Reacting quickly to complaints of caregivers who had their eligibility for Program of Comprehensive Assistance for Family Caregivers (PCAFC) funding revoked, the VA has announced that it will pause revocations while reviewing the program’s implementation. “VA is taking immediate action to review the National Caregiver Support Program to ensure we honor our commitment to enhance the health and well-being of veterans,” said Secretary of Veterans Affairs David J. Shulkin, MD, in a prepared statement. “I have instructed an internal review to evaluate consistency of revocations in the program and standardize communication with veterans and caregivers nationwide.”

An NPR report documented a number of cases of PCAFC support that had been changed recently despite little evidence for change in the veterans’ need for care. According to the NPR analysis, some VA facilities saw significant drops in the number of caregivers who received support; whereas others saw equally significant increases.

According to the VA, veterans who need a VA designated family caregiver to assist with the management of personal care functions that are required for everyday living and are in conjunction with standard care provided by the VA are eligible for the program. A clinical support team evaluates the veteran for eligibility, and the caregiver receives training. The program provides a monthly stipend based on the veterans’ “level of need and required assistance.”

During the review, the VA will continue accepting PCAFC applications, approving applicants based on current eligibility criteria, processing appeals, and monitoring eligible veterans’ well-being at least every 90 days unless otherwise clinically indicated.

 “Caregivers play a critically important role in the health and well-being of veterans, and caring for an injured veteran is a labor of love,” said Dr. Poonam Alaigh, acting VA Under Secretary for Health. “We remain focused on process improvements and support services for our family caregivers so they can take care of our veterans.” 

Reacting quickly to complaints of caregivers who had their eligibility for Program of Comprehensive Assistance for Family Caregivers (PCAFC) funding revoked, the VA has announced that it will pause revocations while reviewing the program’s implementation. “VA is taking immediate action to review the National Caregiver Support Program to ensure we honor our commitment to enhance the health and well-being of veterans,” said Secretary of Veterans Affairs David J. Shulkin, MD, in a prepared statement. “I have instructed an internal review to evaluate consistency of revocations in the program and standardize communication with veterans and caregivers nationwide.”

An NPR report documented a number of cases of PCAFC support that had been changed recently despite little evidence for change in the veterans’ need for care. According to the NPR analysis, some VA facilities saw significant drops in the number of caregivers who received support; whereas others saw equally significant increases.

According to the VA, veterans who need a VA designated family caregiver to assist with the management of personal care functions that are required for everyday living and are in conjunction with standard care provided by the VA are eligible for the program. A clinical support team evaluates the veteran for eligibility, and the caregiver receives training. The program provides a monthly stipend based on the veterans’ “level of need and required assistance.”

During the review, the VA will continue accepting PCAFC applications, approving applicants based on current eligibility criteria, processing appeals, and monitoring eligible veterans’ well-being at least every 90 days unless otherwise clinically indicated.

 “Caregivers play a critically important role in the health and well-being of veterans, and caring for an injured veteran is a labor of love,” said Dr. Poonam Alaigh, acting VA Under Secretary for Health. “We remain focused on process improvements and support services for our family caregivers so they can take care of our veterans.” 

Reacting quickly to complaints of caregivers who had their eligibility for Program of Comprehensive Assistance for Family Caregivers (PCAFC) funding revoked, the VA has announced that it will pause revocations while reviewing the program’s implementation. “VA is taking immediate action to review the National Caregiver Support Program to ensure we honor our commitment to enhance the health and well-being of veterans,” said Secretary of Veterans Affairs David J. Shulkin, MD, in a prepared statement. “I have instructed an internal review to evaluate consistency of revocations in the program and standardize communication with veterans and caregivers nationwide.”

An NPR report documented a number of cases of PCAFC support that had been changed recently despite little evidence for change in the veterans’ need for care. According to the NPR analysis, some VA facilities saw significant drops in the number of caregivers who received support; whereas others saw equally significant increases.

According to the VA, veterans who need a VA designated family caregiver to assist with the management of personal care functions that are required for everyday living and are in conjunction with standard care provided by the VA are eligible for the program. A clinical support team evaluates the veteran for eligibility, and the caregiver receives training. The program provides a monthly stipend based on the veterans’ “level of need and required assistance.”

During the review, the VA will continue accepting PCAFC applications, approving applicants based on current eligibility criteria, processing appeals, and monitoring eligible veterans’ well-being at least every 90 days unless otherwise clinically indicated.

 “Caregivers play a critically important role in the health and well-being of veterans, and caring for an injured veteran is a labor of love,” said Dr. Poonam Alaigh, acting VA Under Secretary for Health. “We remain focused on process improvements and support services for our family caregivers so they can take care of our veterans.” 

This should not come as much of a surprise, but health care made the top-5 list of occupations whose workers are getting too little sleep, according to a study by The National Institute for Occupational Safety and Health (NIOSH) researchers.

The researchers analyzed data from 179,621 working adults who responded to the 2013 or 2014 Behavior Risk Factor Surveillance System annual surveys. Among the 22 major occupation groups, health care support (40.1%) and health care practitioners and technical (40.0%) ranked second and third in “short sleep duration,” after production (42.9%). Among the occupational subgroups, nursing, psychiatric, and home health aides had a high adjusted prevalence of short sleep duration.

Workers in occupations where alternative shiftwork is common were more likely to have a higher adjusted prevalence of short sleep duration.  More than 35% of health care practitioners work shifts. Workers in other occupation groups such as teachers, farmers, or pilots, were more likely to report getting enough sleep.

Time at work also is on the rise in the US where workers have the longest annual working hours among workers in all wealthy industrialized countries, which reduces the time available for sleep, NIOSH says. The researchers point out that lack of sleep has been linked to negative health outcomes including cardiovascular disease, obesity, and depression, as well as safety issues related to drowsy driving and injuries.

To help people get more sleep or improve the quality of the sleep they get, NIOSH offers training and resources about sleep, shiftwork, and fatigue for a variety of audiences including health care workers and emergency responders. Free downloadable materials are available at www.cdc.gov/niosh/topics/workschedules/education.html.

This should not come as much of a surprise, but health care made the top-5 list of occupations whose workers are getting too little sleep, according to a study by The National Institute for Occupational Safety and Health (NIOSH) researchers.

