In this edition of “How I will treat my next patient,” I take a look at two “chemo-free” neoadjuvant studies reported at the annual meeting of the American Society of Clinical Oncology. One summarizes the potential utility of immune checkpoint inhibitors (ICIs) in non–small cell lung cancer (NSCLC) patients who are – or can become – candidates for curative resection and the other highlights the potential utility of neoadjuvant trastuzumab emtansine (T-DM1) for HER2-positive breast cancer patients.

NEOSTAR in NSCLC

With the accumulation of comorbid conditions in an aging population, we all see NSCLC patients who are potential candidates for curative surgery, but for whom we have concerns about standard preoperative chemotherapy plus or minus radiation. At ASCO 2019, abstracts 8503 (atezolizumab, the LCMC3 trial) and 8504 (nivolumab plus or minus ipilimumab, NEOSTAR) addressed the neoadjuvant use of ICIs. I will focus on NEOSTAR, because the major pathologic response (mPR) rate – reduction in viable tumor cells to 10% or less – was higher with the combination of nivolumab plus ipilimumab in NEOSTAR than with single agent nivolumab or atezolizumab in the NEOSTAR or LCMC3 trials, respectively.

Briefly, 44 patients with stage I-IIIA NSCLC were randomized to nivolumab plus or minus ipilimumab. In total, 93% completed 6 weeks of neoadjuvant therapy and 89% were resected. The mPR rate was 33% with nivolumab plus ipilimumab (about twice as high as with nivolumab alone in NEOSTAR or atezolizumab in LCMC3).

Among resected patients, nivolumab plus ipilimumab had a 44% mPR rate and a pathologic complete response rate of 38%. Although RECIST (Response Evaluation Criteria in Solid Tumors) responses were more likely in patients who had an mPR, 11% of patients had radiographic “nodal immune flare” because of noncaseating granulomas in regional (or nonregional) nodes. Elevated baseline programmed death-ligand 1 was associated with a higher rate of mPR. Surgical complications seemed similar to expectations – 1 bronchopleural fistula and 8 air leaks among the 39 resected patients.
 

What this means in practice

Although the mPR endpoint has no validated association with survival and the studies were relatively small, neoadjuvant use of ICIs in patients for whom tolerance to standard chemotherapy plus or minus radiation might be problematic is attractive – especially in view of the reality of an approximately 50% relapse rate after surgical resection with standard therapy.

If I had a potential candidate for neoadjuvant ICI therapy – especially one with a high proportion of cells with PD-L1 or someone with an equivocal distant metastasis on a preoperative PET-CT – I would consider using an ICI as given in LCMC3 or NEOSTAR.

PREDIX in HER2-positive breast cancer

As Mark Pegram, MD, of Stanford (Calif.) University suggested in his discussion at the local/regional/adjuvant breast cancer session at ASCO 2019, the goal of HER2-targeted therapy was originally that it could replace – not supplement – the use of cytotoxic chemotherapy.

Abstracts 500 (the KRISTINE trial: neoadjuvant T-DM1 plus pertuzumab vs. docetaxel, carboplatin, and trastuzumab plus pertuzumab); 501 (the PREDIX study: T-DM1 vs. docetaxel plus trastuzumab plus pertuzumab [DTP] for six cycles); and 502 (HER2 heterogeneity as a predictor of response) addressed the potential for the antibody-drug conjugate to replace standard preoperative cytotoxic chemotherapy plus HER2-targeting.

In PREDIX, it was anticipated that toxicity would be lower with T-DM1 than with DTP – and it was, with better quality of life scores. The authors found a pathologic complete response rate of 45% among 98 participants with stage IIA-IIIA HER2-positive breast cancer, with higher rates among hormone receptor–negative than hormone receptor–positive patients, as expected.

PREDIX patients were allowed to switch from T-DM1 to DTP for progression, lack of clinical/radiographic response, or toxicity. More than twice as many patients switched from DTP to T-DM1 than vice versa for progression or lack of response.

What this means in practice

Although neither DTP nor T-DM1 are National Comprehensive Cancer Network guideline-endorsed neoadjuvant regimens at present, the KRISTINE and PREDIX trials and Abstract 502 advance the discussion about further personalizing therapy for HER2-amplified breast cancer with high HER2 copy number and lack of intratumor heterogeneity for HER2. They also raise questions about de-escalating therapy for patients with good prognosis and HER2-positive cancers, and the creative use of T-DM1 in the neoadjuvant setting.

Neoadjuvant T-DM1 may not be standard of care yet, but watch this space.

Dr. Lyss has been a community-based medical oncologist and clinical researcher for more than 35 years, practicing in St. Louis. His clinical and research interests are in the prevention, diagnosis, and treatment of breast and lung cancers and in expanding access to clinical trials to medically underserved populations.

In this edition of “How I will treat my next patient,” I take a look at two “chemo-free” neoadjuvant studies reported at the annual meeting of the American Society of Clinical Oncology. One summarizes the potential utility of immune checkpoint inhibitors (ICIs) in non–small cell lung cancer (NSCLC) patients who are – or can become – candidates for curative resection and the other highlights the potential utility of neoadjuvant trastuzumab emtansine (T-DM1) for HER2-positive breast cancer patients.

NEOSTAR in NSCLC

With the accumulation of comorbid conditions in an aging population, we all see NSCLC patients who are potential candidates for curative surgery, but for whom we have concerns about standard preoperative chemotherapy plus or minus radiation. At ASCO 2019, abstracts 8503 (atezolizumab, the LCMC3 trial) and 8504 (nivolumab plus or minus ipilimumab, NEOSTAR) addressed the neoadjuvant use of ICIs. I will focus on NEOSTAR, because the major pathologic response (mPR) rate – reduction in viable tumor cells to 10% or less – was higher with the combination of nivolumab plus ipilimumab in NEOSTAR than with single agent nivolumab or atezolizumab in the NEOSTAR or LCMC3 trials, respectively.

Briefly, 44 patients with stage I-IIIA NSCLC were randomized to nivolumab plus or minus ipilimumab. In total, 93% completed 6 weeks of neoadjuvant therapy and 89% were resected. The mPR rate was 33% with nivolumab plus ipilimumab (about twice as high as with nivolumab alone in NEOSTAR or atezolizumab in LCMC3).

Among resected patients, nivolumab plus ipilimumab had a 44% mPR rate and a pathologic complete response rate of 38%. Although RECIST (Response Evaluation Criteria in Solid Tumors) responses were more likely in patients who had an mPR, 11% of patients had radiographic “nodal immune flare” because of noncaseating granulomas in regional (or nonregional) nodes. Elevated baseline programmed death-ligand 1 was associated with a higher rate of mPR. Surgical complications seemed similar to expectations – 1 bronchopleural fistula and 8 air leaks among the 39 resected patients.
 

What this means in practice

Although the mPR endpoint has no validated association with survival and the studies were relatively small, neoadjuvant use of ICIs in patients for whom tolerance to standard chemotherapy plus or minus radiation might be problematic is attractive – especially in view of the reality of an approximately 50% relapse rate after surgical resection with standard therapy.

If I had a potential candidate for neoadjuvant ICI therapy – especially one with a high proportion of cells with PD-L1 or someone with an equivocal distant metastasis on a preoperative PET-CT – I would consider using an ICI as given in LCMC3 or NEOSTAR.

PREDIX in HER2-positive breast cancer

As Mark Pegram, MD, of Stanford (Calif.) University suggested in his discussion at the local/regional/adjuvant breast cancer session at ASCO 2019, the goal of HER2-targeted therapy was originally that it could replace – not supplement – the use of cytotoxic chemotherapy.

Abstracts 500 (the KRISTINE trial: neoadjuvant T-DM1 plus pertuzumab vs. docetaxel, carboplatin, and trastuzumab plus pertuzumab); 501 (the PREDIX study: T-DM1 vs. docetaxel plus trastuzumab plus pertuzumab [DTP] for six cycles); and 502 (HER2 heterogeneity as a predictor of response) addressed the potential for the antibody-drug conjugate to replace standard preoperative cytotoxic chemotherapy plus HER2-targeting.

In PREDIX, it was anticipated that toxicity would be lower with T-DM1 than with DTP – and it was, with better quality of life scores. The authors found a pathologic complete response rate of 45% among 98 participants with stage IIA-IIIA HER2-positive breast cancer, with higher rates among hormone receptor–negative than hormone receptor–positive patients, as expected.

PREDIX patients were allowed to switch from T-DM1 to DTP for progression, lack of clinical/radiographic response, or toxicity. More than twice as many patients switched from DTP to T-DM1 than vice versa for progression or lack of response.

What this means in practice

Although neither DTP nor T-DM1 are National Comprehensive Cancer Network guideline-endorsed neoadjuvant regimens at present, the KRISTINE and PREDIX trials and Abstract 502 advance the discussion about further personalizing therapy for HER2-amplified breast cancer with high HER2 copy number and lack of intratumor heterogeneity for HER2. They also raise questions about de-escalating therapy for patients with good prognosis and HER2-positive cancers, and the creative use of T-DM1 in the neoadjuvant setting.

Neoadjuvant T-DM1 may not be standard of care yet, but watch this space.

Dr. Lyss has been a community-based medical oncologist and clinical researcher for more than 35 years, practicing in St. Louis. His clinical and research interests are in the prevention, diagnosis, and treatment of breast and lung cancers and in expanding access to clinical trials to medically underserved populations.

In this edition of “How I will treat my next patient,” I take a look at two “chemo-free” neoadjuvant studies reported at the annual meeting of the American Society of Clinical Oncology. One summarizes the potential utility of immune checkpoint inhibitors (ICIs) in non–small cell lung cancer (NSCLC) patients who are – or can become – candidates for curative resection and the other highlights the potential utility of neoadjuvant trastuzumab emtansine (T-DM1) for HER2-positive breast cancer patients.

NEOSTAR in NSCLC

With the accumulation of comorbid conditions in an aging population, we all see NSCLC patients who are potential candidates for curative surgery, but for whom we have concerns about standard preoperative chemotherapy plus or minus radiation. At ASCO 2019, abstracts 8503 (atezolizumab, the LCMC3 trial) and 8504 (nivolumab plus or minus ipilimumab, NEOSTAR) addressed the neoadjuvant use of ICIs. I will focus on NEOSTAR, because the major pathologic response (mPR) rate – reduction in viable tumor cells to 10% or less – was higher with the combination of nivolumab plus ipilimumab in NEOSTAR than with single agent nivolumab or atezolizumab in the NEOSTAR or LCMC3 trials, respectively.

Briefly, 44 patients with stage I-IIIA NSCLC were randomized to nivolumab plus or minus ipilimumab. In total, 93% completed 6 weeks of neoadjuvant therapy and 89% were resected. The mPR rate was 33% with nivolumab plus ipilimumab (about twice as high as with nivolumab alone in NEOSTAR or atezolizumab in LCMC3).

Among resected patients, nivolumab plus ipilimumab had a 44% mPR rate and a pathologic complete response rate of 38%. Although RECIST (Response Evaluation Criteria in Solid Tumors) responses were more likely in patients who had an mPR, 11% of patients had radiographic “nodal immune flare” because of noncaseating granulomas in regional (or nonregional) nodes. Elevated baseline programmed death-ligand 1 was associated with a higher rate of mPR. Surgical complications seemed similar to expectations – 1 bronchopleural fistula and 8 air leaks among the 39 resected patients.
 

