TOPLINE:

GPT-4 generated highly accurate pancreatic cancer synoptic reports from original reports, outperforming GPT-3.5. Using GPT-4 reports instead of original reports, surgeons were able to better assess tumor resectability in patients with pancreatic ductal adenocarcinoma and saved time evaluating reports.

METHODOLOGY:

• Compared with original reports, structured imaging reports help surgeons assess tumor resectability in patients with pancreatic ductal adenocarcinoma. However, radiologist uptake of structured reporting remains inconsistent.
• To determine whether converting free-text (ie, original) radiology reports into structured reports can benefit surgeons, researchers evaluated how well GPT-4 and GPT-3.5 were able to generate pancreatic ductal adenocarcinoma synoptic reports from originals.
• The retrospective study included 180 consecutive pancreatic ductal adenocarcinoma staging CT reports, which were reviewed by two radiologists to establish a reference standard for 14 key findings and National Comprehensive Cancer Network resectability category.
• Researchers prompted GPT-3.5 and GPT-4 to create synoptic reports from original reports using the same criteria, and surgeons compared the precision, accuracy, and time to assess the original and artificial intelligence (AI)–generated reports.

TAKEAWAY:

• GPT-4 outperformed GPT-3.5 on all metrics evaluated. For instance, compared with GPT-3.5, GPT-4 achieved equal or higher F1 scores for all 14 key features (F1 scores help assess the precision and recall of a machine-learning model).
• GPT-4 also demonstrated greater precision than GPT-3.5 for extracting superior mesenteric artery involvement (100% vs 88.8%, respectively) and for categorizing resectability.
• Compared with original reports, AI-generated reports helped surgeons better categorize resectability (83% vs 76%, respectively; P = .03), and surgeons spent less time when using AI-generated reports.
• The AI-generated reports did lead to some clinically notable errors. GPT-4, for instance, made errors in extracting common hepatic artery involvement.

IN PRACTICE:

“In our study, GPT-4 was near-perfect at automatically creating pancreatic ductal adenocarcinoma synoptic reports from original reports, outperforming GPT-3.5 overall,” the authors wrote. This “represents a useful application that can increase standardization and improve communication between radiologists and surgeons.” However, the authors cautioned, the “presence of some clinically significant errors highlights the need for implementation in supervised and preliminary contexts, rather than being relied on for management decisions.” 

SOURCE:

The study, with first author Rajesh Bhayana, MD, University Health Network in Toronto, Ontario, Canada, was published online in Radiology. 

LIMITATIONS:

While GPT-4 showed high accuracy in report generation, it did lead to some errors. Researchers also relied on original reports when generating the AI reports, and the original reports can contain ambiguous descriptions and language.

DISCLOSURES:

Dr. Bhayana reported no relevant conflicts of interest. Additional disclosures are noted in the original article.

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

TOPLINE:

GPT-4 generated highly accurate pancreatic cancer synoptic reports from original reports, outperforming GPT-3.5. Using GPT-4 reports instead of original reports, surgeons were able to better assess tumor resectability in patients with pancreatic ductal adenocarcinoma and saved time evaluating reports.

METHODOLOGY:

• Compared with original reports, structured imaging reports help surgeons assess tumor resectability in patients with pancreatic ductal adenocarcinoma. However, radiologist uptake of structured reporting remains inconsistent.
• To determine whether converting free-text (ie, original) radiology reports into structured reports can benefit surgeons, researchers evaluated how well GPT-4 and GPT-3.5 were able to generate pancreatic ductal adenocarcinoma synoptic reports from originals.
• The retrospective study included 180 consecutive pancreatic ductal adenocarcinoma staging CT reports, which were reviewed by two radiologists to establish a reference standard for 14 key findings and National Comprehensive Cancer Network resectability category.
• Researchers prompted GPT-3.5 and GPT-4 to create synoptic reports from original reports using the same criteria, and surgeons compared the precision, accuracy, and time to assess the original and artificial intelligence (AI)–generated reports.

TAKEAWAY:

• GPT-4 outperformed GPT-3.5 on all metrics evaluated. For instance, compared with GPT-3.5, GPT-4 achieved equal or higher F1 scores for all 14 key features (F1 scores help assess the precision and recall of a machine-learning model).
• GPT-4 also demonstrated greater precision than GPT-3.5 for extracting superior mesenteric artery involvement (100% vs 88.8%, respectively) and for categorizing resectability.
• Compared with original reports, AI-generated reports helped surgeons better categorize resectability (83% vs 76%, respectively; P = .03), and surgeons spent less time when using AI-generated reports.
• The AI-generated reports did lead to some clinically notable errors. GPT-4, for instance, made errors in extracting common hepatic artery involvement.

IN PRACTICE:

“In our study, GPT-4 was near-perfect at automatically creating pancreatic ductal adenocarcinoma synoptic reports from original reports, outperforming GPT-3.5 overall,” the authors wrote. This “represents a useful application that can increase standardization and improve communication between radiologists and surgeons.” However, the authors cautioned, the “presence of some clinically significant errors highlights the need for implementation in supervised and preliminary contexts, rather than being relied on for management decisions.” 

SOURCE:

The study, with first author Rajesh Bhayana, MD, University Health Network in Toronto, Ontario, Canada, was published online in Radiology. 

LIMITATIONS:

While GPT-4 showed high accuracy in report generation, it did lead to some errors. Researchers also relied on original reports when generating the AI reports, and the original reports can contain ambiguous descriptions and language.

DISCLOSURES:

Dr. Bhayana reported no relevant conflicts of interest. Additional disclosures are noted in the original article.

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

TOPLINE:

GPT-4 generated highly accurate pancreatic cancer synoptic reports from original reports, outperforming GPT-3.5. Using GPT-4 reports instead of original reports, surgeons were able to better assess tumor resectability in patients with pancreatic ductal adenocarcinoma and saved time evaluating reports.

METHODOLOGY:

• Compared with original reports, structured imaging reports help surgeons assess tumor resectability in patients with pancreatic ductal adenocarcinoma. However, radiologist uptake of structured reporting remains inconsistent.
• To determine whether converting free-text (ie, original) radiology reports into structured reports can benefit surgeons, researchers evaluated how well GPT-4 and GPT-3.5 were able to generate pancreatic ductal adenocarcinoma synoptic reports from originals.
• The retrospective study included 180 consecutive pancreatic ductal adenocarcinoma staging CT reports, which were reviewed by two radiologists to establish a reference standard for 14 key findings and National Comprehensive Cancer Network resectability category.
• Researchers prompted GPT-3.5 and GPT-4 to create synoptic reports from original reports using the same criteria, and surgeons compared the precision, accuracy, and time to assess the original and artificial intelligence (AI)–generated reports.

TAKEAWAY:

• GPT-4 outperformed GPT-3.5 on all metrics evaluated. For instance, compared with GPT-3.5, GPT-4 achieved equal or higher F1 scores for all 14 key features (F1 scores help assess the precision and recall of a machine-learning model).
• GPT-4 also demonstrated greater precision than GPT-3.5 for extracting superior mesenteric artery involvement (100% vs 88.8%, respectively) and for categorizing resectability.
• Compared with original reports, AI-generated reports helped surgeons better categorize resectability (83% vs 76%, respectively; P = .03), and surgeons spent less time when using AI-generated reports.
• The AI-generated reports did lead to some clinically notable errors. GPT-4, for instance, made errors in extracting common hepatic artery involvement.

IN PRACTICE:

“In our study, GPT-4 was near-perfect at automatically creating pancreatic ductal adenocarcinoma synoptic reports from original reports, outperforming GPT-3.5 overall,” the authors wrote. This “represents a useful application that can increase standardization and improve communication between radiologists and surgeons.” However, the authors cautioned, the “presence of some clinically significant errors highlights the need for implementation in supervised and preliminary contexts, rather than being relied on for management decisions.” 

SOURCE:

The study, with first author Rajesh Bhayana, MD, University Health Network in Toronto, Ontario, Canada, was published online in Radiology. 

LIMITATIONS:

While GPT-4 showed high accuracy in report generation, it did lead to some errors. Researchers also relied on original reports when generating the AI reports, and the original reports can contain ambiguous descriptions and language.

DISCLOSURES:

Dr. Bhayana reported no relevant conflicts of interest. Additional disclosures are noted in the original article.

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

Recently, the British Journal of General Practice published a paper that claimed that anxiety may be a prodromal feature of Parkinson’s disease). That news was widely picked up and spread.

The researchers certainly have some interesting data, but this sort of article, once enough general and social media websites get a hold of it, is bound to cause panic in the streets. And phone calls to my office.

An anxious-by-nature friend even emailed me the link with a laconic “Well, I’m screwed” in the subject line.

Is there a correlation between Parkinson’s disease and anxiety? Probably. Any of us practicing neurology have seen it. Some of it is likely from the anxiety of the situation, but the biochemical changes brought by the disease are also likely a big part.

But does that mean everyone with anxiety has Parkinson’s disease? Of course not. Anxiety is common, probably more common in our current era than ever before (this is why I tell patients not to watch the news and to avoid social media — they’re bad for your sanity and blood pressure).

Stories like this, once they start getting forwarded on Facebook (or another social media outlet), only raise anxiety, which results in more forwarding, and the snowball begins rolling downhill before crashing into my office (obviously this is a figure of speech, as it’s July in Phoenix).

The research is interesting. The point is valid. But the leaps the public makes are ... problematic. It’s only a matter of time before someone comes in demanding a DaT scan because they’re anxious. At $4K a test, that’s not happening.

The intersection between medical research and mass media, while not new, becomes increasingly problematic in the social media era, where things that are preliminary in the medical literature make the jump to certainty in the public arena.

Which raises anxiety all around.

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

Recently, the British Journal of General Practice published a paper that claimed that anxiety may be a prodromal feature of Parkinson’s disease). That news was widely picked up and spread.

The researchers certainly have some interesting data, but this sort of article, once enough general and social media websites get a hold of it, is bound to cause panic in the streets. And phone calls to my office.

An anxious-by-nature friend even emailed me the link with a laconic “Well, I’m screwed” in the subject line.

Is there a correlation between Parkinson’s disease and anxiety? Probably. Any of us practicing neurology have seen it. Some of it is likely from the anxiety of the situation, but the biochemical changes brought by the disease are also likely a big part.

But does that mean everyone with anxiety has Parkinson’s disease? Of course not. Anxiety is common, probably more common in our current era than ever before (this is why I tell patients not to watch the news and to avoid social media — they’re bad for your sanity and blood pressure).

Stories like this, once they start getting forwarded on Facebook (or another social media outlet), only raise anxiety, which results in more forwarding, and the snowball begins rolling downhill before crashing into my office (obviously this is a figure of speech, as it’s July in Phoenix).

The research is interesting. The point is valid. But the leaps the public makes are ... problematic. It’s only a matter of time before someone comes in demanding a DaT scan because they’re anxious. At $4K a test, that’s not happening.

The intersection between medical research and mass media, while not new, becomes increasingly problematic in the social media era, where things that are preliminary in the medical literature make the jump to certainty in the public arena.

Which raises anxiety all around.

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

Recently, the British Journal of General Practice published a paper that claimed that anxiety may be a prodromal feature of Parkinson’s disease). That news was widely picked up and spread.

The researchers certainly have some interesting data, but this sort of article, once enough general and social media websites get a hold of it, is bound to cause panic in the streets. And phone calls to my office.

An anxious-by-nature friend even emailed me the link with a laconic “Well, I’m screwed” in the subject line.

Is there a correlation between Parkinson’s disease and anxiety? Probably. Any of us practicing neurology have seen it. Some of it is likely from the anxiety of the situation, but the biochemical changes brought by the disease are also likely a big part.

But does that mean everyone with anxiety has Parkinson’s disease? Of course not. Anxiety is common, probably more common in our current era than ever before (this is why I tell patients not to watch the news and to avoid social media — they’re bad for your sanity and blood pressure).

Stories like this, once they start getting forwarded on Facebook (or another social media outlet), only raise anxiety, which results in more forwarding, and the snowball begins rolling downhill before crashing into my office (obviously this is a figure of speech, as it’s July in Phoenix).

The research is interesting. The point is valid. But the leaps the public makes are ... problematic. It’s only a matter of time before someone comes in demanding a DaT scan because they’re anxious. At $4K a test, that’s not happening.

The intersection between medical research and mass media, while not new, becomes increasingly problematic in the social media era, where things that are preliminary in the medical literature make the jump to certainty in the public arena.

Which raises anxiety all around.

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

More than two-thirds of patients with migraine also suffer from neck pain, a combination that’s linked to higher levels of various forms of disability, an international, prospective, cross-sectional study finds.

Of 51,969 respondents with headache over the past year, the 27.9% with migraine were more likely to have neck pain than those with non-migraine headache (68.3% vs 36.1%, respectively, P < .001), reported Richard B. Lipton, MD, professor of neurology at Albert Einstein College of Medicine, New York City, and colleagues in Headache.

Compared with other patients with migraine, those who also have neck pain have “greater disability, more psychiatric comorbidities, more allodynia, diminished quality of life, decreased work productivity, and reduced response to treatment,” Dr. Lipton said in an interview. “If patients don’t report [neck pain], it is probably worth asking about. And when patients have both migraine and neck pain, they may merit increased therapeutic attention.”

As Dr. Lipton noted, clinicians have long known that neck pain is common in migraine, although it’s been unclear how the two conditions are connected. “One possibility is that the neck pain is actually a manifestation of the migraine headache. Another possibility is that the neck pain is an independent factor unrelated to migraine headaches: Many people have migraine and cervical spine disease. And the third possibility is that neck pain may be an exacerbating factor, that cervical spine disease may make the migraine worse.”

Referred pain is a potential factor too, he said.
 

Assessing Migraine, Neck Pain, and Disability

The new study sought to better understand the role of neck pain in migraine, Dr. Lipton said.

For the CaMEO-I study, researchers surveyed 51,969 adults with headache via the Internet in Canada, France, Germany, Japan, United Kingdom, and the United States from 2021-2022. Most of the 37,477 patients with non-migraine headaches were considered to have tension headaches.

Among the 14,492 patients with migraine, demographics were statistically similar among those who had neck pain or didn’t have it (average age = 40.7 and 42.1, 68.4% and 72.5% female, and average BMIs = 26.0 and 26.4, respectively).

Among patients in the US, 71.4% of patients with migraine reported neck pain versus 35.9% of those with non-migraine headaches. In Canada, the numbers were 69.5% and 37.5%, respectively.

Among all patients with migraine, moderate-to-severe disability was more common among those with neck pain than those without neck pain (47.7% vs 28.9%, respectively, P < .001). Those with both migraine and neck pain had more symptom burden (P < .001), and 28.4% said neck pain was their most bothersome symptom. They also had a higher number of symptoms (P < .001).

