Pediatric News

Cannabis use may lead to thinning of the cerebral cortex in adolescents, research in mice and humans suggested.

The multilevel study demonstrated that tetrahydrocannabinol (THC), an active substance in cannabis, causes shrinkage of dendritic arborization — the neurons’ network of antennae that play a critical role in communication between brain cells.

The connection between dendritic arborization and cortical thickness was hinted at in an earlier study by Tomáš Paus, MD, PhD, professor of psychiatry and addictology at the University of Montreal, Quebec, Canada, and colleagues, who found that cannabis use in early adolescence was associated with lower cortical thickness in boys with a high genetic risk for schizophrenia.

“We speculated at that time that the differences in cortical thickness might be related to differences in dendritic arborization, and our current study confirmed it,” Paus said.

That confirmation came in the mouse part of the study, when coauthor Graciela Piñeyro, MD, PhD, also of the University of Montreal, counted the dendritic branches of mice exposed to THC and compared the total with the number of dendritic branches in unexposed mice. “What surprised me was finding that THC in the mice was targeting the same type of cells and structures that Dr. Paus had predicted would be affected from the human studies,” she said. “Structurally, they were mostly the neurons that contribute to synapses in the cortex, and their branching was reduced.”

Paus explained that in humans, a decrease in input from the affected dendrites “makes it harder for the brain to learn new things, interact with people, cope with new situations, et cetera. In other words, it makes the brain more vulnerable to everything that can happen in a young person’s life.”

The study was published online on October 9 in the Journal of Neuroscience.
 

Of Mice, Men, and Cannabis

Although associations between cannabis use by teenagers and variations in brain maturation have been well studied, the cellular and molecular underpinnings of these associations were unclear, according to the authors.

To investigate further, they conducted this three-step study. First, they exposed adolescent male mice to THC or a synthetic cannabinoid (WIN 55,212-2) and assessed differentially expressed genes, spine numbers, and the extent of dendritic complexity in the frontal cortex of each mouse.

Next, using MRI, they examined differences in cortical thickness in 34 brain regions in 140 male adolescents who experimented with cannabis before age 16 years and 327 who did not.

Then, they again conducted experiments in mice and found that 13 THC-related genes correlated with variations in cortical thickness. Virtual histology revealed that these 13 genes were coexpressed with cell markers of astrocytes, microglia, and a type of pyramidal cell enriched in genes that regulate dendritic expression.

Similarly, the WIN-related genes correlated with differences in cortical thickness and showed coexpression patterns with the same three cell types.

Furthermore, the affected genes were also found in humans, particularly in the thinner cortical regions of the adolescents who experimented with cannabis.

By acting on microglia, THC seems to promote the removal of synapses and, eventually, the reduction of the dendritic tree in mice, Piñeyro explained. That’s important not only because a similar mechanism may be at work in humans but also because “we now might have a model to test different types of cannabis products to see which ones are producing the greatest effect on neurons and therefore greater removal of synapses through the microglia. This could be a way of testing drugs that are out in the street to see which would be the most or least dangerous to the synapses in the brain.”
 

‘Significant Implications’

Commenting on the study, Yasmin Hurd, PhD, Ward-Coleman chair of translational neuroscience at the Icahn School of Medicine at Mount Sinai and director of the Addiction Institute of Mount Sinai in New York City, said, “These findings are in line with previous results, so they are feasible. This study adds more depth by showing that cortical genes that were differentially altered by adolescent THC correlated with cannabis-related changes in cortical thickness based on human neuroimaging data.” Hurd did not participate in the research.

“The results emphasize that consumption of potent cannabis products during adolescence can impact cortical function, which has significant implications for decision-making and risky behavior as well. It also can increase vulnerability to psychiatric disorders such as schizophrenia.”

Although a mouse model is “not truly the same as the human condition, the fact that the animal model also showed evidence of the morphological changes indicative of reduced cortical thickness, [like] the humans, is strong,” she said.

Additional research could include women and assess potential sex differences, she added.

Ronald Ellis, MD, PhD, an investigator in the Center for Medicinal Cannabis Research at the University of California, San Diego School of Medicine, said, “The findings are plausible and extend prior work showing evidence of increased risk for psychotic disorders later in life in adolescents who use cannabis.” Ellis did not participate in the research.

“Future studies should explore how these findings might vary across different demographic groups, which could provide a more inclusive understanding of how cannabis impacts the brain,” he said. “Additionally, longitudinal studies to track changes in the brain over time could help to establish causal relationships more robustly.

“The take-home message to clinicians at this point is to discuss cannabis use history carefully and confidentially with adolescent patients to better provide advice on its potential risks,” he concluded.

Paus added that he would tell patients, “If you’re going to use cannabis, don’t start early. If you have to, then do so in moderation. And if you have family history of mental illness, be very careful.”

No funding for the study was reported. Paus, Piñeyro, Hurd, and Ellis declared having no relevant financial relationships. 
 

A version of this article appeared on Medscape.com.

Cannabis use may lead to thinning of the cerebral cortex in adolescents, research in mice and humans suggested.

The multilevel study demonstrated that tetrahydrocannabinol (THC), an active substance in cannabis, causes shrinkage of dendritic arborization — the neurons’ network of antennae that play a critical role in communication between brain cells.

The connection between dendritic arborization and cortical thickness was hinted at in an earlier study by Tomáš Paus, MD, PhD, professor of psychiatry and addictology at the University of Montreal, Quebec, Canada, and colleagues, who found that cannabis use in early adolescence was associated with lower cortical thickness in boys with a high genetic risk for schizophrenia.

“We speculated at that time that the differences in cortical thickness might be related to differences in dendritic arborization, and our current study confirmed it,” Paus said.

That confirmation came in the mouse part of the study, when coauthor Graciela Piñeyro, MD, PhD, also of the University of Montreal, counted the dendritic branches of mice exposed to THC and compared the total with the number of dendritic branches in unexposed mice. “What surprised me was finding that THC in the mice was targeting the same type of cells and structures that Dr. Paus had predicted would be affected from the human studies,” she said. “Structurally, they were mostly the neurons that contribute to synapses in the cortex, and their branching was reduced.”

Paus explained that in humans, a decrease in input from the affected dendrites “makes it harder for the brain to learn new things, interact with people, cope with new situations, et cetera. In other words, it makes the brain more vulnerable to everything that can happen in a young person’s life.”

The study was published online on October 9 in the Journal of Neuroscience.
 

Of Mice, Men, and Cannabis

Although associations between cannabis use by teenagers and variations in brain maturation have been well studied, the cellular and molecular underpinnings of these associations were unclear, according to the authors.

To investigate further, they conducted this three-step study. First, they exposed adolescent male mice to THC or a synthetic cannabinoid (WIN 55,212-2) and assessed differentially expressed genes, spine numbers, and the extent of dendritic complexity in the frontal cortex of each mouse.

Next, using MRI, they examined differences in cortical thickness in 34 brain regions in 140 male adolescents who experimented with cannabis before age 16 years and 327 who did not.

Then, they again conducted experiments in mice and found that 13 THC-related genes correlated with variations in cortical thickness. Virtual histology revealed that these 13 genes were coexpressed with cell markers of astrocytes, microglia, and a type of pyramidal cell enriched in genes that regulate dendritic expression.

Similarly, the WIN-related genes correlated with differences in cortical thickness and showed coexpression patterns with the same three cell types.

Furthermore, the affected genes were also found in humans, particularly in the thinner cortical regions of the adolescents who experimented with cannabis.

By acting on microglia, THC seems to promote the removal of synapses and, eventually, the reduction of the dendritic tree in mice, Piñeyro explained. That’s important not only because a similar mechanism may be at work in humans but also because “we now might have a model to test different types of cannabis products to see which ones are producing the greatest effect on neurons and therefore greater removal of synapses through the microglia. This could be a way of testing drugs that are out in the street to see which would be the most or least dangerous to the synapses in the brain.”
 

‘Significant Implications’

Commenting on the study, Yasmin Hurd, PhD, Ward-Coleman chair of translational neuroscience at the Icahn School of Medicine at Mount Sinai and director of the Addiction Institute of Mount Sinai in New York City, said, “These findings are in line with previous results, so they are feasible. This study adds more depth by showing that cortical genes that were differentially altered by adolescent THC correlated with cannabis-related changes in cortical thickness based on human neuroimaging data.” Hurd did not participate in the research.

“The results emphasize that consumption of potent cannabis products during adolescence can impact cortical function, which has significant implications for decision-making and risky behavior as well. It also can increase vulnerability to psychiatric disorders such as schizophrenia.”

Although a mouse model is “not truly the same as the human condition, the fact that the animal model also showed evidence of the morphological changes indicative of reduced cortical thickness, [like] the humans, is strong,” she said.

Additional research could include women and assess potential sex differences, she added.

Ronald Ellis, MD, PhD, an investigator in the Center for Medicinal Cannabis Research at the University of California, San Diego School of Medicine, said, “The findings are plausible and extend prior work showing evidence of increased risk for psychotic disorders later in life in adolescents who use cannabis.” Ellis did not participate in the research.

“Future studies should explore how these findings might vary across different demographic groups, which could provide a more inclusive understanding of how cannabis impacts the brain,” he said. “Additionally, longitudinal studies to track changes in the brain over time could help to establish causal relationships more robustly.

“The take-home message to clinicians at this point is to discuss cannabis use history carefully and confidentially with adolescent patients to better provide advice on its potential risks,” he concluded.

Paus added that he would tell patients, “If you’re going to use cannabis, don’t start early. If you have to, then do so in moderation. And if you have family history of mental illness, be very careful.”

No funding for the study was reported. Paus, Piñeyro, Hurd, and Ellis declared having no relevant financial relationships. 
 

A version of this article appeared on Medscape.com.

Cannabis use may lead to thinning of the cerebral cortex in adolescents, research in mice and humans suggested.

The multilevel study demonstrated that tetrahydrocannabinol (THC), an active substance in cannabis, causes shrinkage of dendritic arborization — the neurons’ network of antennae that play a critical role in communication between brain cells.

The connection between dendritic arborization and cortical thickness was hinted at in an earlier study by Tomáš Paus, MD, PhD, professor of psychiatry and addictology at the University of Montreal, Quebec, Canada, and colleagues, who found that cannabis use in early adolescence was associated with lower cortical thickness in boys with a high genetic risk for schizophrenia.

“We speculated at that time that the differences in cortical thickness might be related to differences in dendritic arborization, and our current study confirmed it,” Paus said.

That confirmation came in the mouse part of the study, when coauthor Graciela Piñeyro, MD, PhD, also of the University of Montreal, counted the dendritic branches of mice exposed to THC and compared the total with the number of dendritic branches in unexposed mice. “What surprised me was finding that THC in the mice was targeting the same type of cells and structures that Dr. Paus had predicted would be affected from the human studies,” she said. “Structurally, they were mostly the neurons that contribute to synapses in the cortex, and their branching was reduced.”

Paus explained that in humans, a decrease in input from the affected dendrites “makes it harder for the brain to learn new things, interact with people, cope with new situations, et cetera. In other words, it makes the brain more vulnerable to everything that can happen in a young person’s life.”

The study was published online on October 9 in the Journal of Neuroscience.
 

Of Mice, Men, and Cannabis

Although associations between cannabis use by teenagers and variations in brain maturation have been well studied, the cellular and molecular underpinnings of these associations were unclear, according to the authors.

To investigate further, they conducted this three-step study. First, they exposed adolescent male mice to THC or a synthetic cannabinoid (WIN 55,212-2) and assessed differentially expressed genes, spine numbers, and the extent of dendritic complexity in the frontal cortex of each mouse.

Next, using MRI, they examined differences in cortical thickness in 34 brain regions in 140 male adolescents who experimented with cannabis before age 16 years and 327 who did not.

Then, they again conducted experiments in mice and found that 13 THC-related genes correlated with variations in cortical thickness. Virtual histology revealed that these 13 genes were coexpressed with cell markers of astrocytes, microglia, and a type of pyramidal cell enriched in genes that regulate dendritic expression.

Similarly, the WIN-related genes correlated with differences in cortical thickness and showed coexpression patterns with the same three cell types.

Furthermore, the affected genes were also found in humans, particularly in the thinner cortical regions of the adolescents who experimented with cannabis.

By acting on microglia, THC seems to promote the removal of synapses and, eventually, the reduction of the dendritic tree in mice, Piñeyro explained. That’s important not only because a similar mechanism may be at work in humans but also because “we now might have a model to test different types of cannabis products to see which ones are producing the greatest effect on neurons and therefore greater removal of synapses through the microglia. This could be a way of testing drugs that are out in the street to see which would be the most or least dangerous to the synapses in the brain.”
 

‘Significant Implications’

Commenting on the study, Yasmin Hurd, PhD, Ward-Coleman chair of translational neuroscience at the Icahn School of Medicine at Mount Sinai and director of the Addiction Institute of Mount Sinai in New York City, said, “These findings are in line with previous results, so they are feasible. This study adds more depth by showing that cortical genes that were differentially altered by adolescent THC correlated with cannabis-related changes in cortical thickness based on human neuroimaging data.” Hurd did not participate in the research.

“The results emphasize that consumption of potent cannabis products during adolescence can impact cortical function, which has significant implications for decision-making and risky behavior as well. It also can increase vulnerability to psychiatric disorders such as schizophrenia.”

Although a mouse model is “not truly the same as the human condition, the fact that the animal model also showed evidence of the morphological changes indicative of reduced cortical thickness, [like] the humans, is strong,” she said.

Additional research could include women and assess potential sex differences, she added.

Ronald Ellis, MD, PhD, an investigator in the Center for Medicinal Cannabis Research at the University of California, San Diego School of Medicine, said, “The findings are plausible and extend prior work showing evidence of increased risk for psychotic disorders later in life in adolescents who use cannabis.” Ellis did not participate in the research.

“Future studies should explore how these findings might vary across different demographic groups, which could provide a more inclusive understanding of how cannabis impacts the brain,” he said. “Additionally, longitudinal studies to track changes in the brain over time could help to establish causal relationships more robustly.

“The take-home message to clinicians at this point is to discuss cannabis use history carefully and confidentially with adolescent patients to better provide advice on its potential risks,” he concluded.

Paus added that he would tell patients, “If you’re going to use cannabis, don’t start early. If you have to, then do so in moderation. And if you have family history of mental illness, be very careful.”

No funding for the study was reported. Paus, Piñeyro, Hurd, and Ellis declared having no relevant financial relationships. 
 

A version of this article appeared on Medscape.com.

A growing body of research suggests that clinicians can offer chimeric antigen receptor (CAR) T-cell therapy safely and effectively on an outpatient basis — a positive development as clinicians strive to expand access beyond metropolitan areas.

In one recent study, an industry-funded phase 2 trial, researchers found similar outcomes from outpatient and inpatient CAR T-cell therapy for relapsed/refractory large B-cell lymphoma with lisocabtagene maraleucel (Breyanzi). 

Another recent study reported that outpatient treatment of B cell non-Hodgkin lymphoma with tisagenlecleucel (Kymriah) had similar efficacy to inpatient treatment. Meanwhile, a 2023 review of CAR T-cell therapy in various settings found similar outcomes in outpatient and inpatient treatment. 

“The future of CAR T-cell therapy lies in balancing safety with accessibility,” said Rayne Rouce, MD, a pediatric oncologist at Texas Children’s Cancer Center in Houston, Texas, in an interview. “Expanding CAR T-cell therapy beyond large medical centers is a critical next step.” 
 

Great Outcomes, Low Access

Since 2017, the FDA has approved six CAR T-cell therapies, which target cancer by harnessing the power of a patient’s own T cells. As an Oregon Health & Sciences University/Knight Cancer Center website explains, T cells are removed from the patient’s body, “genetically modified to make the chimeric antigen receptor, or CAR, [which] protein binds to specific proteins on the surface of cancer cells.”

Modified cells are grown and then infused back into the body, where they “multiply and may be able to destroy all the cancer cells.”

As Rouce puts it, “CAR T-cells have revolutionized the treatment of relapsed or refractory blood cancers.” One or more of the therapies have been approved to treat types of lymphoblastic leukemia, B-cell lymphoma, follicular lymphoma, mantle cell lymphoma, and multiple myeloma.

A 2023 review of clinical trial data reported complete response rates of 40%-54% in aggressive B-cell lymphoma, 67% in mantle cell lymphoma, and 69%-74% in indolent B cell lymphoma.

“Commercialization of CAR T-cell therapy brought hope that access would expand beyond the major academic medical centers with the highly specialized infrastructure and advanced laboratories required to manufacture and ultimately treat patients,” Rouce said. “However, it quickly became clear that patients who are underinsured or uninsured — or who live outside the network of the well-resourced institutions that house these therapies — are still unable to access these potentially life-saving therapies.”

A 2024 report estimated the cost of CAR T-cell therapy as $700,000-$1 million and said only a small percentage of those who could benefit from the treatment actually get it. For example, an estimated 10,000 patients with diffuse large B-cell lymphoma alone could benefit from CAR T therapy annually, but a survey of 200 US healthcare centers in 2021 found that 1900 procedures were performed overall for all indications. 
 

Distance to Treatment Is a Major Obstacle

Even if patients have insurance plans willing to cover CAR T-cell therapy, they may not be able get care. While more than 150 US centers are certified to administer the therapy, “distance to major medical centers with CAR T capabilities is a major obstacle,” Yuliya Linhares, MD, chief of lymphoma at Miami Cancer Institute in Miami, Florida, said in an interview. 

“I have had patients who chose to not proceed with CAR T therapy due to inability to travel the distance to the medical center for pre-CAR T appointments and assessments and a lack of caretakers who are available to stay nearby,” Linhares said.

Indeed, the challenges facing patients in rural and underserved urban areas can be overwhelming, Hoda Badr, PhD, professor of medicine at Baylor College of Medicine in Houston, Texas, said in an interview.

“They must take time off work, arrange accommodations near treatment sites, and manage travel costs, all of which strain limited financial resources. The inability to afford these additional expenses can lead to delays in receiving care or patients forgoing the treatment altogether,” Badr said. She added that “the psychological and social burden of being away from family and community support systems during treatment can intensify the stress of an already difficult situation.”

A statistic tells the story of the urban/community divide. CAR T-cell therapy administration at academic centers after leukapheresis — the separation and collection of white blood cells — is reported to be at around 90%, while it’s only 47% in community-based practices that have to refer patients elsewhere, Linhares noted. 
 

Researchers Explore CAR T-Cell Therapy in the Community 

Linhares is lead author of the phase 2 trial that explored administration of lisocabtagene maraleucel in 82 patients with relapsed/refractory large B-cell lymphoma. The findings were published Sept. 30 in Blood Advances.

The OUTREACH trial, funded by Juno/Bristol-Myers Squibb, treated patients in the third line and beyond at community medical centers (outpatient-monitored, 70%; inpatient-monitored, 30%). The trial didn’t require facilities to be certified by the Foundation for the Accreditation of Cellular Therapy (FACT); all had to be non-tertiary cancer centers that weren’t associated with a university. In order to administer therapy on the outpatient basis, the centers had to have phase 1 or hematopoietic stem cell transplant capabilities.