What this means in practice

Although the mPR endpoint has no validated association with survival and the studies were relatively small, neoadjuvant use of ICIs in patients for whom tolerance to standard chemotherapy plus or minus radiation might be problematic is attractive – especially in view of the reality of an approximately 50% relapse rate after surgical resection with standard therapy.

If I had a potential candidate for neoadjuvant ICI therapy – especially one with a high proportion of cells with PD-L1 or someone with an equivocal distant metastasis on a preoperative PET-CT – I would consider using an ICI as given in LCMC3 or NEOSTAR.

PREDIX in HER2-positive breast cancer

As Mark Pegram, MD, of Stanford (Calif.) University suggested in his discussion at the local/regional/adjuvant breast cancer session at ASCO 2019, the goal of HER2-targeted therapy was originally that it could replace – not supplement – the use of cytotoxic chemotherapy.

Abstracts 500 (the KRISTINE trial: neoadjuvant T-DM1 plus pertuzumab vs. docetaxel, carboplatin, and trastuzumab plus pertuzumab); 501 (the PREDIX study: T-DM1 vs. docetaxel plus trastuzumab plus pertuzumab [DTP] for six cycles); and 502 (HER2 heterogeneity as a predictor of response) addressed the potential for the antibody-drug conjugate to replace standard preoperative cytotoxic chemotherapy plus HER2-targeting.

In PREDIX, it was anticipated that toxicity would be lower with T-DM1 than with DTP – and it was, with better quality of life scores. The authors found a pathologic complete response rate of 45% among 98 participants with stage IIA-IIIA HER2-positive breast cancer, with higher rates among hormone receptor–negative than hormone receptor–positive patients, as expected.

PREDIX patients were allowed to switch from T-DM1 to DTP for progression, lack of clinical/radiographic response, or toxicity. More than twice as many patients switched from DTP to T-DM1 than vice versa for progression or lack of response.

What this means in practice

Although neither DTP nor T-DM1 are National Comprehensive Cancer Network guideline-endorsed neoadjuvant regimens at present, the KRISTINE and PREDIX trials and Abstract 502 advance the discussion about further personalizing therapy for HER2-amplified breast cancer with high HER2 copy number and lack of intratumor heterogeneity for HER2. They also raise questions about de-escalating therapy for patients with good prognosis and HER2-positive cancers, and the creative use of T-DM1 in the neoadjuvant setting.

Neoadjuvant T-DM1 may not be standard of care yet, but watch this space.

Dr. Lyss has been a community-based medical oncologist and clinical researcher for more than 35 years, practicing in St. Louis. His clinical and research interests are in the prevention, diagnosis, and treatment of breast and lung cancers and in expanding access to clinical trials to medically underserved populations.

MADRID – Surveys and consensus techniques have been instrumental in identifying much needed candidate criteria toward the classification of chronic nonbacterial osteomyelitis (CNO), according to recent findings from international surveys of pediatric rheumatologists that were presented at the European Congress of Rheumatology.

Melissa Oliver, MD, a pediatric rheumatologist at Riley Hospital for Children, Indianapolis, and colleagues recently undertook the multiphase study as part of an international collaborative effort led by the Childhood Arthritis and Rheumatology Research Alliance to establish consensus-based diagnostic and classification criteria for CNO, an autoinflammatory bone disease of unknown cause that primarily affects children and adolescents. CNO is also known as chronic recurrent multifocal osteomyelitis (CRMO). If this disease is not diagnosed and treated appropriately in a timely fashion, damage and long-term disability is possible. In the absence of widely accepted, consensus-driven criteria, treatment is based largely on expert opinion, Dr. Oliver explained in an interview.

“There is an urgent need for a new and more robust set of classification criteria for CRMO, based on large expert consensus and the analysis of a large sample of patients and controls,” she said.

There are two proposed diagnostic criteria, the 2007 classification of nonbacterial osteitis and the 2016 Bristol diagnostic criteria for CRMO, but both are derived from single-center cohort studies and have not been validated, Dr. Oliver explained.

The list of candidate items that have come out of the study is moving clinicians a step closer toward the design of a practical patient data collection form that appropriately weighs each item included in the classification criteria.

The study employed anonymous survey and nominal group techniques with the goal of developing a set of classification criteria sensitive and specific enough to identify CRMO/CNO patients. In phase 1, a Delphi survey was administered among international rheumatologists to generate candidate criteria items. Phase 2 sought to reduce candidate criteria items through consensus processes via input from physicians managing CNO and patients or caregivers of children with CNO.

Altogether, 259 of 865 pediatric rheumatologists (30%) completed an online questionnaire addressing features key to the classification of CNO, including 77 who practice in Europe (30%), 132 in North America (51%), and 50 on other continents (19%). Of these, 138 (53%) had greater than 10 years of clinical practice experience, and 108 (42%) had managed more than 10 CNO patients.

Initially, Dr. Oliver and colleagues identified 33 candidate criteria items that fell into six domains: clinical presentation, physical exam, laboratory findings, imaging findings, bone biopsy, and treatment response. The top eight weighted items that increased the likelihood of CNO/CRMO were exclusion of malignancy by bone biopsy; multifocal bone lesions; presence of bone pain, swelling, and/or warmth; signs of fibrosis and/or inflammation on bone biopsy; typical location of CNO/CRMO lesion, such as the clavicle, metaphysis of long bones, the mandible, and vertebrae; presence of CNO/CRMO–related comorbidities; normal C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR); and typical MRI findings of CNO/CRMO.

By phase 2, candidate items, which were presented to 39 rheumatologists and 7 parents, were refined or eliminated using item-reduction techniques. A second survey was issued to 77 of 82 members of a work group so that the remaining items could be ranked by their power of distinguishing CNO from conditions that merely mimicked the disease. The greatest mean discriminatory scores were identified with multifocal lesions (ruling out malignancy and infection) and typical location on imaging. Normal C-reactive protein and/or an erythrocyte sedimentation rate more than three times the upper limit of normal had the greatest negative mean discriminatory scores.

The next steps will be to form an expert panel who will use 1000minds software to determine the final criteria and identify a threshold for disease. The investigators hope to build a large multinational case repository of at least 500 patients with CNO/CRMO and 500 patients with mimicking conditions from which to derive a development cohort and an external validation cohort. So far, 10 sites, including 4 in Europe, have obtained approval from an institutional review board. The group has also submitted a proposal for classification criteria to the American College of Rheumatology and the European League Against Rheumatism, Dr. Oliver said.

Dr. Oliver had no disclosures to report, but several coauthors reported financial ties to industry.

[email protected]

SOURCE: Oliver M et al. Ann Rheum Dis. Jun 2019;78(Suppl 2):254-5, Abstract OP0342. doi: 10.1136/annrheumdis-2019-eular.1539.

MADRID – Surveys and consensus techniques have been instrumental in identifying much needed candidate criteria toward the classification of chronic nonbacterial osteomyelitis (CNO), according to recent findings from international surveys of pediatric rheumatologists that were presented at the European Congress of Rheumatology.

Melissa Oliver, MD, a pediatric rheumatologist at Riley Hospital for Children, Indianapolis, and colleagues recently undertook the multiphase study as part of an international collaborative effort led by the Childhood Arthritis and Rheumatology Research Alliance to establish consensus-based diagnostic and classification criteria for CNO, an autoinflammatory bone disease of unknown cause that primarily affects children and adolescents. CNO is also known as chronic recurrent multifocal osteomyelitis (CRMO). If this disease is not diagnosed and treated appropriately in a timely fashion, damage and long-term disability is possible. In the absence of widely accepted, consensus-driven criteria, treatment is based largely on expert opinion, Dr. Oliver explained in an interview.

“There is an urgent need for a new and more robust set of classification criteria for CRMO, based on large expert consensus and the analysis of a large sample of patients and controls,” she said.

There are two proposed diagnostic criteria, the 2007 classification of nonbacterial osteitis and the 2016 Bristol diagnostic criteria for CRMO, but both are derived from single-center cohort studies and have not been validated, Dr. Oliver explained.

The list of candidate items that have come out of the study is moving clinicians a step closer toward the design of a practical patient data collection form that appropriately weighs each item included in the classification criteria.

The study employed anonymous survey and nominal group techniques with the goal of developing a set of classification criteria sensitive and specific enough to identify CRMO/CNO patients. In phase 1, a Delphi survey was administered among international rheumatologists to generate candidate criteria items. Phase 2 sought to reduce candidate criteria items through consensus processes via input from physicians managing CNO and patients or caregivers of children with CNO.

Altogether, 259 of 865 pediatric rheumatologists (30%) completed an online questionnaire addressing features key to the classification of CNO, including 77 who practice in Europe (30%), 132 in North America (51%), and 50 on other continents (19%). Of these, 138 (53%) had greater than 10 years of clinical practice experience, and 108 (42%) had managed more than 10 CNO patients.

Initially, Dr. Oliver and colleagues identified 33 candidate criteria items that fell into six domains: clinical presentation, physical exam, laboratory findings, imaging findings, bone biopsy, and treatment response. The top eight weighted items that increased the likelihood of CNO/CRMO were exclusion of malignancy by bone biopsy; multifocal bone lesions; presence of bone pain, swelling, and/or warmth; signs of fibrosis and/or inflammation on bone biopsy; typical location of CNO/CRMO lesion, such as the clavicle, metaphysis of long bones, the mandible, and vertebrae; presence of CNO/CRMO–related comorbidities; normal C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR); and typical MRI findings of CNO/CRMO.

By phase 2, candidate items, which were presented to 39 rheumatologists and 7 parents, were refined or eliminated using item-reduction techniques. A second survey was issued to 77 of 82 members of a work group so that the remaining items could be ranked by their power of distinguishing CNO from conditions that merely mimicked the disease. The greatest mean discriminatory scores were identified with multifocal lesions (ruling out malignancy and infection) and typical location on imaging. Normal C-reactive protein and/or an erythrocyte sedimentation rate more than three times the upper limit of normal had the greatest negative mean discriminatory scores.

The next steps will be to form an expert panel who will use 1000minds software to determine the final criteria and identify a threshold for disease. The investigators hope to build a large multinational case repository of at least 500 patients with CNO/CRMO and 500 patients with mimicking conditions from which to derive a development cohort and an external validation cohort. So far, 10 sites, including 4 in Europe, have obtained approval from an institutional review board. The group has also submitted a proposal for classification criteria to the American College of Rheumatology and the European League Against Rheumatism, Dr. Oliver said.

Dr. Oliver had no disclosures to report, but several coauthors reported financial ties to industry.

[email protected]

SOURCE: Oliver M et al. Ann Rheum Dis. Jun 2019;78(Suppl 2):254-5, Abstract OP0342. doi: 10.1136/annrheumdis-2019-eular.1539.

MADRID – Surveys and consensus techniques have been instrumental in identifying much needed candidate criteria toward the classification of chronic nonbacterial osteomyelitis (CNO), according to recent findings from international surveys of pediatric rheumatologists that were presented at the European Congress of Rheumatology.

Melissa Oliver, MD, a pediatric rheumatologist at Riley Hospital for Children, Indianapolis, and colleagues recently undertook the multiphase study as part of an international collaborative effort led by the Childhood Arthritis and Rheumatology Research Alliance to establish consensus-based diagnostic and classification criteria for CNO, an autoinflammatory bone disease of unknown cause that primarily affects children and adolescents. CNO is also known as chronic recurrent multifocal osteomyelitis (CRMO). If this disease is not diagnosed and treated appropriately in a timely fashion, damage and long-term disability is possible. In the absence of widely accepted, consensus-driven criteria, treatment is based largely on expert opinion, Dr. Oliver explained in an interview.