Several conditions were more common among patients with migraine who reported neck pain versus those who didn’t (depression/anxiety, 40.2% vs 28.2%; anxiety, 41.2% vs 29.2%; and allodynia, 54.0% vs 36.6%, respectively, all P  <  0.001). Those with neck pain were also more likely to have “poor acute treatment optimization” (61.1% vs 53.3%, respectively, P < .001).

Researchers noted limitations such as the use of self-reported data, the potential for selection bias, limitations regarding survey questions, and an inability to determine causation.
 

Clinical Messages

The findings suggest that patients with both migraine and neck pain have greater activation of second-order neurons in the trigeminocervical complex, Dr. Lipton said.

He added that neck pain is often part of the migraine prodrome or the migraine attack itself, suggesting that it’s “part and parcel of the migraine attack.” However, neck pain may have another cause — such as degenerative disease of the neck — if it’s not directly connected to migraine, he added.

As for clinical messages from the study, “it’s quite likely that the neck pain is a primary manifestation of migraine. Migraine may well be the explanation in the absence of a reason to look further,” Dr. Lipton said.

If neck pain heralds a migraine, treating the prodrome with CGRP receptor antagonists (“gepants”) can be helpful, he said. He highlighted other preventive options include beta blockers, anti-epilepsy drugs, and monoclonal antibodies. There’s also anecdotal support for using botulinum toxin A in patients with chronic migraine and neck pain, he said.

In an interview, Mayo Clinic Arizona associate professor of neurology Rashmi B. Halker Singh, MD, who’s familiar with the study but did not take part in it, praised the research. The findings “help us to better understand the impact of living with neck pain if you are somebody with migraine,” she said. “It alerts us that we need to be more aggressive in how we manage that in patients.”

The study also emphasizes the importance of preventive medication in appropriate patients with migraine, especially those with neck pain who may be living with greater disability, she said. “About 13% of people with migraine are on a preventive medication, but about 40% are eligible. That’s an area where we have a big gap.”

Dr. Halker Singh added that non-medication strategies such as acupuncture and physical therapy can be helpful.

AbbVie funded the study. Dr. Lipton reports support for the study from AbbVie; research support paid to his institution from the Czap Foundation, National Headache Foundation, National Institutes of Health, S&L Marx Foundation, and US Food and Drug Administration; and personal fees from AbbVie/Allergan, American Academy of Neurology, American Headache Society, Amgen, Biohaven, Biovision, Boston, Dr. Reddy’s (Promius), electroCore, Eli Lilly, GlaxoSmithKline, Grifols, Lundbeck (Alder), Merck, Pernix, Pfizer, Teva, Vector, and Vedanta Research. He holds stock/options in Axon, Biohaven, CoolTech, and Manistee. Other authors report various disclosures.

Dr. Halker Singh is deputy editor of Headache, where the study was published, but wasn’t aware of it until it was published.

More than two-thirds of patients with migraine also suffer from neck pain, a combination that’s linked to higher levels of various forms of disability, an international, prospective, cross-sectional study finds.

Of 51,969 respondents with headache over the past year, the 27.9% with migraine were more likely to have neck pain than those with non-migraine headache (68.3% vs 36.1%, respectively, P < .001), reported Richard B. Lipton, MD, professor of neurology at Albert Einstein College of Medicine, New York City, and colleagues in Headache.

Compared with other patients with migraine, those who also have neck pain have “greater disability, more psychiatric comorbidities, more allodynia, diminished quality of life, decreased work productivity, and reduced response to treatment,” Dr. Lipton said in an interview. “If patients don’t report [neck pain], it is probably worth asking about. And when patients have both migraine and neck pain, they may merit increased therapeutic attention.”

As Dr. Lipton noted, clinicians have long known that neck pain is common in migraine, although it’s been unclear how the two conditions are connected. “One possibility is that the neck pain is actually a manifestation of the migraine headache. Another possibility is that the neck pain is an independent factor unrelated to migraine headaches: Many people have migraine and cervical spine disease. And the third possibility is that neck pain may be an exacerbating factor, that cervical spine disease may make the migraine worse.”

Referred pain is a potential factor too, he said.
 

Assessing Migraine, Neck Pain, and Disability

The new study sought to better understand the role of neck pain in migraine, Dr. Lipton said.

For the CaMEO-I study, researchers surveyed 51,969 adults with headache via the Internet in Canada, France, Germany, Japan, United Kingdom, and the United States from 2021-2022. Most of the 37,477 patients with non-migraine headaches were considered to have tension headaches.

Among the 14,492 patients with migraine, demographics were statistically similar among those who had neck pain or didn’t have it (average age = 40.7 and 42.1, 68.4% and 72.5% female, and average BMIs = 26.0 and 26.4, respectively).

Among patients in the US, 71.4% of patients with migraine reported neck pain versus 35.9% of those with non-migraine headaches. In Canada, the numbers were 69.5% and 37.5%, respectively.

Among all patients with migraine, moderate-to-severe disability was more common among those with neck pain than those without neck pain (47.7% vs 28.9%, respectively, P < .001). Those with both migraine and neck pain had more symptom burden (P < .001), and 28.4% said neck pain was their most bothersome symptom. They also had a higher number of symptoms (P < .001).

Several conditions were more common among patients with migraine who reported neck pain versus those who didn’t (depression/anxiety, 40.2% vs 28.2%; anxiety, 41.2% vs 29.2%; and allodynia, 54.0% vs 36.6%, respectively, all P  <  0.001). Those with neck pain were also more likely to have “poor acute treatment optimization” (61.1% vs 53.3%, respectively, P < .001).

Researchers noted limitations such as the use of self-reported data, the potential for selection bias, limitations regarding survey questions, and an inability to determine causation.
 

Clinical Messages

The findings suggest that patients with both migraine and neck pain have greater activation of second-order neurons in the trigeminocervical complex, Dr. Lipton said.

He added that neck pain is often part of the migraine prodrome or the migraine attack itself, suggesting that it’s “part and parcel of the migraine attack.” However, neck pain may have another cause — such as degenerative disease of the neck — if it’s not directly connected to migraine, he added.

As for clinical messages from the study, “it’s quite likely that the neck pain is a primary manifestation of migraine. Migraine may well be the explanation in the absence of a reason to look further,” Dr. Lipton said.

If neck pain heralds a migraine, treating the prodrome with CGRP receptor antagonists (“gepants”) can be helpful, he said. He highlighted other preventive options include beta blockers, anti-epilepsy drugs, and monoclonal antibodies. There’s also anecdotal support for using botulinum toxin A in patients with chronic migraine and neck pain, he said.

In an interview, Mayo Clinic Arizona associate professor of neurology Rashmi B. Halker Singh, MD, who’s familiar with the study but did not take part in it, praised the research. The findings “help us to better understand the impact of living with neck pain if you are somebody with migraine,” she said. “It alerts us that we need to be more aggressive in how we manage that in patients.”

The study also emphasizes the importance of preventive medication in appropriate patients with migraine, especially those with neck pain who may be living with greater disability, she said. “About 13% of people with migraine are on a preventive medication, but about 40% are eligible. That’s an area where we have a big gap.”

Dr. Halker Singh added that non-medication strategies such as acupuncture and physical therapy can be helpful.

AbbVie funded the study. Dr. Lipton reports support for the study from AbbVie; research support paid to his institution from the Czap Foundation, National Headache Foundation, National Institutes of Health, S&L Marx Foundation, and US Food and Drug Administration; and personal fees from AbbVie/Allergan, American Academy of Neurology, American Headache Society, Amgen, Biohaven, Biovision, Boston, Dr. Reddy’s (Promius), electroCore, Eli Lilly, GlaxoSmithKline, Grifols, Lundbeck (Alder), Merck, Pernix, Pfizer, Teva, Vector, and Vedanta Research. He holds stock/options in Axon, Biohaven, CoolTech, and Manistee. Other authors report various disclosures.

Dr. Halker Singh is deputy editor of Headache, where the study was published, but wasn’t aware of it until it was published.

More than two-thirds of patients with migraine also suffer from neck pain, a combination that’s linked to higher levels of various forms of disability, an international, prospective, cross-sectional study finds.

Of 51,969 respondents with headache over the past year, the 27.9% with migraine were more likely to have neck pain than those with non-migraine headache (68.3% vs 36.1%, respectively, P < .001), reported Richard B. Lipton, MD, professor of neurology at Albert Einstein College of Medicine, New York City, and colleagues in Headache.

Compared with other patients with migraine, those who also have neck pain have “greater disability, more psychiatric comorbidities, more allodynia, diminished quality of life, decreased work productivity, and reduced response to treatment,” Dr. Lipton said in an interview. “If patients don’t report [neck pain], it is probably worth asking about. And when patients have both migraine and neck pain, they may merit increased therapeutic attention.”

As Dr. Lipton noted, clinicians have long known that neck pain is common in migraine, although it’s been unclear how the two conditions are connected. “One possibility is that the neck pain is actually a manifestation of the migraine headache. Another possibility is that the neck pain is an independent factor unrelated to migraine headaches: Many people have migraine and cervical spine disease. And the third possibility is that neck pain may be an exacerbating factor, that cervical spine disease may make the migraine worse.”

Referred pain is a potential factor too, he said.
 

Assessing Migraine, Neck Pain, and Disability

The new study sought to better understand the role of neck pain in migraine, Dr. Lipton said.

For the CaMEO-I study, researchers surveyed 51,969 adults with headache via the Internet in Canada, France, Germany, Japan, United Kingdom, and the United States from 2021-2022. Most of the 37,477 patients with non-migraine headaches were considered to have tension headaches.

Among the 14,492 patients with migraine, demographics were statistically similar among those who had neck pain or didn’t have it (average age = 40.7 and 42.1, 68.4% and 72.5% female, and average BMIs = 26.0 and 26.4, respectively).

Among patients in the US, 71.4% of patients with migraine reported neck pain versus 35.9% of those with non-migraine headaches. In Canada, the numbers were 69.5% and 37.5%, respectively.

Among all patients with migraine, moderate-to-severe disability was more common among those with neck pain than those without neck pain (47.7% vs 28.9%, respectively, P < .001). Those with both migraine and neck pain had more symptom burden (P < .001), and 28.4% said neck pain was their most bothersome symptom. They also had a higher number of symptoms (P < .001).

Several conditions were more common among patients with migraine who reported neck pain versus those who didn’t (depression/anxiety, 40.2% vs 28.2%; anxiety, 41.2% vs 29.2%; and allodynia, 54.0% vs 36.6%, respectively, all P  <  0.001). Those with neck pain were also more likely to have “poor acute treatment optimization” (61.1% vs 53.3%, respectively, P < .001).

Researchers noted limitations such as the use of self-reported data, the potential for selection bias, limitations regarding survey questions, and an inability to determine causation.
 

Clinical Messages

The findings suggest that patients with both migraine and neck pain have greater activation of second-order neurons in the trigeminocervical complex, Dr. Lipton said.

He added that neck pain is often part of the migraine prodrome or the migraine attack itself, suggesting that it’s “part and parcel of the migraine attack.” However, neck pain may have another cause — such as degenerative disease of the neck — if it’s not directly connected to migraine, he added.

As for clinical messages from the study, “it’s quite likely that the neck pain is a primary manifestation of migraine. Migraine may well be the explanation in the absence of a reason to look further,” Dr. Lipton said.

If neck pain heralds a migraine, treating the prodrome with CGRP receptor antagonists (“gepants”) can be helpful, he said. He highlighted other preventive options include beta blockers, anti-epilepsy drugs, and monoclonal antibodies. There’s also anecdotal support for using botulinum toxin A in patients with chronic migraine and neck pain, he said.

In an interview, Mayo Clinic Arizona associate professor of neurology Rashmi B. Halker Singh, MD, who’s familiar with the study but did not take part in it, praised the research. The findings “help us to better understand the impact of living with neck pain if you are somebody with migraine,” she said. “It alerts us that we need to be more aggressive in how we manage that in patients.”

The study also emphasizes the importance of preventive medication in appropriate patients with migraine, especially those with neck pain who may be living with greater disability, she said. “About 13% of people with migraine are on a preventive medication, but about 40% are eligible. That’s an area where we have a big gap.”

Dr. Halker Singh added that non-medication strategies such as acupuncture and physical therapy can be helpful.

AbbVie funded the study. Dr. Lipton reports support for the study from AbbVie; research support paid to his institution from the Czap Foundation, National Headache Foundation, National Institutes of Health, S&L Marx Foundation, and US Food and Drug Administration; and personal fees from AbbVie/Allergan, American Academy of Neurology, American Headache Society, Amgen, Biohaven, Biovision, Boston, Dr. Reddy’s (Promius), electroCore, Eli Lilly, GlaxoSmithKline, Grifols, Lundbeck (Alder), Merck, Pernix, Pfizer, Teva, Vector, and Vedanta Research. He holds stock/options in Axon, Biohaven, CoolTech, and Manistee. Other authors report various disclosures.

Dr. Halker Singh is deputy editor of Headache, where the study was published, but wasn’t aware of it until it was published.

Mount Sinai Health System in New York City is forcing part-time physicians to sign employment contracts that violate their labor rights, according to a June 2024 complaint by the National Labor Relations Board (NLRB). 

The complaint stems from no-poaching and confidentiality clauses in the agreements required as a condition of employment, NLRB officials alleged.

The contracts state that, for 1 year following termination, part-time physicians may not recruit, solicit, or induce to terminate the employment of any hospital system employee or independent contractor, according to a copy of the terms included in NLRB’s June 18 complaint. 

By requiring the agreements, NLRB officials claimed, Mount Sinai is “interfering with, restraining, and coercing employees” in violation of the National Labor Relations Act. The health system’s “unfair labor practices” affects commerce as outlined under the law, according to the NLRB. The Act bans employers from burdening or obstructing commerce or the free flow of commerce.

Mount Sinai did not respond to requests for comment.

The NLRB’s complaint follows a landmark decision by the Federal Trade Commission (FTC) to ban noncompete agreements nationwide. In April 2024, the FTC voted to prohibit noncompetes indefinitely in an effort to protect workers.

“Noncompete clauses keep wages low, suppress new ideas, and rob the American economy of dynamism, including from the more than 8500 new startups that would be created a year once noncompetes are banned,” FTC Chair Lina M. Khan said in a statement. “The FTC’s final rule to ban noncompetes will ensure Americans have the freedom to pursue a new job, start a new business, or bring a new idea to market.”

Business groups and agencies have since sued to challenge against the ban, including the Chamber of Commerce. The Chamber and other business groups argue that noncompete agreements are important for companies to protect trade secrets, shield recruiting investments, and hide confidential information. The lawsuits are ongoing. 
 

A Physician Blows the Whistle

An anonymous physician first alerted the NLRB to the contract language in November 2023. The doctor was required the sign the hospital system’s agreement for part-time physicians. The complaint does not say if the employee is still employed by the hospital system. 

To remedy the unfair labor practices alleged, the NLRB seeks an order requiring the health system to rescind the contract language, stop any actions against current or former employees to enforce the provisions, and make whole any employees who suffered financial losses related to the contract terms. 

