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Eltrombopag receives priority review designation for SAA
Eltrombopag (Promacta®) in combination with standard immunosuppressive therapy (IST) has received priority review designation from the US Food and Drug Administration (FDA) for first-line treatment of severe aplastic anemia (SAA).
The drug is already approved for SAA in the refractory setting for patients who have had an insufficient response to IST.
And it is approved for adults and children with chronic immune thrombocytopenia (ITP) who are refractory to other treatments and for patients with chronic hepatitis C virus infection who are thrombocytopenic.
Eltrombopag, an oral thrombopoietin receptor agonist, had received breakthrough therapy designation from the FDA earlier this year for use in combination with IST as first-line treatment of SAA.
The priority review designation for the agent as a first-line treatment for SAA is supported by data from a phase 1/2 trial published in NEJM in April 2017 and subsequent data on file with Novartis.
The FDA intends to take action on a priority review application within 6 months of receiving it, rather than the standard 10 months.
The agency grants priority review to applications for products that may provide significant improvements in the treatment, diagnosis, or prevention of serious conditions.
Trial data
Ninety-two patients with previously untreated SAA were enrolled on the trial and received IST and eltrombopag in 3 different cohorts.
Cohorts varied by start day of eltrombopag and duration of eltrombopag therapy. Patients in cohort 1 received eltrombopag from day 14 to 6 months. Patients in cohort 2 received the drug from day 14 to 3 months. And patients in cohort 3 received eltrombopag from day 1 to 6 months.
The overall response rate (ORR) at 6 months was 80% (cohort 1), 87% (cohort 2), and 94% (cohort 3).
The complete response rate at 6 months was 33%, 26%, and 58% in the 3 cohorts, respectively.
At a median follow-up of 2 years, the overall survival rate was 97%.
In the corporate announcement of the priority review designation, Novartis reported an ORR of 85% at 6 months.
Adverse events included transient elevations in liver enzyme levels (7 patients) and 2 severe adverse events—grades 2 and 3 cutaneous eruption—related to eltrombopag that resulted in patients stopping the drug.
Eltrombopag is marketed as Revolade in countries outside the US.
Eltrombopag (Promacta®) in combination with standard immunosuppressive therapy (IST) has received priority review designation from the US Food and Drug Administration (FDA) for first-line treatment of severe aplastic anemia (SAA).
The drug is already approved for SAA in the refractory setting for patients who have had an insufficient response to IST.
And it is approved for adults and children with chronic immune thrombocytopenia (ITP) who are refractory to other treatments and for patients with chronic hepatitis C virus infection who are thrombocytopenic.
Eltrombopag, an oral thrombopoietin receptor agonist, had received breakthrough therapy designation from the FDA earlier this year for use in combination with IST as first-line treatment of SAA.
The priority review designation for the agent as a first-line treatment for SAA is supported by data from a phase 1/2 trial published in NEJM in April 2017 and subsequent data on file with Novartis.
The FDA intends to take action on a priority review application within 6 months of receiving it, rather than the standard 10 months.
The agency grants priority review to applications for products that may provide significant improvements in the treatment, diagnosis, or prevention of serious conditions.
Trial data
Ninety-two patients with previously untreated SAA were enrolled on the trial and received IST and eltrombopag in 3 different cohorts.
Cohorts varied by start day of eltrombopag and duration of eltrombopag therapy. Patients in cohort 1 received eltrombopag from day 14 to 6 months. Patients in cohort 2 received the drug from day 14 to 3 months. And patients in cohort 3 received eltrombopag from day 1 to 6 months.
The overall response rate (ORR) at 6 months was 80% (cohort 1), 87% (cohort 2), and 94% (cohort 3).
The complete response rate at 6 months was 33%, 26%, and 58% in the 3 cohorts, respectively.
At a median follow-up of 2 years, the overall survival rate was 97%.
In the corporate announcement of the priority review designation, Novartis reported an ORR of 85% at 6 months.
Adverse events included transient elevations in liver enzyme levels (7 patients) and 2 severe adverse events—grades 2 and 3 cutaneous eruption—related to eltrombopag that resulted in patients stopping the drug.
Eltrombopag is marketed as Revolade in countries outside the US.
Eltrombopag (Promacta®) in combination with standard immunosuppressive therapy (IST) has received priority review designation from the US Food and Drug Administration (FDA) for first-line treatment of severe aplastic anemia (SAA).
The drug is already approved for SAA in the refractory setting for patients who have had an insufficient response to IST.
And it is approved for adults and children with chronic immune thrombocytopenia (ITP) who are refractory to other treatments and for patients with chronic hepatitis C virus infection who are thrombocytopenic.
Eltrombopag, an oral thrombopoietin receptor agonist, had received breakthrough therapy designation from the FDA earlier this year for use in combination with IST as first-line treatment of SAA.
The priority review designation for the agent as a first-line treatment for SAA is supported by data from a phase 1/2 trial published in NEJM in April 2017 and subsequent data on file with Novartis.
The FDA intends to take action on a priority review application within 6 months of receiving it, rather than the standard 10 months.
The agency grants priority review to applications for products that may provide significant improvements in the treatment, diagnosis, or prevention of serious conditions.
Trial data
Ninety-two patients with previously untreated SAA were enrolled on the trial and received IST and eltrombopag in 3 different cohorts.
Cohorts varied by start day of eltrombopag and duration of eltrombopag therapy. Patients in cohort 1 received eltrombopag from day 14 to 6 months. Patients in cohort 2 received the drug from day 14 to 3 months. And patients in cohort 3 received eltrombopag from day 1 to 6 months.
The overall response rate (ORR) at 6 months was 80% (cohort 1), 87% (cohort 2), and 94% (cohort 3).
The complete response rate at 6 months was 33%, 26%, and 58% in the 3 cohorts, respectively.
At a median follow-up of 2 years, the overall survival rate was 97%.
In the corporate announcement of the priority review designation, Novartis reported an ORR of 85% at 6 months.
Adverse events included transient elevations in liver enzyme levels (7 patients) and 2 severe adverse events—grades 2 and 3 cutaneous eruption—related to eltrombopag that resulted in patients stopping the drug.
Eltrombopag is marketed as Revolade in countries outside the US.
Equal treatment, equal or better prostate cancer outcomes for black men
CHICAGO – Black men with advanced prostate cancer have survival with chemotherapy that rivals or surpasses that of white men with advanced disease, and black men with castration-resistant prostate cancer have better outcomes with abiraterone than white men.
Those conclusions come from two studies presented here at the annual meeting of the American Society of Clinical Oncology. Taken together, they suggest that although there may be genetic or biologic differences in cancer presentation among different racial groups, receiving the appropriate care can level out those differences.
In the first study, Susan Halabi, PhD, from Duke University in Durham, N.C., and colleagues pooled data from nine randomized phase 3 chemotherapy trials in men with advanced prostate cancer and found that black and white men had the same median survival, 21 months, but black men had an adjusted hazard ratio [HR} for death of 0.81, compared with white men.
For the subpopulation of African Americans who were enrolled in trials funded by the National Cancer Institute (NCI), the HR for death was 0.76 (P less than .0001).
“The bottom line, in a sense, is that African American men with advanced prostate cancer need to get to an oncologist and ideally need to get on a clinical trial, and if they do, their outcomes are every bit as good as Caucasian men, if not even a little bit better,” Richard Schilsky, MD, chief medical officer of ASCO, said at a briefing prior to presentation of the studies.
In the second study, a prospective clinical trial of abiraterone (Zytiga) in 100 men with metastatic castration-resistant prostate cancer (mCRPC), black men were more likely to have a decline in prostate-specific antigen (PSA), and a longer median time to PSA rise than white men (16.6 vs. 11.5 months), reported Daniel George, MD, also from Duke.
“There’s a 1.6 times greater likelihood that African Americans are diagnosed with prostate cancer, but a 2.4 times greater chance they die from that disease, and although there very well may be multi-factorial reasons for that, I think some of this is genetic,” he said.
Pooled analysis
In the United States, black men are more likely to be diagnosed with prostate cancer in their 40s and 50s than white men and are often diagnosed with advanced-stage and higher grade cancers. Black men also have double the rate of prostate cancer-specific deaths as white men.
Black men, however, are underrepresented in clinical trials, making it difficult to draw firm conclusions about racial differences due to small sample sizes.
To overcome this problem, Dr. Halabi and colleagues pooled data on 8,452 patients with mCRPC - including 7,528 white men and 500 African American men – from nine randomized phase 3 trials of docetaxel and prednisone or a regimen containing those agents.
Median overall survival, the primary endpoint, was 21.0 months for black men and 21.2 months for white men.
In multivariate analysis adjusted for age, PSA, performance status, alkaline phosphatase, hemoglobin, and metastatic sites, the pooled hazard ratio (HR) for black vs. white men was 0.81 (P = .001) for all patients in the study, and when the analysis was restricted to those patients who received only docetaxel and prednisone (4,172), the results were similar, Dr. Halabi said.
“I would argue that what this tells us is pretty striking: that African-American men have potentially better survival by getting conventional therapy,” commented ASCO expert Robert Dreicer, MD, MS, from the University of Virginia in Charlottesville.
“The nihilism associated with prostate cancer in African-American men is not supported by this really interesting work,” he continued. “What it says to us is when we treat those with bad prostate cancer, African Americans, they do well.”