As Linhares explained, 72% of participating centers hadn’t provided CAR T-cell therapy before, and 44% did not have FACT accreditation. “About 32% of patients received CAR T at CAR T naive sites, while 70% of patients received CAR T as outpatients. Investigators had to decide whether patients qualified for the outpatient observation or had to be admitted for the inpatient observation,” she noted.
 

Community Outcomes Were Comparable to Major Trial

As for the results, grade 3 or higher adverse events occurred at a similar frequency among outpatients and inpatients at 74% and 76%, Linhares said. There were no grade 5 adverse events, and 25% of patients treated as outpatients were never hospitalized. 

Response rates were similar to those in the major TRANSCEND trial with the objective response rates rate of 80% and complete response rates of 54%.

“Overall,” Linhares said, “our study demonstrated that with the availability of standard operating procedures, specially trained staff and a multidisciplinary team trained in CAR T toxicity management, inpatient and outpatient CAR T administration is feasible at specialized community medical centers.”

In 2023, another study examined patients with B-cell non-Hodgkin lymphoma who were treated on an outpatient basis with tisagenlecleucel. Researchers reported that outpatient therapy was “feasible and associated with similar efficacy outcomes as inpatient treatment.”

And a 2023 systematic literature review identified 11 studies that reported outpatient vs inpatient outcomes in CAR T-cell therapy and found “comparable response rates (80-82% in outpatient and 72-80% in inpatient).” Costs were cheaper in the outpatient setting. 

Research findings like these are good news, Baylor College of Medicine’s Badr said. “Outpatient administration could help to scale the availability of this therapy to a broader range of healthcare settings, including those serving underserved populations. Findings indicate promising safety profiles, which is encouraging for expanding access.”
 

Not Every Patient Can Tolerate Outpatient Care

Linhares noted that the patients who received outpatient care in the lisocabtagene maraleucel study were in better shape than those in the inpatient group. Those selected for inpatient care had “higher disease risk characteristics, including high grade B cell lymphoma histology, higher disease burden, and having received bridging therapy. This points to the fact that the investigators properly selected patients who were at a higher risk of complications for inpatient observation. Additionally, some patients stayed as inpatient due to social factors, which increases length of stay independently of disease characteristics.”

Specifically, reasons for inpatient monitoring were disease characteristics (48%) including tumor burden and risk of adverse events; psychosocial factors (32%) including lack of caregiver support or transportation; COVID-19 precautions (8%); pre-infusion adverse events (8%) of fever and vasovagal reaction; and principal investigator decision (4%) due to limited hospital experience with CAR T-cell therapy.

Texas Children’s Cancer Center’s Rouce said “certain patients, particularly those with higher risk for complications or those who require intensive monitoring, may not be suited for outpatient CAR T-cell therapy. This may be due to other comorbidities or baseline factors known to predispose to CAR T-related toxicities. However, evidence-based risk mitigation algorithms may still allow closely monitored outpatient treatment, with recognition that hospital admission for incipient side effects may be necessary.”
 

What’s Next for Access to Therapy?

Rouce noted that her institution, like many others, is offering CAR T-cell therapy on an outpatient basis. “Additionally, continued scientific innovation, such as immediately available, off-the-shelf cell therapies and inducible safety switches, will ultimately improve access,” she said. 

Linhares noted a recent advance and highlighted research that’s now in progress. “CAR Ts now have an indication as a second-line therapy in relapsed/refractory large B-cell lymphoma, and there are ongoing clinical trials that will potentially move CAR Ts into the first line,” she said. “Some trials are exploring allogeneic, readily available off-the-shelf CAR T for the treatment of minimal residual disease positive large B-cell lymphoma after completion of first-line therapy.”

These potential advances “are increasing the need for CAR T-capable medical centers,” Linhares noted. “More and more medical centers with expert hematology teams are becoming CAR T-certified, with more patients having access to CAR T.”

Still, she said, “I don’t think access is nearly as good as it should be. Many patients in rural areas are still unable to get this life-saving treatment. “However, “it is very possible that other novel targeted therapies, such as bispecific antibodies, will be used in place of CAR T in areas with poor CAR T access. Bispecific antibody efficacy in various B cell lymphoma histologies are being currently explored.”

Rouce discloses relationships with Novartis and Pfizer. Linhares reports ties with Kyowa Kirin, AbbVie, ADC, BeiGene, Genentech, Gilead, GlaxoSmithKline, Seagen, and TG. Badr has no disclosures. 
 

A version of this article appeared on Medscape.com.

A growing body of research suggests that clinicians can offer chimeric antigen receptor (CAR) T-cell therapy safely and effectively on an outpatient basis — a positive development as clinicians strive to expand access beyond metropolitan areas.

In one recent study, an industry-funded phase 2 trial, researchers found similar outcomes from outpatient and inpatient CAR T-cell therapy for relapsed/refractory large B-cell lymphoma with lisocabtagene maraleucel (Breyanzi). 

Another recent study reported that outpatient treatment of B cell non-Hodgkin lymphoma with tisagenlecleucel (Kymriah) had similar efficacy to inpatient treatment. Meanwhile, a 2023 review of CAR T-cell therapy in various settings found similar outcomes in outpatient and inpatient treatment. 

“The future of CAR T-cell therapy lies in balancing safety with accessibility,” said Rayne Rouce, MD, a pediatric oncologist at Texas Children’s Cancer Center in Houston, Texas, in an interview. “Expanding CAR T-cell therapy beyond large medical centers is a critical next step.” 
 

Great Outcomes, Low Access

Since 2017, the FDA has approved six CAR T-cell therapies, which target cancer by harnessing the power of a patient’s own T cells. As an Oregon Health & Sciences University/Knight Cancer Center website explains, T cells are removed from the patient’s body, “genetically modified to make the chimeric antigen receptor, or CAR, [which] protein binds to specific proteins on the surface of cancer cells.”

Modified cells are grown and then infused back into the body, where they “multiply and may be able to destroy all the cancer cells.”

As Rouce puts it, “CAR T-cells have revolutionized the treatment of relapsed or refractory blood cancers.” One or more of the therapies have been approved to treat types of lymphoblastic leukemia, B-cell lymphoma, follicular lymphoma, mantle cell lymphoma, and multiple myeloma.

A 2023 review of clinical trial data reported complete response rates of 40%-54% in aggressive B-cell lymphoma, 67% in mantle cell lymphoma, and 69%-74% in indolent B cell lymphoma.

“Commercialization of CAR T-cell therapy brought hope that access would expand beyond the major academic medical centers with the highly specialized infrastructure and advanced laboratories required to manufacture and ultimately treat patients,” Rouce said. “However, it quickly became clear that patients who are underinsured or uninsured — or who live outside the network of the well-resourced institutions that house these therapies — are still unable to access these potentially life-saving therapies.”

A 2024 report estimated the cost of CAR T-cell therapy as $700,000-$1 million and said only a small percentage of those who could benefit from the treatment actually get it. For example, an estimated 10,000 patients with diffuse large B-cell lymphoma alone could benefit from CAR T therapy annually, but a survey of 200 US healthcare centers in 2021 found that 1900 procedures were performed overall for all indications. 
 

Distance to Treatment Is a Major Obstacle

Even if patients have insurance plans willing to cover CAR T-cell therapy, they may not be able get care. While more than 150 US centers are certified to administer the therapy, “distance to major medical centers with CAR T capabilities is a major obstacle,” Yuliya Linhares, MD, chief of lymphoma at Miami Cancer Institute in Miami, Florida, said in an interview. 

“I have had patients who chose to not proceed with CAR T therapy due to inability to travel the distance to the medical center for pre-CAR T appointments and assessments and a lack of caretakers who are available to stay nearby,” Linhares said.

Indeed, the challenges facing patients in rural and underserved urban areas can be overwhelming, Hoda Badr, PhD, professor of medicine at Baylor College of Medicine in Houston, Texas, said in an interview.

“They must take time off work, arrange accommodations near treatment sites, and manage travel costs, all of which strain limited financial resources. The inability to afford these additional expenses can lead to delays in receiving care or patients forgoing the treatment altogether,” Badr said. She added that “the psychological and social burden of being away from family and community support systems during treatment can intensify the stress of an already difficult situation.”

A statistic tells the story of the urban/community divide. CAR T-cell therapy administration at academic centers after leukapheresis — the separation and collection of white blood cells — is reported to be at around 90%, while it’s only 47% in community-based practices that have to refer patients elsewhere, Linhares noted. 
 

Researchers Explore CAR T-Cell Therapy in the Community 

Linhares is lead author of the phase 2 trial that explored administration of lisocabtagene maraleucel in 82 patients with relapsed/refractory large B-cell lymphoma. The findings were published Sept. 30 in Blood Advances.

The OUTREACH trial, funded by Juno/Bristol-Myers Squibb, treated patients in the third line and beyond at community medical centers (outpatient-monitored, 70%; inpatient-monitored, 30%). The trial didn’t require facilities to be certified by the Foundation for the Accreditation of Cellular Therapy (FACT); all had to be non-tertiary cancer centers that weren’t associated with a university. In order to administer therapy on the outpatient basis, the centers had to have phase 1 or hematopoietic stem cell transplant capabilities.

As Linhares explained, 72% of participating centers hadn’t provided CAR T-cell therapy before, and 44% did not have FACT accreditation. “About 32% of patients received CAR T at CAR T naive sites, while 70% of patients received CAR T as outpatients. Investigators had to decide whether patients qualified for the outpatient observation or had to be admitted for the inpatient observation,” she noted.
 

Community Outcomes Were Comparable to Major Trial

As for the results, grade 3 or higher adverse events occurred at a similar frequency among outpatients and inpatients at 74% and 76%, Linhares said. There were no grade 5 adverse events, and 25% of patients treated as outpatients were never hospitalized. 

Response rates were similar to those in the major TRANSCEND trial with the objective response rates rate of 80% and complete response rates of 54%.

“Overall,” Linhares said, “our study demonstrated that with the availability of standard operating procedures, specially trained staff and a multidisciplinary team trained in CAR T toxicity management, inpatient and outpatient CAR T administration is feasible at specialized community medical centers.”

In 2023, another study examined patients with B-cell non-Hodgkin lymphoma who were treated on an outpatient basis with tisagenlecleucel. Researchers reported that outpatient therapy was “feasible and associated with similar efficacy outcomes as inpatient treatment.”

And a 2023 systematic literature review identified 11 studies that reported outpatient vs inpatient outcomes in CAR T-cell therapy and found “comparable response rates (80-82% in outpatient and 72-80% in inpatient).” Costs were cheaper in the outpatient setting. 

Research findings like these are good news, Baylor College of Medicine’s Badr said. “Outpatient administration could help to scale the availability of this therapy to a broader range of healthcare settings, including those serving underserved populations. Findings indicate promising safety profiles, which is encouraging for expanding access.”
 

Not Every Patient Can Tolerate Outpatient Care

Linhares noted that the patients who received outpatient care in the lisocabtagene maraleucel study were in better shape than those in the inpatient group. Those selected for inpatient care had “higher disease risk characteristics, including high grade B cell lymphoma histology, higher disease burden, and having received bridging therapy. This points to the fact that the investigators properly selected patients who were at a higher risk of complications for inpatient observation. Additionally, some patients stayed as inpatient due to social factors, which increases length of stay independently of disease characteristics.”

Specifically, reasons for inpatient monitoring were disease characteristics (48%) including tumor burden and risk of adverse events; psychosocial factors (32%) including lack of caregiver support or transportation; COVID-19 precautions (8%); pre-infusion adverse events (8%) of fever and vasovagal reaction; and principal investigator decision (4%) due to limited hospital experience with CAR T-cell therapy.

Texas Children’s Cancer Center’s Rouce said “certain patients, particularly those with higher risk for complications or those who require intensive monitoring, may not be suited for outpatient CAR T-cell therapy. This may be due to other comorbidities or baseline factors known to predispose to CAR T-related toxicities. However, evidence-based risk mitigation algorithms may still allow closely monitored outpatient treatment, with recognition that hospital admission for incipient side effects may be necessary.”
 

What’s Next for Access to Therapy?

Rouce noted that her institution, like many others, is offering CAR T-cell therapy on an outpatient basis. “Additionally, continued scientific innovation, such as immediately available, off-the-shelf cell therapies and inducible safety switches, will ultimately improve access,” she said. 

Linhares noted a recent advance and highlighted research that’s now in progress. “CAR Ts now have an indication as a second-line therapy in relapsed/refractory large B-cell lymphoma, and there are ongoing clinical trials that will potentially move CAR Ts into the first line,” she said. “Some trials are exploring allogeneic, readily available off-the-shelf CAR T for the treatment of minimal residual disease positive large B-cell lymphoma after completion of first-line therapy.”

These potential advances “are increasing the need for CAR T-capable medical centers,” Linhares noted. “More and more medical centers with expert hematology teams are becoming CAR T-certified, with more patients having access to CAR T.”

Still, she said, “I don’t think access is nearly as good as it should be. Many patients in rural areas are still unable to get this life-saving treatment. “However, “it is very possible that other novel targeted therapies, such as bispecific antibodies, will be used in place of CAR T in areas with poor CAR T access. Bispecific antibody efficacy in various B cell lymphoma histologies are being currently explored.”

Rouce discloses relationships with Novartis and Pfizer. Linhares reports ties with Kyowa Kirin, AbbVie, ADC, BeiGene, Genentech, Gilead, GlaxoSmithKline, Seagen, and TG. Badr has no disclosures. 
 

A version of this article appeared on Medscape.com.

A growing body of research suggests that clinicians can offer chimeric antigen receptor (CAR) T-cell therapy safely and effectively on an outpatient basis — a positive development as clinicians strive to expand access beyond metropolitan areas.

In one recent study, an industry-funded phase 2 trial, researchers found similar outcomes from outpatient and inpatient CAR T-cell therapy for relapsed/refractory large B-cell lymphoma with lisocabtagene maraleucel (Breyanzi). 

Another recent study reported that outpatient treatment of B cell non-Hodgkin lymphoma with tisagenlecleucel (Kymriah) had similar efficacy to inpatient treatment. Meanwhile, a 2023 review of CAR T-cell therapy in various settings found similar outcomes in outpatient and inpatient treatment. 

“The future of CAR T-cell therapy lies in balancing safety with accessibility,” said Rayne Rouce, MD, a pediatric oncologist at Texas Children’s Cancer Center in Houston, Texas, in an interview. “Expanding CAR T-cell therapy beyond large medical centers is a critical next step.” 
 

Great Outcomes, Low Access

Since 2017, the FDA has approved six CAR T-cell therapies, which target cancer by harnessing the power of a patient’s own T cells. As an Oregon Health & Sciences University/Knight Cancer Center website explains, T cells are removed from the patient’s body, “genetically modified to make the chimeric antigen receptor, or CAR, [which] protein binds to specific proteins on the surface of cancer cells.”

Modified cells are grown and then infused back into the body, where they “multiply and may be able to destroy all the cancer cells.”

As Rouce puts it, “CAR T-cells have revolutionized the treatment of relapsed or refractory blood cancers.” One or more of the therapies have been approved to treat types of lymphoblastic leukemia, B-cell lymphoma, follicular lymphoma, mantle cell lymphoma, and multiple myeloma.

A 2023 review of clinical trial data reported complete response rates of 40%-54% in aggressive B-cell lymphoma, 67% in mantle cell lymphoma, and 69%-74% in indolent B cell lymphoma.

“Commercialization of CAR T-cell therapy brought hope that access would expand beyond the major academic medical centers with the highly specialized infrastructure and advanced laboratories required to manufacture and ultimately treat patients,” Rouce said. “However, it quickly became clear that patients who are underinsured or uninsured — or who live outside the network of the well-resourced institutions that house these therapies — are still unable to access these potentially life-saving therapies.”

A 2024 report estimated the cost of CAR T-cell therapy as $700,000-$1 million and said only a small percentage of those who could benefit from the treatment actually get it. For example, an estimated 10,000 patients with diffuse large B-cell lymphoma alone could benefit from CAR T therapy annually, but a survey of 200 US healthcare centers in 2021 found that 1900 procedures were performed overall for all indications. 
 

Distance to Treatment Is a Major Obstacle

Even if patients have insurance plans willing to cover CAR T-cell therapy, they may not be able get care. While more than 150 US centers are certified to administer the therapy, “distance to major medical centers with CAR T capabilities is a major obstacle,” Yuliya Linhares, MD, chief of lymphoma at Miami Cancer Institute in Miami, Florida, said in an interview. 

“I have had patients who chose to not proceed with CAR T therapy due to inability to travel the distance to the medical center for pre-CAR T appointments and assessments and a lack of caretakers who are available to stay nearby,” Linhares said.

Indeed, the challenges facing patients in rural and underserved urban areas can be overwhelming, Hoda Badr, PhD, professor of medicine at Baylor College of Medicine in Houston, Texas, said in an interview.

“They must take time off work, arrange accommodations near treatment sites, and manage travel costs, all of which strain limited financial resources. The inability to afford these additional expenses can lead to delays in receiving care or patients forgoing the treatment altogether,” Badr said. She added that “the psychological and social burden of being away from family and community support systems during treatment can intensify the stress of an already difficult situation.”

A statistic tells the story of the urban/community divide. CAR T-cell therapy administration at academic centers after leukapheresis — the separation and collection of white blood cells — is reported to be at around 90%, while it’s only 47% in community-based practices that have to refer patients elsewhere, Linhares noted. 
 

Researchers Explore CAR T-Cell Therapy in the Community 

Linhares is lead author of the phase 2 trial that explored administration of lisocabtagene maraleucel in 82 patients with relapsed/refractory large B-cell lymphoma. The findings were published Sept. 30 in Blood Advances.

The OUTREACH trial, funded by Juno/Bristol-Myers Squibb, treated patients in the third line and beyond at community medical centers (outpatient-monitored, 70%; inpatient-monitored, 30%). The trial didn’t require facilities to be certified by the Foundation for the Accreditation of Cellular Therapy (FACT); all had to be non-tertiary cancer centers that weren’t associated with a university. In order to administer therapy on the outpatient basis, the centers had to have phase 1 or hematopoietic stem cell transplant capabilities.

As Linhares explained, 72% of participating centers hadn’t provided CAR T-cell therapy before, and 44% did not have FACT accreditation. “About 32% of patients received CAR T at CAR T naive sites, while 70% of patients received CAR T as outpatients. Investigators had to decide whether patients qualified for the outpatient observation or had to be admitted for the inpatient observation,” she noted.
 

Community Outcomes Were Comparable to Major Trial

As for the results, grade 3 or higher adverse events occurred at a similar frequency among outpatients and inpatients at 74% and 76%, Linhares said. There were no grade 5 adverse events, and 25% of patients treated as outpatients were never hospitalized. 

Response rates were similar to those in the major TRANSCEND trial with the objective response rates rate of 80% and complete response rates of 54%.

“Overall,” Linhares said, “our study demonstrated that with the availability of standard operating procedures, specially trained staff and a multidisciplinary team trained in CAR T toxicity management, inpatient and outpatient CAR T administration is feasible at specialized community medical centers.”

In 2023, another study examined patients with B-cell non-Hodgkin lymphoma who were treated on an outpatient basis with tisagenlecleucel. Researchers reported that outpatient therapy was “feasible and associated with similar efficacy outcomes as inpatient treatment.”