The allegation against Mount Sinai is among a rising number of grievances filed with the NLRB that claim unfair labor practices. During the first 6 months of fiscal year 2024, unfair labor practice charges filed across the NLRB’s field offices increased 7% — from 9612 in 2023 to 10,278 in 2024, according to a news release. 

NLRB, meanwhile has been cracking down on anticompetitive labor practices and confidentiality provisions that prevent employees from speaking out. 

In a February 2023 decision for instance, NLRB ruled that an employer violates the National Labor Relations Act by offering severance agreements to workers that include restrictive confidentiality and nondisparagement terms. In 2022, the NLRB and the Federal Trade Commission forged a partnership to more widely combat unfair, anticompetitive, and deceptive business practices. 

“Noncompete provisions reasonably tend to chill employees in the exercise of Section 7 rights when the provisions could reasonably be construed by employees to deny them the ability to quit or change jobs by cutting off their access to other employment opportunities that they are qualified for,” NLRB General Counsel Jennifer Abruzzo said in a 2023 release. 

Ms. Abruzzo stressed in a memo that NLR Act is committed to an interagency approach to restrictions on the exercise of employee rights, “including limits to workers’ job mobility, information sharing, and referrals to other agencies.” 

Mount Sinai Health System must respond to the NLRB’s complaint by July 16, and an administrative law judge is scheduled to hear the case on September 24.

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

Mount Sinai Health System in New York City is forcing part-time physicians to sign employment contracts that violate their labor rights, according to a June 2024 complaint by the National Labor Relations Board (NLRB). 

The complaint stems from no-poaching and confidentiality clauses in the agreements required as a condition of employment, NLRB officials alleged.

The contracts state that, for 1 year following termination, part-time physicians may not recruit, solicit, or induce to terminate the employment of any hospital system employee or independent contractor, according to a copy of the terms included in NLRB’s June 18 complaint. 

By requiring the agreements, NLRB officials claimed, Mount Sinai is “interfering with, restraining, and coercing employees” in violation of the National Labor Relations Act. The health system’s “unfair labor practices” affects commerce as outlined under the law, according to the NLRB. The Act bans employers from burdening or obstructing commerce or the free flow of commerce.

Mount Sinai did not respond to requests for comment.

The NLRB’s complaint follows a landmark decision by the Federal Trade Commission (FTC) to ban noncompete agreements nationwide. In April 2024, the FTC voted to prohibit noncompetes indefinitely in an effort to protect workers.

“Noncompete clauses keep wages low, suppress new ideas, and rob the American economy of dynamism, including from the more than 8500 new startups that would be created a year once noncompetes are banned,” FTC Chair Lina M. Khan said in a statement. “The FTC’s final rule to ban noncompetes will ensure Americans have the freedom to pursue a new job, start a new business, or bring a new idea to market.”

Business groups and agencies have since sued to challenge against the ban, including the Chamber of Commerce. The Chamber and other business groups argue that noncompete agreements are important for companies to protect trade secrets, shield recruiting investments, and hide confidential information. The lawsuits are ongoing. 
 

A Physician Blows the Whistle

An anonymous physician first alerted the NLRB to the contract language in November 2023. The doctor was required the sign the hospital system’s agreement for part-time physicians. The complaint does not say if the employee is still employed by the hospital system. 

To remedy the unfair labor practices alleged, the NLRB seeks an order requiring the health system to rescind the contract language, stop any actions against current or former employees to enforce the provisions, and make whole any employees who suffered financial losses related to the contract terms. 

The allegation against Mount Sinai is among a rising number of grievances filed with the NLRB that claim unfair labor practices. During the first 6 months of fiscal year 2024, unfair labor practice charges filed across the NLRB’s field offices increased 7% — from 9612 in 2023 to 10,278 in 2024, according to a news release. 

NLRB, meanwhile has been cracking down on anticompetitive labor practices and confidentiality provisions that prevent employees from speaking out. 

In a February 2023 decision for instance, NLRB ruled that an employer violates the National Labor Relations Act by offering severance agreements to workers that include restrictive confidentiality and nondisparagement terms. In 2022, the NLRB and the Federal Trade Commission forged a partnership to more widely combat unfair, anticompetitive, and deceptive business practices. 

“Noncompete provisions reasonably tend to chill employees in the exercise of Section 7 rights when the provisions could reasonably be construed by employees to deny them the ability to quit or change jobs by cutting off their access to other employment opportunities that they are qualified for,” NLRB General Counsel Jennifer Abruzzo said in a 2023 release. 

Ms. Abruzzo stressed in a memo that NLR Act is committed to an interagency approach to restrictions on the exercise of employee rights, “including limits to workers’ job mobility, information sharing, and referrals to other agencies.” 

Mount Sinai Health System must respond to the NLRB’s complaint by July 16, and an administrative law judge is scheduled to hear the case on September 24.

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

Mount Sinai Health System in New York City is forcing part-time physicians to sign employment contracts that violate their labor rights, according to a June 2024 complaint by the National Labor Relations Board (NLRB). 

The complaint stems from no-poaching and confidentiality clauses in the agreements required as a condition of employment, NLRB officials alleged.

The contracts state that, for 1 year following termination, part-time physicians may not recruit, solicit, or induce to terminate the employment of any hospital system employee or independent contractor, according to a copy of the terms included in NLRB’s June 18 complaint. 

By requiring the agreements, NLRB officials claimed, Mount Sinai is “interfering with, restraining, and coercing employees” in violation of the National Labor Relations Act. The health system’s “unfair labor practices” affects commerce as outlined under the law, according to the NLRB. The Act bans employers from burdening or obstructing commerce or the free flow of commerce.

Mount Sinai did not respond to requests for comment.

The NLRB’s complaint follows a landmark decision by the Federal Trade Commission (FTC) to ban noncompete agreements nationwide. In April 2024, the FTC voted to prohibit noncompetes indefinitely in an effort to protect workers.

“Noncompete clauses keep wages low, suppress new ideas, and rob the American economy of dynamism, including from the more than 8500 new startups that would be created a year once noncompetes are banned,” FTC Chair Lina M. Khan said in a statement. “The FTC’s final rule to ban noncompetes will ensure Americans have the freedom to pursue a new job, start a new business, or bring a new idea to market.”

Business groups and agencies have since sued to challenge against the ban, including the Chamber of Commerce. The Chamber and other business groups argue that noncompete agreements are important for companies to protect trade secrets, shield recruiting investments, and hide confidential information. The lawsuits are ongoing. 
 

A Physician Blows the Whistle

An anonymous physician first alerted the NLRB to the contract language in November 2023. The doctor was required the sign the hospital system’s agreement for part-time physicians. The complaint does not say if the employee is still employed by the hospital system. 

To remedy the unfair labor practices alleged, the NLRB seeks an order requiring the health system to rescind the contract language, stop any actions against current or former employees to enforce the provisions, and make whole any employees who suffered financial losses related to the contract terms. 

The allegation against Mount Sinai is among a rising number of grievances filed with the NLRB that claim unfair labor practices. During the first 6 months of fiscal year 2024, unfair labor practice charges filed across the NLRB’s field offices increased 7% — from 9612 in 2023 to 10,278 in 2024, according to a news release. 

NLRB, meanwhile has been cracking down on anticompetitive labor practices and confidentiality provisions that prevent employees from speaking out. 

In a February 2023 decision for instance, NLRB ruled that an employer violates the National Labor Relations Act by offering severance agreements to workers that include restrictive confidentiality and nondisparagement terms. In 2022, the NLRB and the Federal Trade Commission forged a partnership to more widely combat unfair, anticompetitive, and deceptive business practices. 

“Noncompete provisions reasonably tend to chill employees in the exercise of Section 7 rights when the provisions could reasonably be construed by employees to deny them the ability to quit or change jobs by cutting off their access to other employment opportunities that they are qualified for,” NLRB General Counsel Jennifer Abruzzo said in a 2023 release. 

Ms. Abruzzo stressed in a memo that NLR Act is committed to an interagency approach to restrictions on the exercise of employee rights, “including limits to workers’ job mobility, information sharing, and referrals to other agencies.” 

Mount Sinai Health System must respond to the NLRB’s complaint by July 16, and an administrative law judge is scheduled to hear the case on September 24.

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

ORLANDO, FLORIDA — Cannabis users may have a “healthier inflammatory cytokine profile, better insulin sensitivity, and higher levels of physical activity than nonusers,” all of which can be linked to a potentially lower risk for diabetes, ongoing research suggests.

In the findings from the SONIC trial, Angela Bryan, PhD, professor and codirector of CUChange at the University of Colorado, Boulder, and colleagues hypothesized that “those inflammatory profiles would improve over the course of 4 weeks, particularly for those using a CBD [cannabidiol] as opposed to a THC [tetrahydrocannabinol] product.”

She presented the findings at the American Diabetes Association (ADA) 84th Scientific Sessions.

Other recent work by Dr. Bryan and her colleagues focused on the public health implications of cannabis legalization. One study examined the acute effects of legal-market cannabis on regular users’ subjective responses while running and found that cannabis use prior to exercise may lead to more enjoyment and runner’s high symptoms, although it also led to feelings of greater exertion. The positive effects could make exercise more appealing to individuals — including those with or at risk for diabetes — who might not otherwise engage in it, Bryan suggested.

Another study found that CBD-dominant forms of cannabis were associated with acute tension reduction, which might lead to longer-term reductions in anxiety. Bryan said the findings could be relevant in the context of diabetes distress.
 

‘Complicated’ Connection to Diabetes

In the SONIC study, participants who were regular cannabis users had an average age of 30 years and had body mass index (BMI) in the healthy range; 86% were White individuals, and 59% were men. They were matched with a similar group of individuals who had not used cannabis for at least a year. At baseline, participants’ NSDR Healthy Eating Index score overall was 51.24, showing a “need for improvement/poor diet.” 

“Folks were maybe not killing it in the dietary domain,” Dr. Bryan acknowledged. “However, they were absolutely killing it in the physical activity domain.”

The researchers did oral glucose tolerance tests to calculate participants’ Matsuda index of insulin sensitivity and measured inflammatory markers, including tumor necrosis factor alpha, interleukin 6 (IL6), IL1 beta, IL12, interferon gamma, IL4, and monocyte chemoattractant protein 1 (MCP-1). In a “randomized encouragement” design, users were assigned to purchase and use a flower product for 4 weeks, however much they wanted. They completed daily assessments of their cannabis use, alcohol use, diet, and physical activity.

Between-group eating patterns were similar over the 4 weeks, with cannabis users reporting “marginally” more servings of salty snacks and food relative to nonusers. None of the daily associations were moderated by which cannabis product was used.

At 4 weeks, the team repeated the tests and, surprisingly, found no change in participants’ inflammatory markers. But what “popped out,” she said, was the “stark difference” between users and nonusers, with users having significantly lower levels of inflammatory biomarkers, circulating cytokines than the nonusers.

An exception were levels of MCP-1, which increased over time in the users but didn’t change in nonusers. Bryan said the finding is “perplexing” and asked the audience for thoughts, especially given that MCP-1 levels are positively associated with diabetes.

After controlling for BMI and inflammation, “we saw absolutely no effects of group or group by time interaction on the Matsuda index of insulin sensitivity,” she said. “Seemingly, there are no chronic effects of cannabis use on insulin sensitivity.”

Regarding limitations, Dr. Bryan acknowledged that the study is being conducted with “a very healthy sample of individuals who exercise a lot, and that might be factoring into our results, especially on insulin sensitivity.” The team could not use “gold standard” randomization because of the schedule-1 status of CannaVan cannabis, and the MCP-1 findings are difficult to interpret.

Furthermore, she noted, “our day-to-day level data show only slight differences in behavior between those who use cannabis and those who don’t and also very slight differences between users’ behavior on days that they use vs days that they don’t.

“I think all of this put together shows us that the relationship between cannabis use and potential implications for diabetes is a lot more complicated than just couch to couchlock [very deep relaxation/sedation] or runner’s high,” she said.
 

Bring On the CannaVan

The team’s next step, currently underway, is to get an acute response to cannabis with an oral glucose tolerance test that’s done immediately after the participant uses a product. Since cannabis is a schedule-1 drug, it can’t be taken into the laboratory. Therefore, the researchers are using a CannaVan — a mobile lab. “We drive it to their homes, they come out, we draw blood, and we send them back into their homes to use as much of their product as they want,” Bryan explained. “They come back out to the van. They do all the follow-up assessments. We take blood again to verify their exposure. And that’s how we collect those data.”

“Invite me back next year, and I will tell you what we found,” she quipped.

Dr. Bryan had no disclosures to report. 

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

ORLANDO, FLORIDA — Cannabis users may have a “healthier inflammatory cytokine profile, better insulin sensitivity, and higher levels of physical activity than nonusers,” all of which can be linked to a potentially lower risk for diabetes, ongoing research suggests.

In the findings from the SONIC trial, Angela Bryan, PhD, professor and codirector of CUChange at the University of Colorado, Boulder, and colleagues hypothesized that “those inflammatory profiles would improve over the course of 4 weeks, particularly for those using a CBD [cannabidiol] as opposed to a THC [tetrahydrocannabinol] product.”

She presented the findings at the American Diabetes Association (ADA) 84th Scientific Sessions.

Other recent work by Dr. Bryan and her colleagues focused on the public health implications of cannabis legalization. One study examined the acute effects of legal-market cannabis on regular users’ subjective responses while running and found that cannabis use prior to exercise may lead to more enjoyment and runner’s high symptoms, although it also led to feelings of greater exertion. The positive effects could make exercise more appealing to individuals — including those with or at risk for diabetes — who might not otherwise engage in it, Bryan suggested.

Another study found that CBD-dominant forms of cannabis were associated with acute tension reduction, which might lead to longer-term reductions in anxiety. Bryan said the findings could be relevant in the context of diabetes distress.
 

‘Complicated’ Connection to Diabetes

In the SONIC study, participants who were regular cannabis users had an average age of 30 years and had body mass index (BMI) in the healthy range; 86% were White individuals, and 59% were men. They were matched with a similar group of individuals who had not used cannabis for at least a year. At baseline, participants’ NSDR Healthy Eating Index score overall was 51.24, showing a “need for improvement/poor diet.” 

“Folks were maybe not killing it in the dietary domain,” Dr. Bryan acknowledged. “However, they were absolutely killing it in the physical activity domain.”

The researchers did oral glucose tolerance tests to calculate participants’ Matsuda index of insulin sensitivity and measured inflammatory markers, including tumor necrosis factor alpha, interleukin 6 (IL6), IL1 beta, IL12, interferon gamma, IL4, and monocyte chemoattractant protein 1 (MCP-1). In a “randomized encouragement” design, users were assigned to purchase and use a flower product for 4 weeks, however much they wanted. They completed daily assessments of their cannabis use, alcohol use, diet, and physical activity.

