Twenty years into the hospitalist movement, the proven formula for developing high-quality scholarly output in a hospital medicine group remains elusive. In this issue of the Journal of Hospital Medicine, McKinney et al. describe a new model in which an academic research coach—a PhD-trained researcher with 50% protected time to assist with hospitalist scholarly activities—is utilized to support scholarship.¹ Built on the premise that most hospitalist faculty do not have research training and many are embarking on their first academic project, the research coach was available to engage hospitalists at any stage of scholarship from conceptualizing an idea, to submitting one’s first IRB, to data analysis, and grant and manuscript submission. This innovation (and the financial investment required) provides an opportunity to consider how to facilitate scholarship and measure its value in hospital medicine groups.

Academic institutions are built on the premise that scholarship—and research in particular—is of equal value to clinical care and teaching; a perspective that is commonly enshrined in promotion criteria that require scholarship for career advancement. While hospitalists are competent to begin clinical practice and transfer their knowledge to others at the conclusion of their residency, most are not prepared to lead research programs or create academic products from their clinical innovations, quality improvement, or medical education work. Yet, particularly for hospitalists who choose to practice in an academic setting, the leadership of their Section, Division, or Department may naturally expect scholarship to occur, similar to other clinical disciplines. In our experience as the directors of research and faculty development in our hospital medicine group, meeting this expectation requires recognizing that faculty development and scholarship development are intertwined and there must be an investment in both.

We believe that faculty development is required—but not sufficient—for the development of high-quality scholarship. In order for hospitalists to generate new knowledge in clinical, educational, quality improvement, and research domains, they must acquire a new skill set after residency training. These skills can be gained in different formats and time frames such as dedicated hospital medicine fellowships, internal faculty development programs, external programs (eg, Academic Hospitalist Academy), and/or individual mentorship. Descriptions of internal faculty development programs have unfortunately been limited to a single institutions with uncertain generalizability.^2,3 One could argue that faculty development may even be more important in hospital medicine than in clinical subspecialties given the relative youth of the field and the experience level of the entry-level faculty. Pediatric hospital medicine may be farthest along in faculty development and scholarship development after becoming a distinct subspecialty recognized by the American Board of Pediatrics and American Board of Medical Specialties; pediatric hospitalists must now complete fellowship training after residency before independent practice.⁴ Importantly, completion of a scholarly product that advances the field is a required component of the pediatric hospital medicine fellowship curricular framework.⁵ Regardless of what infrastructure a hospital medicine group chooses to build, there is a growing realization that faculty development must be firmly in place in order for scholarship to flourish.

In addition to junior faculty development, there is also a need for scholarship development to translate new skills into products of scholarship. For example, a well-published senior faculty member still may need statistical assistance and a midcareer hospitalist who leads quality improvement may struggle to write an effective manuscript to disseminate their findings. McKinney et al.’s innovation seems intended to meet this need, and the just-in-time and menu-style nature of the academic research coach resource is unique and novel. One can imagine how this approach to increasing scholarship productivity could be effective and utilized by busy junior, midcareer, and senior hospitalists alike. As the authors point out, this model attempts to mitigate the drawbacks that other models for enhancing hospitalist scholarship have faced, such as relying on physician scientists as mentors, holding works-in-progress or research seminars, or funding a consulting statistician. A well-trained scientist who meets hospitalists “where they are” is appealing when placed in the context of an effective faculty development program that enables faculty to take advantage of this resource. We hope that future evaluations of this promising innovation will include a comparison group to measure the effect of the academic research coach and demonstrate a return on the financial investment supporting the academic research coach.

Measuring return on investment requires defining the value of scholarship in hospital medicine. Some things that are easy to measure and have valence for traditional academic productivity are captured in the McKinney manuscript: the number of abstracts, papers, and grants. Indirect costs from extramural funding may be particularly important for the financial “bottom line” of many hospitalist groups, which tend to be clinical cost centers in most academic institutions. However, other outcomes that are more challenging to measure may be equally or more important. Does investment in a model to support scholarly productivity lead to less burnout, higher retention, and greater professional satisfaction for academic hospitalists? Does this investment change group culture from “week on, week off” or “on service, off service” to one that has more balance in clinical and nonclinical pursuits?⁶ How does investment in research development translate into national reputation, the ability to recruit outstanding candidates, or the number of hospitalist faculty who become interested in research careers? Measuring the impact of an academic research coach or other intervention on these factors might offer useful insights to drive further investment in hospitalist scholarship.

Measuring the value of scholarship in hospital medicine touches very near to the core of the value proposition of hospital medicine overall as a specialty. Without high-quality scholarship that demonstrates the influence of hospitalists in improving systems, leading change, educating learners, and advocating for the needs of our patients, why continue to invest in this model? We are struck every year at the Society of Hospital Medicine national conference about how much innovation hospitalists are leading – and how little is systematically evaluated or disseminated. In Beckett’s “Waiting for Godot,” Vladimir and Estragon talk about life and wait for Godot who, of course, never arrives. Instead of patiently waiting for more scholarship to arrive, we suggest that hospital medicine leaders follow the lead of McKinney et al. and take action by investing in it.

Disclosures

The views expressed are those of the authors and not necessarily those of the Department of Veterans Affairs.

Funding

Dr. Burke is funded by a VA HSR&D Career Development Award.

Twenty years into the hospitalist movement, the proven formula for developing high-quality scholarly output in a hospital medicine group remains elusive. In this issue of the Journal of Hospital Medicine, McKinney et al. describe a new model in which an academic research coach—a PhD-trained researcher with 50% protected time to assist with hospitalist scholarly activities—is utilized to support scholarship.¹ Built on the premise that most hospitalist faculty do not have research training and many are embarking on their first academic project, the research coach was available to engage hospitalists at any stage of scholarship from conceptualizing an idea, to submitting one’s first IRB, to data analysis, and grant and manuscript submission. This innovation (and the financial investment required) provides an opportunity to consider how to facilitate scholarship and measure its value in hospital medicine groups.

Academic institutions are built on the premise that scholarship—and research in particular—is of equal value to clinical care and teaching; a perspective that is commonly enshrined in promotion criteria that require scholarship for career advancement. While hospitalists are competent to begin clinical practice and transfer their knowledge to others at the conclusion of their residency, most are not prepared to lead research programs or create academic products from their clinical innovations, quality improvement, or medical education work. Yet, particularly for hospitalists who choose to practice in an academic setting, the leadership of their Section, Division, or Department may naturally expect scholarship to occur, similar to other clinical disciplines. In our experience as the directors of research and faculty development in our hospital medicine group, meeting this expectation requires recognizing that faculty development and scholarship development are intertwined and there must be an investment in both.

We believe that faculty development is required—but not sufficient—for the development of high-quality scholarship. In order for hospitalists to generate new knowledge in clinical, educational, quality improvement, and research domains, they must acquire a new skill set after residency training. These skills can be gained in different formats and time frames such as dedicated hospital medicine fellowships, internal faculty development programs, external programs (eg, Academic Hospitalist Academy), and/or individual mentorship. Descriptions of internal faculty development programs have unfortunately been limited to a single institutions with uncertain generalizability.^2,3 One could argue that faculty development may even be more important in hospital medicine than in clinical subspecialties given the relative youth of the field and the experience level of the entry-level faculty. Pediatric hospital medicine may be farthest along in faculty development and scholarship development after becoming a distinct subspecialty recognized by the American Board of Pediatrics and American Board of Medical Specialties; pediatric hospitalists must now complete fellowship training after residency before independent practice.⁴ Importantly, completion of a scholarly product that advances the field is a required component of the pediatric hospital medicine fellowship curricular framework.⁵ Regardless of what infrastructure a hospital medicine group chooses to build, there is a growing realization that faculty development must be firmly in place in order for scholarship to flourish.

In addition to junior faculty development, there is also a need for scholarship development to translate new skills into products of scholarship. For example, a well-published senior faculty member still may need statistical assistance and a midcareer hospitalist who leads quality improvement may struggle to write an effective manuscript to disseminate their findings. McKinney et al.’s innovation seems intended to meet this need, and the just-in-time and menu-style nature of the academic research coach resource is unique and novel. One can imagine how this approach to increasing scholarship productivity could be effective and utilized by busy junior, midcareer, and senior hospitalists alike. As the authors point out, this model attempts to mitigate the drawbacks that other models for enhancing hospitalist scholarship have faced, such as relying on physician scientists as mentors, holding works-in-progress or research seminars, or funding a consulting statistician. A well-trained scientist who meets hospitalists “where they are” is appealing when placed in the context of an effective faculty development program that enables faculty to take advantage of this resource. We hope that future evaluations of this promising innovation will include a comparison group to measure the effect of the academic research coach and demonstrate a return on the financial investment supporting the academic research coach.

Measuring return on investment requires defining the value of scholarship in hospital medicine. Some things that are easy to measure and have valence for traditional academic productivity are captured in the McKinney manuscript: the number of abstracts, papers, and grants. Indirect costs from extramural funding may be particularly important for the financial “bottom line” of many hospitalist groups, which tend to be clinical cost centers in most academic institutions. However, other outcomes that are more challenging to measure may be equally or more important. Does investment in a model to support scholarly productivity lead to less burnout, higher retention, and greater professional satisfaction for academic hospitalists? Does this investment change group culture from “week on, week off” or “on service, off service” to one that has more balance in clinical and nonclinical pursuits?⁶ How does investment in research development translate into national reputation, the ability to recruit outstanding candidates, or the number of hospitalist faculty who become interested in research careers? Measuring the impact of an academic research coach or other intervention on these factors might offer useful insights to drive further investment in hospitalist scholarship.

Measuring the value of scholarship in hospital medicine touches very near to the core of the value proposition of hospital medicine overall as a specialty. Without high-quality scholarship that demonstrates the influence of hospitalists in improving systems, leading change, educating learners, and advocating for the needs of our patients, why continue to invest in this model? We are struck every year at the Society of Hospital Medicine national conference about how much innovation hospitalists are leading – and how little is systematically evaluated or disseminated. In Beckett’s “Waiting for Godot,” Vladimir and Estragon talk about life and wait for Godot who, of course, never arrives. Instead of patiently waiting for more scholarship to arrive, we suggest that hospital medicine leaders follow the lead of McKinney et al. and take action by investing in it.

Disclosures

The views expressed are those of the authors and not necessarily those of the Department of Veterans Affairs.

Funding

Dr. Burke is funded by a VA HSR&D Career Development Award.

Twenty years into the hospitalist movement, the proven formula for developing high-quality scholarly output in a hospital medicine group remains elusive. In this issue of the Journal of Hospital Medicine, McKinney et al. describe a new model in which an academic research coach—a PhD-trained researcher with 50% protected time to assist with hospitalist scholarly activities—is utilized to support scholarship.¹ Built on the premise that most hospitalist faculty do not have research training and many are embarking on their first academic project, the research coach was available to engage hospitalists at any stage of scholarship from conceptualizing an idea, to submitting one’s first IRB, to data analysis, and grant and manuscript submission. This innovation (and the financial investment required) provides an opportunity to consider how to facilitate scholarship and measure its value in hospital medicine groups.

Academic institutions are built on the premise that scholarship—and research in particular—is of equal value to clinical care and teaching; a perspective that is commonly enshrined in promotion criteria that require scholarship for career advancement. While hospitalists are competent to begin clinical practice and transfer their knowledge to others at the conclusion of their residency, most are not prepared to lead research programs or create academic products from their clinical innovations, quality improvement, or medical education work. Yet, particularly for hospitalists who choose to practice in an academic setting, the leadership of their Section, Division, or Department may naturally expect scholarship to occur, similar to other clinical disciplines. In our experience as the directors of research and faculty development in our hospital medicine group, meeting this expectation requires recognizing that faculty development and scholarship development are intertwined and there must be an investment in both.

