Clinical Endocrinology News

Most physicians oppose the way standardized relative value units (RVUs) are used to determine performance and compensation, according to Medscape’s 2024 Physicians and RVUs Report. About 6 in 10 survey respondents were unhappy with how RVUs affected them financially, while 7 in 10 said RVUs were poor measures of productivity.

The report analyzed 2024 survey data from 1005 practicing physicians who earn RVUs.

“I’m already mad that the medical field is controlled by health insurers and what they pay and authorize,” said an anesthesiologist in New York. “Then [that approach] is transferred to medical offices and hospitals, where physicians are paid by RVUs.”

Most physicians surveyed produced between 4000 and 8000 RVUs per year. Roughly one in six were high RVU generators, generating more than 10,000 annually.

In most cases, the metric influences earning potential — 42% of doctors surveyed said RVUs affect their salaries to some degree. One quarter said their salary was based entirely on RVUs. More than three fourths of physicians who received performance bonuses said they must meet RVU targets to do so.

“The current RVU system encourages unnecessary procedures, hurting patients,” said an orthopedic surgeon in Maine.

Nearly three fourths of practitioners surveyed said they occasionally to frequently felt pressure to take on more patients as a result of this system.

“I know numerous primary care doctors and specialists who have been forced to increase patient volume to meet RVU goals, and none is happy about it,” said Alok Patel, MD, a pediatric hospitalist with Stanford Hospital in Palo Alto, California. “Plus, patients are definitely not happy about being rushed.”

More than half of respondents said they occasionally or frequently felt compelled by their employer to use higher-level coding, which interferes with a physician’s ethical responsibility to the patient, said Arthur L. Caplan, PhD, a bioethicist at NYU Langone Medical Center in New York City.

“Rather than rewarding excellence or good outcomes, you’re kind of rewarding procedures and volume,” said Dr. Caplan. “It’s more than pressure; it’s expected.”

Nearly 6 in 10 physicians said that the method for calculating reimbursements was unfair. Almost half said that they weren’t happy with how their workplace uses RVUs.

A few respondents said that their RVU model, which is often based on what Dr. Patel called an “overly complicated algorithm,” did not account for the time spent on tasks or the fact that some patients miss appointments. RVUs also rely on factors outside the control of a physician, such as location and patient volume, said one doctor.

The model can also lower the level of care patients receive, Dr. Patel said.

“I know primary care doctors who work in RVU-based systems and simply cannot take the necessary time — even if it’s 30-45 minutes — to thoroughly assess a patient, when the model forces them to take on 15-minute encounters.”

Finally, over half of clinicians said alternatives to the RVU system would be more effective, and 77% suggested including qualitative data. One respondent recommended incorporating time spent doing paperwork and communicating with patients, complexity of conditions, and medication management.

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

Most physicians oppose the way standardized relative value units (RVUs) are used to determine performance and compensation, according to Medscape’s 2024 Physicians and RVUs Report. About 6 in 10 survey respondents were unhappy with how RVUs affected them financially, while 7 in 10 said RVUs were poor measures of productivity.

The report analyzed 2024 survey data from 1005 practicing physicians who earn RVUs.

“I’m already mad that the medical field is controlled by health insurers and what they pay and authorize,” said an anesthesiologist in New York. “Then [that approach] is transferred to medical offices and hospitals, where physicians are paid by RVUs.”

Most physicians surveyed produced between 4000 and 8000 RVUs per year. Roughly one in six were high RVU generators, generating more than 10,000 annually.

In most cases, the metric influences earning potential — 42% of doctors surveyed said RVUs affect their salaries to some degree. One quarter said their salary was based entirely on RVUs. More than three fourths of physicians who received performance bonuses said they must meet RVU targets to do so.

“The current RVU system encourages unnecessary procedures, hurting patients,” said an orthopedic surgeon in Maine.

Nearly three fourths of practitioners surveyed said they occasionally to frequently felt pressure to take on more patients as a result of this system.

“I know numerous primary care doctors and specialists who have been forced to increase patient volume to meet RVU goals, and none is happy about it,” said Alok Patel, MD, a pediatric hospitalist with Stanford Hospital in Palo Alto, California. “Plus, patients are definitely not happy about being rushed.”

More than half of respondents said they occasionally or frequently felt compelled by their employer to use higher-level coding, which interferes with a physician’s ethical responsibility to the patient, said Arthur L. Caplan, PhD, a bioethicist at NYU Langone Medical Center in New York City.

“Rather than rewarding excellence or good outcomes, you’re kind of rewarding procedures and volume,” said Dr. Caplan. “It’s more than pressure; it’s expected.”

Nearly 6 in 10 physicians said that the method for calculating reimbursements was unfair. Almost half said that they weren’t happy with how their workplace uses RVUs.

A few respondents said that their RVU model, which is often based on what Dr. Patel called an “overly complicated algorithm,” did not account for the time spent on tasks or the fact that some patients miss appointments. RVUs also rely on factors outside the control of a physician, such as location and patient volume, said one doctor.

The model can also lower the level of care patients receive, Dr. Patel said.

“I know primary care doctors who work in RVU-based systems and simply cannot take the necessary time — even if it’s 30-45 minutes — to thoroughly assess a patient, when the model forces them to take on 15-minute encounters.”

Finally, over half of clinicians said alternatives to the RVU system would be more effective, and 77% suggested including qualitative data. One respondent recommended incorporating time spent doing paperwork and communicating with patients, complexity of conditions, and medication management.

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

Most physicians oppose the way standardized relative value units (RVUs) are used to determine performance and compensation, according to Medscape’s 2024 Physicians and RVUs Report. About 6 in 10 survey respondents were unhappy with how RVUs affected them financially, while 7 in 10 said RVUs were poor measures of productivity.

The report analyzed 2024 survey data from 1005 practicing physicians who earn RVUs.

“I’m already mad that the medical field is controlled by health insurers and what they pay and authorize,” said an anesthesiologist in New York. “Then [that approach] is transferred to medical offices and hospitals, where physicians are paid by RVUs.”

Most physicians surveyed produced between 4000 and 8000 RVUs per year. Roughly one in six were high RVU generators, generating more than 10,000 annually.

In most cases, the metric influences earning potential — 42% of doctors surveyed said RVUs affect their salaries to some degree. One quarter said their salary was based entirely on RVUs. More than three fourths of physicians who received performance bonuses said they must meet RVU targets to do so.

“The current RVU system encourages unnecessary procedures, hurting patients,” said an orthopedic surgeon in Maine.

Nearly three fourths of practitioners surveyed said they occasionally to frequently felt pressure to take on more patients as a result of this system.

“I know numerous primary care doctors and specialists who have been forced to increase patient volume to meet RVU goals, and none is happy about it,” said Alok Patel, MD, a pediatric hospitalist with Stanford Hospital in Palo Alto, California. “Plus, patients are definitely not happy about being rushed.”

More than half of respondents said they occasionally or frequently felt compelled by their employer to use higher-level coding, which interferes with a physician’s ethical responsibility to the patient, said Arthur L. Caplan, PhD, a bioethicist at NYU Langone Medical Center in New York City.

“Rather than rewarding excellence or good outcomes, you’re kind of rewarding procedures and volume,” said Dr. Caplan. “It’s more than pressure; it’s expected.”

Nearly 6 in 10 physicians said that the method for calculating reimbursements was unfair. Almost half said that they weren’t happy with how their workplace uses RVUs.

A few respondents said that their RVU model, which is often based on what Dr. Patel called an “overly complicated algorithm,” did not account for the time spent on tasks or the fact that some patients miss appointments. RVUs also rely on factors outside the control of a physician, such as location and patient volume, said one doctor.

The model can also lower the level of care patients receive, Dr. Patel said.

“I know primary care doctors who work in RVU-based systems and simply cannot take the necessary time — even if it’s 30-45 minutes — to thoroughly assess a patient, when the model forces them to take on 15-minute encounters.”

Finally, over half of clinicians said alternatives to the RVU system would be more effective, and 77% suggested including qualitative data. One respondent recommended incorporating time spent doing paperwork and communicating with patients, complexity of conditions, and medication management.

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

TOPLINE:

Compared with dipeptidyl peptidase 4 (DPP-4) inhibitors, glucagon-like peptide 1 receptor agonists (GLP-1 RAs) are associated with a lower risk for all-cause mortality and major adverse cardiovascular events (MACE) in patients with immune-mediated inflammatory diseases (IMIDs) and type 2 diabetes (T2D).

METHODOLOGY:

• GLP-1 RAs reduce the risk for all-cause mortality, cardiovascular mortality, and stroke in patients with diabetes. However, previous trials have excluded those with IMIDs, leaving a gap in understanding the cardioprotective effects of GLP-1 RAs in this population.
• Researchers conducted a population-based cohort study to assess if patients with an IMID derive greater benefits from GLP-1 RAs than DPP-4 inhibitors.
• They used administrative health data from British Columbia, Canada, to include 10,855 patients with IMIDs (rheumatoid arthritis, psoriatic disease, ankylosing spondylitis, inflammatory bowel disease, or systemic autoimmune rheumatic disease) and T2D who initiated either GLP-1 RA (n = 3570) or DPP-4 inhibitor (n = 7285).
• The mean follow-up was 1.46 and 1.88 years in the GLP-1 RA and DPP-4 inhibitor cohorts, respectively.
• The primary outcome was all-cause mortality, and the secondary outcome was MACE, including cardiovascular death, myocardial infarction, and ischemic stroke.

TAKEAWAY:

• The risk for all-cause mortality was 52% lower in patients who initiated GLP-1 RAs than in those who initiated DPP-4 inhibitors (weighted hazard ratio [HR], 0.48; 95% CI, 0.31-0.75).
• Additionally, patients initiating DPP-4 inhibitors.
• In the subgroup of patients with GLP-1 RAs had a significantly lower risk for MACE (weighted HR, 0.66; 95% CI, 0.50-0.88), particularly myocardial infarction (weighted HR, 0.62; 95% CI, 0.40-0.96), than those initiating rheumatoid arthritis and T2D, those who initiated GLP-1 RAs had a 55% lower risk for all-cause mortality and 61% lower risk for MACE than those who initiated DPP-4 inhibitors.

IN PRACTICE:

“This corresponds to nine fewer deaths and 11 fewer MACE per 1000 person-years, respectively, supporting the hypothesis that these agents have a cardioprotective effect in this high-risk population,” the authors wrote.

SOURCE:

This study was led by Derin Karacabeyli, MD, Division of Rheumatology, Department of Medicine, University of British Columbia, Vancouver, Canada, and was published online on August 8, 2024, in PLOS ONE.

LIMITATIONS:

The study’s dependence on administrative health data might have resulted in incomplete capture of comorbidities, particularly obesity. The mean follow-up period was relatively short, which might have limited the long-term applicability of these findings. The accuracy of the case definitions for IMIDs and T2D, according to International Classification of Diseases codes, could not be fully ascertained.

DISCLOSURES:

The study was supported by grants from the Canadian Institutes of Health Research. Two authors declared receiving research support, consulting fees, or participating in advisory boards outside the submitted work.

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

TOPLINE:

Compared with dipeptidyl peptidase 4 (DPP-4) inhibitors, glucagon-like peptide 1 receptor agonists (GLP-1 RAs) are associated with a lower risk for all-cause mortality and major adverse cardiovascular events (MACE) in patients with immune-mediated inflammatory diseases (IMIDs) and type 2 diabetes (T2D).

METHODOLOGY:

• GLP-1 RAs reduce the risk for all-cause mortality, cardiovascular mortality, and stroke in patients with diabetes. However, previous trials have excluded those with IMIDs, leaving a gap in understanding the cardioprotective effects of GLP-1 RAs in this population.
• Researchers conducted a population-based cohort study to assess if patients with an IMID derive greater benefits from GLP-1 RAs than DPP-4 inhibitors.
• They used administrative health data from British Columbia, Canada, to include 10,855 patients with IMIDs (rheumatoid arthritis, psoriatic disease, ankylosing spondylitis, inflammatory bowel disease, or systemic autoimmune rheumatic disease) and T2D who initiated either GLP-1 RA (n = 3570) or DPP-4 inhibitor (n = 7285).
• The mean follow-up was 1.46 and 1.88 years in the GLP-1 RA and DPP-4 inhibitor cohorts, respectively.
• The primary outcome was all-cause mortality, and the secondary outcome was MACE, including cardiovascular death, myocardial infarction, and ischemic stroke.

TAKEAWAY:

• The risk for all-cause mortality was 52% lower in patients who initiated GLP-1 RAs than in those who initiated DPP-4 inhibitors (weighted hazard ratio [HR], 0.48; 95% CI, 0.31-0.75).
• Additionally, patients initiating DPP-4 inhibitors.
• In the subgroup of patients with GLP-1 RAs had a significantly lower risk for MACE (weighted HR, 0.66; 95% CI, 0.50-0.88), particularly myocardial infarction (weighted HR, 0.62; 95% CI, 0.40-0.96), than those initiating rheumatoid arthritis and T2D, those who initiated GLP-1 RAs had a 55% lower risk for all-cause mortality and 61% lower risk for MACE than those who initiated DPP-4 inhibitors.

IN PRACTICE:

“This corresponds to nine fewer deaths and 11 fewer MACE per 1000 person-years, respectively, supporting the hypothesis that these agents have a cardioprotective effect in this high-risk population,” the authors wrote.

SOURCE:

This study was led by Derin Karacabeyli, MD, Division of Rheumatology, Department of Medicine, University of British Columbia, Vancouver, Canada, and was published online on August 8, 2024, in PLOS ONE.

LIMITATIONS:

The study’s dependence on administrative health data might have resulted in incomplete capture of comorbidities, particularly obesity. The mean follow-up period was relatively short, which might have limited the long-term applicability of these findings. The accuracy of the case definitions for IMIDs and T2D, according to International Classification of Diseases codes, could not be fully ascertained.

DISCLOSURES:

The study was supported by grants from the Canadian Institutes of Health Research. Two authors declared receiving research support, consulting fees, or participating in advisory boards outside the submitted work.

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

TOPLINE:

Compared with dipeptidyl peptidase 4 (DPP-4) inhibitors, glucagon-like peptide 1 receptor agonists (GLP-1 RAs) are associated with a lower risk for all-cause mortality and major adverse cardiovascular events (MACE) in patients with immune-mediated inflammatory diseases (IMIDs) and type 2 diabetes (T2D).

METHODOLOGY:

• GLP-1 RAs reduce the risk for all-cause mortality, cardiovascular mortality, and stroke in patients with diabetes. However, previous trials have excluded those with IMIDs, leaving a gap in understanding the cardioprotective effects of GLP-1 RAs in this population.
• Researchers conducted a population-based cohort study to assess if patients with an IMID derive greater benefits from GLP-1 RAs than DPP-4 inhibitors.
• They used administrative health data from British Columbia, Canada, to include 10,855 patients with IMIDs (rheumatoid arthritis, psoriatic disease, ankylosing spondylitis, inflammatory bowel disease, or systemic autoimmune rheumatic disease) and T2D who initiated either GLP-1 RA (n = 3570) or DPP-4 inhibitor (n = 7285).
• The mean follow-up was 1.46 and 1.88 years in the GLP-1 RA and DPP-4 inhibitor cohorts, respectively.
• The primary outcome was all-cause mortality, and the secondary outcome was MACE, including cardiovascular death, myocardial infarction, and ischemic stroke.

TAKEAWAY:

• The risk for all-cause mortality was 52% lower in patients who initiated GLP-1 RAs than in those who initiated DPP-4 inhibitors (weighted hazard ratio [HR], 0.48; 95% CI, 0.31-0.75).
• Additionally, patients initiating DPP-4 inhibitors.
• In the subgroup of patients with GLP-1 RAs had a significantly lower risk for MACE (weighted HR, 0.66; 95% CI, 0.50-0.88), particularly myocardial infarction (weighted HR, 0.62; 95% CI, 0.40-0.96), than those initiating rheumatoid arthritis and T2D, those who initiated GLP-1 RAs had a 55% lower risk for all-cause mortality and 61% lower risk for MACE than those who initiated DPP-4 inhibitors.

IN PRACTICE:

“This corresponds to nine fewer deaths and 11 fewer MACE per 1000 person-years, respectively, supporting the hypothesis that these agents have a cardioprotective effect in this high-risk population,” the authors wrote.

SOURCE:

This study was led by Derin Karacabeyli, MD, Division of Rheumatology, Department of Medicine, University of British Columbia, Vancouver, Canada, and was published online on August 8, 2024, in PLOS ONE.

LIMITATIONS:

The study’s dependence on administrative health data might have resulted in incomplete capture of comorbidities, particularly obesity. The mean follow-up period was relatively short, which might have limited the long-term applicability of these findings. The accuracy of the case definitions for IMIDs and T2D, according to International Classification of Diseases codes, could not be fully ascertained.

DISCLOSURES:

The study was supported by grants from the Canadian Institutes of Health Research. Two authors declared receiving research support, consulting fees, or participating in advisory boards outside the submitted work.

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

This transcript has been edited for clarity.

Akshay B. Jain, MD: Welcome back to Medscape at ADA 2024, where Dr. James Kim, primary care physician from Calgary, Alberta, will be joining me in deciphering the key highlights at the ADA conference and bringing our own clinical twist into what the relevance would be for people like you and I to take back to our clinics.

Welcome back, Dr. Kim. 

James Kim, MBBCh, PgDip, MScCH: Thank you very much. It’s nice to be back. 

Dr. Jain: This was a diabetes conference, so obviously we are very pancreas focused. At this conference, we went outside our general area of territory, going outside of the pancreas and delving into other organ states. What I found fascinating were some data regarding the effects of incretin therapy on the lung, and in particular, some of the restrictive lung disorders.

Dr. Kim, you attended these sessions as well. Can you tell us a little bit more about the results that were discussed? 

Dr. Kim: This is an interesting field. The moderator of the session went up and said that there has been no time in any previous ADA sessions where the lung issue was actually discussed. This was the first time ever.

They had some of the world leaders in this field, so it was really awesome to see them. Just to paint a picture of these obese asthmatic patients, they are challenging cases because, as you know, the main therapy for any asthmatic patient is inhaled corticosteroid.

