Mixed Topics

In late October, a federal grand jury charged a Detroit-area medical oncologist Naveed Aslam, MD, in an indictment for his part in a scheme to illegally sell cancer drugs.

According to the indictment, Aslam acquired and sold more than $17 million in cancer drugs and personally netted more than $2.5 million during the scheme.

The charges against Aslam, filed on October 23 in the US District Court for the Eastern District of Michigan, include 10 counts of illegally selling or trading prescription drugs and one count of conspiring to do so.

“Dr. Aslam’s alleged participation in this scheme not only allowed him to profit unlawfully from the sale of cancer drugs but it also posed a serious threat by potentially placing these medications into the wrong hands,” Cheyvoryea Gibson, special agent in charge of the FBI in Michigan, said in a press release announcing the indictment.

The investigation is being conducted jointly by the FBI, the US Food and Drug Administration (FDA), the US Department of Health and Human Services Office of Inspector General, and Homeland Security Investigations.

The indictment alleges that Aslam was recruited by an unnamed operator of a Michigan corporation that engaged in business as a retail pharmacy and in the wholesale distribution of expensive prescription drugs, largely oncology drugs.

According to the indictment, Aslam and the operator came to an agreement where Aslam would purchase these expensive drugs from an authorized distributor under the false pretense that he was going to prescribe them to patients.

Instead, Aslam allegedly “sold and transferred the prescription drugs” to or through the Michigan business, with involvement from the unnamed operator and a second unnamed individual.

The unnamed individuals “identified customers interested in buying prescription cancer drugs” and “communicated with Dr. Aslam about what cancer drugs were requested,” according to the press release. “Dr. Aslam used his access to certain cancer drugs through his medical practice, Somerset Hematology and Oncology, P.C., to order and purchase the cancer drugs from his supplier.”

The indictment lays out that Aslam allegedly profited from this scheme in several ways, which included charging the Michigan business more than he paid the distributor for the drugs, sharing the profits when the business resold the drugs at a markup, and receiving rebates and discounts from the distributor “based on the amount of qualifying drugs he purchased and resold.”

According to the indictment, the scheme ran from early 2019 to mid-2023 and included four antibody drug conjugates — trastuzumab deruxtecan (Enhertu), enfortumab vedotin (Padcev), tisotumab vedotin (Tivdak), and sacituzumab govitecan (Trodelvy) — and the monoclonal antibody mogamulizumab (Poteligeo) for cutaneous T-cell lymphoma.

By working with Aslam, the operatives “obtained prescription drugs from an authorized distributor that they would not otherwise have been permitted to purchase, and which they were able to sell at a profit,” according to the indictment.

Both the prosecuting assistant US attorney, Andrew Lievense, and Aslam’s defense lawyer, Daniel Dena, declined to comment for this news organization.

The prosecutor is seeking to recoup the more than $2.5 million Aslam allegedly pocketed, according to the indictment. The press release also noted that an “indictment is only a charge and is not evidence of guilt.”
 

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

In late October, a federal grand jury charged a Detroit-area medical oncologist Naveed Aslam, MD, in an indictment for his part in a scheme to illegally sell cancer drugs.

According to the indictment, Aslam acquired and sold more than $17 million in cancer drugs and personally netted more than $2.5 million during the scheme.

The charges against Aslam, filed on October 23 in the US District Court for the Eastern District of Michigan, include 10 counts of illegally selling or trading prescription drugs and one count of conspiring to do so.

“Dr. Aslam’s alleged participation in this scheme not only allowed him to profit unlawfully from the sale of cancer drugs but it also posed a serious threat by potentially placing these medications into the wrong hands,” Cheyvoryea Gibson, special agent in charge of the FBI in Michigan, said in a press release announcing the indictment.

The investigation is being conducted jointly by the FBI, the US Food and Drug Administration (FDA), the US Department of Health and Human Services Office of Inspector General, and Homeland Security Investigations.

The indictment alleges that Aslam was recruited by an unnamed operator of a Michigan corporation that engaged in business as a retail pharmacy and in the wholesale distribution of expensive prescription drugs, largely oncology drugs.

According to the indictment, Aslam and the operator came to an agreement where Aslam would purchase these expensive drugs from an authorized distributor under the false pretense that he was going to prescribe them to patients.

Instead, Aslam allegedly “sold and transferred the prescription drugs” to or through the Michigan business, with involvement from the unnamed operator and a second unnamed individual.

The unnamed individuals “identified customers interested in buying prescription cancer drugs” and “communicated with Dr. Aslam about what cancer drugs were requested,” according to the press release. “Dr. Aslam used his access to certain cancer drugs through his medical practice, Somerset Hematology and Oncology, P.C., to order and purchase the cancer drugs from his supplier.”

The indictment lays out that Aslam allegedly profited from this scheme in several ways, which included charging the Michigan business more than he paid the distributor for the drugs, sharing the profits when the business resold the drugs at a markup, and receiving rebates and discounts from the distributor “based on the amount of qualifying drugs he purchased and resold.”

According to the indictment, the scheme ran from early 2019 to mid-2023 and included four antibody drug conjugates — trastuzumab deruxtecan (Enhertu), enfortumab vedotin (Padcev), tisotumab vedotin (Tivdak), and sacituzumab govitecan (Trodelvy) — and the monoclonal antibody mogamulizumab (Poteligeo) for cutaneous T-cell lymphoma.

By working with Aslam, the operatives “obtained prescription drugs from an authorized distributor that they would not otherwise have been permitted to purchase, and which they were able to sell at a profit,” according to the indictment.

Both the prosecuting assistant US attorney, Andrew Lievense, and Aslam’s defense lawyer, Daniel Dena, declined to comment for this news organization.

The prosecutor is seeking to recoup the more than $2.5 million Aslam allegedly pocketed, according to the indictment. The press release also noted that an “indictment is only a charge and is not evidence of guilt.”
 

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

In late October, a federal grand jury charged a Detroit-area medical oncologist Naveed Aslam, MD, in an indictment for his part in a scheme to illegally sell cancer drugs.

According to the indictment, Aslam acquired and sold more than $17 million in cancer drugs and personally netted more than $2.5 million during the scheme.

The charges against Aslam, filed on October 23 in the US District Court for the Eastern District of Michigan, include 10 counts of illegally selling or trading prescription drugs and one count of conspiring to do so.

“Dr. Aslam’s alleged participation in this scheme not only allowed him to profit unlawfully from the sale of cancer drugs but it also posed a serious threat by potentially placing these medications into the wrong hands,” Cheyvoryea Gibson, special agent in charge of the FBI in Michigan, said in a press release announcing the indictment.

The investigation is being conducted jointly by the FBI, the US Food and Drug Administration (FDA), the US Department of Health and Human Services Office of Inspector General, and Homeland Security Investigations.

The indictment alleges that Aslam was recruited by an unnamed operator of a Michigan corporation that engaged in business as a retail pharmacy and in the wholesale distribution of expensive prescription drugs, largely oncology drugs.

According to the indictment, Aslam and the operator came to an agreement where Aslam would purchase these expensive drugs from an authorized distributor under the false pretense that he was going to prescribe them to patients.

Instead, Aslam allegedly “sold and transferred the prescription drugs” to or through the Michigan business, with involvement from the unnamed operator and a second unnamed individual.

The unnamed individuals “identified customers interested in buying prescription cancer drugs” and “communicated with Dr. Aslam about what cancer drugs were requested,” according to the press release. “Dr. Aslam used his access to certain cancer drugs through his medical practice, Somerset Hematology and Oncology, P.C., to order and purchase the cancer drugs from his supplier.”

The indictment lays out that Aslam allegedly profited from this scheme in several ways, which included charging the Michigan business more than he paid the distributor for the drugs, sharing the profits when the business resold the drugs at a markup, and receiving rebates and discounts from the distributor “based on the amount of qualifying drugs he purchased and resold.”

According to the indictment, the scheme ran from early 2019 to mid-2023 and included four antibody drug conjugates — trastuzumab deruxtecan (Enhertu), enfortumab vedotin (Padcev), tisotumab vedotin (Tivdak), and sacituzumab govitecan (Trodelvy) — and the monoclonal antibody mogamulizumab (Poteligeo) for cutaneous T-cell lymphoma.

By working with Aslam, the operatives “obtained prescription drugs from an authorized distributor that they would not otherwise have been permitted to purchase, and which they were able to sell at a profit,” according to the indictment.

Both the prosecuting assistant US attorney, Andrew Lievense, and Aslam’s defense lawyer, Daniel Dena, declined to comment for this news organization.

The prosecutor is seeking to recoup the more than $2.5 million Aslam allegedly pocketed, according to the indictment. The press release also noted that an “indictment is only a charge and is not evidence of guilt.”
 

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

In daily practice, physicians need a quick and simple way to assess whether a patient’s weight presents a health risk. For decades, the body mass index (BMI) has been used for this purpose, with calculations based on height and weight. Despite its convenience, BMI has faced increasing criticism. Recent research suggests that another metric, the body roundness index (BRI), might better gauge the health risks associated with obesity.

According to experts, BRI may more accurately identify people with high levels of visceral fat than BMI. It’s well documented that abdominal fat is strongly linked to higher risks for obesity-related diseases.
 

Studies Support BRI

Several studies have suggested that BRI could be a valuable tool for assessing health risks. In June of this year, researchers from China reported a significant U-shaped association between BRI and overall mortality in a paper published in JAMA Network Open. People with very low or very high BRI had an increased risk for death, noted Xiaoqian Zhang, MD, from Beijing University of Chinese Medicine, Beijing, China, and his colleagues.

A study published in September in the Journal of the American Heart Association showed that elevated BRI over several years was associated with an increased risk for cardiovascular diseases. “The BRI can be included as a predictive factor for cardiovascular disease incidence,” stated the authors, led by Man Yang, MD, from Nanjing Medical University in Nanjing, China.
 

Why Replace BMI?

Why is a replacement for BMI necessary? When asked by this news organization, Manfred Müller, MD, senior professor at the Institute of Human Nutrition and Food Science at the University of Kiel, in Germany, explained: “BMI was designed to provide a simple value that was as independent of body size as possible, that could detect obesity and estimate related disease risks. But scientifically, BMI has always been a very crude measure to characterize disease risks.”

Müller was part of a research group led by US mathematician Diana Thomas, PhD, who, at the time, worked at Montclair State University, Montclair, New Jersey, and now holds a position at the US Military Academy at West Point, in New York. The group developed and published the BRI in 2013.
 

BMI Classifies Bodybuilders as Obese

The researchers justified their search for a “better” anthropometric measure with two aspects of BMI that still constitute the main points of criticism of the widely used index today:

BMI incorrectly classifies individuals with significant muscle mass, like bodybuilders, as obese, as it doesn’t distinguish between fat and muscle mass. 

BMI provides no information about fat distribution in the body — whether it’s concentrated in the hips or the abdomen, for example. 

In practice, this means that a person with a normal BMI could already have prediabetes, high blood pressure, and high cholesterol, which might go undetected if no further investigations are conducted based solely on their BMI.

The BRI aims to solve this problem. As the name suggests, this index seeks to capture a person’s “roundness.” The formula for calculating BRI includes waist circumference and height but excludes body weight:

BRI = 364.2 − 365.5 × √(1 − [Waist circumference in cm/2π]²/[0.5 × Height in cm]²)

In their 2013 article, Thomas, Müller, and colleagues wrote that it still needed to be proven whether their newly developed index correlated with mortality and the risk for cardiovascular and metabolic diseases — and whether it was sufficiently better than BMI to justify the more complex calculation.
 

Could BRI Replace BMI?

Opinions differ on whether the BRI should replace the BMI. Zhang’s team concluded that the BRI needs to be validated in additional independent cohorts. If it does, it could become a practical screening tool in patient care.

Yang’s research group is optimistic about the BRI’s future: “The longitudinal trajectory of the BRI could be used as a novel indicator of cardiovascular disease risk, which provides a new possibility for cardiovascular disease prevention,” they wrote.

However, even BRI Co-creator Thomas has concerns. “Our entire medical system has been built around the BMI,” she told JAMA, referring to factors such as children’s growth charts and dosage recommendations for medications. That cannot be changed overnight.

Any anthropometric measure intended to replace BMI would need to be rigorously validated across all age groups, genders, and ethnicities. The impact of interventions such as bariatric surgery, diet, and exercise on the new measure would also need to be demonstrated.
 

Anthropometric Measures Only for Clinical Use

Even if BRI proves to be a “better” metric than BMI for patient care, Müller believes it would be no more suitable for research than BMI. “Regardless of the anthropometric measure, these are practical tools for everyday use,” he stressed.

“A high BRI, like a high BMI, is a risk factor — similar to high blood pressure, high cholesterol levels, or smoking — but it is not a disease,” he added. “In practice, as a physician, I know that a patient with a high BMI or BRI has an increased risk. I need to pay attention to that patient.”

Problems arise when indices like BMI or BRI are used in research. “These ‘invented’ anthropometric measures have no biological basis, which can harm obesity research,” Müller emphasized.

He cited the example of genetic research into obesity, which seeks to identify associations between specific genetic patterns and BMI values. “Why should weight in kilograms divided by height in meters squared be genetically determined?” he asked. “These measures are human-made constructs that have nothing to do with biology.”

Müller believes that the use of BMI has created a “gray area in obesity research” that may account for many of the “unexplained” phenomena in this field.
 

The BMI Might Be Responsible for the ‘Healthy Obese’

One such phenomenon is the much-discussed “healthy obese,” referring to individuals with a BMI over 30 who do not have high blood sugar, high blood pressure, metabolic disorders, or elevated uric acid levels. “It’s speculated that it must be due to genetic factors, but in reality, the classification is simply wrong,” Müller said.

According to Müller, research should rely on other methods to determine obesity or relevant fat. For example, to assess diabetes risk, liver fat needs to be measured through enzyme tests, ultrasonography, CT, or MRI.

Visceral fat is also important in assessing cardiometabolic risk. “In the doctor’s office, it’s acceptable to estimate this by looking at waist circumference or even BRI. But for research, that’s inadequate,” noted Müller. Direct measurement of trunk fat with dual-energy x-ray absorptiometry or visceral fat with CT or MRI is needed.

“You always have to distinguish between research and patient care. In daily practice, measures like BRI or BMI are sufficient for assessing cardiometabolic risk. But in research, they are not,” Müller explained. To accurately study the disease risks associated with obesity, one must be aware that “with BMI, you cannot create scientifically valid patient or population groups because this value is far too imprecise.”
 

This story was translated from Medscape’s German edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

In daily practice, physicians need a quick and simple way to assess whether a patient’s weight presents a health risk. For decades, the body mass index (BMI) has been used for this purpose, with calculations based on height and weight. Despite its convenience, BMI has faced increasing criticism. Recent research suggests that another metric, the body roundness index (BRI), might better gauge the health risks associated with obesity.

According to experts, BRI may more accurately identify people with high levels of visceral fat than BMI. It’s well documented that abdominal fat is strongly linked to higher risks for obesity-related diseases.
 

Studies Support BRI

Several studies have suggested that BRI could be a valuable tool for assessing health risks. In June of this year, researchers from China reported a significant U-shaped association between BRI and overall mortality in a paper published in JAMA Network Open. People with very low or very high BRI had an increased risk for death, noted Xiaoqian Zhang, MD, from Beijing University of Chinese Medicine, Beijing, China, and his colleagues.

A study published in September in the Journal of the American Heart Association showed that elevated BRI over several years was associated with an increased risk for cardiovascular diseases. “The BRI can be included as a predictive factor for cardiovascular disease incidence,” stated the authors, led by Man Yang, MD, from Nanjing Medical University in Nanjing, China.
 

Why Replace BMI?

Why is a replacement for BMI necessary? When asked by this news organization, Manfred Müller, MD, senior professor at the Institute of Human Nutrition and Food Science at the University of Kiel, in Germany, explained: “BMI was designed to provide a simple value that was as independent of body size as possible, that could detect obesity and estimate related disease risks. But scientifically, BMI has always been a very crude measure to characterize disease risks.”

Müller was part of a research group led by US mathematician Diana Thomas, PhD, who, at the time, worked at Montclair State University, Montclair, New Jersey, and now holds a position at the US Military Academy at West Point, in New York. The group developed and published the BRI in 2013.
 

BMI Classifies Bodybuilders as Obese

The researchers justified their search for a “better” anthropometric measure with two aspects of BMI that still constitute the main points of criticism of the widely used index today:

BMI incorrectly classifies individuals with significant muscle mass, like bodybuilders, as obese, as it doesn’t distinguish between fat and muscle mass. 

BMI provides no information about fat distribution in the body — whether it’s concentrated in the hips or the abdomen, for example. 

In practice, this means that a person with a normal BMI could already have prediabetes, high blood pressure, and high cholesterol, which might go undetected if no further investigations are conducted based solely on their BMI.

The BRI aims to solve this problem. As the name suggests, this index seeks to capture a person’s “roundness.” The formula for calculating BRI includes waist circumference and height but excludes body weight:

BRI = 364.2 − 365.5 × √(1 − [Waist circumference in cm/2π]²/[0.5 × Height in cm]²)

In their 2013 article, Thomas, Müller, and colleagues wrote that it still needed to be proven whether their newly developed index correlated with mortality and the risk for cardiovascular and metabolic diseases — and whether it was sufficiently better than BMI to justify the more complex calculation.
 

Could BRI Replace BMI?

Opinions differ on whether the BRI should replace the BMI. Zhang’s team concluded that the BRI needs to be validated in additional independent cohorts. If it does, it could become a practical screening tool in patient care.