The researchers analyzed data from 179,621 working adults who responded to the 2013 or 2014 Behavior Risk Factor Surveillance System annual surveys. Among the 22 major occupation groups, health care support (40.1%) and health care practitioners and technical (40.0%) ranked second and third in “short sleep duration,” after production (42.9%). Among the occupational subgroups, nursing, psychiatric, and home health aides had a high adjusted prevalence of short sleep duration.

Workers in occupations where alternative shiftwork is common were more likely to have a higher adjusted prevalence of short sleep duration.  More than 35% of health care practitioners work shifts. Workers in other occupation groups such as teachers, farmers, or pilots, were more likely to report getting enough sleep.

Time at work also is on the rise in the US where workers have the longest annual working hours among workers in all wealthy industrialized countries, which reduces the time available for sleep, NIOSH says. The researchers point out that lack of sleep has been linked to negative health outcomes including cardiovascular disease, obesity, and depression, as well as safety issues related to drowsy driving and injuries.

To help people get more sleep or improve the quality of the sleep they get, NIOSH offers training and resources about sleep, shiftwork, and fatigue for a variety of audiences including health care workers and emergency responders. Free downloadable materials are available at www.cdc.gov/niosh/topics/workschedules/education.html.

This should not come as much of a surprise, but health care made the top-5 list of occupations whose workers are getting too little sleep, according to a study by The National Institute for Occupational Safety and Health (NIOSH) researchers.

The researchers analyzed data from 179,621 working adults who responded to the 2013 or 2014 Behavior Risk Factor Surveillance System annual surveys. Among the 22 major occupation groups, health care support (40.1%) and health care practitioners and technical (40.0%) ranked second and third in “short sleep duration,” after production (42.9%). Among the occupational subgroups, nursing, psychiatric, and home health aides had a high adjusted prevalence of short sleep duration.

Workers in occupations where alternative shiftwork is common were more likely to have a higher adjusted prevalence of short sleep duration.  More than 35% of health care practitioners work shifts. Workers in other occupation groups such as teachers, farmers, or pilots, were more likely to report getting enough sleep.

Time at work also is on the rise in the US where workers have the longest annual working hours among workers in all wealthy industrialized countries, which reduces the time available for sleep, NIOSH says. The researchers point out that lack of sleep has been linked to negative health outcomes including cardiovascular disease, obesity, and depression, as well as safety issues related to drowsy driving and injuries.

To help people get more sleep or improve the quality of the sleep they get, NIOSH offers training and resources about sleep, shiftwork, and fatigue for a variety of audiences including health care workers and emergency responders. Free downloadable materials are available at www.cdc.gov/niosh/topics/workschedules/education.html.

Image from PLOS ONE

Researchers believe they have found a way to prevent graft-versus-host disease (GVHD) after hematopoietic stem cell transplant (HSCT) while preserving a strong graft-versus-leukemia (GVL) effect.

In experiments with mice, the team found that temporary in vivo depletion of CD4+ T cells soon after HSCT prevented GVHD without inhibiting GVL effects.

The depletion of CD4+ cells essentially caused CD8+ cells to become exhausted in their quest to destroy normal tissue but strengthened in their fight against leukemia, which meant the CD8+ cells could eliminate leukemic cells without causing GVHD.

Defu Zeng, MD, of City of Hope in Duarte, California, and his colleagues recounted these findings in the Journal of Clinical Investigation.

The researchers were able to achieve temporary in vivo depletion of CD4+ T cells by injecting mice with an anti-CD4 monoclonal antibody (mAb).

The team found that a single injection of the mAb given immediately after HSCT prevented acute but not chronic GVHD. Three injections of the mAb—given on days 0, 14, and 28—prevented both types of GVHD.

The researchers said their results suggest GVHD is more effectively prevented by temporary in vivo depletion of donor CD4+ T cells early after HSCT than by ex vivo depletion of donor CD4+ T cells.

This is because treatment with an anti-CD4 mAb temporarily depletes both the injected mature CD4+ T cells and the CD4+ T cells generated de novo from the marrow progenitors early after HSCT.

In explaining the mechanism behind their observations, the researchers noted that the interaction between PD-L1 and CD80 has been shown to exacerbate GVHD, but costimulation of CD80 and PD-1 ameliorates GVHD.

In their experiments, the team found that depleting CD4+ T cells increased serum IFN-γ and reduced IL-2 concentrations. And this led to upregulation of PD-L1 expression by recipient tissues and donor CD8+ T cells.

The researchers said that, in GVHD target tissues, the interactions of PD-L1 and PD-1 on donor CD8+ T cells caused anergy, exhaustion, and apoptosis. These effects prevented the development of GVHD.

On the other hand, in lymphoid tissues, the interactions of PD-L1 and CD80 augmented CD8+ T-cell expansion without increasing anergy, exhaustion, or apoptosis. This allowed for the preservation of GVL effects.

“If successfully translated into clinical application, this [CD4+ T-cell-depleting] regimen may represent one of the novel approaches that allow strong GVL effects without causing GVHD,” Dr Zeng said.

“This kind of regimen has the potential to promote widespread application of allogenic [HSCT] as a curative therapy for hematological malignancies.”

Image from PLOS ONE

Researchers believe they have found a way to prevent graft-versus-host disease (GVHD) after hematopoietic stem cell transplant (HSCT) while preserving a strong graft-versus-leukemia (GVL) effect.

In experiments with mice, the team found that temporary in vivo depletion of CD4+ T cells soon after HSCT prevented GVHD without inhibiting GVL effects.

The depletion of CD4+ cells essentially caused CD8+ cells to become exhausted in their quest to destroy normal tissue but strengthened in their fight against leukemia, which meant the CD8+ cells could eliminate leukemic cells without causing GVHD.

Defu Zeng, MD, of City of Hope in Duarte, California, and his colleagues recounted these findings in the Journal of Clinical Investigation.

The researchers were able to achieve temporary in vivo depletion of CD4+ T cells by injecting mice with an anti-CD4 monoclonal antibody (mAb).

The team found that a single injection of the mAb given immediately after HSCT prevented acute but not chronic GVHD. Three injections of the mAb—given on days 0, 14, and 28—prevented both types of GVHD.

The researchers said their results suggest GVHD is more effectively prevented by temporary in vivo depletion of donor CD4+ T cells early after HSCT than by ex vivo depletion of donor CD4+ T cells.

This is because treatment with an anti-CD4 mAb temporarily depletes both the injected mature CD4+ T cells and the CD4+ T cells generated de novo from the marrow progenitors early after HSCT.