And a 2023 systematic literature review identified 11 studies that reported outpatient vs inpatient outcomes in CAR T-cell therapy and found “comparable response rates (80-82% in outpatient and 72-80% in inpatient).” Costs were cheaper in the outpatient setting. 

Research findings like these are good news, Baylor College of Medicine’s Badr said. “Outpatient administration could help to scale the availability of this therapy to a broader range of healthcare settings, including those serving underserved populations. Findings indicate promising safety profiles, which is encouraging for expanding access.”
 

Not Every Patient Can Tolerate Outpatient Care

Linhares noted that the patients who received outpatient care in the lisocabtagene maraleucel study were in better shape than those in the inpatient group. Those selected for inpatient care had “higher disease risk characteristics, including high grade B cell lymphoma histology, higher disease burden, and having received bridging therapy. This points to the fact that the investigators properly selected patients who were at a higher risk of complications for inpatient observation. Additionally, some patients stayed as inpatient due to social factors, which increases length of stay independently of disease characteristics.”

Specifically, reasons for inpatient monitoring were disease characteristics (48%) including tumor burden and risk of adverse events; psychosocial factors (32%) including lack of caregiver support or transportation; COVID-19 precautions (8%); pre-infusion adverse events (8%) of fever and vasovagal reaction; and principal investigator decision (4%) due to limited hospital experience with CAR T-cell therapy.

Texas Children’s Cancer Center’s Rouce said “certain patients, particularly those with higher risk for complications or those who require intensive monitoring, may not be suited for outpatient CAR T-cell therapy. This may be due to other comorbidities or baseline factors known to predispose to CAR T-related toxicities. However, evidence-based risk mitigation algorithms may still allow closely monitored outpatient treatment, with recognition that hospital admission for incipient side effects may be necessary.”
 

What’s Next for Access to Therapy?

Rouce noted that her institution, like many others, is offering CAR T-cell therapy on an outpatient basis. “Additionally, continued scientific innovation, such as immediately available, off-the-shelf cell therapies and inducible safety switches, will ultimately improve access,” she said. 

Linhares noted a recent advance and highlighted research that’s now in progress. “CAR Ts now have an indication as a second-line therapy in relapsed/refractory large B-cell lymphoma, and there are ongoing clinical trials that will potentially move CAR Ts into the first line,” she said. “Some trials are exploring allogeneic, readily available off-the-shelf CAR T for the treatment of minimal residual disease positive large B-cell lymphoma after completion of first-line therapy.”

These potential advances “are increasing the need for CAR T-capable medical centers,” Linhares noted. “More and more medical centers with expert hematology teams are becoming CAR T-certified, with more patients having access to CAR T.”

Still, she said, “I don’t think access is nearly as good as it should be. Many patients in rural areas are still unable to get this life-saving treatment. “However, “it is very possible that other novel targeted therapies, such as bispecific antibodies, will be used in place of CAR T in areas with poor CAR T access. Bispecific antibody efficacy in various B cell lymphoma histologies are being currently explored.”

Rouce discloses relationships with Novartis and Pfizer. Linhares reports ties with Kyowa Kirin, AbbVie, ADC, BeiGene, Genentech, Gilead, GlaxoSmithKline, Seagen, and TG. Badr has no disclosures. 
 

A version of this article appeared on Medscape.com.

TOPLINE:

Between 2011 and 2023, the US Food and Drug Administration (FDA) reported recalls of 334 cosmetic dermatology products in the United States, affecting over 77 million units, predominantly due to bacterial contamination.

METHODOLOGY:

• Researchers conducted a cross-sectional analysis of the FDA Enforcement Report database for cosmetic dermatology products from 2011 to 2023.
• Cosmetic products are any article “intended for body cleaning or beauty enhancement,” as defined by the FDA.
• Recalls were categorized by product type, reason for the recall, microbial contaminant, inorganic contaminant, distribution, and risk classification.

TAKEAWAY:

• During the study period, 334 voluntary and manufacturer-initiated recalls of cosmetic products were reported, affecting 77,135,700 units.
• A total of 297 recalls (88.9%) were categorized as Class II, indicating that they caused “medically reversible health consequences.” The median recall duration was 307 days.
• Hygiene and cleaning products accounted for most of the recalls (51.5%). Makeup gels, soaps, shampoos, tattoo ink, wipes, and lotions were the most recalled product categories. Nearly 51% of the products were distributed internationally.
• Microbial and inorganic contamination accounted for 76.8% and 10.2% of the recalls (the two most common reasons for the recall), respectively, with bacteria (80%) the most common contaminating pathogen (primarily Pseudomonas and Burkholderia species).

IN PRACTICE:

With 77 million units recalled by the FDA over 12 years, cosmetic recalls have remained common, the authors concluded, adding that “dermatologists should be key voices in pharmacovigilance given scientific expertise and frontline experience managing products and associated concerns.” Dermatologists, they added, “should also be aware of FDA enforcement reports for recall updates given that average recall termination took approximately 1 year.”

SOURCE:

The study was led by Kaushik P. Venkatesh, MBA, MPH, Harvard Medical School, Boston, and was published online on October 29 in the Journal of the American Academy of Dermatology.

LIMITATIONS: 

The study’s limitations include the potential underreporting of Class III recalls (products that are unlikely to cause any adverse health reaction but violate FDA labeling or manufacturing laws) and lack of complete information on contaminants.

DISCLOSURES:

No information on funding was provided in the study. No conflicts of interest were reported.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Between 2011 and 2023, the US Food and Drug Administration (FDA) reported recalls of 334 cosmetic dermatology products in the United States, affecting over 77 million units, predominantly due to bacterial contamination.

METHODOLOGY:

• Researchers conducted a cross-sectional analysis of the FDA Enforcement Report database for cosmetic dermatology products from 2011 to 2023.
• Cosmetic products are any article “intended for body cleaning or beauty enhancement,” as defined by the FDA.
• Recalls were categorized by product type, reason for the recall, microbial contaminant, inorganic contaminant, distribution, and risk classification.

TAKEAWAY:

• During the study period, 334 voluntary and manufacturer-initiated recalls of cosmetic products were reported, affecting 77,135,700 units.
• A total of 297 recalls (88.9%) were categorized as Class II, indicating that they caused “medically reversible health consequences.” The median recall duration was 307 days.
• Hygiene and cleaning products accounted for most of the recalls (51.5%). Makeup gels, soaps, shampoos, tattoo ink, wipes, and lotions were the most recalled product categories. Nearly 51% of the products were distributed internationally.
• Microbial and inorganic contamination accounted for 76.8% and 10.2% of the recalls (the two most common reasons for the recall), respectively, with bacteria (80%) the most common contaminating pathogen (primarily Pseudomonas and Burkholderia species).

IN PRACTICE:

With 77 million units recalled by the FDA over 12 years, cosmetic recalls have remained common, the authors concluded, adding that “dermatologists should be key voices in pharmacovigilance given scientific expertise and frontline experience managing products and associated concerns.” Dermatologists, they added, “should also be aware of FDA enforcement reports for recall updates given that average recall termination took approximately 1 year.”

SOURCE:

The study was led by Kaushik P. Venkatesh, MBA, MPH, Harvard Medical School, Boston, and was published online on October 29 in the Journal of the American Academy of Dermatology.

LIMITATIONS: 

The study’s limitations include the potential underreporting of Class III recalls (products that are unlikely to cause any adverse health reaction but violate FDA labeling or manufacturing laws) and lack of complete information on contaminants.

DISCLOSURES:

No information on funding was provided in the study. No conflicts of interest were reported.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Between 2011 and 2023, the US Food and Drug Administration (FDA) reported recalls of 334 cosmetic dermatology products in the United States, affecting over 77 million units, predominantly due to bacterial contamination.

METHODOLOGY:

• Researchers conducted a cross-sectional analysis of the FDA Enforcement Report database for cosmetic dermatology products from 2011 to 2023.
• Cosmetic products are any article “intended for body cleaning or beauty enhancement,” as defined by the FDA.
• Recalls were categorized by product type, reason for the recall, microbial contaminant, inorganic contaminant, distribution, and risk classification.

TAKEAWAY:

• During the study period, 334 voluntary and manufacturer-initiated recalls of cosmetic products were reported, affecting 77,135,700 units.
• A total of 297 recalls (88.9%) were categorized as Class II, indicating that they caused “medically reversible health consequences.” The median recall duration was 307 days.
• Hygiene and cleaning products accounted for most of the recalls (51.5%). Makeup gels, soaps, shampoos, tattoo ink, wipes, and lotions were the most recalled product categories. Nearly 51% of the products were distributed internationally.
• Microbial and inorganic contamination accounted for 76.8% and 10.2% of the recalls (the two most common reasons for the recall), respectively, with bacteria (80%) the most common contaminating pathogen (primarily Pseudomonas and Burkholderia species).

IN PRACTICE:

With 77 million units recalled by the FDA over 12 years, cosmetic recalls have remained common, the authors concluded, adding that “dermatologists should be key voices in pharmacovigilance given scientific expertise and frontline experience managing products and associated concerns.” Dermatologists, they added, “should also be aware of FDA enforcement reports for recall updates given that average recall termination took approximately 1 year.”

SOURCE:

The study was led by Kaushik P. Venkatesh, MBA, MPH, Harvard Medical School, Boston, and was published online on October 29 in the Journal of the American Academy of Dermatology.

LIMITATIONS: 

The study’s limitations include the potential underreporting of Class III recalls (products that are unlikely to cause any adverse health reaction but violate FDA labeling or manufacturing laws) and lack of complete information on contaminants.

DISCLOSURES:

No information on funding was provided in the study. No conflicts of interest were reported.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

Approximately one third of parents of children with atopic dermatitis reported little or no improvement with elimination diets, and nearly 80% reintroduced the eliminated foods, based on survey data from nearly 300 parents.

Although atopic dermatitis can be associated with an increased risk for food allergies, major allergy organizations do not currently recommend elimination diets as a treatment for atopic dermatitis, said Nadia Makkoukdji, MD, a pediatrician at Jackson Memorial Hospital, Miami, in a presentation at the American College of Allergy, Asthma, and Immunology (ACAAI) Annual Scientific Meeting.

“A fear of drastic dietary changes often prevents families from seeking the care their children need,” Makkoukdji said in an interview. In the clinical setting, Makkoukdji noted that she has seen many patients who have started food elimination diets on their own or as recommended by other doctors, and that these diets can lead to dangers such as the development of immunoglobulin E–mediated food allergies on reintroduction of eliminated foods and malnutrition. They can also produce “emotional stress in children and anxiety or depression, while also adding stress to parents and the entire family.”

Makkoukdji conducted the study to explore parents’ perceptions of these diets in management of their children’s atopic dermatitis, she said.

In the study, Makkoukdji and colleagues sought to understand parents’ perceptions of the role of diet in atopic dermatitis in their children. The researchers reviewed surveys from 298 parents of children with atopic dermatitis who were seen at a single academic center. Parents completed the surveys in the emergency department or in an allergy, dermatology, and general pediatrics clinic.

Overall, 42% of parents identified food triggers for their child’s atopic dermatitis. The most commonly identified triggers were milk (32%), tree nuts/seeds/peanuts (16%), and eggs (11%).

Of the parents who reported food triggers, 23% removed the suspected trigger food from the child’s diet completely, 20% removed suspected trigger foods from their own diets while breastfeeding, and 19% changed their infant’s formula.

In the wake of the elimination diets, 38% of the parents reported no improvement in their child’s atopic dermatitis, 35% reported a 25% improvement, and 9% reported complete resolution. The majority (79%) reintroduced eliminated foods and reported no recurrence of atopic dermatitis symptoms.

The researchers were surprised by how many parents changed their child’s diet in the belief that certain foods exacerbated their child’s atopic dermatitis, “although this perception aligns with the common concern that food allergens can trigger or worsen atopic dermatitis flares,” Makkoukdji said.

The current study highlights the need for more awareness of the limited impact of dietary modifications on atopic dermatitis in the absence of confirmed food allergies, Makkoukdji said. “Our study shows that food elimination diets are still commonly being used by parents in the local Miami population.”

The findings were limited by several factors, including the use of data from a single center and the focus only on pediatric patients, but the primary goal was to assess parental perceptions of AD flares in relation to dietary choices, said Makkoukdji. “Future studies that include larger and more diverse populations would be valuable for the field.”
 

Dietary Modifications Don’t Live Up to Hype

“Food continues to be one of the most discussed aspects of atopic dermatitis,” Peter Lio, MD, clinical assistant professor of dermatology and pediatrics at Northwestern University Feinberg School of Medicine, Chicago, Illinois, said in an interview.

“Almost all of my patients and families ask about dietary modifications, even though almost all of them have experimented with it to some degree,” said Lio. In his experience, diet plays a small role, if any, in the day-to-day management of atopic dermatitis.

This lack of effect of dietary changes is often frustrating to patients because of the persistent “common wisdom” that points to diet as a root cause of atopic dermatitis, Lio said. “Many practitioners continue to recommend excluding foods such as gluten or dairy from the diet, but generally these are only of modest help,” and although patients wish that dietary changes would fix the problem, most are left wondering why these changes didn’t help them.

The current study findings “reflect my own experience after nearly 20 years of being deeply immersed in the world of atopic dermatitis,” Lio said. Although the takeaway message does not argue against eating healthy foods, some foods do seem to make AD worse in some patients and may have nonallergic pro-inflammatory effects.

“In those cases, it is reasonable to limit or avoid those foods. However, it is extremely difficult to tell what food or foods are driving flare-ups when things are out of control, so dietary modification is generally not the best place to start,” he said.

True food allergies are much more common in patients with atopic dermatitis compared with individuals without atopic dermatitis, but the current study is not addressing these types of allergies, Lio emphasized. “If someone has true allergy to peanuts, for example, they should not be eating them; we also know that they are not ‘cheating’ because these patients would not merely have an eczema flare; they would have urticaria, angioedema, or anaphylaxis. There is tremendous confusion around this point and lots of confusion around allergy testing and its limitations.”

In addition, patients with atopic dermatitis are more likely than those without atopic dermatitis to have abnormalities in the gut microbiome and gut barrier, Lio said.

Abnormalities in the gut microbiome are different from the concept of allergy and may fall into the more complex category of barrier and microbiome disruptors, he said. Therefore, “the food category may not be nearly as important as the specific preparation of the food along with the additives (such as preservatives and emulsifiers) that may actually be driving the problem.”

Although in the past many clinicians advised patients to try cutting out certain foods to see whether atopic dermatitis symptoms improved, this strategy is not without risk, said Lio. “There have been incredible advancements in understanding the role of the gut in tolerization to foods.” Recent research has shown that by eating foods regularly, particularly those such as peanuts that seem to have more allergic potential, the body becomes tolerant, and this prevents the development of true food allergies.

As for additional research, many questions remain about the effects of types of foods, processing methods, and timing of introduction of foods on atopic dermatitis, Lio noted.

“Atopic dermatitis is a systemic condition with the immune system, with the skin/gut/respiratory barriers and microbiome involved; I think we now have a broader view of how big and complex the landscape really is,” he said.

The study received no outside funding. The researchers had no financial conflicts to disclose. Lio had no disclosures relevant to elimination diets but disclosed serving on the speakers bureau for AbbVie, Arcutis Biotherapeutics, Eli Lilly, Galderma, Hyphens Pharma, Incyte, La Roche–Posay/L’Oréal, Pfizer, Pierre Fabre Dermatologie, Regeneron/Sanofi Genzyme, and Verrica Pharmaceuticals; serving on consulting/advisory boards; or having stock options for many pharmaceutical companies. Lio also disclosed a patent pending for a Theraplex product with royalties paid and is a board member and Scientific Advisory Committee member emeritus of the National Eczema Association.

A version of this article first appeared on Medscape.com.

Approximately one third of parents of children with atopic dermatitis reported little or no improvement with elimination diets, and nearly 80% reintroduced the eliminated foods, based on survey data from nearly 300 parents.

Although atopic dermatitis can be associated with an increased risk for food allergies, major allergy organizations do not currently recommend elimination diets as a treatment for atopic dermatitis, said Nadia Makkoukdji, MD, a pediatrician at Jackson Memorial Hospital, Miami, in a presentation at the American College of Allergy, Asthma, and Immunology (ACAAI) Annual Scientific Meeting.

“A fear of drastic dietary changes often prevents families from seeking the care their children need,” Makkoukdji said in an interview. In the clinical setting, Makkoukdji noted that she has seen many patients who have started food elimination diets on their own or as recommended by other doctors, and that these diets can lead to dangers such as the development of immunoglobulin E–mediated food allergies on reintroduction of eliminated foods and malnutrition. They can also produce “emotional stress in children and anxiety or depression, while also adding stress to parents and the entire family.”

Makkoukdji conducted the study to explore parents’ perceptions of these diets in management of their children’s atopic dermatitis, she said.

In the study, Makkoukdji and colleagues sought to understand parents’ perceptions of the role of diet in atopic dermatitis in their children. The researchers reviewed surveys from 298 parents of children with atopic dermatitis who were seen at a single academic center. Parents completed the surveys in the emergency department or in an allergy, dermatology, and general pediatrics clinic.

Overall, 42% of parents identified food triggers for their child’s atopic dermatitis. The most commonly identified triggers were milk (32%), tree nuts/seeds/peanuts (16%), and eggs (11%).

Of the parents who reported food triggers, 23% removed the suspected trigger food from the child’s diet completely, 20% removed suspected trigger foods from their own diets while breastfeeding, and 19% changed their infant’s formula.

In the wake of the elimination diets, 38% of the parents reported no improvement in their child’s atopic dermatitis, 35% reported a 25% improvement, and 9% reported complete resolution. The majority (79%) reintroduced eliminated foods and reported no recurrence of atopic dermatitis symptoms.

The researchers were surprised by how many parents changed their child’s diet in the belief that certain foods exacerbated their child’s atopic dermatitis, “although this perception aligns with the common concern that food allergens can trigger or worsen atopic dermatitis flares,” Makkoukdji said.

The current study highlights the need for more awareness of the limited impact of dietary modifications on atopic dermatitis in the absence of confirmed food allergies, Makkoukdji said. “Our study shows that food elimination diets are still commonly being used by parents in the local Miami population.”

The findings were limited by several factors, including the use of data from a single center and the focus only on pediatric patients, but the primary goal was to assess parental perceptions of AD flares in relation to dietary choices, said Makkoukdji. “Future studies that include larger and more diverse populations would be valuable for the field.”
 

Dietary Modifications Don’t Live Up to Hype

“Food continues to be one of the most discussed aspects of atopic dermatitis,” Peter Lio, MD, clinical assistant professor of dermatology and pediatrics at Northwestern University Feinberg School of Medicine, Chicago, Illinois, said in an interview.

“Almost all of my patients and families ask about dietary modifications, even though almost all of them have experimented with it to some degree,” said Lio. In his experience, diet plays a small role, if any, in the day-to-day management of atopic dermatitis.

This lack of effect of dietary changes is often frustrating to patients because of the persistent “common wisdom” that points to diet as a root cause of atopic dermatitis, Lio said. “Many practitioners continue to recommend excluding foods such as gluten or dairy from the diet, but generally these are only of modest help,” and although patients wish that dietary changes would fix the problem, most are left wondering why these changes didn’t help them.