“There is an urgent need for a new and more robust set of classification criteria for CRMO, based on large expert consensus and the analysis of a large sample of patients and controls,” she said.

There are two proposed diagnostic criteria, the 2007 classification of nonbacterial osteitis and the 2016 Bristol diagnostic criteria for CRMO, but both are derived from single-center cohort studies and have not been validated, Dr. Oliver explained.

The list of candidate items that have come out of the study is moving clinicians a step closer toward the design of a practical patient data collection form that appropriately weighs each item included in the classification criteria.

The study employed anonymous survey and nominal group techniques with the goal of developing a set of classification criteria sensitive and specific enough to identify CRMO/CNO patients. In phase 1, a Delphi survey was administered among international rheumatologists to generate candidate criteria items. Phase 2 sought to reduce candidate criteria items through consensus processes via input from physicians managing CNO and patients or caregivers of children with CNO.

Altogether, 259 of 865 pediatric rheumatologists (30%) completed an online questionnaire addressing features key to the classification of CNO, including 77 who practice in Europe (30%), 132 in North America (51%), and 50 on other continents (19%). Of these, 138 (53%) had greater than 10 years of clinical practice experience, and 108 (42%) had managed more than 10 CNO patients.

Initially, Dr. Oliver and colleagues identified 33 candidate criteria items that fell into six domains: clinical presentation, physical exam, laboratory findings, imaging findings, bone biopsy, and treatment response. The top eight weighted items that increased the likelihood of CNO/CRMO were exclusion of malignancy by bone biopsy; multifocal bone lesions; presence of bone pain, swelling, and/or warmth; signs of fibrosis and/or inflammation on bone biopsy; typical location of CNO/CRMO lesion, such as the clavicle, metaphysis of long bones, the mandible, and vertebrae; presence of CNO/CRMO–related comorbidities; normal C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR); and typical MRI findings of CNO/CRMO.

By phase 2, candidate items, which were presented to 39 rheumatologists and 7 parents, were refined or eliminated using item-reduction techniques. A second survey was issued to 77 of 82 members of a work group so that the remaining items could be ranked by their power of distinguishing CNO from conditions that merely mimicked the disease. The greatest mean discriminatory scores were identified with multifocal lesions (ruling out malignancy and infection) and typical location on imaging. Normal C-reactive protein and/or an erythrocyte sedimentation rate more than three times the upper limit of normal had the greatest negative mean discriminatory scores.

The next steps will be to form an expert panel who will use 1000minds software to determine the final criteria and identify a threshold for disease. The investigators hope to build a large multinational case repository of at least 500 patients with CNO/CRMO and 500 patients with mimicking conditions from which to derive a development cohort and an external validation cohort. So far, 10 sites, including 4 in Europe, have obtained approval from an institutional review board. The group has also submitted a proposal for classification criteria to the American College of Rheumatology and the European League Against Rheumatism, Dr. Oliver said.

Dr. Oliver had no disclosures to report, but several coauthors reported financial ties to industry.

[email protected]

SOURCE: Oliver M et al. Ann Rheum Dis. Jun 2019;78(Suppl 2):254-5, Abstract OP0342. doi: 10.1136/annrheumdis-2019-eular.1539.

Contrary to previous research indicating that medical cannabis laws reduced opioid overdose mortality, the association between these two has reversed, with opioid overdose mortality increased in states with comprehensive medical cannabis laws, according to Chelsea L. Shover, PhD, and associates.

Courtesy Wikimedia Commons/Coaster420/Creative Commons License

The original research by Marcus A. Bachhuber, MD, and associates showed that the introduction of state medical cannabis laws was associated with a 24.8% reduction in opioid overdose deaths per 100,000 population between 1999 and 2010. In contrast, the new research – which looked at a longer time period than the original research did – found that the association between state medical cannabis laws and opioid overdose mortality reversed direction, from ­–21% to +23%.

“We find it unlikely that medical cannabis – used by about 2.5% of the U.S. population – has exerted large conflicting effects on opioid overdose mortality,” wrote Dr. Shover, of the department of psychiatry and behavioral sciences at Stanford (Calif.) University, and associates. “A more plausible interpretation is that this association is spurious.” Their study was published in the Proceedings of the National Academy of Sciences.

To conduct their analysis, Dr. Shover and associates extended the timeline reviewed by Dr. Bachhuber and associates to 2017. During 2010-2017, 32 states enacted medical cannabis laws, including 17 allowing only medical cannabis with low levels of tetrahydrocannabinol (THC), and 8 legalized recreational marijuana. In the expanded timeline during 1999-2017, states possessing a comprehensive medical marijuana law saw an increase in opioid overdose mortality of 28.2%. Meanwhile, states with recreational marijuana laws saw a decrease of 14.7% in opioid overdose mortality, and states with low-THC medical cannabis laws saw a decrease of 7.1%. However, the investigators noted that those values had wide confidence intervals, which indicates “compatibility with large range of true associations.”

“The nonrobustness of the earlier findings also highlights the challenges of controlling scientific messages in controversial policy areas. Corporate actors with deep pockets have substantial ability to promote congenial results, and suffering people are desperate for effective solutions. Cannabinoids have demonstrated therapeutic benefits, but reducing population-level opioid overdose mortality does not appear to be among them,” Dr. Shover and associates noted.

Dr. Shover reported receiving support from National Institute on Drug Abuse and the Wu Tsai Neurosciences Institute. Another coauthor received support from the Veterans Health Administration, Wu Tsai Neurosciences Institute, and the Esther Ting Memorial Professorship at Stanford.

[email protected]

SOURCE: Shover CL et al. Proc Natl Acad Sci U S A. 2019 Jun 10. doi: 10.1073/pnas.1903434116.

Contrary to previous research indicating that medical cannabis laws reduced opioid overdose mortality, the association between these two has reversed, with opioid overdose mortality increased in states with comprehensive medical cannabis laws, according to Chelsea L. Shover, PhD, and associates.

Courtesy Wikimedia Commons/Coaster420/Creative Commons License

The original research by Marcus A. Bachhuber, MD, and associates showed that the introduction of state medical cannabis laws was associated with a 24.8% reduction in opioid overdose deaths per 100,000 population between 1999 and 2010. In contrast, the new research – which looked at a longer time period than the original research did – found that the association between state medical cannabis laws and opioid overdose mortality reversed direction, from ­–21% to +23%.

“We find it unlikely that medical cannabis – used by about 2.5% of the U.S. population – has exerted large conflicting effects on opioid overdose mortality,” wrote Dr. Shover, of the department of psychiatry and behavioral sciences at Stanford (Calif.) University, and associates. “A more plausible interpretation is that this association is spurious.” Their study was published in the Proceedings of the National Academy of Sciences.

To conduct their analysis, Dr. Shover and associates extended the timeline reviewed by Dr. Bachhuber and associates to 2017. During 2010-2017, 32 states enacted medical cannabis laws, including 17 allowing only medical cannabis with low levels of tetrahydrocannabinol (THC), and 8 legalized recreational marijuana. In the expanded timeline during 1999-2017, states possessing a comprehensive medical marijuana law saw an increase in opioid overdose mortality of 28.2%. Meanwhile, states with recreational marijuana laws saw a decrease of 14.7% in opioid overdose mortality, and states with low-THC medical cannabis laws saw a decrease of 7.1%. However, the investigators noted that those values had wide confidence intervals, which indicates “compatibility with large range of true associations.”

“The nonrobustness of the earlier findings also highlights the challenges of controlling scientific messages in controversial policy areas. Corporate actors with deep pockets have substantial ability to promote congenial results, and suffering people are desperate for effective solutions. Cannabinoids have demonstrated therapeutic benefits, but reducing population-level opioid overdose mortality does not appear to be among them,” Dr. Shover and associates noted.

Dr. Shover reported receiving support from National Institute on Drug Abuse and the Wu Tsai Neurosciences Institute. Another coauthor received support from the Veterans Health Administration, Wu Tsai Neurosciences Institute, and the Esther Ting Memorial Professorship at Stanford.

[email protected]

SOURCE: Shover CL et al. Proc Natl Acad Sci U S A. 2019 Jun 10. doi: 10.1073/pnas.1903434116.

Contrary to previous research indicating that medical cannabis laws reduced opioid overdose mortality, the association between these two has reversed, with opioid overdose mortality increased in states with comprehensive medical cannabis laws, according to Chelsea L. Shover, PhD, and associates.

Courtesy Wikimedia Commons/Coaster420/Creative Commons License

The original research by Marcus A. Bachhuber, MD, and associates showed that the introduction of state medical cannabis laws was associated with a 24.8% reduction in opioid overdose deaths per 100,000 population between 1999 and 2010. In contrast, the new research – which looked at a longer time period than the original research did – found that the association between state medical cannabis laws and opioid overdose mortality reversed direction, from ­–21% to +23%.

“We find it unlikely that medical cannabis – used by about 2.5% of the U.S. population – has exerted large conflicting effects on opioid overdose mortality,” wrote Dr. Shover, of the department of psychiatry and behavioral sciences at Stanford (Calif.) University, and associates. “A more plausible interpretation is that this association is spurious.” Their study was published in the Proceedings of the National Academy of Sciences.

To conduct their analysis, Dr. Shover and associates extended the timeline reviewed by Dr. Bachhuber and associates to 2017. During 2010-2017, 32 states enacted medical cannabis laws, including 17 allowing only medical cannabis with low levels of tetrahydrocannabinol (THC), and 8 legalized recreational marijuana. In the expanded timeline during 1999-2017, states possessing a comprehensive medical marijuana law saw an increase in opioid overdose mortality of 28.2%. Meanwhile, states with recreational marijuana laws saw a decrease of 14.7% in opioid overdose mortality, and states with low-THC medical cannabis laws saw a decrease of 7.1%. However, the investigators noted that those values had wide confidence intervals, which indicates “compatibility with large range of true associations.”

“The nonrobustness of the earlier findings also highlights the challenges of controlling scientific messages in controversial policy areas. Corporate actors with deep pockets have substantial ability to promote congenial results, and suffering people are desperate for effective solutions. Cannabinoids have demonstrated therapeutic benefits, but reducing population-level opioid overdose mortality does not appear to be among them,” Dr. Shover and associates noted.

Dr. Shover reported receiving support from National Institute on Drug Abuse and the Wu Tsai Neurosciences Institute. Another coauthor received support from the Veterans Health Administration, Wu Tsai Neurosciences Institute, and the Esther Ting Memorial Professorship at Stanford.

[email protected]

SOURCE: Shover CL et al. Proc Natl Acad Sci U S A. 2019 Jun 10. doi: 10.1073/pnas.1903434116.

MADRID – Results from an ongoing study of postmenopausal women who discontinue osteoporosis treatment with denosumab (Prolia) so far support the use of denosumab as a second-line therapy after a bisphosphonate, unless otherwise indicated, in order to reduce the loss of bone mineral density (BMD) after its discontinuation and also to support treatment to reduce bone turnover biomarkers as much as possible after stopping denosumab.

“We saw in our study that, even if you give bisphosphonates after denosumab discontinuation, [patients] could lose bone, and the group that controlled the loss of bone had very high control of bone turnover markers,” study author and presenter Bérengère Rozier Aubry, MD, said in an interview at the European Congress of Rheumatology.