Yang’s research group is optimistic about the BRI’s future: “The longitudinal trajectory of the BRI could be used as a novel indicator of cardiovascular disease risk, which provides a new possibility for cardiovascular disease prevention,” they wrote.

However, even BRI Co-creator Thomas has concerns. “Our entire medical system has been built around the BMI,” she told JAMA, referring to factors such as children’s growth charts and dosage recommendations for medications. That cannot be changed overnight.

Any anthropometric measure intended to replace BMI would need to be rigorously validated across all age groups, genders, and ethnicities. The impact of interventions such as bariatric surgery, diet, and exercise on the new measure would also need to be demonstrated.
 

Anthropometric Measures Only for Clinical Use

Even if BRI proves to be a “better” metric than BMI for patient care, Müller believes it would be no more suitable for research than BMI. “Regardless of the anthropometric measure, these are practical tools for everyday use,” he stressed.

“A high BRI, like a high BMI, is a risk factor — similar to high blood pressure, high cholesterol levels, or smoking — but it is not a disease,” he added. “In practice, as a physician, I know that a patient with a high BMI or BRI has an increased risk. I need to pay attention to that patient.”

Problems arise when indices like BMI or BRI are used in research. “These ‘invented’ anthropometric measures have no biological basis, which can harm obesity research,” Müller emphasized.

He cited the example of genetic research into obesity, which seeks to identify associations between specific genetic patterns and BMI values. “Why should weight in kilograms divided by height in meters squared be genetically determined?” he asked. “These measures are human-made constructs that have nothing to do with biology.”

Müller believes that the use of BMI has created a “gray area in obesity research” that may account for many of the “unexplained” phenomena in this field.
 

The BMI Might Be Responsible for the ‘Healthy Obese’

One such phenomenon is the much-discussed “healthy obese,” referring to individuals with a BMI over 30 who do not have high blood sugar, high blood pressure, metabolic disorders, or elevated uric acid levels. “It’s speculated that it must be due to genetic factors, but in reality, the classification is simply wrong,” Müller said.

According to Müller, research should rely on other methods to determine obesity or relevant fat. For example, to assess diabetes risk, liver fat needs to be measured through enzyme tests, ultrasonography, CT, or MRI.

Visceral fat is also important in assessing cardiometabolic risk. “In the doctor’s office, it’s acceptable to estimate this by looking at waist circumference or even BRI. But for research, that’s inadequate,” noted Müller. Direct measurement of trunk fat with dual-energy x-ray absorptiometry or visceral fat with CT or MRI is needed.

“You always have to distinguish between research and patient care. In daily practice, measures like BRI or BMI are sufficient for assessing cardiometabolic risk. But in research, they are not,” Müller explained. To accurately study the disease risks associated with obesity, one must be aware that “with BMI, you cannot create scientifically valid patient or population groups because this value is far too imprecise.”
 

This story was translated from Medscape’s German edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

In daily practice, physicians need a quick and simple way to assess whether a patient’s weight presents a health risk. For decades, the body mass index (BMI) has been used for this purpose, with calculations based on height and weight. Despite its convenience, BMI has faced increasing criticism. Recent research suggests that another metric, the body roundness index (BRI), might better gauge the health risks associated with obesity.

According to experts, BRI may more accurately identify people with high levels of visceral fat than BMI. It’s well documented that abdominal fat is strongly linked to higher risks for obesity-related diseases.
 

Studies Support BRI

Several studies have suggested that BRI could be a valuable tool for assessing health risks. In June of this year, researchers from China reported a significant U-shaped association between BRI and overall mortality in a paper published in JAMA Network Open. People with very low or very high BRI had an increased risk for death, noted Xiaoqian Zhang, MD, from Beijing University of Chinese Medicine, Beijing, China, and his colleagues.

A study published in September in the Journal of the American Heart Association showed that elevated BRI over several years was associated with an increased risk for cardiovascular diseases. “The BRI can be included as a predictive factor for cardiovascular disease incidence,” stated the authors, led by Man Yang, MD, from Nanjing Medical University in Nanjing, China.
 

Why Replace BMI?

Why is a replacement for BMI necessary? When asked by this news organization, Manfred Müller, MD, senior professor at the Institute of Human Nutrition and Food Science at the University of Kiel, in Germany, explained: “BMI was designed to provide a simple value that was as independent of body size as possible, that could detect obesity and estimate related disease risks. But scientifically, BMI has always been a very crude measure to characterize disease risks.”

Müller was part of a research group led by US mathematician Diana Thomas, PhD, who, at the time, worked at Montclair State University, Montclair, New Jersey, and now holds a position at the US Military Academy at West Point, in New York. The group developed and published the BRI in 2013.
 

BMI Classifies Bodybuilders as Obese

The researchers justified their search for a “better” anthropometric measure with two aspects of BMI that still constitute the main points of criticism of the widely used index today:

BMI incorrectly classifies individuals with significant muscle mass, like bodybuilders, as obese, as it doesn’t distinguish between fat and muscle mass. 

BMI provides no information about fat distribution in the body — whether it’s concentrated in the hips or the abdomen, for example. 

In practice, this means that a person with a normal BMI could already have prediabetes, high blood pressure, and high cholesterol, which might go undetected if no further investigations are conducted based solely on their BMI.

The BRI aims to solve this problem. As the name suggests, this index seeks to capture a person’s “roundness.” The formula for calculating BRI includes waist circumference and height but excludes body weight:

BRI = 364.2 − 365.5 × √(1 − [Waist circumference in cm/2π]²/[0.5 × Height in cm]²)

In their 2013 article, Thomas, Müller, and colleagues wrote that it still needed to be proven whether their newly developed index correlated with mortality and the risk for cardiovascular and metabolic diseases — and whether it was sufficiently better than BMI to justify the more complex calculation.
 

Could BRI Replace BMI?

Opinions differ on whether the BRI should replace the BMI. Zhang’s team concluded that the BRI needs to be validated in additional independent cohorts. If it does, it could become a practical screening tool in patient care.

Yang’s research group is optimistic about the BRI’s future: “The longitudinal trajectory of the BRI could be used as a novel indicator of cardiovascular disease risk, which provides a new possibility for cardiovascular disease prevention,” they wrote.

However, even BRI Co-creator Thomas has concerns. “Our entire medical system has been built around the BMI,” she told JAMA, referring to factors such as children’s growth charts and dosage recommendations for medications. That cannot be changed overnight.

Any anthropometric measure intended to replace BMI would need to be rigorously validated across all age groups, genders, and ethnicities. The impact of interventions such as bariatric surgery, diet, and exercise on the new measure would also need to be demonstrated.
 

Anthropometric Measures Only for Clinical Use

Even if BRI proves to be a “better” metric than BMI for patient care, Müller believes it would be no more suitable for research than BMI. “Regardless of the anthropometric measure, these are practical tools for everyday use,” he stressed.

“A high BRI, like a high BMI, is a risk factor — similar to high blood pressure, high cholesterol levels, or smoking — but it is not a disease,” he added. “In practice, as a physician, I know that a patient with a high BMI or BRI has an increased risk. I need to pay attention to that patient.”

Problems arise when indices like BMI or BRI are used in research. “These ‘invented’ anthropometric measures have no biological basis, which can harm obesity research,” Müller emphasized.

He cited the example of genetic research into obesity, which seeks to identify associations between specific genetic patterns and BMI values. “Why should weight in kilograms divided by height in meters squared be genetically determined?” he asked. “These measures are human-made constructs that have nothing to do with biology.”

Müller believes that the use of BMI has created a “gray area in obesity research” that may account for many of the “unexplained” phenomena in this field.
 

The BMI Might Be Responsible for the ‘Healthy Obese’

One such phenomenon is the much-discussed “healthy obese,” referring to individuals with a BMI over 30 who do not have high blood sugar, high blood pressure, metabolic disorders, or elevated uric acid levels. “It’s speculated that it must be due to genetic factors, but in reality, the classification is simply wrong,” Müller said.

According to Müller, research should rely on other methods to determine obesity or relevant fat. For example, to assess diabetes risk, liver fat needs to be measured through enzyme tests, ultrasonography, CT, or MRI.

Visceral fat is also important in assessing cardiometabolic risk. “In the doctor’s office, it’s acceptable to estimate this by looking at waist circumference or even BRI. But for research, that’s inadequate,” noted Müller. Direct measurement of trunk fat with dual-energy x-ray absorptiometry or visceral fat with CT or MRI is needed.

“You always have to distinguish between research and patient care. In daily practice, measures like BRI or BMI are sufficient for assessing cardiometabolic risk. But in research, they are not,” Müller explained. To accurately study the disease risks associated with obesity, one must be aware that “with BMI, you cannot create scientifically valid patient or population groups because this value is far too imprecise.”
 

This story was translated from Medscape’s German edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

This transcript has been edited for clarity .

Robert A. Harrington, MD: I’m here in London at the European Society of Cardiology meetings, at theheart.org | Medscape Cardiology booth, using the meetings as an opportunity to meet with colleagues to talk about recent things that they’ve been writing about.

Today I’m joined by a good friend and colleague, Dr. Dhruv Kazi from Beth Israel Deaconess in Boston. Thanks for joining us.

Dhruv S. Kazi, MD, MS: Thank you for having me.

Harrington: Dr. Kazi is an associate professor of medicine at Harvard Medical School. He’s also the associate director of the Smith Center, which is an outcomes research center at the Beth Israel Deaconess. Thanks for joining us.

Kazi: Excited to be here.

Harrington: The topic I think you know that I want to discuss is a really important paper. There are two papers. They’re part of the American Heart Association’s 100th anniversary celebration, if you will. Many of the papers looked back at where science taken us.

With your coauthor, Karen Joynt Maddox, your papers are looking forward. They’re about the burden of cardiovascular disease in 2050. One paper really focused on what I would call the clinical and public health issues. Yours is focused on the economics. Is that a good description?

Kazi: Perfect.

Harrington: Tell us what you, Karen, and the other writers set out to do. What were you asked to do?

Kazi: As you know, the American Heart Association is entering its second century. Part of this was an exercise to say, where will the country be in 2050, which is a long enough time horizon for us to start planning for the future. What are the conditions that affect the magnitude of the disease, and the kinds of people who will be affected, that we should be aware of?

We looked back and said, if prior trends remain the same, where will we be in 2050, accounting for changes in demographics, changes in the composition of the population, and knowing that some of the cardiovascular risk factors are getting worse?

Harrington: For me, what was really striking is that, when I first saw the title and read “2050,” I thought, Oh, that’s a long way away. Then as I started reading it, I realized that this is not so far away.

Kazi: Absolutely.

Harrington: If we’re going to make a difference, it might take us 25 years.

Kazi: Especially if we set ourselves ambitious goals, we›re going to have to dig deep. Business-as-usual is not going to get us there.

Harrington: No. What I think has happened is we›ve spent so much time taking care of acute illness. Case fatality rates are fantastic. I was actually making the comment yesterday to a colleague that when I was an intern, the 30-day death rate from acute myocardial infarction was about 20%.

Kazi: Oh, wow.

Harrington: Now it’s 5%. That’s a big difference in a career.
 

Trends in the Wrong Direction

Kazi: There are fundamental trends. The decline in case fatalities is a really positive development, and I would hope that, going forward, that would continue. Those are risk-adjusted death rates and what is happening is that risk is going up. This is a function of the fact that the US population is aging; 2030 will be the first year that all the baby boomers will be over the age of 65.

By the mid-2030s, we’ll have more adults over the age of 65 than kids. That aging of the population is going to increase risk. The second is — and this is a positive development — we are a more diverse population, but the populations that are minoritized have higher cardiovascular risk, for a variety of reasons.

As the population of Asian Americans increases and doubles, in fact, as the population of Hispanic Americans doubles, we’re going to see an increase in risk related to cardiovascular disease. The third is that, over the past decade, there are some risk factors that are going in the wrong direction.

Harrington: Let’s talk about that because that’s humbling. I’m involved, as you know, with the American Heart Association, as are you. Despite all the work on Life’s Simple 7 and now Life’s Essential 8, we still have some issues.

Kazi: The big ones that come to mind are hypertension, diabetes, and obesity, all of which are trending in the wrong direction. Hypertension, we were gaining traction; and then over the past decade, we’ve slipped again. As you know, national blood pressure control rates have declined in many populations.

Harrington: Rather substantially.

Kazi: Substantially so, which has implications, in particular, for stroke rates in the future and stroke rates in young adults in the future. Obesity is a problem that we have very little control over. We’re already at 40% on average, which means that some populations are already in the 60% range.

Harrington: We also have obesity in kids — the burden, I’ll call it, of obesity. It’s not that you become obese in your thirties or your forties; you›re becoming obese as a teenager or even younger.

Kazi: Exactly. Since the 1990s, obesity in US adults has doubled, but obesity in US children has quadrupled. It’s starting from a lower base, but it’s very much an escalating problem.

Harrington: Diabetes is tightly linked to it but not totally explained.

Kazi: Exactly. The increase in diabetes is largely driven by obesity, but it›s probably also driven by changes in diet and lifestyle that don›t go through obesity.

Harrington: Yeah, it’s interesting. I think I have this figure correctly. It used to be rare that you saw a child with type 2 diabetes or what we call type 2 diabetes.

Kazi: Yeah.

Harrington: Now, the vast majority of kids with diabetes have type 2 diabetes.

Kazi: In the adolescents/young adults age group, most of it is type 2.

Harrington: Diabetes going up, obesity up, hypertension not well controlled, smoking combustible cigarettes way down.

Kazi: Yeah.

Harrington: Cholesterol levels. I was surprised. Cholesterol looked better. You said — because I was at a meeting where somebody asked you — that’s not explained by treatment.

Kazi: No, it’s not, at least going back to the ‘70s, but likely even sooner. I think that can only be attributed to substantial dietary changes. We are consuming less fat and less trans-fat. It’s possible that those collectively are improving our cholesterol levels, possibly at the expense of our glucose levels, because we basically substituted fats in our diet with more carbs at a population level.
 

Cigarettes and Vaping

Harrington: Some things certainly trend in the right direction but others in a really difficult direction. It’s going to lead to pretty large changes in risk for coronary disease, atrial fibrillation, and heart failure.

Kazi: I want to go back to the tobacco point. There are definitely marked declines in tobacco, still tightly related to income in the country. You see much higher prevalence of tobacco use in lower-income populations, but it’s unclear to me where it’s going in kids. We know that combustible tobacco use is going down but e-cigarettes went up. What that leads to over the next 30 years is unclear to me.

Harrington: That is a really important comment that’s worth sidebarring. The vaping use has been a terrible epidemic among our high schoolers. What is that going to lead to? Is it going to lead to the use of combustible cigarettes and we’re going to see that go back up? It remains to be seen.

Kazi: Yes, it remains to be seen. Going back to your point about this change in risk factors and this change in demographics, both aging and becoming a more diverse population means that we have large increases in some healthcare conditions.

Coronary heart disease goes up some, there›s a big jump in stroke — nearly a doubling in stroke — which is related to hypertension, obesity, an aging population, and a more diverse population. There are changes in stroke in the young, and atrial fibrillation related to, again, hypertension. We’re seeing these projections, and with them come these pretty large projections in changes in healthcare spending.
 

Healthcare Spending Not Sustainable

Harrington: Big. I mean, it’s not sustainable. Give the audience the number — it’s pretty frightening.

Kazi: We’re talking about a quadrupling of healthcare costs related to cardiovascular disease over 25 years. We’ve gotten used to the narrative that healthcare in the US is expensive and drugs are expensive, but this is an enormous problem — an unsustainable problem, like you called it.

It’s a doubling as a proportion of the economy. I was looking this up this morning. If the US healthcare economy were its own economy, it would be the fourth largest economy in the world.

Harrington: Healthcare as it is today, is it 21% of our economy?

Kazi: It’s 17% now. If it were its own economy, it would be the fourth largest in the world. We are spending more on healthcare than all but two other countries’ total economies. It’s kind of crazy.

Harrington: We’re talking about a quadrupling.

Kazi: Within that, the cardiovascular piece is a big piece, and we›re talking about a quadrupling.

Harrington: That’s both direct and indirect costs.

Kazi: The quadrupling of costs is just the direct costs. Indirect costs, for the listeners, refer to costs unrelated to healthcare but changes in productivity, either because people are disabled and unable to participate fully in the workforce or they die early.

The productivity costs are also increased substantially as a result. If you look at both healthcare and productivity, that goes up threefold. These are very large changes.

Harrington: Let’s now get to what we can do about it. I made the comment to you when I first read the papers that I was very depressed. Then, after I went through my Kübler-Ross stages of depression, death, and dying, I came to acceptance.

What are we going to do about it? This is a focus on policy, but also a focus on how we deliver healthcare, how we think about healthcare, and how we develop drugs and devices.

The drug question is going to be the one the audience is thinking about. They say, well, what about GLP-1 agonists? Aren’t those going to save the day?

Kazi: Yes and no. I’ll say that, early in my career, I used to be very attracted to simple solutions to complex problems. I’ve come to realize that simple solutions are elegant, attractive, and wrong. We›re dealing with a very complex issue and I think we’re going to need a multipronged approach.

The way I think about it is that there was a group of people who are at very high risk today. How do we help those individuals? Then how do we help the future generation so that they’re not dealing with the projections that we’re talking about.

My colleague, Karen Joynt Maddox, who led one of the papers, as you mentioned, has an elegant line in the paper where she says projections are not destiny. These are things we can change.

Harrington: If nothing changes, this is what it’s going to look like.

Kazi: This is where we’re headed.

Harrington: We can change. We’ve got some time to change, but we don’t have forever.