Patients who are obese have quite a bit of a steroid resistance. Therefore, they end up being on many medications that sometimes are off label, and many end up on biologics as well. Therefore, the respiratory world has been seeking therapies for these obese asthmatic patients who are likely to be steroid resistant because these people are also likely to end up on an oral steroid as well.

Dr. Jain, you know the effect of the steroids much better than I do, and it’s like a laundry list. We really don’t want our patients to be on oral steroids. 

In the past few years, GLP-1 has been studied quite extensively in the lung, especially in the world of asthma, and also in COPD. What’s really fascinating is that the GLP-1 receptors have been found to be quite abundant in the airway. Some studies show that the highest concentration of GLP-1 lies in the airway, whereas some studies have said that it’s the third most common area to find the GLP-1. 

It is not a surprise that GLP-1 is being studied in managing the airway, especially airway inflammation in asthma and COPD patients. The preliminary data have been quite encouraging. They also discussed that there are new medications coming out that seem to be incretin based, so we’ll wait to see what those studies show.

There are two current phase 3 trials being held at the moment. One is using semaglutide 2.4 mg subcutaneous and another one is using metformin to reduce the airway inflammation in these asthmatic patients and also in some COPD patients. We’ll look forward to these results.

Dr. Jain: That’s really important to note because we see that there is a high density of these receptors in the airways, and hitherto we had no idea about the overall effect. Now, we’re looking at, as you mentioned, individuals with obesity who have asthma, so there are both the restrictive and obstructive components in the lung coming into play here.

From an endocrinology perspective, I’m thinking that this could be multiple effects of the GLP-1 receptor agonists, where on one hand you’re managing the obesity and you’re working along that line, and on the other hand, it could have local anti-inflammatory effects in the lung. Hence, there could be potential improvement in the overall pulmonary function of these individuals. 

Dr. Kim: We are seeing this in primary care. Ever since I found out this information, I have started numerous patients, who are obese, asthmatic patients who do not have diabetes, on GLP-1 therapies, and their pulmonary function tests have improved significantly.

As a matter of fact, one of my personal friends is a severe asthmatic patient. She ends up being on oral steroids about three times a year. There was even one day when I saw her in one of my classes and she was dyspneic. She was short of breath. 

I introduced her to one of my colleagues who’s a respirologist and very much into the impact of the incretins and asthma, and she was started on a GLP-1 receptor agonist. She lost about 30 pounds of weight, but now she is labeled as a mild asthmatic. Her pulmonary function test is completely normal. She hasn’t touched an oral steroid for a couple of years now.

That is a huge success story and I’m seeing that even in my own clinic as well. It’s a huge win for the respiratory world.

Dr. Jain: I think from an endocrinology perspective as well, if we are initiating GLP-1 receptor agonists or medications in that class, where we use it for management of obesity, sooner or later we do hit a stage where people will plateau with their weight loss. They won’t have any additional weight loss.

We tell individuals at that time that the fact that they’re able to maintain the weight loss still means that the medication is working from the obesity perspective. For individuals who also have asthma, it would be a good point to tell them that it could still have potential effects on reducing inflammation ongoing. Hence, even though they may not be losing any additional weight, it would still be helpful to continue on these medications from a pulmonary perspective. 

Dr. Kim: Right now these pleiotropic effects of GLP-1 agents are absolutely mind-blowing. I mentioned in one of my respiratory presentations to a bunch of respirologists that diabetes is taking over the world, including the respiratory world. Well, you can imagine what their faces were like. However, they were quite impressed at that, and they were very excited with what these two phase 3 trials will show. 

Dr. Jain: I think, based on the ADA 2024 conference, GLP-1 receptor agonists continue to be the gift that keeps giving. We have the effects on diabetes, obesity, kidney function, liver protection, lungs, and Alzheimer’s. We saw some sessions about potential use in people with alcohol misuse disorder or gambling problems. Clearly, there’s a large amount of research that›s being done with these agents. 

Perhaps when you and I talk about ADA 2025, we might be able to talk about some more pleiotropic benefits outside the pancreas. Until then, please do check out our other videos from ADA 2024. Thanks for joining us again, Dr. Kim.

Dr. Kim: Thank you very much for having me.
 

Dr. Jain, clinical instructor, Department of Endocrinology, University of British Columbia, and endocrinologist, TLC Diabetes and Endocrinology, Vancouver, British Columbia, Canada, has disclosed ties with Abbott, Acerus, AstraZeneca, Amgen, Bausch Healthcare, Bayer, Boehringer Ingelheim, Care to Know, CCRN, Connected in Motion, CPD Network, Dexcom, Diabetes Canada, Eli Lilly, GSK, HLS Therapeutics, Janssen, Master Clinician Alliance, MDBriefcase, Merck, Medtronic, Moderna, Novartis, Novo Nordisk, Partners in Progressive Medical Education, Pfizer, Sanofi Aventis, Timed Right, WebMD, Gilead Sciences, Insulet, PocketPills, Roche, and Takeda. Dr. Kim, clinical assistant professor, Department of Family Medicine, University of Calgary, Alberta, has disclosed ties with Abbott, AbbVie, AstraZeneca, Bayer, Boehringer Ingelheim, Eisai, Embecta, Eli Lilly, GSK, Janssen, Linpharma, Novo Nordisk, Miravo, Otsuka, Pfizer, Teva, Takeda, and Sanofi, and Partners in Progressive Medical Education.
 

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

This transcript has been edited for clarity.

Akshay B. Jain, MD: Welcome back to Medscape at ADA 2024, where Dr. James Kim, primary care physician from Calgary, Alberta, will be joining me in deciphering the key highlights at the ADA conference and bringing our own clinical twist into what the relevance would be for people like you and I to take back to our clinics.

Welcome back, Dr. Kim. 

James Kim, MBBCh, PgDip, MScCH: Thank you very much. It’s nice to be back. 

Dr. Jain: This was a diabetes conference, so obviously we are very pancreas focused. At this conference, we went outside our general area of territory, going outside of the pancreas and delving into other organ states. What I found fascinating were some data regarding the effects of incretin therapy on the lung, and in particular, some of the restrictive lung disorders.

Dr. Kim, you attended these sessions as well. Can you tell us a little bit more about the results that were discussed? 

Dr. Kim: This is an interesting field. The moderator of the session went up and said that there has been no time in any previous ADA sessions where the lung issue was actually discussed. This was the first time ever.

They had some of the world leaders in this field, so it was really awesome to see them. Just to paint a picture of these obese asthmatic patients, they are challenging cases because, as you know, the main therapy for any asthmatic patient is inhaled corticosteroid.

Patients who are obese have quite a bit of a steroid resistance. Therefore, they end up being on many medications that sometimes are off label, and many end up on biologics as well. Therefore, the respiratory world has been seeking therapies for these obese asthmatic patients who are likely to be steroid resistant because these people are also likely to end up on an oral steroid as well.

Dr. Jain, you know the effect of the steroids much better than I do, and it’s like a laundry list. We really don’t want our patients to be on oral steroids. 

In the past few years, GLP-1 has been studied quite extensively in the lung, especially in the world of asthma, and also in COPD. What’s really fascinating is that the GLP-1 receptors have been found to be quite abundant in the airway. Some studies show that the highest concentration of GLP-1 lies in the airway, whereas some studies have said that it’s the third most common area to find the GLP-1. 

It is not a surprise that GLP-1 is being studied in managing the airway, especially airway inflammation in asthma and COPD patients. The preliminary data have been quite encouraging. They also discussed that there are new medications coming out that seem to be incretin based, so we’ll wait to see what those studies show.

There are two current phase 3 trials being held at the moment. One is using semaglutide 2.4 mg subcutaneous and another one is using metformin to reduce the airway inflammation in these asthmatic patients and also in some COPD patients. We’ll look forward to these results.

Dr. Jain: That’s really important to note because we see that there is a high density of these receptors in the airways, and hitherto we had no idea about the overall effect. Now, we’re looking at, as you mentioned, individuals with obesity who have asthma, so there are both the restrictive and obstructive components in the lung coming into play here.

From an endocrinology perspective, I’m thinking that this could be multiple effects of the GLP-1 receptor agonists, where on one hand you’re managing the obesity and you’re working along that line, and on the other hand, it could have local anti-inflammatory effects in the lung. Hence, there could be potential improvement in the overall pulmonary function of these individuals. 

Dr. Kim: We are seeing this in primary care. Ever since I found out this information, I have started numerous patients, who are obese, asthmatic patients who do not have diabetes, on GLP-1 therapies, and their pulmonary function tests have improved significantly.

As a matter of fact, one of my personal friends is a severe asthmatic patient. She ends up being on oral steroids about three times a year. There was even one day when I saw her in one of my classes and she was dyspneic. She was short of breath. 

I introduced her to one of my colleagues who’s a respirologist and very much into the impact of the incretins and asthma, and she was started on a GLP-1 receptor agonist. She lost about 30 pounds of weight, but now she is labeled as a mild asthmatic. Her pulmonary function test is completely normal. She hasn’t touched an oral steroid for a couple of years now.

That is a huge success story and I’m seeing that even in my own clinic as well. It’s a huge win for the respiratory world.

Dr. Jain: I think from an endocrinology perspective as well, if we are initiating GLP-1 receptor agonists or medications in that class, where we use it for management of obesity, sooner or later we do hit a stage where people will plateau with their weight loss. They won’t have any additional weight loss.

We tell individuals at that time that the fact that they’re able to maintain the weight loss still means that the medication is working from the obesity perspective. For individuals who also have asthma, it would be a good point to tell them that it could still have potential effects on reducing inflammation ongoing. Hence, even though they may not be losing any additional weight, it would still be helpful to continue on these medications from a pulmonary perspective. 

Dr. Kim: Right now these pleiotropic effects of GLP-1 agents are absolutely mind-blowing. I mentioned in one of my respiratory presentations to a bunch of respirologists that diabetes is taking over the world, including the respiratory world. Well, you can imagine what their faces were like. However, they were quite impressed at that, and they were very excited with what these two phase 3 trials will show. 

Dr. Jain: I think, based on the ADA 2024 conference, GLP-1 receptor agonists continue to be the gift that keeps giving. We have the effects on diabetes, obesity, kidney function, liver protection, lungs, and Alzheimer’s. We saw some sessions about potential use in people with alcohol misuse disorder or gambling problems. Clearly, there’s a large amount of research that›s being done with these agents. 

Perhaps when you and I talk about ADA 2025, we might be able to talk about some more pleiotropic benefits outside the pancreas. Until then, please do check out our other videos from ADA 2024. Thanks for joining us again, Dr. Kim.

Dr. Kim: Thank you very much for having me.
 

Dr. Jain, clinical instructor, Department of Endocrinology, University of British Columbia, and endocrinologist, TLC Diabetes and Endocrinology, Vancouver, British Columbia, Canada, has disclosed ties with Abbott, Acerus, AstraZeneca, Amgen, Bausch Healthcare, Bayer, Boehringer Ingelheim, Care to Know, CCRN, Connected in Motion, CPD Network, Dexcom, Diabetes Canada, Eli Lilly, GSK, HLS Therapeutics, Janssen, Master Clinician Alliance, MDBriefcase, Merck, Medtronic, Moderna, Novartis, Novo Nordisk, Partners in Progressive Medical Education, Pfizer, Sanofi Aventis, Timed Right, WebMD, Gilead Sciences, Insulet, PocketPills, Roche, and Takeda. Dr. Kim, clinical assistant professor, Department of Family Medicine, University of Calgary, Alberta, has disclosed ties with Abbott, AbbVie, AstraZeneca, Bayer, Boehringer Ingelheim, Eisai, Embecta, Eli Lilly, GSK, Janssen, Linpharma, Novo Nordisk, Miravo, Otsuka, Pfizer, Teva, Takeda, and Sanofi, and Partners in Progressive Medical Education.
 

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

This transcript has been edited for clarity.

Akshay B. Jain, MD: Welcome back to Medscape at ADA 2024, where Dr. James Kim, primary care physician from Calgary, Alberta, will be joining me in deciphering the key highlights at the ADA conference and bringing our own clinical twist into what the relevance would be for people like you and I to take back to our clinics.

Welcome back, Dr. Kim. 

James Kim, MBBCh, PgDip, MScCH: Thank you very much. It’s nice to be back. 

Dr. Jain: This was a diabetes conference, so obviously we are very pancreas focused. At this conference, we went outside our general area of territory, going outside of the pancreas and delving into other organ states. What I found fascinating were some data regarding the effects of incretin therapy on the lung, and in particular, some of the restrictive lung disorders.

Dr. Kim, you attended these sessions as well. Can you tell us a little bit more about the results that were discussed? 

Dr. Kim: This is an interesting field. The moderator of the session went up and said that there has been no time in any previous ADA sessions where the lung issue was actually discussed. This was the first time ever.

They had some of the world leaders in this field, so it was really awesome to see them. Just to paint a picture of these obese asthmatic patients, they are challenging cases because, as you know, the main therapy for any asthmatic patient is inhaled corticosteroid.

Patients who are obese have quite a bit of a steroid resistance. Therefore, they end up being on many medications that sometimes are off label, and many end up on biologics as well. Therefore, the respiratory world has been seeking therapies for these obese asthmatic patients who are likely to be steroid resistant because these people are also likely to end up on an oral steroid as well.

Dr. Jain, you know the effect of the steroids much better than I do, and it’s like a laundry list. We really don’t want our patients to be on oral steroids. 

In the past few years, GLP-1 has been studied quite extensively in the lung, especially in the world of asthma, and also in COPD. What’s really fascinating is that the GLP-1 receptors have been found to be quite abundant in the airway. Some studies show that the highest concentration of GLP-1 lies in the airway, whereas some studies have said that it’s the third most common area to find the GLP-1. 

It is not a surprise that GLP-1 is being studied in managing the airway, especially airway inflammation in asthma and COPD patients. The preliminary data have been quite encouraging. They also discussed that there are new medications coming out that seem to be incretin based, so we’ll wait to see what those studies show.

There are two current phase 3 trials being held at the moment. One is using semaglutide 2.4 mg subcutaneous and another one is using metformin to reduce the airway inflammation in these asthmatic patients and also in some COPD patients. We’ll look forward to these results.

Dr. Jain: That’s really important to note because we see that there is a high density of these receptors in the airways, and hitherto we had no idea about the overall effect. Now, we’re looking at, as you mentioned, individuals with obesity who have asthma, so there are both the restrictive and obstructive components in the lung coming into play here.

From an endocrinology perspective, I’m thinking that this could be multiple effects of the GLP-1 receptor agonists, where on one hand you’re managing the obesity and you’re working along that line, and on the other hand, it could have local anti-inflammatory effects in the lung. Hence, there could be potential improvement in the overall pulmonary function of these individuals. 

Dr. Kim: We are seeing this in primary care. Ever since I found out this information, I have started numerous patients, who are obese, asthmatic patients who do not have diabetes, on GLP-1 therapies, and their pulmonary function tests have improved significantly.

As a matter of fact, one of my personal friends is a severe asthmatic patient. She ends up being on oral steroids about three times a year. There was even one day when I saw her in one of my classes and she was dyspneic. She was short of breath. 

I introduced her to one of my colleagues who’s a respirologist and very much into the impact of the incretins and asthma, and she was started on a GLP-1 receptor agonist. She lost about 30 pounds of weight, but now she is labeled as a mild asthmatic. Her pulmonary function test is completely normal. She hasn’t touched an oral steroid for a couple of years now.

That is a huge success story and I’m seeing that even in my own clinic as well. It’s a huge win for the respiratory world.

Dr. Jain: I think from an endocrinology perspective as well, if we are initiating GLP-1 receptor agonists or medications in that class, where we use it for management of obesity, sooner or later we do hit a stage where people will plateau with their weight loss. They won’t have any additional weight loss.

We tell individuals at that time that the fact that they’re able to maintain the weight loss still means that the medication is working from the obesity perspective. For individuals who also have asthma, it would be a good point to tell them that it could still have potential effects on reducing inflammation ongoing. Hence, even though they may not be losing any additional weight, it would still be helpful to continue on these medications from a pulmonary perspective. 

Dr. Kim: Right now these pleiotropic effects of GLP-1 agents are absolutely mind-blowing. I mentioned in one of my respiratory presentations to a bunch of respirologists that diabetes is taking over the world, including the respiratory world. Well, you can imagine what their faces were like. However, they were quite impressed at that, and they were very excited with what these two phase 3 trials will show. 

Dr. Jain: I think, based on the ADA 2024 conference, GLP-1 receptor agonists continue to be the gift that keeps giving. We have the effects on diabetes, obesity, kidney function, liver protection, lungs, and Alzheimer’s. We saw some sessions about potential use in people with alcohol misuse disorder or gambling problems. Clearly, there’s a large amount of research that›s being done with these agents. 

Perhaps when you and I talk about ADA 2025, we might be able to talk about some more pleiotropic benefits outside the pancreas. Until then, please do check out our other videos from ADA 2024. Thanks for joining us again, Dr. Kim.

Dr. Kim: Thank you very much for having me.
 

Dr. Jain, clinical instructor, Department of Endocrinology, University of British Columbia, and endocrinologist, TLC Diabetes and Endocrinology, Vancouver, British Columbia, Canada, has disclosed ties with Abbott, Acerus, AstraZeneca, Amgen, Bausch Healthcare, Bayer, Boehringer Ingelheim, Care to Know, CCRN, Connected in Motion, CPD Network, Dexcom, Diabetes Canada, Eli Lilly, GSK, HLS Therapeutics, Janssen, Master Clinician Alliance, MDBriefcase, Merck, Medtronic, Moderna, Novartis, Novo Nordisk, Partners in Progressive Medical Education, Pfizer, Sanofi Aventis, Timed Right, WebMD, Gilead Sciences, Insulet, PocketPills, Roche, and Takeda. Dr. Kim, clinical assistant professor, Department of Family Medicine, University of Calgary, Alberta, has disclosed ties with Abbott, AbbVie, AstraZeneca, Bayer, Boehringer Ingelheim, Eisai, Embecta, Eli Lilly, GSK, Janssen, Linpharma, Novo Nordisk, Miravo, Otsuka, Pfizer, Teva, Takeda, and Sanofi, and Partners in Progressive Medical Education.
 