She and her colleagues at the Center of Bone Diseases at Lausanne (Switzerland) University Hospital are conducting the ReoLaus (Rebound Effect Observatory in Lausanne) Bone Project to determine whether giving a bisphosphonate to postmenopausal women with osteoporosis after they have discontinued denosumab can stop the loss of bone mineral density (BMD) observed in many patients up to 2 years after stopping denosumab. This postdenosumab BMD loss has also been observed to occur with multiple spontaneous vertebral fractures.

Nearly half of patients who start denosumab discontinue it within 1 year, and 64% by 2 years, according to U.S. administrative claims data (Osteoporos Int. 2017 Apr. doi: 10.1007/s00198-016-3886-y), even though it can be taken for up to 10 years. The discontinuation is either because the patient wishes to do so or there’s a medical indication such as stopping aromatase inhibitor treatment, resolution of osteoporosis, or side effects, Dr. Rozier Aubry said in a press conference at the European Congress of Rheumatology.

Upon discontinuing denosumab, there’s a marked rebound effect in which levels of bone turnover markers rise for 2 years, and some or all of the BMD that was gained is lost (J Clin Endocrinol Metab. 2011 Apr. doi: 10.1210/jc.2010-1502). Multiple spontaneous vertebral fractures also have been reported in 5%-7%, as Dr. Rozier Aubry and colleagues first described in 2016 (Osteoporos Int. 2016 May. doi: 10.1007/s00198-015-3380-y) and others have reported subsequently.

Recommendations from the Endocrine Society in March 2019, a 2017 position statement from the European Calcified Tissue Society, and guidelines from other groups advise giving antiresorptive treatment (bisphosphonates, hormone therapy, or selective estrogen-receptor modulators) but do not say which one, in what dose, when, or for how long, Dr. Rozier Aubry noted.

Treatment with zoledronate 6 months after the last denosumab injection achieves partial preservation of BMD, but multiple vertebral fractures have still been reported when raloxifene, ibandronate, or alendronate have been given after stopping denosumab, she said.

In the ReoLaus Bone Project, Dr. Rozier Aubry and associates are following 170 postmenopausal women with osteoporosis at Lausanne University Hospital who are taking denosumab therapy. At the congress, she reported on the first 71 women in the cohort with 1 year of follow-up. They had a mean age of 64 years, had fewer than one prevalent fracture before starting denosumab, and stopped denosumab after a mean of 7.7 injections. Overall, 8% took glucocorticoids, and 22% took aromatase inhibitors.

The investigators collected data on what treatment was used after denosumab, how bone turnover markers changed 1-3 months after the last denosumab injection and then regularly afterward, how bone mineral density changed after 1 year, and any new osteoporotic fractures.

At the time of denosumab discontinuation, 59% received zoledronate, 24% alendronate, 3% other drugs, and 14% nothing. At a mean of about 17 months after the last denosumab injection, the investigators classified 30 patients as BMD losers (losing at least 3.96%), and 41 had stable BMD. The researchers found that BMD losers were younger (61.4 years vs. 65.5 years), were less likely to use zoledronate before starting denosumab (0% vs. 12%), and had greater serum CTX (C-telopeptide cross-linked type 1 collagen) levels at denosumab initiation (644 ng/mL vs. 474 ng/mL) and 12.8 months after stopping denosumab (592 ng/mL vs. 336 ng/mL) than did those with stable BMD. All differences were statistically significant.

“Our results support the use of denosumab in second line after bisphosphonate therapy to restrain the BMD loss at its discontinuation ... and a strategy to maintain the bone turnover marker serum CTX as low as possible after denosumab discontinuation,” she concluded.

“Our proposition is to start with 1 or 2 years of bisphosphonates, and if the osteoporosis is severe, to switch to denosumab treatment for 4, 6 years. … We can use denosumab for 10 years without side effects, and after that we give bisphosphonates to consolidate the treatment,” she said.

Dr. Rozier Aubry and her associates plan to follow patients in their study for 2 years.

Dr. Rozier Aubry disclosed serving on speakers bureaus for Eli Lilly, Pfizer, Amgen, and Novartis.

[email protected]

SOURCE: Rozier Aubry B et al. Ann Rheum Dis. Jun 2019;78(Suppl 2):115; Abstract OP0085. doi: 10.1136/annrheumdis-2019-eular.4175.

MADRID – Results from an ongoing study of postmenopausal women who discontinue osteoporosis treatment with denosumab (Prolia) so far support the use of denosumab as a second-line therapy after a bisphosphonate, unless otherwise indicated, in order to reduce the loss of bone mineral density (BMD) after its discontinuation and also to support treatment to reduce bone turnover biomarkers as much as possible after stopping denosumab.

“We saw in our study that, even if you give bisphosphonates after denosumab discontinuation, [patients] could lose bone, and the group that controlled the loss of bone had very high control of bone turnover markers,” study author and presenter Bérengère Rozier Aubry, MD, said in an interview at the European Congress of Rheumatology.

She and her colleagues at the Center of Bone Diseases at Lausanne (Switzerland) University Hospital are conducting the ReoLaus (Rebound Effect Observatory in Lausanne) Bone Project to determine whether giving a bisphosphonate to postmenopausal women with osteoporosis after they have discontinued denosumab can stop the loss of bone mineral density (BMD) observed in many patients up to 2 years after stopping denosumab. This postdenosumab BMD loss has also been observed to occur with multiple spontaneous vertebral fractures.

Nearly half of patients who start denosumab discontinue it within 1 year, and 64% by 2 years, according to U.S. administrative claims data (Osteoporos Int. 2017 Apr. doi: 10.1007/s00198-016-3886-y), even though it can be taken for up to 10 years. The discontinuation is either because the patient wishes to do so or there’s a medical indication such as stopping aromatase inhibitor treatment, resolution of osteoporosis, or side effects, Dr. Rozier Aubry said in a press conference at the European Congress of Rheumatology.

Upon discontinuing denosumab, there’s a marked rebound effect in which levels of bone turnover markers rise for 2 years, and some or all of the BMD that was gained is lost (J Clin Endocrinol Metab. 2011 Apr. doi: 10.1210/jc.2010-1502). Multiple spontaneous vertebral fractures also have been reported in 5%-7%, as Dr. Rozier Aubry and colleagues first described in 2016 (Osteoporos Int. 2016 May. doi: 10.1007/s00198-015-3380-y) and others have reported subsequently.

Recommendations from the Endocrine Society in March 2019, a 2017 position statement from the European Calcified Tissue Society, and guidelines from other groups advise giving antiresorptive treatment (bisphosphonates, hormone therapy, or selective estrogen-receptor modulators) but do not say which one, in what dose, when, or for how long, Dr. Rozier Aubry noted.

Treatment with zoledronate 6 months after the last denosumab injection achieves partial preservation of BMD, but multiple vertebral fractures have still been reported when raloxifene, ibandronate, or alendronate have been given after stopping denosumab, she said.

In the ReoLaus Bone Project, Dr. Rozier Aubry and associates are following 170 postmenopausal women with osteoporosis at Lausanne University Hospital who are taking denosumab therapy. At the congress, she reported on the first 71 women in the cohort with 1 year of follow-up. They had a mean age of 64 years, had fewer than one prevalent fracture before starting denosumab, and stopped denosumab after a mean of 7.7 injections. Overall, 8% took glucocorticoids, and 22% took aromatase inhibitors.

The investigators collected data on what treatment was used after denosumab, how bone turnover markers changed 1-3 months after the last denosumab injection and then regularly afterward, how bone mineral density changed after 1 year, and any new osteoporotic fractures.

At the time of denosumab discontinuation, 59% received zoledronate, 24% alendronate, 3% other drugs, and 14% nothing. At a mean of about 17 months after the last denosumab injection, the investigators classified 30 patients as BMD losers (losing at least 3.96%), and 41 had stable BMD. The researchers found that BMD losers were younger (61.4 years vs. 65.5 years), were less likely to use zoledronate before starting denosumab (0% vs. 12%), and had greater serum CTX (C-telopeptide cross-linked type 1 collagen) levels at denosumab initiation (644 ng/mL vs. 474 ng/mL) and 12.8 months after stopping denosumab (592 ng/mL vs. 336 ng/mL) than did those with stable BMD. All differences were statistically significant.

“Our results support the use of denosumab in second line after bisphosphonate therapy to restrain the BMD loss at its discontinuation ... and a strategy to maintain the bone turnover marker serum CTX as low as possible after denosumab discontinuation,” she concluded.

“Our proposition is to start with 1 or 2 years of bisphosphonates, and if the osteoporosis is severe, to switch to denosumab treatment for 4, 6 years. … We can use denosumab for 10 years without side effects, and after that we give bisphosphonates to consolidate the treatment,” she said.

Dr. Rozier Aubry and her associates plan to follow patients in their study for 2 years.

Dr. Rozier Aubry disclosed serving on speakers bureaus for Eli Lilly, Pfizer, Amgen, and Novartis.

[email protected]

SOURCE: Rozier Aubry B et al. Ann Rheum Dis. Jun 2019;78(Suppl 2):115; Abstract OP0085. doi: 10.1136/annrheumdis-2019-eular.4175.

MADRID – Results from an ongoing study of postmenopausal women who discontinue osteoporosis treatment with denosumab (Prolia) so far support the use of denosumab as a second-line therapy after a bisphosphonate, unless otherwise indicated, in order to reduce the loss of bone mineral density (BMD) after its discontinuation and also to support treatment to reduce bone turnover biomarkers as much as possible after stopping denosumab.

“We saw in our study that, even if you give bisphosphonates after denosumab discontinuation, [patients] could lose bone, and the group that controlled the loss of bone had very high control of bone turnover markers,” study author and presenter Bérengère Rozier Aubry, MD, said in an interview at the European Congress of Rheumatology.

She and her colleagues at the Center of Bone Diseases at Lausanne (Switzerland) University Hospital are conducting the ReoLaus (Rebound Effect Observatory in Lausanne) Bone Project to determine whether giving a bisphosphonate to postmenopausal women with osteoporosis after they have discontinued denosumab can stop the loss of bone mineral density (BMD) observed in many patients up to 2 years after stopping denosumab. This postdenosumab BMD loss has also been observed to occur with multiple spontaneous vertebral fractures.

Nearly half of patients who start denosumab discontinue it within 1 year, and 64% by 2 years, according to U.S. administrative claims data (Osteoporos Int. 2017 Apr. doi: 10.1007/s00198-016-3886-y), even though it can be taken for up to 10 years. The discontinuation is either because the patient wishes to do so or there’s a medical indication such as stopping aromatase inhibitor treatment, resolution of osteoporosis, or side effects, Dr. Rozier Aubry said in a press conference at the European Congress of Rheumatology.

Upon discontinuing denosumab, there’s a marked rebound effect in which levels of bone turnover markers rise for 2 years, and some or all of the BMD that was gained is lost (J Clin Endocrinol Metab. 2011 Apr. doi: 10.1210/jc.2010-1502). Multiple spontaneous vertebral fractures also have been reported in 5%-7%, as Dr. Rozier Aubry and colleagues first described in 2016 (Osteoporos Int. 2016 May. doi: 10.1007/s00198-015-3380-y) and others have reported subsequently.

Recommendations from the Endocrine Society in March 2019, a 2017 position statement from the European Calcified Tissue Society, and guidelines from other groups advise giving antiresorptive treatment (bisphosphonates, hormone therapy, or selective estrogen-receptor modulators) but do not say which one, in what dose, when, or for how long, Dr. Rozier Aubry noted.