We believe that faculty development is required—but not sufficient—for the development of high-quality scholarship. In order for hospitalists to generate new knowledge in clinical, educational, quality improvement, and research domains, they must acquire a new skill set after residency training. These skills can be gained in different formats and time frames such as dedicated hospital medicine fellowships, internal faculty development programs, external programs (eg, Academic Hospitalist Academy), and/or individual mentorship. Descriptions of internal faculty development programs have unfortunately been limited to a single institutions with uncertain generalizability.^2,3 One could argue that faculty development may even be more important in hospital medicine than in clinical subspecialties given the relative youth of the field and the experience level of the entry-level faculty. Pediatric hospital medicine may be farthest along in faculty development and scholarship development after becoming a distinct subspecialty recognized by the American Board of Pediatrics and American Board of Medical Specialties; pediatric hospitalists must now complete fellowship training after residency before independent practice.⁴ Importantly, completion of a scholarly product that advances the field is a required component of the pediatric hospital medicine fellowship curricular framework.⁵ Regardless of what infrastructure a hospital medicine group chooses to build, there is a growing realization that faculty development must be firmly in place in order for scholarship to flourish.

In addition to junior faculty development, there is also a need for scholarship development to translate new skills into products of scholarship. For example, a well-published senior faculty member still may need statistical assistance and a midcareer hospitalist who leads quality improvement may struggle to write an effective manuscript to disseminate their findings. McKinney et al.’s innovation seems intended to meet this need, and the just-in-time and menu-style nature of the academic research coach resource is unique and novel. One can imagine how this approach to increasing scholarship productivity could be effective and utilized by busy junior, midcareer, and senior hospitalists alike. As the authors point out, this model attempts to mitigate the drawbacks that other models for enhancing hospitalist scholarship have faced, such as relying on physician scientists as mentors, holding works-in-progress or research seminars, or funding a consulting statistician. A well-trained scientist who meets hospitalists “where they are” is appealing when placed in the context of an effective faculty development program that enables faculty to take advantage of this resource. We hope that future evaluations of this promising innovation will include a comparison group to measure the effect of the academic research coach and demonstrate a return on the financial investment supporting the academic research coach.

Measuring return on investment requires defining the value of scholarship in hospital medicine. Some things that are easy to measure and have valence for traditional academic productivity are captured in the McKinney manuscript: the number of abstracts, papers, and grants. Indirect costs from extramural funding may be particularly important for the financial “bottom line” of many hospitalist groups, which tend to be clinical cost centers in most academic institutions. However, other outcomes that are more challenging to measure may be equally or more important. Does investment in a model to support scholarly productivity lead to less burnout, higher retention, and greater professional satisfaction for academic hospitalists? Does this investment change group culture from “week on, week off” or “on service, off service” to one that has more balance in clinical and nonclinical pursuits?⁶ How does investment in research development translate into national reputation, the ability to recruit outstanding candidates, or the number of hospitalist faculty who become interested in research careers? Measuring the impact of an academic research coach or other intervention on these factors might offer useful insights to drive further investment in hospitalist scholarship.

Measuring the value of scholarship in hospital medicine touches very near to the core of the value proposition of hospital medicine overall as a specialty. Without high-quality scholarship that demonstrates the influence of hospitalists in improving systems, leading change, educating learners, and advocating for the needs of our patients, why continue to invest in this model? We are struck every year at the Society of Hospital Medicine national conference about how much innovation hospitalists are leading – and how little is systematically evaluated or disseminated. In Beckett’s “Waiting for Godot,” Vladimir and Estragon talk about life and wait for Godot who, of course, never arrives. Instead of patiently waiting for more scholarship to arrive, we suggest that hospital medicine leaders follow the lead of McKinney et al. and take action by investing in it.

Disclosures

The views expressed are those of the authors and not necessarily those of the Department of Veterans Affairs.

Funding

Dr. Burke is funded by a VA HSR&D Career Development Award.

Until there’s greater transparency – and greater understanding of the clinical and economic impact – it’s time for dermatologists to stop selling their practices to private equity firms.

South_agency/Getty Images

That’s the opinion of Joshua Sharfstein, MD, and Jamar Slocum, MD, both of Johns Hopkins University, Baltimore, who published their views in an editorial in JAMA Dermatology.

“At current pace, by the time more is understood about the takeover of dermatology practices by private equity firms, it will be too late to change course,” Dr. Sharfstein, former principal deputy commissioner at the Food and Drug Administration, and Dr. Slocum wrote. “Efforts to protect the field of dermatology and the American public from the potential adverse consequences should begin now.”

Investment in dermatology practices has spiked in recent years.

Between May 1, 2012, and May 22, 2018, 17 private equity–backed dermatology management groups (DMG) acquired 184 practices, accounting for 381 dermatology clinics, according to a study by Sally Tan, MD, of Brigham and Women’s Hospital, Boston, and colleagues.

The findings “likely underreported direct acquisitions of small physician-owned practices by small PE [private equity] firms,” Dr. Tan and colleagues wrote. “In addition, the data underestimated the number of clinics transitioning from physician to PE-backed ownership because the specific clinics associated with each DMG at the time of the DMG’s initial PE investment has not been disclosed.”

More than one-third of clinics associated with private equity–acquired practices are in Texas and Florida; however, clinics have been acquired in at least 30 states (JAMA Dermatol. doi: 10.1001/jamadermatol.2019.1634).

Physicians have raised concerns about the loss of autonomy and conflicts of interest from investors more concerned with a return on investment ahead of clinical concerns, Dr. Tan and colleagues noted.

From a clinical perspective, there are a number of things that have raised a red flag, Dr. Sharfstein noted.

There have been reports of inappropriate procedures being conducted, he said in an interview. “Another [concern] is unnecessary marketing of cosmetic procedures – the sale of various products that are not adding much of anything to health. So I think it is the unnecessary procedures on the one end and the huge focus on just driving up revenues without any real benefit.”

The flood of private equity money could, over the long term, create access to care and viability issues, he added.

“If you think of a doctor’s office as a revenue-generating machine, that could have pretty profound implications for the nature of treatment and the nature of access to care for different people,” he said. “There is reason to be worried about the viability of access to care in the ways that has been traditionally understood.”

To that end, Dr. Sharfstein and Dr. Slocum make recommendations on what to do in the near term.

First, they are calling for a moratorium on private equity investment either via a conscious decision by dermatologist to reject private equity investment or legislative/regulatory action preventing it.

“Until meaningful data are available on what happens to the quality of care and affordability for patients and payers, dermatologists should stop selling their practices to private equity firms, and legislators should prohibit such transactions,” they wrote in JAMA Dermatology. Exceptions could be made when “a practice can make a strong and public case to health officials that doing so is in the public interest.”

More transparency around these deals is needed as well.

They call on the American Academy of Dermatology to solicit, curate, and release data on the ownership of all dermatology practices, “as well as core measures related to their use of nonphysicians, access to essential and emergency care, the provision of uncompensated care, and revenue growth.”

Dr. Sharfstein and Dr. Slocum cautioned that “the basic approach and incentives of private equity are not aligned with health and value in dermatology. By focusing on short-term revenue opportunities, private equity acquisitions will likely add to the immense cost and stark inequality of our health care system, with the added risks of unnecessary treatments and significant disruptions in care.”

gtwachtman@mdedge.com

SOURCE: Tan S et al. JAMA Dermatol. 2019 Jul 24. doi: 10.1001/jamadermatol.2019.1634.

Until there’s greater transparency – and greater understanding of the clinical and economic impact – it’s time for dermatologists to stop selling their practices to private equity firms.

South_agency/Getty Images

That’s the opinion of Joshua Sharfstein, MD, and Jamar Slocum, MD, both of Johns Hopkins University, Baltimore, who published their views in an editorial in JAMA Dermatology.

“At current pace, by the time more is understood about the takeover of dermatology practices by private equity firms, it will be too late to change course,” Dr. Sharfstein, former principal deputy commissioner at the Food and Drug Administration, and Dr. Slocum wrote. “Efforts to protect the field of dermatology and the American public from the potential adverse consequences should begin now.”

Investment in dermatology practices has spiked in recent years.

Between May 1, 2012, and May 22, 2018, 17 private equity–backed dermatology management groups (DMG) acquired 184 practices, accounting for 381 dermatology clinics, according to a study by Sally Tan, MD, of Brigham and Women’s Hospital, Boston, and colleagues.

The findings “likely underreported direct acquisitions of small physician-owned practices by small PE [private equity] firms,” Dr. Tan and colleagues wrote. “In addition, the data underestimated the number of clinics transitioning from physician to PE-backed ownership because the specific clinics associated with each DMG at the time of the DMG’s initial PE investment has not been disclosed.”

More than one-third of clinics associated with private equity–acquired practices are in Texas and Florida; however, clinics have been acquired in at least 30 states (JAMA Dermatol. doi: 10.1001/jamadermatol.2019.1634).

Physicians have raised concerns about the loss of autonomy and conflicts of interest from investors more concerned with a return on investment ahead of clinical concerns, Dr. Tan and colleagues noted.

From a clinical perspective, there are a number of things that have raised a red flag, Dr. Sharfstein noted.

There have been reports of inappropriate procedures being conducted, he said in an interview. “Another [concern] is unnecessary marketing of cosmetic procedures – the sale of various products that are not adding much of anything to health. So I think it is the unnecessary procedures on the one end and the huge focus on just driving up revenues without any real benefit.”

The flood of private equity money could, over the long term, create access to care and viability issues, he added.

“If you think of a doctor’s office as a revenue-generating machine, that could have pretty profound implications for the nature of treatment and the nature of access to care for different people,” he said. “There is reason to be worried about the viability of access to care in the ways that has been traditionally understood.”

To that end, Dr. Sharfstein and Dr. Slocum make recommendations on what to do in the near term.

First, they are calling for a moratorium on private equity investment either via a conscious decision by dermatologist to reject private equity investment or legislative/regulatory action preventing it.

“Until meaningful data are available on what happens to the quality of care and affordability for patients and payers, dermatologists should stop selling their practices to private equity firms, and legislators should prohibit such transactions,” they wrote in JAMA Dermatology. Exceptions could be made when “a practice can make a strong and public case to health officials that doing so is in the public interest.”

More transparency around these deals is needed as well.

They call on the American Academy of Dermatology to solicit, curate, and release data on the ownership of all dermatology practices, “as well as core measures related to their use of nonphysicians, access to essential and emergency care, the provision of uncompensated care, and revenue growth.”

Dr. Sharfstein and Dr. Slocum cautioned that “the basic approach and incentives of private equity are not aligned with health and value in dermatology. By focusing on short-term revenue opportunities, private equity acquisitions will likely add to the immense cost and stark inequality of our health care system, with the added risks of unnecessary treatments and significant disruptions in care.”

gtwachtman@mdedge.com

SOURCE: Tan S et al. JAMA Dermatol. 2019 Jul 24. doi: 10.1001/jamadermatol.2019.1634.

Until there’s greater transparency – and greater understanding of the clinical and economic impact – it’s time for dermatologists to stop selling their practices to private equity firms.

South_agency/Getty Images

That’s the opinion of Joshua Sharfstein, MD, and Jamar Slocum, MD, both of Johns Hopkins University, Baltimore, who published their views in an editorial in JAMA Dermatology.