Abiraterone Study
In the abiraterone study, 50 men who self-identified as white and 50 as black were enrolled and treated with abiraterone acetate and prednisone until disease progression or intolerable toxicity.
Radiographic progression-free survival, the primary endpoint, was 16.8 months in each group. As previously noted, however, median PFS was 16.6 months for black patients, vs. 11.5 months for white men. Black men also had a longer median PSA PFS, with 82% of black men having a 30% or greater PSA decline, compared with 78% of white patients. Respective proportions of men having higher declines were 74% vs. 66% experiencing a PSA decline of at least 50%, and 48% vs. 38% having a decline of at least 90%.
Rates of tumor flare, however, were higher among African Americans, at 16% vs. 4%.
Adverse event rates were generally similar between the study arms, although more white than black patients experienced fatigue, and more black than white patients had hypokalemia.
Single-nucletoide polymorphism (SNP) profiling showed differences between the two groups in key genes involved in androgen metabolism and transport, which may explain the improved responses to abiraterone among African Americans.
“We talk about access to care; we have now demonstrated that if you treat African Americans with standard-of-care drugs for advanced prostate cancer, there’s compelling evidence that they respond as well or maybe better than white men,” Dr. Dreicer commented.
“[We are] beginning to understand the differences that drive differential responses,” he continued. “When African-American men are under-represented in clinical trials, the trial outcomes might be different, frankly, because people respond differently to drugs. I think those are the take homes.”
SOURCE: Halabi et al, George et al. ASCO 2018 Abstracts LBA5005 and LBA5009
CHICAGO – Black men with advanced prostate cancer have survival with chemotherapy that rivals or surpasses that of white men with advanced disease, and black men with castration-resistant prostate cancer have better outcomes with abiraterone than white men.
Those conclusions come from two studies presented here at the annual meeting of the American Society of Clinical Oncology. Taken together, they suggest that although there may be genetic or biologic differences in cancer presentation among different racial groups, receiving the appropriate care can level out those differences.
In the first study, Susan Halabi, PhD, from Duke University in Durham, N.C., and colleagues pooled data from nine randomized phase 3 chemotherapy trials in men with advanced prostate cancer and found that black and white men had the same median survival, 21 months, but black men had an adjusted hazard ratio [HR} for death of 0.81, compared with white men.
For the subpopulation of African Americans who were enrolled in trials funded by the National Cancer Institute (NCI), the HR for death was 0.76 (P less than .0001).
“The bottom line, in a sense, is that African American men with advanced prostate cancer need to get to an oncologist and ideally need to get on a clinical trial, and if they do, their outcomes are every bit as good as Caucasian men, if not even a little bit better,” Richard Schilsky, MD, chief medical officer of ASCO, said at a briefing prior to presentation of the studies.
In the second study, a prospective clinical trial of abiraterone (Zytiga) in 100 men with metastatic castration-resistant prostate cancer (mCRPC), black men were more likely to have a decline in prostate-specific antigen (PSA), and a longer median time to PSA rise than white men (16.6 vs. 11.5 months), reported Daniel George, MD, also from Duke.
“There’s a 1.6 times greater likelihood that African Americans are diagnosed with prostate cancer, but a 2.4 times greater chance they die from that disease, and although there very well may be multi-factorial reasons for that, I think some of this is genetic,” he said.
Pooled analysis
In the United States, black men are more likely to be diagnosed with prostate cancer in their 40s and 50s than white men and are often diagnosed with advanced-stage and higher grade cancers. Black men also have double the rate of prostate cancer-specific deaths as white men.
Black men, however, are underrepresented in clinical trials, making it difficult to draw firm conclusions about racial differences due to small sample sizes.
To overcome this problem, Dr. Halabi and colleagues pooled data on 8,452 patients with mCRPC - including 7,528 white men and 500 African American men – from nine randomized phase 3 trials of docetaxel and prednisone or a regimen containing those agents.
Median overall survival, the primary endpoint, was 21.0 months for black men and 21.2 months for white men.
In multivariate analysis adjusted for age, PSA, performance status, alkaline phosphatase, hemoglobin, and metastatic sites, the pooled hazard ratio (HR) for black vs. white men was 0.81 (P = .001) for all patients in the study, and when the analysis was restricted to those patients who received only docetaxel and prednisone (4,172), the results were similar, Dr. Halabi said.
“I would argue that what this tells us is pretty striking: that African-American men have potentially better survival by getting conventional therapy,” commented ASCO expert Robert Dreicer, MD, MS, from the University of Virginia in Charlottesville.
“The nihilism associated with prostate cancer in African-American men is not supported by this really interesting work,” he continued. “What it says to us is when we treat those with bad prostate cancer, African Americans, they do well.”
Abiraterone Study
In the abiraterone study, 50 men who self-identified as white and 50 as black were enrolled and treated with abiraterone acetate and prednisone until disease progression or intolerable toxicity.
Radiographic progression-free survival, the primary endpoint, was 16.8 months in each group. As previously noted, however, median PFS was 16.6 months for black patients, vs. 11.5 months for white men. Black men also had a longer median PSA PFS, with 82% of black men having a 30% or greater PSA decline, compared with 78% of white patients. Respective proportions of men having higher declines were 74% vs. 66% experiencing a PSA decline of at least 50%, and 48% vs. 38% having a decline of at least 90%.
Rates of tumor flare, however, were higher among African Americans, at 16% vs. 4%.
Adverse event rates were generally similar between the study arms, although more white than black patients experienced fatigue, and more black than white patients had hypokalemia.
Single-nucletoide polymorphism (SNP) profiling showed differences between the two groups in key genes involved in androgen metabolism and transport, which may explain the improved responses to abiraterone among African Americans.
“We talk about access to care; we have now demonstrated that if you treat African Americans with standard-of-care drugs for advanced prostate cancer, there’s compelling evidence that they respond as well or maybe better than white men,” Dr. Dreicer commented.
“[We are] beginning to understand the differences that drive differential responses,” he continued. “When African-American men are under-represented in clinical trials, the trial outcomes might be different, frankly, because people respond differently to drugs. I think those are the take homes.”
SOURCE: Halabi et al, George et al. ASCO 2018 Abstracts LBA5005 and LBA5009
CHICAGO – Black men with advanced prostate cancer have survival with chemotherapy that rivals or surpasses that of white men with advanced disease, and black men with castration-resistant prostate cancer have better outcomes with abiraterone than white men.
Those conclusions come from two studies presented here at the annual meeting of the American Society of Clinical Oncology. Taken together, they suggest that although there may be genetic or biologic differences in cancer presentation among different racial groups, receiving the appropriate care can level out those differences.
In the first study, Susan Halabi, PhD, from Duke University in Durham, N.C., and colleagues pooled data from nine randomized phase 3 chemotherapy trials in men with advanced prostate cancer and found that black and white men had the same median survival, 21 months, but black men had an adjusted hazard ratio [HR} for death of 0.81, compared with white men.
For the subpopulation of African Americans who were enrolled in trials funded by the National Cancer Institute (NCI), the HR for death was 0.76 (P less than .0001).
“The bottom line, in a sense, is that African American men with advanced prostate cancer need to get to an oncologist and ideally need to get on a clinical trial, and if they do, their outcomes are every bit as good as Caucasian men, if not even a little bit better,” Richard Schilsky, MD, chief medical officer of ASCO, said at a briefing prior to presentation of the studies.
In the second study, a prospective clinical trial of abiraterone (Zytiga) in 100 men with metastatic castration-resistant prostate cancer (mCRPC), black men were more likely to have a decline in prostate-specific antigen (PSA), and a longer median time to PSA rise than white men (16.6 vs. 11.5 months), reported Daniel George, MD, also from Duke.
“There’s a 1.6 times greater likelihood that African Americans are diagnosed with prostate cancer, but a 2.4 times greater chance they die from that disease, and although there very well may be multi-factorial reasons for that, I think some of this is genetic,” he said.
Pooled analysis
In the United States, black men are more likely to be diagnosed with prostate cancer in their 40s and 50s than white men and are often diagnosed with advanced-stage and higher grade cancers. Black men also have double the rate of prostate cancer-specific deaths as white men.
Black men, however, are underrepresented in clinical trials, making it difficult to draw firm conclusions about racial differences due to small sample sizes.
To overcome this problem, Dr. Halabi and colleagues pooled data on 8,452 patients with mCRPC - including 7,528 white men and 500 African American men – from nine randomized phase 3 trials of docetaxel and prednisone or a regimen containing those agents.
Median overall survival, the primary endpoint, was 21.0 months for black men and 21.2 months for white men.
In multivariate analysis adjusted for age, PSA, performance status, alkaline phosphatase, hemoglobin, and metastatic sites, the pooled hazard ratio (HR) for black vs. white men was 0.81 (P = .001) for all patients in the study, and when the analysis was restricted to those patients who received only docetaxel and prednisone (4,172), the results were similar, Dr. Halabi said.
“I would argue that what this tells us is pretty striking: that African-American men have potentially better survival by getting conventional therapy,” commented ASCO expert Robert Dreicer, MD, MS, from the University of Virginia in Charlottesville.
“The nihilism associated with prostate cancer in African-American men is not supported by this really interesting work,” he continued. “What it says to us is when we treat those with bad prostate cancer, African Americans, they do well.”
Abiraterone Study
In the abiraterone study, 50 men who self-identified as white and 50 as black were enrolled and treated with abiraterone acetate and prednisone until disease progression or intolerable toxicity.