Treatment with zoledronate 6 months after the last denosumab injection achieves partial preservation of BMD, but multiple vertebral fractures have still been reported when raloxifene, ibandronate, or alendronate have been given after stopping denosumab, she said.

In the ReoLaus Bone Project, Dr. Rozier Aubry and associates are following 170 postmenopausal women with osteoporosis at Lausanne University Hospital who are taking denosumab therapy. At the congress, she reported on the first 71 women in the cohort with 1 year of follow-up. They had a mean age of 64 years, had fewer than one prevalent fracture before starting denosumab, and stopped denosumab after a mean of 7.7 injections. Overall, 8% took glucocorticoids, and 22% took aromatase inhibitors.

The investigators collected data on what treatment was used after denosumab, how bone turnover markers changed 1-3 months after the last denosumab injection and then regularly afterward, how bone mineral density changed after 1 year, and any new osteoporotic fractures.

At the time of denosumab discontinuation, 59% received zoledronate, 24% alendronate, 3% other drugs, and 14% nothing. At a mean of about 17 months after the last denosumab injection, the investigators classified 30 patients as BMD losers (losing at least 3.96%), and 41 had stable BMD. The researchers found that BMD losers were younger (61.4 years vs. 65.5 years), were less likely to use zoledronate before starting denosumab (0% vs. 12%), and had greater serum CTX (C-telopeptide cross-linked type 1 collagen) levels at denosumab initiation (644 ng/mL vs. 474 ng/mL) and 12.8 months after stopping denosumab (592 ng/mL vs. 336 ng/mL) than did those with stable BMD. All differences were statistically significant.

“Our results support the use of denosumab in second line after bisphosphonate therapy to restrain the BMD loss at its discontinuation ... and a strategy to maintain the bone turnover marker serum CTX as low as possible after denosumab discontinuation,” she concluded.

“Our proposition is to start with 1 or 2 years of bisphosphonates, and if the osteoporosis is severe, to switch to denosumab treatment for 4, 6 years. … We can use denosumab for 10 years without side effects, and after that we give bisphosphonates to consolidate the treatment,” she said.

Dr. Rozier Aubry and her associates plan to follow patients in their study for 2 years.

Dr. Rozier Aubry disclosed serving on speakers bureaus for Eli Lilly, Pfizer, Amgen, and Novartis.

[email protected]

SOURCE: Rozier Aubry B et al. Ann Rheum Dis. Jun 2019;78(Suppl 2):115; Abstract OP0085. doi: 10.1136/annrheumdis-2019-eular.4175.

Part of Dr. Aletha Maybank’s medical training left a sour taste in her mouth.

Ted Grudzinski, courtesy of the American Medical Association

Her superiors told her not to worry about nonmedical issues affecting her patients’ quality of life, she said, because social workers would handle it. But she didn’t understand how physicians could divorce medical advice from the context of patients’ lives.

“How can you offer advice as recommendations that’s not even relevant to how their day to day plays out?” Dr. Maybank asked.

Today, Dr. Maybank is continuing to question that medical school philosophy. She was recently named the first chief health equity officer for the American Medical Association. In that job, she is responsible for implementing practices among doctors across the country to help end disparities in care. She has a full agenda, including launching the group’s Center for Health Equity and helping the Chicago-based doctors association reach out to people in poor neighborhoods in the city.

A pediatrician, Dr. Maybank previously worked for the New York City government as deputy commissioner for the health department and founding director of the city’s health equity center.

Carmen Heredia Rodriguez of Kaiser Health News recently spoke with Dr. Maybank about her new role and how health inequities affect Americans. This transcript has been edited for length and clarity.

Q: Can you tell me what health equity means to you, and what are some of the main drivers that are keeping health inequitable in this country?

The AMA policy around health equity is optimal health for all people.

But it’s not just an outcome; there’s a process to get there. How do we engage with people? How do we look at and collect our data to make sure our practices and processes are equitable? How do we hire differently to ensure diversity? All these things are processes to achieve health equity.

In order to understand what produces inequities, we have to understand what creates health. Health is created outside of the walls of the doctor’s office and at the hospital. What are patients’ jobs and employment like? The kind of education they have. Income. Their ability to build wealth. All of these are conditions that impact health.

Q: Is there anything along your career path that really surprised you about the state of health care in the United States?

There’s the perception that all of our health is really determined by whether you have a doctor or not, or if you have insurance. What creates health is much beyond that.

So if we really want to work on health and equity, we have to partner with people who are in the education space and the economic space and the housing spaces, because that’s where health inequities are produced. You could have insurance coverage. You could have a primary care doctor. But it doesn’t mean that you’re not going to experience health inequities.

Q: Discrimination based on racial lines is one obvious driver of health inequities. What are some of the other populations that are affected by health inequity?

I think structural racism is a system that affects us all.

It’s not just the black-white issue. So, whether it’s discrimination or inequities that exist among LGBT youth and transgender [or] nonconforming people, or if it’s folks who are immigrants or women, a lot of that is contextualized under the umbrella of white supremacy within the country.

Q: And what are some of your priorities?

A large part of my work will be how I build the organizational capacity to better understand health equity. The reality in this country is folks aren’t comfortable talking about those issues. So, we have to destigmatize talking about all of this.

Q: Are there any particular populations or relationships that you plan to focus on?

The AMA excluded black physicians until the 1960s. So one question is: How do we work to heal relationships as well as understand the impact of our past actions? The AMA definitely issued an apology in the early 2000s, and my new role is also a step in the right direction. However, there is more that we can and should do.

Another priority now is: How do we work, and who do we work with, in our own backyard of Chicago? What can we do to work directly with people experiencing the greatest burden of disease? How do we ensure that we acknowledge the power, assets and expertise of communities so that we have the process and solutions driven and led by communities? To that end, we’ve begun working with West Side United via a relationship at Rush Medical Center. West Side United is a community-driven, collective neighborhood planning, implementation and investment effort geared toward optimizing economic well-being and improved health outcomes.

Q: Is there anything else you feel is important to understand about health equity?

Health equity and social determinants of health have become jargon. But we are talking about people’s lives. We were all born equal. We are clearly not all treated equal, but we all deserve equity. I don’t live outside of it, and none of us really do. I am one of those women who were three to four times more likely to die at childbirth because I’m black. So I don’t live outside of this experience. I’m talking about my own life.

Kaiser Health News is a nonprofit national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation that is not affiliated with Kaiser Permanente.

Part of Dr. Aletha Maybank’s medical training left a sour taste in her mouth.

Ted Grudzinski, courtesy of the American Medical Association

Her superiors told her not to worry about nonmedical issues affecting her patients’ quality of life, she said, because social workers would handle it. But she didn’t understand how physicians could divorce medical advice from the context of patients’ lives.

“How can you offer advice as recommendations that’s not even relevant to how their day to day plays out?” Dr. Maybank asked.

Today, Dr. Maybank is continuing to question that medical school philosophy. She was recently named the first chief health equity officer for the American Medical Association. In that job, she is responsible for implementing practices among doctors across the country to help end disparities in care. She has a full agenda, including launching the group’s Center for Health Equity and helping the Chicago-based doctors association reach out to people in poor neighborhoods in the city.

A pediatrician, Dr. Maybank previously worked for the New York City government as deputy commissioner for the health department and founding director of the city’s health equity center.

Carmen Heredia Rodriguez of Kaiser Health News recently spoke with Dr. Maybank about her new role and how health inequities affect Americans. This transcript has been edited for length and clarity.

Q: Can you tell me what health equity means to you, and what are some of the main drivers that are keeping health inequitable in this country?

The AMA policy around health equity is optimal health for all people.

But it’s not just an outcome; there’s a process to get there. How do we engage with people? How do we look at and collect our data to make sure our practices and processes are equitable? How do we hire differently to ensure diversity? All these things are processes to achieve health equity.

In order to understand what produces inequities, we have to understand what creates health. Health is created outside of the walls of the doctor’s office and at the hospital. What are patients’ jobs and employment like? The kind of education they have. Income. Their ability to build wealth. All of these are conditions that impact health.

Q: Is there anything along your career path that really surprised you about the state of health care in the United States?

There’s the perception that all of our health is really determined by whether you have a doctor or not, or if you have insurance. What creates health is much beyond that.

So if we really want to work on health and equity, we have to partner with people who are in the education space and the economic space and the housing spaces, because that’s where health inequities are produced. You could have insurance coverage. You could have a primary care doctor. But it doesn’t mean that you’re not going to experience health inequities.

Q: Discrimination based on racial lines is one obvious driver of health inequities. What are some of the other populations that are affected by health inequity?

I think structural racism is a system that affects us all.

It’s not just the black-white issue. So, whether it’s discrimination or inequities that exist among LGBT youth and transgender [or] nonconforming people, or if it’s folks who are immigrants or women, a lot of that is contextualized under the umbrella of white supremacy within the country.

Q: And what are some of your priorities?

A large part of my work will be how I build the organizational capacity to better understand health equity. The reality in this country is folks aren’t comfortable talking about those issues. So, we have to destigmatize talking about all of this.

Q: Are there any particular populations or relationships that you plan to focus on?

The AMA excluded black physicians until the 1960s. So one question is: How do we work to heal relationships as well as understand the impact of our past actions? The AMA definitely issued an apology in the early 2000s, and my new role is also a step in the right direction. However, there is more that we can and should do.

Another priority now is: How do we work, and who do we work with, in our own backyard of Chicago? What can we do to work directly with people experiencing the greatest burden of disease? How do we ensure that we acknowledge the power, assets and expertise of communities so that we have the process and solutions driven and led by communities? To that end, we’ve begun working with West Side United via a relationship at Rush Medical Center. West Side United is a community-driven, collective neighborhood planning, implementation and investment effort geared toward optimizing economic well-being and improved health outcomes.

Q: Is there anything else you feel is important to understand about health equity?

Health equity and social determinants of health have become jargon. But we are talking about people’s lives. We were all born equal. We are clearly not all treated equal, but we all deserve equity. I don’t live outside of it, and none of us really do. I am one of those women who were three to four times more likely to die at childbirth because I’m black. So I don’t live outside of this experience. I’m talking about my own life.

Kaiser Health News is a nonprofit national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation that is not affiliated with Kaiser Permanente.

Part of Dr. Aletha Maybank’s medical training left a sour taste in her mouth.

Ted Grudzinski, courtesy of the American Medical Association

Her superiors told her not to worry about nonmedical issues affecting her patients’ quality of life, she said, because social workers would handle it. But she didn’t understand how physicians could divorce medical advice from the context of patients’ lives.

“How can you offer advice as recommendations that’s not even relevant to how their day to day plays out?” Dr. Maybank asked.

Today, Dr. Maybank is continuing to question that medical school philosophy. She was recently named the first chief health equity officer for the American Medical Association. In that job, she is responsible for implementing practices among doctors across the country to help end disparities in care. She has a full agenda, including launching the group’s Center for Health Equity and helping the Chicago-based doctors association reach out to people in poor neighborhoods in the city.

A pediatrician, Dr. Maybank previously worked for the New York City government as deputy commissioner for the health department and founding director of the city’s health equity center.

Carmen Heredia Rodriguez of Kaiser Health News recently spoke with Dr. Maybank about her new role and how health inequities affect Americans. This transcript has been edited for length and clarity.

Q: Can you tell me what health equity means to you, and what are some of the main drivers that are keeping health inequitable in this country?

The AMA policy around health equity is optimal health for all people.