“At current pace, by the time more is understood about the takeover of dermatology practices by private equity firms, it will be too late to change course,” Dr. Sharfstein, former principal deputy commissioner at the Food and Drug Administration, and Dr. Slocum wrote. “Efforts to protect the field of dermatology and the American public from the potential adverse consequences should begin now.”

Investment in dermatology practices has spiked in recent years.

Between May 1, 2012, and May 22, 2018, 17 private equity–backed dermatology management groups (DMG) acquired 184 practices, accounting for 381 dermatology clinics, according to a study by Sally Tan, MD, of Brigham and Women’s Hospital, Boston, and colleagues.

The findings “likely underreported direct acquisitions of small physician-owned practices by small PE [private equity] firms,” Dr. Tan and colleagues wrote. “In addition, the data underestimated the number of clinics transitioning from physician to PE-backed ownership because the specific clinics associated with each DMG at the time of the DMG’s initial PE investment has not been disclosed.”

More than one-third of clinics associated with private equity–acquired practices are in Texas and Florida; however, clinics have been acquired in at least 30 states (JAMA Dermatol. doi: 10.1001/jamadermatol.2019.1634).

Physicians have raised concerns about the loss of autonomy and conflicts of interest from investors more concerned with a return on investment ahead of clinical concerns, Dr. Tan and colleagues noted.

From a clinical perspective, there are a number of things that have raised a red flag, Dr. Sharfstein noted.

There have been reports of inappropriate procedures being conducted, he said in an interview. “Another [concern] is unnecessary marketing of cosmetic procedures – the sale of various products that are not adding much of anything to health. So I think it is the unnecessary procedures on the one end and the huge focus on just driving up revenues without any real benefit.”

The flood of private equity money could, over the long term, create access to care and viability issues, he added.

“If you think of a doctor’s office as a revenue-generating machine, that could have pretty profound implications for the nature of treatment and the nature of access to care for different people,” he said. “There is reason to be worried about the viability of access to care in the ways that has been traditionally understood.”

To that end, Dr. Sharfstein and Dr. Slocum make recommendations on what to do in the near term.

First, they are calling for a moratorium on private equity investment either via a conscious decision by dermatologist to reject private equity investment or legislative/regulatory action preventing it.

“Until meaningful data are available on what happens to the quality of care and affordability for patients and payers, dermatologists should stop selling their practices to private equity firms, and legislators should prohibit such transactions,” they wrote in JAMA Dermatology. Exceptions could be made when “a practice can make a strong and public case to health officials that doing so is in the public interest.”

More transparency around these deals is needed as well.

They call on the American Academy of Dermatology to solicit, curate, and release data on the ownership of all dermatology practices, “as well as core measures related to their use of nonphysicians, access to essential and emergency care, the provision of uncompensated care, and revenue growth.”

Dr. Sharfstein and Dr. Slocum cautioned that “the basic approach and incentives of private equity are not aligned with health and value in dermatology. By focusing on short-term revenue opportunities, private equity acquisitions will likely add to the immense cost and stark inequality of our health care system, with the added risks of unnecessary treatments and significant disruptions in care.”

gtwachtman@mdedge.com

SOURCE: Tan S et al. JAMA Dermatol. 2019 Jul 24. doi: 10.1001/jamadermatol.2019.1634.

The degree of tumor mutational burden can predict whether patients with non–small cell lung cancer will benefit from immunotherapy with a checkpoint inhibitor, but differences in TMB by tumor histology and metastatic sites suggest that clinicians still don’t fully understand the implications of this marker for clinical care, investigators say.

A study of nearly 3,500 unmatched non–small cell lung cancer (NSCLC) samples showed that TMB of 10 mutations per megabase (MB) or higher occurred more frequently in metastases (especially brain metastases) than in primary tumors, in squamous cell carcinomas (SCC), compared with adenocarcinomas, and in poorly differentiated tumors, compared with moderately or well-differentiated tumors, reported Matthew K. Stein, MD, of the University of Tennessee Health Sciences Center in Memphis and colleagues in JCO Precision Oncology.

“Further work is needed to elucidate the mutational differences implied by TMB with the hope of identifying additional ICI [immune checkpoint inhibitor] biomarkers, as well as exploring unique therapeutic approaches for brain metastases and other sites with high TMB,” they wrote.

To get a clearer picture of differences in TMB by biopsy sample location, histology, and other biomarkers, the investigators obtained 3,424 unique, unmatched specimens from multiple U.S. cancer centers. The specimens, including 2,351 adenocarcinomas and 1,073 SCCs, were identified by only age and sex, with histology confirmed by pathology review.

The investigators conducted next-generation sequencing of 592 cancer-related genes on each specimen, as well as programmed death ligand 1 (PD-L1) immunohistochemistry, and TMB. They used a TMB cutoff of 10 mutations/MB, which was established as predictive of response to immune checkpoint inhibitors in the Checkmate 568 and Checkmate 227 trials.

They found that 38% of metastatic adenocarcinoma samples had TMB of 10 mutations/MB or greater, compared with 25% of primary adenocarcinomas (P less than .001), a difference that was greatest for brain metastases, compared with other metastases (61% vs. 35%; P less than .001). The median TMBs were 13 mutations/MB vs. 6 mutations/MB, respectively.

Similarly, TMB above the cutoff was more frequent in SCC metastases than primaries (41% vs. 35%; P = .038).

TMB of 10 mutations/MB occurred significantly more often in SCC primary tumors (35%) than in adenocarcinoma primaries (25%; P less than .001).

They also saw variability in TMB among other sites, with adrenal metastases being the second–most likely site to have high TMB (51%) and bone metastases being least likely (19%).

In an analysis stratified by histology and primary or metastatic sample site, poorly differentiated tumors were significantly more likely to have TMB of 10 mutations/MB or greater both for adenocarcinomas (40% of poorly differentiated primaries vs. 19% for others, and 48% of poorly differentiated metastases vs. 35% for other metastases; P less than .001 for both), and for SCCs (40% vs. 33% of primaries; P = .028; and 42% vs. 31% of metastases; P = .025).

The investigators also detected site-specific differences in PD-L1 positivity, STK11 and KRAS mutation rates, and other markers along the 10 mutations/MB cutoff which they characterized as “clinically informative.”

“Practically, clinicians should consider obtaining metastasis samples when possible if assessing for high TMB. Furthermore, in addition to previously described intratumor heterogeneity, our data highlight significant intertumor heterogeneity in NSCLC. One possible solution to capture tumor heterogeneity is with blood TMB, which theoretically could depict a composite TMB score versus single-site tissue,” Dr. Stein and associates said.

The investigators did not report a study funding source. Dr. Stein reported no relevant disclosures. Several of the coauthors are employees of Caris Life Sciences, which performed the tumor profiling.

SOURCE: Stein MK et al. JCO Precision Oncology. 2019 Jul 26. doi: 10.1200/PO.18.00376.

The degree of tumor mutational burden can predict whether patients with non–small cell lung cancer will benefit from immunotherapy with a checkpoint inhibitor, but differences in TMB by tumor histology and metastatic sites suggest that clinicians still don’t fully understand the implications of this marker for clinical care, investigators say.

A study of nearly 3,500 unmatched non–small cell lung cancer (NSCLC) samples showed that TMB of 10 mutations per megabase (MB) or higher occurred more frequently in metastases (especially brain metastases) than in primary tumors, in squamous cell carcinomas (SCC), compared with adenocarcinomas, and in poorly differentiated tumors, compared with moderately or well-differentiated tumors, reported Matthew K. Stein, MD, of the University of Tennessee Health Sciences Center in Memphis and colleagues in JCO Precision Oncology.

“Further work is needed to elucidate the mutational differences implied by TMB with the hope of identifying additional ICI [immune checkpoint inhibitor] biomarkers, as well as exploring unique therapeutic approaches for brain metastases and other sites with high TMB,” they wrote.

To get a clearer picture of differences in TMB by biopsy sample location, histology, and other biomarkers, the investigators obtained 3,424 unique, unmatched specimens from multiple U.S. cancer centers. The specimens, including 2,351 adenocarcinomas and 1,073 SCCs, were identified by only age and sex, with histology confirmed by pathology review.

The investigators conducted next-generation sequencing of 592 cancer-related genes on each specimen, as well as programmed death ligand 1 (PD-L1) immunohistochemistry, and TMB. They used a TMB cutoff of 10 mutations/MB, which was established as predictive of response to immune checkpoint inhibitors in the Checkmate 568 and Checkmate 227 trials.

They found that 38% of metastatic adenocarcinoma samples had TMB of 10 mutations/MB or greater, compared with 25% of primary adenocarcinomas (P less than .001), a difference that was greatest for brain metastases, compared with other metastases (61% vs. 35%; P less than .001). The median TMBs were 13 mutations/MB vs. 6 mutations/MB, respectively.

Similarly, TMB above the cutoff was more frequent in SCC metastases than primaries (41% vs. 35%; P = .038).

TMB of 10 mutations/MB occurred significantly more often in SCC primary tumors (35%) than in adenocarcinoma primaries (25%; P less than .001).

They also saw variability in TMB among other sites, with adrenal metastases being the second–most likely site to have high TMB (51%) and bone metastases being least likely (19%).

In an analysis stratified by histology and primary or metastatic sample site, poorly differentiated tumors were significantly more likely to have TMB of 10 mutations/MB or greater both for adenocarcinomas (40% of poorly differentiated primaries vs. 19% for others, and 48% of poorly differentiated metastases vs. 35% for other metastases; P less than .001 for both), and for SCCs (40% vs. 33% of primaries; P = .028; and 42% vs. 31% of metastases; P = .025).

The investigators also detected site-specific differences in PD-L1 positivity, STK11 and KRAS mutation rates, and other markers along the 10 mutations/MB cutoff which they characterized as “clinically informative.”

“Practically, clinicians should consider obtaining metastasis samples when possible if assessing for high TMB. Furthermore, in addition to previously described intratumor heterogeneity, our data highlight significant intertumor heterogeneity in NSCLC. One possible solution to capture tumor heterogeneity is with blood TMB, which theoretically could depict a composite TMB score versus single-site tissue,” Dr. Stein and associates said.

The investigators did not report a study funding source. Dr. Stein reported no relevant disclosures. Several of the coauthors are employees of Caris Life Sciences, which performed the tumor profiling.

SOURCE: Stein MK et al. JCO Precision Oncology. 2019 Jul 26. doi: 10.1200/PO.18.00376.

The degree of tumor mutational burden can predict whether patients with non–small cell lung cancer will benefit from immunotherapy with a checkpoint inhibitor, but differences in TMB by tumor histology and metastatic sites suggest that clinicians still don’t fully understand the implications of this marker for clinical care, investigators say.

A study of nearly 3,500 unmatched non–small cell lung cancer (NSCLC) samples showed that TMB of 10 mutations per megabase (MB) or higher occurred more frequently in metastases (especially brain metastases) than in primary tumors, in squamous cell carcinomas (SCC), compared with adenocarcinomas, and in poorly differentiated tumors, compared with moderately or well-differentiated tumors, reported Matthew K. Stein, MD, of the University of Tennessee Health Sciences Center in Memphis and colleagues in JCO Precision Oncology.

“Further work is needed to elucidate the mutational differences implied by TMB with the hope of identifying additional ICI [immune checkpoint inhibitor] biomarkers, as well as exploring unique therapeutic approaches for brain metastases and other sites with high TMB,” they wrote.

To get a clearer picture of differences in TMB by biopsy sample location, histology, and other biomarkers, the investigators obtained 3,424 unique, unmatched specimens from multiple U.S. cancer centers. The specimens, including 2,351 adenocarcinomas and 1,073 SCCs, were identified by only age and sex, with histology confirmed by pathology review.