The current study findings “reflect my own experience after nearly 20 years of being deeply immersed in the world of atopic dermatitis,” Lio said. Although the takeaway message does not argue against eating healthy foods, some foods do seem to make AD worse in some patients and may have nonallergic pro-inflammatory effects.

“In those cases, it is reasonable to limit or avoid those foods. However, it is extremely difficult to tell what food or foods are driving flare-ups when things are out of control, so dietary modification is generally not the best place to start,” he said.

True food allergies are much more common in patients with atopic dermatitis compared with individuals without atopic dermatitis, but the current study is not addressing these types of allergies, Lio emphasized. “If someone has true allergy to peanuts, for example, they should not be eating them; we also know that they are not ‘cheating’ because these patients would not merely have an eczema flare; they would have urticaria, angioedema, or anaphylaxis. There is tremendous confusion around this point and lots of confusion around allergy testing and its limitations.”

In addition, patients with atopic dermatitis are more likely than those without atopic dermatitis to have abnormalities in the gut microbiome and gut barrier, Lio said.

Abnormalities in the gut microbiome are different from the concept of allergy and may fall into the more complex category of barrier and microbiome disruptors, he said. Therefore, “the food category may not be nearly as important as the specific preparation of the food along with the additives (such as preservatives and emulsifiers) that may actually be driving the problem.”

Although in the past many clinicians advised patients to try cutting out certain foods to see whether atopic dermatitis symptoms improved, this strategy is not without risk, said Lio. “There have been incredible advancements in understanding the role of the gut in tolerization to foods.” Recent research has shown that by eating foods regularly, particularly those such as peanuts that seem to have more allergic potential, the body becomes tolerant, and this prevents the development of true food allergies.

As for additional research, many questions remain about the effects of types of foods, processing methods, and timing of introduction of foods on atopic dermatitis, Lio noted.

“Atopic dermatitis is a systemic condition with the immune system, with the skin/gut/respiratory barriers and microbiome involved; I think we now have a broader view of how big and complex the landscape really is,” he said.

The study received no outside funding. The researchers had no financial conflicts to disclose. Lio had no disclosures relevant to elimination diets but disclosed serving on the speakers bureau for AbbVie, Arcutis Biotherapeutics, Eli Lilly, Galderma, Hyphens Pharma, Incyte, La Roche–Posay/L’Oréal, Pfizer, Pierre Fabre Dermatologie, Regeneron/Sanofi Genzyme, and Verrica Pharmaceuticals; serving on consulting/advisory boards; or having stock options for many pharmaceutical companies. Lio also disclosed a patent pending for a Theraplex product with royalties paid and is a board member and Scientific Advisory Committee member emeritus of the National Eczema Association.

A version of this article first appeared on Medscape.com.

Approximately one third of parents of children with atopic dermatitis reported little or no improvement with elimination diets, and nearly 80% reintroduced the eliminated foods, based on survey data from nearly 300 parents.

Although atopic dermatitis can be associated with an increased risk for food allergies, major allergy organizations do not currently recommend elimination diets as a treatment for atopic dermatitis, said Nadia Makkoukdji, MD, a pediatrician at Jackson Memorial Hospital, Miami, in a presentation at the American College of Allergy, Asthma, and Immunology (ACAAI) Annual Scientific Meeting.

“A fear of drastic dietary changes often prevents families from seeking the care their children need,” Makkoukdji said in an interview. In the clinical setting, Makkoukdji noted that she has seen many patients who have started food elimination diets on their own or as recommended by other doctors, and that these diets can lead to dangers such as the development of immunoglobulin E–mediated food allergies on reintroduction of eliminated foods and malnutrition. They can also produce “emotional stress in children and anxiety or depression, while also adding stress to parents and the entire family.”

Makkoukdji conducted the study to explore parents’ perceptions of these diets in management of their children’s atopic dermatitis, she said.

In the study, Makkoukdji and colleagues sought to understand parents’ perceptions of the role of diet in atopic dermatitis in their children. The researchers reviewed surveys from 298 parents of children with atopic dermatitis who were seen at a single academic center. Parents completed the surveys in the emergency department or in an allergy, dermatology, and general pediatrics clinic.

Overall, 42% of parents identified food triggers for their child’s atopic dermatitis. The most commonly identified triggers were milk (32%), tree nuts/seeds/peanuts (16%), and eggs (11%).

Of the parents who reported food triggers, 23% removed the suspected trigger food from the child’s diet completely, 20% removed suspected trigger foods from their own diets while breastfeeding, and 19% changed their infant’s formula.

In the wake of the elimination diets, 38% of the parents reported no improvement in their child’s atopic dermatitis, 35% reported a 25% improvement, and 9% reported complete resolution. The majority (79%) reintroduced eliminated foods and reported no recurrence of atopic dermatitis symptoms.

The researchers were surprised by how many parents changed their child’s diet in the belief that certain foods exacerbated their child’s atopic dermatitis, “although this perception aligns with the common concern that food allergens can trigger or worsen atopic dermatitis flares,” Makkoukdji said.

The current study highlights the need for more awareness of the limited impact of dietary modifications on atopic dermatitis in the absence of confirmed food allergies, Makkoukdji said. “Our study shows that food elimination diets are still commonly being used by parents in the local Miami population.”

The findings were limited by several factors, including the use of data from a single center and the focus only on pediatric patients, but the primary goal was to assess parental perceptions of AD flares in relation to dietary choices, said Makkoukdji. “Future studies that include larger and more diverse populations would be valuable for the field.”
 

Dietary Modifications Don’t Live Up to Hype

“Food continues to be one of the most discussed aspects of atopic dermatitis,” Peter Lio, MD, clinical assistant professor of dermatology and pediatrics at Northwestern University Feinberg School of Medicine, Chicago, Illinois, said in an interview.

“Almost all of my patients and families ask about dietary modifications, even though almost all of them have experimented with it to some degree,” said Lio. In his experience, diet plays a small role, if any, in the day-to-day management of atopic dermatitis.

This lack of effect of dietary changes is often frustrating to patients because of the persistent “common wisdom” that points to diet as a root cause of atopic dermatitis, Lio said. “Many practitioners continue to recommend excluding foods such as gluten or dairy from the diet, but generally these are only of modest help,” and although patients wish that dietary changes would fix the problem, most are left wondering why these changes didn’t help them.

The current study findings “reflect my own experience after nearly 20 years of being deeply immersed in the world of atopic dermatitis,” Lio said. Although the takeaway message does not argue against eating healthy foods, some foods do seem to make AD worse in some patients and may have nonallergic pro-inflammatory effects.

“In those cases, it is reasonable to limit or avoid those foods. However, it is extremely difficult to tell what food or foods are driving flare-ups when things are out of control, so dietary modification is generally not the best place to start,” he said.

True food allergies are much more common in patients with atopic dermatitis compared with individuals without atopic dermatitis, but the current study is not addressing these types of allergies, Lio emphasized. “If someone has true allergy to peanuts, for example, they should not be eating them; we also know that they are not ‘cheating’ because these patients would not merely have an eczema flare; they would have urticaria, angioedema, or anaphylaxis. There is tremendous confusion around this point and lots of confusion around allergy testing and its limitations.”

In addition, patients with atopic dermatitis are more likely than those without atopic dermatitis to have abnormalities in the gut microbiome and gut barrier, Lio said.

Abnormalities in the gut microbiome are different from the concept of allergy and may fall into the more complex category of barrier and microbiome disruptors, he said. Therefore, “the food category may not be nearly as important as the specific preparation of the food along with the additives (such as preservatives and emulsifiers) that may actually be driving the problem.”

Although in the past many clinicians advised patients to try cutting out certain foods to see whether atopic dermatitis symptoms improved, this strategy is not without risk, said Lio. “There have been incredible advancements in understanding the role of the gut in tolerization to foods.” Recent research has shown that by eating foods regularly, particularly those such as peanuts that seem to have more allergic potential, the body becomes tolerant, and this prevents the development of true food allergies.

As for additional research, many questions remain about the effects of types of foods, processing methods, and timing of introduction of foods on atopic dermatitis, Lio noted.

“Atopic dermatitis is a systemic condition with the immune system, with the skin/gut/respiratory barriers and microbiome involved; I think we now have a broader view of how big and complex the landscape really is,” he said.

The study received no outside funding. The researchers had no financial conflicts to disclose. Lio had no disclosures relevant to elimination diets but disclosed serving on the speakers bureau for AbbVie, Arcutis Biotherapeutics, Eli Lilly, Galderma, Hyphens Pharma, Incyte, La Roche–Posay/L’Oréal, Pfizer, Pierre Fabre Dermatologie, Regeneron/Sanofi Genzyme, and Verrica Pharmaceuticals; serving on consulting/advisory boards; or having stock options for many pharmaceutical companies. Lio also disclosed a patent pending for a Theraplex product with royalties paid and is a board member and Scientific Advisory Committee member emeritus of the National Eczema Association.

A version of this article first appeared on Medscape.com.

TOPLINE:

The use of newer biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) for treating juvenile idiopathic arthritis (JIA) rose sharply from 2001 to 2022, while the use of conventional synthetic DMARDs (csDMARDs) plummeted, with adalimumab becoming the most commonly used b/tsDMARD.

METHODOLOGY:

• Researchers performed a serial cross-sectional study using Merative MarketScan Commercial Claims and Encounters data from 2000 to 2022 to describe recent trends in DMARD use for children with JIA in the United States.
• They identified 20,258 new episodes of DMARD use among 13,696 children with JIA (median age, 14 years; 67.5% girls) who newly initiated at least one DMARD.
• Participants were required to have ≥ 365 days of continuous healthcare and pharmacy eligibility prior to the index date, defined as the date of DMARD initiation.

TAKEAWAY:

• The use of csDMARDs declined from 89.5% to 43.2% between 2001 and 2022 (P < .001 for trend), whereas the use of bDMARDs increased from 10.5% to 50.0% over the same period (P < .001).
• Methotrexate was the most commonly used DMARD throughout the study period ; however, as with other csDMARDs, its use declined from 42.1% in 2001 to 21.5% in 2022 (P < .001 ).
• Use of the tumor necrosis factor inhibitor adalimumab doubled from 7% in 2007 to 14% in 2008 and increased further up to 20.5% by 2022; adalimumab also became the most predominantly used b/tsDMARD after csDMARD monotherapy, accounting for 77.8% of prescriptions following csDMARDs in 2022.
• Even though the use of individual TNF inhibitors increased, their overall popularity fell in recent years as the use of newer b/tsDMARDs, such as ustekinumab and secukinumab, increased.

IN PRACTICE:

“These real-world treatment patterns give us insight into how selection of therapies for JIA has evolved with increasing availability of effective agents and help prepare for future studies on comparative DMARD safety and effectiveness,” the authors wrote.

SOURCE:

The study was led by Priyanka Yalamanchili, PharmD, MS, Center for Pharmacoepidemiology and Treatment Science, Institute for Health, Rutgers University, New Brunswick, New Jersey, and was published online October 22, 2024, in Arthritis & Rheumatology.

LIMITATIONS: 

The dependence on commercial claims data may have limited the generalizability of the findings to other populations, such as those with public insurance or without insurance. The study did not have access to demographic data of the participants to investigate the presence of disparities in the use of DMARDs. Moreover, the lack of clinical details about the patients with JIA, including disease severity and specialty of prescribers, may have affected the interpretation of the results.

DISCLOSURES:

The study was supported by funding from the National Institute of Arthritis and Musculoskeletal and Skin Diseases and several other institutes of the National Institutes of Health, as well as the Rheumatology Research Foundation and the Juvenile Diabetes Research Foundation. No conflicts of interest were reported by the authors.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

The use of newer biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) for treating juvenile idiopathic arthritis (JIA) rose sharply from 2001 to 2022, while the use of conventional synthetic DMARDs (csDMARDs) plummeted, with adalimumab becoming the most commonly used b/tsDMARD.

METHODOLOGY:

• Researchers performed a serial cross-sectional study using Merative MarketScan Commercial Claims and Encounters data from 2000 to 2022 to describe recent trends in DMARD use for children with JIA in the United States.
• They identified 20,258 new episodes of DMARD use among 13,696 children with JIA (median age, 14 years; 67.5% girls) who newly initiated at least one DMARD.
• Participants were required to have ≥ 365 days of continuous healthcare and pharmacy eligibility prior to the index date, defined as the date of DMARD initiation.

TAKEAWAY:

• The use of csDMARDs declined from 89.5% to 43.2% between 2001 and 2022 (P < .001 for trend), whereas the use of bDMARDs increased from 10.5% to 50.0% over the same period (P < .001).
• Methotrexate was the most commonly used DMARD throughout the study period ; however, as with other csDMARDs, its use declined from 42.1% in 2001 to 21.5% in 2022 (P < .001 ).
• Use of the tumor necrosis factor inhibitor adalimumab doubled from 7% in 2007 to 14% in 2008 and increased further up to 20.5% by 2022; adalimumab also became the most predominantly used b/tsDMARD after csDMARD monotherapy, accounting for 77.8% of prescriptions following csDMARDs in 2022.
• Even though the use of individual TNF inhibitors increased, their overall popularity fell in recent years as the use of newer b/tsDMARDs, such as ustekinumab and secukinumab, increased.

IN PRACTICE:

“These real-world treatment patterns give us insight into how selection of therapies for JIA has evolved with increasing availability of effective agents and help prepare for future studies on comparative DMARD safety and effectiveness,” the authors wrote.

SOURCE:

The study was led by Priyanka Yalamanchili, PharmD, MS, Center for Pharmacoepidemiology and Treatment Science, Institute for Health, Rutgers University, New Brunswick, New Jersey, and was published online October 22, 2024, in Arthritis & Rheumatology.

LIMITATIONS: 

The dependence on commercial claims data may have limited the generalizability of the findings to other populations, such as those with public insurance or without insurance. The study did not have access to demographic data of the participants to investigate the presence of disparities in the use of DMARDs. Moreover, the lack of clinical details about the patients with JIA, including disease severity and specialty of prescribers, may have affected the interpretation of the results.

DISCLOSURES:

The study was supported by funding from the National Institute of Arthritis and Musculoskeletal and Skin Diseases and several other institutes of the National Institutes of Health, as well as the Rheumatology Research Foundation and the Juvenile Diabetes Research Foundation. No conflicts of interest were reported by the authors.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

The use of newer biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) for treating juvenile idiopathic arthritis (JIA) rose sharply from 2001 to 2022, while the use of conventional synthetic DMARDs (csDMARDs) plummeted, with adalimumab becoming the most commonly used b/tsDMARD.

METHODOLOGY:

• Researchers performed a serial cross-sectional study using Merative MarketScan Commercial Claims and Encounters data from 2000 to 2022 to describe recent trends in DMARD use for children with JIA in the United States.
• They identified 20,258 new episodes of DMARD use among 13,696 children with JIA (median age, 14 years; 67.5% girls) who newly initiated at least one DMARD.
• Participants were required to have ≥ 365 days of continuous healthcare and pharmacy eligibility prior to the index date, defined as the date of DMARD initiation.

TAKEAWAY:

• The use of csDMARDs declined from 89.5% to 43.2% between 2001 and 2022 (P < .001 for trend), whereas the use of bDMARDs increased from 10.5% to 50.0% over the same period (P < .001).
• Methotrexate was the most commonly used DMARD throughout the study period ; however, as with other csDMARDs, its use declined from 42.1% in 2001 to 21.5% in 2022 (P < .001 ).
• Use of the tumor necrosis factor inhibitor adalimumab doubled from 7% in 2007 to 14% in 2008 and increased further up to 20.5% by 2022; adalimumab also became the most predominantly used b/tsDMARD after csDMARD monotherapy, accounting for 77.8% of prescriptions following csDMARDs in 2022.
• Even though the use of individual TNF inhibitors increased, their overall popularity fell in recent years as the use of newer b/tsDMARDs, such as ustekinumab and secukinumab, increased.

IN PRACTICE:

“These real-world treatment patterns give us insight into how selection of therapies for JIA has evolved with increasing availability of effective agents and help prepare for future studies on comparative DMARD safety and effectiveness,” the authors wrote.

SOURCE:

The study was led by Priyanka Yalamanchili, PharmD, MS, Center for Pharmacoepidemiology and Treatment Science, Institute for Health, Rutgers University, New Brunswick, New Jersey, and was published online October 22, 2024, in Arthritis & Rheumatology.

LIMITATIONS: 

The dependence on commercial claims data may have limited the generalizability of the findings to other populations, such as those with public insurance or without insurance. The study did not have access to demographic data of the participants to investigate the presence of disparities in the use of DMARDs. Moreover, the lack of clinical details about the patients with JIA, including disease severity and specialty of prescribers, may have affected the interpretation of the results.

DISCLOSURES:

The study was supported by funding from the National Institute of Arthritis and Musculoskeletal and Skin Diseases and several other institutes of the National Institutes of Health, as well as the Rheumatology Research Foundation and the Juvenile Diabetes Research Foundation. No conflicts of interest were reported by the authors.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

Despite some recent progress in compensation equity, women in medicine continue to be paid significantly lower salaries than men.

According to the Female Compensation Report 2024 by Medscape, male doctors of any kind earned an average salary of about $400,000, whereas female doctors earned approximately $309,000 — a 29% gap.

The report analyzed survey data from 7000 practicing physicians who were recruited over a 4-month period starting in October 2023. The respondents comprised roughly 60% women representing over 29 specialties.

In the 2022 report, the pay gap between the genders was 32%. But some women in the field argued substantial headway is still needed.

“You can try and pick apart the data, but I’d say we’re not really making progress,” said Susan T. Hingle, MD, an internist in Illinois and president of the American Medical Women’s Association. “A decline by a couple of percentage points is not significantly addressing this pay gap that over a lifetime is huge, can be millions of dollars.”

The gender gap was narrower among female primary care physicians (PCPs) vs medical specialists. Female PCPs earned around $253,000 per year, whereas male PCPs earned about $295,000 per year. Hingle suggested that female PCPs may enjoy more pay equity because health systems have a harder time filling these positions.

On the other hand, the gap for specialists rose from 27% in 2022 to 31% in 2023. Differences in how aggressively women and men negotiate compensation packages may play a role, said Hingle.

“Taking negotiation out of the equation would be progress to me,” said Hingle.

Pay disparity did not appear to be the result of time spent on the job — female doctors reported an average of 49 work hours per week, whereas their male counterparts reported 50 work hours per week.

Meanwhile, the pay gap progressively worsened over time. Among doctors aged 28-34 years, men earned an average of $53,000 more than women. By ages 46-49, men earned an average of $157,000 more than women.

“I had to take my employer to court to get equal compensation, sad as it is to say,” said a hospitalist in North Carolina.

Nearly 60% of women surveyed felt they were not being paid fairly for their efforts, up from less than half reported in Medscape’s 2021 report. Hingle said that this figure may not only reflect sentiments about the compensation gap, but also less support on the job, including fewer physician assistants (PAs), nurses, and administrative staff.

“At my job, I do the work of multiple people,” said a survey respondent. “Junior resident, senior resident, social worker, nurse practitioner, PA — as well as try to be a teacher, researcher, [and] an excellent doctor and have the time to make patients feel as if they are not in a rush.”