But it’s not just an outcome; there’s a process to get there. How do we engage with people? How do we look at and collect our data to make sure our practices and processes are equitable? How do we hire differently to ensure diversity? All these things are processes to achieve health equity.

In order to understand what produces inequities, we have to understand what creates health. Health is created outside of the walls of the doctor’s office and at the hospital. What are patients’ jobs and employment like? The kind of education they have. Income. Their ability to build wealth. All of these are conditions that impact health.

Q: Is there anything along your career path that really surprised you about the state of health care in the United States?

There’s the perception that all of our health is really determined by whether you have a doctor or not, or if you have insurance. What creates health is much beyond that.

So if we really want to work on health and equity, we have to partner with people who are in the education space and the economic space and the housing spaces, because that’s where health inequities are produced. You could have insurance coverage. You could have a primary care doctor. But it doesn’t mean that you’re not going to experience health inequities.

Q: Discrimination based on racial lines is one obvious driver of health inequities. What are some of the other populations that are affected by health inequity?

I think structural racism is a system that affects us all.

It’s not just the black-white issue. So, whether it’s discrimination or inequities that exist among LGBT youth and transgender [or] nonconforming people, or if it’s folks who are immigrants or women, a lot of that is contextualized under the umbrella of white supremacy within the country.

Q: And what are some of your priorities?

A large part of my work will be how I build the organizational capacity to better understand health equity. The reality in this country is folks aren’t comfortable talking about those issues. So, we have to destigmatize talking about all of this.

Q: Are there any particular populations or relationships that you plan to focus on?

The AMA excluded black physicians until the 1960s. So one question is: How do we work to heal relationships as well as understand the impact of our past actions? The AMA definitely issued an apology in the early 2000s, and my new role is also a step in the right direction. However, there is more that we can and should do.

Another priority now is: How do we work, and who do we work with, in our own backyard of Chicago? What can we do to work directly with people experiencing the greatest burden of disease? How do we ensure that we acknowledge the power, assets and expertise of communities so that we have the process and solutions driven and led by communities? To that end, we’ve begun working with West Side United via a relationship at Rush Medical Center. West Side United is a community-driven, collective neighborhood planning, implementation and investment effort geared toward optimizing economic well-being and improved health outcomes.

Q: Is there anything else you feel is important to understand about health equity?

Health equity and social determinants of health have become jargon. But we are talking about people’s lives. We were all born equal. We are clearly not all treated equal, but we all deserve equity. I don’t live outside of it, and none of us really do. I am one of those women who were three to four times more likely to die at childbirth because I’m black. So I don’t live outside of this experience. I’m talking about my own life.

Kaiser Health News is a nonprofit national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation that is not affiliated with Kaiser Permanente.

SAN FRANCISCO – Powerful drugs now make it possible to lower LDL cholesterol levels to dramatically low levels. But is this a good idea? There are risks, and a cardiologist urged diabetes professionals to not overdo cholesterol reduction. But a colleague argued in favor of aggressively targeting “bad” cholesterol.

Catherine Hackett

“We used to say you can’t be too rich or too thin. We now say you can’t be too rich or too thin or have a too-low LDL cholesterol,” said cardiologist Steven E. Nissen, MD, chairman of cardiovascular medicine at the Cleveland Clinic Foundation, who spoke at the annual scientific sessions of the American Diabetes Association about the wisdom of extreme LDL cholesterol lowering.

Dr. Nissen faced off in a debate with cardiologist Sanket Dhruva, MD, of the University of California, San Francisco, who doesn’t support aggressive LDL cholesterol lowering.

It is fine, Dr. Dhruva said, to treat patients so their LDL cholesterol levels drop below 100 mg/dL. “I don’t think there’s any argument there.”

But Dr. Dhruva questioned whether it’s a good idea to generally decrease LDL cholesterol well below 70 mg/dL, as is now possible with the use of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors.

SAN FRANCISCO – Powerful drugs now make it possible to lower LDL cholesterol levels to dramatically low levels. But is this a good idea? There are risks, and a cardiologist urged diabetes professionals to not overdo cholesterol reduction. But a colleague argued in favor of aggressively targeting “bad” cholesterol.

Catherine Hackett

“We used to say you can’t be too rich or too thin. We now say you can’t be too rich or too thin or have a too-low LDL cholesterol,” said cardiologist Steven E. Nissen, MD, chairman of cardiovascular medicine at the Cleveland Clinic Foundation, who spoke at the annual scientific sessions of the American Diabetes Association about the wisdom of extreme LDL cholesterol lowering.

Dr. Nissen faced off in a debate with cardiologist Sanket Dhruva, MD, of the University of California, San Francisco, who doesn’t support aggressive LDL cholesterol lowering.

It is fine, Dr. Dhruva said, to treat patients so their LDL cholesterol levels drop below 100 mg/dL. “I don’t think there’s any argument there.”

But Dr. Dhruva questioned whether it’s a good idea to generally decrease LDL cholesterol well below 70 mg/dL, as is now possible with the use of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors.

SAN FRANCISCO – Powerful drugs now make it possible to lower LDL cholesterol levels to dramatically low levels. But is this a good idea? There are risks, and a cardiologist urged diabetes professionals to not overdo cholesterol reduction. But a colleague argued in favor of aggressively targeting “bad” cholesterol.

Catherine Hackett

“We used to say you can’t be too rich or too thin. We now say you can’t be too rich or too thin or have a too-low LDL cholesterol,” said cardiologist Steven E. Nissen, MD, chairman of cardiovascular medicine at the Cleveland Clinic Foundation, who spoke at the annual scientific sessions of the American Diabetes Association about the wisdom of extreme LDL cholesterol lowering.

Dr. Nissen faced off in a debate with cardiologist Sanket Dhruva, MD, of the University of California, San Francisco, who doesn’t support aggressive LDL cholesterol lowering.

It is fine, Dr. Dhruva said, to treat patients so their LDL cholesterol levels drop below 100 mg/dL. “I don’t think there’s any argument there.”

But Dr. Dhruva questioned whether it’s a good idea to generally decrease LDL cholesterol well below 70 mg/dL, as is now possible with the use of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors.

WASHINGTON – Levothyroxine was not effective at decreasing physical fatigue in older adults with hypothyroidism, according to a new study.

Jennifer Reising/MDedge News

The double-blind, randomized, placebo-controlled, parallel-group trial used subsets of data from the TRUST study. This new research, which was presented at the Annual Meeting of the Society of General Internal Medicine, provides further evidence that prescribing levothyroxine to older patients with subclinical hypothyroidism will not reduce fatigue.

Like the findings in the TRUST study, the new study, “Effect of Thyroid Hormone Replacement on Fatigability in Older Adults with Subclinical Hypothyroidism: A Randomized Placebo Controlled Trial,” showed that the use of levothyroxine in subclinical hypothyroidism was not effective in changing physical and mental fatigability in older adults.

“This study shows that levothyroxine treatment may not be necessary and results in high costs and side effects,” noted Mirah Stuber, MD, during her presentation of the findings at the meeting.

The new study examined the effect of levothyroxine on the tiredness of older adults but with a more detailed analysis of fatigue than the full TRUST study provided. In this new study, investigators used a new assessment tool, called the Pittsburgh Fatigability Scale (PFS), a 10-item self-administered questionnaire that can measure both physical and mental fatigability. Perceived fatigability anchors tiredness to a set of activities and has been shown to be a more sensitive measure than global fatigue, explained Dr. Stuber of the University of Chicago.

The scores range from 0-50, with higher scores indicating higher fatigability. The scales were divided between mental and physical activities and measured fatigue in relation to a defined activity of a specific duration and intensity. These activities included a leisurely 30-minute walk and participation in a 1-hour social activity.

This study involved 230 participants from Switzerland and Ireland, with a mean age of 73.4 years, who had persistent hypothyroidism. The population was randomized to 119 patients who were administered levothyroxine and 111 patients who received a placebo.

At baseline, the levothyroxine group had a mean physical PFS score of 14.7 ± 9.3, and the placebo group had a score of 11.1 ± 9.1. The baseline mean mental PFS score for the levothyroxine group was 7.4 ± 8.0, while it was 5.1 ± 6.9 for the placebo group.

After 12 months of the participants’ use of levothyroxine or placebo, the physical PFS scores increased for both the treatment and placebo groups. For the levothyroxine group, the mean physical PFS score was 14.8 ± 9.6, while it was 12.4 ± 9.3 for the placebo group (P = 0.88). The investigators found no significant differences between these scores for the levothyroxine and placebo groups.

The mean mental PFS score slightly decreased to 6.0 ± 7.8 for the levothyroxine group, while it slightly increased to 6.0 ± 8.0 for the placebo group (P = 0.26) at 12 months. The difference between the mental fatigability scores for the levothyroxine and placebo arms at 12 months was also not significant.

The physical fatigability between-group difference was 0.2 (95% confidence interval, –1.8 to 2.1; P = 0.88), while the mental fatigability difference was –1.0 (95% CI, –2.8 to 0.8; P = 0.26).

The study was funded by the European Union FP7 and the Swiss National Science Foundation. Merck KGaA, Darmstadt (Germany) provided levothyroxine and the placebo. Dr. Stuber has no conflicts of interest.

WASHINGTON – Levothyroxine was not effective at decreasing physical fatigue in older adults with hypothyroidism, according to a new study.

Jennifer Reising/MDedge News

The double-blind, randomized, placebo-controlled, parallel-group trial used subsets of data from the TRUST study. This new research, which was presented at the Annual Meeting of the Society of General Internal Medicine, provides further evidence that prescribing levothyroxine to older patients with subclinical hypothyroidism will not reduce fatigue.

Like the findings in the TRUST study, the new study, “Effect of Thyroid Hormone Replacement on Fatigability in Older Adults with Subclinical Hypothyroidism: A Randomized Placebo Controlled Trial,” showed that the use of levothyroxine in subclinical hypothyroidism was not effective in changing physical and mental fatigability in older adults.

“This study shows that levothyroxine treatment may not be necessary and results in high costs and side effects,” noted Mirah Stuber, MD, during her presentation of the findings at the meeting.

The new study examined the effect of levothyroxine on the tiredness of older adults but with a more detailed analysis of fatigue than the full TRUST study provided. In this new study, investigators used a new assessment tool, called the Pittsburgh Fatigability Scale (PFS), a 10-item self-administered questionnaire that can measure both physical and mental fatigability. Perceived fatigability anchors tiredness to a set of activities and has been shown to be a more sensitive measure than global fatigue, explained Dr. Stuber of the University of Chicago.

The scores range from 0-50, with higher scores indicating higher fatigability. The scales were divided between mental and physical activities and measured fatigue in relation to a defined activity of a specific duration and intensity. These activities included a leisurely 30-minute walk and participation in a 1-hour social activity.

This study involved 230 participants from Switzerland and Ireland, with a mean age of 73.4 years, who had persistent hypothyroidism. The population was randomized to 119 patients who were administered levothyroxine and 111 patients who received a placebo.

At baseline, the levothyroxine group had a mean physical PFS score of 14.7 ± 9.3, and the placebo group had a score of 11.1 ± 9.1. The baseline mean mental PFS score for the levothyroxine group was 7.4 ± 8.0, while it was 5.1 ± 6.9 for the placebo group.

After 12 months of the participants’ use of levothyroxine or placebo, the physical PFS scores increased for both the treatment and placebo groups. For the levothyroxine group, the mean physical PFS score was 14.8 ± 9.6, while it was 12.4 ± 9.3 for the placebo group (P = 0.88). The investigators found no significant differences between these scores for the levothyroxine and placebo groups.