The investigators conducted next-generation sequencing of 592 cancer-related genes on each specimen, as well as programmed death ligand 1 (PD-L1) immunohistochemistry, and TMB. They used a TMB cutoff of 10 mutations/MB, which was established as predictive of response to immune checkpoint inhibitors in the Checkmate 568 and Checkmate 227 trials.

They found that 38% of metastatic adenocarcinoma samples had TMB of 10 mutations/MB or greater, compared with 25% of primary adenocarcinomas (P less than .001), a difference that was greatest for brain metastases, compared with other metastases (61% vs. 35%; P less than .001). The median TMBs were 13 mutations/MB vs. 6 mutations/MB, respectively.

Similarly, TMB above the cutoff was more frequent in SCC metastases than primaries (41% vs. 35%; P = .038).

TMB of 10 mutations/MB occurred significantly more often in SCC primary tumors (35%) than in adenocarcinoma primaries (25%; P less than .001).

They also saw variability in TMB among other sites, with adrenal metastases being the second–most likely site to have high TMB (51%) and bone metastases being least likely (19%).

In an analysis stratified by histology and primary or metastatic sample site, poorly differentiated tumors were significantly more likely to have TMB of 10 mutations/MB or greater both for adenocarcinomas (40% of poorly differentiated primaries vs. 19% for others, and 48% of poorly differentiated metastases vs. 35% for other metastases; P less than .001 for both), and for SCCs (40% vs. 33% of primaries; P = .028; and 42% vs. 31% of metastases; P = .025).

The investigators also detected site-specific differences in PD-L1 positivity, STK11 and KRAS mutation rates, and other markers along the 10 mutations/MB cutoff which they characterized as “clinically informative.”

“Practically, clinicians should consider obtaining metastasis samples when possible if assessing for high TMB. Furthermore, in addition to previously described intratumor heterogeneity, our data highlight significant intertumor heterogeneity in NSCLC. One possible solution to capture tumor heterogeneity is with blood TMB, which theoretically could depict a composite TMB score versus single-site tissue,” Dr. Stein and associates said.

The investigators did not report a study funding source. Dr. Stein reported no relevant disclosures. Several of the coauthors are employees of Caris Life Sciences, which performed the tumor profiling.

SOURCE: Stein MK et al. JCO Precision Oncology. 2019 Jul 26. doi: 10.1200/PO.18.00376.

A new guideline from the American Gastroenterological Association (AGA) aims to help physicians diagnose the cause of chronic watery diarrhea, particularly to exclude diagnoses other than functional diarrhea or diarrhea-predominant irritable bowel syndrome (IBS). The guideline, published in Gastroenterology, does not apply to patients with concerning presentations like weight loss/anemia, diarrhea with signs of fat malabsorption, bloody diarrhea, cases with a family history of inflammatory bowel disease (IBD), colon cancer, or celiac disease or to those who have traveled to diarrheal disease–related regions.

To rule out IBD, physicians can use either fecal calprotectin (threshold value of 50 microg/g, sensitivity, 0.81; specificity, 0.87) or fecal lactoferrin (threshold, 4.0-7.25 mcg/g; pooled sensitivity for IBD, 0.79; specificity, 0.93). Neither erythrocyte sedimentation rate (ESR) nor C-reactive protein (CRP) should be used to diagnose IBD because tests have shown low pooled sensitivity and specificity. CRP might be useful in settings in which fecal lactoferrin or calprotectin tests are not available or covered by insurance.

Patients should be tested for giardia infection, using the antigen test or PCR, because this pathogen is common in the United States and easily treated.

Patients who have not recently traveled to or from high-risk areas should not be tested for ova and parasites because this is unlikely to identify a culprit. There are other guidelines for treating patients who have traveled to high-risk countries.

Celiac disease should be tested for using immunoglobulin-A tissue transglutaminase (IgA tTG) and a second test (IgG tTG and IgG or IgA deamidated gliadin peptide, or DGP) in case the patient has IgA deficiency that could lead to a false negative on the primary test. Thresholds of 7-15 AU/mL in IgA tTG typically provide sensitivity and specificity greater than 90%. A quantitative IgA level found to be normal confirms the IgA tTG test. In abnormal findings, either IgG tTG or a test for IgG DGP can be used. If no information on IgA levels is available, IgG tTG or IgG DGP can be combined with IgA tTG. Positive celiac disease tests should be confirmed by duodenal biopsy.

Bile acid diarrhea should be tested for in the United States by measuring total bile acids in a 48-hour stool collection to document increased fecal bile acids, or serum fibroblast growth factor 19, to identify defective feedback of bile acid synthesis. The Selenium HomotauroCholic Acid Test (SeHCAT) has moderate diagnostic efficiency, but it is not available in North America. A measurement of serum levels of 7alpha-hydroxy-4-cholesten-3-one (C4), which measures bile acid synthesis, is not yet available.

No recommendation was made for using available serologic tests for the diagnosis of IBS because existing evidence suggests they lack the diagnostic accuracy needed for routine use.

The guideline development was funded by AGA and had no outside funding.

SOURCE: Smalley W et al. Gastroenterology. 2019 Jul 11. doi: 10.1053/j.gastro.2019.07.004.

A new guideline from the American Gastroenterological Association (AGA) aims to help physicians diagnose the cause of chronic watery diarrhea, particularly to exclude diagnoses other than functional diarrhea or diarrhea-predominant irritable bowel syndrome (IBS). The guideline, published in Gastroenterology, does not apply to patients with concerning presentations like weight loss/anemia, diarrhea with signs of fat malabsorption, bloody diarrhea, cases with a family history of inflammatory bowel disease (IBD), colon cancer, or celiac disease or to those who have traveled to diarrheal disease–related regions.

To rule out IBD, physicians can use either fecal calprotectin (threshold value of 50 microg/g, sensitivity, 0.81; specificity, 0.87) or fecal lactoferrin (threshold, 4.0-7.25 mcg/g; pooled sensitivity for IBD, 0.79; specificity, 0.93). Neither erythrocyte sedimentation rate (ESR) nor C-reactive protein (CRP) should be used to diagnose IBD because tests have shown low pooled sensitivity and specificity. CRP might be useful in settings in which fecal lactoferrin or calprotectin tests are not available or covered by insurance.

Patients should be tested for giardia infection, using the antigen test or PCR, because this pathogen is common in the United States and easily treated.

Patients who have not recently traveled to or from high-risk areas should not be tested for ova and parasites because this is unlikely to identify a culprit. There are other guidelines for treating patients who have traveled to high-risk countries.

Celiac disease should be tested for using immunoglobulin-A tissue transglutaminase (IgA tTG) and a second test (IgG tTG and IgG or IgA deamidated gliadin peptide, or DGP) in case the patient has IgA deficiency that could lead to a false negative on the primary test. Thresholds of 7-15 AU/mL in IgA tTG typically provide sensitivity and specificity greater than 90%. A quantitative IgA level found to be normal confirms the IgA tTG test. In abnormal findings, either IgG tTG or a test for IgG DGP can be used. If no information on IgA levels is available, IgG tTG or IgG DGP can be combined with IgA tTG. Positive celiac disease tests should be confirmed by duodenal biopsy.

Bile acid diarrhea should be tested for in the United States by measuring total bile acids in a 48-hour stool collection to document increased fecal bile acids, or serum fibroblast growth factor 19, to identify defective feedback of bile acid synthesis. The Selenium HomotauroCholic Acid Test (SeHCAT) has moderate diagnostic efficiency, but it is not available in North America. A measurement of serum levels of 7alpha-hydroxy-4-cholesten-3-one (C4), which measures bile acid synthesis, is not yet available.

No recommendation was made for using available serologic tests for the diagnosis of IBS because existing evidence suggests they lack the diagnostic accuracy needed for routine use.

The guideline development was funded by AGA and had no outside funding.

SOURCE: Smalley W et al. Gastroenterology. 2019 Jul 11. doi: 10.1053/j.gastro.2019.07.004.

A new guideline from the American Gastroenterological Association (AGA) aims to help physicians diagnose the cause of chronic watery diarrhea, particularly to exclude diagnoses other than functional diarrhea or diarrhea-predominant irritable bowel syndrome (IBS). The guideline, published in Gastroenterology, does not apply to patients with concerning presentations like weight loss/anemia, diarrhea with signs of fat malabsorption, bloody diarrhea, cases with a family history of inflammatory bowel disease (IBD), colon cancer, or celiac disease or to those who have traveled to diarrheal disease–related regions.

To rule out IBD, physicians can use either fecal calprotectin (threshold value of 50 microg/g, sensitivity, 0.81; specificity, 0.87) or fecal lactoferrin (threshold, 4.0-7.25 mcg/g; pooled sensitivity for IBD, 0.79; specificity, 0.93). Neither erythrocyte sedimentation rate (ESR) nor C-reactive protein (CRP) should be used to diagnose IBD because tests have shown low pooled sensitivity and specificity. CRP might be useful in settings in which fecal lactoferrin or calprotectin tests are not available or covered by insurance.

Patients should be tested for giardia infection, using the antigen test or PCR, because this pathogen is common in the United States and easily treated.

Patients who have not recently traveled to or from high-risk areas should not be tested for ova and parasites because this is unlikely to identify a culprit. There are other guidelines for treating patients who have traveled to high-risk countries.

Celiac disease should be tested for using immunoglobulin-A tissue transglutaminase (IgA tTG) and a second test (IgG tTG and IgG or IgA deamidated gliadin peptide, or DGP) in case the patient has IgA deficiency that could lead to a false negative on the primary test. Thresholds of 7-15 AU/mL in IgA tTG typically provide sensitivity and specificity greater than 90%. A quantitative IgA level found to be normal confirms the IgA tTG test. In abnormal findings, either IgG tTG or a test for IgG DGP can be used. If no information on IgA levels is available, IgG tTG or IgG DGP can be combined with IgA tTG. Positive celiac disease tests should be confirmed by duodenal biopsy.

Bile acid diarrhea should be tested for in the United States by measuring total bile acids in a 48-hour stool collection to document increased fecal bile acids, or serum fibroblast growth factor 19, to identify defective feedback of bile acid synthesis. The Selenium HomotauroCholic Acid Test (SeHCAT) has moderate diagnostic efficiency, but it is not available in North America. A measurement of serum levels of 7alpha-hydroxy-4-cholesten-3-one (C4), which measures bile acid synthesis, is not yet available.

No recommendation was made for using available serologic tests for the diagnosis of IBS because existing evidence suggests they lack the diagnostic accuracy needed for routine use.

The guideline development was funded by AGA and had no outside funding.

SOURCE: Smalley W et al. Gastroenterology. 2019 Jul 11. doi: 10.1053/j.gastro.2019.07.004.

The Food and Drug Administration has issued a safety alert approving new boxed warnings about increased blood clot and mortality risk associated with the 10-mg, twice-daily dose of tofacitinib (Xeljanz), as well as a new limitation for patients with ulcerative colitis receiving the medication.

Tofacitinib, a Janus kinase inhibitor, was first approved by the FDA in 2012 for the treatment of rheumatoid arthritis (RA). An indication for psoriatic arthritis was added in 2017, and one for ulcerative colitis was added in 2018.

After the 2012 approval, the FDA commissioned a postmarketing trial in patients with RA on background methotrexate to evaluate safety and the risk of cancer, heart-related events, and infection. The 5- and 10-mg tofacitinib twice daily doses are being analyzed in an ongoing study in comparison with a tumor necrosis factor (TNF) inhibitor.