In explaining the mechanism behind their observations, the researchers noted that the interaction between PD-L1 and CD80 has been shown to exacerbate GVHD, but costimulation of CD80 and PD-1 ameliorates GVHD.

In their experiments, the team found that depleting CD4+ T cells increased serum IFN-γ and reduced IL-2 concentrations. And this led to upregulation of PD-L1 expression by recipient tissues and donor CD8+ T cells.

The researchers said that, in GVHD target tissues, the interactions of PD-L1 and PD-1 on donor CD8+ T cells caused anergy, exhaustion, and apoptosis. These effects prevented the development of GVHD.

On the other hand, in lymphoid tissues, the interactions of PD-L1 and CD80 augmented CD8+ T-cell expansion without increasing anergy, exhaustion, or apoptosis. This allowed for the preservation of GVL effects.

“If successfully translated into clinical application, this [CD4+ T-cell-depleting] regimen may represent one of the novel approaches that allow strong GVL effects without causing GVHD,” Dr Zeng said.

“This kind of regimen has the potential to promote widespread application of allogenic [HSCT] as a curative therapy for hematological malignancies.”

Image from PLOS ONE

Researchers believe they have found a way to prevent graft-versus-host disease (GVHD) after hematopoietic stem cell transplant (HSCT) while preserving a strong graft-versus-leukemia (GVL) effect.

In experiments with mice, the team found that temporary in vivo depletion of CD4+ T cells soon after HSCT prevented GVHD without inhibiting GVL effects.

The depletion of CD4+ cells essentially caused CD8+ cells to become exhausted in their quest to destroy normal tissue but strengthened in their fight against leukemia, which meant the CD8+ cells could eliminate leukemic cells without causing GVHD.

Defu Zeng, MD, of City of Hope in Duarte, California, and his colleagues recounted these findings in the Journal of Clinical Investigation.

The researchers were able to achieve temporary in vivo depletion of CD4+ T cells by injecting mice with an anti-CD4 monoclonal antibody (mAb).

The team found that a single injection of the mAb given immediately after HSCT prevented acute but not chronic GVHD. Three injections of the mAb—given on days 0, 14, and 28—prevented both types of GVHD.

The researchers said their results suggest GVHD is more effectively prevented by temporary in vivo depletion of donor CD4+ T cells early after HSCT than by ex vivo depletion of donor CD4+ T cells.

This is because treatment with an anti-CD4 mAb temporarily depletes both the injected mature CD4+ T cells and the CD4+ T cells generated de novo from the marrow progenitors early after HSCT.

In explaining the mechanism behind their observations, the researchers noted that the interaction between PD-L1 and CD80 has been shown to exacerbate GVHD, but costimulation of CD80 and PD-1 ameliorates GVHD.

In their experiments, the team found that depleting CD4+ T cells increased serum IFN-γ and reduced IL-2 concentrations. And this led to upregulation of PD-L1 expression by recipient tissues and donor CD8+ T cells.

The researchers said that, in GVHD target tissues, the interactions of PD-L1 and PD-1 on donor CD8+ T cells caused anergy, exhaustion, and apoptosis. These effects prevented the development of GVHD.

On the other hand, in lymphoid tissues, the interactions of PD-L1 and CD80 augmented CD8+ T-cell expansion without increasing anergy, exhaustion, or apoptosis. This allowed for the preservation of GVL effects.

“If successfully translated into clinical application, this [CD4+ T-cell-depleting] regimen may represent one of the novel approaches that allow strong GVL effects without causing GVHD,” Dr Zeng said.

“This kind of regimen has the potential to promote widespread application of allogenic [HSCT] as a curative therapy for hematological malignancies.”

Photo from Penn Medicine

The US Food and Drug Administration (FDA) has granted another breakthrough therapy designation to CTL019 (tisagenlecleucel-T), an investigational chimeric antigen receptor (CAR) T-cell therapy.

CTL019 now has breakthrough designation as a treatment for adults with relapsed or refractory diffuse large B-cell lymphoma (DLBCL) who have failed 2 or more prior therapies.

The FDA previously granted CTL019 breakthrough designation as a treatment for relapsed/refractory B-cell acute lymphoblastic leukemia (ALL) in pediatric and young adult patients.

Breakthrough designation is intended to expedite the development and review of new medicines that treat serious or life-threatening conditions, if those medicines have demonstrated substantial improvement over available therapies.

The breakthrough designation for CTL019 in DLBCL is based on data from the phase 2 JULIET trial (NCT02445248), in which researchers are evaluating the efficacy and safety of CTL019 in adults with relapsed/refractory DLBCL.

Findings from JULIET are expected to be presented at an upcoming medical meeting.

About CTL019

CTL019 consists of autologous T cells expressing a CD19-specific CAR. The therapy was first developed by the University of Pennsylvania.

In 2012, the university and Novartis entered into a global collaboration to further research, develop, and commercialize CAR-T cell therapies, including CTL019. Novartis holds the worldwide rights to CARs developed through the collaboration.

According to Novartis, regulatory submissions for CTL019 in the treatment of relapsed/refractory DLBCL are expected to be filed by the end of the year.

The company has already filed a biologics license application with the FDA for CTL019 as a treatment for patients with relapsed/refractory B-cell ALL. The FDA granted that application priority review.

Photo from Penn Medicine

The US Food and Drug Administration (FDA) has granted another breakthrough therapy designation to CTL019 (tisagenlecleucel-T), an investigational chimeric antigen receptor (CAR) T-cell therapy.

CTL019 now has breakthrough designation as a treatment for adults with relapsed or refractory diffuse large B-cell lymphoma (DLBCL) who have failed 2 or more prior therapies.

The FDA previously granted CTL019 breakthrough designation as a treatment for relapsed/refractory B-cell acute lymphoblastic leukemia (ALL) in pediatric and young adult patients.

Breakthrough designation is intended to expedite the development and review of new medicines that treat serious or life-threatening conditions, if those medicines have demonstrated substantial improvement over available therapies.

The breakthrough designation for CTL019 in DLBCL is based on data from the phase 2 JULIET trial (NCT02445248), in which researchers are evaluating the efficacy and safety of CTL019 in adults with relapsed/refractory DLBCL.

Findings from JULIET are expected to be presented at an upcoming medical meeting.

About CTL019

CTL019 consists of autologous T cells expressing a CD19-specific CAR. The therapy was first developed by the University of Pennsylvania.