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

Childhood cancers represent a diverse group of neoplasms, and thanks to advances in treatment, survival rates have improved significantly. Today, more than 80%-85% of children diagnosed with cancer in developed countries survive into adulthood.

This increase in survival has brought new challenges, however. Compared with the general population, childhood cancer survivors (CCS) are at a notably higher risk for early mortality, developing secondary cancers, and experiencing various long-term clinical and psychosocial issues stemming from their disease or its treatment.

Long-term follow-up care for CCS is a complex and evolving field. Despite ongoing efforts to establish global and national guidelines, current evidence indicates that the care and management of these patients remain suboptimal.

Sexual dysfunction is a common and significant late effect among CCS. The disruptions caused by cancer and its treatment can interfere with normal physiological and psychological development, leading to issues with sexual function. This aspect of health is critical as it influences not just physical well-being but also psychosocial, developmental, and emotional health.
 

Characteristics and Mechanisms

Sexual functioning encompasses the physiological and psychological aspects of sexual behavior, including desire, arousal, orgasm, sexual pleasure, and overall satisfaction.

As CCS reach adolescence or adulthood, they often face sexual and reproductive issues, particularly as they enter romantic relationships.

Sexual functioning is a complex process that relies on the interaction of various factors, including physiological health, psychosexual development, romantic relationships, body image, and desire.

Despite its importance, the impact of childhood cancer on sexual function is often overlooked, even though cancer and its treatments can have lifelong effects. 
 

Sexual Function in CCS

A recent review aimed to summarize the existing research on sexual function among CCS, highlighting assessment tools, key stages of psychosexual development, common sexual problems, and the prevalence of sexual dysfunction.

The review study included 22 studies published between 2000 and 2022, comprising two qualitative, six cohort, and 14 cross-sectional studies.

Most CCS reached all key stages of psychosexual development at an average age of 29.8 years. Although some milestones were achieved later than is typical, many survivors felt they reached these stages at the appropriate time. Sexual initiation was less common among those who had undergone intensive neurotoxic treatments, such as those diagnosed with brain tumors or leukemia in childhood.

In a cross-sectional study of CCS aged 17-39 years, about one third had never engaged in sexual intercourse, 41.4% reported never experiencing sexual attraction, 44.8% were dissatisfied with their sex lives, and many rarely felt sexually attractive to others. Another study found that common issues among CCS included a lack of interest in sex (30%), difficulty enjoying sex (24%), and difficulty becoming aroused (23%). However, comparing and analyzing these problems was challenging due to the lack of standardized assessment criteria.

The prevalence of sexual dysfunction among CCS ranged from 12.3% to 46.5%. For males, the prevalence ranged from 12.3% to 54.0%, while for females, it ranged from 19.9% to 57.0%.
 

Factors Influencing Sexual Function

The review identified the following four categories of factors influencing sexual function in CCS: Demographic, treatment-related, psychological, and physiological.

Demographic factors: Gender, age, education level, relationship status, income level, and race all play roles in sexual function.

Female survivors reported more severe sexual dysfunction and poorer sexual health than did male survivors. Age at cancer diagnosis, age at evaluation, and the time since diagnosis were closely linked to sexual experiences. Patients diagnosed with cancer during childhood tended to report better sexual function than those diagnosed during adolescence.

Treatment-related factors: The type of cancer and intensity of treatment, along with surgical history, were significant factors. Surgeries involving the spinal cord or sympathetic nerves, as well as a history of prostate or pelvic surgery, were strongly associated with erectile dysfunction in men. In women, pelvic surgeries and treatments to the pelvic area were commonly linked to sexual dysfunction.

The association between treatment intensity and sexual function was noted across several studies, although the results were not always consistent. For example, testicular radiation above 10 Gy was positively correlated with sexual dysfunction. Women who underwent more intensive treatments were more likely to report issues in multiple areas of sexual function, while men in this group were less likely to have children.

Among female CCS, certain types of cancer, such as germ cell tumors, renal tumors, and leukemia, present a higher risk for sexual dysfunction. Women who had CNS tumors in childhood frequently reported problems like difficulty in sexual arousal, low sexual satisfaction, infrequent sexual activity, and fewer sexual partners, compared with survivors of other cancers. Survivors of acute lymphoblastic leukemia and those who underwent hematopoietic stem cell transplantation (HSCT) also showed varying degrees of impaired sexual function, compared with the general population. The HSCT group showed significant testicular damage, including reduced testicular volumes, low testosterone levels, and low sperm counts.

Psychological factors: These factors, such as emotional distress, play a significant role in sexual dysfunction among CCS. Symptoms like anxiety, nervousness during sexual activity, and depression are commonly reported by those with sexual dysfunction. The connection between body image and sexual function is complex. Many CCS with sexual dysfunction express concern about how others, particularly their partners, perceived their altered body image due to cancer and its treatment.

Physiological factors: In male CCS, low serum testosterone levels and low lean muscle mass are linked to an increased risk for sexual dysfunction. Treatments involving alkylating agents or testicular radiation, and surgery or radiotherapy targeting the genitourinary organs or the hypothalamic-pituitary region, can lead to various physiological and endocrine disorders, contributing to sexual dysfunction. Despite these risks, there is a lack of research evaluating sexual function through the lens of the hypothalamic-pituitary-gonadal axis and neuroendocrine pathways.
 

This story was translated from Univadis Italy 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.

Childhood cancers represent a diverse group of neoplasms, and thanks to advances in treatment, survival rates have improved significantly. Today, more than 80%-85% of children diagnosed with cancer in developed countries survive into adulthood.

This increase in survival has brought new challenges, however. Compared with the general population, childhood cancer survivors (CCS) are at a notably higher risk for early mortality, developing secondary cancers, and experiencing various long-term clinical and psychosocial issues stemming from their disease or its treatment.

Long-term follow-up care for CCS is a complex and evolving field. Despite ongoing efforts to establish global and national guidelines, current evidence indicates that the care and management of these patients remain suboptimal.

Sexual dysfunction is a common and significant late effect among CCS. The disruptions caused by cancer and its treatment can interfere with normal physiological and psychological development, leading to issues with sexual function. This aspect of health is critical as it influences not just physical well-being but also psychosocial, developmental, and emotional health.
 

Characteristics and Mechanisms

Sexual functioning encompasses the physiological and psychological aspects of sexual behavior, including desire, arousal, orgasm, sexual pleasure, and overall satisfaction.

As CCS reach adolescence or adulthood, they often face sexual and reproductive issues, particularly as they enter romantic relationships.

Sexual functioning is a complex process that relies on the interaction of various factors, including physiological health, psychosexual development, romantic relationships, body image, and desire.

Despite its importance, the impact of childhood cancer on sexual function is often overlooked, even though cancer and its treatments can have lifelong effects. 
 

Sexual Function in CCS

A recent review aimed to summarize the existing research on sexual function among CCS, highlighting assessment tools, key stages of psychosexual development, common sexual problems, and the prevalence of sexual dysfunction.

The review study included 22 studies published between 2000 and 2022, comprising two qualitative, six cohort, and 14 cross-sectional studies.

Most CCS reached all key stages of psychosexual development at an average age of 29.8 years. Although some milestones were achieved later than is typical, many survivors felt they reached these stages at the appropriate time. Sexual initiation was less common among those who had undergone intensive neurotoxic treatments, such as those diagnosed with brain tumors or leukemia in childhood.

In a cross-sectional study of CCS aged 17-39 years, about one third had never engaged in sexual intercourse, 41.4% reported never experiencing sexual attraction, 44.8% were dissatisfied with their sex lives, and many rarely felt sexually attractive to others. Another study found that common issues among CCS included a lack of interest in sex (30%), difficulty enjoying sex (24%), and difficulty becoming aroused (23%). However, comparing and analyzing these problems was challenging due to the lack of standardized assessment criteria.

The prevalence of sexual dysfunction among CCS ranged from 12.3% to 46.5%. For males, the prevalence ranged from 12.3% to 54.0%, while for females, it ranged from 19.9% to 57.0%.
 

Factors Influencing Sexual Function

The review identified the following four categories of factors influencing sexual function in CCS: Demographic, treatment-related, psychological, and physiological.

Demographic factors: Gender, age, education level, relationship status, income level, and race all play roles in sexual function.

Female survivors reported more severe sexual dysfunction and poorer sexual health than did male survivors. Age at cancer diagnosis, age at evaluation, and the time since diagnosis were closely linked to sexual experiences. Patients diagnosed with cancer during childhood tended to report better sexual function than those diagnosed during adolescence.

Treatment-related factors: The type of cancer and intensity of treatment, along with surgical history, were significant factors. Surgeries involving the spinal cord or sympathetic nerves, as well as a history of prostate or pelvic surgery, were strongly associated with erectile dysfunction in men. In women, pelvic surgeries and treatments to the pelvic area were commonly linked to sexual dysfunction.

The association between treatment intensity and sexual function was noted across several studies, although the results were not always consistent. For example, testicular radiation above 10 Gy was positively correlated with sexual dysfunction. Women who underwent more intensive treatments were more likely to report issues in multiple areas of sexual function, while men in this group were less likely to have children.

Among female CCS, certain types of cancer, such as germ cell tumors, renal tumors, and leukemia, present a higher risk for sexual dysfunction. Women who had CNS tumors in childhood frequently reported problems like difficulty in sexual arousal, low sexual satisfaction, infrequent sexual activity, and fewer sexual partners, compared with survivors of other cancers. Survivors of acute lymphoblastic leukemia and those who underwent hematopoietic stem cell transplantation (HSCT) also showed varying degrees of impaired sexual function, compared with the general population. The HSCT group showed significant testicular damage, including reduced testicular volumes, low testosterone levels, and low sperm counts.

Psychological factors: These factors, such as emotional distress, play a significant role in sexual dysfunction among CCS. Symptoms like anxiety, nervousness during sexual activity, and depression are commonly reported by those with sexual dysfunction. The connection between body image and sexual function is complex. Many CCS with sexual dysfunction express concern about how others, particularly their partners, perceived their altered body image due to cancer and its treatment.

Physiological factors: In male CCS, low serum testosterone levels and low lean muscle mass are linked to an increased risk for sexual dysfunction. Treatments involving alkylating agents or testicular radiation, and surgery or radiotherapy targeting the genitourinary organs or the hypothalamic-pituitary region, can lead to various physiological and endocrine disorders, contributing to sexual dysfunction. Despite these risks, there is a lack of research evaluating sexual function through the lens of the hypothalamic-pituitary-gonadal axis and neuroendocrine pathways.
 

This story was translated from Univadis Italy 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.

Childhood cancers represent a diverse group of neoplasms, and thanks to advances in treatment, survival rates have improved significantly. Today, more than 80%-85% of children diagnosed with cancer in developed countries survive into adulthood.

This increase in survival has brought new challenges, however. Compared with the general population, childhood cancer survivors (CCS) are at a notably higher risk for early mortality, developing secondary cancers, and experiencing various long-term clinical and psychosocial issues stemming from their disease or its treatment.

Long-term follow-up care for CCS is a complex and evolving field. Despite ongoing efforts to establish global and national guidelines, current evidence indicates that the care and management of these patients remain suboptimal.

Sexual dysfunction is a common and significant late effect among CCS. The disruptions caused by cancer and its treatment can interfere with normal physiological and psychological development, leading to issues with sexual function. This aspect of health is critical as it influences not just physical well-being but also psychosocial, developmental, and emotional health.
 

Characteristics and Mechanisms

Sexual functioning encompasses the physiological and psychological aspects of sexual behavior, including desire, arousal, orgasm, sexual pleasure, and overall satisfaction.

As CCS reach adolescence or adulthood, they often face sexual and reproductive issues, particularly as they enter romantic relationships.

Sexual functioning is a complex process that relies on the interaction of various factors, including physiological health, psychosexual development, romantic relationships, body image, and desire.

Despite its importance, the impact of childhood cancer on sexual function is often overlooked, even though cancer and its treatments can have lifelong effects. 
 

Sexual Function in CCS

A recent review aimed to summarize the existing research on sexual function among CCS, highlighting assessment tools, key stages of psychosexual development, common sexual problems, and the prevalence of sexual dysfunction.

The review study included 22 studies published between 2000 and 2022, comprising two qualitative, six cohort, and 14 cross-sectional studies.

Most CCS reached all key stages of psychosexual development at an average age of 29.8 years. Although some milestones were achieved later than is typical, many survivors felt they reached these stages at the appropriate time. Sexual initiation was less common among those who had undergone intensive neurotoxic treatments, such as those diagnosed with brain tumors or leukemia in childhood.

In a cross-sectional study of CCS aged 17-39 years, about one third had never engaged in sexual intercourse, 41.4% reported never experiencing sexual attraction, 44.8% were dissatisfied with their sex lives, and many rarely felt sexually attractive to others. Another study found that common issues among CCS included a lack of interest in sex (30%), difficulty enjoying sex (24%), and difficulty becoming aroused (23%). However, comparing and analyzing these problems was challenging due to the lack of standardized assessment criteria.

The prevalence of sexual dysfunction among CCS ranged from 12.3% to 46.5%. For males, the prevalence ranged from 12.3% to 54.0%, while for females, it ranged from 19.9% to 57.0%.
 

Factors Influencing Sexual Function

The review identified the following four categories of factors influencing sexual function in CCS: Demographic, treatment-related, psychological, and physiological.

Demographic factors: Gender, age, education level, relationship status, income level, and race all play roles in sexual function.

Female survivors reported more severe sexual dysfunction and poorer sexual health than did male survivors. Age at cancer diagnosis, age at evaluation, and the time since diagnosis were closely linked to sexual experiences. Patients diagnosed with cancer during childhood tended to report better sexual function than those diagnosed during adolescence.

Treatment-related factors: The type of cancer and intensity of treatment, along with surgical history, were significant factors. Surgeries involving the spinal cord or sympathetic nerves, as well as a history of prostate or pelvic surgery, were strongly associated with erectile dysfunction in men. In women, pelvic surgeries and treatments to the pelvic area were commonly linked to sexual dysfunction.

The association between treatment intensity and sexual function was noted across several studies, although the results were not always consistent. For example, testicular radiation above 10 Gy was positively correlated with sexual dysfunction. Women who underwent more intensive treatments were more likely to report issues in multiple areas of sexual function, while men in this group were less likely to have children.

Among female CCS, certain types of cancer, such as germ cell tumors, renal tumors, and leukemia, present a higher risk for sexual dysfunction. Women who had CNS tumors in childhood frequently reported problems like difficulty in sexual arousal, low sexual satisfaction, infrequent sexual activity, and fewer sexual partners, compared with survivors of other cancers. Survivors of acute lymphoblastic leukemia and those who underwent hematopoietic stem cell transplantation (HSCT) also showed varying degrees of impaired sexual function, compared with the general population. The HSCT group showed significant testicular damage, including reduced testicular volumes, low testosterone levels, and low sperm counts.

Psychological factors: These factors, such as emotional distress, play a significant role in sexual dysfunction among CCS. Symptoms like anxiety, nervousness during sexual activity, and depression are commonly reported by those with sexual dysfunction. The connection between body image and sexual function is complex. Many CCS with sexual dysfunction express concern about how others, particularly their partners, perceived their altered body image due to cancer and its treatment.

Physiological factors: In male CCS, low serum testosterone levels and low lean muscle mass are linked to an increased risk for sexual dysfunction. Treatments involving alkylating agents or testicular radiation, and surgery or radiotherapy targeting the genitourinary organs or the hypothalamic-pituitary region, can lead to various physiological and endocrine disorders, contributing to sexual dysfunction. Despite these risks, there is a lack of research evaluating sexual function through the lens of the hypothalamic-pituitary-gonadal axis and neuroendocrine pathways.
 

This story was translated from Univadis Italy 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.

A new “best practices” guide released by the Alliance for Pharmacy Compounding (APC) aims to educate compounding pharmacists and reassure prescribers about the ethical, legal, and practical considerations that must be addressed to ensure quality standards and protect patients’ health.

Endocrinologists have expressed skepticism about the quality of compounded drugs, particularly the popular glucagon-like peptide 1 (GLP-1) semaglutide. The Food and Drug Administration (FDA) recently issued an alert linking hospitalizations to overdoses of compounded semaglutide.

“This document goes beyond today’s media-grabbing shortages,” APC Board Chair-Elect Gina Besteman, RPh, of Belmar Pharma Solutions told this news organization. “We developed these best practices to apply to all shortage drug compounding, and especially in this moment when so many are compounding GLP-1s. These serve as a reminder about what compliance and care look like.”

Prescribers determine whether a patient needs a compounded medication, not pharmacists, Ms. Besteman noted. “A patient-specific prescription order must be authorized for a compounded medication to be dispensed. Prescribers should ensure pharmacies they work with regularly check the FDA Drug Shortage List, as compounding of ‘essential copies’ of FDA-approved drugs is only allowed when a drug is listed as ‘currently in shortage.’ ”
 

Framework for Compounding

“With fake and illegal online stores popping up, it’s critical for legitimate, state-licensed compounding pharmacies to maintain the profession’s high standards,” the APC said in a media communication.

Highlights of its best practices, which are directed toward 503A state-licensed compounding pharmacies, include the following, among others:

• Pharmacies should check the FDA drug shortage list prior to preparing a copy of an FDA-approved drug and maintain documentation to demonstrate to regulators that the drug was in shortage at the time it was compounded.
• Pharmacies may only source active pharmaceutical ingredients (APIs) from state-licensed wholesalers who purchase from FDA-registered manufacturers or order directly from FDA-registered manufacturers.
• Verify from the wholesaler that the manufacturer is registered with the FDA and the API meets all the requirements of section 503A, and that both hold the appropriate permits or licenses in their home state and the shipped to state.
• Adhere to USP Chapter <797> testing requirements for sterility, endotoxin, stability, particulate, antimicrobial effectiveness, and container closure integrity studies.
• Counseling must be offered to the patient or the patient’s agent/caregiver. Providing written information that assists in the understanding of how to properly use the compounded medication is advised.
• Instructions should be written in a way that a layperson can understand (especially directions including dosage titrations and conversions between milligrams and milliliters or units).
• Like all medications, compounded drugs can only be prescribed in the presence of a valid patient-practitioner relationship and can only be dispensed by a pharmacy after receipt of a valid patient-specific prescription order.
• When marketing, never make claims of safety or efficacy of the compounded product.
• Advertising that patients will/may save money using compounded medications, compared with manufactured products is not allowed.