Radiographic progression-free survival, the primary endpoint, was 16.8 months in each group. As previously noted, however, median PFS was 16.6 months for black patients, vs. 11.5 months for white men. Black men also had a longer median PSA PFS, with 82% of black men having a 30% or greater PSA decline, compared with 78% of white patients. Respective proportions of men having higher declines were 74% vs. 66% experiencing a PSA decline of at least 50%, and 48% vs. 38% having a decline of at least 90%.
Rates of tumor flare, however, were higher among African Americans, at 16% vs. 4%.
Adverse event rates were generally similar between the study arms, although more white than black patients experienced fatigue, and more black than white patients had hypokalemia.
Single-nucletoide polymorphism (SNP) profiling showed differences between the two groups in key genes involved in androgen metabolism and transport, which may explain the improved responses to abiraterone among African Americans.
“We talk about access to care; we have now demonstrated that if you treat African Americans with standard-of-care drugs for advanced prostate cancer, there’s compelling evidence that they respond as well or maybe better than white men,” Dr. Dreicer commented.
“[We are] beginning to understand the differences that drive differential responses,” he continued. “When African-American men are under-represented in clinical trials, the trial outcomes might be different, frankly, because people respond differently to drugs. I think those are the take homes.”
SOURCE: Halabi et al, George et al. ASCO 2018 Abstracts LBA5005 and LBA5009
REPORTING FROM ASCO 2018
Key clinical point: Apparent racial disparities in prostate cancer care may be reduced or eliminated with proper care and access to clinical trials.
Major finding: In a pooled analysis, black men with advanced prostate cancer treated with docetaxel prednisone had a 19% lower risk for death than white men,
Study details: Pooled analysis of 9 randomized phase III trials with a total of 8,452 men and a prospective trial with 100 men with advanced prostate cancer.
Disclosures: The study by Halabi et al was funded by Congressionally Directed Medical Research Programs. The study by George et al was funded by Janssen. Dr. Halabi disclosed a consulting or advisory role with Tokai Pharmaceuticals, Eisai, and Bayer, and travel expenses from Bayer. Dr. George disclosed consulting/advising with Janssen and several other pharmaceutical companies, in addition to speakers’ bureau, travel expenses, and honoraria from various companies. He has also received institutional research funding from Exelixis, Genentech/Roche, Janssen Oncology, Novartis, Pfizer, Astellas Pharma, Bristol-Myers Squibb, Millennium, Acerta Pharma, Bayer, Dendreon, and Innocrin Pharma.
Source: Halabi et al, George et al. ASCO 2018 Abstracts LBA5005 and LBA5009.
Post-traumatic osteoarthritis needs to be prevention focus
, Jackie Whittaker, PT, PhD, said at the World Congress of Osteoarthritis.
“We all know that the burden of this disease is enormous and it’s expanding at an alarming rate,” she said at the congress, sponsored by the Osteoarthritis Research Society International.
“The only way that we have at this moment to try to reduce the burden of this disease is to shift our approach to management upstream and focus on prevention,” said Dr. Whittaker, who is an associate professor and research director at the University of Alberta, Edmonton, Canada.
According to the World Health Organization, OA is expected to become the fourth leading cause of disability worldwide by 2020. Furthermore, there will be a projected rise in prevalence from 12% to 25% in North America by 2030.
Dr. Whittaker suggested that it was time to try to identify those at risk of developing OA, such as after a joint injury, and ran through some suggestions on how posttraumatic OA (PTOA) might be preventable.
Secondary prevention of posttraumatic osteoarthritis
The prevention of PTOA can be split into primary, secondary and tertiary prevention, with primary prevention trying to prevent injuries from occurring in the first place.
“Strategies aimed at identifying and slowing down the onset of symptomatic osteoarthritis in preclinical populations would be referred to as secondary prevention,” Dr. Whittaker explained, adding that tertiary prevention would then be strategies aimed at improving function and reducing disability in those who already have symptomatic PTOA.
While there are programs that address primary and tertiary prevention – such as Footy First, an exercise training program adopted by the Australian Football League to reduce the risk of common leg injuries and the Good Life with osteoArthritis in Denmark (GLA:D®) education and supervised exercise program for those with symptomatic OA – there is more of a gap for secondary prevention.
Some of the first steps to developing a secondary prevention model would be to determine the extent of PTOA after joint injury and then identify risk factors or causal mechanisms. Then, prevention strategies could be developed and tested before implementation and effectiveness studies are performed.
Performing the necessary prospective cohort studies, however, is when things get challenging – PTOA can take 10–15 years to manifest and studies would potentially need to run for long periods of time, which comes at a cost. Other challenges are that there is no commonly agree definition. PTOA is multifactorial, and because people may be in their 20s, there could be other contributing factors to the disease course.
Identifying modifiable risk factors
There are a “fair number” of prospective and retrospective studies that have been done to try to identify patients at risk for OA after joint injury. Several have looked at unmodifiable risk factors, such as age and sex, and the type of injury. Others have looked at potentially modifiable factors such as the treatment approach and avoiding re-injury, joint mechanics and strength, body composition and aerobic fitness and behavioral characteristics such as physical activity and return to sport.
Data from the Alberta Youth PrE-OA Study, an ongoing longitudinal cohort study, have shown that structural changes consistent with OA are not unique to tears in the anterior cruciate ligament or to meniscal tears, which are known to up the risk of PTOA. Furthermore, the odds of having MRI-defined OA 3–10 years after a knee injury varies by the injury history, type, and surgery.
Other findings from the Alberta Youth PrE-OA Study data have shown that previously injured subjects have a 30% risk for re-injury, with weaker knee extensors and flexors and poorer dynamic balance than uninjured study participants. The results have also shown that there is reduced physical activity and avoidance in those who have been injured.
Who is the population at risk?
“Although the supporting evidence and the level of evidence for some of the risk factors is not as thorough as we would like it, there are some common themes across the literature, that are consistent to what we see in clinical practice, and what we know from primary and tertiary prevention,” Dr. Whittaker said. “Based upon that, we can start to hypothesize who’s at greatest risk of developing posttraumatic osteoarthritis and what we might start doing about it right now.”
Dr. Whittaker proposed the following risk factors could be used to “build a profile” of someone at risk of PTOA:
- Having sustained an anterior cruciate ligament (ACL) tear with or without a damaged meniscus
- Elevated body mass index (BMI) or adiposity, and low grade systemic inflammation
- Weak knee muscles, and poor dynamic balance
- Reduced or disengaged from physical activity
- Insufficient rehabilitation, pain or stiffness, or fear of movement
There is also an argument for nutrition being involved, Dr. Whittaker said, with levels of micronutrients such as vitamins D and K and calcium playing an integral role in bone health.
What could secondary prevention look like?
“So, with this risk profile, what can be done?” Dr. Whittaker asked rhetorically. Exercise therapy is key, and increasing the muscle strength of the knee and lower extremity are an important component of this strategy. Strength alone may not be enough, so exercise programs will need to increase the neuromuscular control of functional movements. Tackling people’s fear of movement will also be a priority. “I think it’s very important that we promote, if not implement, physical activity guidelines.”
Education is also going to be an important part of any secondary prevention program for PTOA, ensuring that people have realistic expectations about re-injury and their risk of developing osteoarthritis and the importance of remaining physically active. Balancing physical activity against their likelihood of flare-ups and learning how to avoid re-injury if at all possible. Weight control and diet will also be a component to include.
One final component is how clinicians work with patients to minimize their risk of PTOA. “We need to co-manage these patients,” Dr. Whittaker said. “We need to have difficult conversations with them and really balance giving them a picture of reality without over medicalizing the situation.”
Dr. Whitaker stated that she had no financial relationships or commercial interests to disclose.
SOURCE: Whittaker J, et al. Osteoarthritis Cartilage 2018:26(1):S7-8. Abstract I-22.
, Jackie Whittaker, PT, PhD, said at the World Congress of Osteoarthritis.
“We all know that the burden of this disease is enormous and it’s expanding at an alarming rate,” she said at the congress, sponsored by the Osteoarthritis Research Society International.
“The only way that we have at this moment to try to reduce the burden of this disease is to shift our approach to management upstream and focus on prevention,” said Dr. Whittaker, who is an associate professor and research director at the University of Alberta, Edmonton, Canada.
According to the World Health Organization, OA is expected to become the fourth leading cause of disability worldwide by 2020. Furthermore, there will be a projected rise in prevalence from 12% to 25% in North America by 2030.
Dr. Whittaker suggested that it was time to try to identify those at risk of developing OA, such as after a joint injury, and ran through some suggestions on how posttraumatic OA (PTOA) might be preventable.
Secondary prevention of posttraumatic osteoarthritis
The prevention of PTOA can be split into primary, secondary and tertiary prevention, with primary prevention trying to prevent injuries from occurring in the first place.
“Strategies aimed at identifying and slowing down the onset of symptomatic osteoarthritis in preclinical populations would be referred to as secondary prevention,” Dr. Whittaker explained, adding that tertiary prevention would then be strategies aimed at improving function and reducing disability in those who already have symptomatic PTOA.
While there are programs that address primary and tertiary prevention – such as Footy First, an exercise training program adopted by the Australian Football League to reduce the risk of common leg injuries and the Good Life with osteoArthritis in Denmark (GLA:D®) education and supervised exercise program for those with symptomatic OA – there is more of a gap for secondary prevention.