In 2012, the university and Novartis entered into a global collaboration to further research, develop, and commercialize CAR-T cell therapies, including CTL019. Novartis holds the worldwide rights to CARs developed through the collaboration.

According to Novartis, regulatory submissions for CTL019 in the treatment of relapsed/refractory DLBCL are expected to be filed by the end of the year.

The company has already filed a biologics license application with the FDA for CTL019 as a treatment for patients with relapsed/refractory B-cell ALL. The FDA granted that application priority review.

Photo from Penn Medicine

The US Food and Drug Administration (FDA) has granted another breakthrough therapy designation to CTL019 (tisagenlecleucel-T), an investigational chimeric antigen receptor (CAR) T-cell therapy.

CTL019 now has breakthrough designation as a treatment for adults with relapsed or refractory diffuse large B-cell lymphoma (DLBCL) who have failed 2 or more prior therapies.

The FDA previously granted CTL019 breakthrough designation as a treatment for relapsed/refractory B-cell acute lymphoblastic leukemia (ALL) in pediatric and young adult patients.

Breakthrough designation is intended to expedite the development and review of new medicines that treat serious or life-threatening conditions, if those medicines have demonstrated substantial improvement over available therapies.

The breakthrough designation for CTL019 in DLBCL is based on data from the phase 2 JULIET trial (NCT02445248), in which researchers are evaluating the efficacy and safety of CTL019 in adults with relapsed/refractory DLBCL.

Findings from JULIET are expected to be presented at an upcoming medical meeting.

About CTL019

CTL019 consists of autologous T cells expressing a CD19-specific CAR. The therapy was first developed by the University of Pennsylvania.

In 2012, the university and Novartis entered into a global collaboration to further research, develop, and commercialize CAR-T cell therapies, including CTL019. Novartis holds the worldwide rights to CARs developed through the collaboration.

According to Novartis, regulatory submissions for CTL019 in the treatment of relapsed/refractory DLBCL are expected to be filed by the end of the year.

The company has already filed a biologics license application with the FDA for CTL019 as a treatment for patients with relapsed/refractory B-cell ALL. The FDA granted that application priority review.

AML cells

A large study of adults with acute myeloid leukemia (AML) correlates cancer-related genetic mutations with subtypes of AML defined by the presence of specific cytogenetic abnormalities.

Researchers combined the cytogenetic abnormalities that define each of 34 AML subgroups with the mutation status of 80 cancer-related genes to produce an “oncoprint,” a tabular summary of the mutations associated with each cytogenetic group.

This allowed the researchers to identify genetic differences among the 34 subgroups and unexpected associations between the AML subsets and specific genetic mutations as well as gene functional groups.

The researchers believe their findings, published in Leukemia, might help guide mutation testing and treatment decisions in the future.

The study involved 1603 newly diagnosed adult AML patients who were treated on Cancer and Leukemia Group B/Alliance for Clinical Trials in Oncology trials in multiple centers across the US. Most patients (n=1080) were under age 60.

The researchers classified the patients into 34 karyotype subgroups within 5 major cytogenetic groups—cytogenetically normal (CN) AML, complex karyotype (CK) AML, core-binding factor (CBF) AML, AML with balanced translocations or inversions other than those associated with CBF-AML, and AML with unbalanced chromosomal abnormalities detected in non-complex karyotypes.

The team sequenced pretreatment bone marrow or peripheral blood samples from each patient to learn the mutational status of 80 cancer- and leukemia-related genes.

The mutations were assigned to 1 of 9 categories based on the gene’s biological function—for example, methylation-related, cohesin complex, chromatin remodeling, and tumor-suppressor genes.

The researchers identified 4390 mutations, with a median of 3 mutations per patient.

Overall, the most frequently mutated genes that contributed to AML in this cohort belonged to the methylation group.

The researchers observed a high incidence of mutations in methylation-related genes in patients with CN-AML, CK-AML, or unbalanced chromosomal abnormalities.

In contrast, mutations in methylation-related genes were almost absent in CBF-AML patients and were rather rare in patients with non-CBF-AML-related balanced translocations or inversions.

Mutations in spliceosome genes were frequent in patients with unbalanced chromosomal abnormalities, especially those with sole trisomy of chromosomes 4, 8, 11, 13, or 21.

“Our study summarizes cytogenetic and mutational information of 1603 AML patients in a single image,” said Ann-Kathrin Eisfeld, MD, of The Ohio State University Comprehensive Cancer Center in Columbus.

“The identification of key mutational features of each subgroup may help us to better understand the pathogenesis of the different AML types and provides a wealth of information for ongoing and future research.”

AML cells

A large study of adults with acute myeloid leukemia (AML) correlates cancer-related genetic mutations with subtypes of AML defined by the presence of specific cytogenetic abnormalities.

Researchers combined the cytogenetic abnormalities that define each of 34 AML subgroups with the mutation status of 80 cancer-related genes to produce an “oncoprint,” a tabular summary of the mutations associated with each cytogenetic group.

This allowed the researchers to identify genetic differences among the 34 subgroups and unexpected associations between the AML subsets and specific genetic mutations as well as gene functional groups.

The researchers believe their findings, published in Leukemia, might help guide mutation testing and treatment decisions in the future.

The study involved 1603 newly diagnosed adult AML patients who were treated on Cancer and Leukemia Group B/Alliance for Clinical Trials in Oncology trials in multiple centers across the US. Most patients (n=1080) were under age 60.

The researchers classified the patients into 34 karyotype subgroups within 5 major cytogenetic groups—cytogenetically normal (CN) AML, complex karyotype (CK) AML, core-binding factor (CBF) AML, AML with balanced translocations or inversions other than those associated with CBF-AML, and AML with unbalanced chromosomal abnormalities detected in non-complex karyotypes.

The team sequenced pretreatment bone marrow or peripheral blood samples from each patient to learn the mutational status of 80 cancer- and leukemia-related genes.

The mutations were assigned to 1 of 9 categories based on the gene’s biological function—for example, methylation-related, cohesin complex, chromatin remodeling, and tumor-suppressor genes.

The researchers identified 4390 mutations, with a median of 3 mutations per patient.

Overall, the most frequently mutated genes that contributed to AML in this cohort belonged to the methylation group.

The researchers observed a high incidence of mutations in methylation-related genes in patients with CN-AML, CK-AML, or unbalanced chromosomal abnormalities.

In contrast, mutations in methylation-related genes were almost absent in CBF-AML patients and were rather rare in patients with non-CBF-AML-related balanced translocations or inversions.