Roughly 30% of women physicians said they would not choose to go into medicine again if given the chance compared with 26% of male physicians.

“Gender inequities in our profession have a direct impact,” said Shikha Jain, MD, an oncologist in Chicago and founder of the Women in Medicine nonprofit. “I think women in general don’t feel valued in the care they’re providing.” 

Jain cited bullying, harassment, and fewer opportunities for leadership and recognition as factors beyond pay that affect female physicians’ feelings of being valued.

A version of this article first appeared on Medscape.com.

Despite some recent progress in compensation equity, women in medicine continue to be paid significantly lower salaries than men.

According to the Female Compensation Report 2024 by Medscape, male doctors of any kind earned an average salary of about $400,000, whereas female doctors earned approximately $309,000 — a 29% gap.

The report analyzed survey data from 7000 practicing physicians who were recruited over a 4-month period starting in October 2023. The respondents comprised roughly 60% women representing over 29 specialties.

In the 2022 report, the pay gap between the genders was 32%. But some women in the field argued substantial headway is still needed.

“You can try and pick apart the data, but I’d say we’re not really making progress,” said Susan T. Hingle, MD, an internist in Illinois and president of the American Medical Women’s Association. “A decline by a couple of percentage points is not significantly addressing this pay gap that over a lifetime is huge, can be millions of dollars.”

The gender gap was narrower among female primary care physicians (PCPs) vs medical specialists. Female PCPs earned around $253,000 per year, whereas male PCPs earned about $295,000 per year. Hingle suggested that female PCPs may enjoy more pay equity because health systems have a harder time filling these positions.

On the other hand, the gap for specialists rose from 27% in 2022 to 31% in 2023. Differences in how aggressively women and men negotiate compensation packages may play a role, said Hingle.

“Taking negotiation out of the equation would be progress to me,” said Hingle.

Pay disparity did not appear to be the result of time spent on the job — female doctors reported an average of 49 work hours per week, whereas their male counterparts reported 50 work hours per week.

Meanwhile, the pay gap progressively worsened over time. Among doctors aged 28-34 years, men earned an average of $53,000 more than women. By ages 46-49, men earned an average of $157,000 more than women.

“I had to take my employer to court to get equal compensation, sad as it is to say,” said a hospitalist in North Carolina.

Nearly 60% of women surveyed felt they were not being paid fairly for their efforts, up from less than half reported in Medscape’s 2021 report. Hingle said that this figure may not only reflect sentiments about the compensation gap, but also less support on the job, including fewer physician assistants (PAs), nurses, and administrative staff.

“At my job, I do the work of multiple people,” said a survey respondent. “Junior resident, senior resident, social worker, nurse practitioner, PA — as well as try to be a teacher, researcher, [and] an excellent doctor and have the time to make patients feel as if they are not in a rush.”

Roughly 30% of women physicians said they would not choose to go into medicine again if given the chance compared with 26% of male physicians.

“Gender inequities in our profession have a direct impact,” said Shikha Jain, MD, an oncologist in Chicago and founder of the Women in Medicine nonprofit. “I think women in general don’t feel valued in the care they’re providing.” 

Jain cited bullying, harassment, and fewer opportunities for leadership and recognition as factors beyond pay that affect female physicians’ feelings of being valued.

A version of this article first appeared on Medscape.com.

Despite some recent progress in compensation equity, women in medicine continue to be paid significantly lower salaries than men.

According to the Female Compensation Report 2024 by Medscape, male doctors of any kind earned an average salary of about $400,000, whereas female doctors earned approximately $309,000 — a 29% gap.

The report analyzed survey data from 7000 practicing physicians who were recruited over a 4-month period starting in October 2023. The respondents comprised roughly 60% women representing over 29 specialties.

In the 2022 report, the pay gap between the genders was 32%. But some women in the field argued substantial headway is still needed.

“You can try and pick apart the data, but I’d say we’re not really making progress,” said Susan T. Hingle, MD, an internist in Illinois and president of the American Medical Women’s Association. “A decline by a couple of percentage points is not significantly addressing this pay gap that over a lifetime is huge, can be millions of dollars.”

The gender gap was narrower among female primary care physicians (PCPs) vs medical specialists. Female PCPs earned around $253,000 per year, whereas male PCPs earned about $295,000 per year. Hingle suggested that female PCPs may enjoy more pay equity because health systems have a harder time filling these positions.

On the other hand, the gap for specialists rose from 27% in 2022 to 31% in 2023. Differences in how aggressively women and men negotiate compensation packages may play a role, said Hingle.

“Taking negotiation out of the equation would be progress to me,” said Hingle.

Pay disparity did not appear to be the result of time spent on the job — female doctors reported an average of 49 work hours per week, whereas their male counterparts reported 50 work hours per week.

Meanwhile, the pay gap progressively worsened over time. Among doctors aged 28-34 years, men earned an average of $53,000 more than women. By ages 46-49, men earned an average of $157,000 more than women.

“I had to take my employer to court to get equal compensation, sad as it is to say,” said a hospitalist in North Carolina.

Nearly 60% of women surveyed felt they were not being paid fairly for their efforts, up from less than half reported in Medscape’s 2021 report. Hingle said that this figure may not only reflect sentiments about the compensation gap, but also less support on the job, including fewer physician assistants (PAs), nurses, and administrative staff.

“At my job, I do the work of multiple people,” said a survey respondent. “Junior resident, senior resident, social worker, nurse practitioner, PA — as well as try to be a teacher, researcher, [and] an excellent doctor and have the time to make patients feel as if they are not in a rush.”

Roughly 30% of women physicians said they would not choose to go into medicine again if given the chance compared with 26% of male physicians.

“Gender inequities in our profession have a direct impact,” said Shikha Jain, MD, an oncologist in Chicago and founder of the Women in Medicine nonprofit. “I think women in general don’t feel valued in the care they’re providing.” 

Jain cited bullying, harassment, and fewer opportunities for leadership and recognition as factors beyond pay that affect female physicians’ feelings of being valued.

A version of this article first appeared on Medscape.com.

TOPLINE:

Children of mothers who had obesity or eating disorders before or during pregnancy may face higher risks for neurodevelopmental and psychiatric disorders.

METHODOLOGY:

• Researchers conducted a population-based cohort study to investigate the association of maternal eating disorders and high prepregnancy body mass index (BMI) with psychiatric disorder and neurodevelopmental diagnoses in offspring.
• They used Finnish national registers to assess all live births from 2004 through 2014, with follow-up until 2021.
• Data of 392,098 mothers (mean age, 30.15 years) and 649,956 offspring (48.86% girls) were included.
• Maternal eating disorders and prepregnancy BMI were the main exposures, with 1.60% of mothers having a history of eating disorders; 5.89% were underweight and 53.13% had obesity.
• Diagnoses of children were identified and grouped by ICD-10 codes of mental, behavioral, and neurodevelopmental disorders, mood disorders, anxiety disorders, sleep disorders, attention-deficit/hyperactivity disorder, and conduct disorders, among several others.

TAKEAWAY:

• From birth until 7-17 years of age, 16.43% of offspring were diagnosed with a neurodevelopmental or psychiatric disorder.
• Maternal eating disorders were associated with psychiatric disorders in the offspring, with the largest effect sizes observed for sleep disorders (hazard ratio [HR], 2.36) and social functioning and tic disorders (HR, 2.18; P < .001 for both).
• The offspring of mothers with severe prepregnancy obesity had a more than twofold increased risk for intellectual disabilities (HR, 2.04; 95% CI, 1.83-2.28); being underweight before pregnancy was also linked to many psychiatric disorders in offspring.
• The occurrence of adverse birth outcomes along with maternal eating disorders or high BMI further increased the risk for neurodevelopmental and psychiatric disorders in the offspring.

IN PRACTICE:

“The findings underline the risk of offspring mental illness associated with maternal eating disorders and prepregnancy BMI and suggest the need to consider these exposures clinically to help prevent offspring mental illness,” the authors wrote.

SOURCE:

This study was led by Ida A.K. Nilsson, PhD, of the Department of Molecular Medicine and Surgery at the Karolinska Institutet in Stockholm, Sweden, and was published online in JAMA Network Open.

LIMITATIONS:

A limitation of the study was the relatively short follow-up time, which restricted the inclusion of late-onset psychiatric disorder diagnoses, such as schizophrenia spectrum disorders. Paternal data and genetic information, which may have influenced the interpretation of the data, were not available. Another potential bias was that mothers with eating disorders may have been more perceptive to their child’s eating behavior, leading to greater access to care and diagnosis for these children.

DISCLOSURES:

This work was supported by the Swedish Research Council, the regional agreement on medical training and clinical research between Region Stockholm and the Karolinska Institutet, the Swedish Brain Foundation, and other sources. The authors declared no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Children of mothers who had obesity or eating disorders before or during pregnancy may face higher risks for neurodevelopmental and psychiatric disorders.

METHODOLOGY:

• Researchers conducted a population-based cohort study to investigate the association of maternal eating disorders and high prepregnancy body mass index (BMI) with psychiatric disorder and neurodevelopmental diagnoses in offspring.
• They used Finnish national registers to assess all live births from 2004 through 2014, with follow-up until 2021.
• Data of 392,098 mothers (mean age, 30.15 years) and 649,956 offspring (48.86% girls) were included.
• Maternal eating disorders and prepregnancy BMI were the main exposures, with 1.60% of mothers having a history of eating disorders; 5.89% were underweight and 53.13% had obesity.
• Diagnoses of children were identified and grouped by ICD-10 codes of mental, behavioral, and neurodevelopmental disorders, mood disorders, anxiety disorders, sleep disorders, attention-deficit/hyperactivity disorder, and conduct disorders, among several others.

TAKEAWAY:

• From birth until 7-17 years of age, 16.43% of offspring were diagnosed with a neurodevelopmental or psychiatric disorder.
• Maternal eating disorders were associated with psychiatric disorders in the offspring, with the largest effect sizes observed for sleep disorders (hazard ratio [HR], 2.36) and social functioning and tic disorders (HR, 2.18; P < .001 for both).
• The offspring of mothers with severe prepregnancy obesity had a more than twofold increased risk for intellectual disabilities (HR, 2.04; 95% CI, 1.83-2.28); being underweight before pregnancy was also linked to many psychiatric disorders in offspring.
• The occurrence of adverse birth outcomes along with maternal eating disorders or high BMI further increased the risk for neurodevelopmental and psychiatric disorders in the offspring.

IN PRACTICE:

“The findings underline the risk of offspring mental illness associated with maternal eating disorders and prepregnancy BMI and suggest the need to consider these exposures clinically to help prevent offspring mental illness,” the authors wrote.

SOURCE:

This study was led by Ida A.K. Nilsson, PhD, of the Department of Molecular Medicine and Surgery at the Karolinska Institutet in Stockholm, Sweden, and was published online in JAMA Network Open.

LIMITATIONS:

A limitation of the study was the relatively short follow-up time, which restricted the inclusion of late-onset psychiatric disorder diagnoses, such as schizophrenia spectrum disorders. Paternal data and genetic information, which may have influenced the interpretation of the data, were not available. Another potential bias was that mothers with eating disorders may have been more perceptive to their child’s eating behavior, leading to greater access to care and diagnosis for these children.

DISCLOSURES:

This work was supported by the Swedish Research Council, the regional agreement on medical training and clinical research between Region Stockholm and the Karolinska Institutet, the Swedish Brain Foundation, and other sources. The authors declared no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Children of mothers who had obesity or eating disorders before or during pregnancy may face higher risks for neurodevelopmental and psychiatric disorders.

METHODOLOGY:

• Researchers conducted a population-based cohort study to investigate the association of maternal eating disorders and high prepregnancy body mass index (BMI) with psychiatric disorder and neurodevelopmental diagnoses in offspring.
• They used Finnish national registers to assess all live births from 2004 through 2014, with follow-up until 2021.
• Data of 392,098 mothers (mean age, 30.15 years) and 649,956 offspring (48.86% girls) were included.
• Maternal eating disorders and prepregnancy BMI were the main exposures, with 1.60% of mothers having a history of eating disorders; 5.89% were underweight and 53.13% had obesity.
• Diagnoses of children were identified and grouped by ICD-10 codes of mental, behavioral, and neurodevelopmental disorders, mood disorders, anxiety disorders, sleep disorders, attention-deficit/hyperactivity disorder, and conduct disorders, among several others.

TAKEAWAY:

• From birth until 7-17 years of age, 16.43% of offspring were diagnosed with a neurodevelopmental or psychiatric disorder.
• Maternal eating disorders were associated with psychiatric disorders in the offspring, with the largest effect sizes observed for sleep disorders (hazard ratio [HR], 2.36) and social functioning and tic disorders (HR, 2.18; P < .001 for both).
• The offspring of mothers with severe prepregnancy obesity had a more than twofold increased risk for intellectual disabilities (HR, 2.04; 95% CI, 1.83-2.28); being underweight before pregnancy was also linked to many psychiatric disorders in offspring.
• The occurrence of adverse birth outcomes along with maternal eating disorders or high BMI further increased the risk for neurodevelopmental and psychiatric disorders in the offspring.

IN PRACTICE:

“The findings underline the risk of offspring mental illness associated with maternal eating disorders and prepregnancy BMI and suggest the need to consider these exposures clinically to help prevent offspring mental illness,” the authors wrote.

SOURCE:

This study was led by Ida A.K. Nilsson, PhD, of the Department of Molecular Medicine and Surgery at the Karolinska Institutet in Stockholm, Sweden, and was published online in JAMA Network Open.

LIMITATIONS:

A limitation of the study was the relatively short follow-up time, which restricted the inclusion of late-onset psychiatric disorder diagnoses, such as schizophrenia spectrum disorders. Paternal data and genetic information, which may have influenced the interpretation of the data, were not available. Another potential bias was that mothers with eating disorders may have been more perceptive to their child’s eating behavior, leading to greater access to care and diagnosis for these children.

DISCLOSURES:

This work was supported by the Swedish Research Council, the regional agreement on medical training and clinical research between Region Stockholm and the Karolinska Institutet, the Swedish Brain Foundation, and other sources. The authors declared no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

When she was 5 years old, Katherine Edson, LCSW, tried to end her life by drowning herself. “I was enduring severe physical and sexual abuse, and it had become unbearable,” she said. “I waded into a lake, knowing there was a point when it would become too deep and I’d go under.”

As she was walking toward the deeper water, it occurred to her that if she died, she wouldn’t be able to eat Rice Krispies again. “I thought, ‘no more Snap, Crackle, and Pop’ — the three little mascots on the cereal box — and I felt sad,” said Edson, a New York–based retired therapist. “But I still kept walking.”

A man on the shore saw her disappear under the water and pulled her out. “I remember vomiting a lot of water and I remember that the man had tattoos, but I don’t remember how I felt to be alive. I was just numb.”

Edson thinks there were clues her pediatrician missed. “We lived in a small Southern town. Everyone knew my parents were alcoholics. I was very dissociated and withdrawn in general and during pediatric visits. My affect broadcasted that something was wrong, but no one asked if I was okay.”

She acknowledged that professionals in those days “weren’t tuned in to mental health issues in kids. At least there’s more awareness today and hopefully more training — especially since it seems like more kids are trying to end their lives today than when I was growing up.”
 

Alarming Statistics

According to the American Academy of Pediatrics (AAP), suicide is the second leading cause of death for people aged 10-24 years. Data from Children’s Hospital Association’s Pediatric Health Information System revealed that suicide attempts, ideation, and self-injury have become the most common mental health conditions seen in the emergency departments (EDs) of children’s hospitals, with a 166% increase in ED visits for suicide attempts in children aged 5-18 years, between 2016 and 2022.

Psychiatrist Helen Egger, MD, chief medical officer and co-founder of Little Otter, a specialty pediatric and whole family digital mental health company, recently coauthored a report analyzing data on 1434 children who completed a screening session and comprehensive diagnostic assessment at Little Otter from May 2023 to February 2024 (n = 1016 children aged 8-14 years and n = 418 aged 3-7 years).

Little Otter

Points of Contact

“It’s known that most children who die by suicide had a recent visit with a health professional — a pediatrician or child mental health professional. It’s unlikely that the child was fine and then, a few weeks later, stopped being fine. The likelihood is that the child wasn’t fine during that visit, but the clinician didn’t ask about mental health,” Egger said.

Christine Crawford, MD, MPH, associate medical director of the National Alliance on Mental Illness (NAMI), said that awareness of pediatric and adolescent suicidality is relevant to all physicians who treat children. “When you’re working with kids, anything can come up. Be prepared to navigate the conversation. You can never predict who the patient will feel most comfortable disclosing these thoughts to.”

NAMI

Don’t Be Afraid to Ask

According to the AAP, all children aged 12 years or older should be screened for suicidal risk, and children aged 8-11 years should be screened “when clinically indicated.” AAP also recommends annual screening for depression in children aged 12 years or older. However, Egger thinks that screening for depression should start sooner.

Katherine Kay Greydanus

It can be tempting to screen by merely giving a youngster a form to fill out in the waiting room, but Greydanus strongly advises against this approach. “The important thing is having rapport with the child, being in the same room together. You can ask some simple questions. ‘How are you doing? How are things at school? How are things with your family?’”

“When you’re screening for depression and have a kid who’s talking about sadness or low mood for more than 2 weeks and endorsing other symptoms, such as problems with sleep or appetite, difficulty concentrating, anhedonia, losing interest in things they’d usually enjoy, feeling they’re a burden to others, hopelessness about the future, being unable to function the way they used to — that person meets criteria for depression and you should have a high suspicion and concern about potential suicide,” said Crawford, assistant professor of psychiatry, Boston University School of Medicine.

She suggested probing further and being direct. “It sounds like you’ve been having a tough time. You talk about being sad. I wonder if you’re feeling so sad that you might not want to be alive anymore.” Some healthcare providers “tiptoe around when it comes to suicide, but it’s better to be direct and communicate the question in simple, plain language: ‘Have you ever had thoughts about hurting or killing yourself, that life is no longer worth living, or life would be easier for your family if you weren’t alive?’”

It’s a common myth that asking about depression or suicidality will “plant a seed” or “put ideas in people’s heads,” potentially leading to suicidality. “What we know to be true is that asking about suicide doesn’t put lives at risk. In fact, the contrary is true,” according to Crawford. Several studies have refuted this myth.

Two screening tools that might be helpful in ascertaining the presence of depression and suicidality are the PHQ-9 modified for Adolescents and the four-question Ask Suicide-Screening Questions.
 

Probe for More Details

If a child or adolescent affirms suicidal ideation, it’s important to ask if they have a plan, Crawford advised. “If they say, ‘yes,’ don’t run out of the office or shut down the conversation by picking up the phone and calling the closest child psychiatrist. We want kids to open up as much as possible when they’ve already opened up a little. So continue the conversation.”

If a child has a plan, the risk for following through on that plan is “high,” Crawford emphasized. “You want the maximum amount of information at your fingertips because this will equip you to navigate the next step in getting the child help.”