Some of the first steps to developing a secondary prevention model would be to determine the extent of PTOA after joint injury and then identify risk factors or causal mechanisms. Then, prevention strategies could be developed and tested before implementation and effectiveness studies are performed.
Performing the necessary prospective cohort studies, however, is when things get challenging – PTOA can take 10–15 years to manifest and studies would potentially need to run for long periods of time, which comes at a cost. Other challenges are that there is no commonly agree definition. PTOA is multifactorial, and because people may be in their 20s, there could be other contributing factors to the disease course.
Identifying modifiable risk factors
There are a “fair number” of prospective and retrospective studies that have been done to try to identify patients at risk for OA after joint injury. Several have looked at unmodifiable risk factors, such as age and sex, and the type of injury. Others have looked at potentially modifiable factors such as the treatment approach and avoiding re-injury, joint mechanics and strength, body composition and aerobic fitness and behavioral characteristics such as physical activity and return to sport.
Data from the Alberta Youth PrE-OA Study, an ongoing longitudinal cohort study, have shown that structural changes consistent with OA are not unique to tears in the anterior cruciate ligament or to meniscal tears, which are known to up the risk of PTOA. Furthermore, the odds of having MRI-defined OA 3–10 years after a knee injury varies by the injury history, type, and surgery.
Other findings from the Alberta Youth PrE-OA Study data have shown that previously injured subjects have a 30% risk for re-injury, with weaker knee extensors and flexors and poorer dynamic balance than uninjured study participants. The results have also shown that there is reduced physical activity and avoidance in those who have been injured.
Who is the population at risk?
“Although the supporting evidence and the level of evidence for some of the risk factors is not as thorough as we would like it, there are some common themes across the literature, that are consistent to what we see in clinical practice, and what we know from primary and tertiary prevention,” Dr. Whittaker said. “Based upon that, we can start to hypothesize who’s at greatest risk of developing posttraumatic osteoarthritis and what we might start doing about it right now.”
Dr. Whittaker proposed the following risk factors could be used to “build a profile” of someone at risk of PTOA:
- Having sustained an anterior cruciate ligament (ACL) tear with or without a damaged meniscus
- Elevated body mass index (BMI) or adiposity, and low grade systemic inflammation
- Weak knee muscles, and poor dynamic balance
- Reduced or disengaged from physical activity
- Insufficient rehabilitation, pain or stiffness, or fear of movement
There is also an argument for nutrition being involved, Dr. Whittaker said, with levels of micronutrients such as vitamins D and K and calcium playing an integral role in bone health.
What could secondary prevention look like?
“So, with this risk profile, what can be done?” Dr. Whittaker asked rhetorically. Exercise therapy is key, and increasing the muscle strength of the knee and lower extremity are an important component of this strategy. Strength alone may not be enough, so exercise programs will need to increase the neuromuscular control of functional movements. Tackling people’s fear of movement will also be a priority. “I think it’s very important that we promote, if not implement, physical activity guidelines.”
Education is also going to be an important part of any secondary prevention program for PTOA, ensuring that people have realistic expectations about re-injury and their risk of developing osteoarthritis and the importance of remaining physically active. Balancing physical activity against their likelihood of flare-ups and learning how to avoid re-injury if at all possible. Weight control and diet will also be a component to include.
One final component is how clinicians work with patients to minimize their risk of PTOA. “We need to co-manage these patients,” Dr. Whittaker said. “We need to have difficult conversations with them and really balance giving them a picture of reality without over medicalizing the situation.”
Dr. Whitaker stated that she had no financial relationships or commercial interests to disclose.
SOURCE: Whittaker J, et al. Osteoarthritis Cartilage 2018:26(1):S7-8. Abstract I-22.
, Jackie Whittaker, PT, PhD, said at the World Congress of Osteoarthritis.
“We all know that the burden of this disease is enormous and it’s expanding at an alarming rate,” she said at the congress, sponsored by the Osteoarthritis Research Society International.
“The only way that we have at this moment to try to reduce the burden of this disease is to shift our approach to management upstream and focus on prevention,” said Dr. Whittaker, who is an associate professor and research director at the University of Alberta, Edmonton, Canada.
According to the World Health Organization, OA is expected to become the fourth leading cause of disability worldwide by 2020. Furthermore, there will be a projected rise in prevalence from 12% to 25% in North America by 2030.
Dr. Whittaker suggested that it was time to try to identify those at risk of developing OA, such as after a joint injury, and ran through some suggestions on how posttraumatic OA (PTOA) might be preventable.
Secondary prevention of posttraumatic osteoarthritis
The prevention of PTOA can be split into primary, secondary and tertiary prevention, with primary prevention trying to prevent injuries from occurring in the first place.
“Strategies aimed at identifying and slowing down the onset of symptomatic osteoarthritis in preclinical populations would be referred to as secondary prevention,” Dr. Whittaker explained, adding that tertiary prevention would then be strategies aimed at improving function and reducing disability in those who already have symptomatic PTOA.
While there are programs that address primary and tertiary prevention – such as Footy First, an exercise training program adopted by the Australian Football League to reduce the risk of common leg injuries and the Good Life with osteoArthritis in Denmark (GLA:D®) education and supervised exercise program for those with symptomatic OA – there is more of a gap for secondary prevention.
Some of the first steps to developing a secondary prevention model would be to determine the extent of PTOA after joint injury and then identify risk factors or causal mechanisms. Then, prevention strategies could be developed and tested before implementation and effectiveness studies are performed.
Performing the necessary prospective cohort studies, however, is when things get challenging – PTOA can take 10–15 years to manifest and studies would potentially need to run for long periods of time, which comes at a cost. Other challenges are that there is no commonly agree definition. PTOA is multifactorial, and because people may be in their 20s, there could be other contributing factors to the disease course.
Identifying modifiable risk factors
There are a “fair number” of prospective and retrospective studies that have been done to try to identify patients at risk for OA after joint injury. Several have looked at unmodifiable risk factors, such as age and sex, and the type of injury. Others have looked at potentially modifiable factors such as the treatment approach and avoiding re-injury, joint mechanics and strength, body composition and aerobic fitness and behavioral characteristics such as physical activity and return to sport.
Data from the Alberta Youth PrE-OA Study, an ongoing longitudinal cohort study, have shown that structural changes consistent with OA are not unique to tears in the anterior cruciate ligament or to meniscal tears, which are known to up the risk of PTOA. Furthermore, the odds of having MRI-defined OA 3–10 years after a knee injury varies by the injury history, type, and surgery.
Other findings from the Alberta Youth PrE-OA Study data have shown that previously injured subjects have a 30% risk for re-injury, with weaker knee extensors and flexors and poorer dynamic balance than uninjured study participants. The results have also shown that there is reduced physical activity and avoidance in those who have been injured.
Who is the population at risk?
“Although the supporting evidence and the level of evidence for some of the risk factors is not as thorough as we would like it, there are some common themes across the literature, that are consistent to what we see in clinical practice, and what we know from primary and tertiary prevention,” Dr. Whittaker said. “Based upon that, we can start to hypothesize who’s at greatest risk of developing posttraumatic osteoarthritis and what we might start doing about it right now.”
Dr. Whittaker proposed the following risk factors could be used to “build a profile” of someone at risk of PTOA:
- Having sustained an anterior cruciate ligament (ACL) tear with or without a damaged meniscus
- Elevated body mass index (BMI) or adiposity, and low grade systemic inflammation
- Weak knee muscles, and poor dynamic balance
- Reduced or disengaged from physical activity
- Insufficient rehabilitation, pain or stiffness, or fear of movement
There is also an argument for nutrition being involved, Dr. Whittaker said, with levels of micronutrients such as vitamins D and K and calcium playing an integral role in bone health.
What could secondary prevention look like?
“So, with this risk profile, what can be done?” Dr. Whittaker asked rhetorically. Exercise therapy is key, and increasing the muscle strength of the knee and lower extremity are an important component of this strategy. Strength alone may not be enough, so exercise programs will need to increase the neuromuscular control of functional movements. Tackling people’s fear of movement will also be a priority. “I think it’s very important that we promote, if not implement, physical activity guidelines.”
Education is also going to be an important part of any secondary prevention program for PTOA, ensuring that people have realistic expectations about re-injury and their risk of developing osteoarthritis and the importance of remaining physically active. Balancing physical activity against their likelihood of flare-ups and learning how to avoid re-injury if at all possible. Weight control and diet will also be a component to include.
One final component is how clinicians work with patients to minimize their risk of PTOA. “We need to co-manage these patients,” Dr. Whittaker said. “We need to have difficult conversations with them and really balance giving them a picture of reality without over medicalizing the situation.”
Dr. Whitaker stated that she had no financial relationships or commercial interests to disclose.
SOURCE: Whittaker J, et al. Osteoarthritis Cartilage 2018:26(1):S7-8. Abstract I-22.
REPORTING FROM OARSI 2018
A blood test to detect lung cancer inches toward the clinic
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
CHICAGO - Uptake of recommended low-dose CT for lung cancer screening has been dismal. Blood-based assays are an attractive alternative being explored by the Circulating Cell–Free Genome Atlas (CCGA) project. Interim results of a CCGA study of 561 individuals without cancer and 118 patients with lung cancers of all stages have found that a trio of assays searching for molecular signatures in plasma cell-free DNA achieved roughly 50% sensitivity for detection of early-stage (stage I-IIIA) lung cancers and 91% sensitivity for detection of late-stage (stage IIIB-IV) lung cancers.