Mutations in spliceosome genes were frequent in patients with unbalanced chromosomal abnormalities, especially those with sole trisomy of chromosomes 4, 8, 11, 13, or 21.

“Our study summarizes cytogenetic and mutational information of 1603 AML patients in a single image,” said Ann-Kathrin Eisfeld, MD, of The Ohio State University Comprehensive Cancer Center in Columbus.

“The identification of key mutational features of each subgroup may help us to better understand the pathogenesis of the different AML types and provides a wealth of information for ongoing and future research.”

AML cells

A large study of adults with acute myeloid leukemia (AML) correlates cancer-related genetic mutations with subtypes of AML defined by the presence of specific cytogenetic abnormalities.

Researchers combined the cytogenetic abnormalities that define each of 34 AML subgroups with the mutation status of 80 cancer-related genes to produce an “oncoprint,” a tabular summary of the mutations associated with each cytogenetic group.

This allowed the researchers to identify genetic differences among the 34 subgroups and unexpected associations between the AML subsets and specific genetic mutations as well as gene functional groups.

The researchers believe their findings, published in Leukemia, might help guide mutation testing and treatment decisions in the future.

The study involved 1603 newly diagnosed adult AML patients who were treated on Cancer and Leukemia Group B/Alliance for Clinical Trials in Oncology trials in multiple centers across the US. Most patients (n=1080) were under age 60.

The researchers classified the patients into 34 karyotype subgroups within 5 major cytogenetic groups—cytogenetically normal (CN) AML, complex karyotype (CK) AML, core-binding factor (CBF) AML, AML with balanced translocations or inversions other than those associated with CBF-AML, and AML with unbalanced chromosomal abnormalities detected in non-complex karyotypes.

The team sequenced pretreatment bone marrow or peripheral blood samples from each patient to learn the mutational status of 80 cancer- and leukemia-related genes.

The mutations were assigned to 1 of 9 categories based on the gene’s biological function—for example, methylation-related, cohesin complex, chromatin remodeling, and tumor-suppressor genes.

The researchers identified 4390 mutations, with a median of 3 mutations per patient.

Overall, the most frequently mutated genes that contributed to AML in this cohort belonged to the methylation group.

The researchers observed a high incidence of mutations in methylation-related genes in patients with CN-AML, CK-AML, or unbalanced chromosomal abnormalities.

In contrast, mutations in methylation-related genes were almost absent in CBF-AML patients and were rather rare in patients with non-CBF-AML-related balanced translocations or inversions.

Mutations in spliceosome genes were frequent in patients with unbalanced chromosomal abnormalities, especially those with sole trisomy of chromosomes 4, 8, 11, 13, or 21.

“Our study summarizes cytogenetic and mutational information of 1603 AML patients in a single image,” said Ann-Kathrin Eisfeld, MD, of The Ohio State University Comprehensive Cancer Center in Columbus.

“The identification of key mutational features of each subgroup may help us to better understand the pathogenesis of the different AML types and provides a wealth of information for ongoing and future research.”

Photo by Daniel Sone

A recent study suggested that bias in research varies across scientific disciplines, but there are some common factors the different fields share.

The data consistently showed that small studies, early studies, and highly cited studies overestimated effect size.

In addition, a scientist’s early career status, isolation from other researchers, and involvement in misconduct appeared to be risk factors for unreliable results.

John P. A. Ioannidis, MD, of Stanford University School of Medicine in Stanford, California, and his colleagues reported these findings in PNAS.

The team reviewed more than 3000 meta-analyses that included nearly 50,000 individual studies across 22 scientific fields.

“I think that this is a mapping exercise,” Dr Ioannidis said. “It maps all the main biases that have been proposed across all 22 scientific disciplines. Now, we have a map for each scientific discipline, which biases are important, and which have a bigger impact, and, therefore, scientists can think about where do they want to go next with their field.”

Types of bias

The researchers examined several hypothesized kinds of scientific bias, including:

• Small-study effect: When studies with small sample sizes report large effect sizes.
• Gray literature bias: The tendency of smaller or statistically insignificant effects to be reported in PhD theses, conference proceedings, or personal communications rather than in peer-reviewed literature.
• Early extremes effect: When extreme or controversial findings are published early just because they are astonishing.
• Decline effect: When reports of extreme effects are followed by subsequent reports of reduced effects.
• Citation bias: The larger the effect size, the more likely the study will be cited.
• United States effect: When US researchers overestimate effect sizes.
• Industry bias: When industry sponsorship and affiliation affect the direction and size of reported effects.

Dr Ioannidis and his colleagues also looked at other factors that might potentially affect the risk of bias, such as size and types of collaborations, the gender of the researchers, and pressure to publish.

Results

Small studies, highly cited studies, and those published in peer-reviewed journals seemed more likely to overestimate effects. US studies and early studies seemed to report more extreme effects.

Early career researchers and researchers working in small or long-distance collaborations were more likely to overestimate effect sizes. And researchers with a history of misconduct tended to overestimate effect sizes.

On the other hand, studies by highly cited authors who published frequently were not more affected by bias than average. And there was no difference in bias according to gender.

In addition, scientists in countries with strong incentives to publish were not more affected by bias than scientists from countries where there was less pressure to publish.

Dr Ioannidis said that, in the data he and his colleagues examined, the influence of different kinds of bias changed over time and seemed to depend on the individual scientist.

“We show that some of the patterns and risk factors seem to be getting worse in intensity over time,” he said. “This is particularly driven by the social sciences . . . . It seems that the social sciences are seeing the more prominent worsening of these biases over time.”

Another finding of this study is that the kinds and amounts of bias were irregularly distributed across the literature.

“Although bias may be worryingly high in specific research areas, it is nonexistent in many others,” said study author Daniele Fanelli, PhD, of the Meta-Research Innovation Center at Stanford (METRICS), Stanford University in Palo Alto. “So bias does not undermine the scientific enterprise as a whole.”

Yet another finding is that the relative magnitude of biases closely reflects the level of attention they receive in the literature. That is, the kinds of biases researchers are most concerned about are, in fact, the ones they should be concerned about.

“Our understanding of bias is improving, and our priorities are set on the right targets,” Dr Fanelli said, though he noted that researchers should not become complacent when it comes to bias.

“We perhaps understand bias better, but we are far from having rid science of it. Indeed, our results suggest that the challenge might be greater than many think because interventions might need to be tailored to the needs and problems of individual disciplines of fields. One-size-fits all solutions are unlikely to work.”