An interim analysis of the trial’s data, as of January 2019, found an increased risk of blood clots and death in patients receiving 10-mg tofacitinib twice daily, compared with the TNF inhibitor and the twice-daily, 5-mg dose. Overall, there were 19 cases of blood clots in the lung out of 3,884 patient-years of follow-up in patients who received tofacitinib 10 mg twice daily, compared with 3 cases out of 3,982 patient-years in patients who received TNF inhibitors. There were also 45 cases of death from all causes during follow-up for tofacitinib 10 mg twice daily, compared with 25 cases in patients who received TNF inhibitors.

Patients with symptoms of thrombosis also receiving tofacitinib should immediately discontinue the medication. Tofacitinib should not be given to patients with ulcerative colitis unless they are not treated effectively with a TNF inhibitor or do not tolerate TNF inhibitors; ulcerative colitis patients should receive the lowest effective dosage, and if the higher dosage is necessary, it should be limited to the shortest amount of time possible, the FDA noted.

lfranki@mdedge.com

The Food and Drug Administration has issued a safety alert approving new boxed warnings about increased blood clot and mortality risk associated with the 10-mg, twice-daily dose of tofacitinib (Xeljanz), as well as a new limitation for patients with ulcerative colitis receiving the medication.

Tofacitinib, a Janus kinase inhibitor, was first approved by the FDA in 2012 for the treatment of rheumatoid arthritis (RA). An indication for psoriatic arthritis was added in 2017, and one for ulcerative colitis was added in 2018.

After the 2012 approval, the FDA commissioned a postmarketing trial in patients with RA on background methotrexate to evaluate safety and the risk of cancer, heart-related events, and infection. The 5- and 10-mg tofacitinib twice daily doses are being analyzed in an ongoing study in comparison with a tumor necrosis factor (TNF) inhibitor.

An interim analysis of the trial’s data, as of January 2019, found an increased risk of blood clots and death in patients receiving 10-mg tofacitinib twice daily, compared with the TNF inhibitor and the twice-daily, 5-mg dose. Overall, there were 19 cases of blood clots in the lung out of 3,884 patient-years of follow-up in patients who received tofacitinib 10 mg twice daily, compared with 3 cases out of 3,982 patient-years in patients who received TNF inhibitors. There were also 45 cases of death from all causes during follow-up for tofacitinib 10 mg twice daily, compared with 25 cases in patients who received TNF inhibitors.

Patients with symptoms of thrombosis also receiving tofacitinib should immediately discontinue the medication. Tofacitinib should not be given to patients with ulcerative colitis unless they are not treated effectively with a TNF inhibitor or do not tolerate TNF inhibitors; ulcerative colitis patients should receive the lowest effective dosage, and if the higher dosage is necessary, it should be limited to the shortest amount of time possible, the FDA noted.

lfranki@mdedge.com

The Food and Drug Administration has issued a safety alert approving new boxed warnings about increased blood clot and mortality risk associated with the 10-mg, twice-daily dose of tofacitinib (Xeljanz), as well as a new limitation for patients with ulcerative colitis receiving the medication.

Tofacitinib, a Janus kinase inhibitor, was first approved by the FDA in 2012 for the treatment of rheumatoid arthritis (RA). An indication for psoriatic arthritis was added in 2017, and one for ulcerative colitis was added in 2018.

After the 2012 approval, the FDA commissioned a postmarketing trial in patients with RA on background methotrexate to evaluate safety and the risk of cancer, heart-related events, and infection. The 5- and 10-mg tofacitinib twice daily doses are being analyzed in an ongoing study in comparison with a tumor necrosis factor (TNF) inhibitor.

An interim analysis of the trial’s data, as of January 2019, found an increased risk of blood clots and death in patients receiving 10-mg tofacitinib twice daily, compared with the TNF inhibitor and the twice-daily, 5-mg dose. Overall, there were 19 cases of blood clots in the lung out of 3,884 patient-years of follow-up in patients who received tofacitinib 10 mg twice daily, compared with 3 cases out of 3,982 patient-years in patients who received TNF inhibitors. There were also 45 cases of death from all causes during follow-up for tofacitinib 10 mg twice daily, compared with 25 cases in patients who received TNF inhibitors.

Patients with symptoms of thrombosis also receiving tofacitinib should immediately discontinue the medication. Tofacitinib should not be given to patients with ulcerative colitis unless they are not treated effectively with a TNF inhibitor or do not tolerate TNF inhibitors; ulcerative colitis patients should receive the lowest effective dosage, and if the higher dosage is necessary, it should be limited to the shortest amount of time possible, the FDA noted.

lfranki@mdedge.com

In 2016, two researchers published a meta-analysis on gray matter abnormalities in youth who had conduct problems.

The study by Jack C. Rogers, PhD, and Stephane A. De Brito, PhD, found 13 well-done studies that included 394 youth with conduct problems and 390 typically developing youth. Compared with the typically developing youth, the conduct-disordered youth had decreased gray matter volume (JAMA Psychiatry. 2016 Jan;73[1]:64-72).

As I knew one of the researchers in one of the studies that made the cut, I called him up and asked whether their research had controlled for fetal alcohol exposure. They had not. I found this very curious because my experience is that youth who have been labeled with conduct disorder often have histories of prenatal fetal alcohol exposure. In addition, my understanding is that youth who have been exposed to prenatal alcohol often have symptoms of conduct disorder. Furthermore, research has shown that such youth have smaller brains (Dev Med Child Neurol. 2001 Mar;43[3]:148-54). I wondered whether the youth studied in that trial had been exposed to alcohol prenatally.

More recently, this problem has resurfaced. An article by Antonia N. Kaczkurkin, PhD, and associates about a large sample of youth was nicely done. But again, the variable of fetal alcohol exposure was not considered. The study was an elegant one that provides a strong rationale for consideration of a “psychopathology factor” in human life (Am J Psychiatry. 2019 Jun 24. doi: 10.1176/appi.ajp.2019.1807035). It shored up that argument by doing neuroimaging studies on a reasonably large sample of youth and showed that reduced cortical thickness (gray matter volume) was associated with overall psychopathology. With the exception of failing to consider the variable of fetal alcohol exposure, the study is a valuable addition to our understanding of what might be going on with psychiatric disorders.

Unfortunately – while hating to sound like a broken record – I noticed that there was no consideration of fetal alcohol exposure as a cause for the findings of the study. It does not seem like a large leap to hypothesize some of these brain imaging studies that find smaller brain components associated with psychopathology and conduct disorder to be a dynamic of fetal alcohol exposure.

It seems to me that we made a huge mistake in public health in asking women only whether they were drinking while they were pregnant because it was the wrong question. The right question is – “When did you realize you were pregnant, and were you doing any social drinking before you knew you were pregnant?”

Without understanding the etiology of the smaller brains in patients with conduct disorder or psychopathology, we are missing a golden opportunity to prevent such problems. The former editor of the American Journal of Psychiatry – Robert A. Freedman, MD – suggests that by giving phosphatidyl choline to pregnant women, such problems could be prevented.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. In 2019, he was awarded the Adolph Meyer Award by the American Psychiatric Association for lifetime achievement in psychiatric research.

In 2016, two researchers published a meta-analysis on gray matter abnormalities in youth who had conduct problems.

The study by Jack C. Rogers, PhD, and Stephane A. De Brito, PhD, found 13 well-done studies that included 394 youth with conduct problems and 390 typically developing youth. Compared with the typically developing youth, the conduct-disordered youth had decreased gray matter volume (JAMA Psychiatry. 2016 Jan;73[1]:64-72).

As I knew one of the researchers in one of the studies that made the cut, I called him up and asked whether their research had controlled for fetal alcohol exposure. They had not. I found this very curious because my experience is that youth who have been labeled with conduct disorder often have histories of prenatal fetal alcohol exposure. In addition, my understanding is that youth who have been exposed to prenatal alcohol often have symptoms of conduct disorder. Furthermore, research has shown that such youth have smaller brains (Dev Med Child Neurol. 2001 Mar;43[3]:148-54). I wondered whether the youth studied in that trial had been exposed to alcohol prenatally.

More recently, this problem has resurfaced. An article by Antonia N. Kaczkurkin, PhD, and associates about a large sample of youth was nicely done. But again, the variable of fetal alcohol exposure was not considered. The study was an elegant one that provides a strong rationale for consideration of a “psychopathology factor” in human life (Am J Psychiatry. 2019 Jun 24. doi: 10.1176/appi.ajp.2019.1807035). It shored up that argument by doing neuroimaging studies on a reasonably large sample of youth and showed that reduced cortical thickness (gray matter volume) was associated with overall psychopathology. With the exception of failing to consider the variable of fetal alcohol exposure, the study is a valuable addition to our understanding of what might be going on with psychiatric disorders.

Unfortunately – while hating to sound like a broken record – I noticed that there was no consideration of fetal alcohol exposure as a cause for the findings of the study. It does not seem like a large leap to hypothesize some of these brain imaging studies that find smaller brain components associated with psychopathology and conduct disorder to be a dynamic of fetal alcohol exposure.

It seems to me that we made a huge mistake in public health in asking women only whether they were drinking while they were pregnant because it was the wrong question. The right question is – “When did you realize you were pregnant, and were you doing any social drinking before you knew you were pregnant?”

Without understanding the etiology of the smaller brains in patients with conduct disorder or psychopathology, we are missing a golden opportunity to prevent such problems. The former editor of the American Journal of Psychiatry – Robert A. Freedman, MD – suggests that by giving phosphatidyl choline to pregnant women, such problems could be prevented.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. In 2019, he was awarded the Adolph Meyer Award by the American Psychiatric Association for lifetime achievement in psychiatric research.

In 2016, two researchers published a meta-analysis on gray matter abnormalities in youth who had conduct problems.

The study by Jack C. Rogers, PhD, and Stephane A. De Brito, PhD, found 13 well-done studies that included 394 youth with conduct problems and 390 typically developing youth. Compared with the typically developing youth, the conduct-disordered youth had decreased gray matter volume (JAMA Psychiatry. 2016 Jan;73[1]:64-72).

As I knew one of the researchers in one of the studies that made the cut, I called him up and asked whether their research had controlled for fetal alcohol exposure. They had not. I found this very curious because my experience is that youth who have been labeled with conduct disorder often have histories of prenatal fetal alcohol exposure. In addition, my understanding is that youth who have been exposed to prenatal alcohol often have symptoms of conduct disorder. Furthermore, research has shown that such youth have smaller brains (Dev Med Child Neurol. 2001 Mar;43[3]:148-54). I wondered whether the youth studied in that trial had been exposed to alcohol prenatally.

More recently, this problem has resurfaced. An article by Antonia N. Kaczkurkin, PhD, and associates about a large sample of youth was nicely done. But again, the variable of fetal alcohol exposure was not considered. The study was an elegant one that provides a strong rationale for consideration of a “psychopathology factor” in human life (Am J Psychiatry. 2019 Jun 24. doi: 10.1176/appi.ajp.2019.1807035). It shored up that argument by doing neuroimaging studies on a reasonably large sample of youth and showed that reduced cortical thickness (gray matter volume) was associated with overall psychopathology. With the exception of failing to consider the variable of fetal alcohol exposure, the study is a valuable addition to our understanding of what might be going on with psychiatric disorders.

Unfortunately – while hating to sound like a broken record – I noticed that there was no consideration of fetal alcohol exposure as a cause for the findings of the study. It does not seem like a large leap to hypothesize some of these brain imaging studies that find smaller brain components associated with psychopathology and conduct disorder to be a dynamic of fetal alcohol exposure.

It seems to me that we made a huge mistake in public health in asking women only whether they were drinking while they were pregnant because it was the wrong question. The right question is – “When did you realize you were pregnant, and were you doing any social drinking before you knew you were pregnant?”

