy. The studies showing an association between estrogen therapy and decreased bone mass were those that followed patients for longer periods of time – 2 years or longer, she said.
Dr. Fighera explained that in Brazil, individuals with gender dysphoria have free access to hormone therapy and gender-affirming surgery through the public health service.
A total of 142 transgender women enrolled in the study, conducted at outpatient endocrine clinics for transgender people in Porto Alegre, Brazil. The clinics’ standardized hormone therapy protocol used daily estradiol valerate 1-4 mg, daily conjugated equine estrogen 0.625-2.5 mg, or daily transdermal 17 beta estradiol 0.5-2 mg. The estrogen therapy was accompanied by either spironolactone 50-150 mg per day, or cyproterone acetate 50-100 mg per day.
For comparison, the investigators enrolled 22 men and 17 women aged 18-40 years. All participants received a dual-energy x-ray absorptiometry (DXA) scan 3 months after those in the transgender arm began hormone therapy, and a second scan at 12 months. For the first year, participants were seen for clinical evaluation and lab studies every 3 months; they were seen every 6 months thereafter.
Although ranges were wide, estradiol levels in transgender women were, on average, approximately intermediate between the female and male control values. Total testosterone for transgender women was an average 1.17 nmol/L, closer to female (0.79 nmol/L) than male (16.39 nmol/L) values.
In a subgroup of 46 participants, Dr. Fighera and her colleagues also examined change over time for transgender women who remained on hormone therapy. Though they did find that appendicular lean mass declined and total fat mass increased from baseline, these changes in body composition were not associated with significant decreases in any BMD measurement when the DXA scan was repeated at 31 months.
Participants’ mean age was 33.7 years, and the mean BMI was 25.4 kg/m2. One-third of participants had already undergone gender-affirming surgery , and most (86.6%) had some previous exposure to hormone therapy. Almost all (96%) of study participants were white.
At 18%, “the prevalence of low bone mass for age was fairly high in this sample of [transgender women] from southern Brazil,” said Dr. Fighera. She called for more work to track change over time in hormone therapy–related bone loss for transgender women. “Until then, monitoring of bone mass should be considered in this population; nonpharmacological lifestyle-related strategies for preventing bone loss may benefit transgender women” who receive long-term hormone therapy, she said.
None of the study authors had disclosures to report.
SOURCE: Fighera T et al. ENDO 2018, Abstract OR 25-5.
REPORTING FROM ENDO 2018
Key clinical point: Transgender women on hormone therapy have bone mass more similar to women than men.
Major finding: Lower lumbar spine density was associated with higher total fat mass (P = .001).
Study details: Study of 142 transgender women receiving hormone therapy, tracked over time and compared with 22 men and 17 women for reference.
Disclosures: The study was sponsored by the Brazilian government. The authors reported that they have no conflicts of interest.
Source: Fighera T et al. ENDO 2018, Abstract OR 25-5.