Between-group eating patterns were similar over the 4 weeks, with cannabis users reporting “marginally” more servings of salty snacks and food relative to nonusers. None of the daily associations were moderated by which cannabis product was used.

At 4 weeks, the team repeated the tests and, surprisingly, found no change in participants’ inflammatory markers. But what “popped out,” she said, was the “stark difference” between users and nonusers, with users having significantly lower levels of inflammatory biomarkers, circulating cytokines than the nonusers.

An exception were levels of MCP-1, which increased over time in the users but didn’t change in nonusers. Bryan said the finding is “perplexing” and asked the audience for thoughts, especially given that MCP-1 levels are positively associated with diabetes.

After controlling for BMI and inflammation, “we saw absolutely no effects of group or group by time interaction on the Matsuda index of insulin sensitivity,” she said. “Seemingly, there are no chronic effects of cannabis use on insulin sensitivity.”

Regarding limitations, Dr. Bryan acknowledged that the study is being conducted with “a very healthy sample of individuals who exercise a lot, and that might be factoring into our results, especially on insulin sensitivity.” The team could not use “gold standard” randomization because of the schedule-1 status of CannaVan cannabis, and the MCP-1 findings are difficult to interpret.

Furthermore, she noted, “our day-to-day level data show only slight differences in behavior between those who use cannabis and those who don’t and also very slight differences between users’ behavior on days that they use vs days that they don’t.

“I think all of this put together shows us that the relationship between cannabis use and potential implications for diabetes is a lot more complicated than just couch to couchlock [very deep relaxation/sedation] or runner’s high,” she said.
 

Bring On the CannaVan

The team’s next step, currently underway, is to get an acute response to cannabis with an oral glucose tolerance test that’s done immediately after the participant uses a product. Since cannabis is a schedule-1 drug, it can’t be taken into the laboratory. Therefore, the researchers are using a CannaVan — a mobile lab. “We drive it to their homes, they come out, we draw blood, and we send them back into their homes to use as much of their product as they want,” Bryan explained. “They come back out to the van. They do all the follow-up assessments. We take blood again to verify their exposure. And that’s how we collect those data.”

“Invite me back next year, and I will tell you what we found,” she quipped.

Dr. Bryan had no disclosures to report. 

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

ORLANDO, FLORIDA — Cannabis users may have a “healthier inflammatory cytokine profile, better insulin sensitivity, and higher levels of physical activity than nonusers,” all of which can be linked to a potentially lower risk for diabetes, ongoing research suggests.

In the findings from the SONIC trial, Angela Bryan, PhD, professor and codirector of CUChange at the University of Colorado, Boulder, and colleagues hypothesized that “those inflammatory profiles would improve over the course of 4 weeks, particularly for those using a CBD [cannabidiol] as opposed to a THC [tetrahydrocannabinol] product.”

She presented the findings at the American Diabetes Association (ADA) 84th Scientific Sessions.

Other recent work by Dr. Bryan and her colleagues focused on the public health implications of cannabis legalization. One study examined the acute effects of legal-market cannabis on regular users’ subjective responses while running and found that cannabis use prior to exercise may lead to more enjoyment and runner’s high symptoms, although it also led to feelings of greater exertion. The positive effects could make exercise more appealing to individuals — including those with or at risk for diabetes — who might not otherwise engage in it, Bryan suggested.

Another study found that CBD-dominant forms of cannabis were associated with acute tension reduction, which might lead to longer-term reductions in anxiety. Bryan said the findings could be relevant in the context of diabetes distress.
 

‘Complicated’ Connection to Diabetes

In the SONIC study, participants who were regular cannabis users had an average age of 30 years and had body mass index (BMI) in the healthy range; 86% were White individuals, and 59% were men. They were matched with a similar group of individuals who had not used cannabis for at least a year. At baseline, participants’ NSDR Healthy Eating Index score overall was 51.24, showing a “need for improvement/poor diet.” 

“Folks were maybe not killing it in the dietary domain,” Dr. Bryan acknowledged. “However, they were absolutely killing it in the physical activity domain.”

The researchers did oral glucose tolerance tests to calculate participants’ Matsuda index of insulin sensitivity and measured inflammatory markers, including tumor necrosis factor alpha, interleukin 6 (IL6), IL1 beta, IL12, interferon gamma, IL4, and monocyte chemoattractant protein 1 (MCP-1). In a “randomized encouragement” design, users were assigned to purchase and use a flower product for 4 weeks, however much they wanted. They completed daily assessments of their cannabis use, alcohol use, diet, and physical activity.

Between-group eating patterns were similar over the 4 weeks, with cannabis users reporting “marginally” more servings of salty snacks and food relative to nonusers. None of the daily associations were moderated by which cannabis product was used.

At 4 weeks, the team repeated the tests and, surprisingly, found no change in participants’ inflammatory markers. But what “popped out,” she said, was the “stark difference” between users and nonusers, with users having significantly lower levels of inflammatory biomarkers, circulating cytokines than the nonusers.

An exception were levels of MCP-1, which increased over time in the users but didn’t change in nonusers. Bryan said the finding is “perplexing” and asked the audience for thoughts, especially given that MCP-1 levels are positively associated with diabetes.

After controlling for BMI and inflammation, “we saw absolutely no effects of group or group by time interaction on the Matsuda index of insulin sensitivity,” she said. “Seemingly, there are no chronic effects of cannabis use on insulin sensitivity.”

Regarding limitations, Dr. Bryan acknowledged that the study is being conducted with “a very healthy sample of individuals who exercise a lot, and that might be factoring into our results, especially on insulin sensitivity.” The team could not use “gold standard” randomization because of the schedule-1 status of CannaVan cannabis, and the MCP-1 findings are difficult to interpret.

Furthermore, she noted, “our day-to-day level data show only slight differences in behavior between those who use cannabis and those who don’t and also very slight differences between users’ behavior on days that they use vs days that they don’t.

“I think all of this put together shows us that the relationship between cannabis use and potential implications for diabetes is a lot more complicated than just couch to couchlock [very deep relaxation/sedation] or runner’s high,” she said.
 

Bring On the CannaVan

The team’s next step, currently underway, is to get an acute response to cannabis with an oral glucose tolerance test that’s done immediately after the participant uses a product. Since cannabis is a schedule-1 drug, it can’t be taken into the laboratory. Therefore, the researchers are using a CannaVan — a mobile lab. “We drive it to their homes, they come out, we draw blood, and we send them back into their homes to use as much of their product as they want,” Bryan explained. “They come back out to the van. They do all the follow-up assessments. We take blood again to verify their exposure. And that’s how we collect those data.”

“Invite me back next year, and I will tell you what we found,” she quipped.

Dr. Bryan had no disclosures to report. 

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

People who have recovered from long COVID can suffer relapses or flare-ups from new viral infections — not just from COVID but from cold, flu, and other viral pathogens, researchers have found.

In some cases, they may be experiencing what researchers call viral interference, something also experienced by people with HIV and other infections associated with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).

Clinical studies on the issue are limited, but patients, doctors, and researchers report many people who previously had long COVID have developed recurring symptoms after consequent viral infections.

Viral persistence — where bits of virus linger in the body — and viral reactivation remain two of the leading suspects for Yale researchers. Viral activation occurs when the immune system responds to an infection by triggering a dormant virus.

Anecdotally, these flare-ups occur more commonly in patients with long COVID with autonomic dysfunction — severe dizziness when standing up — and other symptoms of ME/CFS, said Alba Azola, MD, a Johns Hopkins Medicine rehabilitation specialist in Baltimore, Maryland, who works with patients with long COVID and other “fatiguing illnesses.”

At last count, about 18% of those surveyed by the Centers for Disease Control and Prevention said they had experienced long COVID. Nearly 60% of those surveyed said they had contracted COVID-19 at least once.

Dr. Azola said that very afternoon she had seen a patient with the flu and a recurrence of previous long COVID symptoms. Not much data exist about cases like this.

“I can’t say there is a specific study looking at this, but anecdotally, we see it all the time,” Dr. Azola said.

She has not seen completely different symptoms; more commonly, she sees a flare-up of previously existing symptoms.

David Putrino, PhD, is director of rehabilitation innovation for the Mount Sinai Health System in New York City. He treats and studies patients with long COVID and echoes what others have seen.

Patients can “recover (or feel recovered) from long COVID until the next immune challenge — another COVID infection, flu infection, pregnancy, food poisoning (all examples we have seen in the clinic) — and experience a significant flare-up of your initial COVID infection,” he said.

“Relapse” is a better term than reinfection, said Jeffrey Parsonnet, MD, an infectious diseases specialist and director of the Dartmouth Hitchcock Post-Acute COVID Syndrome Clinic, Lebanon, New Hampshire.

“We see patients who had COVID-19 followed by long COVID who then get better — either completely or mostly better. Then they’ve gotten COVID again, and this is followed by recurrence of long COVID symptoms,” he said.

“Every patient looks different in terms of what gets better and how quickly. And again, some patients are not better (or even minimally so) after a couple of years,” he said.
 

Patients Tell Their Stories

On the COVID-19 Long Haulers Support Facebook group, many of the 100,000 followers ask about viral reactivation. Delainne “Laney” Bond, RN, who has battled postinfection chronic illness herself, runs the Facebook group. From what she sees, “each time a person is infected or reinfected with SARS-CoV-2, they have a risk of developing long COVID or experiencing worse long COVID. Multiple infections can lead to progressive health complications.”

The posts on her site include many queries about reinfections. A post from December included nearly 80 comments with people describing the full range of symptoms. Some stories relayed how the reinfection symptoms were short lived. Some report returning to their baseline — not completely symptom free but improved.

Doctors and patients say long COVID comes and goes — relapsing-remitting — and shares many features with other complex multisystem chronic conditions, according to a new National Academy of Sciences report. Those include ME/CFS and the Epstein-Barr virus.

As far as how to treat, Dr. Putrino is one of the clinical researchers testing antivirals. One is Paxlovid; the others are drugs developed for the AIDS virus.

“A plausible mechanism for long COVID is persistence of the SARS-CoV-2 virus in tissue and/or the reactivation of latent pathogens,” according to an explanation of the research on the PolyBio Institute website, which is involved with the research.

In the meantime, “long COVID appears to be a chronic condition with few patients achieving full remission,” according to a new Academy of Sciences report. The report concludes that long COVID recovery can plateau at 6-12 months. They also note that 18%-22% of people who have long COVID symptoms at 5 months are still ill at 1 year.

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

People who have recovered from long COVID can suffer relapses or flare-ups from new viral infections — not just from COVID but from cold, flu, and other viral pathogens, researchers have found.

In some cases, they may be experiencing what researchers call viral interference, something also experienced by people with HIV and other infections associated with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).

Clinical studies on the issue are limited, but patients, doctors, and researchers report many people who previously had long COVID have developed recurring symptoms after consequent viral infections.

Viral persistence — where bits of virus linger in the body — and viral reactivation remain two of the leading suspects for Yale researchers. Viral activation occurs when the immune system responds to an infection by triggering a dormant virus.

Anecdotally, these flare-ups occur more commonly in patients with long COVID with autonomic dysfunction — severe dizziness when standing up — and other symptoms of ME/CFS, said Alba Azola, MD, a Johns Hopkins Medicine rehabilitation specialist in Baltimore, Maryland, who works with patients with long COVID and other “fatiguing illnesses.”

At last count, about 18% of those surveyed by the Centers for Disease Control and Prevention said they had experienced long COVID. Nearly 60% of those surveyed said they had contracted COVID-19 at least once.

Dr. Azola said that very afternoon she had seen a patient with the flu and a recurrence of previous long COVID symptoms. Not much data exist about cases like this.

“I can’t say there is a specific study looking at this, but anecdotally, we see it all the time,” Dr. Azola said.

She has not seen completely different symptoms; more commonly, she sees a flare-up of previously existing symptoms.

David Putrino, PhD, is director of rehabilitation innovation for the Mount Sinai Health System in New York City. He treats and studies patients with long COVID and echoes what others have seen.

Patients can “recover (or feel recovered) from long COVID until the next immune challenge — another COVID infection, flu infection, pregnancy, food poisoning (all examples we have seen in the clinic) — and experience a significant flare-up of your initial COVID infection,” he said.

“Relapse” is a better term than reinfection, said Jeffrey Parsonnet, MD, an infectious diseases specialist and director of the Dartmouth Hitchcock Post-Acute COVID Syndrome Clinic, Lebanon, New Hampshire.

“We see patients who had COVID-19 followed by long COVID who then get better — either completely or mostly better. Then they’ve gotten COVID again, and this is followed by recurrence of long COVID symptoms,” he said.

“Every patient looks different in terms of what gets better and how quickly. And again, some patients are not better (or even minimally so) after a couple of years,” he said.
 

Patients Tell Their Stories

On the COVID-19 Long Haulers Support Facebook group, many of the 100,000 followers ask about viral reactivation. Delainne “Laney” Bond, RN, who has battled postinfection chronic illness herself, runs the Facebook group. From what she sees, “each time a person is infected or reinfected with SARS-CoV-2, they have a risk of developing long COVID or experiencing worse long COVID. Multiple infections can lead to progressive health complications.”

The posts on her site include many queries about reinfections. A post from December included nearly 80 comments with people describing the full range of symptoms. Some stories relayed how the reinfection symptoms were short lived. Some report returning to their baseline — not completely symptom free but improved.

Doctors and patients say long COVID comes and goes — relapsing-remitting — and shares many features with other complex multisystem chronic conditions, according to a new National Academy of Sciences report. Those include ME/CFS and the Epstein-Barr virus.

As far as how to treat, Dr. Putrino is one of the clinical researchers testing antivirals. One is Paxlovid; the others are drugs developed for the AIDS virus.

“A plausible mechanism for long COVID is persistence of the SARS-CoV-2 virus in tissue and/or the reactivation of latent pathogens,” according to an explanation of the research on the PolyBio Institute website, which is involved with the research.

In the meantime, “long COVID appears to be a chronic condition with few patients achieving full remission,” according to a new Academy of Sciences report. The report concludes that long COVID recovery can plateau at 6-12 months. They also note that 18%-22% of people who have long COVID symptoms at 5 months are still ill at 1 year.

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

People who have recovered from long COVID can suffer relapses or flare-ups from new viral infections — not just from COVID but from cold, flu, and other viral pathogens, researchers have found.

In some cases, they may be experiencing what researchers call viral interference, something also experienced by people with HIV and other infections associated with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).

Clinical studies on the issue are limited, but patients, doctors, and researchers report many people who previously had long COVID have developed recurring symptoms after consequent viral infections.

Viral persistence — where bits of virus linger in the body — and viral reactivation remain two of the leading suspects for Yale researchers. Viral activation occurs when the immune system responds to an infection by triggering a dormant virus.