Without understanding the etiology of the smaller brains in patients with conduct disorder or psychopathology, we are missing a golden opportunity to prevent such problems. The former editor of the American Journal of Psychiatry – Robert A. Freedman, MD – suggests that by giving phosphatidyl choline to pregnant women, such problems could be prevented.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. In 2019, he was awarded the Adolph Meyer Award by the American Psychiatric Association for lifetime achievement in psychiatric research.

The general fertility rate in the United States decreased 2% between 2017 and 2018, according to a report from the Centers for Disease Control and Prevention.

©fotolia

Fertility rates, defined as births per 1,000 women aged 15-44 years, declined for all racial/ethnic groups studied.

Teen birth rates, or births among girls aged 15-19 years, declined from 2017 to 2018 as well.

These data come from the National Vital Statistics System’s Natality Data File, which includes information from birth certificates for all births in the United States.

The data show a decline in the general fertility rate from 60.3 per 1,000 women in 2017 to 59.1 per 1,000 women in 2018, a significant decrease (P less than .05).

Fertility rates declined across the three largest racial/ethnic groups studied, decreasing:

• 3% in Hispanic women, from 67.6 to 65.9 per 1,000.
• 2% in non-Hispanic black women, from 63.1 to 62.0 per 1,000.
• 2% in non-Hispanic white women, from 57.2 to 56.3 per 1,000.

Similarly, teen birth rates declined 7% from 2017 to 2018, decreasing from 18.8 to 17.4 births per 1,000 girls aged 15-19 years (P less than .05). Rates decreased:

• 8% in Hispanic teens, from 28.9 to 26.7 per 1,000.
• 4% in non-Hispanic black teens, from 27.5 to 26.3 per 1,000.
• 8% in non-Hispanic white teens, from 13.2 to 12.1 per 1,000.

The data also show an increase in the rate of vaginal births after previous cesarean (VBAC) delivery. The percentage of VBAC deliveries increased from 12.8% in 2017 to 13.3% in 2018 (P less than .05).

VBAC delivery rates increased across all racial/ethnic groups studied, although the increase among non-Hispanic back women was not significant.

Finally, the report shows an increase in preterm and early term births from 2017 to 2018. Preterm deliveries (less than 37 weeks of gestation) increased from 9.93% to 10.02%, and early term deliveries (37-38 weeks) increased from 26.00% to 26.53% (P less than .05).

At the same time, full-term births (39-40 weeks) decreased from 57.49% to 57.24%, and late- and post-term births (41 weeks or more) decreased from 6.58 % to 6.20% (P less than .05). These findings were consistent across the racial/ethnic groups studied.

jensmith@mdedge.com

SOURCE: Martin JA et al. NCHS Data Brief. 2019 July; no 346.

The general fertility rate in the United States decreased 2% between 2017 and 2018, according to a report from the Centers for Disease Control and Prevention.

©fotolia

Fertility rates, defined as births per 1,000 women aged 15-44 years, declined for all racial/ethnic groups studied.

Teen birth rates, or births among girls aged 15-19 years, declined from 2017 to 2018 as well.

These data come from the National Vital Statistics System’s Natality Data File, which includes information from birth certificates for all births in the United States.

The data show a decline in the general fertility rate from 60.3 per 1,000 women in 2017 to 59.1 per 1,000 women in 2018, a significant decrease (P less than .05).

Fertility rates declined across the three largest racial/ethnic groups studied, decreasing:

• 3% in Hispanic women, from 67.6 to 65.9 per 1,000.
• 2% in non-Hispanic black women, from 63.1 to 62.0 per 1,000.
• 2% in non-Hispanic white women, from 57.2 to 56.3 per 1,000.

Similarly, teen birth rates declined 7% from 2017 to 2018, decreasing from 18.8 to 17.4 births per 1,000 girls aged 15-19 years (P less than .05). Rates decreased:

• 8% in Hispanic teens, from 28.9 to 26.7 per 1,000.
• 4% in non-Hispanic black teens, from 27.5 to 26.3 per 1,000.
• 8% in non-Hispanic white teens, from 13.2 to 12.1 per 1,000.

The data also show an increase in the rate of vaginal births after previous cesarean (VBAC) delivery. The percentage of VBAC deliveries increased from 12.8% in 2017 to 13.3% in 2018 (P less than .05).

VBAC delivery rates increased across all racial/ethnic groups studied, although the increase among non-Hispanic back women was not significant.

Finally, the report shows an increase in preterm and early term births from 2017 to 2018. Preterm deliveries (less than 37 weeks of gestation) increased from 9.93% to 10.02%, and early term deliveries (37-38 weeks) increased from 26.00% to 26.53% (P less than .05).

At the same time, full-term births (39-40 weeks) decreased from 57.49% to 57.24%, and late- and post-term births (41 weeks or more) decreased from 6.58 % to 6.20% (P less than .05). These findings were consistent across the racial/ethnic groups studied.

jensmith@mdedge.com

SOURCE: Martin JA et al. NCHS Data Brief. 2019 July; no 346.

The general fertility rate in the United States decreased 2% between 2017 and 2018, according to a report from the Centers for Disease Control and Prevention.

©fotolia

Fertility rates, defined as births per 1,000 women aged 15-44 years, declined for all racial/ethnic groups studied.

Teen birth rates, or births among girls aged 15-19 years, declined from 2017 to 2018 as well.

These data come from the National Vital Statistics System’s Natality Data File, which includes information from birth certificates for all births in the United States.

The data show a decline in the general fertility rate from 60.3 per 1,000 women in 2017 to 59.1 per 1,000 women in 2018, a significant decrease (P less than .05).

Fertility rates declined across the three largest racial/ethnic groups studied, decreasing:

• 3% in Hispanic women, from 67.6 to 65.9 per 1,000.
• 2% in non-Hispanic black women, from 63.1 to 62.0 per 1,000.
• 2% in non-Hispanic white women, from 57.2 to 56.3 per 1,000.

Similarly, teen birth rates declined 7% from 2017 to 2018, decreasing from 18.8 to 17.4 births per 1,000 girls aged 15-19 years (P less than .05). Rates decreased:

• 8% in Hispanic teens, from 28.9 to 26.7 per 1,000.
• 4% in non-Hispanic black teens, from 27.5 to 26.3 per 1,000.
• 8% in non-Hispanic white teens, from 13.2 to 12.1 per 1,000.

The data also show an increase in the rate of vaginal births after previous cesarean (VBAC) delivery. The percentage of VBAC deliveries increased from 12.8% in 2017 to 13.3% in 2018 (P less than .05).

VBAC delivery rates increased across all racial/ethnic groups studied, although the increase among non-Hispanic back women was not significant.

Finally, the report shows an increase in preterm and early term births from 2017 to 2018. Preterm deliveries (less than 37 weeks of gestation) increased from 9.93% to 10.02%, and early term deliveries (37-38 weeks) increased from 26.00% to 26.53% (P less than .05).

At the same time, full-term births (39-40 weeks) decreased from 57.49% to 57.24%, and late- and post-term births (41 weeks or more) decreased from 6.58 % to 6.20% (P less than .05). These findings were consistent across the racial/ethnic groups studied.

jensmith@mdedge.com

SOURCE: Martin JA et al. NCHS Data Brief. 2019 July; no 346.

The DTaP, hepatitis B virus, and Haemophilus influenzae type b (Hib) vaccine was found to be noninferior to a similar, commercially available vaccine in infants, according to a study in Vaccine.

MarianVejcik/Getty Images

In this phase 3, randomized, single-blind, multicenter, noninferiority study, Sai Krishna Susarla of Human Biologicals Institute, which developed the test vaccine, and colleagues randomized 405 infants aged 6-8 weeks 2:1 to three doses of either the test vaccine or the comparator, Pentavac SD (Serum Institute of India). The percentages of seroconversion for diphtheria, pertussis, hepatitis B, and Hib were 98.44%, 92.61%, 99.22%, and 95.72% for the test vaccine, respectively, and 90.0%, 89.23%, 100%, and 90.77% for the comparator. In keeping with some previous studies, the percentages for tetanus were low at 50.97% with the test vaccine and 30.23% with the comparator. Despite the low seroconversion for tetanus, the test vaccine was determined to be noninferior to the comparator for it and the other four diseases it targets. The safety profile was also found to be comparable.

Although the study’s major limitation is that it was conducted in only one country, “the strength of the study is considered to be good” because “compliance to protocol was good, deviations were minimal, and ... very few subjects were withdrawn,” the researchers wrote.

Some of the researchers were employees of the sponsor, Human Biologicals Institute, which developed the test vaccine. Other researchers had no financial interest in the test vaccine and were unrelated to the sponsor, but did receive research grants for conducting the study at their respective sites.

cpalmer@mdedge.com

SOURCE: Susarla SK et al. Vaccine. 2019 Jul 19. doi: 10.1016/j.vaccine.2019.06.067.

The DTaP, hepatitis B virus, and Haemophilus influenzae type b (Hib) vaccine was found to be noninferior to a similar, commercially available vaccine in infants, according to a study in Vaccine.

MarianVejcik/Getty Images

In this phase 3, randomized, single-blind, multicenter, noninferiority study, Sai Krishna Susarla of Human Biologicals Institute, which developed the test vaccine, and colleagues randomized 405 infants aged 6-8 weeks 2:1 to three doses of either the test vaccine or the comparator, Pentavac SD (Serum Institute of India). The percentages of seroconversion for diphtheria, pertussis, hepatitis B, and Hib were 98.44%, 92.61%, 99.22%, and 95.72% for the test vaccine, respectively, and 90.0%, 89.23%, 100%, and 90.77% for the comparator. In keeping with some previous studies, the percentages for tetanus were low at 50.97% with the test vaccine and 30.23% with the comparator. Despite the low seroconversion for tetanus, the test vaccine was determined to be noninferior to the comparator for it and the other four diseases it targets. The safety profile was also found to be comparable.

Although the study’s major limitation is that it was conducted in only one country, “the strength of the study is considered to be good” because “compliance to protocol was good, deviations were minimal, and ... very few subjects were withdrawn,” the researchers wrote.

Some of the researchers were employees of the sponsor, Human Biologicals Institute, which developed the test vaccine. Other researchers had no financial interest in the test vaccine and were unrelated to the sponsor, but did receive research grants for conducting the study at their respective sites.

cpalmer@mdedge.com

SOURCE: Susarla SK et al. Vaccine. 2019 Jul 19. doi: 10.1016/j.vaccine.2019.06.067.

The DTaP, hepatitis B virus, and Haemophilus influenzae type b (Hib) vaccine was found to be noninferior to a similar, commercially available vaccine in infants, according to a study in Vaccine.

MarianVejcik/Getty Images

In this phase 3, randomized, single-blind, multicenter, noninferiority study, Sai Krishna Susarla of Human Biologicals Institute, which developed the test vaccine, and colleagues randomized 405 infants aged 6-8 weeks 2:1 to three doses of either the test vaccine or the comparator, Pentavac SD (Serum Institute of India). The percentages of seroconversion for diphtheria, pertussis, hepatitis B, and Hib were 98.44%, 92.61%, 99.22%, and 95.72% for the test vaccine, respectively, and 90.0%, 89.23%, 100%, and 90.77% for the comparator. In keeping with some previous studies, the percentages for tetanus were low at 50.97% with the test vaccine and 30.23% with the comparator. Despite the low seroconversion for tetanus, the test vaccine was determined to be noninferior to the comparator for it and the other four diseases it targets. The safety profile was also found to be comparable.