“Compounding FDA-approved drugs during shortages is nothing new — pharmacies have been doing it well before GLP-1s came on the scene, and they’ll continue long after this current shortage ends,” Ms. Besteman said. “Prescribers should be aware of APC’s guidelines because they provide a framework for ethically and legally compounding medications during drug shortages.

“To paraphrase The Police,” she concluded, “every move you make, every step you take, they’ll be watching you. Make sure they see those best practices in action.”
 

‘Reduces the Risks’

Commenting on the best practices guidance, Ivania Rizo, MD, director of Obesity Medicine and Diabetes and clinical colead at Boston Medical Center’s Health Equity Accelerator in Massachusetts, said: “These best practices will hopefully make a difference in the quality of compounded drugs.”

“The emphasis on rigorous testing of APIs and adherence to USP standards is particularly important for maintaining drug quality,” she noted. “This structured approach reduces the risk of variability and ensures that compounded drugs meet high-quality standards, thus enhancing their reliability.”

“Knowing that compounding pharmacies are adhering to rigorous standards for sourcing, testing, and compounding can at least reassure clinicians that specific steps are being taken for the safety and efficacy of these medications,” she said. “The transparency in documenting compliance with FDA guidelines and maintaining high-quality control measures can enhance trust among healthcare providers.”

Although clinicians are likely to have more confidence in compounded drugs when these best practices are followed, she said, “overall, we all hope that the shortages of medications such as tirzepatide are resolved promptly, allowing patients to access FDA-approved drugs without the need for compounding.”

“While the implementation of best practices for compounding during shortages is a positive and necessary step, our ultimate goal remains to address and resolve these shortages in the near future,” she concluded.

Dr. Rizo declared no competing interests.

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

A new “best practices” guide released by the Alliance for Pharmacy Compounding (APC) aims to educate compounding pharmacists and reassure prescribers about the ethical, legal, and practical considerations that must be addressed to ensure quality standards and protect patients’ health.

Endocrinologists have expressed skepticism about the quality of compounded drugs, particularly the popular glucagon-like peptide 1 (GLP-1) semaglutide. The Food and Drug Administration (FDA) recently issued an alert linking hospitalizations to overdoses of compounded semaglutide.

“This document goes beyond today’s media-grabbing shortages,” APC Board Chair-Elect Gina Besteman, RPh, of Belmar Pharma Solutions told this news organization. “We developed these best practices to apply to all shortage drug compounding, and especially in this moment when so many are compounding GLP-1s. These serve as a reminder about what compliance and care look like.”

Prescribers determine whether a patient needs a compounded medication, not pharmacists, Ms. Besteman noted. “A patient-specific prescription order must be authorized for a compounded medication to be dispensed. Prescribers should ensure pharmacies they work with regularly check the FDA Drug Shortage List, as compounding of ‘essential copies’ of FDA-approved drugs is only allowed when a drug is listed as ‘currently in shortage.’ ”
 

Framework for Compounding

“With fake and illegal online stores popping up, it’s critical for legitimate, state-licensed compounding pharmacies to maintain the profession’s high standards,” the APC said in a media communication.

Highlights of its best practices, which are directed toward 503A state-licensed compounding pharmacies, include the following, among others:

• Pharmacies should check the FDA drug shortage list prior to preparing a copy of an FDA-approved drug and maintain documentation to demonstrate to regulators that the drug was in shortage at the time it was compounded.
• Pharmacies may only source active pharmaceutical ingredients (APIs) from state-licensed wholesalers who purchase from FDA-registered manufacturers or order directly from FDA-registered manufacturers.
• Verify from the wholesaler that the manufacturer is registered with the FDA and the API meets all the requirements of section 503A, and that both hold the appropriate permits or licenses in their home state and the shipped to state.
• Adhere to USP Chapter <797> testing requirements for sterility, endotoxin, stability, particulate, antimicrobial effectiveness, and container closure integrity studies.
• Counseling must be offered to the patient or the patient’s agent/caregiver. Providing written information that assists in the understanding of how to properly use the compounded medication is advised.
• Instructions should be written in a way that a layperson can understand (especially directions including dosage titrations and conversions between milligrams and milliliters or units).
• Like all medications, compounded drugs can only be prescribed in the presence of a valid patient-practitioner relationship and can only be dispensed by a pharmacy after receipt of a valid patient-specific prescription order.
• When marketing, never make claims of safety or efficacy of the compounded product.
• Advertising that patients will/may save money using compounded medications, compared with manufactured products is not allowed.

“Compounding FDA-approved drugs during shortages is nothing new — pharmacies have been doing it well before GLP-1s came on the scene, and they’ll continue long after this current shortage ends,” Ms. Besteman said. “Prescribers should be aware of APC’s guidelines because they provide a framework for ethically and legally compounding medications during drug shortages.

“To paraphrase The Police,” she concluded, “every move you make, every step you take, they’ll be watching you. Make sure they see those best practices in action.”
 

‘Reduces the Risks’

Commenting on the best practices guidance, Ivania Rizo, MD, director of Obesity Medicine and Diabetes and clinical colead at Boston Medical Center’s Health Equity Accelerator in Massachusetts, said: “These best practices will hopefully make a difference in the quality of compounded drugs.”

“The emphasis on rigorous testing of APIs and adherence to USP standards is particularly important for maintaining drug quality,” she noted. “This structured approach reduces the risk of variability and ensures that compounded drugs meet high-quality standards, thus enhancing their reliability.”

“Knowing that compounding pharmacies are adhering to rigorous standards for sourcing, testing, and compounding can at least reassure clinicians that specific steps are being taken for the safety and efficacy of these medications,” she said. “The transparency in documenting compliance with FDA guidelines and maintaining high-quality control measures can enhance trust among healthcare providers.”

Although clinicians are likely to have more confidence in compounded drugs when these best practices are followed, she said, “overall, we all hope that the shortages of medications such as tirzepatide are resolved promptly, allowing patients to access FDA-approved drugs without the need for compounding.”

“While the implementation of best practices for compounding during shortages is a positive and necessary step, our ultimate goal remains to address and resolve these shortages in the near future,” she concluded.

Dr. Rizo declared no competing interests.

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

A new “best practices” guide released by the Alliance for Pharmacy Compounding (APC) aims to educate compounding pharmacists and reassure prescribers about the ethical, legal, and practical considerations that must be addressed to ensure quality standards and protect patients’ health.

Endocrinologists have expressed skepticism about the quality of compounded drugs, particularly the popular glucagon-like peptide 1 (GLP-1) semaglutide. The Food and Drug Administration (FDA) recently issued an alert linking hospitalizations to overdoses of compounded semaglutide.

“This document goes beyond today’s media-grabbing shortages,” APC Board Chair-Elect Gina Besteman, RPh, of Belmar Pharma Solutions told this news organization. “We developed these best practices to apply to all shortage drug compounding, and especially in this moment when so many are compounding GLP-1s. These serve as a reminder about what compliance and care look like.”

Prescribers determine whether a patient needs a compounded medication, not pharmacists, Ms. Besteman noted. “A patient-specific prescription order must be authorized for a compounded medication to be dispensed. Prescribers should ensure pharmacies they work with regularly check the FDA Drug Shortage List, as compounding of ‘essential copies’ of FDA-approved drugs is only allowed when a drug is listed as ‘currently in shortage.’ ”
 

Framework for Compounding

“With fake and illegal online stores popping up, it’s critical for legitimate, state-licensed compounding pharmacies to maintain the profession’s high standards,” the APC said in a media communication.

Highlights of its best practices, which are directed toward 503A state-licensed compounding pharmacies, include the following, among others:

• Pharmacies should check the FDA drug shortage list prior to preparing a copy of an FDA-approved drug and maintain documentation to demonstrate to regulators that the drug was in shortage at the time it was compounded.
• Pharmacies may only source active pharmaceutical ingredients (APIs) from state-licensed wholesalers who purchase from FDA-registered manufacturers or order directly from FDA-registered manufacturers.
• Verify from the wholesaler that the manufacturer is registered with the FDA and the API meets all the requirements of section 503A, and that both hold the appropriate permits or licenses in their home state and the shipped to state.
• Adhere to USP Chapter <797> testing requirements for sterility, endotoxin, stability, particulate, antimicrobial effectiveness, and container closure integrity studies.
• Counseling must be offered to the patient or the patient’s agent/caregiver. Providing written information that assists in the understanding of how to properly use the compounded medication is advised.
• Instructions should be written in a way that a layperson can understand (especially directions including dosage titrations and conversions between milligrams and milliliters or units).
• Like all medications, compounded drugs can only be prescribed in the presence of a valid patient-practitioner relationship and can only be dispensed by a pharmacy after receipt of a valid patient-specific prescription order.
• When marketing, never make claims of safety or efficacy of the compounded product.
• Advertising that patients will/may save money using compounded medications, compared with manufactured products is not allowed.

“Compounding FDA-approved drugs during shortages is nothing new — pharmacies have been doing it well before GLP-1s came on the scene, and they’ll continue long after this current shortage ends,” Ms. Besteman said. “Prescribers should be aware of APC’s guidelines because they provide a framework for ethically and legally compounding medications during drug shortages.

“To paraphrase The Police,” she concluded, “every move you make, every step you take, they’ll be watching you. Make sure they see those best practices in action.”
 

‘Reduces the Risks’

Commenting on the best practices guidance, Ivania Rizo, MD, director of Obesity Medicine and Diabetes and clinical colead at Boston Medical Center’s Health Equity Accelerator in Massachusetts, said: “These best practices will hopefully make a difference in the quality of compounded drugs.”

“The emphasis on rigorous testing of APIs and adherence to USP standards is particularly important for maintaining drug quality,” she noted. “This structured approach reduces the risk of variability and ensures that compounded drugs meet high-quality standards, thus enhancing their reliability.”

“Knowing that compounding pharmacies are adhering to rigorous standards for sourcing, testing, and compounding can at least reassure clinicians that specific steps are being taken for the safety and efficacy of these medications,” she said. “The transparency in documenting compliance with FDA guidelines and maintaining high-quality control measures can enhance trust among healthcare providers.”

Although clinicians are likely to have more confidence in compounded drugs when these best practices are followed, she said, “overall, we all hope that the shortages of medications such as tirzepatide are resolved promptly, allowing patients to access FDA-approved drugs without the need for compounding.”

“While the implementation of best practices for compounding during shortages is a positive and necessary step, our ultimate goal remains to address and resolve these shortages in the near future,” she concluded.

Dr. Rizo declared no competing interests.

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

Edema in the feet and legs is a common complaint in our practices. It can cause pain, weakness, heaviness, discomfort, limited movement, and a negative body image. Medications can contribute to edema, either alone or in combination with other health issues.

Edema is also associated with advanced age, female sex, obesity, diabetes, hypertension, pain, lack of physical activity, and mobility limitations. These factors often necessitate medication prescriptions, which can aggravate the problem. Therefore, it is important to know how to treat or prevent medication-induced edema.

There are four main causes of edema, and all can facilitate medication-induced edema.

• Increased capillary pressure. Conditions such as heart failure, renal dysfunction, venous insufficiency, deep vein thrombosis, and cirrhosis can increase capillary pressure, leading to edema.
• Decreased oncotic pressure. Hypoalbuminemia, a primary cause of reduced colloid oncotic pressure, can result from nephrotic syndrome, diabetic nephropathy, lupus nephropathy, amyloidosis, nephropathies, cirrhosis, chronic liver disease, and malabsorption or malnutrition.
• Increased capillary permeability. Vascular injury, often associated with diabetes, can increase capillary permeability and contribute to edema.
• Impaired lymphatic drainage. Lymphatic obstruction is common in patients with lymphedema, tumors, inflammation, fibrosis, certain infections, surgery, and congenital anomalies. Conditions such as thyroid disorders can also cause an increase in interstitial albumin and other proteins without a corresponding increase in lymphatic flow, leading to lymphedema.

Medications That Can Cause Edema

• Calcium channel blockers (CCBs). Drugs such as nifedipine and amlodipine can increase hydrostatic pressure by causing selective vasodilation of precapillary vessels, leading to increased intracapillary pressures. Newer lipophilic CCBs (eg, levamlodipine) exhibit lower rates of edema. Reducing the dose is often effective. Diuretics are not very effective for vasodilation-induced edema. Combining CCBs with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), which induce postcapillary dilation and normalize intracapillary pressure, may reduce fluid leakage into the interstitial space. This combination may be more beneficial than high-dose CCB monotherapy.
• Thiazolidinedione (eg, pioglitazone). These increase vascular permeability and hydrostatic pressure. They work by stimulating the peroxisome proliferator–activated gamma receptor, increasing vascular endothelial permeability, vascular endothelial growth factor secretion, and renal retention of sodium and fluids. Because of other adverse effects, their use is now limited.
• Agents for neuropathic pain (gabapentin and pregabalin). These drugs can induce selective vasodilation of arterioles through a mechanism similar to that of CCBs, causing increased intracapillary pressures. Edema usually begins within the first month of treatment or dose increase and often regresses after dose reduction or drug discontinuation.
• Antiparkinsonian dopamine agonists. These increase hydrostatic pressure by reducing sympathetic tone and dilating arterioles through alpha-2 adrenergic receptor activity.
• New antipsychotics. Drugs like clozapine, iloperidone, lurasidone, olanzapine, quetiapine, risperidone, and ziprasidone can increase hydrostatic pressure through antagonistic effects on alpha-1 adrenergic receptors, causing vasodilation.
• Nitrates. These drugs increase hydrostatic pressure by causing preferential venous dilation, leading to increased venous pooling.
• Nonsteroidal anti-inflammatory drugs (NSAIDs). These drugs can increase hydrostatic pressure by inhibiting vasodilation of afferent renal arterioles, decreasing the glomerular filtration rate, and stimulating the renin-angiotensin-aldosterone system, which leads to sodium and water retention. These adverse effects warrant cautious use of these agents.
• ACE inhibitors. Drugs such as enalapril and ramipril can increase vascular permeability. They reduce the metabolism and accumulation of bradykinin, which increases vascular permeability and fluid leakage. These effects are rare and are usually related to allergic responses.
• Insulin. Insulin decreases capillary oncotic pressure and increases vascular permeability. Rapid correction of hyperglycemia can cause a loss of oncotic pressure, while chronic hyperglycemia can damage vascular membranes, increasing permeability. These effects are generally benign and can be managed with careful dose titration, sodium restriction, or diuretics.
• Steroids. Steroids with mineralocorticoid activity can increase renal sodium and water retention, leading to increased blood volume. Fludrocortisone has the highest mineralocorticoid activity, while dexamethasone and methylprednisolone have negligible activity.

Implications

Understanding how these medications cause edema is important for effective management. For example, in the case of those causing edema due to reduced oncotic pressure, like insulin, slow dose titrations can help adapt to osmolarity changes. For drugs causing edema due to increased hydrostatic pressure, diuretics are more effective in acute management.

The key takeaways from this review are:

• Awareness of drug-induced edema. Many drugs besides CCBs can cause edema.
• Combination therapy. Combining ACE inhibitors or ARBs with CCBs can prevent or reduce CCB-induced edema.
• Edema management strategies. Strategies to manage or prevent edema should include dose reductions or replacement of the problematic medication, especially in severe or refractory cases.

Dr. Wajngarten, professor of cardiology, University of São Paulo, Brazil, has disclosed no relevant financial relationships.

This story was translated from the Medscape Portuguese 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.

Edema in the feet and legs is a common complaint in our practices. It can cause pain, weakness, heaviness, discomfort, limited movement, and a negative body image. Medications can contribute to edema, either alone or in combination with other health issues.

Edema is also associated with advanced age, female sex, obesity, diabetes, hypertension, pain, lack of physical activity, and mobility limitations. These factors often necessitate medication prescriptions, which can aggravate the problem. Therefore, it is important to know how to treat or prevent medication-induced edema.

There are four main causes of edema, and all can facilitate medication-induced edema.

• Increased capillary pressure. Conditions such as heart failure, renal dysfunction, venous insufficiency, deep vein thrombosis, and cirrhosis can increase capillary pressure, leading to edema.
• Decreased oncotic pressure. Hypoalbuminemia, a primary cause of reduced colloid oncotic pressure, can result from nephrotic syndrome, diabetic nephropathy, lupus nephropathy, amyloidosis, nephropathies, cirrhosis, chronic liver disease, and malabsorption or malnutrition.
• Increased capillary permeability. Vascular injury, often associated with diabetes, can increase capillary permeability and contribute to edema.
• Impaired lymphatic drainage. Lymphatic obstruction is common in patients with lymphedema, tumors, inflammation, fibrosis, certain infections, surgery, and congenital anomalies. Conditions such as thyroid disorders can also cause an increase in interstitial albumin and other proteins without a corresponding increase in lymphatic flow, leading to lymphedema.