Anecdotally, these flare-ups occur more commonly in patients with long COVID with autonomic dysfunction — severe dizziness when standing up — and other symptoms of ME/CFS, said Alba Azola, MD, a Johns Hopkins Medicine rehabilitation specialist in Baltimore, Maryland, who works with patients with long COVID and other “fatiguing illnesses.”

At last count, about 18% of those surveyed by the Centers for Disease Control and Prevention said they had experienced long COVID. Nearly 60% of those surveyed said they had contracted COVID-19 at least once.

Dr. Azola said that very afternoon she had seen a patient with the flu and a recurrence of previous long COVID symptoms. Not much data exist about cases like this.

“I can’t say there is a specific study looking at this, but anecdotally, we see it all the time,” Dr. Azola said.

She has not seen completely different symptoms; more commonly, she sees a flare-up of previously existing symptoms.

David Putrino, PhD, is director of rehabilitation innovation for the Mount Sinai Health System in New York City. He treats and studies patients with long COVID and echoes what others have seen.

Patients can “recover (or feel recovered) from long COVID until the next immune challenge — another COVID infection, flu infection, pregnancy, food poisoning (all examples we have seen in the clinic) — and experience a significant flare-up of your initial COVID infection,” he said.

“Relapse” is a better term than reinfection, said Jeffrey Parsonnet, MD, an infectious diseases specialist and director of the Dartmouth Hitchcock Post-Acute COVID Syndrome Clinic, Lebanon, New Hampshire.

“We see patients who had COVID-19 followed by long COVID who then get better — either completely or mostly better. Then they’ve gotten COVID again, and this is followed by recurrence of long COVID symptoms,” he said.

“Every patient looks different in terms of what gets better and how quickly. And again, some patients are not better (or even minimally so) after a couple of years,” he said.
 

Patients Tell Their Stories

On the COVID-19 Long Haulers Support Facebook group, many of the 100,000 followers ask about viral reactivation. Delainne “Laney” Bond, RN, who has battled postinfection chronic illness herself, runs the Facebook group. From what she sees, “each time a person is infected or reinfected with SARS-CoV-2, they have a risk of developing long COVID or experiencing worse long COVID. Multiple infections can lead to progressive health complications.”

The posts on her site include many queries about reinfections. A post from December included nearly 80 comments with people describing the full range of symptoms. Some stories relayed how the reinfection symptoms were short lived. Some report returning to their baseline — not completely symptom free but improved.

Doctors and patients say long COVID comes and goes — relapsing-remitting — and shares many features with other complex multisystem chronic conditions, according to a new National Academy of Sciences report. Those include ME/CFS and the Epstein-Barr virus.

As far as how to treat, Dr. Putrino is one of the clinical researchers testing antivirals. One is Paxlovid; the others are drugs developed for the AIDS virus.

“A plausible mechanism for long COVID is persistence of the SARS-CoV-2 virus in tissue and/or the reactivation of latent pathogens,” according to an explanation of the research on the PolyBio Institute website, which is involved with the research.

In the meantime, “long COVID appears to be a chronic condition with few patients achieving full remission,” according to a new Academy of Sciences report. The report concludes that long COVID recovery can plateau at 6-12 months. They also note that 18%-22% of people who have long COVID symptoms at 5 months are still ill at 1 year.

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

ORLANDO, FLORIDA — An analysis of data from 137 patients suggested testing whether people have a trait known as abnormal postprandial satiety (APS), or hungry gut, can predict how well they may respond to the obesity drug semaglutide, although it failed to establish this link for the somewhat similar tirzepatide.

At the American Diabetes Association (ADA) Scientific Sessions, Maria Daniela Hurtado Andrade, MD, PhD, of the Mayo Clinic, Jacksonville, Florida, presented results of a study using the MyPhenome Hungry Gut test, which was developed through machine learning, a form of artificial intelligence. 

The test is part of the MyPhenome obesity phenotyping portfolio from Phenomix Sciences, a company founded by Mayo Clinic physicians, scientists, and researchers Andres Acosta, MD, PhD, and Michael Camilleri, MD, DSc. 

At the ADA meeting, Dr. Hurtado Andrade discussed a test of 137 adults: 91 were considered to have a positive biomarker for abnormal postprandial satiety (APS+), and 46 who did not have it were classified as APS−. These were patients of the Mayo Clinic who were already taking obesity drugs and agreed to phenotyping. Of this group, 113 were on semaglutide and 24 on tirzepatide.

At 12 months, among those taking semaglutide, patients classified as APS+ achieved a mean 18% body weight loss compared with 10% in those classified as APS−. But the test didn’t find these kinds of differences for the tirzepatide group, with a mean 19.4% body weight loss in the APS+ group and a mean loss of 22.1% in the APS− group.

Further studies are warranted to assess the clinical utility of these biomarkers, Dr. Hurtado Andrade said. But these findings do support “the use of precision medicine for obesity based on an individual’s genetic background,” she said.

Dr. Hurtado Andrade’s presentation impressed fellow researchers who noted it as an early step toward the long-sought goal of more personalized medicine.

Daniel S. Hsia, MD, of Emory University, Atlanta, who led the ADA session at which Dr. Hurtado Andrade presented, said it was good to see new information being presented about using genetic risk scoring in obesity.

“The numbers were very small for the tirzepatide group as compared to the semaglutide group, so it’s a little hard to really come to any significant conclusions,” Dr. Hsia said in an interview.

At the ADA meeting, Ajay D. Rao, MD, MMSc, of Temple University, Philadelphia, said clinicians are excited about the idea of having biomarkers to aid in decisions about approaches to obesity.

In a follow-up interview with this news organization, Dr. Rao said he too is looking to see more testing of this approach to care, while describing Hurtado Andrade’s work as a “very well-done study.”

“We still need to see more large-scale studies of responsiveness to certain interventions,” he said. 

Dr. Hurtado Andrade noted that researchers at academic centers such as Mayo can try to hone in the combination of genetic and other factors that led to obesity, such as emotional eating patterns and abnormal postprandial satiety. 

But this approach is not widely scalable, as it demands resources of time and staffing that not all clinicians and patients enjoy.

“To overcome this challenge, our team has been working on developing biomarkers” such as the machine-learning gene risk score used to predict abnormal postprandial satiety, she said.

Findings for a related project were presented in May at Digestive Disease Week, as this news organization reported earlier. In that study, researchers calculated the genetic risk score for 84 adults undergoing weight loss interventions at Mayo Clinic who were prescribed the glucagon-like peptide 1 receptor agonist semaglutide.

This news organization separately asked Phenomix about the sales of MyPhenome Test kits. These cost $499, and about 500 tests have been sold since commercialization started last year, a spokesperson said.

The study was funded by Phenomix Sciences. Separately, Dr. Hurtado Andrade has worked as a consultant for Novo Nordisk and received research support from the National Institutes of Health. 

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

ORLANDO, FLORIDA — An analysis of data from 137 patients suggested testing whether people have a trait known as abnormal postprandial satiety (APS), or hungry gut, can predict how well they may respond to the obesity drug semaglutide, although it failed to establish this link for the somewhat similar tirzepatide.

At the American Diabetes Association (ADA) Scientific Sessions, Maria Daniela Hurtado Andrade, MD, PhD, of the Mayo Clinic, Jacksonville, Florida, presented results of a study using the MyPhenome Hungry Gut test, which was developed through machine learning, a form of artificial intelligence. 

The test is part of the MyPhenome obesity phenotyping portfolio from Phenomix Sciences, a company founded by Mayo Clinic physicians, scientists, and researchers Andres Acosta, MD, PhD, and Michael Camilleri, MD, DSc. 

At the ADA meeting, Dr. Hurtado Andrade discussed a test of 137 adults: 91 were considered to have a positive biomarker for abnormal postprandial satiety (APS+), and 46 who did not have it were classified as APS−. These were patients of the Mayo Clinic who were already taking obesity drugs and agreed to phenotyping. Of this group, 113 were on semaglutide and 24 on tirzepatide.

At 12 months, among those taking semaglutide, patients classified as APS+ achieved a mean 18% body weight loss compared with 10% in those classified as APS−. But the test didn’t find these kinds of differences for the tirzepatide group, with a mean 19.4% body weight loss in the APS+ group and a mean loss of 22.1% in the APS− group.

Further studies are warranted to assess the clinical utility of these biomarkers, Dr. Hurtado Andrade said. But these findings do support “the use of precision medicine for obesity based on an individual’s genetic background,” she said.

Dr. Hurtado Andrade’s presentation impressed fellow researchers who noted it as an early step toward the long-sought goal of more personalized medicine.

Daniel S. Hsia, MD, of Emory University, Atlanta, who led the ADA session at which Dr. Hurtado Andrade presented, said it was good to see new information being presented about using genetic risk scoring in obesity.

“The numbers were very small for the tirzepatide group as compared to the semaglutide group, so it’s a little hard to really come to any significant conclusions,” Dr. Hsia said in an interview.

At the ADA meeting, Ajay D. Rao, MD, MMSc, of Temple University, Philadelphia, said clinicians are excited about the idea of having biomarkers to aid in decisions about approaches to obesity.

In a follow-up interview with this news organization, Dr. Rao said he too is looking to see more testing of this approach to care, while describing Hurtado Andrade’s work as a “very well-done study.”

“We still need to see more large-scale studies of responsiveness to certain interventions,” he said. 

Dr. Hurtado Andrade noted that researchers at academic centers such as Mayo can try to hone in the combination of genetic and other factors that led to obesity, such as emotional eating patterns and abnormal postprandial satiety. 

But this approach is not widely scalable, as it demands resources of time and staffing that not all clinicians and patients enjoy.

“To overcome this challenge, our team has been working on developing biomarkers” such as the machine-learning gene risk score used to predict abnormal postprandial satiety, she said.

Findings for a related project were presented in May at Digestive Disease Week, as this news organization reported earlier. In that study, researchers calculated the genetic risk score for 84 adults undergoing weight loss interventions at Mayo Clinic who were prescribed the glucagon-like peptide 1 receptor agonist semaglutide.

This news organization separately asked Phenomix about the sales of MyPhenome Test kits. These cost $499, and about 500 tests have been sold since commercialization started last year, a spokesperson said.

The study was funded by Phenomix Sciences. Separately, Dr. Hurtado Andrade has worked as a consultant for Novo Nordisk and received research support from the National Institutes of Health. 

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

ORLANDO, FLORIDA — An analysis of data from 137 patients suggested testing whether people have a trait known as abnormal postprandial satiety (APS), or hungry gut, can predict how well they may respond to the obesity drug semaglutide, although it failed to establish this link for the somewhat similar tirzepatide.

At the American Diabetes Association (ADA) Scientific Sessions, Maria Daniela Hurtado Andrade, MD, PhD, of the Mayo Clinic, Jacksonville, Florida, presented results of a study using the MyPhenome Hungry Gut test, which was developed through machine learning, a form of artificial intelligence. 

The test is part of the MyPhenome obesity phenotyping portfolio from Phenomix Sciences, a company founded by Mayo Clinic physicians, scientists, and researchers Andres Acosta, MD, PhD, and Michael Camilleri, MD, DSc. 

At the ADA meeting, Dr. Hurtado Andrade discussed a test of 137 adults: 91 were considered to have a positive biomarker for abnormal postprandial satiety (APS+), and 46 who did not have it were classified as APS−. These were patients of the Mayo Clinic who were already taking obesity drugs and agreed to phenotyping. Of this group, 113 were on semaglutide and 24 on tirzepatide.

At 12 months, among those taking semaglutide, patients classified as APS+ achieved a mean 18% body weight loss compared with 10% in those classified as APS−. But the test didn’t find these kinds of differences for the tirzepatide group, with a mean 19.4% body weight loss in the APS+ group and a mean loss of 22.1% in the APS− group.

Further studies are warranted to assess the clinical utility of these biomarkers, Dr. Hurtado Andrade said. But these findings do support “the use of precision medicine for obesity based on an individual’s genetic background,” she said.

Dr. Hurtado Andrade’s presentation impressed fellow researchers who noted it as an early step toward the long-sought goal of more personalized medicine.

Daniel S. Hsia, MD, of Emory University, Atlanta, who led the ADA session at which Dr. Hurtado Andrade presented, said it was good to see new information being presented about using genetic risk scoring in obesity.

“The numbers were very small for the tirzepatide group as compared to the semaglutide group, so it’s a little hard to really come to any significant conclusions,” Dr. Hsia said in an interview.

At the ADA meeting, Ajay D. Rao, MD, MMSc, of Temple University, Philadelphia, said clinicians are excited about the idea of having biomarkers to aid in decisions about approaches to obesity.

In a follow-up interview with this news organization, Dr. Rao said he too is looking to see more testing of this approach to care, while describing Hurtado Andrade’s work as a “very well-done study.”

“We still need to see more large-scale studies of responsiveness to certain interventions,” he said. 

Dr. Hurtado Andrade noted that researchers at academic centers such as Mayo can try to hone in the combination of genetic and other factors that led to obesity, such as emotional eating patterns and abnormal postprandial satiety. 

But this approach is not widely scalable, as it demands resources of time and staffing that not all clinicians and patients enjoy.

“To overcome this challenge, our team has been working on developing biomarkers” such as the machine-learning gene risk score used to predict abnormal postprandial satiety, she said.

Findings for a related project were presented in May at Digestive Disease Week, as this news organization reported earlier. In that study, researchers calculated the genetic risk score for 84 adults undergoing weight loss interventions at Mayo Clinic who were prescribed the glucagon-like peptide 1 receptor agonist semaglutide.

This news organization separately asked Phenomix about the sales of MyPhenome Test kits. These cost $499, and about 500 tests have been sold since commercialization started last year, a spokesperson said.

The study was funded by Phenomix Sciences. Separately, Dr. Hurtado Andrade has worked as a consultant for Novo Nordisk and received research support from the National Institutes of Health. 

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

Patients with early, triple negative breast cancer (TNBC) and high risk of recurrence after initial therapy had significantly better 3-year overall survival (OS) when given adjuvant avelumab compared with those who were observed without further treatment, in the A-BRAVE trial.

“The 30% reduction in the risk of distant metastasis, and 34% reduction in the risk of death suggests that avelumab may have a role in early triple negative breast cancer patients at high risk of relapse after primary surgery or with invasive residual disease after neoadjuvant chemotherapy,” Pierfranco Conte, MD, from the department of surgery, oncology, and gastroenterology at the University of Padua, Italy, reported at the annual meeting of the American Society of Clinical Oncology.

A-BRAVE is the first randomized phase 3 trial patients with TNBC, treated with adjuvant avelumab, explained Dr. Conte. “Neoadjuvant chemotherapy is recommended for stage cT1c or larger, or cN+ disease. However, in case of invasive residual disease at surgery, prognosis is still very poor.”

TNBC is more immunogenic compared with other breast cancer subtypes, suggesting a role for immune checkpoint inhibitors such as avelumab in this setting, he said.
 