Kazi: Yes, exactly. We picked the 25-year timeline instead of a “let’s plan for the next century” timeline because we want something concrete and actionable. It’s close enough to be meaningful but far enough to give us the runway we need to act.

Harrington: Give me two things from the policy perspective, because it’s mostly policy.

Kazi: There are policy and clinical interventions. From the policy perspective, if I had to list two things, one is expansion of access to care. As we talk about this big increase in the burden of disease and risk factors, if you have a large proportion of your population that has hypertension or diabetes, you’re going to have to expand access to care to ensure that people get treated so they can get access to this care before they develop the complications that we worry about, like stroke and heart disease, that are very expensive to treat downstream.

The second, more broadly related to access to care, is the access to medications that are effective. You bring up GLP-1s. I think we need a real strategy for how we can give people access to GLP-1s at a price that is affordable to individuals but also affordable to the health system, and to help them stay on the drugs.

GLP-1s are transformative in what they do for weight loss and for diabetes, but more than 50% of people who start one are off it at 12 months. There’s something fundamentally wrong about how we’re delivering GLP-1s today. It’s not just about the cost of the drugs but the support system people need to stay on.

Harrington: I’ve made the comment, in many forms now, that we know the drugs work. We have to figure out how to use them.

Kazi: Exactly, yes.

Harrington: Using them includes chronicity. This is a chronic condition. Some people can come off the drugs, but many can’t. We’re going to have to figure this out, and maybe the newer generations of drugs will help us address what people call the off-ramping. How are we going to do that? I think you’re spot-on. Those are critically important questions.

Kazi: As we looked at this modeling, I’ll tell you — I had a come-to-Jesus moment where I was like, there is no way to fix cardiovascular disease in the US without going through obesity and diabetes. We have to address obesity in the US. We can’t just treat our way out of it. Obesity is fundamentally a food problem and we’ve got to engage again with food policy in a meaningful way.

Harrington: As you know, with the American Heart Association, we›re doing a large amount of work now on food as medicine and food is medicine. We are trying to figure out what the levers are that we can pull to actually help people eat healthier diets.

Kazi: Yes. Rather than framing it as an individual choice that people are eating poorly, it’s, how do we make healthy diets the default in the environment?

Harrington: This is where you get to the children as well.

Kazi: Exactly.

Harrington: I could talk about this all day. I’ve had the benefit of reading the papers now a few times and talking to you on several occasions. Thank you for joining us.

Kazi: Thank you.
 

Dr. Harrington, Stephen and Suzanne Weiss Dean, Weill Cornell Medicine; Provost for Medical Affairs, Cornell University, New York, NY, disclosed ties with Baim Institute (DSMB); CSL (RCT Executive Committee); Janssen (RCT Char), NHLBI (RCT Executive Committee, DSMB Chair); PCORI (RCT Co-Chair); DCRI, Atropos Health; Bitterroot Bio; Bristol Myers Squibb; BridgeBio; Element Science; Edwards Lifesciences; Foresite Labs; Medscape/WebMD Board of Directors for: American Heart Association; College of the Holy Cross; and Cytokinetics. Dr. Kazi, Associate Director, Smith Center for Outcomes Research, Associate Professor, Department of Medicine (Cardiology), Harvard Medical School, Director, Department of Cardiac Critical Care Unit, Beth Israel Deaconess Medical Center, Boston, Massachusetts, has disclosed receiving a research grant from Boston Scientific (grant to examine the economics of stroke prevention).

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity .

Robert A. Harrington, MD: I’m here in London at the European Society of Cardiology meetings, at theheart.org | Medscape Cardiology booth, using the meetings as an opportunity to meet with colleagues to talk about recent things that they’ve been writing about.

Today I’m joined by a good friend and colleague, Dr. Dhruv Kazi from Beth Israel Deaconess in Boston. Thanks for joining us.

Dhruv S. Kazi, MD, MS: Thank you for having me.

Harrington: Dr. Kazi is an associate professor of medicine at Harvard Medical School. He’s also the associate director of the Smith Center, which is an outcomes research center at the Beth Israel Deaconess. Thanks for joining us.

Kazi: Excited to be here.

Harrington: The topic I think you know that I want to discuss is a really important paper. There are two papers. They’re part of the American Heart Association’s 100th anniversary celebration, if you will. Many of the papers looked back at where science taken us.

With your coauthor, Karen Joynt Maddox, your papers are looking forward. They’re about the burden of cardiovascular disease in 2050. One paper really focused on what I would call the clinical and public health issues. Yours is focused on the economics. Is that a good description?

Kazi: Perfect.

Harrington: Tell us what you, Karen, and the other writers set out to do. What were you asked to do?

Kazi: As you know, the American Heart Association is entering its second century. Part of this was an exercise to say, where will the country be in 2050, which is a long enough time horizon for us to start planning for the future. What are the conditions that affect the magnitude of the disease, and the kinds of people who will be affected, that we should be aware of?

We looked back and said, if prior trends remain the same, where will we be in 2050, accounting for changes in demographics, changes in the composition of the population, and knowing that some of the cardiovascular risk factors are getting worse?

Harrington: For me, what was really striking is that, when I first saw the title and read “2050,” I thought, Oh, that’s a long way away. Then as I started reading it, I realized that this is not so far away.

Kazi: Absolutely.

Harrington: If we’re going to make a difference, it might take us 25 years.

Kazi: Especially if we set ourselves ambitious goals, we›re going to have to dig deep. Business-as-usual is not going to get us there.

Harrington: No. What I think has happened is we›ve spent so much time taking care of acute illness. Case fatality rates are fantastic. I was actually making the comment yesterday to a colleague that when I was an intern, the 30-day death rate from acute myocardial infarction was about 20%.

Kazi: Oh, wow.

Harrington: Now it’s 5%. That’s a big difference in a career.
 

Trends in the Wrong Direction

Kazi: There are fundamental trends. The decline in case fatalities is a really positive development, and I would hope that, going forward, that would continue. Those are risk-adjusted death rates and what is happening is that risk is going up. This is a function of the fact that the US population is aging; 2030 will be the first year that all the baby boomers will be over the age of 65.

By the mid-2030s, we’ll have more adults over the age of 65 than kids. That aging of the population is going to increase risk. The second is — and this is a positive development — we are a more diverse population, but the populations that are minoritized have higher cardiovascular risk, for a variety of reasons.

As the population of Asian Americans increases and doubles, in fact, as the population of Hispanic Americans doubles, we’re going to see an increase in risk related to cardiovascular disease. The third is that, over the past decade, there are some risk factors that are going in the wrong direction.

Harrington: Let’s talk about that because that’s humbling. I’m involved, as you know, with the American Heart Association, as are you. Despite all the work on Life’s Simple 7 and now Life’s Essential 8, we still have some issues.

Kazi: The big ones that come to mind are hypertension, diabetes, and obesity, all of which are trending in the wrong direction. Hypertension, we were gaining traction; and then over the past decade, we’ve slipped again. As you know, national blood pressure control rates have declined in many populations.

Harrington: Rather substantially.

Kazi: Substantially so, which has implications, in particular, for stroke rates in the future and stroke rates in young adults in the future. Obesity is a problem that we have very little control over. We’re already at 40% on average, which means that some populations are already in the 60% range.

Harrington: We also have obesity in kids — the burden, I’ll call it, of obesity. It’s not that you become obese in your thirties or your forties; you›re becoming obese as a teenager or even younger.

Kazi: Exactly. Since the 1990s, obesity in US adults has doubled, but obesity in US children has quadrupled. It’s starting from a lower base, but it’s very much an escalating problem.

Harrington: Diabetes is tightly linked to it but not totally explained.

Kazi: Exactly. The increase in diabetes is largely driven by obesity, but it›s probably also driven by changes in diet and lifestyle that don›t go through obesity.

Harrington: Yeah, it’s interesting. I think I have this figure correctly. It used to be rare that you saw a child with type 2 diabetes or what we call type 2 diabetes.

Kazi: Yeah.

Harrington: Now, the vast majority of kids with diabetes have type 2 diabetes.

Kazi: In the adolescents/young adults age group, most of it is type 2.

Harrington: Diabetes going up, obesity up, hypertension not well controlled, smoking combustible cigarettes way down.

Kazi: Yeah.

Harrington: Cholesterol levels. I was surprised. Cholesterol looked better. You said — because I was at a meeting where somebody asked you — that’s not explained by treatment.

Kazi: No, it’s not, at least going back to the ‘70s, but likely even sooner. I think that can only be attributed to substantial dietary changes. We are consuming less fat and less trans-fat. It’s possible that those collectively are improving our cholesterol levels, possibly at the expense of our glucose levels, because we basically substituted fats in our diet with more carbs at a population level.
 

Cigarettes and Vaping

Harrington: Some things certainly trend in the right direction but others in a really difficult direction. It’s going to lead to pretty large changes in risk for coronary disease, atrial fibrillation, and heart failure.

Kazi: I want to go back to the tobacco point. There are definitely marked declines in tobacco, still tightly related to income in the country. You see much higher prevalence of tobacco use in lower-income populations, but it’s unclear to me where it’s going in kids. We know that combustible tobacco use is going down but e-cigarettes went up. What that leads to over the next 30 years is unclear to me.

Harrington: That is a really important comment that’s worth sidebarring. The vaping use has been a terrible epidemic among our high schoolers. What is that going to lead to? Is it going to lead to the use of combustible cigarettes and we’re going to see that go back up? It remains to be seen.

Kazi: Yes, it remains to be seen. Going back to your point about this change in risk factors and this change in demographics, both aging and becoming a more diverse population means that we have large increases in some healthcare conditions.

Coronary heart disease goes up some, there›s a big jump in stroke — nearly a doubling in stroke — which is related to hypertension, obesity, an aging population, and a more diverse population. There are changes in stroke in the young, and atrial fibrillation related to, again, hypertension. We’re seeing these projections, and with them come these pretty large projections in changes in healthcare spending.
 

Healthcare Spending Not Sustainable

Harrington: Big. I mean, it’s not sustainable. Give the audience the number — it’s pretty frightening.

Kazi: We’re talking about a quadrupling of healthcare costs related to cardiovascular disease over 25 years. We’ve gotten used to the narrative that healthcare in the US is expensive and drugs are expensive, but this is an enormous problem — an unsustainable problem, like you called it.

It’s a doubling as a proportion of the economy. I was looking this up this morning. If the US healthcare economy were its own economy, it would be the fourth largest economy in the world.

Harrington: Healthcare as it is today, is it 21% of our economy?

Kazi: It’s 17% now. If it were its own economy, it would be the fourth largest in the world. We are spending more on healthcare than all but two other countries’ total economies. It’s kind of crazy.

Harrington: We’re talking about a quadrupling.

Kazi: Within that, the cardiovascular piece is a big piece, and we›re talking about a quadrupling.

Harrington: That’s both direct and indirect costs.

Kazi: The quadrupling of costs is just the direct costs. Indirect costs, for the listeners, refer to costs unrelated to healthcare but changes in productivity, either because people are disabled and unable to participate fully in the workforce or they die early.

The productivity costs are also increased substantially as a result. If you look at both healthcare and productivity, that goes up threefold. These are very large changes.

Harrington: Let’s now get to what we can do about it. I made the comment to you when I first read the papers that I was very depressed. Then, after I went through my Kübler-Ross stages of depression, death, and dying, I came to acceptance.

What are we going to do about it? This is a focus on policy, but also a focus on how we deliver healthcare, how we think about healthcare, and how we develop drugs and devices.

The drug question is going to be the one the audience is thinking about. They say, well, what about GLP-1 agonists? Aren’t those going to save the day?

Kazi: Yes and no. I’ll say that, early in my career, I used to be very attracted to simple solutions to complex problems. I’ve come to realize that simple solutions are elegant, attractive, and wrong. We›re dealing with a very complex issue and I think we’re going to need a multipronged approach.

The way I think about it is that there was a group of people who are at very high risk today. How do we help those individuals? Then how do we help the future generation so that they’re not dealing with the projections that we’re talking about.

My colleague, Karen Joynt Maddox, who led one of the papers, as you mentioned, has an elegant line in the paper where she says projections are not destiny. These are things we can change.

Harrington: If nothing changes, this is what it’s going to look like.

Kazi: This is where we’re headed.

Harrington: We can change. We’ve got some time to change, but we don’t have forever.

Kazi: Yes, exactly. We picked the 25-year timeline instead of a “let’s plan for the next century” timeline because we want something concrete and actionable. It’s close enough to be meaningful but far enough to give us the runway we need to act.

Harrington: Give me two things from the policy perspective, because it’s mostly policy.

Kazi: There are policy and clinical interventions. From the policy perspective, if I had to list two things, one is expansion of access to care. As we talk about this big increase in the burden of disease and risk factors, if you have a large proportion of your population that has hypertension or diabetes, you’re going to have to expand access to care to ensure that people get treated so they can get access to this care before they develop the complications that we worry about, like stroke and heart disease, that are very expensive to treat downstream.

The second, more broadly related to access to care, is the access to medications that are effective. You bring up GLP-1s. I think we need a real strategy for how we can give people access to GLP-1s at a price that is affordable to individuals but also affordable to the health system, and to help them stay on the drugs.

GLP-1s are transformative in what they do for weight loss and for diabetes, but more than 50% of people who start one are off it at 12 months. There’s something fundamentally wrong about how we’re delivering GLP-1s today. It’s not just about the cost of the drugs but the support system people need to stay on.

Harrington: I’ve made the comment, in many forms now, that we know the drugs work. We have to figure out how to use them.

Kazi: Exactly, yes.

Harrington: Using them includes chronicity. This is a chronic condition. Some people can come off the drugs, but many can’t. We’re going to have to figure this out, and maybe the newer generations of drugs will help us address what people call the off-ramping. How are we going to do that? I think you’re spot-on. Those are critically important questions.

Kazi: As we looked at this modeling, I’ll tell you — I had a come-to-Jesus moment where I was like, there is no way to fix cardiovascular disease in the US without going through obesity and diabetes. We have to address obesity in the US. We can’t just treat our way out of it. Obesity is fundamentally a food problem and we’ve got to engage again with food policy in a meaningful way.

Harrington: As you know, with the American Heart Association, we›re doing a large amount of work now on food as medicine and food is medicine. We are trying to figure out what the levers are that we can pull to actually help people eat healthier diets.

Kazi: Yes. Rather than framing it as an individual choice that people are eating poorly, it’s, how do we make healthy diets the default in the environment?

Harrington: This is where you get to the children as well.

Kazi: Exactly.

Harrington: I could talk about this all day. I’ve had the benefit of reading the papers now a few times and talking to you on several occasions. Thank you for joining us.

Kazi: Thank you.
 

Dr. Harrington, Stephen and Suzanne Weiss Dean, Weill Cornell Medicine; Provost for Medical Affairs, Cornell University, New York, NY, disclosed ties with Baim Institute (DSMB); CSL (RCT Executive Committee); Janssen (RCT Char), NHLBI (RCT Executive Committee, DSMB Chair); PCORI (RCT Co-Chair); DCRI, Atropos Health; Bitterroot Bio; Bristol Myers Squibb; BridgeBio; Element Science; Edwards Lifesciences; Foresite Labs; Medscape/WebMD Board of Directors for: American Heart Association; College of the Holy Cross; and Cytokinetics. Dr. Kazi, Associate Director, Smith Center for Outcomes Research, Associate Professor, Department of Medicine (Cardiology), Harvard Medical School, Director, Department of Cardiac Critical Care Unit, Beth Israel Deaconess Medical Center, Boston, Massachusetts, has disclosed receiving a research grant from Boston Scientific (grant to examine the economics of stroke prevention).

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity .

Robert A. Harrington, MD: I’m here in London at the European Society of Cardiology meetings, at theheart.org | Medscape Cardiology booth, using the meetings as an opportunity to meet with colleagues to talk about recent things that they’ve been writing about.

Today I’m joined by a good friend and colleague, Dr. Dhruv Kazi from Beth Israel Deaconess in Boston. Thanks for joining us.

Dhruv S. Kazi, MD, MS: Thank you for having me.

Harrington: Dr. Kazi is an associate professor of medicine at Harvard Medical School. He’s also the associate director of the Smith Center, which is an outcomes research center at the Beth Israel Deaconess. Thanks for joining us.

Kazi: Excited to be here.

Harrington: The topic I think you know that I want to discuss is a really important paper. There are two papers. They’re part of the American Heart Association’s 100th anniversary celebration, if you will. Many of the papers looked back at where science taken us.

With your coauthor, Karen Joynt Maddox, your papers are looking forward. They’re about the burden of cardiovascular disease in 2050. One paper really focused on what I would call the clinical and public health issues. Yours is focused on the economics. Is that a good description?

Kazi: Perfect.

Harrington: Tell us what you, Karen, and the other writers set out to do. What were you asked to do?

Kazi: As you know, the American Heart Association is entering its second century. Part of this was an exercise to say, where will the country be in 2050, which is a long enough time horizon for us to start planning for the future. What are the conditions that affect the magnitude of the disease, and the kinds of people who will be affected, that we should be aware of?

We looked back and said, if prior trends remain the same, where will we be in 2050, accounting for changes in demographics, changes in the composition of the population, and knowing that some of the cardiovascular risk factors are getting worse?

Harrington: For me, what was really striking is that, when I first saw the title and read “2050,” I thought, Oh, that’s a long way away. Then as I started reading it, I realized that this is not so far away.

Kazi: Absolutely.

Harrington: If we’re going to make a difference, it might take us 25 years.

Kazi: Especially if we set ourselves ambitious goals, we›re going to have to dig deep. Business-as-usual is not going to get us there.