Although the study’s major limitation is that it was conducted in only one country, “the strength of the study is considered to be good” because “compliance to protocol was good, deviations were minimal, and ... very few subjects were withdrawn,” the researchers wrote.

Some of the researchers were employees of the sponsor, Human Biologicals Institute, which developed the test vaccine. Other researchers had no financial interest in the test vaccine and were unrelated to the sponsor, but did receive research grants for conducting the study at their respective sites.

cpalmer@mdedge.com

SOURCE: Susarla SK et al. Vaccine. 2019 Jul 19. doi: 10.1016/j.vaccine.2019.06.067.

ORLANDO – Inhaler choice for patients with chronic obstructive pulmonary disease (COPD) should be chosen on the basis of access, cost, prescriber, patient ability, and patient preference.

That’s according to Gabriel Ortiz, MPAS, PA-C, DFAAPA, a speaker at the Cardiovascular & Respiratory Summit by Global Academy for Medical Education.

There are several treatment options available in inhaler form for patients with COPD, including short-acting and long-acting beta₂-agonists (SABA/LABA), short-acting and long-acting antimuscarinics (SAMA/LAMA), combination therapy, and triple therapy. But education and training on how to use an inhaler is also important, Mr. Ortiz said in his presentation.

Providers should help a patient choose an inhaler they are most likely to use. “It’s difficult to actuate and inhale, so there’s a lot of education that goes into that,” said Mr. Ortiz, of Pediatric Pulmonary Services in El Paso, Texas. “What we do for our patients is, we educate them, we tell them to demonstrate it, then bring [the] inhaler back on the next visit and demonstrate to us every time.”

“Make sure that they demonstrate because, as patients get older, they may lose their ability to actuate and inhale,” he added.

Adherence to therapy should also be considered before changing from a current therapy, he added. Mr. Ortiz described a scenario in which a prescription was filled, but because of the cost, the patient reduced the dose by half to make the therapy last longer.

“We could be the best providers in the world, prescribing the best medication in the world. If the medication doesn’t get to where we need it, it’s not going to help anybody,” he said.

Providers should also use nonpharmacological treatments to prevent or keep COPD from progressing. Smoking cessation is key to reducing the risk of developing COPD, and it is not clear whether e-cigarettes aid in smoking cessation, despite companies that market these products making that claim. “We have a huge e-cigarette epidemic here,” he said.

Instead, Mr. Ortiz recommended identifying which patients are current tobacco users, encouraging them to quit, determining whether the patient is willing to make a commitment to cut down on tobacco use or stop entirely, helping draft a quit plan and obtaining intra- and extratreatment social support for smoking cessation, and scheduling follow-up. Providers should discuss smoking cessation at each visit, and it may take multiple visits before a patient is willing to consider quitting, he said.

Another measure providers can take is making sure patients with COPD have received influenza and pneumococcal vaccinations because this can lower the risk of respiratory tract infections. Physical activity, training in exercise, nutritional support, and pulmonary rehabilitation can improve their health status, dyspnea, and exercise tolerance. While C-level evidence shows education alone is not effective according to Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines, providers working with patients through self-management interventions have been shown to improve health status and decrease COPD-related hospitalizations.

Oxygen therapy has been effective for patients with severe resting chronic hypoxia and improves survival, said Mr. Ortiz. For patients who gradually decline in health despite treatment, palliative, hospice, and end-of-life care may be an option. “Remember that as acute exacerbations continue, that increases the risk of death,” he said. “We want to try and prevent [those] exacerbations and improve quality of life.”

During follow-up visits, providers should continue performing spirometry tests annually to measure decline in forced expiratory volume in 1 second, information on symptoms that have presented since the previous visit, details of any exacerbations that occurred, and current smoking status. When making decisions to adjust therapy, providers should examine the effectiveness of the current regimen and consider the dose of prescribed medications, whether the patient is adhering to the regimen, inhaler technique, and any side effects.

Mr. Ortiz reports also being a paid employee for Thermo Fisher, a biotechnology product development company based in Waltham, Mass. Global Academy for Medical Education and this news organization are owned by the same parent company.


 

ORLANDO – Inhaler choice for patients with chronic obstructive pulmonary disease (COPD) should be chosen on the basis of access, cost, prescriber, patient ability, and patient preference.

That’s according to Gabriel Ortiz, MPAS, PA-C, DFAAPA, a speaker at the Cardiovascular & Respiratory Summit by Global Academy for Medical Education.

There are several treatment options available in inhaler form for patients with COPD, including short-acting and long-acting beta₂-agonists (SABA/LABA), short-acting and long-acting antimuscarinics (SAMA/LAMA), combination therapy, and triple therapy. But education and training on how to use an inhaler is also important, Mr. Ortiz said in his presentation.

Providers should help a patient choose an inhaler they are most likely to use. “It’s difficult to actuate and inhale, so there’s a lot of education that goes into that,” said Mr. Ortiz, of Pediatric Pulmonary Services in El Paso, Texas. “What we do for our patients is, we educate them, we tell them to demonstrate it, then bring [the] inhaler back on the next visit and demonstrate to us every time.”

“Make sure that they demonstrate because, as patients get older, they may lose their ability to actuate and inhale,” he added.

Adherence to therapy should also be considered before changing from a current therapy, he added. Mr. Ortiz described a scenario in which a prescription was filled, but because of the cost, the patient reduced the dose by half to make the therapy last longer.

“We could be the best providers in the world, prescribing the best medication in the world. If the medication doesn’t get to where we need it, it’s not going to help anybody,” he said.

Providers should also use nonpharmacological treatments to prevent or keep COPD from progressing. Smoking cessation is key to reducing the risk of developing COPD, and it is not clear whether e-cigarettes aid in smoking cessation, despite companies that market these products making that claim. “We have a huge e-cigarette epidemic here,” he said.

Instead, Mr. Ortiz recommended identifying which patients are current tobacco users, encouraging them to quit, determining whether the patient is willing to make a commitment to cut down on tobacco use or stop entirely, helping draft a quit plan and obtaining intra- and extratreatment social support for smoking cessation, and scheduling follow-up. Providers should discuss smoking cessation at each visit, and it may take multiple visits before a patient is willing to consider quitting, he said.

Another measure providers can take is making sure patients with COPD have received influenza and pneumococcal vaccinations because this can lower the risk of respiratory tract infections. Physical activity, training in exercise, nutritional support, and pulmonary rehabilitation can improve their health status, dyspnea, and exercise tolerance. While C-level evidence shows education alone is not effective according to Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines, providers working with patients through self-management interventions have been shown to improve health status and decrease COPD-related hospitalizations.

Oxygen therapy has been effective for patients with severe resting chronic hypoxia and improves survival, said Mr. Ortiz. For patients who gradually decline in health despite treatment, palliative, hospice, and end-of-life care may be an option. “Remember that as acute exacerbations continue, that increases the risk of death,” he said. “We want to try and prevent [those] exacerbations and improve quality of life.”

During follow-up visits, providers should continue performing spirometry tests annually to measure decline in forced expiratory volume in 1 second, information on symptoms that have presented since the previous visit, details of any exacerbations that occurred, and current smoking status. When making decisions to adjust therapy, providers should examine the effectiveness of the current regimen and consider the dose of prescribed medications, whether the patient is adhering to the regimen, inhaler technique, and any side effects.

Mr. Ortiz reports also being a paid employee for Thermo Fisher, a biotechnology product development company based in Waltham, Mass. Global Academy for Medical Education and this news organization are owned by the same parent company.


 

ORLANDO – Inhaler choice for patients with chronic obstructive pulmonary disease (COPD) should be chosen on the basis of access, cost, prescriber, patient ability, and patient preference.

That’s according to Gabriel Ortiz, MPAS, PA-C, DFAAPA, a speaker at the Cardiovascular & Respiratory Summit by Global Academy for Medical Education.

There are several treatment options available in inhaler form for patients with COPD, including short-acting and long-acting beta₂-agonists (SABA/LABA), short-acting and long-acting antimuscarinics (SAMA/LAMA), combination therapy, and triple therapy. But education and training on how to use an inhaler is also important, Mr. Ortiz said in his presentation.

Providers should help a patient choose an inhaler they are most likely to use. “It’s difficult to actuate and inhale, so there’s a lot of education that goes into that,” said Mr. Ortiz, of Pediatric Pulmonary Services in El Paso, Texas. “What we do for our patients is, we educate them, we tell them to demonstrate it, then bring [the] inhaler back on the next visit and demonstrate to us every time.”

“Make sure that they demonstrate because, as patients get older, they may lose their ability to actuate and inhale,” he added.

Adherence to therapy should also be considered before changing from a current therapy, he added. Mr. Ortiz described a scenario in which a prescription was filled, but because of the cost, the patient reduced the dose by half to make the therapy last longer.

“We could be the best providers in the world, prescribing the best medication in the world. If the medication doesn’t get to where we need it, it’s not going to help anybody,” he said.

Providers should also use nonpharmacological treatments to prevent or keep COPD from progressing. Smoking cessation is key to reducing the risk of developing COPD, and it is not clear whether e-cigarettes aid in smoking cessation, despite companies that market these products making that claim. “We have a huge e-cigarette epidemic here,” he said.

Instead, Mr. Ortiz recommended identifying which patients are current tobacco users, encouraging them to quit, determining whether the patient is willing to make a commitment to cut down on tobacco use or stop entirely, helping draft a quit plan and obtaining intra- and extratreatment social support for smoking cessation, and scheduling follow-up. Providers should discuss smoking cessation at each visit, and it may take multiple visits before a patient is willing to consider quitting, he said.

Another measure providers can take is making sure patients with COPD have received influenza and pneumococcal vaccinations because this can lower the risk of respiratory tract infections. Physical activity, training in exercise, nutritional support, and pulmonary rehabilitation can improve their health status, dyspnea, and exercise tolerance. While C-level evidence shows education alone is not effective according to Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines, providers working with patients through self-management interventions have been shown to improve health status and decrease COPD-related hospitalizations.

Oxygen therapy has been effective for patients with severe resting chronic hypoxia and improves survival, said Mr. Ortiz. For patients who gradually decline in health despite treatment, palliative, hospice, and end-of-life care may be an option. “Remember that as acute exacerbations continue, that increases the risk of death,” he said. “We want to try and prevent [those] exacerbations and improve quality of life.”

During follow-up visits, providers should continue performing spirometry tests annually to measure decline in forced expiratory volume in 1 second, information on symptoms that have presented since the previous visit, details of any exacerbations that occurred, and current smoking status. When making decisions to adjust therapy, providers should examine the effectiveness of the current regimen and consider the dose of prescribed medications, whether the patient is adhering to the regimen, inhaler technique, and any side effects.

Mr. Ortiz reports also being a paid employee for Thermo Fisher, a biotechnology product development company based in Waltham, Mass. Global Academy for Medical Education and this news organization are owned by the same parent company.


 

The Florida Society of Rheumatology is an excellent state conference that is very well attended because of the comprehensive clinical topics covered by esteemed faculty. Every year, there is a balance of patient care lectures and updates in advocacy, billing, and coding. Clinicians need a combination of both arenas to be successful with the day-to-day practice of rheumatology and to render evidenced-based patient care. This year, the FSR certainly delivered on this mission as reflected by articles on these presentations published at MDedge Rheumatology. An added focus this year was how to leverage technology in a rheumatology practice to capture patient-reported outcomes (PROs) to better understand issues affecting our patient population and improve therapy plans where indicated.