A-BRAVE Methods and Results

The trial enrolled 477 patients, median age 51 years, between June 2016 and October 2020, after their disease had progressed following initial treatment. There were two strata of patients: those who had received upfront surgery and then adjuvant chemotherapy before disease progression (stratum A, 18%); and those who received neoadjuvant chemotherapy, surgery, and then adjuvant chemo, but still had residual disease (stratum B, 82%).

Patients were randomized to either observation (n = 239) or treatment with avelumab (n = 238), at a dose of 10 mg/kg every 2 weeks for one year.

At a median follow-up of 52.1 months, avelumab did not show an advantage for the primary endpoint of 3-year disease-free survival (DFS), with 68.3% of treated patients meeting this endpoint, compared to 63.2% of observed patients (hazard ratio [HR 0.81, P = .172].

However, the treatment did show statistically significant benefits for the secondary 3-year OS endpoint (84.8% vs 76.3%, HR 0.66, P = .035).

“Trying to understand why we did observe a greater benefit with avelumab in overall survival compared to disease-free survival, we also made a post-hoc exploratory analysis on distant disease-free survival,” explained Dr. Conte.

There was a statistically significant 3-year distant disease-free survival (DDFS) benefit for treated patients compared with controls (75.4% vs 67.9%, HR 0.7, P = .0277), translating to a 30% reduction in the risk of distant metastasis, he noted.
 

Findings Are ‘Hypothesis-Generating’

The results are “hypothesis-generating at this point,” Alexandra Thomas, MD, a breast medical oncologist who was not involved in the research, said in an interview. “These results suggest that the story on how to best utilize checkpoint blockade as adjuvant therapy in triple negative breast cancer may not yet be fully written.”

She emphasized the study did not meet its primary endpoint, “though the results for secondary endpoints OS and the exploratory endpoint DDFS are intriguing.

“A-BRAVE is a smaller study, especially relative to Impassion030 (ALEXANDRA), which enrolled over 2,000 patients,” she explained. “It is notable that avelumab has slightly different properties than atezolizumab, which was used in Impassion030.”

“Avelumab is also a weak PD-L2 inhibitor. Could this be important? Notably, today most patients with clinical stage II-III triple negative breast cancer will receive pembrolizumab as per KEYNOTE-522, so the potential for clinical impact is greatly reduced,” added Dr. Thomas, professor and assistant director in the department of internal medicine at Duke Cancer Institute, in Durham, North Carolina.

SWOG1814, which has not been reported yet, “also looks at pembrolizumab in patients with residual disease post neoadjuvant chemotherapy and will provide further important information on in this space,” she said.

Merck KGaA funded the study.

Dr. Conte disclosed consulting or advisory roles with Daiichi Sankyo/Lilly, Gilead Sciences, Reveal Genomics; a HER2Dx patient; and providing expert testimony for AstraZeneca.

Dr. Thomas disclosed research grants from Sanofi and Merck.

Patients with early, triple negative breast cancer (TNBC) and high risk of recurrence after initial therapy had significantly better 3-year overall survival (OS) when given adjuvant avelumab compared with those who were observed without further treatment, in the A-BRAVE trial.

“The 30% reduction in the risk of distant metastasis, and 34% reduction in the risk of death suggests that avelumab may have a role in early triple negative breast cancer patients at high risk of relapse after primary surgery or with invasive residual disease after neoadjuvant chemotherapy,” Pierfranco Conte, MD, from the department of surgery, oncology, and gastroenterology at the University of Padua, Italy, reported at the annual meeting of the American Society of Clinical Oncology.

A-BRAVE is the first randomized phase 3 trial patients with TNBC, treated with adjuvant avelumab, explained Dr. Conte. “Neoadjuvant chemotherapy is recommended for stage cT1c or larger, or cN+ disease. However, in case of invasive residual disease at surgery, prognosis is still very poor.”

TNBC is more immunogenic compared with other breast cancer subtypes, suggesting a role for immune checkpoint inhibitors such as avelumab in this setting, he said.
 

A-BRAVE Methods and Results

The trial enrolled 477 patients, median age 51 years, between June 2016 and October 2020, after their disease had progressed following initial treatment. There were two strata of patients: those who had received upfront surgery and then adjuvant chemotherapy before disease progression (stratum A, 18%); and those who received neoadjuvant chemotherapy, surgery, and then adjuvant chemo, but still had residual disease (stratum B, 82%).

Patients were randomized to either observation (n = 239) or treatment with avelumab (n = 238), at a dose of 10 mg/kg every 2 weeks for one year.

At a median follow-up of 52.1 months, avelumab did not show an advantage for the primary endpoint of 3-year disease-free survival (DFS), with 68.3% of treated patients meeting this endpoint, compared to 63.2% of observed patients (hazard ratio [HR 0.81, P = .172].

However, the treatment did show statistically significant benefits for the secondary 3-year OS endpoint (84.8% vs 76.3%, HR 0.66, P = .035).

“Trying to understand why we did observe a greater benefit with avelumab in overall survival compared to disease-free survival, we also made a post-hoc exploratory analysis on distant disease-free survival,” explained Dr. Conte.

There was a statistically significant 3-year distant disease-free survival (DDFS) benefit for treated patients compared with controls (75.4% vs 67.9%, HR 0.7, P = .0277), translating to a 30% reduction in the risk of distant metastasis, he noted.
 

Findings Are ‘Hypothesis-Generating’

The results are “hypothesis-generating at this point,” Alexandra Thomas, MD, a breast medical oncologist who was not involved in the research, said in an interview. “These results suggest that the story on how to best utilize checkpoint blockade as adjuvant therapy in triple negative breast cancer may not yet be fully written.”

She emphasized the study did not meet its primary endpoint, “though the results for secondary endpoints OS and the exploratory endpoint DDFS are intriguing.

“A-BRAVE is a smaller study, especially relative to Impassion030 (ALEXANDRA), which enrolled over 2,000 patients,” she explained. “It is notable that avelumab has slightly different properties than atezolizumab, which was used in Impassion030.”

“Avelumab is also a weak PD-L2 inhibitor. Could this be important? Notably, today most patients with clinical stage II-III triple negative breast cancer will receive pembrolizumab as per KEYNOTE-522, so the potential for clinical impact is greatly reduced,” added Dr. Thomas, professor and assistant director in the department of internal medicine at Duke Cancer Institute, in Durham, North Carolina.

SWOG1814, which has not been reported yet, “also looks at pembrolizumab in patients with residual disease post neoadjuvant chemotherapy and will provide further important information on in this space,” she said.

Merck KGaA funded the study.

Dr. Conte disclosed consulting or advisory roles with Daiichi Sankyo/Lilly, Gilead Sciences, Reveal Genomics; a HER2Dx patient; and providing expert testimony for AstraZeneca.

Dr. Thomas disclosed research grants from Sanofi and Merck.

Patients with early, triple negative breast cancer (TNBC) and high risk of recurrence after initial therapy had significantly better 3-year overall survival (OS) when given adjuvant avelumab compared with those who were observed without further treatment, in the A-BRAVE trial.

“The 30% reduction in the risk of distant metastasis, and 34% reduction in the risk of death suggests that avelumab may have a role in early triple negative breast cancer patients at high risk of relapse after primary surgery or with invasive residual disease after neoadjuvant chemotherapy,” Pierfranco Conte, MD, from the department of surgery, oncology, and gastroenterology at the University of Padua, Italy, reported at the annual meeting of the American Society of Clinical Oncology.

A-BRAVE is the first randomized phase 3 trial patients with TNBC, treated with adjuvant avelumab, explained Dr. Conte. “Neoadjuvant chemotherapy is recommended for stage cT1c or larger, or cN+ disease. However, in case of invasive residual disease at surgery, prognosis is still very poor.”

TNBC is more immunogenic compared with other breast cancer subtypes, suggesting a role for immune checkpoint inhibitors such as avelumab in this setting, he said.
 

A-BRAVE Methods and Results

The trial enrolled 477 patients, median age 51 years, between June 2016 and October 2020, after their disease had progressed following initial treatment. There were two strata of patients: those who had received upfront surgery and then adjuvant chemotherapy before disease progression (stratum A, 18%); and those who received neoadjuvant chemotherapy, surgery, and then adjuvant chemo, but still had residual disease (stratum B, 82%).

Patients were randomized to either observation (n = 239) or treatment with avelumab (n = 238), at a dose of 10 mg/kg every 2 weeks for one year.

At a median follow-up of 52.1 months, avelumab did not show an advantage for the primary endpoint of 3-year disease-free survival (DFS), with 68.3% of treated patients meeting this endpoint, compared to 63.2% of observed patients (hazard ratio [HR 0.81, P = .172].

However, the treatment did show statistically significant benefits for the secondary 3-year OS endpoint (84.8% vs 76.3%, HR 0.66, P = .035).

“Trying to understand why we did observe a greater benefit with avelumab in overall survival compared to disease-free survival, we also made a post-hoc exploratory analysis on distant disease-free survival,” explained Dr. Conte.

There was a statistically significant 3-year distant disease-free survival (DDFS) benefit for treated patients compared with controls (75.4% vs 67.9%, HR 0.7, P = .0277), translating to a 30% reduction in the risk of distant metastasis, he noted.
 

Findings Are ‘Hypothesis-Generating’

The results are “hypothesis-generating at this point,” Alexandra Thomas, MD, a breast medical oncologist who was not involved in the research, said in an interview. “These results suggest that the story on how to best utilize checkpoint blockade as adjuvant therapy in triple negative breast cancer may not yet be fully written.”

She emphasized the study did not meet its primary endpoint, “though the results for secondary endpoints OS and the exploratory endpoint DDFS are intriguing.

“A-BRAVE is a smaller study, especially relative to Impassion030 (ALEXANDRA), which enrolled over 2,000 patients,” she explained. “It is notable that avelumab has slightly different properties than atezolizumab, which was used in Impassion030.”

“Avelumab is also a weak PD-L2 inhibitor. Could this be important? Notably, today most patients with clinical stage II-III triple negative breast cancer will receive pembrolizumab as per KEYNOTE-522, so the potential for clinical impact is greatly reduced,” added Dr. Thomas, professor and assistant director in the department of internal medicine at Duke Cancer Institute, in Durham, North Carolina.

SWOG1814, which has not been reported yet, “also looks at pembrolizumab in patients with residual disease post neoadjuvant chemotherapy and will provide further important information on in this space,” she said.

Merck KGaA funded the study.

Dr. Conte disclosed consulting or advisory roles with Daiichi Sankyo/Lilly, Gilead Sciences, Reveal Genomics; a HER2Dx patient; and providing expert testimony for AstraZeneca.

Dr. Thomas disclosed research grants from Sanofi and Merck.

Should 5 mg of tamoxifen — known as “baby TAM” — or the usual 20 mg dose be standard of care for breast cancer prevention in high-risk women?

Research to date clearly shows that tamoxifen can reduce the risk for breast cancer in high-risk individuals by 30%-50%. Recent evidence also indicates that this chemoprevention approach can reduce the risk of dying from breast cancer by as much as 57%.

In 2019, the US Preventive Services Task Force issued updated recommendations that clinicians offer risk-reducing medications, such as tamoxifen, raloxifene, or aromatase inhibitors, to women at an increased risk for breast cancer and a low risk for adverse medication effects.

However, this prophylactic strategy remains underused.

A major roadblock: The drugs’ side effects, which include venous thromboembolic events and endometrial cancer as well as symptoms of menopause, such as hot flashes and sexual issues, have made uptake and adherence a challenge.

Offering women a lower dose of tamoxifen could allay fears about toxicities and improve uptake as well as reduce side effects and boost long-term adherence among those receiving baby TAM.

However, experts remain uncertain about whether patients need the standard dose to experience the full prevention benefit.
 

The Debate

Years ago, Andrea De Censi, MD, a breast cancer researcher at the Galliera Hospital in Genova, Italy, and his colleagues reasoned that, because tamoxifen is a competitive estrogen receptor inhibitor, it may indeed have a minimal effective dose below 20 mg/d.

The fruits of that line of thought were presented to the world in the TAM-01 trial, first published in 2019, which pitted tamoxifen 5 mg/d for 3 years against placebo in 500 women with high-risk lesions, including lobular and ductal carcinoma in situ.

Dr. De Censi and colleagues found that baby TAM reduced the risk for invasive breast cancer by 52% and the risk for contralateral breast cancer by 75%.

Treatment adherence was slightly higher in the baby TAM group at 65% vs 61% in the placebo group.

A recent 10-year follow-up showed ongoing benefits associated with baby TAM vs placebo — a 42% reduction in breast cancer and a 64% drop in contralateral lesions.

The baby TAM group vs placebo experienced a slight increase in hot flashes but no significant increase in other common side effects.

Regarding serious adverse events, the baby TAM arm had one case of stage 1 endometrial cancer (0.4% of patients) and 20 cases of endometrial polyps (5%) vs 13 cases of endometrial polyps in the placebo arm. But there were no significant differences in thrombosis, cataracts, bone fractures, and other serious events.

Dr. De Censi said he’s surprised the baby TAM vs tamoxifen topic is still being debated. “Baby TAM, in my opinion, is a new standard of care for endocrine prevention of breast cancer in high-risk [women],” and baby TAM over 3 years is enough, said Dr. De Censi during a debate on the topic at the 2024 European Society for Medical Oncology Breast Cancer Congress in Berlin.

Gareth Evans, MD, a cancer genetics and prevention specialist at the University of Manchester, Manchester, England, however, isn’t convinced.

During the debate, Dr. Evans explained that  his main concern was that the baby TAM trial was limited to women with high-risk lesions, not other common reasons for tamoxifen prophylaxis, such as a positive family history or BRCA mutations.

“In Manchester, we have put over a thousand women on tamoxifen who have a family history or other risk factors, not high-risk lesions,” and there simply isn’t definitive evidence for baby TAM in these women, Dr. Evans said.

The vast weight of evidence for tamoxifen prophylaxis, he added, is in trials involving tens of thousands of women, followed in some cases for 20 years, who received the 20 mg dose for 5 years.

As a result, women in Manchester are started on 20 mg and dropped down to 5 mg only for side effects. That way, Evans explained, we are not taking away the benefit among women who can tolerate 20 mg.

Meanwhile, there’s no evidence that baby TAM improves medication adherence, he noted. Trials have reported similar adherence rates to baby TAM and standard dose tamoxifen as well as no definitive evidence that the risk for cancer and thrombosis is less with baby TAM, he said.

In fact, Dr. Evans noted, “many women take tamoxifen 20 mg for 5 years with no side effects.”

Overall, “I don’t think we’ve got the evidence yet to drop” dosages, particularly in women without high-risk lesions, Dr. Evans said. A real concern, he added, is poor metabolizers for whom 5 mg won’t be enough to have a preventive effect.

Dr. De Censi noted, however, that there will likely never be a definitive answer to the question of baby TAM vs standard dosing because industry has no financial incentive to do a head-to-head trial; tamoxifen went off patent over 30 years ago.