Harrington: No. What I think has happened is we›ve spent so much time taking care of acute illness. Case fatality rates are fantastic. I was actually making the comment yesterday to a colleague that when I was an intern, the 30-day death rate from acute myocardial infarction was about 20%.

Kazi: Oh, wow.

Harrington: Now it’s 5%. That’s a big difference in a career.
 

Trends in the Wrong Direction

Kazi: There are fundamental trends. The decline in case fatalities is a really positive development, and I would hope that, going forward, that would continue. Those are risk-adjusted death rates and what is happening is that risk is going up. This is a function of the fact that the US population is aging; 2030 will be the first year that all the baby boomers will be over the age of 65.

By the mid-2030s, we’ll have more adults over the age of 65 than kids. That aging of the population is going to increase risk. The second is — and this is a positive development — we are a more diverse population, but the populations that are minoritized have higher cardiovascular risk, for a variety of reasons.

As the population of Asian Americans increases and doubles, in fact, as the population of Hispanic Americans doubles, we’re going to see an increase in risk related to cardiovascular disease. The third is that, over the past decade, there are some risk factors that are going in the wrong direction.

Harrington: Let’s talk about that because that’s humbling. I’m involved, as you know, with the American Heart Association, as are you. Despite all the work on Life’s Simple 7 and now Life’s Essential 8, we still have some issues.

Kazi: The big ones that come to mind are hypertension, diabetes, and obesity, all of which are trending in the wrong direction. Hypertension, we were gaining traction; and then over the past decade, we’ve slipped again. As you know, national blood pressure control rates have declined in many populations.

Harrington: Rather substantially.

Kazi: Substantially so, which has implications, in particular, for stroke rates in the future and stroke rates in young adults in the future. Obesity is a problem that we have very little control over. We’re already at 40% on average, which means that some populations are already in the 60% range.

Harrington: We also have obesity in kids — the burden, I’ll call it, of obesity. It’s not that you become obese in your thirties or your forties; you›re becoming obese as a teenager or even younger.

Kazi: Exactly. Since the 1990s, obesity in US adults has doubled, but obesity in US children has quadrupled. It’s starting from a lower base, but it’s very much an escalating problem.

Harrington: Diabetes is tightly linked to it but not totally explained.

Kazi: Exactly. The increase in diabetes is largely driven by obesity, but it›s probably also driven by changes in diet and lifestyle that don›t go through obesity.

Harrington: Yeah, it’s interesting. I think I have this figure correctly. It used to be rare that you saw a child with type 2 diabetes or what we call type 2 diabetes.

Kazi: Yeah.

Harrington: Now, the vast majority of kids with diabetes have type 2 diabetes.

Kazi: In the adolescents/young adults age group, most of it is type 2.

Harrington: Diabetes going up, obesity up, hypertension not well controlled, smoking combustible cigarettes way down.

Kazi: Yeah.

Harrington: Cholesterol levels. I was surprised. Cholesterol looked better. You said — because I was at a meeting where somebody asked you — that’s not explained by treatment.

Kazi: No, it’s not, at least going back to the ‘70s, but likely even sooner. I think that can only be attributed to substantial dietary changes. We are consuming less fat and less trans-fat. It’s possible that those collectively are improving our cholesterol levels, possibly at the expense of our glucose levels, because we basically substituted fats in our diet with more carbs at a population level.
 

Cigarettes and Vaping

Harrington: Some things certainly trend in the right direction but others in a really difficult direction. It’s going to lead to pretty large changes in risk for coronary disease, atrial fibrillation, and heart failure.

Kazi: I want to go back to the tobacco point. There are definitely marked declines in tobacco, still tightly related to income in the country. You see much higher prevalence of tobacco use in lower-income populations, but it’s unclear to me where it’s going in kids. We know that combustible tobacco use is going down but e-cigarettes went up. What that leads to over the next 30 years is unclear to me.

Harrington: That is a really important comment that’s worth sidebarring. The vaping use has been a terrible epidemic among our high schoolers. What is that going to lead to? Is it going to lead to the use of combustible cigarettes and we’re going to see that go back up? It remains to be seen.

Kazi: Yes, it remains to be seen. Going back to your point about this change in risk factors and this change in demographics, both aging and becoming a more diverse population means that we have large increases in some healthcare conditions.

Coronary heart disease goes up some, there›s a big jump in stroke — nearly a doubling in stroke — which is related to hypertension, obesity, an aging population, and a more diverse population. There are changes in stroke in the young, and atrial fibrillation related to, again, hypertension. We’re seeing these projections, and with them come these pretty large projections in changes in healthcare spending.
 

Healthcare Spending Not Sustainable

Harrington: Big. I mean, it’s not sustainable. Give the audience the number — it’s pretty frightening.

Kazi: We’re talking about a quadrupling of healthcare costs related to cardiovascular disease over 25 years. We’ve gotten used to the narrative that healthcare in the US is expensive and drugs are expensive, but this is an enormous problem — an unsustainable problem, like you called it.

It’s a doubling as a proportion of the economy. I was looking this up this morning. If the US healthcare economy were its own economy, it would be the fourth largest economy in the world.

Harrington: Healthcare as it is today, is it 21% of our economy?

Kazi: It’s 17% now. If it were its own economy, it would be the fourth largest in the world. We are spending more on healthcare than all but two other countries’ total economies. It’s kind of crazy.

Harrington: We’re talking about a quadrupling.

Kazi: Within that, the cardiovascular piece is a big piece, and we›re talking about a quadrupling.

Harrington: That’s both direct and indirect costs.

Kazi: The quadrupling of costs is just the direct costs. Indirect costs, for the listeners, refer to costs unrelated to healthcare but changes in productivity, either because people are disabled and unable to participate fully in the workforce or they die early.

The productivity costs are also increased substantially as a result. If you look at both healthcare and productivity, that goes up threefold. These are very large changes.

Harrington: Let’s now get to what we can do about it. I made the comment to you when I first read the papers that I was very depressed. Then, after I went through my Kübler-Ross stages of depression, death, and dying, I came to acceptance.

What are we going to do about it? This is a focus on policy, but also a focus on how we deliver healthcare, how we think about healthcare, and how we develop drugs and devices.

The drug question is going to be the one the audience is thinking about. They say, well, what about GLP-1 agonists? Aren’t those going to save the day?

Kazi: Yes and no. I’ll say that, early in my career, I used to be very attracted to simple solutions to complex problems. I’ve come to realize that simple solutions are elegant, attractive, and wrong. We›re dealing with a very complex issue and I think we’re going to need a multipronged approach.

The way I think about it is that there was a group of people who are at very high risk today. How do we help those individuals? Then how do we help the future generation so that they’re not dealing with the projections that we’re talking about.

My colleague, Karen Joynt Maddox, who led one of the papers, as you mentioned, has an elegant line in the paper where she says projections are not destiny. These are things we can change.

Harrington: If nothing changes, this is what it’s going to look like.

Kazi: This is where we’re headed.

Harrington: We can change. We’ve got some time to change, but we don’t have forever.

Kazi: Yes, exactly. We picked the 25-year timeline instead of a “let’s plan for the next century” timeline because we want something concrete and actionable. It’s close enough to be meaningful but far enough to give us the runway we need to act.

Harrington: Give me two things from the policy perspective, because it’s mostly policy.

Kazi: There are policy and clinical interventions. From the policy perspective, if I had to list two things, one is expansion of access to care. As we talk about this big increase in the burden of disease and risk factors, if you have a large proportion of your population that has hypertension or diabetes, you’re going to have to expand access to care to ensure that people get treated so they can get access to this care before they develop the complications that we worry about, like stroke and heart disease, that are very expensive to treat downstream.

The second, more broadly related to access to care, is the access to medications that are effective. You bring up GLP-1s. I think we need a real strategy for how we can give people access to GLP-1s at a price that is affordable to individuals but also affordable to the health system, and to help them stay on the drugs.

GLP-1s are transformative in what they do for weight loss and for diabetes, but more than 50% of people who start one are off it at 12 months. There’s something fundamentally wrong about how we’re delivering GLP-1s today. It’s not just about the cost of the drugs but the support system people need to stay on.

Harrington: I’ve made the comment, in many forms now, that we know the drugs work. We have to figure out how to use them.

Kazi: Exactly, yes.

Harrington: Using them includes chronicity. This is a chronic condition. Some people can come off the drugs, but many can’t. We’re going to have to figure this out, and maybe the newer generations of drugs will help us address what people call the off-ramping. How are we going to do that? I think you’re spot-on. Those are critically important questions.

Kazi: As we looked at this modeling, I’ll tell you — I had a come-to-Jesus moment where I was like, there is no way to fix cardiovascular disease in the US without going through obesity and diabetes. We have to address obesity in the US. We can’t just treat our way out of it. Obesity is fundamentally a food problem and we’ve got to engage again with food policy in a meaningful way.

Harrington: As you know, with the American Heart Association, we›re doing a large amount of work now on food as medicine and food is medicine. We are trying to figure out what the levers are that we can pull to actually help people eat healthier diets.

Kazi: Yes. Rather than framing it as an individual choice that people are eating poorly, it’s, how do we make healthy diets the default in the environment?

Harrington: This is where you get to the children as well.

Kazi: Exactly.

Harrington: I could talk about this all day. I’ve had the benefit of reading the papers now a few times and talking to you on several occasions. Thank you for joining us.

Kazi: Thank you.
 

Dr. Harrington, Stephen and Suzanne Weiss Dean, Weill Cornell Medicine; Provost for Medical Affairs, Cornell University, New York, NY, disclosed ties with Baim Institute (DSMB); CSL (RCT Executive Committee); Janssen (RCT Char), NHLBI (RCT Executive Committee, DSMB Chair); PCORI (RCT Co-Chair); DCRI, Atropos Health; Bitterroot Bio; Bristol Myers Squibb; BridgeBio; Element Science; Edwards Lifesciences; Foresite Labs; Medscape/WebMD Board of Directors for: American Heart Association; College of the Holy Cross; and Cytokinetics. Dr. Kazi, Associate Director, Smith Center for Outcomes Research, Associate Professor, Department of Medicine (Cardiology), Harvard Medical School, Director, Department of Cardiac Critical Care Unit, Beth Israel Deaconess Medical Center, Boston, Massachusetts, has disclosed receiving a research grant from Boston Scientific (grant to examine the economics of stroke prevention).

A version of this article appeared on Medscape.com.

On October 1, 2024, International Classification of Diseases, 10th Revision, Clinical Modification (ICD-10-CM) codes for central centrifugal cicatricial alopecia (CCCA) and frontal fibrosing alopecia (FFA) took effect for the first time, a development characterized as a critical advancement in the field of hair loss disorders.

“CCCA and FFA are conditions that require early diagnosis and intervention to prevent irreversible hair loss,” Maria Hordinsky, MD, professor of dermatology at the University of Minnesota, Minneapolis, and a member of the Board of Directors, Scarring Alopecia Foundation (SAF), said in an interview.

Ms. Jefferson

For her part, Jefferson said that she will continue to advocate for patients with scarring alopecia as a medical student and when she becomes a physician. “I hope in the near future we will see an externally led FDA Patient-Focused Drug Development meeting for both CCCA and FFA, further advancing care and research for these conditions,” she said in an interview.

McMichael, Hordinsky, and Jefferson had no relevant disclosures to report.

A version of this article appeared on Medscape.com.

On October 1, 2024, International Classification of Diseases, 10th Revision, Clinical Modification (ICD-10-CM) codes for central centrifugal cicatricial alopecia (CCCA) and frontal fibrosing alopecia (FFA) took effect for the first time, a development characterized as a critical advancement in the field of hair loss disorders.

“CCCA and FFA are conditions that require early diagnosis and intervention to prevent irreversible hair loss,” Maria Hordinsky, MD, professor of dermatology at the University of Minnesota, Minneapolis, and a member of the Board of Directors, Scarring Alopecia Foundation (SAF), said in an interview.

Ms. Jefferson

For her part, Jefferson said that she will continue to advocate for patients with scarring alopecia as a medical student and when she becomes a physician. “I hope in the near future we will see an externally led FDA Patient-Focused Drug Development meeting for both CCCA and FFA, further advancing care and research for these conditions,” she said in an interview.

McMichael, Hordinsky, and Jefferson had no relevant disclosures to report.

A version of this article appeared on Medscape.com.

On October 1, 2024, International Classification of Diseases, 10th Revision, Clinical Modification (ICD-10-CM) codes for central centrifugal cicatricial alopecia (CCCA) and frontal fibrosing alopecia (FFA) took effect for the first time, a development characterized as a critical advancement in the field of hair loss disorders.

“CCCA and FFA are conditions that require early diagnosis and intervention to prevent irreversible hair loss,” Maria Hordinsky, MD, professor of dermatology at the University of Minnesota, Minneapolis, and a member of the Board of Directors, Scarring Alopecia Foundation (SAF), said in an interview.

Ms. Jefferson

For her part, Jefferson said that she will continue to advocate for patients with scarring alopecia as a medical student and when she becomes a physician. “I hope in the near future we will see an externally led FDA Patient-Focused Drug Development meeting for both CCCA and FFA, further advancing care and research for these conditions,” she said in an interview.

McMichael, Hordinsky, and Jefferson had no relevant disclosures to report.

A version of this article appeared on Medscape.com.

TOPLINE: 

More than half of the US peer reviewers for four major medical journals received industry payments between 2020-2022, new research shows. Altogether they received more than $64 million in general, non-research payments, with a median payment per physician of $7614. Research payments — including money paid directly to physicians as well as funds related to research for which a physician was registered as a principal investigator — exceeded $1 billion.

METHODOLOGY:

• Researchers identified peer reviewers in 2022 for The BMJ, JAMA, The Lancet, and The New England Journal of Medicine using each journal’s list of reviewers for that year. They included 1962 US-based physicians in their analysis.
• General and research payments made to the peer reviewers between 2020-2022 were extracted from the Open Payments database.

TAKEAWAY:

• Nearly 59% of the peer reviewers received industry payments between 2020-2022.
• Payments included $34.31 million in consulting fees and $11.8 million for speaking compensation unrelated to continuing medical education programs.
• Male reviewers received a significantly higher median total payment than did female reviewers ($38,959 vs $19,586). General payments were higher for men as well ($8663 vs $4183).
• For comparison, the median general payment to all physicians in 2018 was $216, the researchers noted.

IN PRACTICE:

“Additional research and transparency regarding industry payments in the peer review process are needed,” the authors of the study wrote.

SOURCE:

Christopher J. D. Wallis, MD, PhD, with the division of urology at the University of Toronto, Canada, was the corresponding author for the study. The article was published online October 10 in JAMA.

LIMITATIONS: 

Whether the financial ties were relevant to any of the papers that the peer reviewers critiqued is not known. Some reviewers might have received additional payments from insurance and technology companies that were not captured in this study. The findings might not apply to other journals, the researchers noted. 

DISCLOSURES:

Wallis disclosed personal fees from Janssen Oncology, Nanostics, Precision Point Specialty, Sesen Bio, AbbVie, Astellas, AstraZeneca, Bayer, EMD Serono, Knight Therapeutics, Merck, Science and Medicine Canada, TerSera, and Tolmar. He and some coauthors also disclosed support and grants from foundations and government institutions.

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

TOPLINE: 

More than half of the US peer reviewers for four major medical journals received industry payments between 2020-2022, new research shows. Altogether they received more than $64 million in general, non-research payments, with a median payment per physician of $7614. Research payments — including money paid directly to physicians as well as funds related to research for which a physician was registered as a principal investigator — exceeded $1 billion.

METHODOLOGY:

• Researchers identified peer reviewers in 2022 for The BMJ, JAMA, The Lancet, and The New England Journal of Medicine using each journal’s list of reviewers for that year. They included 1962 US-based physicians in their analysis.
• General and research payments made to the peer reviewers between 2020-2022 were extracted from the Open Payments database.

TAKEAWAY:

• Nearly 59% of the peer reviewers received industry payments between 2020-2022.
• Payments included $34.31 million in consulting fees and $11.8 million for speaking compensation unrelated to continuing medical education programs.
• Male reviewers received a significantly higher median total payment than did female reviewers ($38,959 vs $19,586). General payments were higher for men as well ($8663 vs $4183).
• For comparison, the median general payment to all physicians in 2018 was $216, the researchers noted.

IN PRACTICE:

“Additional research and transparency regarding industry payments in the peer review process are needed,” the authors of the study wrote.

SOURCE:

Christopher J. D. Wallis, MD, PhD, with the division of urology at the University of Toronto, Canada, was the corresponding author for the study. The article was published online October 10 in JAMA.

LIMITATIONS: 

Whether the financial ties were relevant to any of the papers that the peer reviewers critiqued is not known. Some reviewers might have received additional payments from insurance and technology companies that were not captured in this study. The findings might not apply to other journals, the researchers noted. 

DISCLOSURES:

Wallis disclosed personal fees from Janssen Oncology, Nanostics, Precision Point Specialty, Sesen Bio, AbbVie, Astellas, AstraZeneca, Bayer, EMD Serono, Knight Therapeutics, Merck, Science and Medicine Canada, TerSera, and Tolmar. He and some coauthors also disclosed support and grants from foundations and government institutions.

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

TOPLINE: 

More than half of the US peer reviewers for four major medical journals received industry payments between 2020-2022, new research shows. Altogether they received more than $64 million in general, non-research payments, with a median payment per physician of $7614. Research payments — including money paid directly to physicians as well as funds related to research for which a physician was registered as a principal investigator — exceeded $1 billion.