In this video interview from the annual meeting of the American Society of Clinical Oncology, lead study author Geoffrey R. Oxnard, MD, of the Dana-Farber Cancer Institute, Boston, discusses the science behind these assays, how they may fill an unmet medical need, and ongoing work to bring them into the clinic.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
CHICAGO - Uptake of recommended low-dose CT for lung cancer screening has been dismal. Blood-based assays are an attractive alternative being explored by the Circulating Cell–Free Genome Atlas (CCGA) project. Interim results of a CCGA study of 561 individuals without cancer and 118 patients with lung cancers of all stages have found that a trio of assays searching for molecular signatures in plasma cell-free DNA achieved roughly 50% sensitivity for detection of early-stage (stage I-IIIA) lung cancers and 91% sensitivity for detection of late-stage (stage IIIB-IV) lung cancers.
In this video interview from the annual meeting of the American Society of Clinical Oncology, lead study author Geoffrey R. Oxnard, MD, of the Dana-Farber Cancer Institute, Boston, discusses the science behind these assays, how they may fill an unmet medical need, and ongoing work to bring them into the clinic.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
CHICAGO - Uptake of recommended low-dose CT for lung cancer screening has been dismal. Blood-based assays are an attractive alternative being explored by the Circulating Cell–Free Genome Atlas (CCGA) project. Interim results of a CCGA study of 561 individuals without cancer and 118 patients with lung cancers of all stages have found that a trio of assays searching for molecular signatures in plasma cell-free DNA achieved roughly 50% sensitivity for detection of early-stage (stage I-IIIA) lung cancers and 91% sensitivity for detection of late-stage (stage IIIB-IV) lung cancers.
In this video interview from the annual meeting of the American Society of Clinical Oncology, lead study author Geoffrey R. Oxnard, MD, of the Dana-Farber Cancer Institute, Boston, discusses the science behind these assays, how they may fill an unmet medical need, and ongoing work to bring them into the clinic.
REPORTING FROM ASCO 2018
Heading down the wrong pathway in advanced breast cancer?
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
CHICAGO – In the SANDPIPER trial, the combination of the phosphatidylinositol 3-kinase (PI3K) inhibitor taselisib and the selective estrogen receptor modifier fulvestrant (Faslodex) was associated with a small but significant progression-free survival (PFS) benefit, compared with fulvestrant alone in women with advanced estrogen-receptor positive, HER2-negative breast cancer.
That 2-month PFS benefit, described as “modest” by investigators, came at the cost of significant toxicities, with nearly 50% of patients treated with the combination having grade 3 or greater toxicities, compared with 16% of patients treated with fulvestrant alone.
In this video interview from the annual meeting of the American Society of Clinical Oncology, ASCO expert Harold Burstein, MD, PhD, from the Dana-Farber Cancer Institute in Boston, questions whether the PI3K pathway, shown to be targetable in hematologic malignancies, is worth continuing to pursue in breast cancer.
Dr. Burstein had no disclosures.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
CHICAGO – In the SANDPIPER trial, the combination of the phosphatidylinositol 3-kinase (PI3K) inhibitor taselisib and the selective estrogen receptor modifier fulvestrant (Faslodex) was associated with a small but significant progression-free survival (PFS) benefit, compared with fulvestrant alone in women with advanced estrogen-receptor positive, HER2-negative breast cancer.
That 2-month PFS benefit, described as “modest” by investigators, came at the cost of significant toxicities, with nearly 50% of patients treated with the combination having grade 3 or greater toxicities, compared with 16% of patients treated with fulvestrant alone.
In this video interview from the annual meeting of the American Society of Clinical Oncology, ASCO expert Harold Burstein, MD, PhD, from the Dana-Farber Cancer Institute in Boston, questions whether the PI3K pathway, shown to be targetable in hematologic malignancies, is worth continuing to pursue in breast cancer.
Dr. Burstein had no disclosures.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
CHICAGO – In the SANDPIPER trial, the combination of the phosphatidylinositol 3-kinase (PI3K) inhibitor taselisib and the selective estrogen receptor modifier fulvestrant (Faslodex) was associated with a small but significant progression-free survival (PFS) benefit, compared with fulvestrant alone in women with advanced estrogen-receptor positive, HER2-negative breast cancer.
That 2-month PFS benefit, described as “modest” by investigators, came at the cost of significant toxicities, with nearly 50% of patients treated with the combination having grade 3 or greater toxicities, compared with 16% of patients treated with fulvestrant alone.
In this video interview from the annual meeting of the American Society of Clinical Oncology, ASCO expert Harold Burstein, MD, PhD, from the Dana-Farber Cancer Institute in Boston, questions whether the PI3K pathway, shown to be targetable in hematologic malignancies, is worth continuing to pursue in breast cancer.
Dr. Burstein had no disclosures.
REPORTING FROM ASCO 2018
Mediterranean diet cut fatty liver risk
Middle-aged and older adults who closely followed a Mediterranean-style diet for 6 years were at significantly lower risk of developing fatty liver disease than others in a large prospective study.
Each 1-standard-deviation rise in Mediterranean-style Diet Score (MDS) correlated with significantly decreased hepatic fat accumulation and a 26% lower odds of new onset fatty liver disease (P = .002). “To our knowledge, ours is the first prospective study to examine the relations of long-term habitual diet to fatty liver,” Jiantao Ma, MBBS, PhD, and his associates wrote in Gastroenterology. “Our findings indicate that improved diet quality may be particularly important for those with high genetic risk for NAFLD.”
Over a median 6 years of follow-up, each 1-standard deviation rise in MDS correlated with a 26% decrease in odds of new-onset fatty liver (95% CI, 10% to 39%; P = .002) and with a significant increase in liver phantom ratio (0.57; 95% confidence interval, 0.27 to 0.86; P less than .001), which signifies lower accumulation of liver fat. Similarly, every 1-standard deviation rise in the AHEI dietary score correlated with a 0.56 rise in liver phantom ratio (95% CI, 0.29 to 0.84; P less than .001) and with a 21% lower odds of incident fatty liver disease (95% CI, 5% to 35%; P = .02).
Individuals whose diets improved the most (those in the highest quartile of dietary score change) over time had about 80% less liver fat accumulate between baseline and follow-up compared with those whose diets worsened the most (those in the lowest quartile of dietary score change). Furthermore, relationship between diet and liver fat remained statistically significant (P = .02) even after accounting for changes in body mass index.
The investigators also studied whether the presence of single nucleotide polymorphisms (SNPs) linked with NAFLD modified dietary effects. High genetic risk for NAFLD did not appear to lead to increased liver fat as long as diet improved or remained stable over time, they found. But when diet worsened over time, high genetic NAFLD risk did correlate with significantly greater accumulation of liver fat (P less than .001).
“Future intervention studies are needed to test the efficacy and efficiency of diet-based approaches for NAFLD prevention as well as to examine mechanisms underlying the association between diet and NAFLD,” the researchers wrote.
The National Heart, Lung and Blood Institute’s Framingham Heart Study provided funding. Affymetrix provided genotyping. The researchers reported having no financial conflicts of interest.
SOURCE: Ma J, et al. Gastroenterology. 2018 Mar 28. doi: 10.1053/j.gastro.2018.03.038
Middle-aged and older adults who closely followed a Mediterranean-style diet for 6 years were at significantly lower risk of developing fatty liver disease than others in a large prospective study.
Each 1-standard-deviation rise in Mediterranean-style Diet Score (MDS) correlated with significantly decreased hepatic fat accumulation and a 26% lower odds of new onset fatty liver disease (P = .002). “To our knowledge, ours is the first prospective study to examine the relations of long-term habitual diet to fatty liver,” Jiantao Ma, MBBS, PhD, and his associates wrote in Gastroenterology. “Our findings indicate that improved diet quality may be particularly important for those with high genetic risk for NAFLD.”
Over a median 6 years of follow-up, each 1-standard deviation rise in MDS correlated with a 26% decrease in odds of new-onset fatty liver (95% CI, 10% to 39%; P = .002) and with a significant increase in liver phantom ratio (0.57; 95% confidence interval, 0.27 to 0.86; P less than .001), which signifies lower accumulation of liver fat. Similarly, every 1-standard deviation rise in the AHEI dietary score correlated with a 0.56 rise in liver phantom ratio (95% CI, 0.29 to 0.84; P less than .001) and with a 21% lower odds of incident fatty liver disease (95% CI, 5% to 35%; P = .02).
Individuals whose diets improved the most (those in the highest quartile of dietary score change) over time had about 80% less liver fat accumulate between baseline and follow-up compared with those whose diets worsened the most (those in the lowest quartile of dietary score change). Furthermore, relationship between diet and liver fat remained statistically significant (P = .02) even after accounting for changes in body mass index.
The investigators also studied whether the presence of single nucleotide polymorphisms (SNPs) linked with NAFLD modified dietary effects. High genetic risk for NAFLD did not appear to lead to increased liver fat as long as diet improved or remained stable over time, they found. But when diet worsened over time, high genetic NAFLD risk did correlate with significantly greater accumulation of liver fat (P less than .001).
“Future intervention studies are needed to test the efficacy and efficiency of diet-based approaches for NAFLD prevention as well as to examine mechanisms underlying the association between diet and NAFLD,” the researchers wrote.