The suicide plan may not be realistic and, if carried out, might not actually end in death, especially in younger children. “A 6-year-old might say, ‘I’m gonna drink a whole bottle of apple juice and my belly will explode.’ Or ‘I’ll take 10 extra vitamins.’ The objective lethality of the plan doesn’t matter in that moment. What matters is that the child believes it’s going to work, and it provides a window into how depressed that child is.”

Greydanus added that it’s important to understand what might be going on in the child’s life. Could there be abuse in the family? Is the child being bullied? Bullying can take place at school or online, he noted. The overall risk for suicidal thoughts is elevated for youth who are involved in bullying, whether they’re the bully or the one being bullied.

Kirk Smalley, president and co-founder of Stand for the Silent, an organization designed to bring awareness about the devastating effects of bullying, agreed that pediatricians a should ask children if they’re being bullied. “Sometimes, kids will open up to someone who isn’t a parent or a teacher, who might be seen as ‘too close’ to the situation,” Smalley said.

“Let them know you’re a trusted adult they can confide in and you’re willing to help them navigate this — and then follow through,” advised Smalley, whose 11-year-old son died by suicide after being subjected to bullying.
 

Painting a Complete Picture

Crawford advises clinicians to “look at the whole picture and piece it together.”

For example, “if the child is functioning, going to school, maintaining relationships with other people, and not experiencing symptoms of depression but discloses the desire to kill him/herself, understand the context.” Sometimes, adolescents can be impulsive. Decision-making “can be driven by emotion.” The teen may have experienced emotional distress, such as “conflict with a peer, arguments with a parent, or romantic heartbreak. She might say, ‘I’m going to kill myself if I ever see him holding hands with another girl.’”

In the setting of an acute stressor, such as a breakup, the child might not need a higher level of care such as hospitalization. “But for non-psychiatry providers, it’s unclear if the child might act on it, so it’s important to have the child evaluated; talk to collateral supports, such as parents, teachers, or a therapist if they have one; and see what makes sense for that specific child.”

She also recommended “getting a sense if the kid is future-oriented in thinking. If they’re talking about an upcoming concert this weekend, or wanting to get to basketball practice, that’s reassuring. It suggests the likelihood of following through [on suicide] is low.”

And assess coping strategies. “You can say, ‘I see you’re really going through a lot. I worry that these thoughts will come up in school. What do you think you’d do in the moment if these thoughts come up?’ If there’s a coping strategy — for example, ‘I’d talk to my friend during lunch’ — that’s also reassuring,” Crawford said.

Of course, that doesn’t mean the statement should be ignored or dismissed. Rather, it informs the next preventive steps and how intensive the level of care should be.
 

Next Steps: Involving the Family, Getting Help

It’s particularly concerning if the child is unable to identify strategies other than suicide, said Crawford. “You can say, ‘I’m concerned because it’s highly likely that you’ll run into this guy and I wouldn’t want you to die. You have so much to live for.’”

Then, you can ask if it’s okay to bring in the parent or caregiver to talk about what the child just revealed. “If the kid says no — especially a teen — you can respond, ‘I hear what you’re saying, but I actually do have to bring your parent in because of your safety and we can discuss together how to keep you safe.’”

In advance, Crawford tells the patient what she plans to share with the parent. “That way, we’re on the same page and the kid has a sense of agency about how the conversation with the parent will go.” If the teen doesn’t want certain information revealed, “you can ask, ‘What would you leave out, and why?’ This lends itself to a helpful conversation about what the child is thinking about.”

Once the provider has received the green light, it’s time to bring the parent into the room. “Especially in the primary care or pediatric setting, the parent is often shocked, worried, and caught off-guard,” Crawford said.

“You can start by thanking the patient for being open and honest. Then you can tell the parent, ‘Your daughter shared she’s been having some difficult emotions and experiences, and she’s thought of ending her life because she doesn’t know how to cope. I wanted to talk to you about this because it’s important to look at resources we can connect her to and effective coping strategies.’”

Further interventions can include referring the patient to a child psychiatrist or therapist, or both. “Have a list of referrals readily available,” Greydanus advised. If you suspect or if the child reveals abuse, you’re a mandated reporter and need to inform Child Protective Services (CPS). “But don’t stop there,” he warned. “Make sure the child is indeed getting help through CPS and appropriate intervention has been taken regarding the abuse and potential suicide attempt.” Or you may send the child to the ED, where ED physicians are “trained in what to do if they suspect abuse. But make sure that when you ‘throw the ball,’ there’s someone who can ‘catch’ it and accept responsibility for the child’s safety.”

Crawford noted that many primary care settings — especially in under-resourced areas — lack child psychiatrists or therapists. “You need to know what’s feasible in the community you’re practicing in,” she advised. “Be aware of the local crisis line — 988 — and mental health resources in the school and community. There are often school psychologists, social workers, or counselors who can become involved.”

Greydanus emphasized that it’s critical to assess for the presence of firearms in the home and address it with the parents. “If a child is sad or angry and gets impulsive, it’s amazingly common for them to get their hands in a firearm and use it.”

As previously reported, pediatricians and other healthcare providers have a valuable role to play in screening parents for firearm ownership and offering counseling on safe storage practices, according to research presented on September 28 at the AAP 2024 National Conference.
 

Sometimes, Even the Best Efforts Aren’t Successful

“Suicide is complicated, and parents or doctors can take all the ‘right’ steps to get counseling for the child — hospitalization, medication, and support — and children might still take their lives,” said Ronnie Susan Walker, MS, LCPC, founder and executive director of Alliance of Hope for Suicide Loss Survivors. The organization was launched as a “postvention campaign” 7 years ago to provide support to survivors of suicide loss, who are themselves a high-risk population for suicide.

Walker alluded to the concept of a “ suicide trance” — a term coined by Richard Heckler, PhD, in his book Waking Up, Alive. This trance “is a state of mind and body that receives only the kind of input that reinforces the pain and corroborates the person’s conviction that the only way out is through death,” Heckler wrote.

Walker, whose stepson died by suicide, said physicians and other healthcare professionals who have lost a patient to suicide “should focus on postvention — finding support from other professionals and managing their own grief and guilt.”

It’s natural to feel guilt and second-guess yourself, Greydanus said. “You question whether you missed something or could have done more, so acknowledge that even with the best care and intentions, some suicides aren’t preventable,” he said.

Walker recommends reaching out to the family. “When I lost my stepson, his doctor came to the funeral and wrote us a very meaningful note. That meant so much to us.”

Greydanus agreed it’s appropriate for the clinician to offer comfort to the family “if he or she feels it necessary or feels moved to do so.” However, he cautioned, there’s “often a fear of malpractice charges that may interfere in certain cases.”

Egger added that records should always be “very detailed,” with clear documentation of how you interacted with the child and the rationale behind your interventions. “I’m not a legal expert, but I would always err on the side of connecting with family and sharing grief and compassion. My experience with physician-patient relationships is that the more connected, transparent, and empathetic they are, the better the outcome will be for everyone.”

Losing a patient to suicide is traumatic, so give yourself time to grieve, Egger advised. “Unfortunately, this is an experience that almost everyone in the field will likely go through at some point. Reach out for professional counseling or peer support.”

Physicians who have lost a patient to suicide may turn to an online forum, the Coalition of Clinician Survivors, designed to create a safe anonymous space for discussion, education, testimonials, and one-on-one support.

Greydanus emphasized that the most important role in working with suicidal youngsters is to provide hope. “Yes, you can’t help everyone, but you can help most of them. That’s why you’re there.”

Greydanus, Crawford, Egger, Edson, Smalley, and Walker reported no financial conflicts of interest.
 

A version of this article appeared on Medscape.com.

When she was 5 years old, Katherine Edson, LCSW, tried to end her life by drowning herself. “I was enduring severe physical and sexual abuse, and it had become unbearable,” she said. “I waded into a lake, knowing there was a point when it would become too deep and I’d go under.”

As she was walking toward the deeper water, it occurred to her that if she died, she wouldn’t be able to eat Rice Krispies again. “I thought, ‘no more Snap, Crackle, and Pop’ — the three little mascots on the cereal box — and I felt sad,” said Edson, a New York–based retired therapist. “But I still kept walking.”

A man on the shore saw her disappear under the water and pulled her out. “I remember vomiting a lot of water and I remember that the man had tattoos, but I don’t remember how I felt to be alive. I was just numb.”

Edson thinks there were clues her pediatrician missed. “We lived in a small Southern town. Everyone knew my parents were alcoholics. I was very dissociated and withdrawn in general and during pediatric visits. My affect broadcasted that something was wrong, but no one asked if I was okay.”

She acknowledged that professionals in those days “weren’t tuned in to mental health issues in kids. At least there’s more awareness today and hopefully more training — especially since it seems like more kids are trying to end their lives today than when I was growing up.”
 

Alarming Statistics

According to the American Academy of Pediatrics (AAP), suicide is the second leading cause of death for people aged 10-24 years. Data from Children’s Hospital Association’s Pediatric Health Information System revealed that suicide attempts, ideation, and self-injury have become the most common mental health conditions seen in the emergency departments (EDs) of children’s hospitals, with a 166% increase in ED visits for suicide attempts in children aged 5-18 years, between 2016 and 2022.

Psychiatrist Helen Egger, MD, chief medical officer and co-founder of Little Otter, a specialty pediatric and whole family digital mental health company, recently coauthored a report analyzing data on 1434 children who completed a screening session and comprehensive diagnostic assessment at Little Otter from May 2023 to February 2024 (n = 1016 children aged 8-14 years and n = 418 aged 3-7 years).

Little Otter

Points of Contact

“It’s known that most children who die by suicide had a recent visit with a health professional — a pediatrician or child mental health professional. It’s unlikely that the child was fine and then, a few weeks later, stopped being fine. The likelihood is that the child wasn’t fine during that visit, but the clinician didn’t ask about mental health,” Egger said.

Christine Crawford, MD, MPH, associate medical director of the National Alliance on Mental Illness (NAMI), said that awareness of pediatric and adolescent suicidality is relevant to all physicians who treat children. “When you’re working with kids, anything can come up. Be prepared to navigate the conversation. You can never predict who the patient will feel most comfortable disclosing these thoughts to.”

NAMI

Don’t Be Afraid to Ask

According to the AAP, all children aged 12 years or older should be screened for suicidal risk, and children aged 8-11 years should be screened “when clinically indicated.” AAP also recommends annual screening for depression in children aged 12 years or older. However, Egger thinks that screening for depression should start sooner.

Katherine Kay Greydanus

It can be tempting to screen by merely giving a youngster a form to fill out in the waiting room, but Greydanus strongly advises against this approach. “The important thing is having rapport with the child, being in the same room together. You can ask some simple questions. ‘How are you doing? How are things at school? How are things with your family?’”

“When you’re screening for depression and have a kid who’s talking about sadness or low mood for more than 2 weeks and endorsing other symptoms, such as problems with sleep or appetite, difficulty concentrating, anhedonia, losing interest in things they’d usually enjoy, feeling they’re a burden to others, hopelessness about the future, being unable to function the way they used to — that person meets criteria for depression and you should have a high suspicion and concern about potential suicide,” said Crawford, assistant professor of psychiatry, Boston University School of Medicine.

She suggested probing further and being direct. “It sounds like you’ve been having a tough time. You talk about being sad. I wonder if you’re feeling so sad that you might not want to be alive anymore.” Some healthcare providers “tiptoe around when it comes to suicide, but it’s better to be direct and communicate the question in simple, plain language: ‘Have you ever had thoughts about hurting or killing yourself, that life is no longer worth living, or life would be easier for your family if you weren’t alive?’”

It’s a common myth that asking about depression or suicidality will “plant a seed” or “put ideas in people’s heads,” potentially leading to suicidality. “What we know to be true is that asking about suicide doesn’t put lives at risk. In fact, the contrary is true,” according to Crawford. Several studies have refuted this myth.

Two screening tools that might be helpful in ascertaining the presence of depression and suicidality are the PHQ-9 modified for Adolescents and the four-question Ask Suicide-Screening Questions.
 

Probe for More Details

If a child or adolescent affirms suicidal ideation, it’s important to ask if they have a plan, Crawford advised. “If they say, ‘yes,’ don’t run out of the office or shut down the conversation by picking up the phone and calling the closest child psychiatrist. We want kids to open up as much as possible when they’ve already opened up a little. So continue the conversation.”

If a child has a plan, the risk for following through on that plan is “high,” Crawford emphasized. “You want the maximum amount of information at your fingertips because this will equip you to navigate the next step in getting the child help.”

The suicide plan may not be realistic and, if carried out, might not actually end in death, especially in younger children. “A 6-year-old might say, ‘I’m gonna drink a whole bottle of apple juice and my belly will explode.’ Or ‘I’ll take 10 extra vitamins.’ The objective lethality of the plan doesn’t matter in that moment. What matters is that the child believes it’s going to work, and it provides a window into how depressed that child is.”

Greydanus added that it’s important to understand what might be going on in the child’s life. Could there be abuse in the family? Is the child being bullied? Bullying can take place at school or online, he noted. The overall risk for suicidal thoughts is elevated for youth who are involved in bullying, whether they’re the bully or the one being bullied.

Kirk Smalley, president and co-founder of Stand for the Silent, an organization designed to bring awareness about the devastating effects of bullying, agreed that pediatricians a should ask children if they’re being bullied. “Sometimes, kids will open up to someone who isn’t a parent or a teacher, who might be seen as ‘too close’ to the situation,” Smalley said.

“Let them know you’re a trusted adult they can confide in and you’re willing to help them navigate this — and then follow through,” advised Smalley, whose 11-year-old son died by suicide after being subjected to bullying.
 

Painting a Complete Picture

Crawford advises clinicians to “look at the whole picture and piece it together.”

For example, “if the child is functioning, going to school, maintaining relationships with other people, and not experiencing symptoms of depression but discloses the desire to kill him/herself, understand the context.” Sometimes, adolescents can be impulsive. Decision-making “can be driven by emotion.” The teen may have experienced emotional distress, such as “conflict with a peer, arguments with a parent, or romantic heartbreak. She might say, ‘I’m going to kill myself if I ever see him holding hands with another girl.’”

In the setting of an acute stressor, such as a breakup, the child might not need a higher level of care such as hospitalization. “But for non-psychiatry providers, it’s unclear if the child might act on it, so it’s important to have the child evaluated; talk to collateral supports, such as parents, teachers, or a therapist if they have one; and see what makes sense for that specific child.”

She also recommended “getting a sense if the kid is future-oriented in thinking. If they’re talking about an upcoming concert this weekend, or wanting to get to basketball practice, that’s reassuring. It suggests the likelihood of following through [on suicide] is low.”

And assess coping strategies. “You can say, ‘I see you’re really going through a lot. I worry that these thoughts will come up in school. What do you think you’d do in the moment if these thoughts come up?’ If there’s a coping strategy — for example, ‘I’d talk to my friend during lunch’ — that’s also reassuring,” Crawford said.

Of course, that doesn’t mean the statement should be ignored or dismissed. Rather, it informs the next preventive steps and how intensive the level of care should be.
 

Next Steps: Involving the Family, Getting Help

It’s particularly concerning if the child is unable to identify strategies other than suicide, said Crawford. “You can say, ‘I’m concerned because it’s highly likely that you’ll run into this guy and I wouldn’t want you to die. You have so much to live for.’”

Then, you can ask if it’s okay to bring in the parent or caregiver to talk about what the child just revealed. “If the kid says no — especially a teen — you can respond, ‘I hear what you’re saying, but I actually do have to bring your parent in because of your safety and we can discuss together how to keep you safe.’”

In advance, Crawford tells the patient what she plans to share with the parent. “That way, we’re on the same page and the kid has a sense of agency about how the conversation with the parent will go.” If the teen doesn’t want certain information revealed, “you can ask, ‘What would you leave out, and why?’ This lends itself to a helpful conversation about what the child is thinking about.”

Once the provider has received the green light, it’s time to bring the parent into the room. “Especially in the primary care or pediatric setting, the parent is often shocked, worried, and caught off-guard,” Crawford said.

“You can start by thanking the patient for being open and honest. Then you can tell the parent, ‘Your daughter shared she’s been having some difficult emotions and experiences, and she’s thought of ending her life because she doesn’t know how to cope. I wanted to talk to you about this because it’s important to look at resources we can connect her to and effective coping strategies.’”

Further interventions can include referring the patient to a child psychiatrist or therapist, or both. “Have a list of referrals readily available,” Greydanus advised. If you suspect or if the child reveals abuse, you’re a mandated reporter and need to inform Child Protective Services (CPS). “But don’t stop there,” he warned. “Make sure the child is indeed getting help through CPS and appropriate intervention has been taken regarding the abuse and potential suicide attempt.” Or you may send the child to the ED, where ED physicians are “trained in what to do if they suspect abuse. But make sure that when you ‘throw the ball,’ there’s someone who can ‘catch’ it and accept responsibility for the child’s safety.”

Crawford noted that many primary care settings — especially in under-resourced areas — lack child psychiatrists or therapists. “You need to know what’s feasible in the community you’re practicing in,” she advised. “Be aware of the local crisis line — 988 — and mental health resources in the school and community. There are often school psychologists, social workers, or counselors who can become involved.”

Greydanus emphasized that it’s critical to assess for the presence of firearms in the home and address it with the parents. “If a child is sad or angry and gets impulsive, it’s amazingly common for them to get their hands in a firearm and use it.”

As previously reported, pediatricians and other healthcare providers have a valuable role to play in screening parents for firearm ownership and offering counseling on safe storage practices, according to research presented on September 28 at the AAP 2024 National Conference.
 

Sometimes, Even the Best Efforts Aren’t Successful

“Suicide is complicated, and parents or doctors can take all the ‘right’ steps to get counseling for the child — hospitalization, medication, and support — and children might still take their lives,” said Ronnie Susan Walker, MS, LCPC, founder and executive director of Alliance of Hope for Suicide Loss Survivors. The organization was launched as a “postvention campaign” 7 years ago to provide support to survivors of suicide loss, who are themselves a high-risk population for suicide.

Walker alluded to the concept of a “ suicide trance” — a term coined by Richard Heckler, PhD, in his book Waking Up, Alive. This trance “is a state of mind and body that receives only the kind of input that reinforces the pain and corroborates the person’s conviction that the only way out is through death,” Heckler wrote.

Walker, whose stepson died by suicide, said physicians and other healthcare professionals who have lost a patient to suicide “should focus on postvention — finding support from other professionals and managing their own grief and guilt.”

It’s natural to feel guilt and second-guess yourself, Greydanus said. “You question whether you missed something or could have done more, so acknowledge that even with the best care and intentions, some suicides aren’t preventable,” he said.

Walker recommends reaching out to the family. “When I lost my stepson, his doctor came to the funeral and wrote us a very meaningful note. That meant so much to us.”

Greydanus agreed it’s appropriate for the clinician to offer comfort to the family “if he or she feels it necessary or feels moved to do so.” However, he cautioned, there’s “often a fear of malpractice charges that may interfere in certain cases.”

Egger added that records should always be “very detailed,” with clear documentation of how you interacted with the child and the rationale behind your interventions. “I’m not a legal expert, but I would always err on the side of connecting with family and sharing grief and compassion. My experience with physician-patient relationships is that the more connected, transparent, and empathetic they are, the better the outcome will be for everyone.”