Medications That Can Cause Edema

• Calcium channel blockers (CCBs). Drugs such as nifedipine and amlodipine can increase hydrostatic pressure by causing selective vasodilation of precapillary vessels, leading to increased intracapillary pressures. Newer lipophilic CCBs (eg, levamlodipine) exhibit lower rates of edema. Reducing the dose is often effective. Diuretics are not very effective for vasodilation-induced edema. Combining CCBs with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), which induce postcapillary dilation and normalize intracapillary pressure, may reduce fluid leakage into the interstitial space. This combination may be more beneficial than high-dose CCB monotherapy.
• Thiazolidinedione (eg, pioglitazone). These increase vascular permeability and hydrostatic pressure. They work by stimulating the peroxisome proliferator–activated gamma receptor, increasing vascular endothelial permeability, vascular endothelial growth factor secretion, and renal retention of sodium and fluids. Because of other adverse effects, their use is now limited.
• Agents for neuropathic pain (gabapentin and pregabalin). These drugs can induce selective vasodilation of arterioles through a mechanism similar to that of CCBs, causing increased intracapillary pressures. Edema usually begins within the first month of treatment or dose increase and often regresses after dose reduction or drug discontinuation.
• Antiparkinsonian dopamine agonists. These increase hydrostatic pressure by reducing sympathetic tone and dilating arterioles through alpha-2 adrenergic receptor activity.
• New antipsychotics. Drugs like clozapine, iloperidone, lurasidone, olanzapine, quetiapine, risperidone, and ziprasidone can increase hydrostatic pressure through antagonistic effects on alpha-1 adrenergic receptors, causing vasodilation.
• Nitrates. These drugs increase hydrostatic pressure by causing preferential venous dilation, leading to increased venous pooling.
• Nonsteroidal anti-inflammatory drugs (NSAIDs). These drugs can increase hydrostatic pressure by inhibiting vasodilation of afferent renal arterioles, decreasing the glomerular filtration rate, and stimulating the renin-angiotensin-aldosterone system, which leads to sodium and water retention. These adverse effects warrant cautious use of these agents.
• ACE inhibitors. Drugs such as enalapril and ramipril can increase vascular permeability. They reduce the metabolism and accumulation of bradykinin, which increases vascular permeability and fluid leakage. These effects are rare and are usually related to allergic responses.
• Insulin. Insulin decreases capillary oncotic pressure and increases vascular permeability. Rapid correction of hyperglycemia can cause a loss of oncotic pressure, while chronic hyperglycemia can damage vascular membranes, increasing permeability. These effects are generally benign and can be managed with careful dose titration, sodium restriction, or diuretics.
• Steroids. Steroids with mineralocorticoid activity can increase renal sodium and water retention, leading to increased blood volume. Fludrocortisone has the highest mineralocorticoid activity, while dexamethasone and methylprednisolone have negligible activity.

Implications

Understanding how these medications cause edema is important for effective management. For example, in the case of those causing edema due to reduced oncotic pressure, like insulin, slow dose titrations can help adapt to osmolarity changes. For drugs causing edema due to increased hydrostatic pressure, diuretics are more effective in acute management.

The key takeaways from this review are:

• Awareness of drug-induced edema. Many drugs besides CCBs can cause edema.
• Combination therapy. Combining ACE inhibitors or ARBs with CCBs can prevent or reduce CCB-induced edema.
• Edema management strategies. Strategies to manage or prevent edema should include dose reductions or replacement of the problematic medication, especially in severe or refractory cases.

Dr. Wajngarten, professor of cardiology, University of São Paulo, Brazil, has disclosed no relevant financial relationships.

This story was translated from the Medscape Portuguese 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.

Edema in the feet and legs is a common complaint in our practices. It can cause pain, weakness, heaviness, discomfort, limited movement, and a negative body image. Medications can contribute to edema, either alone or in combination with other health issues.

Edema is also associated with advanced age, female sex, obesity, diabetes, hypertension, pain, lack of physical activity, and mobility limitations. These factors often necessitate medication prescriptions, which can aggravate the problem. Therefore, it is important to know how to treat or prevent medication-induced edema.

There are four main causes of edema, and all can facilitate medication-induced edema.

• Increased capillary pressure. Conditions such as heart failure, renal dysfunction, venous insufficiency, deep vein thrombosis, and cirrhosis can increase capillary pressure, leading to edema.
• Decreased oncotic pressure. Hypoalbuminemia, a primary cause of reduced colloid oncotic pressure, can result from nephrotic syndrome, diabetic nephropathy, lupus nephropathy, amyloidosis, nephropathies, cirrhosis, chronic liver disease, and malabsorption or malnutrition.
• Increased capillary permeability. Vascular injury, often associated with diabetes, can increase capillary permeability and contribute to edema.
• Impaired lymphatic drainage. Lymphatic obstruction is common in patients with lymphedema, tumors, inflammation, fibrosis, certain infections, surgery, and congenital anomalies. Conditions such as thyroid disorders can also cause an increase in interstitial albumin and other proteins without a corresponding increase in lymphatic flow, leading to lymphedema.

Medications That Can Cause Edema

• Calcium channel blockers (CCBs). Drugs such as nifedipine and amlodipine can increase hydrostatic pressure by causing selective vasodilation of precapillary vessels, leading to increased intracapillary pressures. Newer lipophilic CCBs (eg, levamlodipine) exhibit lower rates of edema. Reducing the dose is often effective. Diuretics are not very effective for vasodilation-induced edema. Combining CCBs with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), which induce postcapillary dilation and normalize intracapillary pressure, may reduce fluid leakage into the interstitial space. This combination may be more beneficial than high-dose CCB monotherapy.
• Thiazolidinedione (eg, pioglitazone). These increase vascular permeability and hydrostatic pressure. They work by stimulating the peroxisome proliferator–activated gamma receptor, increasing vascular endothelial permeability, vascular endothelial growth factor secretion, and renal retention of sodium and fluids. Because of other adverse effects, their use is now limited.
• Agents for neuropathic pain (gabapentin and pregabalin). These drugs can induce selective vasodilation of arterioles through a mechanism similar to that of CCBs, causing increased intracapillary pressures. Edema usually begins within the first month of treatment or dose increase and often regresses after dose reduction or drug discontinuation.
• Antiparkinsonian dopamine agonists. These increase hydrostatic pressure by reducing sympathetic tone and dilating arterioles through alpha-2 adrenergic receptor activity.
• New antipsychotics. Drugs like clozapine, iloperidone, lurasidone, olanzapine, quetiapine, risperidone, and ziprasidone can increase hydrostatic pressure through antagonistic effects on alpha-1 adrenergic receptors, causing vasodilation.
• Nitrates. These drugs increase hydrostatic pressure by causing preferential venous dilation, leading to increased venous pooling.
• Nonsteroidal anti-inflammatory drugs (NSAIDs). These drugs can increase hydrostatic pressure by inhibiting vasodilation of afferent renal arterioles, decreasing the glomerular filtration rate, and stimulating the renin-angiotensin-aldosterone system, which leads to sodium and water retention. These adverse effects warrant cautious use of these agents.
• ACE inhibitors. Drugs such as enalapril and ramipril can increase vascular permeability. They reduce the metabolism and accumulation of bradykinin, which increases vascular permeability and fluid leakage. These effects are rare and are usually related to allergic responses.
• Insulin. Insulin decreases capillary oncotic pressure and increases vascular permeability. Rapid correction of hyperglycemia can cause a loss of oncotic pressure, while chronic hyperglycemia can damage vascular membranes, increasing permeability. These effects are generally benign and can be managed with careful dose titration, sodium restriction, or diuretics.
• Steroids. Steroids with mineralocorticoid activity can increase renal sodium and water retention, leading to increased blood volume. Fludrocortisone has the highest mineralocorticoid activity, while dexamethasone and methylprednisolone have negligible activity.

Implications

Understanding how these medications cause edema is important for effective management. For example, in the case of those causing edema due to reduced oncotic pressure, like insulin, slow dose titrations can help adapt to osmolarity changes. For drugs causing edema due to increased hydrostatic pressure, diuretics are more effective in acute management.

The key takeaways from this review are:

• Awareness of drug-induced edema. Many drugs besides CCBs can cause edema.
• Combination therapy. Combining ACE inhibitors or ARBs with CCBs can prevent or reduce CCB-induced edema.
• Edema management strategies. Strategies to manage or prevent edema should include dose reductions or replacement of the problematic medication, especially in severe or refractory cases.

Dr. Wajngarten, professor of cardiology, University of São Paulo, Brazil, has disclosed no relevant financial relationships.

This story was translated from the Medscape Portuguese 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.

STOCKHOLM — At the American Society of Retina Specialists (ASRS) 2024 Annual Meeting, researchers discussed how insights into potential risk factors and new treatments could improve outcomes for patients with diabetic retinopathy.

Jennifer Lim, MD, an ophthalmologist and director of the Retina Service at the University of Illinois Hospital & Health Sciences System in Chicago, told this news organization that emerging approaches to treating diabetic retinopathy offer hope because they address the root causes of the disease beyond just targeting vascular endothelial growth factor (VEGF). She said innovative methods and add-on treatments could lead to more durable and effective drugs.

Exploration of risk factors and treatment options for diabetic retinopathy could lead to more effective management strategies for the condition, agreed David Boyer, MD, an ophthalmologist at Retina Vitreous Associates Medical Group in Los Angeles, speaking with this news organization.
 

Risk Factors for Diabetic Retinopathy

Sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide 1 receptor agonists (GLP-1 RAs) have gained popularity because of their benefits beyond glycemic control, including weight loss, and cardiovascular and kidney protection. However, the impact of these medications on vision-threatening retinal complications is not fully understood. “There has always been a question about whether these newer diabetes medications might exacerbate diabetic eye disease,” said Dr. Boyer.

In a retrospective observational study, researchers included adults with type 2 diabetes and moderate cardiovascular disease risk who had no history of advanced diabetic retinal complications. These patients initiated treatment with GLP-1 RA, SGLT2 inhibitors, DPP-4 inhibitors, or sulfonylureas. The study used inverse probability of treatment weighting to mimic randomization and compared the time to the first treatment for diabetic macular edema or proliferative diabetic retinopathy across the treatment groups.

Results, presented by Andrew J. Barkmeier, MD, an associate professor of ophthalmology at the Mayo Clinic, showed that among 371,698 patients, those who initiated therapy with SGLT2 inhibitors had a lower risk of requiring treatment for sight-threatening retinopathy compared with those using other medication classes. GLP-1 RA did not increase retinopathy risk relative to dipeptidyl peptidase 4 inhibitors and sulfonylurea medications.

“[This study] told us that we do have to keep an eye on patients’ retinopathy when they start on these new inhibitors. But the progression is minimal and, overall, I think most people today favor keeping blood sugar levels as good as possible,” said Dr. Boyer, who was not involved in the study.

Another factor that might increase diabetic retinopathy progression is obstructive sleep apnea. This underdiagnosed condition is linked to several health issues, including dementia, stroke, and myocardial infarctions. Although not easily treated, obstructive sleep apnea is manageable, Dr. Boyer explained.

Researchers utilized the TriNetX electronic health records research network to identify patients with nonproliferative diabetic retinopathy, both with and without obstructive sleep apnea. 

The results, presented by Ehsan Rahimy, MD, a retinal specialist at Palo Alto Medical Foundation and a professor at Stanford University, showed that patients with obstructive sleep apnea had a significantly higher risk of progressing to proliferative diabetic retinopathy and developing new-onset diabetic macular edema. These patients were more likely to require ocular interventions, such as intravitreal injections and laser photocoagulation. They also had greater risks for stroke, myocardial infarction, and death compared with those who did not have obstructive sleep apnea.

“It was good to bring this to everybody’s attention,” said Dr. Boyer, who was not involved in the study. “It’s an easy question to ask someone if they snore.”
 

New Treatments on the Horizon

In another presentation, Nathan C. Steinle, MD, of California Retina Consultants, presented a study that assessed the durability of response to sozinibercept in patients with retinal vascular diseases. This novel therapeutic agent is designed to inhibit VEGF-C and VEGF-D in conditions where VEGF-A suppression alone is insufficient. 

Sozinibercept was combined with standard anti–VEGF-A therapies such as ranibizumab or aflibercept. It involved a prospective, post hoc analysis of two phase 1b, open-label, dose-escalation studies, including 40 patients with neovascular age-related macular degeneration (nAMD; 31 patients) or diabetic macular edema (nine patients). These patients, either treatment-naive or previously treated, received three intravitreal injections of ranibizumab or aflibercept in combination with sozinibercept at various doses.

Results indicated that sozinibercept combination therapy was well tolerated, with no dose-limiting toxicities. In treatment-naive nAMD patients, the mean best-corrected visual acuity (BCVA) improved significantly from baseline at months 3 and 6. Previously treated nAMD patients also showed BCVA improvements, although to a lesser extent. For patients with persistent diabetic macular edema, switching to sozinibercept plus aflibercept resulted in notable BCVA gains. The mean time to requiring retreatment was longer in treatment-naive patients than in those previously treated, indicating a durable response. 

“Combination therapy with sozinibercept is going to be really important,” said Dr. Lim, who was not involved in the study, “because it attacks with a dual mechanism of action.”

Oral agents promise a potentially easier alternative for patients compared with frequent injections. CU06-1004 is a novel orally administered endothelial dysfunction blocker that has shown promise in stabilizing damaged capillaries, reducing abnormal angiogenesis, and inhibiting inflammatory activation in preclinical studies. “CU06 is very interesting to me because by preventing endothelial loss, it gets to the pathophysiology of why the blood vessels break down,” Dr. Lim said.

In a proof-of-concept phase 2a, multicenter, open-label, parallel-group trial, investigators randomly assigned 67 patients with diabetic macular edema to receive 100 mg, 200 mg, or 300 mg of CU06-1004 once daily for 12 weeks, followed by a 4-week follow-up. 

Results presented by Victor Gonzalez, MD, of Valley Retina Institute in Texas, indicated that the oral agent improved BCVA, stabilized central subfield thickness, and showed positive anatomical changes in optical coherence tomography images. CU06-1004 was well tolerated, with no drug-related serious adverse events. 

“The number [of patients] was very small, and we will need a much longer, larger trial to see if [CU06-1004] has benefits long term,” said Dr. Boyer, who was not involved in the study. “But I think we’re all very excited if we can find an oral agent for treating diabetic retinopathy. It would be easier for the patient to take a pill than having to come in for injections.” 

The sustained-release axitinib implant, OTX-TKI, is also generating significant interest, particularly for nonproliferative diabetic retinopathy. Axitinib, a tyrosine kinase inhibitor (TKI), targets signaling pathways crucial in cellular processes, providing a novel approach to managing diseases where traditional therapies might fall short. Unlike traditional anti-VEGF treatments that focus solely on cytokine levels, TKIs block the activation of signaling pathways, preventing downstream signaling regardless of cytokine levels. This mechanism is particularly important because it effectively inhibits disease progression even if levels of VEGF are high, Dr. Lim explained.

In the phase 1 HELIOS trial, OTX-TKI was assessed in patients with nonproliferative diabetic retinopathy. This multicenter, double-masked, parallel-group clinical study included 21 patients who had not received anti-VEGF treatment, dexamethasone intravitreal implants in the previous 12 months, or intraocular steroid injections in the prior 4 months. Patients were randomly assigned to receive either OTX-TKI or sham treatment.

Results presented by Dilsher S. Dhoot, MD, of California Retina Consultants, indicated that OTX-TKI was generally well tolerated, with no serious ocular adverse events. At 48 weeks, 46.2% of eyes treated with OTX-TKI showed a 1- or 2-step improvement on the Diabetic Retinopathy Severity Scale (DRSS) compared with none in the sham arm. Additionally, no eyes treated with OTX-TKI experienced a worsening on the DRSS, whereas 25% of eyes in the sham arm did. Vision-threatening complications, such as proliferative diabetic retinopathy or diabetic macular edema, developed in 37.5% of the sham group but in none of the OTX-TKI treated eyes. A single injection of OTX-TKI provided durable DRSS improvement for up to 48 weeks, with no patients in either arm requiring rescue therapy.

“This is a really exciting add-on treatment,” Dr. Lim said, who was not involved in the study. She explained that it is initially necessary to control the disease with standard treatments, because TKIs may take longer to exhibit their effects. Once the disease is stabilized, TKIs can be used alongside other therapies, potentially reducing the reliance on frequent anti-VEGF injections. “These are preliminary results, but that’s the hope going forward.”

Dr. Lim and Dr. Boyer report no relevant financial relationships.

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

STOCKHOLM — At the American Society of Retina Specialists (ASRS) 2024 Annual Meeting, researchers discussed how insights into potential risk factors and new treatments could improve outcomes for patients with diabetic retinopathy.

Jennifer Lim, MD, an ophthalmologist and director of the Retina Service at the University of Illinois Hospital & Health Sciences System in Chicago, told this news organization that emerging approaches to treating diabetic retinopathy offer hope because they address the root causes of the disease beyond just targeting vascular endothelial growth factor (VEGF). She said innovative methods and add-on treatments could lead to more durable and effective drugs.

Exploration of risk factors and treatment options for diabetic retinopathy could lead to more effective management strategies for the condition, agreed David Boyer, MD, an ophthalmologist at Retina Vitreous Associates Medical Group in Los Angeles, speaking with this news organization.
 

Risk Factors for Diabetic Retinopathy

Sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide 1 receptor agonists (GLP-1 RAs) have gained popularity because of their benefits beyond glycemic control, including weight loss, and cardiovascular and kidney protection. However, the impact of these medications on vision-threatening retinal complications is not fully understood. “There has always been a question about whether these newer diabetes medications might exacerbate diabetic eye disease,” said Dr. Boyer.

In a retrospective observational study, researchers included adults with type 2 diabetes and moderate cardiovascular disease risk who had no history of advanced diabetic retinal complications. These patients initiated treatment with GLP-1 RA, SGLT2 inhibitors, DPP-4 inhibitors, or sulfonylureas. The study used inverse probability of treatment weighting to mimic randomization and compared the time to the first treatment for diabetic macular edema or proliferative diabetic retinopathy across the treatment groups.

Results, presented by Andrew J. Barkmeier, MD, an associate professor of ophthalmology at the Mayo Clinic, showed that among 371,698 patients, those who initiated therapy with SGLT2 inhibitors had a lower risk of requiring treatment for sight-threatening retinopathy compared with those using other medication classes. GLP-1 RA did not increase retinopathy risk relative to dipeptidyl peptidase 4 inhibitors and sulfonylurea medications.

“[This study] told us that we do have to keep an eye on patients’ retinopathy when they start on these new inhibitors. But the progression is minimal and, overall, I think most people today favor keeping blood sugar levels as good as possible,” said Dr. Boyer, who was not involved in the study.

Another factor that might increase diabetic retinopathy progression is obstructive sleep apnea. This underdiagnosed condition is linked to several health issues, including dementia, stroke, and myocardial infarctions. Although not easily treated, obstructive sleep apnea is manageable, Dr. Boyer explained.

Researchers utilized the TriNetX electronic health records research network to identify patients with nonproliferative diabetic retinopathy, both with and without obstructive sleep apnea. 

The results, presented by Ehsan Rahimy, MD, a retinal specialist at Palo Alto Medical Foundation and a professor at Stanford University, showed that patients with obstructive sleep apnea had a significantly higher risk of progressing to proliferative diabetic retinopathy and developing new-onset diabetic macular edema. These patients were more likely to require ocular interventions, such as intravitreal injections and laser photocoagulation. They also had greater risks for stroke, myocardial infarction, and death compared with those who did not have obstructive sleep apnea.