The mean mental PFS score slightly decreased to 6.0 ± 7.8 for the levothyroxine group, while it slightly increased to 6.0 ± 8.0 for the placebo group (P = 0.26) at 12 months. The difference between the mental fatigability scores for the levothyroxine and placebo arms at 12 months was also not significant.

The physical fatigability between-group difference was 0.2 (95% confidence interval, –1.8 to 2.1; P = 0.88), while the mental fatigability difference was –1.0 (95% CI, –2.8 to 0.8; P = 0.26).

The study was funded by the European Union FP7 and the Swiss National Science Foundation. Merck KGaA, Darmstadt (Germany) provided levothyroxine and the placebo. Dr. Stuber has no conflicts of interest.

WASHINGTON – Levothyroxine was not effective at decreasing physical fatigue in older adults with hypothyroidism, according to a new study.

Jennifer Reising/MDedge News

The double-blind, randomized, placebo-controlled, parallel-group trial used subsets of data from the TRUST study. This new research, which was presented at the Annual Meeting of the Society of General Internal Medicine, provides further evidence that prescribing levothyroxine to older patients with subclinical hypothyroidism will not reduce fatigue.

Like the findings in the TRUST study, the new study, “Effect of Thyroid Hormone Replacement on Fatigability in Older Adults with Subclinical Hypothyroidism: A Randomized Placebo Controlled Trial,” showed that the use of levothyroxine in subclinical hypothyroidism was not effective in changing physical and mental fatigability in older adults.

“This study shows that levothyroxine treatment may not be necessary and results in high costs and side effects,” noted Mirah Stuber, MD, during her presentation of the findings at the meeting.

The new study examined the effect of levothyroxine on the tiredness of older adults but with a more detailed analysis of fatigue than the full TRUST study provided. In this new study, investigators used a new assessment tool, called the Pittsburgh Fatigability Scale (PFS), a 10-item self-administered questionnaire that can measure both physical and mental fatigability. Perceived fatigability anchors tiredness to a set of activities and has been shown to be a more sensitive measure than global fatigue, explained Dr. Stuber of the University of Chicago.

The scores range from 0-50, with higher scores indicating higher fatigability. The scales were divided between mental and physical activities and measured fatigue in relation to a defined activity of a specific duration and intensity. These activities included a leisurely 30-minute walk and participation in a 1-hour social activity.

This study involved 230 participants from Switzerland and Ireland, with a mean age of 73.4 years, who had persistent hypothyroidism. The population was randomized to 119 patients who were administered levothyroxine and 111 patients who received a placebo.

At baseline, the levothyroxine group had a mean physical PFS score of 14.7 ± 9.3, and the placebo group had a score of 11.1 ± 9.1. The baseline mean mental PFS score for the levothyroxine group was 7.4 ± 8.0, while it was 5.1 ± 6.9 for the placebo group.

After 12 months of the participants’ use of levothyroxine or placebo, the physical PFS scores increased for both the treatment and placebo groups. For the levothyroxine group, the mean physical PFS score was 14.8 ± 9.6, while it was 12.4 ± 9.3 for the placebo group (P = 0.88). The investigators found no significant differences between these scores for the levothyroxine and placebo groups.

The mean mental PFS score slightly decreased to 6.0 ± 7.8 for the levothyroxine group, while it slightly increased to 6.0 ± 8.0 for the placebo group (P = 0.26) at 12 months. The difference between the mental fatigability scores for the levothyroxine and placebo arms at 12 months was also not significant.

The physical fatigability between-group difference was 0.2 (95% confidence interval, –1.8 to 2.1; P = 0.88), while the mental fatigability difference was –1.0 (95% CI, –2.8 to 0.8; P = 0.26).

The study was funded by the European Union FP7 and the Swiss National Science Foundation. Merck KGaA, Darmstadt (Germany) provided levothyroxine and the placebo. Dr. Stuber has no conflicts of interest.

My vet sells cannabidiol (CBD) oil for dogs and cats.

Anatoliy Sizov/Getty Images

So does the vape store down the street, the pharmacy around the corner ... and pretty much every place these days.

I probably have more patients ask me about CBD than any other drug, usually because a friend/cousin/in-law/child/parent/spouse/neighbor/coworker “said I should ask you about this.” That’s the power of the Internet: The most marginally proven treatments are portrayed as definitive cures, while some of the most effective treatments (like vaccines) are treated like a lethal-injection drug.

I really don’t have anything against CBD oil, or medical marijuana in general. If they help you, great. But I don’t like the way they’re portrayed as miracle cures for pretty much whatever ails you.

Nothing is, or ever will be, a miracle cure. There will always be nonresponders and those who have adverse effects. In that respect, what goes for one treatment goes for all of them.

But that doesn’t stop these things from being pushed in the most unreliable ways. On Yelp, Groupon, Facebook, and countless other nonmedical sites that aren’t required to back up their claims with hard evidence.

Anything I prescribe, and all over-the-counter medications, are subject to far more scrutiny. They have known risks and benefits. They’ve been through trials, and most have years of data to review when questions arise.

Granted, CBD oil has been approved, as Epidiolex, for different forms of epilepsy. That kind of regulation is a step forward, but the majority of people selling CBD oil are doing so with unregulated OTC forms.

These may work, but the lack of regulation means every one of these places can make their own formulations, purities, and strengths. In some respects it’s a throwback to the era of patent medicines, where each pharmacy was free to whip up their own concoctions, label them as treatments for whatever they wished, and advertise and sell them.

The Food and Drug Administration, however, continues to take an ostrich approach. At their level these OTC agents are illegal and cannot be sold or marketed. At the same time, though, the restrictions overall are not being enforced. This gives the impression that there is nothing wrong with selling them.

Let’s look at morphine, an effective pain reliever and controlled substance. It’s tightly regulated, as it should be. But what if those regulations were ignored? What if, in addition to it being available by prescription, it were sold OTC in perhaps weaker but unregulated strengths and forms, with a variety of unscientific claims made for its benefits?

I don’t see anyone getting away with doing that.

Like I said earlier, I have nothing against CBD oil. But I do think it should have to go through the same approval process as any other medication, with specific strengths, dosing, benefits, and side effects determined, and enforceable regulations around its manufacturing, sale, and use.

Anything less is snake oil.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

My vet sells cannabidiol (CBD) oil for dogs and cats.

Anatoliy Sizov/Getty Images

So does the vape store down the street, the pharmacy around the corner ... and pretty much every place these days.

I probably have more patients ask me about CBD than any other drug, usually because a friend/cousin/in-law/child/parent/spouse/neighbor/coworker “said I should ask you about this.” That’s the power of the Internet: The most marginally proven treatments are portrayed as definitive cures, while some of the most effective treatments (like vaccines) are treated like a lethal-injection drug.

I really don’t have anything against CBD oil, or medical marijuana in general. If they help you, great. But I don’t like the way they’re portrayed as miracle cures for pretty much whatever ails you.

Nothing is, or ever will be, a miracle cure. There will always be nonresponders and those who have adverse effects. In that respect, what goes for one treatment goes for all of them.

But that doesn’t stop these things from being pushed in the most unreliable ways. On Yelp, Groupon, Facebook, and countless other nonmedical sites that aren’t required to back up their claims with hard evidence.

Anything I prescribe, and all over-the-counter medications, are subject to far more scrutiny. They have known risks and benefits. They’ve been through trials, and most have years of data to review when questions arise.

Granted, CBD oil has been approved, as Epidiolex, for different forms of epilepsy. That kind of regulation is a step forward, but the majority of people selling CBD oil are doing so with unregulated OTC forms.

These may work, but the lack of regulation means every one of these places can make their own formulations, purities, and strengths. In some respects it’s a throwback to the era of patent medicines, where each pharmacy was free to whip up their own concoctions, label them as treatments for whatever they wished, and advertise and sell them.

The Food and Drug Administration, however, continues to take an ostrich approach. At their level these OTC agents are illegal and cannot be sold or marketed. At the same time, though, the restrictions overall are not being enforced. This gives the impression that there is nothing wrong with selling them.

Let’s look at morphine, an effective pain reliever and controlled substance. It’s tightly regulated, as it should be. But what if those regulations were ignored? What if, in addition to it being available by prescription, it were sold OTC in perhaps weaker but unregulated strengths and forms, with a variety of unscientific claims made for its benefits?

I don’t see anyone getting away with doing that.

Like I said earlier, I have nothing against CBD oil. But I do think it should have to go through the same approval process as any other medication, with specific strengths, dosing, benefits, and side effects determined, and enforceable regulations around its manufacturing, sale, and use.

Anything less is snake oil.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

My vet sells cannabidiol (CBD) oil for dogs and cats.

Anatoliy Sizov/Getty Images

So does the vape store down the street, the pharmacy around the corner ... and pretty much every place these days.

I probably have more patients ask me about CBD than any other drug, usually because a friend/cousin/in-law/child/parent/spouse/neighbor/coworker “said I should ask you about this.” That’s the power of the Internet: The most marginally proven treatments are portrayed as definitive cures, while some of the most effective treatments (like vaccines) are treated like a lethal-injection drug.

I really don’t have anything against CBD oil, or medical marijuana in general. If they help you, great. But I don’t like the way they’re portrayed as miracle cures for pretty much whatever ails you.

Nothing is, or ever will be, a miracle cure. There will always be nonresponders and those who have adverse effects. In that respect, what goes for one treatment goes for all of them.

But that doesn’t stop these things from being pushed in the most unreliable ways. On Yelp, Groupon, Facebook, and countless other nonmedical sites that aren’t required to back up their claims with hard evidence.

Anything I prescribe, and all over-the-counter medications, are subject to far more scrutiny. They have known risks and benefits. They’ve been through trials, and most have years of data to review when questions arise.

Granted, CBD oil has been approved, as Epidiolex, for different forms of epilepsy. That kind of regulation is a step forward, but the majority of people selling CBD oil are doing so with unregulated OTC forms.

These may work, but the lack of regulation means every one of these places can make their own formulations, purities, and strengths. In some respects it’s a throwback to the era of patent medicines, where each pharmacy was free to whip up their own concoctions, label them as treatments for whatever they wished, and advertise and sell them.

The Food and Drug Administration, however, continues to take an ostrich approach. At their level these OTC agents are illegal and cannot be sold or marketed. At the same time, though, the restrictions overall are not being enforced. This gives the impression that there is nothing wrong with selling them.

Let’s look at morphine, an effective pain reliever and controlled substance. It’s tightly regulated, as it should be. But what if those regulations were ignored? What if, in addition to it being available by prescription, it were sold OTC in perhaps weaker but unregulated strengths and forms, with a variety of unscientific claims made for its benefits?

I don’t see anyone getting away with doing that.

Like I said earlier, I have nothing against CBD oil. But I do think it should have to go through the same approval process as any other medication, with specific strengths, dosing, benefits, and side effects determined, and enforceable regulations around its manufacturing, sale, and use.

Anything less is snake oil.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Chronic obstructive pulmonary disease (COPD) prevalence among adults is strongly correlated with their state’s current smoking prevalence, according to a Centers for Disease Control and Prevention analysis of respondents to a behavioral risk factor survey.

“Population-based strategies for smoking prevention and control have the potential to decrease the prevalence of COPD in the United States,” wrote Anne G. Wheaton, PhD, of the CDC’s National Center for Chronic Disease Prevention and Health Promotion and coauthors. The study was published in the Morbidity and Mortality Weekly Report.