Still, a poll of the audience favored Evans’ approach — 80% said they would start high-risk women on 20 mg for breast cancer prophylaxis and reduce for side effects as needed.

Dr. De Censi didn’t have any disclosures. Dr. Evans is a consultant/advisor for AstraZeneca, SpringWorks, Recursion, Everything Genetic, and Syantra.

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

Should 5 mg of tamoxifen — known as “baby TAM” — or the usual 20 mg dose be standard of care for breast cancer prevention in high-risk women?

Research to date clearly shows that tamoxifen can reduce the risk for breast cancer in high-risk individuals by 30%-50%. Recent evidence also indicates that this chemoprevention approach can reduce the risk of dying from breast cancer by as much as 57%.

In 2019, the US Preventive Services Task Force issued updated recommendations that clinicians offer risk-reducing medications, such as tamoxifen, raloxifene, or aromatase inhibitors, to women at an increased risk for breast cancer and a low risk for adverse medication effects.

However, this prophylactic strategy remains underused.

A major roadblock: The drugs’ side effects, which include venous thromboembolic events and endometrial cancer as well as symptoms of menopause, such as hot flashes and sexual issues, have made uptake and adherence a challenge.

Offering women a lower dose of tamoxifen could allay fears about toxicities and improve uptake as well as reduce side effects and boost long-term adherence among those receiving baby TAM.

However, experts remain uncertain about whether patients need the standard dose to experience the full prevention benefit.
 

The Debate

Years ago, Andrea De Censi, MD, a breast cancer researcher at the Galliera Hospital in Genova, Italy, and his colleagues reasoned that, because tamoxifen is a competitive estrogen receptor inhibitor, it may indeed have a minimal effective dose below 20 mg/d.

The fruits of that line of thought were presented to the world in the TAM-01 trial, first published in 2019, which pitted tamoxifen 5 mg/d for 3 years against placebo in 500 women with high-risk lesions, including lobular and ductal carcinoma in situ.

Dr. De Censi and colleagues found that baby TAM reduced the risk for invasive breast cancer by 52% and the risk for contralateral breast cancer by 75%.

Treatment adherence was slightly higher in the baby TAM group at 65% vs 61% in the placebo group.

A recent 10-year follow-up showed ongoing benefits associated with baby TAM vs placebo — a 42% reduction in breast cancer and a 64% drop in contralateral lesions.

The baby TAM group vs placebo experienced a slight increase in hot flashes but no significant increase in other common side effects.

Regarding serious adverse events, the baby TAM arm had one case of stage 1 endometrial cancer (0.4% of patients) and 20 cases of endometrial polyps (5%) vs 13 cases of endometrial polyps in the placebo arm. But there were no significant differences in thrombosis, cataracts, bone fractures, and other serious events.

Dr. De Censi said he’s surprised the baby TAM vs tamoxifen topic is still being debated. “Baby TAM, in my opinion, is a new standard of care for endocrine prevention of breast cancer in high-risk [women],” and baby TAM over 3 years is enough, said Dr. De Censi during a debate on the topic at the 2024 European Society for Medical Oncology Breast Cancer Congress in Berlin.

Gareth Evans, MD, a cancer genetics and prevention specialist at the University of Manchester, Manchester, England, however, isn’t convinced.

During the debate, Dr. Evans explained that  his main concern was that the baby TAM trial was limited to women with high-risk lesions, not other common reasons for tamoxifen prophylaxis, such as a positive family history or BRCA mutations.

“In Manchester, we have put over a thousand women on tamoxifen who have a family history or other risk factors, not high-risk lesions,” and there simply isn’t definitive evidence for baby TAM in these women, Dr. Evans said.

The vast weight of evidence for tamoxifen prophylaxis, he added, is in trials involving tens of thousands of women, followed in some cases for 20 years, who received the 20 mg dose for 5 years.

As a result, women in Manchester are started on 20 mg and dropped down to 5 mg only for side effects. That way, Evans explained, we are not taking away the benefit among women who can tolerate 20 mg.

Meanwhile, there’s no evidence that baby TAM improves medication adherence, he noted. Trials have reported similar adherence rates to baby TAM and standard dose tamoxifen as well as no definitive evidence that the risk for cancer and thrombosis is less with baby TAM, he said.

In fact, Dr. Evans noted, “many women take tamoxifen 20 mg for 5 years with no side effects.”

Overall, “I don’t think we’ve got the evidence yet to drop” dosages, particularly in women without high-risk lesions, Dr. Evans said. A real concern, he added, is poor metabolizers for whom 5 mg won’t be enough to have a preventive effect.

Dr. De Censi noted, however, that there will likely never be a definitive answer to the question of baby TAM vs standard dosing because industry has no financial incentive to do a head-to-head trial; tamoxifen went off patent over 30 years ago.

Still, a poll of the audience favored Evans’ approach — 80% said they would start high-risk women on 20 mg for breast cancer prophylaxis and reduce for side effects as needed.

Dr. De Censi didn’t have any disclosures. Dr. Evans is a consultant/advisor for AstraZeneca, SpringWorks, Recursion, Everything Genetic, and Syantra.

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

Should 5 mg of tamoxifen — known as “baby TAM” — or the usual 20 mg dose be standard of care for breast cancer prevention in high-risk women?

Research to date clearly shows that tamoxifen can reduce the risk for breast cancer in high-risk individuals by 30%-50%. Recent evidence also indicates that this chemoprevention approach can reduce the risk of dying from breast cancer by as much as 57%.

In 2019, the US Preventive Services Task Force issued updated recommendations that clinicians offer risk-reducing medications, such as tamoxifen, raloxifene, or aromatase inhibitors, to women at an increased risk for breast cancer and a low risk for adverse medication effects.

However, this prophylactic strategy remains underused.

A major roadblock: The drugs’ side effects, which include venous thromboembolic events and endometrial cancer as well as symptoms of menopause, such as hot flashes and sexual issues, have made uptake and adherence a challenge.

Offering women a lower dose of tamoxifen could allay fears about toxicities and improve uptake as well as reduce side effects and boost long-term adherence among those receiving baby TAM.

However, experts remain uncertain about whether patients need the standard dose to experience the full prevention benefit.
 

The Debate

Years ago, Andrea De Censi, MD, a breast cancer researcher at the Galliera Hospital in Genova, Italy, and his colleagues reasoned that, because tamoxifen is a competitive estrogen receptor inhibitor, it may indeed have a minimal effective dose below 20 mg/d.

The fruits of that line of thought were presented to the world in the TAM-01 trial, first published in 2019, which pitted tamoxifen 5 mg/d for 3 years against placebo in 500 women with high-risk lesions, including lobular and ductal carcinoma in situ.

Dr. De Censi and colleagues found that baby TAM reduced the risk for invasive breast cancer by 52% and the risk for contralateral breast cancer by 75%.

Treatment adherence was slightly higher in the baby TAM group at 65% vs 61% in the placebo group.

A recent 10-year follow-up showed ongoing benefits associated with baby TAM vs placebo — a 42% reduction in breast cancer and a 64% drop in contralateral lesions.

The baby TAM group vs placebo experienced a slight increase in hot flashes but no significant increase in other common side effects.

Regarding serious adverse events, the baby TAM arm had one case of stage 1 endometrial cancer (0.4% of patients) and 20 cases of endometrial polyps (5%) vs 13 cases of endometrial polyps in the placebo arm. But there were no significant differences in thrombosis, cataracts, bone fractures, and other serious events.

Dr. De Censi said he’s surprised the baby TAM vs tamoxifen topic is still being debated. “Baby TAM, in my opinion, is a new standard of care for endocrine prevention of breast cancer in high-risk [women],” and baby TAM over 3 years is enough, said Dr. De Censi during a debate on the topic at the 2024 European Society for Medical Oncology Breast Cancer Congress in Berlin.

Gareth Evans, MD, a cancer genetics and prevention specialist at the University of Manchester, Manchester, England, however, isn’t convinced.

During the debate, Dr. Evans explained that  his main concern was that the baby TAM trial was limited to women with high-risk lesions, not other common reasons for tamoxifen prophylaxis, such as a positive family history or BRCA mutations.

“In Manchester, we have put over a thousand women on tamoxifen who have a family history or other risk factors, not high-risk lesions,” and there simply isn’t definitive evidence for baby TAM in these women, Dr. Evans said.

The vast weight of evidence for tamoxifen prophylaxis, he added, is in trials involving tens of thousands of women, followed in some cases for 20 years, who received the 20 mg dose for 5 years.

As a result, women in Manchester are started on 20 mg and dropped down to 5 mg only for side effects. That way, Evans explained, we are not taking away the benefit among women who can tolerate 20 mg.

Meanwhile, there’s no evidence that baby TAM improves medication adherence, he noted. Trials have reported similar adherence rates to baby TAM and standard dose tamoxifen as well as no definitive evidence that the risk for cancer and thrombosis is less with baby TAM, he said.

In fact, Dr. Evans noted, “many women take tamoxifen 20 mg for 5 years with no side effects.”

Overall, “I don’t think we’ve got the evidence yet to drop” dosages, particularly in women without high-risk lesions, Dr. Evans said. A real concern, he added, is poor metabolizers for whom 5 mg won’t be enough to have a preventive effect.

Dr. De Censi noted, however, that there will likely never be a definitive answer to the question of baby TAM vs standard dosing because industry has no financial incentive to do a head-to-head trial; tamoxifen went off patent over 30 years ago.

Still, a poll of the audience favored Evans’ approach — 80% said they would start high-risk women on 20 mg for breast cancer prophylaxis and reduce for side effects as needed.

Dr. De Censi didn’t have any disclosures. Dr. Evans is a consultant/advisor for AstraZeneca, SpringWorks, Recursion, Everything Genetic, and Syantra.

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

In one of several recently published studies on the relationship between COVID-19 infection and asthma, asthma symptoms in children declined as the proportion of the US population vaccinated against COVID-19 increased, according to data drawn from the National Survey of Children’s Health (NSCH).

The inverse correlation between symptoms and vaccination was strong and statistically significant, according to investigators led by Matthew M. Davis, MD, Physician in Chief and Chief Scientific Officer, Nemours Children’s Health, Wilmington, Delaware.

“With each increase of 10 percentage points in COVID-19 vaccination coverage, the parent-reported child asthma symptoms prevalence decreased by 0.36 percentage points (P < .05),” Dr. Davis and his coinvestigators reported in a research letter published in JAMA Network Open.
 

Studies Explore Relationship of COVID and Asthma

The reduced risk of asthma symptoms with COVID-19 vaccination in children at the population level is just one of several recently published studies exploring the interaction between COVID-19 infection and asthma, but two studies that posed the same question did not reach the same conclusion.

In one, COVID-19 infection in children was not found to be a trigger for new-onset asthma, but the second found that it was. In a third study, the preponderance of evidence from a meta-analysis found that patients with asthma – whether children or adults – did not necessarily experience a more severe course of COVID-19 infection than in those without asthma.

The NSCH database study calculated state-level change in scores for patient-reported childhood asthma symptoms in the years in the years 2018-2019, which preceded the pandemic and the years 2020-2021, when the pandemic began. The hypothesis was that the proportion of the population 5 years of age or older who completed the COVID-19 primary vaccination would be inversely related to asthma symptom prevalence.

Relative to the 2018-2019 years, the mean rate of parent-reported asthma symptoms was 0.85% lower (6.93% vs 7.77%; P < .001) in 2020-2021, when the mean primary series COVID-19 vaccination rate was 72.3%.

The study was not able to evaluate the impact of COVID-19 vaccination specifically in children with asthma, because history of asthma is not captured in the NSCH data, but Dr. Davis contended that the reduction in symptomatic asthma among children with increased vaccination offers validation for the state-level findings.

“Moreover, the absence of an association of COVID-19 vaccination administered predominantly in 2021 with population-level COVID-19 mortality in 2020 serves as a negative control,” he and his colleagues wrote in their research letter.
 

Protection from Respiratory Viruses Seen for Asthma Patients

In an interview, Dr. Davis reported that these data are consistent with previous evidence that immunization against influenza also reduces risk of asthma symptoms. In a meta-analysis published in 2017, it was estimated that live vaccines reduced risk of influenza by 81% and prevented 59%-72% of asthma attacks leading to hospitalizations or emergency room visits.

“The similarity of our findings regarding COVID-19 vaccination to prior data regarding influenza vaccination underscores the importance of preventing viral illnesses in individuals with a history of asthma,” Dr. Davis said. It is not yet clear if this is true of respiratory syncytial virus (RSV). Because of the short time that the RSV vaccine has been available, it is too soon to conduct an analysis.

One message from this study is that “clinicians should continue to encourage COVID-19 vaccination for children because of its general benefits in preventing coronavirus-related illness and the apparent specific benefits for children with a history of asthma,” he said.

While vaccination appears to reduce asthmatic symptoms related to COVID-19 infection, one study suggests that COVID-19 does not trigger new-onset asthma. In a retrospective study published in Pediatrics, no association between COVID-19 infection and new-onset asthma could be made in an analysis of 27,423 children (ages, 1-16 years) from the Children’s Hospital of Philadelphia (CHOP) Care Network.

Across all the pediatric age groups evaluated, the consistent finding was “SARS-CoV-2 positivity does not confer an additional risk for asthma diagnosis at least within the first 18 months after a [polymerase chain reaction] test,” concluded the investigators, led by David A. Hill, MD, PhD, Division of Allergy and Immunology, CHOP, Philadelphia, Pennsylvania.
 

Risk of Asthma Doubled After COVID-19 Infection

However, the opposite conclusion was reached by investigators evaluating data from two cohorts of children ages 5-18 drawn from the TriNetX database, a global health research network with data on more than 250 million individuals. Cohort 1 included more than 250,000 children. These children had never received COVID-19 vaccination. The 50,000 patients in cohort 2 had all received COVID19 vaccination.

To compare the impact of COVID-19 infection on new-onset asthma, the patients who were infected with COVID-19 were compared with those who were not infected after propensity score matching over 18 months of follow-up.

In cohort 1, the rate of new onset asthma was more than twofold greater among those with COVID-19 infection (4.7% vs 2.0%). The hazard ratio (HR) of 2.25 had tight confidence intervals (95% CI, 2.158-2.367).

In cohort 2, the risk of new-onset asthma at 18 months among those who had a COVID-19 infection relative to those without was even greater (8.3% vs 3.1%). The relative risk approached a 3-fold increase (HR 2.745; 95% CI, 2.521-2.99).

The conclusion of these investigators, led by Chia-Chi Lung, PhD, Department of Public Health, Chung Shan Medical University, Taichung City, Taiwan, was that there is “a critical need for ongoing monitoring and customized healthcare strategies to mitigate the long-term respiratory impacts of COVID-19 in children.”

These health risks might not be as significant as once feared. In the recently published study from Environmental Health Insights, the goal of a meta-analysis was to determine if patients with asthma relative to those without asthma face a higher risk of serious disease from COVID-19 infection. The meta-analysis included studies of children and adults. The answer, according an in-depth analysis of 21 articles in a “scoping review,” was a qualified no.