Losing a patient to suicide is traumatic, so give yourself time to grieve, Egger advised. “Unfortunately, this is an experience that almost everyone in the field will likely go through at some point. Reach out for professional counseling or peer support.”

Physicians who have lost a patient to suicide may turn to an online forum, the Coalition of Clinician Survivors, designed to create a safe anonymous space for discussion, education, testimonials, and one-on-one support.

Greydanus emphasized that the most important role in working with suicidal youngsters is to provide hope. “Yes, you can’t help everyone, but you can help most of them. That’s why you’re there.”

Greydanus, Crawford, Egger, Edson, Smalley, and Walker reported no financial conflicts of interest.
 

A version of this article appeared on Medscape.com.

When she was 5 years old, Katherine Edson, LCSW, tried to end her life by drowning herself. “I was enduring severe physical and sexual abuse, and it had become unbearable,” she said. “I waded into a lake, knowing there was a point when it would become too deep and I’d go under.”

As she was walking toward the deeper water, it occurred to her that if she died, she wouldn’t be able to eat Rice Krispies again. “I thought, ‘no more Snap, Crackle, and Pop’ — the three little mascots on the cereal box — and I felt sad,” said Edson, a New York–based retired therapist. “But I still kept walking.”

A man on the shore saw her disappear under the water and pulled her out. “I remember vomiting a lot of water and I remember that the man had tattoos, but I don’t remember how I felt to be alive. I was just numb.”

Edson thinks there were clues her pediatrician missed. “We lived in a small Southern town. Everyone knew my parents were alcoholics. I was very dissociated and withdrawn in general and during pediatric visits. My affect broadcasted that something was wrong, but no one asked if I was okay.”

She acknowledged that professionals in those days “weren’t tuned in to mental health issues in kids. At least there’s more awareness today and hopefully more training — especially since it seems like more kids are trying to end their lives today than when I was growing up.”
 

Alarming Statistics

According to the American Academy of Pediatrics (AAP), suicide is the second leading cause of death for people aged 10-24 years. Data from Children’s Hospital Association’s Pediatric Health Information System revealed that suicide attempts, ideation, and self-injury have become the most common mental health conditions seen in the emergency departments (EDs) of children’s hospitals, with a 166% increase in ED visits for suicide attempts in children aged 5-18 years, between 2016 and 2022.

Psychiatrist Helen Egger, MD, chief medical officer and co-founder of Little Otter, a specialty pediatric and whole family digital mental health company, recently coauthored a report analyzing data on 1434 children who completed a screening session and comprehensive diagnostic assessment at Little Otter from May 2023 to February 2024 (n = 1016 children aged 8-14 years and n = 418 aged 3-7 years).

Little Otter

Points of Contact

“It’s known that most children who die by suicide had a recent visit with a health professional — a pediatrician or child mental health professional. It’s unlikely that the child was fine and then, a few weeks later, stopped being fine. The likelihood is that the child wasn’t fine during that visit, but the clinician didn’t ask about mental health,” Egger said.

Christine Crawford, MD, MPH, associate medical director of the National Alliance on Mental Illness (NAMI), said that awareness of pediatric and adolescent suicidality is relevant to all physicians who treat children. “When you’re working with kids, anything can come up. Be prepared to navigate the conversation. You can never predict who the patient will feel most comfortable disclosing these thoughts to.”

NAMI

Don’t Be Afraid to Ask

According to the AAP, all children aged 12 years or older should be screened for suicidal risk, and children aged 8-11 years should be screened “when clinically indicated.” AAP also recommends annual screening for depression in children aged 12 years or older. However, Egger thinks that screening for depression should start sooner.

Katherine Kay Greydanus

It can be tempting to screen by merely giving a youngster a form to fill out in the waiting room, but Greydanus strongly advises against this approach. “The important thing is having rapport with the child, being in the same room together. You can ask some simple questions. ‘How are you doing? How are things at school? How are things with your family?’”

“When you’re screening for depression and have a kid who’s talking about sadness or low mood for more than 2 weeks and endorsing other symptoms, such as problems with sleep or appetite, difficulty concentrating, anhedonia, losing interest in things they’d usually enjoy, feeling they’re a burden to others, hopelessness about the future, being unable to function the way they used to — that person meets criteria for depression and you should have a high suspicion and concern about potential suicide,” said Crawford, assistant professor of psychiatry, Boston University School of Medicine.

She suggested probing further and being direct. “It sounds like you’ve been having a tough time. You talk about being sad. I wonder if you’re feeling so sad that you might not want to be alive anymore.” Some healthcare providers “tiptoe around when it comes to suicide, but it’s better to be direct and communicate the question in simple, plain language: ‘Have you ever had thoughts about hurting or killing yourself, that life is no longer worth living, or life would be easier for your family if you weren’t alive?’”

It’s a common myth that asking about depression or suicidality will “plant a seed” or “put ideas in people’s heads,” potentially leading to suicidality. “What we know to be true is that asking about suicide doesn’t put lives at risk. In fact, the contrary is true,” according to Crawford. Several studies have refuted this myth.

Two screening tools that might be helpful in ascertaining the presence of depression and suicidality are the PHQ-9 modified for Adolescents and the four-question Ask Suicide-Screening Questions.
 

Probe for More Details

If a child or adolescent affirms suicidal ideation, it’s important to ask if they have a plan, Crawford advised. “If they say, ‘yes,’ don’t run out of the office or shut down the conversation by picking up the phone and calling the closest child psychiatrist. We want kids to open up as much as possible when they’ve already opened up a little. So continue the conversation.”

If a child has a plan, the risk for following through on that plan is “high,” Crawford emphasized. “You want the maximum amount of information at your fingertips because this will equip you to navigate the next step in getting the child help.”

The suicide plan may not be realistic and, if carried out, might not actually end in death, especially in younger children. “A 6-year-old might say, ‘I’m gonna drink a whole bottle of apple juice and my belly will explode.’ Or ‘I’ll take 10 extra vitamins.’ The objective lethality of the plan doesn’t matter in that moment. What matters is that the child believes it’s going to work, and it provides a window into how depressed that child is.”

Greydanus added that it’s important to understand what might be going on in the child’s life. Could there be abuse in the family? Is the child being bullied? Bullying can take place at school or online, he noted. The overall risk for suicidal thoughts is elevated for youth who are involved in bullying, whether they’re the bully or the one being bullied.

Kirk Smalley, president and co-founder of Stand for the Silent, an organization designed to bring awareness about the devastating effects of bullying, agreed that pediatricians a should ask children if they’re being bullied. “Sometimes, kids will open up to someone who isn’t a parent or a teacher, who might be seen as ‘too close’ to the situation,” Smalley said.

“Let them know you’re a trusted adult they can confide in and you’re willing to help them navigate this — and then follow through,” advised Smalley, whose 11-year-old son died by suicide after being subjected to bullying.
 

Painting a Complete Picture

Crawford advises clinicians to “look at the whole picture and piece it together.”

For example, “if the child is functioning, going to school, maintaining relationships with other people, and not experiencing symptoms of depression but discloses the desire to kill him/herself, understand the context.” Sometimes, adolescents can be impulsive. Decision-making “can be driven by emotion.” The teen may have experienced emotional distress, such as “conflict with a peer, arguments with a parent, or romantic heartbreak. She might say, ‘I’m going to kill myself if I ever see him holding hands with another girl.’”

In the setting of an acute stressor, such as a breakup, the child might not need a higher level of care such as hospitalization. “But for non-psychiatry providers, it’s unclear if the child might act on it, so it’s important to have the child evaluated; talk to collateral supports, such as parents, teachers, or a therapist if they have one; and see what makes sense for that specific child.”

She also recommended “getting a sense if the kid is future-oriented in thinking. If they’re talking about an upcoming concert this weekend, or wanting to get to basketball practice, that’s reassuring. It suggests the likelihood of following through [on suicide] is low.”

And assess coping strategies. “You can say, ‘I see you’re really going through a lot. I worry that these thoughts will come up in school. What do you think you’d do in the moment if these thoughts come up?’ If there’s a coping strategy — for example, ‘I’d talk to my friend during lunch’ — that’s also reassuring,” Crawford said.

Of course, that doesn’t mean the statement should be ignored or dismissed. Rather, it informs the next preventive steps and how intensive the level of care should be.
 

Next Steps: Involving the Family, Getting Help

It’s particularly concerning if the child is unable to identify strategies other than suicide, said Crawford. “You can say, ‘I’m concerned because it’s highly likely that you’ll run into this guy and I wouldn’t want you to die. You have so much to live for.’”

Then, you can ask if it’s okay to bring in the parent or caregiver to talk about what the child just revealed. “If the kid says no — especially a teen — you can respond, ‘I hear what you’re saying, but I actually do have to bring your parent in because of your safety and we can discuss together how to keep you safe.’”

In advance, Crawford tells the patient what she plans to share with the parent. “That way, we’re on the same page and the kid has a sense of agency about how the conversation with the parent will go.” If the teen doesn’t want certain information revealed, “you can ask, ‘What would you leave out, and why?’ This lends itself to a helpful conversation about what the child is thinking about.”

Once the provider has received the green light, it’s time to bring the parent into the room. “Especially in the primary care or pediatric setting, the parent is often shocked, worried, and caught off-guard,” Crawford said.

“You can start by thanking the patient for being open and honest. Then you can tell the parent, ‘Your daughter shared she’s been having some difficult emotions and experiences, and she’s thought of ending her life because she doesn’t know how to cope. I wanted to talk to you about this because it’s important to look at resources we can connect her to and effective coping strategies.’”

Further interventions can include referring the patient to a child psychiatrist or therapist, or both. “Have a list of referrals readily available,” Greydanus advised. If you suspect or if the child reveals abuse, you’re a mandated reporter and need to inform Child Protective Services (CPS). “But don’t stop there,” he warned. “Make sure the child is indeed getting help through CPS and appropriate intervention has been taken regarding the abuse and potential suicide attempt.” Or you may send the child to the ED, where ED physicians are “trained in what to do if they suspect abuse. But make sure that when you ‘throw the ball,’ there’s someone who can ‘catch’ it and accept responsibility for the child’s safety.”

Crawford noted that many primary care settings — especially in under-resourced areas — lack child psychiatrists or therapists. “You need to know what’s feasible in the community you’re practicing in,” she advised. “Be aware of the local crisis line — 988 — and mental health resources in the school and community. There are often school psychologists, social workers, or counselors who can become involved.”

Greydanus emphasized that it’s critical to assess for the presence of firearms in the home and address it with the parents. “If a child is sad or angry and gets impulsive, it’s amazingly common for them to get their hands in a firearm and use it.”

As previously reported, pediatricians and other healthcare providers have a valuable role to play in screening parents for firearm ownership and offering counseling on safe storage practices, according to research presented on September 28 at the AAP 2024 National Conference.
 

Sometimes, Even the Best Efforts Aren’t Successful

“Suicide is complicated, and parents or doctors can take all the ‘right’ steps to get counseling for the child — hospitalization, medication, and support — and children might still take their lives,” said Ronnie Susan Walker, MS, LCPC, founder and executive director of Alliance of Hope for Suicide Loss Survivors. The organization was launched as a “postvention campaign” 7 years ago to provide support to survivors of suicide loss, who are themselves a high-risk population for suicide.

Walker alluded to the concept of a “ suicide trance” — a term coined by Richard Heckler, PhD, in his book Waking Up, Alive. This trance “is a state of mind and body that receives only the kind of input that reinforces the pain and corroborates the person’s conviction that the only way out is through death,” Heckler wrote.

Walker, whose stepson died by suicide, said physicians and other healthcare professionals who have lost a patient to suicide “should focus on postvention — finding support from other professionals and managing their own grief and guilt.”

It’s natural to feel guilt and second-guess yourself, Greydanus said. “You question whether you missed something or could have done more, so acknowledge that even with the best care and intentions, some suicides aren’t preventable,” he said.

Walker recommends reaching out to the family. “When I lost my stepson, his doctor came to the funeral and wrote us a very meaningful note. That meant so much to us.”

Greydanus agreed it’s appropriate for the clinician to offer comfort to the family “if he or she feels it necessary or feels moved to do so.” However, he cautioned, there’s “often a fear of malpractice charges that may interfere in certain cases.”

Egger added that records should always be “very detailed,” with clear documentation of how you interacted with the child and the rationale behind your interventions. “I’m not a legal expert, but I would always err on the side of connecting with family and sharing grief and compassion. My experience with physician-patient relationships is that the more connected, transparent, and empathetic they are, the better the outcome will be for everyone.”

Losing a patient to suicide is traumatic, so give yourself time to grieve, Egger advised. “Unfortunately, this is an experience that almost everyone in the field will likely go through at some point. Reach out for professional counseling or peer support.”

Physicians who have lost a patient to suicide may turn to an online forum, the Coalition of Clinician Survivors, designed to create a safe anonymous space for discussion, education, testimonials, and one-on-one support.

Greydanus emphasized that the most important role in working with suicidal youngsters is to provide hope. “Yes, you can’t help everyone, but you can help most of them. That’s why you’re there.”

Greydanus, Crawford, Egger, Edson, Smalley, and Walker reported no financial conflicts of interest.
 

A version of this article appeared on Medscape.com.

Sometime in the last year or 2 I wrote that, despite my considerable reservations, I had finally come to the conclusion that the American Medical Association’s decision to designate obesity as a disease was appropriate. My rationalization was that the disease label would open more opportunities for funding obesity treatments. However, the explosive growth and popularity of glucagon-like peptide 1 (GLP-1) agonists over the last year has had me rethinking my decision to suppress my long-held reservations about the disease designation.

So, if it’s not a disease, then what should we call it? How do we explain its surge in high-income countries that began in the 1980s? While there are still some folks who see obesity as a character flaw, I think you and I as healthcare providers have difficulty explaining the increase prevalence of obesity as either global breakdown of willpower or a widespread genetic shift as the result of burst of radiation from solar flares.

However, if we want to continue our search and finger-pointing we need to have a better definition of exactly what obesity is. If we’re going to continue calling it a disease we have done a pretty sloppy job of creating diagnostic criteria. To be honest, we aren’t doing such a hot job with “long COVID” either.

A recent article in the New York Times makes it clear that I’m not the only physician who is feeling uncomfortable with this lack of diagnostic specificity.

We know that using body mass index (BMI) as a criteria is imprecise. There are healthy individuals with elevated BMIs and there are others who are carrying an unhealthy amount of fat who have normal BMIs. And, there are individuals who have what might appear to be an excess amount of fat who are fit and healthy by other criteria.

Some investigators feel that a set of measurements that includes a waist and/or hip measurement may be a more accurate way of determining visceral adipose tissue. However, this body roundness index (BRI) currently relies on a tape measurement. Until the technique can be preformed by an inexpensive and readily available scanner, the BRI cannot be considered a practical tool for determining obesity.

Dr. Francisco Rubino, the chair of metabolic and bariatric surgery at Kings College in London, England, has been quoted as saying that, “if one defines a disease inaccurately, everything that stems from that – from diagnosis to treatment to policies – will be distorted and biased.”

Denmark has been forced to relabel obesity as a risk factor because the disease designation was stressing the financial viability of their healthcare system as more and more patients were being prescribe GLP-1 agonists, sometimes off label. A rationing strategy was resulting in suboptimal treatment of a significant portion of the obese population.

Spearheaded by Dr. Rubino, a Lancet Commission composed of physicians has tasked itself to define an “evidence-based diagnosis for obesity. Instead of relying on a single metric such as the BMI or BRI, diagnosing “clinical obesity” would involve a broad array of observations including a history, physical examination, standard laboratory and additional testing, “naming signs and symptoms, organ by organ, tissue by tissue, with plausible mechanisms for each one.” In other words, treating each patient as an individual using evidence-based criteria to make a diagnosis. While likely to be time consuming, this strategy feels like a more scientific approach. I suspect once clinical obesity is more rigorously defined it could be divided into several subtypes. For example, there would be a few conditions that were genetic; Prader-Willi syndrome being the best known.

However, I think the Lancet Commission’s strategy will find that the majority of individuals who make up this half-century global surge have become clinically obese because they have been unable to adapt to the obeseogenic forces in our society, which include diet, autocentricity, and attractive sedentary forms of entertainment, to name just three.

In some cases these unfortunate individuals are more vulnerable because there were born into an economically disadvantaged situation. In other scenarios a lack of foresight and/or political will may have left individuals with no other choice but to rely on automobiles to get around. Still others may find themselves living in a nutritional desert because all of the grocery stores have closed.

I recently encountered a descriptor in a story about the Federal Emergency Management Agency which could easily be adapted to describe this large and growing subtype of individuals with clinical obesity. “Social vulnerability” is measure of how well a community can withstand external stressors that impact human health. For example, the emergency management folks are thinking in terms of natural disaster such as hurricanes, floods, and tornadoes and are asking how well a given community can meet the challenges one would create.

But, the term social vulnerability can easily be applied to individuals living in a society in which unhealthy food is abundant, an infrastructure that discourages or outright prevents non-motorized travel, and the temptation of sedentary entertainment options is unavoidable. Fortunately, not every citizen living in an obesogenic society becomes obese. What factors have protected the non-obese individuals from these obeseogenic stressors? What are the characteristics of the unfortunate “vulnerables” living in the same society who end up being obese?

It is time to shift our focus away from a poorly defined disease model to one in which we begin looking at our society to find out why we have so many socially vulnerable individuals. The toll of obesity as it is currently defined is many order of magnitudes greater than any natural disaster. We have become communities that can no longer withstand the its obesogenic stressors many of which we have created and/or allowed to accumulate over the last century.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

Sometime in the last year or 2 I wrote that, despite my considerable reservations, I had finally come to the conclusion that the American Medical Association’s decision to designate obesity as a disease was appropriate. My rationalization was that the disease label would open more opportunities for funding obesity treatments. However, the explosive growth and popularity of glucagon-like peptide 1 (GLP-1) agonists over the last year has had me rethinking my decision to suppress my long-held reservations about the disease designation.

So, if it’s not a disease, then what should we call it? How do we explain its surge in high-income countries that began in the 1980s? While there are still some folks who see obesity as a character flaw, I think you and I as healthcare providers have difficulty explaining the increase prevalence of obesity as either global breakdown of willpower or a widespread genetic shift as the result of burst of radiation from solar flares.

However, if we want to continue our search and finger-pointing we need to have a better definition of exactly what obesity is. If we’re going to continue calling it a disease we have done a pretty sloppy job of creating diagnostic criteria. To be honest, we aren’t doing such a hot job with “long COVID” either.

A recent article in the New York Times makes it clear that I’m not the only physician who is feeling uncomfortable with this lack of diagnostic specificity.

We know that using body mass index (BMI) as a criteria is imprecise. There are healthy individuals with elevated BMIs and there are others who are carrying an unhealthy amount of fat who have normal BMIs. And, there are individuals who have what might appear to be an excess amount of fat who are fit and healthy by other criteria.

Some investigators feel that a set of measurements that includes a waist and/or hip measurement may be a more accurate way of determining visceral adipose tissue. However, this body roundness index (BRI) currently relies on a tape measurement. Until the technique can be preformed by an inexpensive and readily available scanner, the BRI cannot be considered a practical tool for determining obesity.