METHODOLOGY:

• Researchers identified peer reviewers in 2022 for The BMJ, JAMA, The Lancet, and The New England Journal of Medicine using each journal’s list of reviewers for that year. They included 1962 US-based physicians in their analysis.
• General and research payments made to the peer reviewers between 2020-2022 were extracted from the Open Payments database.

TAKEAWAY:

• Nearly 59% of the peer reviewers received industry payments between 2020-2022.
• Payments included $34.31 million in consulting fees and $11.8 million for speaking compensation unrelated to continuing medical education programs.
• Male reviewers received a significantly higher median total payment than did female reviewers ($38,959 vs $19,586). General payments were higher for men as well ($8663 vs $4183).
• For comparison, the median general payment to all physicians in 2018 was $216, the researchers noted.

IN PRACTICE:

“Additional research and transparency regarding industry payments in the peer review process are needed,” the authors of the study wrote.

SOURCE:

Christopher J. D. Wallis, MD, PhD, with the division of urology at the University of Toronto, Canada, was the corresponding author for the study. The article was published online October 10 in JAMA.

LIMITATIONS: 

Whether the financial ties were relevant to any of the papers that the peer reviewers critiqued is not known. Some reviewers might have received additional payments from insurance and technology companies that were not captured in this study. The findings might not apply to other journals, the researchers noted. 

DISCLOSURES:

Wallis disclosed personal fees from Janssen Oncology, Nanostics, Precision Point Specialty, Sesen Bio, AbbVie, Astellas, AstraZeneca, Bayer, EMD Serono, Knight Therapeutics, Merck, Science and Medicine Canada, TerSera, and Tolmar. He and some coauthors also disclosed support and grants from foundations and government institutions.

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

Many patients use cannabis to manage their cancer-related symptoms. However, research indicates that patients often do so without speaking to their oncologists first, and oncologists may be hesitant to broach the topic with their patients.

Updated guidelines from the American Society of Clinical Oncology (ASCO) on the use of cannabis and cannabinoids in adults with cancer stress that it’s an important conversation to have.

According to the ASCO expert panel, access to and use of cannabis alongside cancer care have outpaced the science on evidence-based indications, and overall high-quality data on the effects of cannabis during cancer care are lacking. While several observational studies support cannabis use to help ease chemotherapy-related nausea and vomiting, the literature remains more divided on other potential benefits, such as alleviating cancer pain and sleep problems, and some evidence points to potential downsides of cannabis use.

Oncologists should “absolutely talk to patients” about cannabis, Brooke Worster, MD, medical director for the Master of Science in Medical Cannabis Science & Business program at Thomas Jefferson University, Philadelphia, told Medscape Medical News.

“Patients are interested, and they are going to find access to information. As a medical professional, it’s our job to help guide them through these spaces in a safe, nonjudgmental way.”

But, Worster noted, oncologists don’t have to be experts on cannabis to begin the conversation with patients.

So, “let yourself off the hook,” Worster urged.

Plus, avoiding the conversation won’t stop patients from using cannabis. In a recent study, Worster and her colleagues found that nearly one third of patients at 12 National Cancer Institute-designated cancer centers had used cannabis since their diagnosis — most often for sleep disturbance, pain, stress, and anxiety. Most (60%) felt somewhat or extremely comfortable talking to their healthcare provider about it, but only 21.5% said they had done so. Even fewer — about 10% — had talked to their treating oncologist.

Because patients may not discuss cannabis use, it’s especially important for oncologists to open up a line of communication, said Worster, also the enterprise director of supportive oncology at the Thomas Jefferson University.
 

Evidence on Cannabis During Cancer Care

A substantial proportion of people with cancer believe cannabis can help manage cancer-related symptoms.

In Worster’s recent survey study, regardless of whether patients had used cannabis, almost 90% of those surveyed reported a perceived benefit. Although 65% also reported perceived risks for cannabis use, including difficulty concentrating, lung damage, and impaired memory, the perceived benefits outweighed the risks.

Despite generally positive perceptions, the overall literature on the benefits of cannabis in patients with cancer paints a less clear picture.

The ASCO guidelines, which were based on 13 systematic reviews and five additional primary studies, reported that cannabis can improve refractory, chemotherapy-induced nausea or vomiting when added to guideline-concordant antiemetic regimens, but that there is no clear evidence of benefit or harm for other supportive care outcomes.

The “certainty of evidence for most outcomes was low or very low,” the ASCO authors wrote.

The ASCO experts explained that, outside the context of a clinical trial, the evidence is not sufficient to recommend cannabis or cannabinoids for managing cancer pain, sleep issues, appetite loss, or anxiety and depression. For these outcomes, some studies indicate a benefit, while others don’t.

Real-world data from a large registry study, for instance, have indicated that medical cannabis is “a safe and effective complementary treatment for pain relief in patients with cancer.” However, a 2020 meta-analysis found that, in studies with a low risk for bias, adding cannabinoids to opioids did not reduce cancer pain in adults with advanced cancer.

There can be downsides to cannabis use, too. In one recent study, some patients reported feeling worse physically and psychologically compared with those who didn’t use cannabis. Another study found that oral cannabis was associated with “bothersome” side effects, including sedation, dizziness, and transient anxiety.

The ASCO guidelines also made it clear that cannabis or cannabinoids should not be used as cancer-directed treatment, outside of a clinical trial.
 

Talking to Patients About Cannabis

Given the level of evidence and patient interest in cannabis, it is important for oncologists to raise the topic of cannabis use with their patients.

To help inform decision-making and approaches to care, the ASCO guidelines suggest that oncologists can guide care themselves or direct patients to appropriate “unbiased, evidence-based” resources. For those who use cannabis or cannabinoids outside of evidence-based indications or clinician recommendations, it’s important to explore patients’ goals, educate them, and try to minimize harm.

One strategy for broaching the topic, Worster suggested, is to simply ask patients if they have tried or considered trying cannabis to control symptoms like nausea and vomiting, loss of appetite, or cancer pain.

The conversation with patients should then include an overview of the potential benefits and potential risks for cannabis use as well as risk reduction strategies, Worster noted.

But “approach it in an open and nonjudgmental frame of mind,” she said. “Just have a conversation.”

Discussing the formulation and concentration of tetrahydrocannabinol (THC) and cannabidiol (CBD) in products matters as well.

Will the product be inhaled, ingested, or topical? Inhaled cannabis is not ideal but is sometimes what patients have access to, Worster explained. Inhaled formulations tend to have faster onset, which might be preferable for treating chemotherapy-related nausea and vomiting, whereas edible formulations may take a while to start working.

It’s also important to warn patients about taking too much, she said, explaining that inhaling THC at higher doses can increase the risk for cardiovascular effects, anxiety, paranoia, panic, and psychosis.

CBD, on the other hand, is anti-inflammatory, but early data suggest it may blunt immune responses in high doses and should be used cautiously by patients receiving immunotherapy.

Worster noted that as laws change and the science advances, new cannabis products and formulations will emerge, as will artificial intelligence tools for helping to guide patients and clinicians in optimal use of cannabis for cancer care. State websites are a particularly helpful tool for providing state-specific medical education related to cannabis laws and use, as well, she said.

The bottom line, she said, is that talking to patients about the ins and outs of cannabis use “really matters.”

Worster disclosed that she is a medical consultant for EO Care.
 

A version of this article appeared on Medscape.com.

Many patients use cannabis to manage their cancer-related symptoms. However, research indicates that patients often do so without speaking to their oncologists first, and oncologists may be hesitant to broach the topic with their patients.

Updated guidelines from the American Society of Clinical Oncology (ASCO) on the use of cannabis and cannabinoids in adults with cancer stress that it’s an important conversation to have.

According to the ASCO expert panel, access to and use of cannabis alongside cancer care have outpaced the science on evidence-based indications, and overall high-quality data on the effects of cannabis during cancer care are lacking. While several observational studies support cannabis use to help ease chemotherapy-related nausea and vomiting, the literature remains more divided on other potential benefits, such as alleviating cancer pain and sleep problems, and some evidence points to potential downsides of cannabis use.

Oncologists should “absolutely talk to patients” about cannabis, Brooke Worster, MD, medical director for the Master of Science in Medical Cannabis Science & Business program at Thomas Jefferson University, Philadelphia, told Medscape Medical News.

“Patients are interested, and they are going to find access to information. As a medical professional, it’s our job to help guide them through these spaces in a safe, nonjudgmental way.”

But, Worster noted, oncologists don’t have to be experts on cannabis to begin the conversation with patients.

So, “let yourself off the hook,” Worster urged.

Plus, avoiding the conversation won’t stop patients from using cannabis. In a recent study, Worster and her colleagues found that nearly one third of patients at 12 National Cancer Institute-designated cancer centers had used cannabis since their diagnosis — most often for sleep disturbance, pain, stress, and anxiety. Most (60%) felt somewhat or extremely comfortable talking to their healthcare provider about it, but only 21.5% said they had done so. Even fewer — about 10% — had talked to their treating oncologist.

Because patients may not discuss cannabis use, it’s especially important for oncologists to open up a line of communication, said Worster, also the enterprise director of supportive oncology at the Thomas Jefferson University.
 

Evidence on Cannabis During Cancer Care

A substantial proportion of people with cancer believe cannabis can help manage cancer-related symptoms.

In Worster’s recent survey study, regardless of whether patients had used cannabis, almost 90% of those surveyed reported a perceived benefit. Although 65% also reported perceived risks for cannabis use, including difficulty concentrating, lung damage, and impaired memory, the perceived benefits outweighed the risks.

Despite generally positive perceptions, the overall literature on the benefits of cannabis in patients with cancer paints a less clear picture.

The ASCO guidelines, which were based on 13 systematic reviews and five additional primary studies, reported that cannabis can improve refractory, chemotherapy-induced nausea or vomiting when added to guideline-concordant antiemetic regimens, but that there is no clear evidence of benefit or harm for other supportive care outcomes.

The “certainty of evidence for most outcomes was low or very low,” the ASCO authors wrote.

The ASCO experts explained that, outside the context of a clinical trial, the evidence is not sufficient to recommend cannabis or cannabinoids for managing cancer pain, sleep issues, appetite loss, or anxiety and depression. For these outcomes, some studies indicate a benefit, while others don’t.

Real-world data from a large registry study, for instance, have indicated that medical cannabis is “a safe and effective complementary treatment for pain relief in patients with cancer.” However, a 2020 meta-analysis found that, in studies with a low risk for bias, adding cannabinoids to opioids did not reduce cancer pain in adults with advanced cancer.

There can be downsides to cannabis use, too. In one recent study, some patients reported feeling worse physically and psychologically compared with those who didn’t use cannabis. Another study found that oral cannabis was associated with “bothersome” side effects, including sedation, dizziness, and transient anxiety.

The ASCO guidelines also made it clear that cannabis or cannabinoids should not be used as cancer-directed treatment, outside of a clinical trial.
 

Talking to Patients About Cannabis

Given the level of evidence and patient interest in cannabis, it is important for oncologists to raise the topic of cannabis use with their patients.

To help inform decision-making and approaches to care, the ASCO guidelines suggest that oncologists can guide care themselves or direct patients to appropriate “unbiased, evidence-based” resources. For those who use cannabis or cannabinoids outside of evidence-based indications or clinician recommendations, it’s important to explore patients’ goals, educate them, and try to minimize harm.

One strategy for broaching the topic, Worster suggested, is to simply ask patients if they have tried or considered trying cannabis to control symptoms like nausea and vomiting, loss of appetite, or cancer pain.

The conversation with patients should then include an overview of the potential benefits and potential risks for cannabis use as well as risk reduction strategies, Worster noted.

But “approach it in an open and nonjudgmental frame of mind,” she said. “Just have a conversation.”

Discussing the formulation and concentration of tetrahydrocannabinol (THC) and cannabidiol (CBD) in products matters as well.

Will the product be inhaled, ingested, or topical? Inhaled cannabis is not ideal but is sometimes what patients have access to, Worster explained. Inhaled formulations tend to have faster onset, which might be preferable for treating chemotherapy-related nausea and vomiting, whereas edible formulations may take a while to start working.

It’s also important to warn patients about taking too much, she said, explaining that inhaling THC at higher doses can increase the risk for cardiovascular effects, anxiety, paranoia, panic, and psychosis.

CBD, on the other hand, is anti-inflammatory, but early data suggest it may blunt immune responses in high doses and should be used cautiously by patients receiving immunotherapy.

Worster noted that as laws change and the science advances, new cannabis products and formulations will emerge, as will artificial intelligence tools for helping to guide patients and clinicians in optimal use of cannabis for cancer care. State websites are a particularly helpful tool for providing state-specific medical education related to cannabis laws and use, as well, she said.

The bottom line, she said, is that talking to patients about the ins and outs of cannabis use “really matters.”

Worster disclosed that she is a medical consultant for EO Care.
 

A version of this article appeared on Medscape.com.

Many patients use cannabis to manage their cancer-related symptoms. However, research indicates that patients often do so without speaking to their oncologists first, and oncologists may be hesitant to broach the topic with their patients.

Updated guidelines from the American Society of Clinical Oncology (ASCO) on the use of cannabis and cannabinoids in adults with cancer stress that it’s an important conversation to have.

According to the ASCO expert panel, access to and use of cannabis alongside cancer care have outpaced the science on evidence-based indications, and overall high-quality data on the effects of cannabis during cancer care are lacking. While several observational studies support cannabis use to help ease chemotherapy-related nausea and vomiting, the literature remains more divided on other potential benefits, such as alleviating cancer pain and sleep problems, and some evidence points to potential downsides of cannabis use.

Oncologists should “absolutely talk to patients” about cannabis, Brooke Worster, MD, medical director for the Master of Science in Medical Cannabis Science & Business program at Thomas Jefferson University, Philadelphia, told Medscape Medical News.

“Patients are interested, and they are going to find access to information. As a medical professional, it’s our job to help guide them through these spaces in a safe, nonjudgmental way.”

But, Worster noted, oncologists don’t have to be experts on cannabis to begin the conversation with patients.

So, “let yourself off the hook,” Worster urged.

Plus, avoiding the conversation won’t stop patients from using cannabis. In a recent study, Worster and her colleagues found that nearly one third of patients at 12 National Cancer Institute-designated cancer centers had used cannabis since their diagnosis — most often for sleep disturbance, pain, stress, and anxiety. Most (60%) felt somewhat or extremely comfortable talking to their healthcare provider about it, but only 21.5% said they had done so. Even fewer — about 10% — had talked to their treating oncologist.

Because patients may not discuss cannabis use, it’s especially important for oncologists to open up a line of communication, said Worster, also the enterprise director of supportive oncology at the Thomas Jefferson University.
 

Evidence on Cannabis During Cancer Care

A substantial proportion of people with cancer believe cannabis can help manage cancer-related symptoms.

In Worster’s recent survey study, regardless of whether patients had used cannabis, almost 90% of those surveyed reported a perceived benefit. Although 65% also reported perceived risks for cannabis use, including difficulty concentrating, lung damage, and impaired memory, the perceived benefits outweighed the risks.

Despite generally positive perceptions, the overall literature on the benefits of cannabis in patients with cancer paints a less clear picture.

The ASCO guidelines, which were based on 13 systematic reviews and five additional primary studies, reported that cannabis can improve refractory, chemotherapy-induced nausea or vomiting when added to guideline-concordant antiemetic regimens, but that there is no clear evidence of benefit or harm for other supportive care outcomes.

The “certainty of evidence for most outcomes was low or very low,” the ASCO authors wrote.

The ASCO experts explained that, outside the context of a clinical trial, the evidence is not sufficient to recommend cannabis or cannabinoids for managing cancer pain, sleep issues, appetite loss, or anxiety and depression. For these outcomes, some studies indicate a benefit, while others don’t.

Real-world data from a large registry study, for instance, have indicated that medical cannabis is “a safe and effective complementary treatment for pain relief in patients with cancer.” However, a 2020 meta-analysis found that, in studies with a low risk for bias, adding cannabinoids to opioids did not reduce cancer pain in adults with advanced cancer.

There can be downsides to cannabis use, too. In one recent study, some patients reported feeling worse physically and psychologically compared with those who didn’t use cannabis. Another study found that oral cannabis was associated with “bothersome” side effects, including sedation, dizziness, and transient anxiety.

The ASCO guidelines also made it clear that cannabis or cannabinoids should not be used as cancer-directed treatment, outside of a clinical trial.
 

Talking to Patients About Cannabis

Given the level of evidence and patient interest in cannabis, it is important for oncologists to raise the topic of cannabis use with their patients.

To help inform decision-making and approaches to care, the ASCO guidelines suggest that oncologists can guide care themselves or direct patients to appropriate “unbiased, evidence-based” resources. For those who use cannabis or cannabinoids outside of evidence-based indications or clinician recommendations, it’s important to explore patients’ goals, educate them, and try to minimize harm.

One strategy for broaching the topic, Worster suggested, is to simply ask patients if they have tried or considered trying cannabis to control symptoms like nausea and vomiting, loss of appetite, or cancer pain.

The conversation with patients should then include an overview of the potential benefits and potential risks for cannabis use as well as risk reduction strategies, Worster noted.

But “approach it in an open and nonjudgmental frame of mind,” she said. “Just have a conversation.”

Discussing the formulation and concentration of tetrahydrocannabinol (THC) and cannabidiol (CBD) in products matters as well.

Will the product be inhaled, ingested, or topical? Inhaled cannabis is not ideal but is sometimes what patients have access to, Worster explained. Inhaled formulations tend to have faster onset, which might be preferable for treating chemotherapy-related nausea and vomiting, whereas edible formulations may take a while to start working.

It’s also important to warn patients about taking too much, she said, explaining that inhaling THC at higher doses can increase the risk for cardiovascular effects, anxiety, paranoia, panic, and psychosis.