“It was good to bring this to everybody’s attention,” said Dr. Boyer, who was not involved in the study. “It’s an easy question to ask someone if they snore.”
 

New Treatments on the Horizon

In another presentation, Nathan C. Steinle, MD, of California Retina Consultants, presented a study that assessed the durability of response to sozinibercept in patients with retinal vascular diseases. This novel therapeutic agent is designed to inhibit VEGF-C and VEGF-D in conditions where VEGF-A suppression alone is insufficient. 

Sozinibercept was combined with standard anti–VEGF-A therapies such as ranibizumab or aflibercept. It involved a prospective, post hoc analysis of two phase 1b, open-label, dose-escalation studies, including 40 patients with neovascular age-related macular degeneration (nAMD; 31 patients) or diabetic macular edema (nine patients). These patients, either treatment-naive or previously treated, received three intravitreal injections of ranibizumab or aflibercept in combination with sozinibercept at various doses.

Results indicated that sozinibercept combination therapy was well tolerated, with no dose-limiting toxicities. In treatment-naive nAMD patients, the mean best-corrected visual acuity (BCVA) improved significantly from baseline at months 3 and 6. Previously treated nAMD patients also showed BCVA improvements, although to a lesser extent. For patients with persistent diabetic macular edema, switching to sozinibercept plus aflibercept resulted in notable BCVA gains. The mean time to requiring retreatment was longer in treatment-naive patients than in those previously treated, indicating a durable response. 

“Combination therapy with sozinibercept is going to be really important,” said Dr. Lim, who was not involved in the study, “because it attacks with a dual mechanism of action.”

Oral agents promise a potentially easier alternative for patients compared with frequent injections. CU06-1004 is a novel orally administered endothelial dysfunction blocker that has shown promise in stabilizing damaged capillaries, reducing abnormal angiogenesis, and inhibiting inflammatory activation in preclinical studies. “CU06 is very interesting to me because by preventing endothelial loss, it gets to the pathophysiology of why the blood vessels break down,” Dr. Lim said.

In a proof-of-concept phase 2a, multicenter, open-label, parallel-group trial, investigators randomly assigned 67 patients with diabetic macular edema to receive 100 mg, 200 mg, or 300 mg of CU06-1004 once daily for 12 weeks, followed by a 4-week follow-up. 

Results presented by Victor Gonzalez, MD, of Valley Retina Institute in Texas, indicated that the oral agent improved BCVA, stabilized central subfield thickness, and showed positive anatomical changes in optical coherence tomography images. CU06-1004 was well tolerated, with no drug-related serious adverse events. 

“The number [of patients] was very small, and we will need a much longer, larger trial to see if [CU06-1004] has benefits long term,” said Dr. Boyer, who was not involved in the study. “But I think we’re all very excited if we can find an oral agent for treating diabetic retinopathy. It would be easier for the patient to take a pill than having to come in for injections.” 

The sustained-release axitinib implant, OTX-TKI, is also generating significant interest, particularly for nonproliferative diabetic retinopathy. Axitinib, a tyrosine kinase inhibitor (TKI), targets signaling pathways crucial in cellular processes, providing a novel approach to managing diseases where traditional therapies might fall short. Unlike traditional anti-VEGF treatments that focus solely on cytokine levels, TKIs block the activation of signaling pathways, preventing downstream signaling regardless of cytokine levels. This mechanism is particularly important because it effectively inhibits disease progression even if levels of VEGF are high, Dr. Lim explained.

In the phase 1 HELIOS trial, OTX-TKI was assessed in patients with nonproliferative diabetic retinopathy. This multicenter, double-masked, parallel-group clinical study included 21 patients who had not received anti-VEGF treatment, dexamethasone intravitreal implants in the previous 12 months, or intraocular steroid injections in the prior 4 months. Patients were randomly assigned to receive either OTX-TKI or sham treatment.

Results presented by Dilsher S. Dhoot, MD, of California Retina Consultants, indicated that OTX-TKI was generally well tolerated, with no serious ocular adverse events. At 48 weeks, 46.2% of eyes treated with OTX-TKI showed a 1- or 2-step improvement on the Diabetic Retinopathy Severity Scale (DRSS) compared with none in the sham arm. Additionally, no eyes treated with OTX-TKI experienced a worsening on the DRSS, whereas 25% of eyes in the sham arm did. Vision-threatening complications, such as proliferative diabetic retinopathy or diabetic macular edema, developed in 37.5% of the sham group but in none of the OTX-TKI treated eyes. A single injection of OTX-TKI provided durable DRSS improvement for up to 48 weeks, with no patients in either arm requiring rescue therapy.

“This is a really exciting add-on treatment,” Dr. Lim said, who was not involved in the study. She explained that it is initially necessary to control the disease with standard treatments, because TKIs may take longer to exhibit their effects. Once the disease is stabilized, TKIs can be used alongside other therapies, potentially reducing the reliance on frequent anti-VEGF injections. “These are preliminary results, but that’s the hope going forward.”

Dr. Lim and Dr. Boyer report no relevant financial relationships.

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

STOCKHOLM — At the American Society of Retina Specialists (ASRS) 2024 Annual Meeting, researchers discussed how insights into potential risk factors and new treatments could improve outcomes for patients with diabetic retinopathy.

Jennifer Lim, MD, an ophthalmologist and director of the Retina Service at the University of Illinois Hospital & Health Sciences System in Chicago, told this news organization that emerging approaches to treating diabetic retinopathy offer hope because they address the root causes of the disease beyond just targeting vascular endothelial growth factor (VEGF). She said innovative methods and add-on treatments could lead to more durable and effective drugs.

Exploration of risk factors and treatment options for diabetic retinopathy could lead to more effective management strategies for the condition, agreed David Boyer, MD, an ophthalmologist at Retina Vitreous Associates Medical Group in Los Angeles, speaking with this news organization.
 

Risk Factors for Diabetic Retinopathy

Sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide 1 receptor agonists (GLP-1 RAs) have gained popularity because of their benefits beyond glycemic control, including weight loss, and cardiovascular and kidney protection. However, the impact of these medications on vision-threatening retinal complications is not fully understood. “There has always been a question about whether these newer diabetes medications might exacerbate diabetic eye disease,” said Dr. Boyer.

In a retrospective observational study, researchers included adults with type 2 diabetes and moderate cardiovascular disease risk who had no history of advanced diabetic retinal complications. These patients initiated treatment with GLP-1 RA, SGLT2 inhibitors, DPP-4 inhibitors, or sulfonylureas. The study used inverse probability of treatment weighting to mimic randomization and compared the time to the first treatment for diabetic macular edema or proliferative diabetic retinopathy across the treatment groups.

Results, presented by Andrew J. Barkmeier, MD, an associate professor of ophthalmology at the Mayo Clinic, showed that among 371,698 patients, those who initiated therapy with SGLT2 inhibitors had a lower risk of requiring treatment for sight-threatening retinopathy compared with those using other medication classes. GLP-1 RA did not increase retinopathy risk relative to dipeptidyl peptidase 4 inhibitors and sulfonylurea medications.

“[This study] told us that we do have to keep an eye on patients’ retinopathy when they start on these new inhibitors. But the progression is minimal and, overall, I think most people today favor keeping blood sugar levels as good as possible,” said Dr. Boyer, who was not involved in the study.

Another factor that might increase diabetic retinopathy progression is obstructive sleep apnea. This underdiagnosed condition is linked to several health issues, including dementia, stroke, and myocardial infarctions. Although not easily treated, obstructive sleep apnea is manageable, Dr. Boyer explained.

Researchers utilized the TriNetX electronic health records research network to identify patients with nonproliferative diabetic retinopathy, both with and without obstructive sleep apnea. 

The results, presented by Ehsan Rahimy, MD, a retinal specialist at Palo Alto Medical Foundation and a professor at Stanford University, showed that patients with obstructive sleep apnea had a significantly higher risk of progressing to proliferative diabetic retinopathy and developing new-onset diabetic macular edema. These patients were more likely to require ocular interventions, such as intravitreal injections and laser photocoagulation. They also had greater risks for stroke, myocardial infarction, and death compared with those who did not have obstructive sleep apnea.

“It was good to bring this to everybody’s attention,” said Dr. Boyer, who was not involved in the study. “It’s an easy question to ask someone if they snore.”
 

New Treatments on the Horizon

In another presentation, Nathan C. Steinle, MD, of California Retina Consultants, presented a study that assessed the durability of response to sozinibercept in patients with retinal vascular diseases. This novel therapeutic agent is designed to inhibit VEGF-C and VEGF-D in conditions where VEGF-A suppression alone is insufficient. 

Sozinibercept was combined with standard anti–VEGF-A therapies such as ranibizumab or aflibercept. It involved a prospective, post hoc analysis of two phase 1b, open-label, dose-escalation studies, including 40 patients with neovascular age-related macular degeneration (nAMD; 31 patients) or diabetic macular edema (nine patients). These patients, either treatment-naive or previously treated, received three intravitreal injections of ranibizumab or aflibercept in combination with sozinibercept at various doses.

Results indicated that sozinibercept combination therapy was well tolerated, with no dose-limiting toxicities. In treatment-naive nAMD patients, the mean best-corrected visual acuity (BCVA) improved significantly from baseline at months 3 and 6. Previously treated nAMD patients also showed BCVA improvements, although to a lesser extent. For patients with persistent diabetic macular edema, switching to sozinibercept plus aflibercept resulted in notable BCVA gains. The mean time to requiring retreatment was longer in treatment-naive patients than in those previously treated, indicating a durable response. 

“Combination therapy with sozinibercept is going to be really important,” said Dr. Lim, who was not involved in the study, “because it attacks with a dual mechanism of action.”

Oral agents promise a potentially easier alternative for patients compared with frequent injections. CU06-1004 is a novel orally administered endothelial dysfunction blocker that has shown promise in stabilizing damaged capillaries, reducing abnormal angiogenesis, and inhibiting inflammatory activation in preclinical studies. “CU06 is very interesting to me because by preventing endothelial loss, it gets to the pathophysiology of why the blood vessels break down,” Dr. Lim said.

In a proof-of-concept phase 2a, multicenter, open-label, parallel-group trial, investigators randomly assigned 67 patients with diabetic macular edema to receive 100 mg, 200 mg, or 300 mg of CU06-1004 once daily for 12 weeks, followed by a 4-week follow-up. 

Results presented by Victor Gonzalez, MD, of Valley Retina Institute in Texas, indicated that the oral agent improved BCVA, stabilized central subfield thickness, and showed positive anatomical changes in optical coherence tomography images. CU06-1004 was well tolerated, with no drug-related serious adverse events. 

“The number [of patients] was very small, and we will need a much longer, larger trial to see if [CU06-1004] has benefits long term,” said Dr. Boyer, who was not involved in the study. “But I think we’re all very excited if we can find an oral agent for treating diabetic retinopathy. It would be easier for the patient to take a pill than having to come in for injections.” 

The sustained-release axitinib implant, OTX-TKI, is also generating significant interest, particularly for nonproliferative diabetic retinopathy. Axitinib, a tyrosine kinase inhibitor (TKI), targets signaling pathways crucial in cellular processes, providing a novel approach to managing diseases where traditional therapies might fall short. Unlike traditional anti-VEGF treatments that focus solely on cytokine levels, TKIs block the activation of signaling pathways, preventing downstream signaling regardless of cytokine levels. This mechanism is particularly important because it effectively inhibits disease progression even if levels of VEGF are high, Dr. Lim explained.

In the phase 1 HELIOS trial, OTX-TKI was assessed in patients with nonproliferative diabetic retinopathy. This multicenter, double-masked, parallel-group clinical study included 21 patients who had not received anti-VEGF treatment, dexamethasone intravitreal implants in the previous 12 months, or intraocular steroid injections in the prior 4 months. Patients were randomly assigned to receive either OTX-TKI or sham treatment.

Results presented by Dilsher S. Dhoot, MD, of California Retina Consultants, indicated that OTX-TKI was generally well tolerated, with no serious ocular adverse events. At 48 weeks, 46.2% of eyes treated with OTX-TKI showed a 1- or 2-step improvement on the Diabetic Retinopathy Severity Scale (DRSS) compared with none in the sham arm. Additionally, no eyes treated with OTX-TKI experienced a worsening on the DRSS, whereas 25% of eyes in the sham arm did. Vision-threatening complications, such as proliferative diabetic retinopathy or diabetic macular edema, developed in 37.5% of the sham group but in none of the OTX-TKI treated eyes. A single injection of OTX-TKI provided durable DRSS improvement for up to 48 weeks, with no patients in either arm requiring rescue therapy.

“This is a really exciting add-on treatment,” Dr. Lim said, who was not involved in the study. She explained that it is initially necessary to control the disease with standard treatments, because TKIs may take longer to exhibit their effects. Once the disease is stabilized, TKIs can be used alongside other therapies, potentially reducing the reliance on frequent anti-VEGF injections. “These are preliminary results, but that’s the hope going forward.”

Dr. Lim and Dr. Boyer report no relevant financial relationships.

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

Take a look at any of the evidence-based US obesity treatment guidelines. The key criteria for diagnosing overweight and obesity is based on the body mass index (BMI). 

The guidelines also use BMI to stratify care options to decrease cardiovascular risk. For example, persons with BMI ≥30 are classified as having obesity, and antiobesity medications are recommended. Those with BMI ≥ 40 are classified as having severe obesity, and metabolic bariatric surgery may be appropriate. 

But where did these cutoff points for more and less aggressive treatments come from? These BMI cutoffs are based primarily on mortality data collected from large non-Hispanic White populations, without data on potential differences by gender and ethnicity. In fact, by itself, BMI is an incomplete measure of cardiometabolic risk, especially in a multiethnic clinic with all genders represented.

For example, it is certainly true that those with BMI ≥ 30 have more cardiovascular risk factors than those with BMI < 30. But Asian American individuals have more risk factors at lower BMIs than do White or African American individuals likely because of more visceral fat accumulation at lower BMIs.

Besides the variation in gender and ethnicity, BMI does not take the type and location of body fat into consideration. Adipose tissue in visceral or ectopic areas have much higher risks for disease than subcutaneous adipose tissue because of the associated inflammation. Measures such as waist circumference, waist-to-hip ratio, and skinfold measurements aim to capture this aspect but often fall short because of variation in techniques.

BMI does not account for muscle mass either, so fit athletes and bodybuilders can be classified as having obesity by BMI alone. More accurate body fat percent measures, such as dual-energy X-ray absorptiometry or MRI specifically for ectopic fat, are labor intensive, expensive, and not feasible to perform in a busy primary care or endocrinology clinic.
 

Assessing Risks From Obesity Beyond BMI

Clearly, better risk measures than BMI are needed, but until they are available, supplemental clinical tools can aid diagnosis and treatment decisions at obesity medicine specialty centers, endocrinology and diabetes centers, and those centers that focus on the treatment of obesity.

For example, a seca scale can measure percent body fat by bioelectric impedance analysis. This technique also has its limitations, but for persons who are well hydrated, it can be used as a baseline to determine efficacy of behavioral interventions, such as resistance-exercise training and a high-protein diet to protect muscle mass as the patient loses weight.

A lot also can be gleaned from diet and exercise history, social history, family history, and physical exam as well as laboratory analyses. For example, an Asian American patient with a BMI of 26 who has been gaining weight mostly in the abdominal region after age 35 years is likely to have cardiometabolic risk, and a family history can solidify that. An exam can show signs of acanthosis nigricans or an enlarged liver and generous abdominal adipose tissue. This would be the patient in whom you would want to obtain a hemoglobin A1c measurement in the chance that it is elevated at > 5.7 mg/dL, suggesting high risk for type 2 diabetes. 

A Fibrosis-4 score can assess the risk for liver disease from aspartate transaminase and alanine aminotransferase and platelet count and age, providing clues to cardiometabolic disease risk.

In the next 10, years there may be a better measure for cardiometabolic risk that is more accurate than BMI is. It could be the sagittal abdominal diameter, which has been purported to more accurately measure visceral abdominal fat. But this has not made it to be one of the vital signs in a busy primary care clinic, however. 
 

Will New Body Fat Tools Change Practice?

In the next 10 years, there may be an affordable gadget to scan the body to determine visceral vs subcutaneous deposition of fat — like radiography for tissue. Now, three-dimensional (3D) total-body scanners can obtain body composition, but they are extremely expensive. The more important clinical question is: How will the use of these imaging modalities change your practice protocol for a particular patient? 

Think about the FibroScan, a type of ultrasound used to determine fatty liver disease and fibrosis. We order the test for those patients in whom we already have a strong suspicion for liver disease and, in obesity practices, for fatty liver and metabolic-associated fatty liver disease or metabolic associated steatohepatitis.

The test results do much to educate the patient and help the patient understand the need for aggressive treatment for their obesity. But it doesn’t necessarily change the clinician’s practice protocols and decisions. We would still recommend weight management and medications or surgery to patients regardless of the findings. 

A FibroScan is an expense, and not all primary care or endocrine practitioners may feel it necessary to purchase one for the added benefit of patient education. And I would argue that a 3D body scanner is a great tool but more for educational purposes than to really determine practice decision-making or outcomes. 

In the meantime, an old-fashioned physical examination, along with a thorough medical, social, and family history should give even the busiest primary care provider enough information to decide whether their patient is a candidate for preventive measures to reduce body fat with diet, exercise, and medication as well as whether the patient is a candidate for metabolic bariatric surgery. Higher suspicion of cardiovascular risk at lower BMI ranges for various ethnicities can help primary care providers pick up on the patients with low BMI but who are at higher risk for type 2 diabetes or prediabetes and cardiovascular disease. 

So the answer to whether we need a better measure than the BMI: Yes, we do. We need a physical examination on all patients.

Dr. Apovian, professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, both in Boston, Massachusetts, disclosed ties with Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, L-Nutra, NeuroBo Pharm, Novo, OptumRx, Pain Script, Palatin, Pursuit by You, Roman Health, Xeno, and Riverview School.

A version of this article appeared on Medscape.com.

Take a look at any of the evidence-based US obesity treatment guidelines. The key criteria for diagnosing overweight and obesity is based on the body mass index (BMI). 