Of the 21 articles, 4 concluded that asthma is a risk factor for serious COVID-19 infection, but 17 did not, according to Chukwudi S. Ubah, PhD, Department of Public Health, Brody School of Medicine, East Caroline University, Greenville, North Carolina.
 

None of These Questions are Fully Resolved

However, given the disparity in the results and the fact that many of the studies included in this analysis had small sample sizes, Dr. Ubah called for larger studies and studies with better controls. He noted, for example, that the studies did not consistently evaluate mitigating factors, such as used of inhaled or oral corticosteroids, which might affect risk of the severity of a COVID-19 infection.

Rather, “our findings pointed out that the type of medication prescribed for asthma may have implications for the severity of COVID-19 infection in these patients,” Dr. Ubah said in an interview.

Overall, the data do not support a major interaction between asthma and COVID-19, even if the data are not conclusive. Each of the senior authors of these studies called for larger and better investigations to further explore whether COVID-19 infection and preexisting asthma interact. So far, the data indicate that if COVID-19 infection poses a risk of precipitating new-onset asthma or inducing a more severe infection in children with asthma, it is low, but the degree of risk, if any, remains unresolved in subgroups defined by asthma treatment or asthma severity.

Dr. Davis, Dr. Hill, Dr. Lung, and Dr. Ubah reported no potential conflicts of interest. None of these studies received funding from commercial interests.

In one of several recently published studies on the relationship between COVID-19 infection and asthma, asthma symptoms in children declined as the proportion of the US population vaccinated against COVID-19 increased, according to data drawn from the National Survey of Children’s Health (NSCH).

The inverse correlation between symptoms and vaccination was strong and statistically significant, according to investigators led by Matthew M. Davis, MD, Physician in Chief and Chief Scientific Officer, Nemours Children’s Health, Wilmington, Delaware.

“With each increase of 10 percentage points in COVID-19 vaccination coverage, the parent-reported child asthma symptoms prevalence decreased by 0.36 percentage points (P < .05),” Dr. Davis and his coinvestigators reported in a research letter published in JAMA Network Open.
 

Studies Explore Relationship of COVID and Asthma

The reduced risk of asthma symptoms with COVID-19 vaccination in children at the population level is just one of several recently published studies exploring the interaction between COVID-19 infection and asthma, but two studies that posed the same question did not reach the same conclusion.

In one, COVID-19 infection in children was not found to be a trigger for new-onset asthma, but the second found that it was. In a third study, the preponderance of evidence from a meta-analysis found that patients with asthma – whether children or adults – did not necessarily experience a more severe course of COVID-19 infection than in those without asthma.

The NSCH database study calculated state-level change in scores for patient-reported childhood asthma symptoms in the years in the years 2018-2019, which preceded the pandemic and the years 2020-2021, when the pandemic began. The hypothesis was that the proportion of the population 5 years of age or older who completed the COVID-19 primary vaccination would be inversely related to asthma symptom prevalence.

Relative to the 2018-2019 years, the mean rate of parent-reported asthma symptoms was 0.85% lower (6.93% vs 7.77%; P < .001) in 2020-2021, when the mean primary series COVID-19 vaccination rate was 72.3%.

The study was not able to evaluate the impact of COVID-19 vaccination specifically in children with asthma, because history of asthma is not captured in the NSCH data, but Dr. Davis contended that the reduction in symptomatic asthma among children with increased vaccination offers validation for the state-level findings.

“Moreover, the absence of an association of COVID-19 vaccination administered predominantly in 2021 with population-level COVID-19 mortality in 2020 serves as a negative control,” he and his colleagues wrote in their research letter.
 

Protection from Respiratory Viruses Seen for Asthma Patients

In an interview, Dr. Davis reported that these data are consistent with previous evidence that immunization against influenza also reduces risk of asthma symptoms. In a meta-analysis published in 2017, it was estimated that live vaccines reduced risk of influenza by 81% and prevented 59%-72% of asthma attacks leading to hospitalizations or emergency room visits.

“The similarity of our findings regarding COVID-19 vaccination to prior data regarding influenza vaccination underscores the importance of preventing viral illnesses in individuals with a history of asthma,” Dr. Davis said. It is not yet clear if this is true of respiratory syncytial virus (RSV). Because of the short time that the RSV vaccine has been available, it is too soon to conduct an analysis.

One message from this study is that “clinicians should continue to encourage COVID-19 vaccination for children because of its general benefits in preventing coronavirus-related illness and the apparent specific benefits for children with a history of asthma,” he said.

While vaccination appears to reduce asthmatic symptoms related to COVID-19 infection, one study suggests that COVID-19 does not trigger new-onset asthma. In a retrospective study published in Pediatrics, no association between COVID-19 infection and new-onset asthma could be made in an analysis of 27,423 children (ages, 1-16 years) from the Children’s Hospital of Philadelphia (CHOP) Care Network.

Across all the pediatric age groups evaluated, the consistent finding was “SARS-CoV-2 positivity does not confer an additional risk for asthma diagnosis at least within the first 18 months after a [polymerase chain reaction] test,” concluded the investigators, led by David A. Hill, MD, PhD, Division of Allergy and Immunology, CHOP, Philadelphia, Pennsylvania.
 

Risk of Asthma Doubled After COVID-19 Infection

However, the opposite conclusion was reached by investigators evaluating data from two cohorts of children ages 5-18 drawn from the TriNetX database, a global health research network with data on more than 250 million individuals. Cohort 1 included more than 250,000 children. These children had never received COVID-19 vaccination. The 50,000 patients in cohort 2 had all received COVID19 vaccination.

To compare the impact of COVID-19 infection on new-onset asthma, the patients who were infected with COVID-19 were compared with those who were not infected after propensity score matching over 18 months of follow-up.

In cohort 1, the rate of new onset asthma was more than twofold greater among those with COVID-19 infection (4.7% vs 2.0%). The hazard ratio (HR) of 2.25 had tight confidence intervals (95% CI, 2.158-2.367).

In cohort 2, the risk of new-onset asthma at 18 months among those who had a COVID-19 infection relative to those without was even greater (8.3% vs 3.1%). The relative risk approached a 3-fold increase (HR 2.745; 95% CI, 2.521-2.99).

The conclusion of these investigators, led by Chia-Chi Lung, PhD, Department of Public Health, Chung Shan Medical University, Taichung City, Taiwan, was that there is “a critical need for ongoing monitoring and customized healthcare strategies to mitigate the long-term respiratory impacts of COVID-19 in children.”

These health risks might not be as significant as once feared. In the recently published study from Environmental Health Insights, the goal of a meta-analysis was to determine if patients with asthma relative to those without asthma face a higher risk of serious disease from COVID-19 infection. The meta-analysis included studies of children and adults. The answer, according an in-depth analysis of 21 articles in a “scoping review,” was a qualified no.

Of the 21 articles, 4 concluded that asthma is a risk factor for serious COVID-19 infection, but 17 did not, according to Chukwudi S. Ubah, PhD, Department of Public Health, Brody School of Medicine, East Caroline University, Greenville, North Carolina.
 

None of These Questions are Fully Resolved

However, given the disparity in the results and the fact that many of the studies included in this analysis had small sample sizes, Dr. Ubah called for larger studies and studies with better controls. He noted, for example, that the studies did not consistently evaluate mitigating factors, such as used of inhaled or oral corticosteroids, which might affect risk of the severity of a COVID-19 infection.

Rather, “our findings pointed out that the type of medication prescribed for asthma may have implications for the severity of COVID-19 infection in these patients,” Dr. Ubah said in an interview.

Overall, the data do not support a major interaction between asthma and COVID-19, even if the data are not conclusive. Each of the senior authors of these studies called for larger and better investigations to further explore whether COVID-19 infection and preexisting asthma interact. So far, the data indicate that if COVID-19 infection poses a risk of precipitating new-onset asthma or inducing a more severe infection in children with asthma, it is low, but the degree of risk, if any, remains unresolved in subgroups defined by asthma treatment or asthma severity.

Dr. Davis, Dr. Hill, Dr. Lung, and Dr. Ubah reported no potential conflicts of interest. None of these studies received funding from commercial interests.

In one of several recently published studies on the relationship between COVID-19 infection and asthma, asthma symptoms in children declined as the proportion of the US population vaccinated against COVID-19 increased, according to data drawn from the National Survey of Children’s Health (NSCH).

The inverse correlation between symptoms and vaccination was strong and statistically significant, according to investigators led by Matthew M. Davis, MD, Physician in Chief and Chief Scientific Officer, Nemours Children’s Health, Wilmington, Delaware.

“With each increase of 10 percentage points in COVID-19 vaccination coverage, the parent-reported child asthma symptoms prevalence decreased by 0.36 percentage points (P < .05),” Dr. Davis and his coinvestigators reported in a research letter published in JAMA Network Open.
 

Studies Explore Relationship of COVID and Asthma

The reduced risk of asthma symptoms with COVID-19 vaccination in children at the population level is just one of several recently published studies exploring the interaction between COVID-19 infection and asthma, but two studies that posed the same question did not reach the same conclusion.

In one, COVID-19 infection in children was not found to be a trigger for new-onset asthma, but the second found that it was. In a third study, the preponderance of evidence from a meta-analysis found that patients with asthma – whether children or adults – did not necessarily experience a more severe course of COVID-19 infection than in those without asthma.

The NSCH database study calculated state-level change in scores for patient-reported childhood asthma symptoms in the years in the years 2018-2019, which preceded the pandemic and the years 2020-2021, when the pandemic began. The hypothesis was that the proportion of the population 5 years of age or older who completed the COVID-19 primary vaccination would be inversely related to asthma symptom prevalence.

Relative to the 2018-2019 years, the mean rate of parent-reported asthma symptoms was 0.85% lower (6.93% vs 7.77%; P < .001) in 2020-2021, when the mean primary series COVID-19 vaccination rate was 72.3%.

The study was not able to evaluate the impact of COVID-19 vaccination specifically in children with asthma, because history of asthma is not captured in the NSCH data, but Dr. Davis contended that the reduction in symptomatic asthma among children with increased vaccination offers validation for the state-level findings.

“Moreover, the absence of an association of COVID-19 vaccination administered predominantly in 2021 with population-level COVID-19 mortality in 2020 serves as a negative control,” he and his colleagues wrote in their research letter.
 

Protection from Respiratory Viruses Seen for Asthma Patients

In an interview, Dr. Davis reported that these data are consistent with previous evidence that immunization against influenza also reduces risk of asthma symptoms. In a meta-analysis published in 2017, it was estimated that live vaccines reduced risk of influenza by 81% and prevented 59%-72% of asthma attacks leading to hospitalizations or emergency room visits.

“The similarity of our findings regarding COVID-19 vaccination to prior data regarding influenza vaccination underscores the importance of preventing viral illnesses in individuals with a history of asthma,” Dr. Davis said. It is not yet clear if this is true of respiratory syncytial virus (RSV). Because of the short time that the RSV vaccine has been available, it is too soon to conduct an analysis.

One message from this study is that “clinicians should continue to encourage COVID-19 vaccination for children because of its general benefits in preventing coronavirus-related illness and the apparent specific benefits for children with a history of asthma,” he said.

While vaccination appears to reduce asthmatic symptoms related to COVID-19 infection, one study suggests that COVID-19 does not trigger new-onset asthma. In a retrospective study published in Pediatrics, no association between COVID-19 infection and new-onset asthma could be made in an analysis of 27,423 children (ages, 1-16 years) from the Children’s Hospital of Philadelphia (CHOP) Care Network.

Across all the pediatric age groups evaluated, the consistent finding was “SARS-CoV-2 positivity does not confer an additional risk for asthma diagnosis at least within the first 18 months after a [polymerase chain reaction] test,” concluded the investigators, led by David A. Hill, MD, PhD, Division of Allergy and Immunology, CHOP, Philadelphia, Pennsylvania.
 

Risk of Asthma Doubled After COVID-19 Infection

However, the opposite conclusion was reached by investigators evaluating data from two cohorts of children ages 5-18 drawn from the TriNetX database, a global health research network with data on more than 250 million individuals. Cohort 1 included more than 250,000 children. These children had never received COVID-19 vaccination. The 50,000 patients in cohort 2 had all received COVID19 vaccination.

To compare the impact of COVID-19 infection on new-onset asthma, the patients who were infected with COVID-19 were compared with those who were not infected after propensity score matching over 18 months of follow-up.

In cohort 1, the rate of new onset asthma was more than twofold greater among those with COVID-19 infection (4.7% vs 2.0%). The hazard ratio (HR) of 2.25 had tight confidence intervals (95% CI, 2.158-2.367).

In cohort 2, the risk of new-onset asthma at 18 months among those who had a COVID-19 infection relative to those without was even greater (8.3% vs 3.1%). The relative risk approached a 3-fold increase (HR 2.745; 95% CI, 2.521-2.99).

The conclusion of these investigators, led by Chia-Chi Lung, PhD, Department of Public Health, Chung Shan Medical University, Taichung City, Taiwan, was that there is “a critical need for ongoing monitoring and customized healthcare strategies to mitigate the long-term respiratory impacts of COVID-19 in children.”

These health risks might not be as significant as once feared. In the recently published study from Environmental Health Insights, the goal of a meta-analysis was to determine if patients with asthma relative to those without asthma face a higher risk of serious disease from COVID-19 infection. The meta-analysis included studies of children and adults. The answer, according an in-depth analysis of 21 articles in a “scoping review,” was a qualified no.

Of the 21 articles, 4 concluded that asthma is a risk factor for serious COVID-19 infection, but 17 did not, according to Chukwudi S. Ubah, PhD, Department of Public Health, Brody School of Medicine, East Caroline University, Greenville, North Carolina.
 

None of These Questions are Fully Resolved

However, given the disparity in the results and the fact that many of the studies included in this analysis had small sample sizes, Dr. Ubah called for larger studies and studies with better controls. He noted, for example, that the studies did not consistently evaluate mitigating factors, such as used of inhaled or oral corticosteroids, which might affect risk of the severity of a COVID-19 infection.

Rather, “our findings pointed out that the type of medication prescribed for asthma may have implications for the severity of COVID-19 infection in these patients,” Dr. Ubah said in an interview.

Overall, the data do not support a major interaction between asthma and COVID-19, even if the data are not conclusive. Each of the senior authors of these studies called for larger and better investigations to further explore whether COVID-19 infection and preexisting asthma interact. So far, the data indicate that if COVID-19 infection poses a risk of precipitating new-onset asthma or inducing a more severe infection in children with asthma, it is low, but the degree of risk, if any, remains unresolved in subgroups defined by asthma treatment or asthma severity.

Dr. Davis, Dr. Hill, Dr. Lung, and Dr. Ubah reported no potential conflicts of interest. None of these studies received funding from commercial interests.