CBD, on the other hand, is anti-inflammatory, but early data suggest it may blunt immune responses in high doses and should be used cautiously by patients receiving immunotherapy.

Worster noted that as laws change and the science advances, new cannabis products and formulations will emerge, as will artificial intelligence tools for helping to guide patients and clinicians in optimal use of cannabis for cancer care. State websites are a particularly helpful tool for providing state-specific medical education related to cannabis laws and use, as well, she said.

The bottom line, she said, is that talking to patients about the ins and outs of cannabis use “really matters.”

Worster disclosed that she is a medical consultant for EO Care.
 

A version of this article appeared on Medscape.com.

THE DIAGNOSIS: Ectopic (Accessory) Breast Tissue

Ectopic (accessory) breast tissue (EBT) is a phenomenon caused by failed regression of one or more components of the embryonic mammary ridges— paired ectodermal thickenings that eventually develop into definitive breast tissue including the nipples, areolae, and parenchyma. Ectopic breast tissue is more common in women than men and is believed to be sporadic, although an autosomal-dominant inheritance mechanism with incomplete penetrance has been proposed for some cases.¹ The reported incidence of EBT varies greatly among racial and ethnic groups but is most common in individuals of Asian descent. The incidence across all types of EBT is estimated at 0.25% to 6% in the general population.²

Observed clinical variations of EBT range from simple polythelia (additional nipple[s] without associated parenchyma) to complete polymastia (organized and differentiated accessory breasts). Some types of EBT are rarer than others: One report of gynecologic cancer screenings in 1660 patients found polymastia and polythelia incidences of 0.12% and 5.48%, respectively.³ Of the symptomatic variations, isolated parenchymal EBT without a nipple or areolar complex is the most common and may manifest clinically as unilateral or bilateral tender, mildly erythematous nodules or masses often located in the axillae. Ectopic breast tissue generally is observed along the milk line, a developmental regional designation corresponding to the embryologic mammary ridge and extending linearly from the anterior axilla to the inguinal fold on both sides of the body; however, there have been rare reports of EBT manifesting in areas outside the milk line, such as the face, neck, back, vulva, and extremities.^2,3

Given that the underlying elements of EBT usually are hormone responsive (as with normal breast tissue), the initial symptom onset and subsequent manifestation frequently coincide with pubertal milestones, pregnancy, or lactation. Furthermore, some patients with EBT may experience symptom fluctuations in concordance with monthly menstrual phases. Many cases of EBT are selflimited and resolve within weeks to months after the end of a pregnancy or lactation, but some cases may persist. Continued observation and follow-up are advisable in all patients, as EBT symptoms often recur and the tissue is susceptible to the same disease processes that affect normal breasts, the most concerning of which is malignancy.⁴ Although the true incidence is limited by available data, primary ectopic breast malignancy has been estimated to account for 0.3% to 3.8% of diagnosed breast malignancies.² Cases of malignancy arising from EBT often are of higher grade and poorer prognosis, a finding that may be attributable to diagnostic delays caused by oversight or misdiagnosis of EBT rather than inherent differences in the biologic profile of the tumors.^2,4 Patients with a documented history of EBT may benefit from having their routine breast cancer screenings expanded to include areas with EBT foci.

Potential misdiagnoses for EBT include subcutaneous lipoma, axillary lymphadenopathy, abscess, hidradenitis suppurativa, or malignancy. Features that are suggestive of EBT include symptom association with hormone fluctuations (eg, menstrual phases), absence of fever, and lactescent rather than purulent drainage. Among reported EBT cases, spontaneous lactation rarely is described and, if present, often is associated with a history of prior trauma (eg, core needle biopsy or local abscess formation).⁵ This trauma creates an aberrant connection known as a milk fistula between the underlying parenchyma and the skin surface. Interestingly, our patient denied any history of axillary trauma, but she was noted to be lactating from an apparent milk fistula rather than an organized secretory duct system.

Though a patient history and clinical examination may be sufficient to diagnose EBT cases that are more physically apparent and well correlated with hormone fluctuations, many cases require additional diagnostic studies for confirmation. Of the tools available, ultrasonography generally is considered first-line due to its noninvasive nature, low cost, minimal risk, and high diagnostic value.² Ultrasonography quickly differentiates between abscesses and cystlike processes, which may appear as discrete areas of decreased echogenicity, and breast tissue, which manifests with fibroglandular tissue and lobules of fat.^2,6 Additionally, ultrasonography may demonstrate the secretion of milk through ducts or fistulae, if present. Should examination with ultrasonography prove inconclusive, follow-up studies using conventional radiographic mammography or magnetic resonance imaging may be warranted. Biopsy of EBT foci generally is not indicated unless first-line noninvasive studies fail to yield a conclusive diagnosis; however, biopsy also may be warranted if initial imaging is suggestive of malignancy arising from EBT.²

Management of EBT generally is conservative, and symptoms often resolve without intervention.⁴ Symptomatic relief may be achieved through techniques such as application of warm/cold compresses, avoidance of mechanical stimulation, and use of over-the-counter pain medicine. In cases that are persistent, frequently recurrent, or associated with severe symptoms or that cause considerable cosmetic impact, management with surgical excision and/or liposuction may be warranted.⁷ In our patient, the symptoms were not bothersome enough to warrant surgical intervention, so she was managed conservatively and did not return for follow-up.

THE DIAGNOSIS: Ectopic (Accessory) Breast Tissue

Ectopic (accessory) breast tissue (EBT) is a phenomenon caused by failed regression of one or more components of the embryonic mammary ridges— paired ectodermal thickenings that eventually develop into definitive breast tissue including the nipples, areolae, and parenchyma. Ectopic breast tissue is more common in women than men and is believed to be sporadic, although an autosomal-dominant inheritance mechanism with incomplete penetrance has been proposed for some cases.¹ The reported incidence of EBT varies greatly among racial and ethnic groups but is most common in individuals of Asian descent. The incidence across all types of EBT is estimated at 0.25% to 6% in the general population.²

Observed clinical variations of EBT range from simple polythelia (additional nipple[s] without associated parenchyma) to complete polymastia (organized and differentiated accessory breasts). Some types of EBT are rarer than others: One report of gynecologic cancer screenings in 1660 patients found polymastia and polythelia incidences of 0.12% and 5.48%, respectively.³ Of the symptomatic variations, isolated parenchymal EBT without a nipple or areolar complex is the most common and may manifest clinically as unilateral or bilateral tender, mildly erythematous nodules or masses often located in the axillae. Ectopic breast tissue generally is observed along the milk line, a developmental regional designation corresponding to the embryologic mammary ridge and extending linearly from the anterior axilla to the inguinal fold on both sides of the body; however, there have been rare reports of EBT manifesting in areas outside the milk line, such as the face, neck, back, vulva, and extremities.^2,3

Given that the underlying elements of EBT usually are hormone responsive (as with normal breast tissue), the initial symptom onset and subsequent manifestation frequently coincide with pubertal milestones, pregnancy, or lactation. Furthermore, some patients with EBT may experience symptom fluctuations in concordance with monthly menstrual phases. Many cases of EBT are selflimited and resolve within weeks to months after the end of a pregnancy or lactation, but some cases may persist. Continued observation and follow-up are advisable in all patients, as EBT symptoms often recur and the tissue is susceptible to the same disease processes that affect normal breasts, the most concerning of which is malignancy.⁴ Although the true incidence is limited by available data, primary ectopic breast malignancy has been estimated to account for 0.3% to 3.8% of diagnosed breast malignancies.² Cases of malignancy arising from EBT often are of higher grade and poorer prognosis, a finding that may be attributable to diagnostic delays caused by oversight or misdiagnosis of EBT rather than inherent differences in the biologic profile of the tumors.^2,4 Patients with a documented history of EBT may benefit from having their routine breast cancer screenings expanded to include areas with EBT foci.

Potential misdiagnoses for EBT include subcutaneous lipoma, axillary lymphadenopathy, abscess, hidradenitis suppurativa, or malignancy. Features that are suggestive of EBT include symptom association with hormone fluctuations (eg, menstrual phases), absence of fever, and lactescent rather than purulent drainage. Among reported EBT cases, spontaneous lactation rarely is described and, if present, often is associated with a history of prior trauma (eg, core needle biopsy or local abscess formation).⁵ This trauma creates an aberrant connection known as a milk fistula between the underlying parenchyma and the skin surface. Interestingly, our patient denied any history of axillary trauma, but she was noted to be lactating from an apparent milk fistula rather than an organized secretory duct system.

Though a patient history and clinical examination may be sufficient to diagnose EBT cases that are more physically apparent and well correlated with hormone fluctuations, many cases require additional diagnostic studies for confirmation. Of the tools available, ultrasonography generally is considered first-line due to its noninvasive nature, low cost, minimal risk, and high diagnostic value.² Ultrasonography quickly differentiates between abscesses and cystlike processes, which may appear as discrete areas of decreased echogenicity, and breast tissue, which manifests with fibroglandular tissue and lobules of fat.^2,6 Additionally, ultrasonography may demonstrate the secretion of milk through ducts or fistulae, if present. Should examination with ultrasonography prove inconclusive, follow-up studies using conventional radiographic mammography or magnetic resonance imaging may be warranted. Biopsy of EBT foci generally is not indicated unless first-line noninvasive studies fail to yield a conclusive diagnosis; however, biopsy also may be warranted if initial imaging is suggestive of malignancy arising from EBT.²

Management of EBT generally is conservative, and symptoms often resolve without intervention.⁴ Symptomatic relief may be achieved through techniques such as application of warm/cold compresses, avoidance of mechanical stimulation, and use of over-the-counter pain medicine. In cases that are persistent, frequently recurrent, or associated with severe symptoms or that cause considerable cosmetic impact, management with surgical excision and/or liposuction may be warranted.⁷ In our patient, the symptoms were not bothersome enough to warrant surgical intervention, so she was managed conservatively and did not return for follow-up.

THE DIAGNOSIS: Ectopic (Accessory) Breast Tissue

Ectopic (accessory) breast tissue (EBT) is a phenomenon caused by failed regression of one or more components of the embryonic mammary ridges— paired ectodermal thickenings that eventually develop into definitive breast tissue including the nipples, areolae, and parenchyma. Ectopic breast tissue is more common in women than men and is believed to be sporadic, although an autosomal-dominant inheritance mechanism with incomplete penetrance has been proposed for some cases.¹ The reported incidence of EBT varies greatly among racial and ethnic groups but is most common in individuals of Asian descent. The incidence across all types of EBT is estimated at 0.25% to 6% in the general population.²

Observed clinical variations of EBT range from simple polythelia (additional nipple[s] without associated parenchyma) to complete polymastia (organized and differentiated accessory breasts). Some types of EBT are rarer than others: One report of gynecologic cancer screenings in 1660 patients found polymastia and polythelia incidences of 0.12% and 5.48%, respectively.³ Of the symptomatic variations, isolated parenchymal EBT without a nipple or areolar complex is the most common and may manifest clinically as unilateral or bilateral tender, mildly erythematous nodules or masses often located in the axillae. Ectopic breast tissue generally is observed along the milk line, a developmental regional designation corresponding to the embryologic mammary ridge and extending linearly from the anterior axilla to the inguinal fold on both sides of the body; however, there have been rare reports of EBT manifesting in areas outside the milk line, such as the face, neck, back, vulva, and extremities.^2,3

Given that the underlying elements of EBT usually are hormone responsive (as with normal breast tissue), the initial symptom onset and subsequent manifestation frequently coincide with pubertal milestones, pregnancy, or lactation. Furthermore, some patients with EBT may experience symptom fluctuations in concordance with monthly menstrual phases. Many cases of EBT are selflimited and resolve within weeks to months after the end of a pregnancy or lactation, but some cases may persist. Continued observation and follow-up are advisable in all patients, as EBT symptoms often recur and the tissue is susceptible to the same disease processes that affect normal breasts, the most concerning of which is malignancy.⁴ Although the true incidence is limited by available data, primary ectopic breast malignancy has been estimated to account for 0.3% to 3.8% of diagnosed breast malignancies.² Cases of malignancy arising from EBT often are of higher grade and poorer prognosis, a finding that may be attributable to diagnostic delays caused by oversight or misdiagnosis of EBT rather than inherent differences in the biologic profile of the tumors.^2,4 Patients with a documented history of EBT may benefit from having their routine breast cancer screenings expanded to include areas with EBT foci.

Potential misdiagnoses for EBT include subcutaneous lipoma, axillary lymphadenopathy, abscess, hidradenitis suppurativa, or malignancy. Features that are suggestive of EBT include symptom association with hormone fluctuations (eg, menstrual phases), absence of fever, and lactescent rather than purulent drainage. Among reported EBT cases, spontaneous lactation rarely is described and, if present, often is associated with a history of prior trauma (eg, core needle biopsy or local abscess formation).⁵ This trauma creates an aberrant connection known as a milk fistula between the underlying parenchyma and the skin surface. Interestingly, our patient denied any history of axillary trauma, but she was noted to be lactating from an apparent milk fistula rather than an organized secretory duct system.

Though a patient history and clinical examination may be sufficient to diagnose EBT cases that are more physically apparent and well correlated with hormone fluctuations, many cases require additional diagnostic studies for confirmation. Of the tools available, ultrasonography generally is considered first-line due to its noninvasive nature, low cost, minimal risk, and high diagnostic value.² Ultrasonography quickly differentiates between abscesses and cystlike processes, which may appear as discrete areas of decreased echogenicity, and breast tissue, which manifests with fibroglandular tissue and lobules of fat.^2,6 Additionally, ultrasonography may demonstrate the secretion of milk through ducts or fistulae, if present. Should examination with ultrasonography prove inconclusive, follow-up studies using conventional radiographic mammography or magnetic resonance imaging may be warranted. Biopsy of EBT foci generally is not indicated unless first-line noninvasive studies fail to yield a conclusive diagnosis; however, biopsy also may be warranted if initial imaging is suggestive of malignancy arising from EBT.²

Management of EBT generally is conservative, and symptoms often resolve without intervention.⁴ Symptomatic relief may be achieved through techniques such as application of warm/cold compresses, avoidance of mechanical stimulation, and use of over-the-counter pain medicine. In cases that are persistent, frequently recurrent, or associated with severe symptoms or that cause considerable cosmetic impact, management with surgical excision and/or liposuction may be warranted.⁷ In our patient, the symptoms were not bothersome enough to warrant surgical intervention, so she was managed conservatively and did not return for follow-up.

A new serum containing 2-mercaptonicotinoyl glycine (Melasyl) as its main ingredient was at least as good as, if not better than, cysteamine 5% cream in treating facial melasma in a randomized controlled study presented at the European Academy of Dermatology and Venereology (EADV) 2024 Congress.

“Melasyl is a new potent melanogenesis inhibitor that exhibits a unique mode of action while preserving melanocyte integrity,” Mukta Sachdev, MD, head of the Department of Dermatology at Manipal Hospital in Bangalore, India, said at a late-breaking news session.

Both the serum and the cysteamine cream lightened participants’ skin to a similar extent, according to the modified Melasma Area and Severity Index (mMASI), with respective reductions of 4.19 and 3.81 points over a period of 4 months from baseline values of 11.15 and 10.93. 

Toa55/iStock/Getty Images

The mMASI score ranges from 0 to 24, with the lowest score representing the least and the highest score the most severe hyperpigmentation of the skin.

But the serum performed better than the cream by another measure. Judged by investigators blinded to which preparation study participants had been using, there was a significantly higher reduction in the Investigator Global Assessment (IGA) score from baseline among those treated with the serum than among those treated with the cream (−51.85% vs −39.06%; P = .0163). 

Moreover, after 4 months of treatment, there were significantly more participants with clear or almost clear skin with the serum than with the cream (17.46% vs 7.81%; P = .0163), Sachdev reported.

Other skin parameters relative to melasma, such as the brightness of skin tone and evenness of the improvement, improved more in the participants using the serum vs cream, she said. 

With “no side effects, no local skin reactions,” Sachdev said, “quality of life improved significantly and similarly, and almost all subjects in both groups were very satisfied with their treatment options.”
 

Active Ingredients

Margarida Gonçalo, MD, PhD, professor of dermatology at the University of Coimbra, in Portugal, who co-chaired the late-breaking news session, commented: “It’s really nice to have new products to treat such a devastating disease.”

Session co-chair, Lidia Rudnicka, MD, head of the Department of Dermatology, Medical University of Warsaw, in Poland, and president of the Polish Dermatological Society, wanted to know more about the active ingredients of the serum and the study’s design. 

Sachdev replied that the serum also contains other ingredients that provide “antioxidant protection” and moisturization. These include retinyl palmitate, which works on the dermal-epidermal junction, and hyaluronic acid, as well as “soothing agents,” such as the medicinal herb Centella asiatica, she said.
 

Study Design

Conducted at a single center in India, the study involved 127 adults aged 20-50 years with melasma. For inclusion, the participants had to have facial epidermal or mixed melasma (phototypes III-V) for more than 1 year; those with dermal melasma were excluded. 

Participants were randomly allocated to receive either the serum, which was applied topically to the areas of interest twice a day in the morning and then at bedtime (n = 63), or cysteamine cream (n = 64), which was applied once a day in addition to a neutral moisturizer. Treatment was for 4 months, with an on-site visit every month. 

All participants were supplied with the same sunscreen/ultraviolet protector applied twice a day (once in the morning and again at midday) and a neutral hydrating cleanser that was used in the morning and evening. 
 

Practical Implications

Over 4 months, both products showed significant improvement in melasma without reaching a plateau, Sachdev reported, with the serum demonstrating superior efficacy and tolerability, as judged by the investigators. 