The National Heart, Lung and Blood Institute’s Framingham Heart Study provided funding. Affymetrix provided genotyping. The researchers reported having no financial conflicts of interest.
SOURCE: Ma J, et al. Gastroenterology. 2018 Mar 28. doi: 10.1053/j.gastro.2018.03.038
Middle-aged and older adults who closely followed a Mediterranean-style diet for 6 years were at significantly lower risk of developing fatty liver disease than others in a large prospective study.
Each 1-standard-deviation rise in Mediterranean-style Diet Score (MDS) correlated with significantly decreased hepatic fat accumulation and a 26% lower odds of new onset fatty liver disease (P = .002). “To our knowledge, ours is the first prospective study to examine the relations of long-term habitual diet to fatty liver,” Jiantao Ma, MBBS, PhD, and his associates wrote in Gastroenterology. “Our findings indicate that improved diet quality may be particularly important for those with high genetic risk for NAFLD.”
Over a median 6 years of follow-up, each 1-standard deviation rise in MDS correlated with a 26% decrease in odds of new-onset fatty liver (95% CI, 10% to 39%; P = .002) and with a significant increase in liver phantom ratio (0.57; 95% confidence interval, 0.27 to 0.86; P less than .001), which signifies lower accumulation of liver fat. Similarly, every 1-standard deviation rise in the AHEI dietary score correlated with a 0.56 rise in liver phantom ratio (95% CI, 0.29 to 0.84; P less than .001) and with a 21% lower odds of incident fatty liver disease (95% CI, 5% to 35%; P = .02).
Individuals whose diets improved the most (those in the highest quartile of dietary score change) over time had about 80% less liver fat accumulate between baseline and follow-up compared with those whose diets worsened the most (those in the lowest quartile of dietary score change). Furthermore, relationship between diet and liver fat remained statistically significant (P = .02) even after accounting for changes in body mass index.
The investigators also studied whether the presence of single nucleotide polymorphisms (SNPs) linked with NAFLD modified dietary effects. High genetic risk for NAFLD did not appear to lead to increased liver fat as long as diet improved or remained stable over time, they found. But when diet worsened over time, high genetic NAFLD risk did correlate with significantly greater accumulation of liver fat (P less than .001).
“Future intervention studies are needed to test the efficacy and efficiency of diet-based approaches for NAFLD prevention as well as to examine mechanisms underlying the association between diet and NAFLD,” the researchers wrote.
The National Heart, Lung and Blood Institute’s Framingham Heart Study provided funding. Affymetrix provided genotyping. The researchers reported having no financial conflicts of interest.
SOURCE: Ma J, et al. Gastroenterology. 2018 Mar 28. doi: 10.1053/j.gastro.2018.03.038
FROM GASTROENTEROLOGY
Key clinical point: A Mediterranean-style diet was associated with significantly less liver fat accumulation and significantly lower risk of fatty liver disease.
Major finding: Each 1-standard-deviation increase in the Mediterranean Diet Score (MDS) correlated with a 26% lower odds of de novo NAFLD (P = .002).
Study details: Prospective study of 1,521 adults from the Framingham Heart Study.
Disclosures: The National Heart, Lung and Blood Institute’s Framingham Heart Study provided funding. Affymetrix provided genotyping. The researchers reported having no conflicts of interest.
Source: Ma J, et al. Gastroenterology. 2018 Mar 28.
Global MS trends: A chaotic picture with risk as the central theme
NASHVILLE, Tenn. – Recent epidemiologic studies of multiple sclerosis from around the globe paint a confusing picture, with incidence up in some countries and down in others, latitudinal associations strong in some regions and waning in others, and an overall lack of well-managed databases to bring order to these findings.
Alberto Ascherio, MD, who moderated a global epidemiology session during the annual meeting of the Consortium of Multiple Sclerosis Centers, said it’s tough to draw firm conclusions from the vastly varied studies assessing epidemiologic patterns of MS around the world. Most researchers are trying to extrapolate population data from smaller groups – a process always fraught with the potential for misinterpretation.
Global data, however, converge on some of the most well-established risk factors for the disease, he said. “There seems to be no doubt that vitamin D deficiency, teenager obesity, Epstein-Barr virus infection, and smoking remain strong risk factors for MS in every database in every country that has examined this,” said Dr. Ascherio, a professor of epidemiology and nutrition at Harvard University, Boston.
He sat down for a video interview to pick apart some of the findings from studies in Australia, New Zealand, Western Europe, Canada, and the United States.
Dr. Ascherio had no financial disclosures.
NASHVILLE, Tenn. – Recent epidemiologic studies of multiple sclerosis from around the globe paint a confusing picture, with incidence up in some countries and down in others, latitudinal associations strong in some regions and waning in others, and an overall lack of well-managed databases to bring order to these findings.
Alberto Ascherio, MD, who moderated a global epidemiology session during the annual meeting of the Consortium of Multiple Sclerosis Centers, said it’s tough to draw firm conclusions from the vastly varied studies assessing epidemiologic patterns of MS around the world. Most researchers are trying to extrapolate population data from smaller groups – a process always fraught with the potential for misinterpretation.
Global data, however, converge on some of the most well-established risk factors for the disease, he said. “There seems to be no doubt that vitamin D deficiency, teenager obesity, Epstein-Barr virus infection, and smoking remain strong risk factors for MS in every database in every country that has examined this,” said Dr. Ascherio, a professor of epidemiology and nutrition at Harvard University, Boston.
He sat down for a video interview to pick apart some of the findings from studies in Australia, New Zealand, Western Europe, Canada, and the United States.
Dr. Ascherio had no financial disclosures.
NASHVILLE, Tenn. – Recent epidemiologic studies of multiple sclerosis from around the globe paint a confusing picture, with incidence up in some countries and down in others, latitudinal associations strong in some regions and waning in others, and an overall lack of well-managed databases to bring order to these findings.
Alberto Ascherio, MD, who moderated a global epidemiology session during the annual meeting of the Consortium of Multiple Sclerosis Centers, said it’s tough to draw firm conclusions from the vastly varied studies assessing epidemiologic patterns of MS around the world. Most researchers are trying to extrapolate population data from smaller groups – a process always fraught with the potential for misinterpretation.
Global data, however, converge on some of the most well-established risk factors for the disease, he said. “There seems to be no doubt that vitamin D deficiency, teenager obesity, Epstein-Barr virus infection, and smoking remain strong risk factors for MS in every database in every country that has examined this,” said Dr. Ascherio, a professor of epidemiology and nutrition at Harvard University, Boston.
He sat down for a video interview to pick apart some of the findings from studies in Australia, New Zealand, Western Europe, Canada, and the United States.
Dr. Ascherio had no financial disclosures.
REPORTING FROM THE CMSC ANNUAL MEETING
Focus on preventing comorbidities in MS, physician urges
NASHVILLE, TENN. – Some patients use multiple sclerosis as an excuse to make poor health choices, but Allen C. Bowling, MD, PhD, of the Colorado Neurological Institute has seen another kind of story unfold. Fifteen to 20 years ago, Dr. Bowling said, he treated patients who took the development of MS in their 20s as a sign they needed to take better care of themselves. “They said MS was the best thing that happened to them ‘because it motivated me to make these healthy lifestyle changes I wouldn’t have made otherwise.’ ”
These patients have maintained their lifestyle changes, he said, lowering their risk of comorbidities and – perhaps – changing the course of their MS for the better.
“It’s all one machine, and sometimes we lose sight of that in our sub-sub-specialized world of treating MS ... You’re caring for a whole person. If you start thinking about that, it does make you think differently about how you treat the person, how you try to prevent disease in terms of certain pathways,” Dr. Bowling said in an interview at the annual meeting of the Consortium of Multiple Sclerosis Centers, where he spoke to colleagues about the importance of helping patients to adopt lifestyle changes.
According to Dr. Bowling, there’s evidence linking lifestyle-related comorbidities, poorer food quality, and tobacco use to higher levels of overall MS risk, relapses, disability, and symptoms.
Researchers have also linked other life factors to higher MS risks: obesity (linked to overall MS risk, disability, symptoms); lack of physical activity (linked to relapses, disability, symptoms); emotional factors (relapses, symptoms); and alcohol overuse (linked to overall risk, disability, symptoms).
“Data is mild to moderate to strong in all those areas for lifestyle approaches like diet, physical activity, emotional health, alcohol in moderation or less, and no tobacco smoking,” Dr. Bowling said.
He said he believes physical activity leads to “much higher and earlier success than diet” in MS patients, although there’s no confirmed “best exercise.”
As for nutrition, he said vitamins D and B12 are possibly beneficial. But he cautioned against the potential for harm from supplements and added that there’s no proven best diet for MS.
As for finding time to address these issues in clinic, Dr. Bowling recommended mentioning various lifestyle issues over multiple office visits.
“Some of the effort should be switched to the primary care doctor,” he said, “but you can use a strong collection of words to convey to the person with MS that this is serious: ‘It’s not MS, but it’s a serious issue, and you must see your primary care doctor.’ ”
He believes that this approach can have a significant impact, “especially for those aged 20-40, because the doctor they pay the most attention to may be their MS clinician.”
Dr. Bowling said that he receives royalties from a book he authored, “Optimal Health With Multiple Sclerosis.”