In his lecture on digital PROs, Jeffrey Curtis, MD, explained the difference between active capture of data through tools such as the Routine Assessment of Patient Index Data 3 (RAPID3) or Health Assessment Questionnaire (HAQ) and passive capture through wearable devices such as a Fitbit or Apple watch. A key point for the audience was that this information improves clinical care and improves medical decision making, and thus all rheumatologists should consider using these tools in practice. Dr. Curtis, William J. Koopman Endowed Professor in Rheumatology and Immunology and director of the UAB Arthritis Clinical Intervention Program at the University of Alabama at Birmingham, is well aware of the practical concerns that face clinicians, namely that this is time consuming. He suggests to keep it short and find a tool that works for you in your practice to understand how your patients are progressing on a treatment regimen. He was clear that “data for the sake of data is not compelling for patients [or clinicians].” The ideal is not to paralyze your practice and drown in patient questionnaires but rather to empower patients to report using standardized tools so we can effect change that will help us to treat rheumatic diseases.

An important point mentioned during this lecture was to keep in mind that, if a patient appears to be a “nonresponder” on RAPID3, for example, it is important to understand whether the patient has a confounding comorbidity, such as fibromyalgia, that may account for the limited improvement.

Michelle Petri, MD, gave two excellent talks at FSR this year. Her lectures are packed with excellent pearls about treating patients with systemic lupus erythematosus. Interestingly, she said to never underestimate the prognostic factor of a low C3. This can indicate a worse clinical course is ahead. In addition, she reminds us as clinicians to protect the kidneys of our lupus patients who have renal disease by avoiding common toxins such as NSAIDs and CT contrast. Of course, she reminds us to use the lowest dose of steroids possible during flares, as prednisone is directly or indirectly responsible for 80% of organ damage over 15 years. She reminds us that lupus patients do not die of lupus. They have a 2.66-fold higher risk of cardiovascular events than the general public. In addition to maintaining lupus patients on hydroxychloroquine, Dr. Petri, professor of medicine and director of the Hopkins Lupus Center at Johns Hopkins University, Baltimore, noted that vitamin D can have cardiovascular and hematologic benefits along with reducing thrombosis in some clinical studies. Low vitamin D was significantly associated with deep venous thrombosis.

In his lecture, Leonard Calabrese, DO, made a compelling argument for the rheumatologists in the audience to call the local oncologists with whom they work. We need to discuss and collaborate on the care of patients experiencing immune-mediated adverse events from exposure to checkpoint inhibitors used to treat malignancy. There is a limited mechanistic understanding of these adverse events, but as rheumatologists we need to get involved and help these patients. We are the experts in managing these newly emerging autoimmune events. We can help to create the best possible therapeutic interventions to help our oncology colleagues with these challenging cases, Dr. Calabrese, professor of medicine and chair of clinical immunology at the Cleveland Clinic, said.

Besides paying our dues to be members of the FSR, it is important for us as rheumatologists to get involved at the state legislature and national level to bring about change for our practices and patients. Currently, the climate can be hostile for reimbursement and for our patients to get the therapies they need. In another presentation, Angus Worthing, MD, chair of the American College of Rheumatology’s Government Affairs Committee, described recent successes at the national level, and he also discussed how we can have our voices heard at the state and national level to protect our profession and the people who rely on our expertise. The FSR and other state rheumatology organizations, as well as the ACR, need our support to continue to be the collective voice for what is right for clinicians and patients alike.
 

Dr. Oberstein is a practicing rheumatologist at the University of Miami Health System and is senior medical director of musculoskeletal at Modernizing Medicine in Boca Raton, Fla. She has no relevant disclosures to report.

The Florida Society of Rheumatology is an excellent state conference that is very well attended because of the comprehensive clinical topics covered by esteemed faculty. Every year, there is a balance of patient care lectures and updates in advocacy, billing, and coding. Clinicians need a combination of both arenas to be successful with the day-to-day practice of rheumatology and to render evidenced-based patient care. This year, the FSR certainly delivered on this mission as reflected by articles on these presentations published at MDedge Rheumatology. An added focus this year was how to leverage technology in a rheumatology practice to capture patient-reported outcomes (PROs) to better understand issues affecting our patient population and improve therapy plans where indicated.

In his lecture on digital PROs, Jeffrey Curtis, MD, explained the difference between active capture of data through tools such as the Routine Assessment of Patient Index Data 3 (RAPID3) or Health Assessment Questionnaire (HAQ) and passive capture through wearable devices such as a Fitbit or Apple watch. A key point for the audience was that this information improves clinical care and improves medical decision making, and thus all rheumatologists should consider using these tools in practice. Dr. Curtis, William J. Koopman Endowed Professor in Rheumatology and Immunology and director of the UAB Arthritis Clinical Intervention Program at the University of Alabama at Birmingham, is well aware of the practical concerns that face clinicians, namely that this is time consuming. He suggests to keep it short and find a tool that works for you in your practice to understand how your patients are progressing on a treatment regimen. He was clear that “data for the sake of data is not compelling for patients [or clinicians].” The ideal is not to paralyze your practice and drown in patient questionnaires but rather to empower patients to report using standardized tools so we can effect change that will help us to treat rheumatic diseases.

An important point mentioned during this lecture was to keep in mind that, if a patient appears to be a “nonresponder” on RAPID3, for example, it is important to understand whether the patient has a confounding comorbidity, such as fibromyalgia, that may account for the limited improvement.

Michelle Petri, MD, gave two excellent talks at FSR this year. Her lectures are packed with excellent pearls about treating patients with systemic lupus erythematosus. Interestingly, she said to never underestimate the prognostic factor of a low C3. This can indicate a worse clinical course is ahead. In addition, she reminds us as clinicians to protect the kidneys of our lupus patients who have renal disease by avoiding common toxins such as NSAIDs and CT contrast. Of course, she reminds us to use the lowest dose of steroids possible during flares, as prednisone is directly or indirectly responsible for 80% of organ damage over 15 years. She reminds us that lupus patients do not die of lupus. They have a 2.66-fold higher risk of cardiovascular events than the general public. In addition to maintaining lupus patients on hydroxychloroquine, Dr. Petri, professor of medicine and director of the Hopkins Lupus Center at Johns Hopkins University, Baltimore, noted that vitamin D can have cardiovascular and hematologic benefits along with reducing thrombosis in some clinical studies. Low vitamin D was significantly associated with deep venous thrombosis.

In his lecture, Leonard Calabrese, DO, made a compelling argument for the rheumatologists in the audience to call the local oncologists with whom they work. We need to discuss and collaborate on the care of patients experiencing immune-mediated adverse events from exposure to checkpoint inhibitors used to treat malignancy. There is a limited mechanistic understanding of these adverse events, but as rheumatologists we need to get involved and help these patients. We are the experts in managing these newly emerging autoimmune events. We can help to create the best possible therapeutic interventions to help our oncology colleagues with these challenging cases, Dr. Calabrese, professor of medicine and chair of clinical immunology at the Cleveland Clinic, said.

Besides paying our dues to be members of the FSR, it is important for us as rheumatologists to get involved at the state legislature and national level to bring about change for our practices and patients. Currently, the climate can be hostile for reimbursement and for our patients to get the therapies they need. In another presentation, Angus Worthing, MD, chair of the American College of Rheumatology’s Government Affairs Committee, described recent successes at the national level, and he also discussed how we can have our voices heard at the state and national level to protect our profession and the people who rely on our expertise. The FSR and other state rheumatology organizations, as well as the ACR, need our support to continue to be the collective voice for what is right for clinicians and patients alike.
 

Dr. Oberstein is a practicing rheumatologist at the University of Miami Health System and is senior medical director of musculoskeletal at Modernizing Medicine in Boca Raton, Fla. She has no relevant disclosures to report.

The Florida Society of Rheumatology is an excellent state conference that is very well attended because of the comprehensive clinical topics covered by esteemed faculty. Every year, there is a balance of patient care lectures and updates in advocacy, billing, and coding. Clinicians need a combination of both arenas to be successful with the day-to-day practice of rheumatology and to render evidenced-based patient care. This year, the FSR certainly delivered on this mission as reflected by articles on these presentations published at MDedge Rheumatology. An added focus this year was how to leverage technology in a rheumatology practice to capture patient-reported outcomes (PROs) to better understand issues affecting our patient population and improve therapy plans where indicated.

In his lecture on digital PROs, Jeffrey Curtis, MD, explained the difference between active capture of data through tools such as the Routine Assessment of Patient Index Data 3 (RAPID3) or Health Assessment Questionnaire (HAQ) and passive capture through wearable devices such as a Fitbit or Apple watch. A key point for the audience was that this information improves clinical care and improves medical decision making, and thus all rheumatologists should consider using these tools in practice. Dr. Curtis, William J. Koopman Endowed Professor in Rheumatology and Immunology and director of the UAB Arthritis Clinical Intervention Program at the University of Alabama at Birmingham, is well aware of the practical concerns that face clinicians, namely that this is time consuming. He suggests to keep it short and find a tool that works for you in your practice to understand how your patients are progressing on a treatment regimen. He was clear that “data for the sake of data is not compelling for patients [or clinicians].” The ideal is not to paralyze your practice and drown in patient questionnaires but rather to empower patients to report using standardized tools so we can effect change that will help us to treat rheumatic diseases.

An important point mentioned during this lecture was to keep in mind that, if a patient appears to be a “nonresponder” on RAPID3, for example, it is important to understand whether the patient has a confounding comorbidity, such as fibromyalgia, that may account for the limited improvement.

Michelle Petri, MD, gave two excellent talks at FSR this year. Her lectures are packed with excellent pearls about treating patients with systemic lupus erythematosus. Interestingly, she said to never underestimate the prognostic factor of a low C3. This can indicate a worse clinical course is ahead. In addition, she reminds us as clinicians to protect the kidneys of our lupus patients who have renal disease by avoiding common toxins such as NSAIDs and CT contrast. Of course, she reminds us to use the lowest dose of steroids possible during flares, as prednisone is directly or indirectly responsible for 80% of organ damage over 15 years. She reminds us that lupus patients do not die of lupus. They have a 2.66-fold higher risk of cardiovascular events than the general public. In addition to maintaining lupus patients on hydroxychloroquine, Dr. Petri, professor of medicine and director of the Hopkins Lupus Center at Johns Hopkins University, Baltimore, noted that vitamin D can have cardiovascular and hematologic benefits along with reducing thrombosis in some clinical studies. Low vitamin D was significantly associated with deep venous thrombosis.

In his lecture, Leonard Calabrese, DO, made a compelling argument for the rheumatologists in the audience to call the local oncologists with whom they work. We need to discuss and collaborate on the care of patients experiencing immune-mediated adverse events from exposure to checkpoint inhibitors used to treat malignancy. There is a limited mechanistic understanding of these adverse events, but as rheumatologists we need to get involved and help these patients. We are the experts in managing these newly emerging autoimmune events. We can help to create the best possible therapeutic interventions to help our oncology colleagues with these challenging cases, Dr. Calabrese, professor of medicine and chair of clinical immunology at the Cleveland Clinic, said.

Besides paying our dues to be members of the FSR, it is important for us as rheumatologists to get involved at the state legislature and national level to bring about change for our practices and patients. Currently, the climate can be hostile for reimbursement and for our patients to get the therapies they need. In another presentation, Angus Worthing, MD, chair of the American College of Rheumatology’s Government Affairs Committee, described recent successes at the national level, and he also discussed how we can have our voices heard at the state and national level to protect our profession and the people who rely on our expertise. The FSR and other state rheumatology organizations, as well as the ACR, need our support to continue to be the collective voice for what is right for clinicians and patients alike.
 

Dr. Oberstein is a practicing rheumatologist at the University of Miami Health System and is senior medical director of musculoskeletal at Modernizing Medicine in Boca Raton, Fla. She has no relevant disclosures to report.