The guidelines also use BMI to stratify care options to decrease cardiovascular risk. For example, persons with BMI ≥30 are classified as having obesity, and antiobesity medications are recommended. Those with BMI ≥ 40 are classified as having severe obesity, and metabolic bariatric surgery may be appropriate. 

But where did these cutoff points for more and less aggressive treatments come from? These BMI cutoffs are based primarily on mortality data collected from large non-Hispanic White populations, without data on potential differences by gender and ethnicity. In fact, by itself, BMI is an incomplete measure of cardiometabolic risk, especially in a multiethnic clinic with all genders represented.

For example, it is certainly true that those with BMI ≥ 30 have more cardiovascular risk factors than those with BMI < 30. But Asian American individuals have more risk factors at lower BMIs than do White or African American individuals likely because of more visceral fat accumulation at lower BMIs.

Besides the variation in gender and ethnicity, BMI does not take the type and location of body fat into consideration. Adipose tissue in visceral or ectopic areas have much higher risks for disease than subcutaneous adipose tissue because of the associated inflammation. Measures such as waist circumference, waist-to-hip ratio, and skinfold measurements aim to capture this aspect but often fall short because of variation in techniques.

BMI does not account for muscle mass either, so fit athletes and bodybuilders can be classified as having obesity by BMI alone. More accurate body fat percent measures, such as dual-energy X-ray absorptiometry or MRI specifically for ectopic fat, are labor intensive, expensive, and not feasible to perform in a busy primary care or endocrinology clinic.
 

Assessing Risks From Obesity Beyond BMI

Clearly, better risk measures than BMI are needed, but until they are available, supplemental clinical tools can aid diagnosis and treatment decisions at obesity medicine specialty centers, endocrinology and diabetes centers, and those centers that focus on the treatment of obesity.

For example, a seca scale can measure percent body fat by bioelectric impedance analysis. This technique also has its limitations, but for persons who are well hydrated, it can be used as a baseline to determine efficacy of behavioral interventions, such as resistance-exercise training and a high-protein diet to protect muscle mass as the patient loses weight.

A lot also can be gleaned from diet and exercise history, social history, family history, and physical exam as well as laboratory analyses. For example, an Asian American patient with a BMI of 26 who has been gaining weight mostly in the abdominal region after age 35 years is likely to have cardiometabolic risk, and a family history can solidify that. An exam can show signs of acanthosis nigricans or an enlarged liver and generous abdominal adipose tissue. This would be the patient in whom you would want to obtain a hemoglobin A1c measurement in the chance that it is elevated at > 5.7 mg/dL, suggesting high risk for type 2 diabetes. 

A Fibrosis-4 score can assess the risk for liver disease from aspartate transaminase and alanine aminotransferase and platelet count and age, providing clues to cardiometabolic disease risk.

In the next 10, years there may be a better measure for cardiometabolic risk that is more accurate than BMI is. It could be the sagittal abdominal diameter, which has been purported to more accurately measure visceral abdominal fat. But this has not made it to be one of the vital signs in a busy primary care clinic, however. 
 

Will New Body Fat Tools Change Practice?

In the next 10 years, there may be an affordable gadget to scan the body to determine visceral vs subcutaneous deposition of fat — like radiography for tissue. Now, three-dimensional (3D) total-body scanners can obtain body composition, but they are extremely expensive. The more important clinical question is: How will the use of these imaging modalities change your practice protocol for a particular patient? 

Think about the FibroScan, a type of ultrasound used to determine fatty liver disease and fibrosis. We order the test for those patients in whom we already have a strong suspicion for liver disease and, in obesity practices, for fatty liver and metabolic-associated fatty liver disease or metabolic associated steatohepatitis.

The test results do much to educate the patient and help the patient understand the need for aggressive treatment for their obesity. But it doesn’t necessarily change the clinician’s practice protocols and decisions. We would still recommend weight management and medications or surgery to patients regardless of the findings. 

A FibroScan is an expense, and not all primary care or endocrine practitioners may feel it necessary to purchase one for the added benefit of patient education. And I would argue that a 3D body scanner is a great tool but more for educational purposes than to really determine practice decision-making or outcomes. 

In the meantime, an old-fashioned physical examination, along with a thorough medical, social, and family history should give even the busiest primary care provider enough information to decide whether their patient is a candidate for preventive measures to reduce body fat with diet, exercise, and medication as well as whether the patient is a candidate for metabolic bariatric surgery. Higher suspicion of cardiovascular risk at lower BMI ranges for various ethnicities can help primary care providers pick up on the patients with low BMI but who are at higher risk for type 2 diabetes or prediabetes and cardiovascular disease. 

So the answer to whether we need a better measure than the BMI: Yes, we do. We need a physical examination on all patients.

Dr. Apovian, professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, both in Boston, Massachusetts, disclosed ties with Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, L-Nutra, NeuroBo Pharm, Novo, OptumRx, Pain Script, Palatin, Pursuit by You, Roman Health, Xeno, and Riverview School.

A version of this article appeared on Medscape.com.

Take a look at any of the evidence-based US obesity treatment guidelines. The key criteria for diagnosing overweight and obesity is based on the body mass index (BMI). 

The guidelines also use BMI to stratify care options to decrease cardiovascular risk. For example, persons with BMI ≥30 are classified as having obesity, and antiobesity medications are recommended. Those with BMI ≥ 40 are classified as having severe obesity, and metabolic bariatric surgery may be appropriate. 

But where did these cutoff points for more and less aggressive treatments come from? These BMI cutoffs are based primarily on mortality data collected from large non-Hispanic White populations, without data on potential differences by gender and ethnicity. In fact, by itself, BMI is an incomplete measure of cardiometabolic risk, especially in a multiethnic clinic with all genders represented.

For example, it is certainly true that those with BMI ≥ 30 have more cardiovascular risk factors than those with BMI < 30. But Asian American individuals have more risk factors at lower BMIs than do White or African American individuals likely because of more visceral fat accumulation at lower BMIs.

Besides the variation in gender and ethnicity, BMI does not take the type and location of body fat into consideration. Adipose tissue in visceral or ectopic areas have much higher risks for disease than subcutaneous adipose tissue because of the associated inflammation. Measures such as waist circumference, waist-to-hip ratio, and skinfold measurements aim to capture this aspect but often fall short because of variation in techniques.

BMI does not account for muscle mass either, so fit athletes and bodybuilders can be classified as having obesity by BMI alone. More accurate body fat percent measures, such as dual-energy X-ray absorptiometry or MRI specifically for ectopic fat, are labor intensive, expensive, and not feasible to perform in a busy primary care or endocrinology clinic.
 

Assessing Risks From Obesity Beyond BMI

Clearly, better risk measures than BMI are needed, but until they are available, supplemental clinical tools can aid diagnosis and treatment decisions at obesity medicine specialty centers, endocrinology and diabetes centers, and those centers that focus on the treatment of obesity.

For example, a seca scale can measure percent body fat by bioelectric impedance analysis. This technique also has its limitations, but for persons who are well hydrated, it can be used as a baseline to determine efficacy of behavioral interventions, such as resistance-exercise training and a high-protein diet to protect muscle mass as the patient loses weight.

A lot also can be gleaned from diet and exercise history, social history, family history, and physical exam as well as laboratory analyses. For example, an Asian American patient with a BMI of 26 who has been gaining weight mostly in the abdominal region after age 35 years is likely to have cardiometabolic risk, and a family history can solidify that. An exam can show signs of acanthosis nigricans or an enlarged liver and generous abdominal adipose tissue. This would be the patient in whom you would want to obtain a hemoglobin A1c measurement in the chance that it is elevated at > 5.7 mg/dL, suggesting high risk for type 2 diabetes. 

A Fibrosis-4 score can assess the risk for liver disease from aspartate transaminase and alanine aminotransferase and platelet count and age, providing clues to cardiometabolic disease risk.

In the next 10, years there may be a better measure for cardiometabolic risk that is more accurate than BMI is. It could be the sagittal abdominal diameter, which has been purported to more accurately measure visceral abdominal fat. But this has not made it to be one of the vital signs in a busy primary care clinic, however. 
 

Will New Body Fat Tools Change Practice?

In the next 10 years, there may be an affordable gadget to scan the body to determine visceral vs subcutaneous deposition of fat — like radiography for tissue. Now, three-dimensional (3D) total-body scanners can obtain body composition, but they are extremely expensive. The more important clinical question is: How will the use of these imaging modalities change your practice protocol for a particular patient? 

Think about the FibroScan, a type of ultrasound used to determine fatty liver disease and fibrosis. We order the test for those patients in whom we already have a strong suspicion for liver disease and, in obesity practices, for fatty liver and metabolic-associated fatty liver disease or metabolic associated steatohepatitis.

The test results do much to educate the patient and help the patient understand the need for aggressive treatment for their obesity. But it doesn’t necessarily change the clinician’s practice protocols and decisions. We would still recommend weight management and medications or surgery to patients regardless of the findings. 

A FibroScan is an expense, and not all primary care or endocrine practitioners may feel it necessary to purchase one for the added benefit of patient education. And I would argue that a 3D body scanner is a great tool but more for educational purposes than to really determine practice decision-making or outcomes. 

In the meantime, an old-fashioned physical examination, along with a thorough medical, social, and family history should give even the busiest primary care provider enough information to decide whether their patient is a candidate for preventive measures to reduce body fat with diet, exercise, and medication as well as whether the patient is a candidate for metabolic bariatric surgery. Higher suspicion of cardiovascular risk at lower BMI ranges for various ethnicities can help primary care providers pick up on the patients with low BMI but who are at higher risk for type 2 diabetes or prediabetes and cardiovascular disease. 

So the answer to whether we need a better measure than the BMI: Yes, we do. We need a physical examination on all patients.

Dr. Apovian, professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, both in Boston, Massachusetts, disclosed ties with Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, L-Nutra, NeuroBo Pharm, Novo, OptumRx, Pain Script, Palatin, Pursuit by You, Roman Health, Xeno, and Riverview School.

A version of this article appeared on Medscape.com.

The allegations against Algerian boxer Imane Khelif at the Paris Olympics raised the questions of intersexuality and its implications in competitive sports. This news organization has decided to delve into the topic to assist doctors who suspect a similar condition in their patients. No certain clinical data about Ms. Khelif have been made public, so this article does not concern the boxer but rather takes inspiration from the media controversy.

What Is Intersexuality?

Intersexuality encompasses a spectrum of variations in sexual development that lead to the simultaneous presence of typical male and female characteristics. As reiterated by the United Nations Office of the High Commissioner for Human Rights, the medical definition does not affect the patient’s self-identification of gender or sexual orientation.

“The percentage of people who fall within the intersexuality spectrum is less than 0.5 per thousand of the general population, but there are no precise statistics, given the difficulty of definition,” said Roberto Lala, MD, pediatric endocrinologist and president of the Federation of Rare Childhood Diseases.

Indeed, there is not only a strict definition of intersexuality that involves a significant presence of these mixed physical characteristics in a way that conditions the self-image of the subject but also a broad definition, said Dr. Lala. “For example, clitoral hypertrophy in a female otherwise conforming to the female gender, which does not raise doubts about identity,” he said.
 

Chromosomes, Genes, and Hormones

A patient’s sexual characteristics are determined by the complex interaction of chromosomal, genetic, and hormonal factors. “The human body is, so to speak, programmed to take on female appearances in development and shifts toward male ones only if exposed to testosterone and other factors. For this to happen, testosterone must be produced during embryonic development, and it must function properly,” said Paolo Moghetti, full professor of endocrinology at the University of Verona, Italy.

The protein encoded by SRY, which is located on the Y chromosome, determines the development of the testicles from undifferentiated tissue of the embryonic gonads. The testicles of the embryo then produce testosterone. The absence of the Y chromosome is a common characteristic of most female individuals. However, there are individuals with a female phenotype who have X and Y chromosomes but lack SRY or have a variant of it that is not entirely functional.

Numerous other chromosomal or genetic variations can lead to alterations in sexual differentiation. “In phenotypically male adult subjects (with a chromosomal makeup of 46XY) with complete androgen insensitivity (so-called Morris syndrome), testosterone levels in the blood are elevated, above normal even for a male, but the hormone is totally ineffective, and the phenotype is totally female at birth, with completely female development of secondary sexual characteristics at puberty,” said Dr. Moghetti.

This means that affected individuals have well-developed breasts and a complete lack or extremely reduced presence of hair, including underarm and pubic hair. Menstruation is also completely absent because there is no uterus, and there are testes, not visible because they are considered in the abdomen.

“There are syndromes that are currently considered congenital but not genetic, of which a genetic origin will probably be identified in the future,” said Dr. Lala.

Some variations in sexual development can be diagnosed prenatally, such as an alteration of the number of sex chromosomes or a discordance between the morphologic characteristics highlighted by ultrasound and the genotype detected by amniocentesis. Some variations are evident at birth because of atypical anatomical characteristics. Others are diagnosed during puberty or later in adulthood, in the presence of infertility. The Italian National Institute of Health details these variations on its website, describing the characteristics that determine diagnosis and treatment.
 

Pathologies or Variations?

Some anomalies in sexual development negatively affect the patient’s physical health. One example is congenital adrenal hyperplasia. “It results from an inherited defect of the adrenal glands, which reduces cortisol production while increasing testosterone production,” said Dr. Lala. “In addition to the appearance of male characteristics in females, in more severe forms, it carries the risk of collapse and shock and requires pharmacological treatment.” It is undoubtedly a pathology.

Other variations in sexual characteristics do not affect the patient’s physical health negatively. They may, however, have a psychologic effect, sometimes a significant one, because of the lack of social acceptance of a person who cannot be classified within the binary classification of sexes.

“Conditions in which mixed male and female aspects are clearly evident have been and are still pathologized by the family, the treating physician, and society,” said Dr. Lala. “In the late 1970s, when a child was born with intersexual anatomical characteristics, it was common practice to surgically intervene, making them female, because it was technically easier.”

Over the years, patients who, as they grew up, were dissatisfied with the solution adopted at birth began to make their voices heard, Dr. Lala added. Scientific societies and international organizations have spoken out against subjecting intersexual newborns to surgical interventions that are not medically necessary. “Nowadays, decisions are made on a case-by-case basis, taking into account the families’ wishes. Interventions are justified with medical reasons, which are often very nuanced,” Dr. Lala concluded.
 

Implications for Sports

Traditionally, athletes participating in competitions in certain sports have been divided into male and female categories to ensure a certain equity and uniformity in performance. Over the years, the emergence of new information about sexual development has made it necessary to update the criteria used in this division.

The main factor responsible for the performance diversity between males and females is the action of testosterone on the male and female organism. “Testosterone has important effects on muscle mass and enhances training results,” said Dr. Moghetti. “As a demonstration of this fact, before puberty, the best performances in athletics or swimming by males and females are similar, then males gain a significant advantage of around 10%-20%.”

A few years ago, the World Athletics Federation conducted widespread screening of athletes participating in its world championships. “It identified a small group of individuals with potentially abnormal testosterone levels for the female sex,” said Dr. Moghetti. “Some were found to be doping, others had genetic defects, and for some, an interpretation was not even possible.”

Some of the individuals had a male genotype but a defect in 5-alpha-reductase, an enzyme essential for the formation of male genitals and hair growth. An athlete with these characteristics, assigned female sex at birth, has a male level of testosterone that stimulates the accumulation of muscle mass, Dr. Moghetti explained. Therefore, the individual has a considerable advantage in performances influenced by this hormone.

“In the end, the Federation decided to set limits on the testosterone levels of athletes participating in certain types of races, especially those in middle distance, that appeared to be more sensitive to differences in hormone levels,” said Dr. Moghetti. “The limitation does not apply to athletes with Morris syndrome, ie, with a male genotype and complete resistance to testosterone, for whom the high level of this hormone does not provide any advantage.” Given the complexity of the problem, he hopes for a case-by-case policy that considers the needs of patients with genetic alterations and those of athletes who have to compete with them.
 

Not the First Time

A recent incident underscored the difficulty of regulating such complex issues. The World Athletics Federation excluded South African middle-distance runner Caster Semenya from competitions years ago because of excessively high testosterone levels.

“The Federation’s regulations recommend that athletes in these cases reduce hormone levels to values below the threshold of 5 nmol/L of blood for a period of at least 6 months before the race by using hormonal contraceptives. The use of such drugs does not pose a health risk, as they are substances normally taken by women for contraception purposes,” said Amelia Filippelli, a pharmacologist at the University of Salerno in Italy. The South African middle-distance runner refused the drug and appealed to the Court of Arbitration for Sport and later to the Swiss Federal Court. Both rejected her appeal. Finally, Ms. Semenya appealed to the European Court of Human Rights, which in 2023 recognized a violation of her rights but does not have the authority to order a change in the Federation’s regulations.

Beyond the ideologic positions of nonexperts, therefore, the issue is still the subject of debate in the scientific community, which is evaluating not only its medical aspects but also its ethical implications.
 

This story was translated from Univadis Italy, which is part of the Medscape professional network, 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.

The allegations against Algerian boxer Imane Khelif at the Paris Olympics raised the questions of intersexuality and its implications in competitive sports. This news organization has decided to delve into the topic to assist doctors who suspect a similar condition in their patients. No certain clinical data about Ms. Khelif have been made public, so this article does not concern the boxer but rather takes inspiration from the media controversy.

What Is Intersexuality?

Intersexuality encompasses a spectrum of variations in sexual development that lead to the simultaneous presence of typical male and female characteristics. As reiterated by the United Nations Office of the High Commissioner for Human Rights, the medical definition does not affect the patient’s self-identification of gender or sexual orientation.

“The percentage of people who fall within the intersexuality spectrum is less than 0.5 per thousand of the general population, but there are no precise statistics, given the difficulty of definition,” said Roberto Lala, MD, pediatric endocrinologist and president of the Federation of Rare Childhood Diseases.

Indeed, there is not only a strict definition of intersexuality that involves a significant presence of these mixed physical characteristics in a way that conditions the self-image of the subject but also a broad definition, said Dr. Lala. “For example, clitoral hypertrophy in a female otherwise conforming to the female gender, which does not raise doubts about identity,” he said.
 