Dr. Francisco Rubino, the chair of metabolic and bariatric surgery at Kings College in London, England, has been quoted as saying that, “if one defines a disease inaccurately, everything that stems from that – from diagnosis to treatment to policies – will be distorted and biased.”

Denmark has been forced to relabel obesity as a risk factor because the disease designation was stressing the financial viability of their healthcare system as more and more patients were being prescribe GLP-1 agonists, sometimes off label. A rationing strategy was resulting in suboptimal treatment of a significant portion of the obese population.

Spearheaded by Dr. Rubino, a Lancet Commission composed of physicians has tasked itself to define an “evidence-based diagnosis for obesity. Instead of relying on a single metric such as the BMI or BRI, diagnosing “clinical obesity” would involve a broad array of observations including a history, physical examination, standard laboratory and additional testing, “naming signs and symptoms, organ by organ, tissue by tissue, with plausible mechanisms for each one.” In other words, treating each patient as an individual using evidence-based criteria to make a diagnosis. While likely to be time consuming, this strategy feels like a more scientific approach. I suspect once clinical obesity is more rigorously defined it could be divided into several subtypes. For example, there would be a few conditions that were genetic; Prader-Willi syndrome being the best known.

However, I think the Lancet Commission’s strategy will find that the majority of individuals who make up this half-century global surge have become clinically obese because they have been unable to adapt to the obeseogenic forces in our society, which include diet, autocentricity, and attractive sedentary forms of entertainment, to name just three.

In some cases these unfortunate individuals are more vulnerable because there were born into an economically disadvantaged situation. In other scenarios a lack of foresight and/or political will may have left individuals with no other choice but to rely on automobiles to get around. Still others may find themselves living in a nutritional desert because all of the grocery stores have closed.

I recently encountered a descriptor in a story about the Federal Emergency Management Agency which could easily be adapted to describe this large and growing subtype of individuals with clinical obesity. “Social vulnerability” is measure of how well a community can withstand external stressors that impact human health. For example, the emergency management folks are thinking in terms of natural disaster such as hurricanes, floods, and tornadoes and are asking how well a given community can meet the challenges one would create.

But, the term social vulnerability can easily be applied to individuals living in a society in which unhealthy food is abundant, an infrastructure that discourages or outright prevents non-motorized travel, and the temptation of sedentary entertainment options is unavoidable. Fortunately, not every citizen living in an obesogenic society becomes obese. What factors have protected the non-obese individuals from these obeseogenic stressors? What are the characteristics of the unfortunate “vulnerables” living in the same society who end up being obese?

It is time to shift our focus away from a poorly defined disease model to one in which we begin looking at our society to find out why we have so many socially vulnerable individuals. The toll of obesity as it is currently defined is many order of magnitudes greater than any natural disaster. We have become communities that can no longer withstand the its obesogenic stressors many of which we have created and/or allowed to accumulate over the last century.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

Sometime in the last year or 2 I wrote that, despite my considerable reservations, I had finally come to the conclusion that the American Medical Association’s decision to designate obesity as a disease was appropriate. My rationalization was that the disease label would open more opportunities for funding obesity treatments. However, the explosive growth and popularity of glucagon-like peptide 1 (GLP-1) agonists over the last year has had me rethinking my decision to suppress my long-held reservations about the disease designation.

So, if it’s not a disease, then what should we call it? How do we explain its surge in high-income countries that began in the 1980s? While there are still some folks who see obesity as a character flaw, I think you and I as healthcare providers have difficulty explaining the increase prevalence of obesity as either global breakdown of willpower or a widespread genetic shift as the result of burst of radiation from solar flares.

However, if we want to continue our search and finger-pointing we need to have a better definition of exactly what obesity is. If we’re going to continue calling it a disease we have done a pretty sloppy job of creating diagnostic criteria. To be honest, we aren’t doing such a hot job with “long COVID” either.

A recent article in the New York Times makes it clear that I’m not the only physician who is feeling uncomfortable with this lack of diagnostic specificity.

We know that using body mass index (BMI) as a criteria is imprecise. There are healthy individuals with elevated BMIs and there are others who are carrying an unhealthy amount of fat who have normal BMIs. And, there are individuals who have what might appear to be an excess amount of fat who are fit and healthy by other criteria.

Some investigators feel that a set of measurements that includes a waist and/or hip measurement may be a more accurate way of determining visceral adipose tissue. However, this body roundness index (BRI) currently relies on a tape measurement. Until the technique can be preformed by an inexpensive and readily available scanner, the BRI cannot be considered a practical tool for determining obesity.

Dr. Francisco Rubino, the chair of metabolic and bariatric surgery at Kings College in London, England, has been quoted as saying that, “if one defines a disease inaccurately, everything that stems from that – from diagnosis to treatment to policies – will be distorted and biased.”

Denmark has been forced to relabel obesity as a risk factor because the disease designation was stressing the financial viability of their healthcare system as more and more patients were being prescribe GLP-1 agonists, sometimes off label. A rationing strategy was resulting in suboptimal treatment of a significant portion of the obese population.

Spearheaded by Dr. Rubino, a Lancet Commission composed of physicians has tasked itself to define an “evidence-based diagnosis for obesity. Instead of relying on a single metric such as the BMI or BRI, diagnosing “clinical obesity” would involve a broad array of observations including a history, physical examination, standard laboratory and additional testing, “naming signs and symptoms, organ by organ, tissue by tissue, with plausible mechanisms for each one.” In other words, treating each patient as an individual using evidence-based criteria to make a diagnosis. While likely to be time consuming, this strategy feels like a more scientific approach. I suspect once clinical obesity is more rigorously defined it could be divided into several subtypes. For example, there would be a few conditions that were genetic; Prader-Willi syndrome being the best known.

However, I think the Lancet Commission’s strategy will find that the majority of individuals who make up this half-century global surge have become clinically obese because they have been unable to adapt to the obeseogenic forces in our society, which include diet, autocentricity, and attractive sedentary forms of entertainment, to name just three.

In some cases these unfortunate individuals are more vulnerable because there were born into an economically disadvantaged situation. In other scenarios a lack of foresight and/or political will may have left individuals with no other choice but to rely on automobiles to get around. Still others may find themselves living in a nutritional desert because all of the grocery stores have closed.

I recently encountered a descriptor in a story about the Federal Emergency Management Agency which could easily be adapted to describe this large and growing subtype of individuals with clinical obesity. “Social vulnerability” is measure of how well a community can withstand external stressors that impact human health. For example, the emergency management folks are thinking in terms of natural disaster such as hurricanes, floods, and tornadoes and are asking how well a given community can meet the challenges one would create.

But, the term social vulnerability can easily be applied to individuals living in a society in which unhealthy food is abundant, an infrastructure that discourages or outright prevents non-motorized travel, and the temptation of sedentary entertainment options is unavoidable. Fortunately, not every citizen living in an obesogenic society becomes obese. What factors have protected the non-obese individuals from these obeseogenic stressors? What are the characteristics of the unfortunate “vulnerables” living in the same society who end up being obese?

It is time to shift our focus away from a poorly defined disease model to one in which we begin looking at our society to find out why we have so many socially vulnerable individuals. The toll of obesity as it is currently defined is many order of magnitudes greater than any natural disaster. We have become communities that can no longer withstand the its obesogenic stressors many of which we have created and/or allowed to accumulate over the last century.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

I suspect you all have some experience with childhood migraine. It can mean a painful several hours for the patient, arriving often without warning, with recurrences spaced months or sometimes even years apart. It may be accompanied by vomiting, which in some cases overshadows the severity of the headache. It can result in lost days from school and ruin family activities. It can occur so infrequently that the family can’t recall accurately when the last episode happened. In some ways it is a different animal than the adult version.

Most of the pediatric patients with migraine I have seen have experienced attacks that were occurring so infrequently that the families and I seldom discussed medication as an option. Back then imipramine was the only choice. However, currently there are more than a half dozen medications and combinations that have been tried. Recently a review of 45 clinical trials of these medications was published in JAMA Network Open.

I will let you review for yourself the details of these Iranian investigators’ network meta-analysis, but the bottom line is that some medications were associated with a reduction in migraine frequency. Others were associated with headache intensity. “However, no treatments were associated with significant improvements in quality of life or reduction of the duration of migraine attacks.”

Obviously, this paper illustrates clearly that we have not yet discovered the medicinal magic bullet for pediatric migraine prophylaxis. This doesn’t surprise me. After listening to scores of families tell their migraine stories, it became apparent to me that there was often a pattern in which the child’s headache had arrived after a period of acute sleep deprivation. For example, a trip to an amusement park in which travel or excitement may have resulted in the child going to bed later and/or getting up earlier. By afternoon the child’s reserves of something (currently unknown) were depleted to a point that the headache and/or vomiting struck.

Because these episodes were often so infrequent, separated by months, that taking a history demonstrating a recurring pattern could take considerable patience on the part of the family and the provider, even for a physician like myself who believes that better sleep is the answer for everything. However, once I could convince a family of the connection between the sleep deprivation and the headaches, they could often recall other episodes in the past that substantiated my explanation.

In some cases there was no obvious history of acute sleep deprivation, or at least it was so subtle that even a history taker with a sleep obsession couldn’t detect it. However, in these cases I could usually elicit a history of chronic sleep deprivation. For example, falling asleep instantly on automobile rides, difficulty with waking in the morning, or unhealthy bedtime routines. With this underlying vulnerability of chronic sleep deprivation, a slightly more exciting or vigorous day was all that was necessary to trigger the headache.

For those of you who don’t share my contention that childhood migraine is usually the result of sleep deprivation, consider the similarity between an epileptic seizure, which can be triggered by fatigue. Both events are usually followed by a deep sleep from which the child wakes refreshed and symptom free.

I think it is interesting that this recent meta-analysis could find no benefit in the quality of life for any of the medications. The explanation may be that the child with migraine already had a somewhat diminished quality of life as a result of the sleep deprivation, either acute or chronic.

When speaking with parents of migraine sufferers, I would tell them that once the headache had started there was little I had to offer to forestall the inevitable pain and vomiting. Certainly not in the form of an oral medication. While many adults will have an aura that warns them of the headache onset, I have found that most children don’t describe an aura. It may be they simply lack the ability to express it. Occasionally an observant parent may detect pallor or a behavior change that indicates a migraine is beginning. On rare occasions a parent may be able to abort the attack by quickly getting the child to a quiet, dark, and calm environment.

Although this recent meta-analysis review of treatment options is discouraging, it may be providing a clue to effective prophylaxis. Some of the medications that decrease the frequency of the attacks may be doing so because they improve the patient’s sleep patterns. Those that decrease the intensity of the pain are probably working on pain pathway that is not specific to migraine.

Continuing a search for a prophylactic medication is a worthy goal, particularly for those patients in which their migraines are debilitating. However, based on my experience, enhanced by my bias, the safest and most effective prophylaxis results from increasing the family’s awareness of the role that sleep deprivation plays in the illness. Even when the family buys into the message and attempts to avoid situations that will tax their vulnerable children, parents will need to accept that sometimes stuff happens even though siblings and peers may be able to tolerate the situation. Spontaneous activities can converge on a day when for whatever reason the migraine-prone child is overtired and the headache and vomiting will erupt.

A lifestyle change is always preferable to a pharmacological intervention. However, that doesn’t mean it is always easy to achieve.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

I suspect you all have some experience with childhood migraine. It can mean a painful several hours for the patient, arriving often without warning, with recurrences spaced months or sometimes even years apart. It may be accompanied by vomiting, which in some cases overshadows the severity of the headache. It can result in lost days from school and ruin family activities. It can occur so infrequently that the family can’t recall accurately when the last episode happened. In some ways it is a different animal than the adult version.

Most of the pediatric patients with migraine I have seen have experienced attacks that were occurring so infrequently that the families and I seldom discussed medication as an option. Back then imipramine was the only choice. However, currently there are more than a half dozen medications and combinations that have been tried. Recently a review of 45 clinical trials of these medications was published in JAMA Network Open.

I will let you review for yourself the details of these Iranian investigators’ network meta-analysis, but the bottom line is that some medications were associated with a reduction in migraine frequency. Others were associated with headache intensity. “However, no treatments were associated with significant improvements in quality of life or reduction of the duration of migraine attacks.”

Obviously, this paper illustrates clearly that we have not yet discovered the medicinal magic bullet for pediatric migraine prophylaxis. This doesn’t surprise me. After listening to scores of families tell their migraine stories, it became apparent to me that there was often a pattern in which the child’s headache had arrived after a period of acute sleep deprivation. For example, a trip to an amusement park in which travel or excitement may have resulted in the child going to bed later and/or getting up earlier. By afternoon the child’s reserves of something (currently unknown) were depleted to a point that the headache and/or vomiting struck.

Because these episodes were often so infrequent, separated by months, that taking a history demonstrating a recurring pattern could take considerable patience on the part of the family and the provider, even for a physician like myself who believes that better sleep is the answer for everything. However, once I could convince a family of the connection between the sleep deprivation and the headaches, they could often recall other episodes in the past that substantiated my explanation.

In some cases there was no obvious history of acute sleep deprivation, or at least it was so subtle that even a history taker with a sleep obsession couldn’t detect it. However, in these cases I could usually elicit a history of chronic sleep deprivation. For example, falling asleep instantly on automobile rides, difficulty with waking in the morning, or unhealthy bedtime routines. With this underlying vulnerability of chronic sleep deprivation, a slightly more exciting or vigorous day was all that was necessary to trigger the headache.

For those of you who don’t share my contention that childhood migraine is usually the result of sleep deprivation, consider the similarity between an epileptic seizure, which can be triggered by fatigue. Both events are usually followed by a deep sleep from which the child wakes refreshed and symptom free.

I think it is interesting that this recent meta-analysis could find no benefit in the quality of life for any of the medications. The explanation may be that the child with migraine already had a somewhat diminished quality of life as a result of the sleep deprivation, either acute or chronic.

When speaking with parents of migraine sufferers, I would tell them that once the headache had started there was little I had to offer to forestall the inevitable pain and vomiting. Certainly not in the form of an oral medication. While many adults will have an aura that warns them of the headache onset, I have found that most children don’t describe an aura. It may be they simply lack the ability to express it. Occasionally an observant parent may detect pallor or a behavior change that indicates a migraine is beginning. On rare occasions a parent may be able to abort the attack by quickly getting the child to a quiet, dark, and calm environment.

Although this recent meta-analysis review of treatment options is discouraging, it may be providing a clue to effective prophylaxis. Some of the medications that decrease the frequency of the attacks may be doing so because they improve the patient’s sleep patterns. Those that decrease the intensity of the pain are probably working on pain pathway that is not specific to migraine.

Continuing a search for a prophylactic medication is a worthy goal, particularly for those patients in which their migraines are debilitating. However, based on my experience, enhanced by my bias, the safest and most effective prophylaxis results from increasing the family’s awareness of the role that sleep deprivation plays in the illness. Even when the family buys into the message and attempts to avoid situations that will tax their vulnerable children, parents will need to accept that sometimes stuff happens even though siblings and peers may be able to tolerate the situation. Spontaneous activities can converge on a day when for whatever reason the migraine-prone child is overtired and the headache and vomiting will erupt.

A lifestyle change is always preferable to a pharmacological intervention. However, that doesn’t mean it is always easy to achieve.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

I suspect you all have some experience with childhood migraine. It can mean a painful several hours for the patient, arriving often without warning, with recurrences spaced months or sometimes even years apart. It may be accompanied by vomiting, which in some cases overshadows the severity of the headache. It can result in lost days from school and ruin family activities. It can occur so infrequently that the family can’t recall accurately when the last episode happened. In some ways it is a different animal than the adult version.

Most of the pediatric patients with migraine I have seen have experienced attacks that were occurring so infrequently that the families and I seldom discussed medication as an option. Back then imipramine was the only choice. However, currently there are more than a half dozen medications and combinations that have been tried. Recently a review of 45 clinical trials of these medications was published in JAMA Network Open.

I will let you review for yourself the details of these Iranian investigators’ network meta-analysis, but the bottom line is that some medications were associated with a reduction in migraine frequency. Others were associated with headache intensity. “However, no treatments were associated with significant improvements in quality of life or reduction of the duration of migraine attacks.”

Obviously, this paper illustrates clearly that we have not yet discovered the medicinal magic bullet for pediatric migraine prophylaxis. This doesn’t surprise me. After listening to scores of families tell their migraine stories, it became apparent to me that there was often a pattern in which the child’s headache had arrived after a period of acute sleep deprivation. For example, a trip to an amusement park in which travel or excitement may have resulted in the child going to bed later and/or getting up earlier. By afternoon the child’s reserves of something (currently unknown) were depleted to a point that the headache and/or vomiting struck.

Because these episodes were often so infrequent, separated by months, that taking a history demonstrating a recurring pattern could take considerable patience on the part of the family and the provider, even for a physician like myself who believes that better sleep is the answer for everything. However, once I could convince a family of the connection between the sleep deprivation and the headaches, they could often recall other episodes in the past that substantiated my explanation.

In some cases there was no obvious history of acute sleep deprivation, or at least it was so subtle that even a history taker with a sleep obsession couldn’t detect it. However, in these cases I could usually elicit a history of chronic sleep deprivation. For example, falling asleep instantly on automobile rides, difficulty with waking in the morning, or unhealthy bedtime routines. With this underlying vulnerability of chronic sleep deprivation, a slightly more exciting or vigorous day was all that was necessary to trigger the headache.

For those of you who don’t share my contention that childhood migraine is usually the result of sleep deprivation, consider the similarity between an epileptic seizure, which can be triggered by fatigue. Both events are usually followed by a deep sleep from which the child wakes refreshed and symptom free.

I think it is interesting that this recent meta-analysis could find no benefit in the quality of life for any of the medications. The explanation may be that the child with migraine already had a somewhat diminished quality of life as a result of the sleep deprivation, either acute or chronic.

When speaking with parents of migraine sufferers, I would tell them that once the headache had started there was little I had to offer to forestall the inevitable pain and vomiting. Certainly not in the form of an oral medication. While many adults will have an aura that warns them of the headache onset, I have found that most children don’t describe an aura. It may be they simply lack the ability to express it. Occasionally an observant parent may detect pallor or a behavior change that indicates a migraine is beginning. On rare occasions a parent may be able to abort the attack by quickly getting the child to a quiet, dark, and calm environment.

Although this recent meta-analysis review of treatment options is discouraging, it may be providing a clue to effective prophylaxis. Some of the medications that decrease the frequency of the attacks may be doing so because they improve the patient’s sleep patterns. Those that decrease the intensity of the pain are probably working on pain pathway that is not specific to migraine.

Continuing a search for a prophylactic medication is a worthy goal, particularly for those patients in which their migraines are debilitating. However, based on my experience, enhanced by my bias, the safest and most effective prophylaxis results from increasing the family’s awareness of the role that sleep deprivation plays in the illness. Even when the family buys into the message and attempts to avoid situations that will tax their vulnerable children, parents will need to accept that sometimes stuff happens even though siblings and peers may be able to tolerate the situation. Spontaneous activities can converge on a day when for whatever reason the migraine-prone child is overtired and the headache and vomiting will erupt.

A lifestyle change is always preferable to a pharmacological intervention. However, that doesn’t mean it is always easy to achieve.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.