The study suggests that the serum is a promising non-hydroquinone treatment for melasma, she said. Hydroquinone-containing topical preparations are used to depigment the skin, but their long-term use can be limited for safety reasons. 

“When products like this demonstrate improvement, it is something for the dermatologist to think about because we now have newer ingredients, which are safer and well tolerated,” she continued, noting that there appeared to be no risk for exogenous ochronosis, which can occur with long-term application of hydroquinone.

“So, I think the armamentarium of non-hydroquinone products for the treatment of melasma is rapidly expanding, and there are studies now with clinically proven efficacy,” Sachdev concluded. 

The study was supported by L’Oréal France La Roche-Posay, which launched Melasyl in March 2024. Sachdev reported receipt of research support and honoraria from the company. Gonçalo and Rudnicka were not involved in the study and had no relevant conflicts of interest to report. 
 

A version of this article appeared on Medscape.com.

A new serum containing 2-mercaptonicotinoyl glycine (Melasyl) as its main ingredient was at least as good as, if not better than, cysteamine 5% cream in treating facial melasma in a randomized controlled study presented at the European Academy of Dermatology and Venereology (EADV) 2024 Congress.

“Melasyl is a new potent melanogenesis inhibitor that exhibits a unique mode of action while preserving melanocyte integrity,” Mukta Sachdev, MD, head of the Department of Dermatology at Manipal Hospital in Bangalore, India, said at a late-breaking news session.

Both the serum and the cysteamine cream lightened participants’ skin to a similar extent, according to the modified Melasma Area and Severity Index (mMASI), with respective reductions of 4.19 and 3.81 points over a period of 4 months from baseline values of 11.15 and 10.93. 

Toa55/iStock/Getty Images

The mMASI score ranges from 0 to 24, with the lowest score representing the least and the highest score the most severe hyperpigmentation of the skin.

But the serum performed better than the cream by another measure. Judged by investigators blinded to which preparation study participants had been using, there was a significantly higher reduction in the Investigator Global Assessment (IGA) score from baseline among those treated with the serum than among those treated with the cream (−51.85% vs −39.06%; P = .0163). 

Moreover, after 4 months of treatment, there were significantly more participants with clear or almost clear skin with the serum than with the cream (17.46% vs 7.81%; P = .0163), Sachdev reported.

Other skin parameters relative to melasma, such as the brightness of skin tone and evenness of the improvement, improved more in the participants using the serum vs cream, she said. 

With “no side effects, no local skin reactions,” Sachdev said, “quality of life improved significantly and similarly, and almost all subjects in both groups were very satisfied with their treatment options.”
 

Active Ingredients

Margarida Gonçalo, MD, PhD, professor of dermatology at the University of Coimbra, in Portugal, who co-chaired the late-breaking news session, commented: “It’s really nice to have new products to treat such a devastating disease.”

Session co-chair, Lidia Rudnicka, MD, head of the Department of Dermatology, Medical University of Warsaw, in Poland, and president of the Polish Dermatological Society, wanted to know more about the active ingredients of the serum and the study’s design. 

Sachdev replied that the serum also contains other ingredients that provide “antioxidant protection” and moisturization. These include retinyl palmitate, which works on the dermal-epidermal junction, and hyaluronic acid, as well as “soothing agents,” such as the medicinal herb Centella asiatica, she said.
 

Study Design

Conducted at a single center in India, the study involved 127 adults aged 20-50 years with melasma. For inclusion, the participants had to have facial epidermal or mixed melasma (phototypes III-V) for more than 1 year; those with dermal melasma were excluded. 

Participants were randomly allocated to receive either the serum, which was applied topically to the areas of interest twice a day in the morning and then at bedtime (n = 63), or cysteamine cream (n = 64), which was applied once a day in addition to a neutral moisturizer. Treatment was for 4 months, with an on-site visit every month. 

All participants were supplied with the same sunscreen/ultraviolet protector applied twice a day (once in the morning and again at midday) and a neutral hydrating cleanser that was used in the morning and evening. 
 

Practical Implications

Over 4 months, both products showed significant improvement in melasma without reaching a plateau, Sachdev reported, with the serum demonstrating superior efficacy and tolerability, as judged by the investigators. 

The study suggests that the serum is a promising non-hydroquinone treatment for melasma, she said. Hydroquinone-containing topical preparations are used to depigment the skin, but their long-term use can be limited for safety reasons. 

“When products like this demonstrate improvement, it is something for the dermatologist to think about because we now have newer ingredients, which are safer and well tolerated,” she continued, noting that there appeared to be no risk for exogenous ochronosis, which can occur with long-term application of hydroquinone.

“So, I think the armamentarium of non-hydroquinone products for the treatment of melasma is rapidly expanding, and there are studies now with clinically proven efficacy,” Sachdev concluded. 

The study was supported by L’Oréal France La Roche-Posay, which launched Melasyl in March 2024. Sachdev reported receipt of research support and honoraria from the company. Gonçalo and Rudnicka were not involved in the study and had no relevant conflicts of interest to report. 
 

A version of this article appeared on Medscape.com.

A new serum containing 2-mercaptonicotinoyl glycine (Melasyl) as its main ingredient was at least as good as, if not better than, cysteamine 5% cream in treating facial melasma in a randomized controlled study presented at the European Academy of Dermatology and Venereology (EADV) 2024 Congress.

“Melasyl is a new potent melanogenesis inhibitor that exhibits a unique mode of action while preserving melanocyte integrity,” Mukta Sachdev, MD, head of the Department of Dermatology at Manipal Hospital in Bangalore, India, said at a late-breaking news session.

Both the serum and the cysteamine cream lightened participants’ skin to a similar extent, according to the modified Melasma Area and Severity Index (mMASI), with respective reductions of 4.19 and 3.81 points over a period of 4 months from baseline values of 11.15 and 10.93. 

Toa55/iStock/Getty Images

The mMASI score ranges from 0 to 24, with the lowest score representing the least and the highest score the most severe hyperpigmentation of the skin.

But the serum performed better than the cream by another measure. Judged by investigators blinded to which preparation study participants had been using, there was a significantly higher reduction in the Investigator Global Assessment (IGA) score from baseline among those treated with the serum than among those treated with the cream (−51.85% vs −39.06%; P = .0163). 

Moreover, after 4 months of treatment, there were significantly more participants with clear or almost clear skin with the serum than with the cream (17.46% vs 7.81%; P = .0163), Sachdev reported.

Other skin parameters relative to melasma, such as the brightness of skin tone and evenness of the improvement, improved more in the participants using the serum vs cream, she said. 

With “no side effects, no local skin reactions,” Sachdev said, “quality of life improved significantly and similarly, and almost all subjects in both groups were very satisfied with their treatment options.”
 

Active Ingredients

Margarida Gonçalo, MD, PhD, professor of dermatology at the University of Coimbra, in Portugal, who co-chaired the late-breaking news session, commented: “It’s really nice to have new products to treat such a devastating disease.”

Session co-chair, Lidia Rudnicka, MD, head of the Department of Dermatology, Medical University of Warsaw, in Poland, and president of the Polish Dermatological Society, wanted to know more about the active ingredients of the serum and the study’s design. 

Sachdev replied that the serum also contains other ingredients that provide “antioxidant protection” and moisturization. These include retinyl palmitate, which works on the dermal-epidermal junction, and hyaluronic acid, as well as “soothing agents,” such as the medicinal herb Centella asiatica, she said.
 

Study Design

Conducted at a single center in India, the study involved 127 adults aged 20-50 years with melasma. For inclusion, the participants had to have facial epidermal or mixed melasma (phototypes III-V) for more than 1 year; those with dermal melasma were excluded. 

Participants were randomly allocated to receive either the serum, which was applied topically to the areas of interest twice a day in the morning and then at bedtime (n = 63), or cysteamine cream (n = 64), which was applied once a day in addition to a neutral moisturizer. Treatment was for 4 months, with an on-site visit every month. 

All participants were supplied with the same sunscreen/ultraviolet protector applied twice a day (once in the morning and again at midday) and a neutral hydrating cleanser that was used in the morning and evening. 
 

Practical Implications

Over 4 months, both products showed significant improvement in melasma without reaching a plateau, Sachdev reported, with the serum demonstrating superior efficacy and tolerability, as judged by the investigators. 

The study suggests that the serum is a promising non-hydroquinone treatment for melasma, she said. Hydroquinone-containing topical preparations are used to depigment the skin, but their long-term use can be limited for safety reasons. 

“When products like this demonstrate improvement, it is something for the dermatologist to think about because we now have newer ingredients, which are safer and well tolerated,” she continued, noting that there appeared to be no risk for exogenous ochronosis, which can occur with long-term application of hydroquinone.

“So, I think the armamentarium of non-hydroquinone products for the treatment of melasma is rapidly expanding, and there are studies now with clinically proven efficacy,” Sachdev concluded. 

The study was supported by L’Oréal France La Roche-Posay, which launched Melasyl in March 2024. Sachdev reported receipt of research support and honoraria from the company. Gonçalo and Rudnicka were not involved in the study and had no relevant conflicts of interest to report. 
 

A version of this article appeared on Medscape.com.

TOPLINE:

The Fracture Risk Assessment Tool (FRAX), with bone mineral density, predicts the risk for major osteoporotic fractures and hip fractures in patients with cancer, but FRAX without bone mineral density slightly overestimates these risks, a new analysis found.

METHODOLOGY:

• Cancer-specific guidelines recommend using FRAX to assess fracture risk, but its applicability in patients with cancer remains unclear.
• This retrospective cohort study included 9877 patients with cancer (mean age, 67.1 years) and 45,875 matched control individuals without cancer (mean age, 66.2 years). All participants had dual-energy x-ray absorptiometry (DXA) scans.
• Researchers collected data on bone mineral density and fractures. The 10-year probabilities of major osteoporotic fractures and hip fractures were calculated using FRAX, and the observed 10-year probabilities of these fractures were compared with FRAX-derived probabilities.
• Compared with individuals without cancer, patients with cancer had a shorter mean follow-up duration (8.5 vs 7.6 years), a slightly higher mean body mass index, and a higher percentage of parental hip fractures (7.0% vs 8.2%); additionally, patients with cancer were more likely to have secondary causes of osteoporosis (10% vs 38.4%) and less likely to receive osteoporosis medication (9.9% vs 4.2%).

TAKEAWAY:

• Compared with individuals without cancer, patients with cancer had a significantly higher incidence rate of major fractures (12.9 vs 14.5 per 1000 person-years) and hip fractures (3.5 vs 4.2 per 1000 person-years).
• FRAX with bone mineral density exhibited excellent calibration for predicting major osteoporotic fractures (slope, 1.03) and hip fractures (0.97) in patients with cancer, regardless of the site of cancer diagnosis. FRAX without bone mineral density, however, underestimated the risk for both major (0.87) and hip fractures (0.72).
• In patients with cancer, FRAX with bone mineral density findings were associated with incident major osteoporotic fractures (hazard ratio [HR] per SD, 1.84) and hip fractures (HR per SD, 3.61).
• When models were adjusted for FRAX with bone mineral density, patients with cancer had an increased risk for both major osteoporotic fractures (HR, 1.17) and hip fractures (HR, 1.30). No difference was found in the risk for fracture between patients with and individuals without cancer when the models were adjusted for FRAX without bone mineral density, even when considering osteoporosis medication use.

IN PRACTICE:

“This retrospective cohort study demonstrates that individuals with cancer are at higher risk of fracture than individuals without cancer and that FRAX, particularly with BMD [bone mineral density], may accurately predict fracture risk in this population. These results, along with the known mortality risk of osteoporotic fractures among cancer survivors, further emphasize the clinical importance of closing the current osteoporosis care gap among cancer survivors,” the authors wrote.

SOURCE:

This study, led by Carrie Ye, MD, MPH, University of Alberta, Edmonton, Alberta, Canada, was published online in JAMA Oncology.

LIMITATIONS:

This study cohort included a selected group of cancer survivors who were referred for DXA scans and may not represent the general cancer population. The cohort consisted predominantly of women, limiting the generalizability to men with cancer. Given the heterogeneity of the population, the findings may not be applicable to all cancer subgroups. Information on cancer stage or the presence of bone metastases at the time of fracture risk assessment was lacking, which could have affected the findings.

DISCLOSURES:

This study was funded by the CancerCare Manitoba Foundation. Three authors reported having ties with various sources, including two who received grants from various organizations.
 

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

TOPLINE:

The Fracture Risk Assessment Tool (FRAX), with bone mineral density, predicts the risk for major osteoporotic fractures and hip fractures in patients with cancer, but FRAX without bone mineral density slightly overestimates these risks, a new analysis found.

METHODOLOGY:

• Cancer-specific guidelines recommend using FRAX to assess fracture risk, but its applicability in patients with cancer remains unclear.
• This retrospective cohort study included 9877 patients with cancer (mean age, 67.1 years) and 45,875 matched control individuals without cancer (mean age, 66.2 years). All participants had dual-energy x-ray absorptiometry (DXA) scans.
• Researchers collected data on bone mineral density and fractures. The 10-year probabilities of major osteoporotic fractures and hip fractures were calculated using FRAX, and the observed 10-year probabilities of these fractures were compared with FRAX-derived probabilities.
• Compared with individuals without cancer, patients with cancer had a shorter mean follow-up duration (8.5 vs 7.6 years), a slightly higher mean body mass index, and a higher percentage of parental hip fractures (7.0% vs 8.2%); additionally, patients with cancer were more likely to have secondary causes of osteoporosis (10% vs 38.4%) and less likely to receive osteoporosis medication (9.9% vs 4.2%).

TAKEAWAY:

• Compared with individuals without cancer, patients with cancer had a significantly higher incidence rate of major fractures (12.9 vs 14.5 per 1000 person-years) and hip fractures (3.5 vs 4.2 per 1000 person-years).
• FRAX with bone mineral density exhibited excellent calibration for predicting major osteoporotic fractures (slope, 1.03) and hip fractures (0.97) in patients with cancer, regardless of the site of cancer diagnosis. FRAX without bone mineral density, however, underestimated the risk for both major (0.87) and hip fractures (0.72).
• In patients with cancer, FRAX with bone mineral density findings were associated with incident major osteoporotic fractures (hazard ratio [HR] per SD, 1.84) and hip fractures (HR per SD, 3.61).
• When models were adjusted for FRAX with bone mineral density, patients with cancer had an increased risk for both major osteoporotic fractures (HR, 1.17) and hip fractures (HR, 1.30). No difference was found in the risk for fracture between patients with and individuals without cancer when the models were adjusted for FRAX without bone mineral density, even when considering osteoporosis medication use.

IN PRACTICE:

“This retrospective cohort study demonstrates that individuals with cancer are at higher risk of fracture than individuals without cancer and that FRAX, particularly with BMD [bone mineral density], may accurately predict fracture risk in this population. These results, along with the known mortality risk of osteoporotic fractures among cancer survivors, further emphasize the clinical importance of closing the current osteoporosis care gap among cancer survivors,” the authors wrote.

SOURCE:

This study, led by Carrie Ye, MD, MPH, University of Alberta, Edmonton, Alberta, Canada, was published online in JAMA Oncology.

LIMITATIONS:

This study cohort included a selected group of cancer survivors who were referred for DXA scans and may not represent the general cancer population. The cohort consisted predominantly of women, limiting the generalizability to men with cancer. Given the heterogeneity of the population, the findings may not be applicable to all cancer subgroups. Information on cancer stage or the presence of bone metastases at the time of fracture risk assessment was lacking, which could have affected the findings.

DISCLOSURES:

This study was funded by the CancerCare Manitoba Foundation. Three authors reported having ties with various sources, including two who received grants from various organizations.
 

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

TOPLINE:

The Fracture Risk Assessment Tool (FRAX), with bone mineral density, predicts the risk for major osteoporotic fractures and hip fractures in patients with cancer, but FRAX without bone mineral density slightly overestimates these risks, a new analysis found.

METHODOLOGY:

• Cancer-specific guidelines recommend using FRAX to assess fracture risk, but its applicability in patients with cancer remains unclear.
• This retrospective cohort study included 9877 patients with cancer (mean age, 67.1 years) and 45,875 matched control individuals without cancer (mean age, 66.2 years). All participants had dual-energy x-ray absorptiometry (DXA) scans.
• Researchers collected data on bone mineral density and fractures. The 10-year probabilities of major osteoporotic fractures and hip fractures were calculated using FRAX, and the observed 10-year probabilities of these fractures were compared with FRAX-derived probabilities.
• Compared with individuals without cancer, patients with cancer had a shorter mean follow-up duration (8.5 vs 7.6 years), a slightly higher mean body mass index, and a higher percentage of parental hip fractures (7.0% vs 8.2%); additionally, patients with cancer were more likely to have secondary causes of osteoporosis (10% vs 38.4%) and less likely to receive osteoporosis medication (9.9% vs 4.2%).

TAKEAWAY:

• Compared with individuals without cancer, patients with cancer had a significantly higher incidence rate of major fractures (12.9 vs 14.5 per 1000 person-years) and hip fractures (3.5 vs 4.2 per 1000 person-years).
• FRAX with bone mineral density exhibited excellent calibration for predicting major osteoporotic fractures (slope, 1.03) and hip fractures (0.97) in patients with cancer, regardless of the site of cancer diagnosis. FRAX without bone mineral density, however, underestimated the risk for both major (0.87) and hip fractures (0.72).
• In patients with cancer, FRAX with bone mineral density findings were associated with incident major osteoporotic fractures (hazard ratio [HR] per SD, 1.84) and hip fractures (HR per SD, 3.61).
• When models were adjusted for FRAX with bone mineral density, patients with cancer had an increased risk for both major osteoporotic fractures (HR, 1.17) and hip fractures (HR, 1.30). No difference was found in the risk for fracture between patients with and individuals without cancer when the models were adjusted for FRAX without bone mineral density, even when considering osteoporosis medication use.