Dr. Wheaton and her fellow researchers analyzed data from 418,378 adult respondents to the 2017 Behavioral Risk Factor Surveillance System survey. Responses came from all 50 states and Washington, D.C.; respondents who had smoked less than 100 lifetime cigarettes were categorized as “never smoked,” while those who had smoked at least 100 cigarettes but no longer smoked were categorized as “former smokers.” Anyone who had smoked at least 100 cigarettes and currently smoked was categorized as a “current smoker.”

The age-adjusted prevalence of COPD among U.S. adults was 6.2% (95% confidence interval, 6.0%-6.3%) in 2017. Current cigarette smokers had a prevalence of 15.2% (95% CI, 14.7%-15.7%); this dipped to 7.6% (95% CI, 7.3%-8.0%) among former smokers and 2.8% (95% CI, 2.7%-2.9%) among adults who had never smoked. Patterns were visible within states: Current smokers had a state-level prevalence of COPD that was strongly correlated with state-level current smoking prevalence (Pearson correlation coefficient, 0.69; P less than .001). State-level COPD prevalence among former smokers (Pearson correlation coefficient, 0.71; P less than .001) and those who never smoked (Pearson correlation coefficient, 0.64; P less than .001) were also strongly correlated with the current smoking prevalence, indicating secondhand smoke as a risk factor for COPD.

The coauthors acknowledged the study’s limitations, including relying on self-reporting for both COPD and smoking status. They also noted that there was no way to measure exposure to secondhand smoke, other indoor or outdoor air pollutants, or respiratory infection history, “all of which might contribute to COPD risk.”

No conflicts of interest were reported.

SOURCE: Wheaton AG et al. MMWR Morb Mortal Wkly Rep. 2019 Jun 21;68(24):533-8.

Chronic obstructive pulmonary disease (COPD) prevalence among adults is strongly correlated with their state’s current smoking prevalence, according to a Centers for Disease Control and Prevention analysis of respondents to a behavioral risk factor survey.

“Population-based strategies for smoking prevention and control have the potential to decrease the prevalence of COPD in the United States,” wrote Anne G. Wheaton, PhD, of the CDC’s National Center for Chronic Disease Prevention and Health Promotion and coauthors. The study was published in the Morbidity and Mortality Weekly Report.

Dr. Wheaton and her fellow researchers analyzed data from 418,378 adult respondents to the 2017 Behavioral Risk Factor Surveillance System survey. Responses came from all 50 states and Washington, D.C.; respondents who had smoked less than 100 lifetime cigarettes were categorized as “never smoked,” while those who had smoked at least 100 cigarettes but no longer smoked were categorized as “former smokers.” Anyone who had smoked at least 100 cigarettes and currently smoked was categorized as a “current smoker.”

The age-adjusted prevalence of COPD among U.S. adults was 6.2% (95% confidence interval, 6.0%-6.3%) in 2017. Current cigarette smokers had a prevalence of 15.2% (95% CI, 14.7%-15.7%); this dipped to 7.6% (95% CI, 7.3%-8.0%) among former smokers and 2.8% (95% CI, 2.7%-2.9%) among adults who had never smoked. Patterns were visible within states: Current smokers had a state-level prevalence of COPD that was strongly correlated with state-level current smoking prevalence (Pearson correlation coefficient, 0.69; P less than .001). State-level COPD prevalence among former smokers (Pearson correlation coefficient, 0.71; P less than .001) and those who never smoked (Pearson correlation coefficient, 0.64; P less than .001) were also strongly correlated with the current smoking prevalence, indicating secondhand smoke as a risk factor for COPD.

The coauthors acknowledged the study’s limitations, including relying on self-reporting for both COPD and smoking status. They also noted that there was no way to measure exposure to secondhand smoke, other indoor or outdoor air pollutants, or respiratory infection history, “all of which might contribute to COPD risk.”

No conflicts of interest were reported.

SOURCE: Wheaton AG et al. MMWR Morb Mortal Wkly Rep. 2019 Jun 21;68(24):533-8.

Chronic obstructive pulmonary disease (COPD) prevalence among adults is strongly correlated with their state’s current smoking prevalence, according to a Centers for Disease Control and Prevention analysis of respondents to a behavioral risk factor survey.

“Population-based strategies for smoking prevention and control have the potential to decrease the prevalence of COPD in the United States,” wrote Anne G. Wheaton, PhD, of the CDC’s National Center for Chronic Disease Prevention and Health Promotion and coauthors. The study was published in the Morbidity and Mortality Weekly Report.

Dr. Wheaton and her fellow researchers analyzed data from 418,378 adult respondents to the 2017 Behavioral Risk Factor Surveillance System survey. Responses came from all 50 states and Washington, D.C.; respondents who had smoked less than 100 lifetime cigarettes were categorized as “never smoked,” while those who had smoked at least 100 cigarettes but no longer smoked were categorized as “former smokers.” Anyone who had smoked at least 100 cigarettes and currently smoked was categorized as a “current smoker.”

The age-adjusted prevalence of COPD among U.S. adults was 6.2% (95% confidence interval, 6.0%-6.3%) in 2017. Current cigarette smokers had a prevalence of 15.2% (95% CI, 14.7%-15.7%); this dipped to 7.6% (95% CI, 7.3%-8.0%) among former smokers and 2.8% (95% CI, 2.7%-2.9%) among adults who had never smoked. Patterns were visible within states: Current smokers had a state-level prevalence of COPD that was strongly correlated with state-level current smoking prevalence (Pearson correlation coefficient, 0.69; P less than .001). State-level COPD prevalence among former smokers (Pearson correlation coefficient, 0.71; P less than .001) and those who never smoked (Pearson correlation coefficient, 0.64; P less than .001) were also strongly correlated with the current smoking prevalence, indicating secondhand smoke as a risk factor for COPD.

The coauthors acknowledged the study’s limitations, including relying on self-reporting for both COPD and smoking status. They also noted that there was no way to measure exposure to secondhand smoke, other indoor or outdoor air pollutants, or respiratory infection history, “all of which might contribute to COPD risk.”

No conflicts of interest were reported.

SOURCE: Wheaton AG et al. MMWR Morb Mortal Wkly Rep. 2019 Jun 21;68(24):533-8.

Clinical question: Is physician burnout associated with more patient safety issues, low professionalism, or poor patient satisfaction?

Background: Burnout is common among physicians and has a negative effect on their personal lives. It is unclear whether physician burnout is associated with poor outcomes for patients.

Study design: Meta-analysis.

Setting: Forty-seven published studies from 19 countries assessing inpatient and outpatient physicians and the relationship between physician burnout and patient care.

Synopsis: After a systematic review of the published literature, 47 studies were included to pool data from 42,473 physicians. Study subjects included residents, early-career and late-career physicians, and both hospital and outpatient physicians. All studies used validated measures of physician burnout.

Burnout was associated with a two-fold increased risk of physician-reported safety incidents (odds ratio, 1.96; 95% confidence interval, 1.59-2.40), low professionalism (OR, 2.31; 95% CI, 1.87-2.85), and likelihood of low patient-reported satisfaction (OR, 2.28; 95% CI, 1.42-3.68). There were no significant differences in these results based on country of origin of the study. Early-career physicians were more likely to have burnout associated with low professionalism than were late-career physicians.

Of the components of burnout, depersonalization was most strongly associated with these negative outcomes. Interestingly, the increased risk of patient safety incidents was associated with physician-reported, but not health care system–reported, patient safety outcomes. This raises concerns that the health care systems may not be capturing “near misses” in their metrics.

Bottom line: Physician burnout doubles the risk of being involved in a patient safety incident, low professionalism, and poor patient satisfaction.

Citation: Panagioti M et al. Association between physician burnout and patient safety, professionalism, and patient satisfaction. JAMA Intern Med. 2018;178(10):1317-30.
 

Dr. Gabriel is assistant professor of medicine and director of Pre-operative Medicine and Medicine Consult Service in the division of hospital medicine at Mount Sinai Hospital, New York.

Clinical question: Is physician burnout associated with more patient safety issues, low professionalism, or poor patient satisfaction?

Background: Burnout is common among physicians and has a negative effect on their personal lives. It is unclear whether physician burnout is associated with poor outcomes for patients.

Study design: Meta-analysis.

Setting: Forty-seven published studies from 19 countries assessing inpatient and outpatient physicians and the relationship between physician burnout and patient care.

Synopsis: After a systematic review of the published literature, 47 studies were included to pool data from 42,473 physicians. Study subjects included residents, early-career and late-career physicians, and both hospital and outpatient physicians. All studies used validated measures of physician burnout.

Burnout was associated with a two-fold increased risk of physician-reported safety incidents (odds ratio, 1.96; 95% confidence interval, 1.59-2.40), low professionalism (OR, 2.31; 95% CI, 1.87-2.85), and likelihood of low patient-reported satisfaction (OR, 2.28; 95% CI, 1.42-3.68). There were no significant differences in these results based on country of origin of the study. Early-career physicians were more likely to have burnout associated with low professionalism than were late-career physicians.

Of the components of burnout, depersonalization was most strongly associated with these negative outcomes. Interestingly, the increased risk of patient safety incidents was associated with physician-reported, but not health care system–reported, patient safety outcomes. This raises concerns that the health care systems may not be capturing “near misses” in their metrics.

Bottom line: Physician burnout doubles the risk of being involved in a patient safety incident, low professionalism, and poor patient satisfaction.

Citation: Panagioti M et al. Association between physician burnout and patient safety, professionalism, and patient satisfaction. JAMA Intern Med. 2018;178(10):1317-30.
 

Dr. Gabriel is assistant professor of medicine and director of Pre-operative Medicine and Medicine Consult Service in the division of hospital medicine at Mount Sinai Hospital, New York.

Clinical question: Is physician burnout associated with more patient safety issues, low professionalism, or poor patient satisfaction?

Background: Burnout is common among physicians and has a negative effect on their personal lives. It is unclear whether physician burnout is associated with poor outcomes for patients.

Study design: Meta-analysis.

Setting: Forty-seven published studies from 19 countries assessing inpatient and outpatient physicians and the relationship between physician burnout and patient care.

Synopsis: After a systematic review of the published literature, 47 studies were included to pool data from 42,473 physicians. Study subjects included residents, early-career and late-career physicians, and both hospital and outpatient physicians. All studies used validated measures of physician burnout.

Burnout was associated with a two-fold increased risk of physician-reported safety incidents (odds ratio, 1.96; 95% confidence interval, 1.59-2.40), low professionalism (OR, 2.31; 95% CI, 1.87-2.85), and likelihood of low patient-reported satisfaction (OR, 2.28; 95% CI, 1.42-3.68). There were no significant differences in these results based on country of origin of the study. Early-career physicians were more likely to have burnout associated with low professionalism than were late-career physicians.

Of the components of burnout, depersonalization was most strongly associated with these negative outcomes. Interestingly, the increased risk of patient safety incidents was associated with physician-reported, but not health care system–reported, patient safety outcomes. This raises concerns that the health care systems may not be capturing “near misses” in their metrics.

Bottom line: Physician burnout doubles the risk of being involved in a patient safety incident, low professionalism, and poor patient satisfaction.

Citation: Panagioti M et al. Association between physician burnout and patient safety, professionalism, and patient satisfaction. JAMA Intern Med. 2018;178(10):1317-30.
 

Dr. Gabriel is assistant professor of medicine and director of Pre-operative Medicine and Medicine Consult Service in the division of hospital medicine at Mount Sinai Hospital, New York.