NASHVILLE, TENN. – Some patients use multiple sclerosis as an excuse to make poor health choices, but Allen C. Bowling, MD, PhD, of the Colorado Neurological Institute has seen another kind of story unfold. Fifteen to 20 years ago, Dr. Bowling said, he treated patients who took the development of MS in their 20s as a sign they needed to take better care of themselves. “They said MS was the best thing that happened to them ‘because it motivated me to make these healthy lifestyle changes I wouldn’t have made otherwise.’ ”
These patients have maintained their lifestyle changes, he said, lowering their risk of comorbidities and – perhaps – changing the course of their MS for the better.
“It’s all one machine, and sometimes we lose sight of that in our sub-sub-specialized world of treating MS ... You’re caring for a whole person. If you start thinking about that, it does make you think differently about how you treat the person, how you try to prevent disease in terms of certain pathways,” Dr. Bowling said in an interview at the annual meeting of the Consortium of Multiple Sclerosis Centers, where he spoke to colleagues about the importance of helping patients to adopt lifestyle changes.
According to Dr. Bowling, there’s evidence linking lifestyle-related comorbidities, poorer food quality, and tobacco use to higher levels of overall MS risk, relapses, disability, and symptoms.
Researchers have also linked other life factors to higher MS risks: obesity (linked to overall MS risk, disability, symptoms); lack of physical activity (linked to relapses, disability, symptoms); emotional factors (relapses, symptoms); and alcohol overuse (linked to overall risk, disability, symptoms).
“Data is mild to moderate to strong in all those areas for lifestyle approaches like diet, physical activity, emotional health, alcohol in moderation or less, and no tobacco smoking,” Dr. Bowling said.
He said he believes physical activity leads to “much higher and earlier success than diet” in MS patients, although there’s no confirmed “best exercise.”
As for nutrition, he said vitamins D and B12 are possibly beneficial. But he cautioned against the potential for harm from supplements and added that there’s no proven best diet for MS.
As for finding time to address these issues in clinic, Dr. Bowling recommended mentioning various lifestyle issues over multiple office visits.
“Some of the effort should be switched to the primary care doctor,” he said, “but you can use a strong collection of words to convey to the person with MS that this is serious: ‘It’s not MS, but it’s a serious issue, and you must see your primary care doctor.’ ”
He believes that this approach can have a significant impact, “especially for those aged 20-40, because the doctor they pay the most attention to may be their MS clinician.”
Dr. Bowling said that he receives royalties from a book he authored, “Optimal Health With Multiple Sclerosis.”
NASHVILLE, TENN. – Some patients use multiple sclerosis as an excuse to make poor health choices, but Allen C. Bowling, MD, PhD, of the Colorado Neurological Institute has seen another kind of story unfold. Fifteen to 20 years ago, Dr. Bowling said, he treated patients who took the development of MS in their 20s as a sign they needed to take better care of themselves. “They said MS was the best thing that happened to them ‘because it motivated me to make these healthy lifestyle changes I wouldn’t have made otherwise.’ ”
These patients have maintained their lifestyle changes, he said, lowering their risk of comorbidities and – perhaps – changing the course of their MS for the better.
“It’s all one machine, and sometimes we lose sight of that in our sub-sub-specialized world of treating MS ... You’re caring for a whole person. If you start thinking about that, it does make you think differently about how you treat the person, how you try to prevent disease in terms of certain pathways,” Dr. Bowling said in an interview at the annual meeting of the Consortium of Multiple Sclerosis Centers, where he spoke to colleagues about the importance of helping patients to adopt lifestyle changes.
According to Dr. Bowling, there’s evidence linking lifestyle-related comorbidities, poorer food quality, and tobacco use to higher levels of overall MS risk, relapses, disability, and symptoms.
Researchers have also linked other life factors to higher MS risks: obesity (linked to overall MS risk, disability, symptoms); lack of physical activity (linked to relapses, disability, symptoms); emotional factors (relapses, symptoms); and alcohol overuse (linked to overall risk, disability, symptoms).
“Data is mild to moderate to strong in all those areas for lifestyle approaches like diet, physical activity, emotional health, alcohol in moderation or less, and no tobacco smoking,” Dr. Bowling said.
He said he believes physical activity leads to “much higher and earlier success than diet” in MS patients, although there’s no confirmed “best exercise.”
As for nutrition, he said vitamins D and B12 are possibly beneficial. But he cautioned against the potential for harm from supplements and added that there’s no proven best diet for MS.
As for finding time to address these issues in clinic, Dr. Bowling recommended mentioning various lifestyle issues over multiple office visits.
“Some of the effort should be switched to the primary care doctor,” he said, “but you can use a strong collection of words to convey to the person with MS that this is serious: ‘It’s not MS, but it’s a serious issue, and you must see your primary care doctor.’ ”
He believes that this approach can have a significant impact, “especially for those aged 20-40, because the doctor they pay the most attention to may be their MS clinician.”
Dr. Bowling said that he receives royalties from a book he authored, “Optimal Health With Multiple Sclerosis.”
REPORTING FROM THE CMSC ANNUAL MEETING
Pregnancy may be ideal time to consider switching MS drugs
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
NASHVILLE, TENN – Women with multiple sclerosis who fare poorly on specific medications before pregnancy don’t tend to do any better afterward, a new study finds. This suggests that pregnancy – a period when many women with MS stop taking their medication – should trigger discussions about switching from drugs that aren’t doing the job, the study’s lead author said.
“It’s a good time to consider the therapy that the individual is on, whether it’s one that’s effective for them, and whether it’s one they should return to when they start up therapy post-partum. It’s likely it will affect them the same way” after pregnancy as before, Caila Vaughn, MPH, PhD, of the University of Buffalo, said in an interview at the 2018 annual meeting of the Consortium of Multiple Sclerosis Clinics.
From 2012-2017, the study authors sent surveys to 1,651 women in the New York State Multiple Sclerosis Consortium as part of an effort to understand how pregnancy affects women with MS, especially when relapses return in the post-partum period.
Of the 1,651 women, 635 (38% of the total) agreed to answer questions about their reproductive history.
Pregnancy data was available for 627 patients of whom 490 (78%) had been pregnant. Of those, 109 said they became pregnant after their MS diagnosis.
Fifty-three (49%) reported relapses in the 2 years prior to pregnancy and 46% reported them in the 2 subsequent years. Just 12% reported relapses during pregnancy, and 16% said they took disease-modifying drugs during pregnancy (60% had taken them before pregnancy).
Why does MS become less severe during pregnancy? “We believe the dormancy of the disease is related to an immune system that is naturally decreased and depressed during pregnancy,” Dr. Vaughn said. Afterward, she said, “the relapses are related to the recovery of the immune system post-partum.”
The researchers didn’t find any links between the use of disease-modifying drugs and relapses before, during, or after pregnancy.
Those who had relapses prior to pregnancy were more likely (P = 0.011) to have them afterward too. But researchers didn’t find a statistically significant link between relapses that occurred during and after pregnancy.
More than three-quarters of those who took disease-modifying drugs before pregnancy returned to using them afterward, in most cases within 3 months.
The study findings suggest that pregnancy is a helpful decision point when patients should take a closer look at the effects of their medications, Dr. Vaughn said. “In conjunction with a physician, they should decide if it’s a good one they should return to.”
Reflecting the findings of other research that suggests pregnancy is safe in women with MS, the study shows no sign that pregnancy – either before or after diagnosis of MS – boosts the risk that MS will get worse.
As for the possible effects of disease-modifying drugs on new mothers who breast-feed, the researchers found no evidence of adverse outcomes in 5 patients who took the medications while breast-feeding.
The study was funded by Teva. Dr. Vaughn reported no relevant disclosures. Several other study authors report various disclosures, including relationships with Teva.
SOURCE: Vaughn C. et al. Abstract FC04, 2018 annual meeting, Consortium of Multiple Sclerosis Centers.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
NASHVILLE, TENN – Women with multiple sclerosis who fare poorly on specific medications before pregnancy don’t tend to do any better afterward, a new study finds. This suggests that pregnancy – a period when many women with MS stop taking their medication – should trigger discussions about switching from drugs that aren’t doing the job, the study’s lead author said.
“It’s a good time to consider the therapy that the individual is on, whether it’s one that’s effective for them, and whether it’s one they should return to when they start up therapy post-partum. It’s likely it will affect them the same way” after pregnancy as before, Caila Vaughn, MPH, PhD, of the University of Buffalo, said in an interview at the 2018 annual meeting of the Consortium of Multiple Sclerosis Clinics.
From 2012-2017, the study authors sent surveys to 1,651 women in the New York State Multiple Sclerosis Consortium as part of an effort to understand how pregnancy affects women with MS, especially when relapses return in the post-partum period.
Of the 1,651 women, 635 (38% of the total) agreed to answer questions about their reproductive history.
Pregnancy data was available for 627 patients of whom 490 (78%) had been pregnant. Of those, 109 said they became pregnant after their MS diagnosis.
Fifty-three (49%) reported relapses in the 2 years prior to pregnancy and 46% reported them in the 2 subsequent years. Just 12% reported relapses during pregnancy, and 16% said they took disease-modifying drugs during pregnancy (60% had taken them before pregnancy).
Why does MS become less severe during pregnancy? “We believe the dormancy of the disease is related to an immune system that is naturally decreased and depressed during pregnancy,” Dr. Vaughn said. Afterward, she said, “the relapses are related to the recovery of the immune system post-partum.”