Photo by Daniel Sone

A recent study suggested that bias in research varies across scientific disciplines, but there are some common factors the different fields share.

The data consistently showed that small studies, early studies, and highly cited studies overestimated effect size.

In addition, a scientist’s early career status, isolation from other researchers, and involvement in misconduct appeared to be risk factors for unreliable results.

John P. A. Ioannidis, MD, of Stanford University School of Medicine in Stanford, California, and his colleagues reported these findings in PNAS.

The team reviewed more than 3000 meta-analyses that included nearly 50,000 individual studies across 22 scientific fields.

“I think that this is a mapping exercise,” Dr Ioannidis said. “It maps all the main biases that have been proposed across all 22 scientific disciplines. Now, we have a map for each scientific discipline, which biases are important, and which have a bigger impact, and, therefore, scientists can think about where do they want to go next with their field.”

Types of bias

The researchers examined several hypothesized kinds of scientific bias, including:

• Small-study effect: When studies with small sample sizes report large effect sizes.
• Gray literature bias: The tendency of smaller or statistically insignificant effects to be reported in PhD theses, conference proceedings, or personal communications rather than in peer-reviewed literature.
• Early extremes effect: When extreme or controversial findings are published early just because they are astonishing.
• Decline effect: When reports of extreme effects are followed by subsequent reports of reduced effects.
• Citation bias: The larger the effect size, the more likely the study will be cited.
• United States effect: When US researchers overestimate effect sizes.
• Industry bias: When industry sponsorship and affiliation affect the direction and size of reported effects.

Dr Ioannidis and his colleagues also looked at other factors that might potentially affect the risk of bias, such as size and types of collaborations, the gender of the researchers, and pressure to publish.

Results

Small studies, highly cited studies, and those published in peer-reviewed journals seemed more likely to overestimate effects. US studies and early studies seemed to report more extreme effects.

Early career researchers and researchers working in small or long-distance collaborations were more likely to overestimate effect sizes. And researchers with a history of misconduct tended to overestimate effect sizes.

On the other hand, studies by highly cited authors who published frequently were not more affected by bias than average. And there was no difference in bias according to gender.

In addition, scientists in countries with strong incentives to publish were not more affected by bias than scientists from countries where there was less pressure to publish.

Dr Ioannidis said that, in the data he and his colleagues examined, the influence of different kinds of bias changed over time and seemed to depend on the individual scientist.

“We show that some of the patterns and risk factors seem to be getting worse in intensity over time,” he said. “This is particularly driven by the social sciences . . . . It seems that the social sciences are seeing the more prominent worsening of these biases over time.”

Another finding of this study is that the kinds and amounts of bias were irregularly distributed across the literature.

“Although bias may be worryingly high in specific research areas, it is nonexistent in many others,” said study author Daniele Fanelli, PhD, of the Meta-Research Innovation Center at Stanford (METRICS), Stanford University in Palo Alto. “So bias does not undermine the scientific enterprise as a whole.”

Yet another finding is that the relative magnitude of biases closely reflects the level of attention they receive in the literature. That is, the kinds of biases researchers are most concerned about are, in fact, the ones they should be concerned about.

“Our understanding of bias is improving, and our priorities are set on the right targets,” Dr Fanelli said, though he noted that researchers should not become complacent when it comes to bias.

“We perhaps understand bias better, but we are far from having rid science of it. Indeed, our results suggest that the challenge might be greater than many think because interventions might need to be tailored to the needs and problems of individual disciplines of fields. One-size-fits all solutions are unlikely to work.”

Photo by Daniel Sone

A recent study suggested that bias in research varies across scientific disciplines, but there are some common factors the different fields share.

The data consistently showed that small studies, early studies, and highly cited studies overestimated effect size.

In addition, a scientist’s early career status, isolation from other researchers, and involvement in misconduct appeared to be risk factors for unreliable results.

John P. A. Ioannidis, MD, of Stanford University School of Medicine in Stanford, California, and his colleagues reported these findings in PNAS.

The team reviewed more than 3000 meta-analyses that included nearly 50,000 individual studies across 22 scientific fields.

“I think that this is a mapping exercise,” Dr Ioannidis said. “It maps all the main biases that have been proposed across all 22 scientific disciplines. Now, we have a map for each scientific discipline, which biases are important, and which have a bigger impact, and, therefore, scientists can think about where do they want to go next with their field.”

Types of bias

The researchers examined several hypothesized kinds of scientific bias, including:

• Small-study effect: When studies with small sample sizes report large effect sizes.
• Gray literature bias: The tendency of smaller or statistically insignificant effects to be reported in PhD theses, conference proceedings, or personal communications rather than in peer-reviewed literature.
• Early extremes effect: When extreme or controversial findings are published early just because they are astonishing.
• Decline effect: When reports of extreme effects are followed by subsequent reports of reduced effects.
• Citation bias: The larger the effect size, the more likely the study will be cited.
• United States effect: When US researchers overestimate effect sizes.
• Industry bias: When industry sponsorship and affiliation affect the direction and size of reported effects.

Dr Ioannidis and his colleagues also looked at other factors that might potentially affect the risk of bias, such as size and types of collaborations, the gender of the researchers, and pressure to publish.

Results

Small studies, highly cited studies, and those published in peer-reviewed journals seemed more likely to overestimate effects. US studies and early studies seemed to report more extreme effects.

Early career researchers and researchers working in small or long-distance collaborations were more likely to overestimate effect sizes. And researchers with a history of misconduct tended to overestimate effect sizes.

On the other hand, studies by highly cited authors who published frequently were not more affected by bias than average. And there was no difference in bias according to gender.

In addition, scientists in countries with strong incentives to publish were not more affected by bias than scientists from countries where there was less pressure to publish.

Dr Ioannidis said that, in the data he and his colleagues examined, the influence of different kinds of bias changed over time and seemed to depend on the individual scientist.

“We show that some of the patterns and risk factors seem to be getting worse in intensity over time,” he said. “This is particularly driven by the social sciences . . . . It seems that the social sciences are seeing the more prominent worsening of these biases over time.”

Another finding of this study is that the kinds and amounts of bias were irregularly distributed across the literature.

“Although bias may be worryingly high in specific research areas, it is nonexistent in many others,” said study author Daniele Fanelli, PhD, of the Meta-Research Innovation Center at Stanford (METRICS), Stanford University in Palo Alto. “So bias does not undermine the scientific enterprise as a whole.”