IN PRACTICE:

“This retrospective cohort study demonstrates that individuals with cancer are at higher risk of fracture than individuals without cancer and that FRAX, particularly with BMD [bone mineral density], may accurately predict fracture risk in this population. These results, along with the known mortality risk of osteoporotic fractures among cancer survivors, further emphasize the clinical importance of closing the current osteoporosis care gap among cancer survivors,” the authors wrote.

SOURCE:

This study, led by Carrie Ye, MD, MPH, University of Alberta, Edmonton, Alberta, Canada, was published online in JAMA Oncology.

LIMITATIONS:

This study cohort included a selected group of cancer survivors who were referred for DXA scans and may not represent the general cancer population. The cohort consisted predominantly of women, limiting the generalizability to men with cancer. Given the heterogeneity of the population, the findings may not be applicable to all cancer subgroups. Information on cancer stage or the presence of bone metastases at the time of fracture risk assessment was lacking, which could have affected the findings.

DISCLOSURES:

This study was funded by the CancerCare Manitoba Foundation. Three authors reported having ties with various sources, including two who received grants from various organizations.
 

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

AMSTERDAM — For frontal fibrosing alopecia (FFA), a disease with no approved therapies, topical delgocitinib attenuated inflammation and generated hair regrowth in women in a controlled phase 2a trial.

“This is an exciting avenue for FFA if the data are recapitulated in a larger population. It could be an important new treatment option,” said Maryanne Senna, MD, director at Lahey Hospital & Medical Center’s Hair Loss Center of Excellence, Burlington, Massachusetts, and assistant dermatology professor at Harvard Medical School, Boston, Massachusetts.

In a design characterized as “exploratory,” the trial had two parts: a randomized, double-blind, vehicle-controlled intervention for 12 weeks, followed by an open-label extension of topical delgocitinib for all participants for another 12 weeks. 

The primary efficacy endpoint was change in the molecular signature of FFA inflammation at 12 weeks. Clinical improvement was monitored with both trichoscopic images capturing the numbers of hairs and follicular units at 12 weeks and clinical severity scores through week 24. In a topical cream formulation, the Janus kinase inhibitor (JAKi) delgocitinib was associated with favorable activity for both. 
 

Some Hair Regrowth for All

“At 24 weeks, all patients achieved some degree of hair regrowth and a stabilization of disease based on hairline measurements,” Senna reported in a late-breaking news session at the 2024 European Academy of Dermatology and Venereology (EADV) Congress. 

On the clinical endpoints, Senna noted an upward trajectory in clinical improvement at the completion of the study.

The 30 participants were randomly assigned in a 1:1 ratio to receive delgocitinib cream in a concentration of 20 mg/g or vehicle cream applied twice daily for 12 weeks. At the end of this double-blind period, patients on vehicle were crossed over to the active therapy, and all patients were monitored for another 12 weeks in an open-label extension. 

The change from baseline in FFA biomarkers was selected as the primary endpoint based on previous work showing up-regulation in the expression of the Th1 biomarkers CXCL9, CXCL10, and interferon gamma in lesional vs nonlesional scalp in patients with FFA. 

When biopsies at the end of 12 weeks in the double-blind phase of the study were compared with the baseline biopsies, researchers found a decrease in expression of the three local inflammation markers in all patients receiving the JAKi, but not in those receiving the vehicle cream. In this small patient sample, only the reduction in expression of CXCL9, a cytokine known for differentiation and promotion of leukocytes, reached statistical significance (P < .05).

But in an analysis involving the expression of multiple genes, “lesions treated with delgocitinib had a 4% improvement in normalization toward a nonlesional transcriptomic profile, while patients treated with vehicle had a 33% worsening,” Senna reported. The difference was highly significant (P < .001).

Furthermore, the decrease in total Lichen Planopilaris Activity Index and FFA severity scores were numerically and statistically greater (P = .023) in the active-treatment arm than in the vehicle arm by the end of the double-blind part of the trial, she said.

On trichoscopy, there was an increased number of hairs and follicular units at 12 weeks relative to baseline among those treated with topical delgocitinib but a reduction in those treated with vehicle.
 

JAKi Patients Gained Hair, Vehicle Patients Lost Hair

On the basis of hair count per square centimeter from baseline, delgocitinib-treated patients gained on average of seven hairs whereas vehicle recipients lost an average of 11 hairs at 24 weeks, Senna reported.

Patients originally treated with vehicle did improve in most outcome measures in the open-label extension of the experimental treatment after crossover, but they did not catch up to those initially randomized to delgocitinib because of further accrual of favorable changes in the active-treatment group over time.

“There were no adverse events associated with active therapy or vehicle, including application-site reactions,” Senna said. The one between-group difference was a higher rate of COVID-19, but this was greater in the control arm.

All 30 of the participants in this study were women, and all had moderate to severe disease at enrollment. The median age was 64 years. Because of the predominant population at the hair loss center, all but one of the participants were White, and one participant was Asian. 

Characterizing FFA as “devastating and disfiguring,” Senna, who specializes in the care of alopecia, noted that this a difficult disease to control with the off-label strategies that are now used. The slow progress to identify treatments for FFA is illustrated by the fact that only one other double-blind and randomized trial has ever been conducted in FFA, she said.
 

Exploratory Study Supports Anecdotal Experience

On the basis of prior anecdotal experience with JAKi treatment for FFA, Senna said, “I do think that it is possible to get largely clear skin with this therapy.” However, she is now hoping for definitive trials to better characterize the efficacy and safety of oral and topical therapies, perhaps used sequentially to maintain clinical improvement.

In light of the limited current options, Menno de Rie, MD, PhD, professor of dermatology at the University of Amsterdam in the Netherlands, called these data “very inspiring and hopeful.” He suggested the promise of this therapy was reinforced by the upward trajectory of the biomarkers and clinical improvement over the study period. 

“Any improvement in treatment options would be welcome, because we do not [have] any reliable therapies for this condition,” de Rie, who was not an investigator, said in an interview after the presentation. 

Ultimately, Senna said, once effective therapy is established, the goal will be to start as early as possible in the disease process. She noted that there is evidence that prompt therapy can reverse the disorder, not just prevent progression.

“If you can get to the hair follicles before the point of no return, there is [a] chance [of] follicular rescue,” she said.

Delgocitinib cream (Anzupgo) was approved in Europe for treating chronic hand eczema in late September and is under review for the same indication in the United States. 

Senna has financial relationships with Arena, Concert, Eli Lilly, Pfizer, and Leo Pharma, which provided funding for this study. de Rie reported no potential conflicts of interest.

A version of this article appeared on Medscape.com.

AMSTERDAM — For frontal fibrosing alopecia (FFA), a disease with no approved therapies, topical delgocitinib attenuated inflammation and generated hair regrowth in women in a controlled phase 2a trial.

“This is an exciting avenue for FFA if the data are recapitulated in a larger population. It could be an important new treatment option,” said Maryanne Senna, MD, director at Lahey Hospital & Medical Center’s Hair Loss Center of Excellence, Burlington, Massachusetts, and assistant dermatology professor at Harvard Medical School, Boston, Massachusetts.

In a design characterized as “exploratory,” the trial had two parts: a randomized, double-blind, vehicle-controlled intervention for 12 weeks, followed by an open-label extension of topical delgocitinib for all participants for another 12 weeks. 

The primary efficacy endpoint was change in the molecular signature of FFA inflammation at 12 weeks. Clinical improvement was monitored with both trichoscopic images capturing the numbers of hairs and follicular units at 12 weeks and clinical severity scores through week 24. In a topical cream formulation, the Janus kinase inhibitor (JAKi) delgocitinib was associated with favorable activity for both. 
 

Some Hair Regrowth for All

“At 24 weeks, all patients achieved some degree of hair regrowth and a stabilization of disease based on hairline measurements,” Senna reported in a late-breaking news session at the 2024 European Academy of Dermatology and Venereology (EADV) Congress. 

On the clinical endpoints, Senna noted an upward trajectory in clinical improvement at the completion of the study.

The 30 participants were randomly assigned in a 1:1 ratio to receive delgocitinib cream in a concentration of 20 mg/g or vehicle cream applied twice daily for 12 weeks. At the end of this double-blind period, patients on vehicle were crossed over to the active therapy, and all patients were monitored for another 12 weeks in an open-label extension. 

The change from baseline in FFA biomarkers was selected as the primary endpoint based on previous work showing up-regulation in the expression of the Th1 biomarkers CXCL9, CXCL10, and interferon gamma in lesional vs nonlesional scalp in patients with FFA. 

When biopsies at the end of 12 weeks in the double-blind phase of the study were compared with the baseline biopsies, researchers found a decrease in expression of the three local inflammation markers in all patients receiving the JAKi, but not in those receiving the vehicle cream. In this small patient sample, only the reduction in expression of CXCL9, a cytokine known for differentiation and promotion of leukocytes, reached statistical significance (P < .05).

But in an analysis involving the expression of multiple genes, “lesions treated with delgocitinib had a 4% improvement in normalization toward a nonlesional transcriptomic profile, while patients treated with vehicle had a 33% worsening,” Senna reported. The difference was highly significant (P < .001).

Furthermore, the decrease in total Lichen Planopilaris Activity Index and FFA severity scores were numerically and statistically greater (P = .023) in the active-treatment arm than in the vehicle arm by the end of the double-blind part of the trial, she said.

On trichoscopy, there was an increased number of hairs and follicular units at 12 weeks relative to baseline among those treated with topical delgocitinib but a reduction in those treated with vehicle.
 

JAKi Patients Gained Hair, Vehicle Patients Lost Hair

On the basis of hair count per square centimeter from baseline, delgocitinib-treated patients gained on average of seven hairs whereas vehicle recipients lost an average of 11 hairs at 24 weeks, Senna reported.

Patients originally treated with vehicle did improve in most outcome measures in the open-label extension of the experimental treatment after crossover, but they did not catch up to those initially randomized to delgocitinib because of further accrual of favorable changes in the active-treatment group over time.

“There were no adverse events associated with active therapy or vehicle, including application-site reactions,” Senna said. The one between-group difference was a higher rate of COVID-19, but this was greater in the control arm.

All 30 of the participants in this study were women, and all had moderate to severe disease at enrollment. The median age was 64 years. Because of the predominant population at the hair loss center, all but one of the participants were White, and one participant was Asian. 

Characterizing FFA as “devastating and disfiguring,” Senna, who specializes in the care of alopecia, noted that this a difficult disease to control with the off-label strategies that are now used. The slow progress to identify treatments for FFA is illustrated by the fact that only one other double-blind and randomized trial has ever been conducted in FFA, she said.
 

Exploratory Study Supports Anecdotal Experience

On the basis of prior anecdotal experience with JAKi treatment for FFA, Senna said, “I do think that it is possible to get largely clear skin with this therapy.” However, she is now hoping for definitive trials to better characterize the efficacy and safety of oral and topical therapies, perhaps used sequentially to maintain clinical improvement.

In light of the limited current options, Menno de Rie, MD, PhD, professor of dermatology at the University of Amsterdam in the Netherlands, called these data “very inspiring and hopeful.” He suggested the promise of this therapy was reinforced by the upward trajectory of the biomarkers and clinical improvement over the study period. 

“Any improvement in treatment options would be welcome, because we do not [have] any reliable therapies for this condition,” de Rie, who was not an investigator, said in an interview after the presentation. 

Ultimately, Senna said, once effective therapy is established, the goal will be to start as early as possible in the disease process. She noted that there is evidence that prompt therapy can reverse the disorder, not just prevent progression.

“If you can get to the hair follicles before the point of no return, there is [a] chance [of] follicular rescue,” she said.

Delgocitinib cream (Anzupgo) was approved in Europe for treating chronic hand eczema in late September and is under review for the same indication in the United States. 

Senna has financial relationships with Arena, Concert, Eli Lilly, Pfizer, and Leo Pharma, which provided funding for this study. de Rie reported no potential conflicts of interest.

A version of this article appeared on Medscape.com.

AMSTERDAM — For frontal fibrosing alopecia (FFA), a disease with no approved therapies, topical delgocitinib attenuated inflammation and generated hair regrowth in women in a controlled phase 2a trial.

“This is an exciting avenue for FFA if the data are recapitulated in a larger population. It could be an important new treatment option,” said Maryanne Senna, MD, director at Lahey Hospital & Medical Center’s Hair Loss Center of Excellence, Burlington, Massachusetts, and assistant dermatology professor at Harvard Medical School, Boston, Massachusetts.

In a design characterized as “exploratory,” the trial had two parts: a randomized, double-blind, vehicle-controlled intervention for 12 weeks, followed by an open-label extension of topical delgocitinib for all participants for another 12 weeks. 

The primary efficacy endpoint was change in the molecular signature of FFA inflammation at 12 weeks. Clinical improvement was monitored with both trichoscopic images capturing the numbers of hairs and follicular units at 12 weeks and clinical severity scores through week 24. In a topical cream formulation, the Janus kinase inhibitor (JAKi) delgocitinib was associated with favorable activity for both. 
 

Some Hair Regrowth for All

“At 24 weeks, all patients achieved some degree of hair regrowth and a stabilization of disease based on hairline measurements,” Senna reported in a late-breaking news session at the 2024 European Academy of Dermatology and Venereology (EADV) Congress. 

On the clinical endpoints, Senna noted an upward trajectory in clinical improvement at the completion of the study.

The 30 participants were randomly assigned in a 1:1 ratio to receive delgocitinib cream in a concentration of 20 mg/g or vehicle cream applied twice daily for 12 weeks. At the end of this double-blind period, patients on vehicle were crossed over to the active therapy, and all patients were monitored for another 12 weeks in an open-label extension. 

The change from baseline in FFA biomarkers was selected as the primary endpoint based on previous work showing up-regulation in the expression of the Th1 biomarkers CXCL9, CXCL10, and interferon gamma in lesional vs nonlesional scalp in patients with FFA. 

When biopsies at the end of 12 weeks in the double-blind phase of the study were compared with the baseline biopsies, researchers found a decrease in expression of the three local inflammation markers in all patients receiving the JAKi, but not in those receiving the vehicle cream. In this small patient sample, only the reduction in expression of CXCL9, a cytokine known for differentiation and promotion of leukocytes, reached statistical significance (P < .05).

But in an analysis involving the expression of multiple genes, “lesions treated with delgocitinib had a 4% improvement in normalization toward a nonlesional transcriptomic profile, while patients treated with vehicle had a 33% worsening,” Senna reported. The difference was highly significant (P < .001).

Furthermore, the decrease in total Lichen Planopilaris Activity Index and FFA severity scores were numerically and statistically greater (P = .023) in the active-treatment arm than in the vehicle arm by the end of the double-blind part of the trial, she said.

On trichoscopy, there was an increased number of hairs and follicular units at 12 weeks relative to baseline among those treated with topical delgocitinib but a reduction in those treated with vehicle.
 

JAKi Patients Gained Hair, Vehicle Patients Lost Hair

On the basis of hair count per square centimeter from baseline, delgocitinib-treated patients gained on average of seven hairs whereas vehicle recipients lost an average of 11 hairs at 24 weeks, Senna reported.

Patients originally treated with vehicle did improve in most outcome measures in the open-label extension of the experimental treatment after crossover, but they did not catch up to those initially randomized to delgocitinib because of further accrual of favorable changes in the active-treatment group over time.

“There were no adverse events associated with active therapy or vehicle, including application-site reactions,” Senna said. The one between-group difference was a higher rate of COVID-19, but this was greater in the control arm.

All 30 of the participants in this study were women, and all had moderate to severe disease at enrollment. The median age was 64 years. Because of the predominant population at the hair loss center, all but one of the participants were White, and one participant was Asian. 

Characterizing FFA as “devastating and disfiguring,” Senna, who specializes in the care of alopecia, noted that this a difficult disease to control with the off-label strategies that are now used. The slow progress to identify treatments for FFA is illustrated by the fact that only one other double-blind and randomized trial has ever been conducted in FFA, she said.
 

Exploratory Study Supports Anecdotal Experience

On the basis of prior anecdotal experience with JAKi treatment for FFA, Senna said, “I do think that it is possible to get largely clear skin with this therapy.” However, she is now hoping for definitive trials to better characterize the efficacy and safety of oral and topical therapies, perhaps used sequentially to maintain clinical improvement.

In light of the limited current options, Menno de Rie, MD, PhD, professor of dermatology at the University of Amsterdam in the Netherlands, called these data “very inspiring and hopeful.” He suggested the promise of this therapy was reinforced by the upward trajectory of the biomarkers and clinical improvement over the study period. 

“Any improvement in treatment options would be welcome, because we do not [have] any reliable therapies for this condition,” de Rie, who was not an investigator, said in an interview after the presentation. 

Ultimately, Senna said, once effective therapy is established, the goal will be to start as early as possible in the disease process. She noted that there is evidence that prompt therapy can reverse the disorder, not just prevent progression.

“If you can get to the hair follicles before the point of no return, there is [a] chance [of] follicular rescue,” she said.

Delgocitinib cream (Anzupgo) was approved in Europe for treating chronic hand eczema in late September and is under review for the same indication in the United States. 

Senna has financial relationships with Arena, Concert, Eli Lilly, Pfizer, and Leo Pharma, which provided funding for this study. de Rie reported no potential conflicts of interest.

A version of this article appeared on Medscape.com.