The researchers didn’t find any links between the use of disease-modifying drugs and relapses before, during, or after pregnancy.
Those who had relapses prior to pregnancy were more likely (P = 0.011) to have them afterward too. But researchers didn’t find a statistically significant link between relapses that occurred during and after pregnancy.
More than three-quarters of those who took disease-modifying drugs before pregnancy returned to using them afterward, in most cases within 3 months.
The study findings suggest that pregnancy is a helpful decision point when patients should take a closer look at the effects of their medications, Dr. Vaughn said. “In conjunction with a physician, they should decide if it’s a good one they should return to.”
Reflecting the findings of other research that suggests pregnancy is safe in women with MS, the study shows no sign that pregnancy – either before or after diagnosis of MS – boosts the risk that MS will get worse.
As for the possible effects of disease-modifying drugs on new mothers who breast-feed, the researchers found no evidence of adverse outcomes in 5 patients who took the medications while breast-feeding.
The study was funded by Teva. Dr. Vaughn reported no relevant disclosures. Several other study authors report various disclosures, including relationships with Teva.
SOURCE: Vaughn C. et al. Abstract FC04, 2018 annual meeting, Consortium of Multiple Sclerosis Centers.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
NASHVILLE, TENN – Women with multiple sclerosis who fare poorly on specific medications before pregnancy don’t tend to do any better afterward, a new study finds. This suggests that pregnancy – a period when many women with MS stop taking their medication – should trigger discussions about switching from drugs that aren’t doing the job, the study’s lead author said.
“It’s a good time to consider the therapy that the individual is on, whether it’s one that’s effective for them, and whether it’s one they should return to when they start up therapy post-partum. It’s likely it will affect them the same way” after pregnancy as before, Caila Vaughn, MPH, PhD, of the University of Buffalo, said in an interview at the 2018 annual meeting of the Consortium of Multiple Sclerosis Clinics.
From 2012-2017, the study authors sent surveys to 1,651 women in the New York State Multiple Sclerosis Consortium as part of an effort to understand how pregnancy affects women with MS, especially when relapses return in the post-partum period.
Of the 1,651 women, 635 (38% of the total) agreed to answer questions about their reproductive history.
Pregnancy data was available for 627 patients of whom 490 (78%) had been pregnant. Of those, 109 said they became pregnant after their MS diagnosis.
Fifty-three (49%) reported relapses in the 2 years prior to pregnancy and 46% reported them in the 2 subsequent years. Just 12% reported relapses during pregnancy, and 16% said they took disease-modifying drugs during pregnancy (60% had taken them before pregnancy).
Why does MS become less severe during pregnancy? “We believe the dormancy of the disease is related to an immune system that is naturally decreased and depressed during pregnancy,” Dr. Vaughn said. Afterward, she said, “the relapses are related to the recovery of the immune system post-partum.”
The researchers didn’t find any links between the use of disease-modifying drugs and relapses before, during, or after pregnancy.
Those who had relapses prior to pregnancy were more likely (P = 0.011) to have them afterward too. But researchers didn’t find a statistically significant link between relapses that occurred during and after pregnancy.
More than three-quarters of those who took disease-modifying drugs before pregnancy returned to using them afterward, in most cases within 3 months.
The study findings suggest that pregnancy is a helpful decision point when patients should take a closer look at the effects of their medications, Dr. Vaughn said. “In conjunction with a physician, they should decide if it’s a good one they should return to.”
Reflecting the findings of other research that suggests pregnancy is safe in women with MS, the study shows no sign that pregnancy – either before or after diagnosis of MS – boosts the risk that MS will get worse.
As for the possible effects of disease-modifying drugs on new mothers who breast-feed, the researchers found no evidence of adverse outcomes in 5 patients who took the medications while breast-feeding.
The study was funded by Teva. Dr. Vaughn reported no relevant disclosures. Several other study authors report various disclosures, including relationships with Teva.
SOURCE: Vaughn C. et al. Abstract FC04, 2018 annual meeting, Consortium of Multiple Sclerosis Centers.
REPORTING FROM THE CMSC ANNUAL MEETING
Key clinical point: Multiple sclerosis relapse rates are similar before and after pregnancy, suggesting it may be a good time to consider switching medications if feasible.
Major finding: 49% of women who were pregnant after MS diagnosis reported relapses in the 2 years prior to pregnancy and 46% reported them in the 2 subsequent years. Those who had relapses prior to pregnancy were more likely to have them afterward, too.
Study details: Survey of 109 women who became pregnant after MS diagnosis.
Disclosures: Teva funded the study. Several study authors report various disclosures, including relationships with Teva.
Source: Vaughn C. et al. Abstract FC04, 2018 annual meeting, Consortium of Multiple Sclerosis Centers.
MS clinic thrives by making regular care a ‘loss leader’
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
NASHVILLE, TENN. – Care for MS patients is expensive, and even non-profit treatment centers can’t survive on reimbursements alone. The solution, according to Terry Smith, CEO of the Multiple Sclerosis Center of Atlanta, is to transform regular care into a “loss leader” and embrace other revenue sources.
“The reimbursements for that 20- minute or 30-minute follow-up just really don’t cover all the resources necessary for comprehensive care,” Mr. Smith said in a video interview at the 2018 annual meeting of the Consortium of Multiple Sclerosis Clinics.
Mr. Smith said his involvement in the MS community was sparked about 2 decades ago when his wife developed the condition. “I have seen what the center gets reimbursed for her office visit, and then what her neurologist gets reimbursed.”
The reimbursement for an MS patient’s follow-up, 25-minute appointment with a physician is $104.25, according to Mr. Smith. Yet these MS visits are “the cornerstone of treatment ... set the tone for how successful the care is.”
To make make up for losses, the Atlanta center has begun offering its own ancillary services. “Our doctors are at the forefront of telling patients we have a group of neurologists that handle both emergent as well as non-emergent neurology,” he said. “That offers a revenue stream beyond the patient encounter.”
Other sources include imaging and an infusion clinic managed for a local hospital through a professional service agreement. The Atlanta center also has created its own specialty pharmacy focused on MS. “We buy disease-modifying drugs, develop personal contact with patients on a regular basis, then develop an ongoing compliance-monitoring program,” he said.
Mr. Smith discloses a consulting fee from Novartis.
Watch the interview to learn more about the center’s efforts.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
NASHVILLE, TENN. – Care for MS patients is expensive, and even non-profit treatment centers can’t survive on reimbursements alone. The solution, according to Terry Smith, CEO of the Multiple Sclerosis Center of Atlanta, is to transform regular care into a “loss leader” and embrace other revenue sources.
“The reimbursements for that 20- minute or 30-minute follow-up just really don’t cover all the resources necessary for comprehensive care,” Mr. Smith said in a video interview at the 2018 annual meeting of the Consortium of Multiple Sclerosis Clinics.
Mr. Smith said his involvement in the MS community was sparked about 2 decades ago when his wife developed the condition. “I have seen what the center gets reimbursed for her office visit, and then what her neurologist gets reimbursed.”
The reimbursement for an MS patient’s follow-up, 25-minute appointment with a physician is $104.25, according to Mr. Smith. Yet these MS visits are “the cornerstone of treatment ... set the tone for how successful the care is.”
To make make up for losses, the Atlanta center has begun offering its own ancillary services. “Our doctors are at the forefront of telling patients we have a group of neurologists that handle both emergent as well as non-emergent neurology,” he said. “That offers a revenue stream beyond the patient encounter.”
Other sources include imaging and an infusion clinic managed for a local hospital through a professional service agreement. The Atlanta center also has created its own specialty pharmacy focused on MS. “We buy disease-modifying drugs, develop personal contact with patients on a regular basis, then develop an ongoing compliance-monitoring program,” he said.
Mr. Smith discloses a consulting fee from Novartis.
Watch the interview to learn more about the center’s efforts.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
NASHVILLE, TENN. – Care for MS patients is expensive, and even non-profit treatment centers can’t survive on reimbursements alone. The solution, according to Terry Smith, CEO of the Multiple Sclerosis Center of Atlanta, is to transform regular care into a “loss leader” and embrace other revenue sources.
“The reimbursements for that 20- minute or 30-minute follow-up just really don’t cover all the resources necessary for comprehensive care,” Mr. Smith said in a video interview at the 2018 annual meeting of the Consortium of Multiple Sclerosis Clinics.
Mr. Smith said his involvement in the MS community was sparked about 2 decades ago when his wife developed the condition. “I have seen what the center gets reimbursed for her office visit, and then what her neurologist gets reimbursed.”
The reimbursement for an MS patient’s follow-up, 25-minute appointment with a physician is $104.25, according to Mr. Smith. Yet these MS visits are “the cornerstone of treatment ... set the tone for how successful the care is.”
To make make up for losses, the Atlanta center has begun offering its own ancillary services. “Our doctors are at the forefront of telling patients we have a group of neurologists that handle both emergent as well as non-emergent neurology,” he said. “That offers a revenue stream beyond the patient encounter.”
Other sources include imaging and an infusion clinic managed for a local hospital through a professional service agreement. The Atlanta center also has created its own specialty pharmacy focused on MS. “We buy disease-modifying drugs, develop personal contact with patients on a regular basis, then develop an ongoing compliance-monitoring program,” he said.
Mr. Smith discloses a consulting fee from Novartis.
Watch the interview to learn more about the center’s efforts.
REPORTING FROM THE CMSC ANNUAL MEETING