Yet another finding is that the relative magnitude of biases closely reflects the level of attention they receive in the literature. That is, the kinds of biases researchers are most concerned about are, in fact, the ones they should be concerned about.

“Our understanding of bias is improving, and our priorities are set on the right targets,” Dr Fanelli said, though he noted that researchers should not become complacent when it comes to bias.

“We perhaps understand bias better, but we are far from having rid science of it. Indeed, our results suggest that the challenge might be greater than many think because interventions might need to be tailored to the needs and problems of individual disciplines of fields. One-size-fits all solutions are unlikely to work.”

CLINICAL QUESTION: Is there variation in patient-to-intensivist ratios (PIR) across ICUs, and does that ratio affect hospital mortality?

BACKGROUND: Most studies show that intensivists improve ICU patient outcomes. With increasing ICU patients but stable intensivist staffing, patient-to-intensivist ratios are increasing. It is unclear if that rising ratio is adversely affecting patient mortality.

STUDY DESIGN: Multicenter retrospective cohort analysis.

SETTING: ICUs in the United Kingdom from 2010 to 2013.

The median PIR was 8.5 but varied substantially – PIRs were often larger. The association between PIR and mortality was U shaped. There was a decrease in mortality as the PIR reached 7.5, after which the mortality increased again. The higher mortality with very low PIRs could reflect a volume-outcome relationship. Less patients could mean less experience, different levels of ancillary staff, and so on.

This study did not take into account the possible differences in the multidisciplinary makeup of the ICU teams that would affect the intensivist’s level of responsibility.

BOTTOM LINE: There seems to be an optimal PIR for mortality, though that optimal number would likely depend on the ancillary staff, level of trainees, and patient acuity.

CITATIONS: Gershengorn HB, Harrison DA, Garland A, et al. “Association of Intensive Care Unit Patient-to-Intensivist Ratios With Hospital Mortality.” JAMA Intern Med. 2017 Mar 1;177(3):388-96.

Dr. Tsien is assistant professor in the division of hospital medicine, Loyola University Chicago, Maywood, Ill.

CLINICAL QUESTION: Is there variation in patient-to-intensivist ratios (PIR) across ICUs, and does that ratio affect hospital mortality?

BACKGROUND: Most studies show that intensivists improve ICU patient outcomes. With increasing ICU patients but stable intensivist staffing, patient-to-intensivist ratios are increasing. It is unclear if that rising ratio is adversely affecting patient mortality.

STUDY DESIGN: Multicenter retrospective cohort analysis.

SETTING: ICUs in the United Kingdom from 2010 to 2013.

The median PIR was 8.5 but varied substantially – PIRs were often larger. The association between PIR and mortality was U shaped. There was a decrease in mortality as the PIR reached 7.5, after which the mortality increased again. The higher mortality with very low PIRs could reflect a volume-outcome relationship. Less patients could mean less experience, different levels of ancillary staff, and so on.

This study did not take into account the possible differences in the multidisciplinary makeup of the ICU teams that would affect the intensivist’s level of responsibility.

BOTTOM LINE: There seems to be an optimal PIR for mortality, though that optimal number would likely depend on the ancillary staff, level of trainees, and patient acuity.

CITATIONS: Gershengorn HB, Harrison DA, Garland A, et al. “Association of Intensive Care Unit Patient-to-Intensivist Ratios With Hospital Mortality.” JAMA Intern Med. 2017 Mar 1;177(3):388-96.

Dr. Tsien is assistant professor in the division of hospital medicine, Loyola University Chicago, Maywood, Ill.

CLINICAL QUESTION: Is there variation in patient-to-intensivist ratios (PIR) across ICUs, and does that ratio affect hospital mortality?

BACKGROUND: Most studies show that intensivists improve ICU patient outcomes. With increasing ICU patients but stable intensivist staffing, patient-to-intensivist ratios are increasing. It is unclear if that rising ratio is adversely affecting patient mortality.

STUDY DESIGN: Multicenter retrospective cohort analysis.

SETTING: ICUs in the United Kingdom from 2010 to 2013.

The median PIR was 8.5 but varied substantially – PIRs were often larger. The association between PIR and mortality was U shaped. There was a decrease in mortality as the PIR reached 7.5, after which the mortality increased again. The higher mortality with very low PIRs could reflect a volume-outcome relationship. Less patients could mean less experience, different levels of ancillary staff, and so on.

This study did not take into account the possible differences in the multidisciplinary makeup of the ICU teams that would affect the intensivist’s level of responsibility.

BOTTOM LINE: There seems to be an optimal PIR for mortality, though that optimal number would likely depend on the ancillary staff, level of trainees, and patient acuity.

CITATIONS: Gershengorn HB, Harrison DA, Garland A, et al. “Association of Intensive Care Unit Patient-to-Intensivist Ratios With Hospital Mortality.” JAMA Intern Med. 2017 Mar 1;177(3):388-96.

Dr. Tsien is assistant professor in the division of hospital medicine, Loyola University Chicago, Maywood, Ill.

CLINICAL QUESTION: What are the accuracy and clinical utility of risk scoring systems in the assessment of patients with upper gastrointestinal (GI) bleeding?

BACKGROUND: There are several pre- and postendoscopy risk scores to predict clinically relevant outcomes such as transfusion, mortality, endoscopy treatment, surgery, and length of hospital stay for upper GI bleeding. The accuracy and applicability of these risk scores has not been well established.

STUDY DESIGN: International multicenter prospective study.

SETTING: Six large hospitals in Europe, North America, Asia, and Oceania.

SYNOPSIS: This is a prospective study comparing three pre-endoscopy scoring systems (Rockall, AIMS65, Glasgow Blatchford) and two postendoscopy scoring systems (PNED, full Rockall) in 3,012 patients with upper GI bleeding over six hospitals. It examined clinically relevant outcomes: intervention (transfusion, endoscopy, interventional radiology, surgery), mortality, rebleeding, and length of hospital stay.

The Glasgow Blatchford risk score was the most accurate at predicting the need for hospitalization and death across all hospitals, compared with the other scoring systems. It was determined that a Glasgow Blatchford score of less than 1 is an optimal threshold for outpatient management, with a 98.6% sensitivity in identifying those who would not require intervention or die. The utility of these scores to direct management in high-risk patients is limited and needs further studies. No scoring system predicted rebleeding or length of hospital stay.

A weakness of the study is that patients who bled while already inpatients were excluded.

BOTTOM LINE: The Glasgow Blatchford risk score can help direct care of very low risk patients (score, less than 1) with upper GI bleeding toward outpatient management.

CITATIONS: Stanley AJ, Laine L, Dalton HR, et al. “Comparison of risk scoring systems for patients presenting with upper gastrointestinal bleeding: International multicenter prospective study.” BMJ. 2017 Jan 4;356:i6432.
 

Dr. Tsien is assistant professor in the division of hospital medicine, Loyola University Chicago, Maywood, Ill.

CLINICAL QUESTION: What are the accuracy and clinical utility of risk scoring systems in the assessment of patients with upper gastrointestinal (GI) bleeding?

BACKGROUND: There are several pre- and postendoscopy risk scores to predict clinically relevant outcomes such as transfusion, mortality, endoscopy treatment, surgery, and length of hospital stay for upper GI bleeding. The accuracy and applicability of these risk scores has not been well established.

STUDY DESIGN: International multicenter prospective study.

SETTING: Six large hospitals in Europe, North America, Asia, and Oceania.

SYNOPSIS: This is a prospective study comparing three pre-endoscopy scoring systems (Rockall, AIMS65, Glasgow Blatchford) and two postendoscopy scoring systems (PNED, full Rockall) in 3,012 patients with upper GI bleeding over six hospitals. It examined clinically relevant outcomes: intervention (transfusion, endoscopy, interventional radiology, surgery), mortality, rebleeding, and length of hospital stay.

The Glasgow Blatchford risk score was the most accurate at predicting the need for hospitalization and death across all hospitals, compared with the other scoring systems. It was determined that a Glasgow Blatchford score of less than 1 is an optimal threshold for outpatient management, with a 98.6% sensitivity in identifying those who would not require intervention or die. The utility of these scores to direct management in high-risk patients is limited and needs further studies. No scoring system predicted rebleeding or length of hospital stay.

A weakness of the study is that patients who bled while already inpatients were excluded.

BOTTOM LINE: The Glasgow Blatchford risk score can help direct care of very low risk patients (score, less than 1) with upper GI bleeding toward outpatient management.

CITATIONS: Stanley AJ, Laine L, Dalton HR, et al. “Comparison of risk scoring systems for patients presenting with upper gastrointestinal bleeding: International multicenter prospective study.” BMJ. 2017 Jan 4;356:i6432.
 

Dr. Tsien is assistant professor in the division of hospital medicine, Loyola University Chicago, Maywood, Ill.

CLINICAL QUESTION: What are the accuracy and clinical utility of risk scoring systems in the assessment of patients with upper gastrointestinal (GI) bleeding?

BACKGROUND: There are several pre- and postendoscopy risk scores to predict clinically relevant outcomes such as transfusion, mortality, endoscopy treatment, surgery, and length of hospital stay for upper GI bleeding. The accuracy and applicability of these risk scores has not been well established.

STUDY DESIGN: International multicenter prospective study.

SETTING: Six large hospitals in Europe, North America, Asia, and Oceania.

SYNOPSIS: This is a prospective study comparing three pre-endoscopy scoring systems (Rockall, AIMS65, Glasgow Blatchford) and two postendoscopy scoring systems (PNED, full Rockall) in 3,012 patients with upper GI bleeding over six hospitals. It examined clinically relevant outcomes: intervention (transfusion, endoscopy, interventional radiology, surgery), mortality, rebleeding, and length of hospital stay.

The Glasgow Blatchford risk score was the most accurate at predicting the need for hospitalization and death across all hospitals, compared with the other scoring systems. It was determined that a Glasgow Blatchford score of less than 1 is an optimal threshold for outpatient management, with a 98.6% sensitivity in identifying those who would not require intervention or die. The utility of these scores to direct management in high-risk patients is limited and needs further studies. No scoring system predicted rebleeding or length of hospital stay.

A weakness of the study is that patients who bled while already inpatients were excluded.

BOTTOM LINE: The Glasgow Blatchford risk score can help direct care of very low risk patients (score, less than 1) with upper GI bleeding toward outpatient management.

CITATIONS: Stanley AJ, Laine L, Dalton HR, et al. “Comparison of risk scoring systems for patients presenting with upper gastrointestinal bleeding: International multicenter prospective study.” BMJ. 2017 Jan 4;356:i6432.
 

Dr. Tsien is assistant professor in the division of hospital medicine, Loyola University Chicago, Maywood, Ill.

Her visit seemed uneventful enough. Back for the semester break of her senior year, Jenna came in for acne follow-up.

She seemed to be doing pretty well: just a couple of active papules on each cheek, as well as some residual fading red marks from old lesions. Still, Jenna was not happy with her situation.

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at [email protected].

Her visit seemed uneventful enough. Back for the semester break of her senior year, Jenna came in for acne follow-up.

She seemed to be doing pretty well: just a couple of active papules on each cheek, as well as some residual fading red marks from old lesions. Still, Jenna was not happy with her situation.

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at [email protected].

Her visit seemed uneventful enough. Back for the semester break of her senior year, Jenna came in for acne follow-up.

She seemed to be doing pretty well: just a couple of active papules on each cheek, as well as some residual fading red marks from old lesions. Still, Jenna was not happy with her situation.

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at [email protected].

In the struggle to understand and comply with new regulations, it’s easy to neglect older ones. Recently, I suggested reviewing your practice for potential Occupational Safety and Health Administration violations, which can be far more costly than anything MACRA has in store.

The same goes for HIPAA since HIPAA violations can be just as costly, in view of renewed governmental enforcement and some disturbing trends in completely unrelated government agencies.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

In the struggle to understand and comply with new regulations, it’s easy to neglect older ones. Recently, I suggested reviewing your practice for potential Occupational Safety and Health Administration violations, which can be far more costly than anything MACRA has in store.

The same goes for HIPAA since HIPAA violations can be just as costly, in view of renewed governmental enforcement and some disturbing trends in completely unrelated government agencies.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

In the struggle to understand and comply with new regulations, it’s easy to neglect older ones. Recently, I suggested reviewing your practice for potential Occupational Safety and Health Administration violations, which can be far more costly than anything MACRA has in store.

The same goes for HIPAA since HIPAA violations can be just as costly, in view of renewed governmental enforcement and some disturbing trends in completely unrelated government agencies.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].