Chromosomes, Genes, and Hormones

A patient’s sexual characteristics are determined by the complex interaction of chromosomal, genetic, and hormonal factors. “The human body is, so to speak, programmed to take on female appearances in development and shifts toward male ones only if exposed to testosterone and other factors. For this to happen, testosterone must be produced during embryonic development, and it must function properly,” said Paolo Moghetti, full professor of endocrinology at the University of Verona, Italy.

The protein encoded by SRY, which is located on the Y chromosome, determines the development of the testicles from undifferentiated tissue of the embryonic gonads. The testicles of the embryo then produce testosterone. The absence of the Y chromosome is a common characteristic of most female individuals. However, there are individuals with a female phenotype who have X and Y chromosomes but lack SRY or have a variant of it that is not entirely functional.

Numerous other chromosomal or genetic variations can lead to alterations in sexual differentiation. “In phenotypically male adult subjects (with a chromosomal makeup of 46XY) with complete androgen insensitivity (so-called Morris syndrome), testosterone levels in the blood are elevated, above normal even for a male, but the hormone is totally ineffective, and the phenotype is totally female at birth, with completely female development of secondary sexual characteristics at puberty,” said Dr. Moghetti.

This means that affected individuals have well-developed breasts and a complete lack or extremely reduced presence of hair, including underarm and pubic hair. Menstruation is also completely absent because there is no uterus, and there are testes, not visible because they are considered in the abdomen.

“There are syndromes that are currently considered congenital but not genetic, of which a genetic origin will probably be identified in the future,” said Dr. Lala.

Some variations in sexual development can be diagnosed prenatally, such as an alteration of the number of sex chromosomes or a discordance between the morphologic characteristics highlighted by ultrasound and the genotype detected by amniocentesis. Some variations are evident at birth because of atypical anatomical characteristics. Others are diagnosed during puberty or later in adulthood, in the presence of infertility. The Italian National Institute of Health details these variations on its website, describing the characteristics that determine diagnosis and treatment.
 

Pathologies or Variations?

Some anomalies in sexual development negatively affect the patient’s physical health. One example is congenital adrenal hyperplasia. “It results from an inherited defect of the adrenal glands, which reduces cortisol production while increasing testosterone production,” said Dr. Lala. “In addition to the appearance of male characteristics in females, in more severe forms, it carries the risk of collapse and shock and requires pharmacological treatment.” It is undoubtedly a pathology.

Other variations in sexual characteristics do not affect the patient’s physical health negatively. They may, however, have a psychologic effect, sometimes a significant one, because of the lack of social acceptance of a person who cannot be classified within the binary classification of sexes.

“Conditions in which mixed male and female aspects are clearly evident have been and are still pathologized by the family, the treating physician, and society,” said Dr. Lala. “In the late 1970s, when a child was born with intersexual anatomical characteristics, it was common practice to surgically intervene, making them female, because it was technically easier.”

Over the years, patients who, as they grew up, were dissatisfied with the solution adopted at birth began to make their voices heard, Dr. Lala added. Scientific societies and international organizations have spoken out against subjecting intersexual newborns to surgical interventions that are not medically necessary. “Nowadays, decisions are made on a case-by-case basis, taking into account the families’ wishes. Interventions are justified with medical reasons, which are often very nuanced,” Dr. Lala concluded.
 

Implications for Sports

Traditionally, athletes participating in competitions in certain sports have been divided into male and female categories to ensure a certain equity and uniformity in performance. Over the years, the emergence of new information about sexual development has made it necessary to update the criteria used in this division.

The main factor responsible for the performance diversity between males and females is the action of testosterone on the male and female organism. “Testosterone has important effects on muscle mass and enhances training results,” said Dr. Moghetti. “As a demonstration of this fact, before puberty, the best performances in athletics or swimming by males and females are similar, then males gain a significant advantage of around 10%-20%.”

A few years ago, the World Athletics Federation conducted widespread screening of athletes participating in its world championships. “It identified a small group of individuals with potentially abnormal testosterone levels for the female sex,” said Dr. Moghetti. “Some were found to be doping, others had genetic defects, and for some, an interpretation was not even possible.”

Some of the individuals had a male genotype but a defect in 5-alpha-reductase, an enzyme essential for the formation of male genitals and hair growth. An athlete with these characteristics, assigned female sex at birth, has a male level of testosterone that stimulates the accumulation of muscle mass, Dr. Moghetti explained. Therefore, the individual has a considerable advantage in performances influenced by this hormone.

“In the end, the Federation decided to set limits on the testosterone levels of athletes participating in certain types of races, especially those in middle distance, that appeared to be more sensitive to differences in hormone levels,” said Dr. Moghetti. “The limitation does not apply to athletes with Morris syndrome, ie, with a male genotype and complete resistance to testosterone, for whom the high level of this hormone does not provide any advantage.” Given the complexity of the problem, he hopes for a case-by-case policy that considers the needs of patients with genetic alterations and those of athletes who have to compete with them.
 

Not the First Time

A recent incident underscored the difficulty of regulating such complex issues. The World Athletics Federation excluded South African middle-distance runner Caster Semenya from competitions years ago because of excessively high testosterone levels.

“The Federation’s regulations recommend that athletes in these cases reduce hormone levels to values below the threshold of 5 nmol/L of blood for a period of at least 6 months before the race by using hormonal contraceptives. The use of such drugs does not pose a health risk, as they are substances normally taken by women for contraception purposes,” said Amelia Filippelli, a pharmacologist at the University of Salerno in Italy. The South African middle-distance runner refused the drug and appealed to the Court of Arbitration for Sport and later to the Swiss Federal Court. Both rejected her appeal. Finally, Ms. Semenya appealed to the European Court of Human Rights, which in 2023 recognized a violation of her rights but does not have the authority to order a change in the Federation’s regulations.

Beyond the ideologic positions of nonexperts, therefore, the issue is still the subject of debate in the scientific community, which is evaluating not only its medical aspects but also its ethical implications.
 

This story was translated from Univadis Italy, which is part of the Medscape professional network, 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.

The allegations against Algerian boxer Imane Khelif at the Paris Olympics raised the questions of intersexuality and its implications in competitive sports. This news organization has decided to delve into the topic to assist doctors who suspect a similar condition in their patients. No certain clinical data about Ms. Khelif have been made public, so this article does not concern the boxer but rather takes inspiration from the media controversy.

What Is Intersexuality?

Intersexuality encompasses a spectrum of variations in sexual development that lead to the simultaneous presence of typical male and female characteristics. As reiterated by the United Nations Office of the High Commissioner for Human Rights, the medical definition does not affect the patient’s self-identification of gender or sexual orientation.

“The percentage of people who fall within the intersexuality spectrum is less than 0.5 per thousand of the general population, but there are no precise statistics, given the difficulty of definition,” said Roberto Lala, MD, pediatric endocrinologist and president of the Federation of Rare Childhood Diseases.

Indeed, there is not only a strict definition of intersexuality that involves a significant presence of these mixed physical characteristics in a way that conditions the self-image of the subject but also a broad definition, said Dr. Lala. “For example, clitoral hypertrophy in a female otherwise conforming to the female gender, which does not raise doubts about identity,” he said.
 

Chromosomes, Genes, and Hormones

A patient’s sexual characteristics are determined by the complex interaction of chromosomal, genetic, and hormonal factors. “The human body is, so to speak, programmed to take on female appearances in development and shifts toward male ones only if exposed to testosterone and other factors. For this to happen, testosterone must be produced during embryonic development, and it must function properly,” said Paolo Moghetti, full professor of endocrinology at the University of Verona, Italy.

The protein encoded by SRY, which is located on the Y chromosome, determines the development of the testicles from undifferentiated tissue of the embryonic gonads. The testicles of the embryo then produce testosterone. The absence of the Y chromosome is a common characteristic of most female individuals. However, there are individuals with a female phenotype who have X and Y chromosomes but lack SRY or have a variant of it that is not entirely functional.

Numerous other chromosomal or genetic variations can lead to alterations in sexual differentiation. “In phenotypically male adult subjects (with a chromosomal makeup of 46XY) with complete androgen insensitivity (so-called Morris syndrome), testosterone levels in the blood are elevated, above normal even for a male, but the hormone is totally ineffective, and the phenotype is totally female at birth, with completely female development of secondary sexual characteristics at puberty,” said Dr. Moghetti.

This means that affected individuals have well-developed breasts and a complete lack or extremely reduced presence of hair, including underarm and pubic hair. Menstruation is also completely absent because there is no uterus, and there are testes, not visible because they are considered in the abdomen.

“There are syndromes that are currently considered congenital but not genetic, of which a genetic origin will probably be identified in the future,” said Dr. Lala.

Some variations in sexual development can be diagnosed prenatally, such as an alteration of the number of sex chromosomes or a discordance between the morphologic characteristics highlighted by ultrasound and the genotype detected by amniocentesis. Some variations are evident at birth because of atypical anatomical characteristics. Others are diagnosed during puberty or later in adulthood, in the presence of infertility. The Italian National Institute of Health details these variations on its website, describing the characteristics that determine diagnosis and treatment.
 

Pathologies or Variations?

Some anomalies in sexual development negatively affect the patient’s physical health. One example is congenital adrenal hyperplasia. “It results from an inherited defect of the adrenal glands, which reduces cortisol production while increasing testosterone production,” said Dr. Lala. “In addition to the appearance of male characteristics in females, in more severe forms, it carries the risk of collapse and shock and requires pharmacological treatment.” It is undoubtedly a pathology.

Other variations in sexual characteristics do not affect the patient’s physical health negatively. They may, however, have a psychologic effect, sometimes a significant one, because of the lack of social acceptance of a person who cannot be classified within the binary classification of sexes.

“Conditions in which mixed male and female aspects are clearly evident have been and are still pathologized by the family, the treating physician, and society,” said Dr. Lala. “In the late 1970s, when a child was born with intersexual anatomical characteristics, it was common practice to surgically intervene, making them female, because it was technically easier.”

Over the years, patients who, as they grew up, were dissatisfied with the solution adopted at birth began to make their voices heard, Dr. Lala added. Scientific societies and international organizations have spoken out against subjecting intersexual newborns to surgical interventions that are not medically necessary. “Nowadays, decisions are made on a case-by-case basis, taking into account the families’ wishes. Interventions are justified with medical reasons, which are often very nuanced,” Dr. Lala concluded.
 

Implications for Sports

Traditionally, athletes participating in competitions in certain sports have been divided into male and female categories to ensure a certain equity and uniformity in performance. Over the years, the emergence of new information about sexual development has made it necessary to update the criteria used in this division.

The main factor responsible for the performance diversity between males and females is the action of testosterone on the male and female organism. “Testosterone has important effects on muscle mass and enhances training results,” said Dr. Moghetti. “As a demonstration of this fact, before puberty, the best performances in athletics or swimming by males and females are similar, then males gain a significant advantage of around 10%-20%.”

A few years ago, the World Athletics Federation conducted widespread screening of athletes participating in its world championships. “It identified a small group of individuals with potentially abnormal testosterone levels for the female sex,” said Dr. Moghetti. “Some were found to be doping, others had genetic defects, and for some, an interpretation was not even possible.”

Some of the individuals had a male genotype but a defect in 5-alpha-reductase, an enzyme essential for the formation of male genitals and hair growth. An athlete with these characteristics, assigned female sex at birth, has a male level of testosterone that stimulates the accumulation of muscle mass, Dr. Moghetti explained. Therefore, the individual has a considerable advantage in performances influenced by this hormone.

“In the end, the Federation decided to set limits on the testosterone levels of athletes participating in certain types of races, especially those in middle distance, that appeared to be more sensitive to differences in hormone levels,” said Dr. Moghetti. “The limitation does not apply to athletes with Morris syndrome, ie, with a male genotype and complete resistance to testosterone, for whom the high level of this hormone does not provide any advantage.” Given the complexity of the problem, he hopes for a case-by-case policy that considers the needs of patients with genetic alterations and those of athletes who have to compete with them.
 

Not the First Time

A recent incident underscored the difficulty of regulating such complex issues. The World Athletics Federation excluded South African middle-distance runner Caster Semenya from competitions years ago because of excessively high testosterone levels.

“The Federation’s regulations recommend that athletes in these cases reduce hormone levels to values below the threshold of 5 nmol/L of blood for a period of at least 6 months before the race by using hormonal contraceptives. The use of such drugs does not pose a health risk, as they are substances normally taken by women for contraception purposes,” said Amelia Filippelli, a pharmacologist at the University of Salerno in Italy. The South African middle-distance runner refused the drug and appealed to the Court of Arbitration for Sport and later to the Swiss Federal Court. Both rejected her appeal. Finally, Ms. Semenya appealed to the European Court of Human Rights, which in 2023 recognized a violation of her rights but does not have the authority to order a change in the Federation’s regulations.

Beyond the ideologic positions of nonexperts, therefore, the issue is still the subject of debate in the scientific community, which is evaluating not only its medical aspects but also its ethical implications.
 

This story was translated from Univadis Italy, which is part of the Medscape professional network, 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.

When Andrea Austin, MD, an emergency medicine specialist, left the military in 2020, she knew the adjustment to civilian life and practice might be difficult. To help smooth the transition, she reached out to a physician mentor who also had a professional coaching certificate. After a conversation, Dr. Austin signed up for 6 months of career coaching. 

It was time well spent, according to Dr. Austin, who today is a coach herself. “It was really the first time I had the ability to choose what I wanted to do, and that required a mindset shift,” she explains. “A big part of coaching is helping physicians discover their agency so that they can make the best career choices.” 

courtesy Dr. Andrea Austin

Physicians have long lacked the coaching resources typically made available to corporate executives. But that’s changing. In today’s high-pressure environment, where doctors are burning out at a rapid pace, coaching can sometimes be an avenue to staying in the field, especially if that coach is a fellow physician who understands what you’re facing. 

With a physician shortage that the Association of American Medical Colleges expects to hit 86,000 in the next decade or so, coaching could be a stone worth turning over. A 2024 report in JAMA Network Open found that coaching provided by physician peers led to a significant reduction in interpersonal disengagement and burnout. 

“What I think is exciting about coaching is that it allows you to better understand yourself and know your strengths and weaknesses,” said Dr. Austin. “It might seem simple, but many ‘soft skills’ aren’t considered mainstream in medicine. Coaching allows us to understand them and ourselves better.” 
 

Why Are Doctors Using Coaches?

Although it’s hard to put a number on how many physicians are turning to coaches, the number of coaches available for doctors is growing rapidly. The American Medical Women’s Association maintains a database of physician coaches. According to deputy director Jodi Godfrey, MS, RDN, the number of members who have added coaching to their skill set has tripled in the past 4 years. “Many cite burnout as the reason they sought coaching support, and then they decided to go on to get certified in coaching.”

courtesy Michael Hanlon

The pandemic is one reason physician coaching has grown, said Elizabeth Esparaz, MD, an ophthalmologist and physician coach. “Since the pandemic, the word ‘burnout’ is thrown around a good deal.” And the causes are clear. “Doctors are facing longer hours, they must make split-second decisions, they’re multitasking, and they have less support staff.”

Among her coaching clients, Dr. Austin has noticed other common struggles: fears of litigation, time scarcity with patients, declining reimbursement that hasn’t kept up with inflation, and loss of autonomy because of the corporatization of healthcare. 

Coaching, Dr. Esparaz believes, can be an antidote to many of these issues. “Coaches help doctors see their strengths and find better ways of applying them,” she said. “We help them move forward, and also see their blind spots.”
 

Clarity, Goals, and Making the Right Choices

Physician coaching comes in a variety of flavors — some one on one, and others in the form of group sessions. All, however, serve the purpose of helping physicians gain career clarity. “Sometimes clients realize their job may not be working for them, but that there are things they can do to change that without having to leave the field,” said Jattu Senesie, MD, a former ob.gyn. who is now a physician coach. 

Dr. Esparaz works with doctors to establish SMART goals: specific, measurable, attainable, realistic, and time based. She gave the example of learning how to set boundaries. “If a physician is asked to create a presentation for work, I encourage them to ask for compensation or administrative time before committing to unpaid tasks.”

Another big issue: charting. It’s increasingly burdensome, and many doctors find it encroaching on their home lives. “If we can identify a problem like that, we can come up with a strategy for mitigating it,” Dr. Esparaz said. This might include setting a goal of getting 80% of charting completed immediately after the patient encounter on the busiest clinic day of the week. The client tests the experiment and then revisits it with the coach to discuss what worked and what didn’t, refining the process until it has freed up the physician’s home life. 

courtesy Dr. Jattu Senesie

The younger generation of doctors often struggles with career choices, too, because it’s the first time they are without structure, said Dr. Senesie. There’s med school and residency, which puts a framework around every move a doctor makes. But once they become attending physicians, the choices are endless. “Coaching can help them find a new structure and systems that will allow them to thrive.”

Although mentoring has been a well-embraced concept for decades, it “hits a wall,” at some point in terms of what it can offer, Dr. Austin said. That’s where coaching can take over. “There’s a point where a mentor cannot help someone self-actualize. As a coach, you don’t need to know everything about a doctor’s life, but you can help them learn to ask themselves the right questions to solve problems.”
 

Should You Stay or Should You Go?

Dr. Austin’s approach begins with the premise that healthcare today is challenging and dysfunctional — but doctors still have agency. She has worked with clients on the verge of leaving the field and helped them find their way back. 

“They have a light bulb moment and open up to the idea that they have much to give still,” she said. “We take an inventory to help them better communicate their needs and make changes, and I help them connect to their values. Sometimes that exercise allows them to reframe their current work environment.” 

Not every doctor who goes through coaching remains in the field. But “that’s the exception, not the rule,” Dr. Austin said. And that’s okay. “If that’s the outcome, coaching probably helped them get to that point faster, and with an informed decision.” 

Dr. Senesie has been coaching for about a decade, and in that time, she’s seen a shift that goes beyond figuring out career goals. “Doctors are more aware of the need for well-being today. The pandemic made it impossible to ignore what doesn’t work for us. When I work with clients, we look for ways to make the job more tenable.” 

According to Dr. Senesie, younger doctors are looking for that balance at the outset. “They want to be physicians, but they also want a life,” she said. “It’s a challenge for them because in addition to that mindset, they’re also coming out with more debt than older generations. They want out from underneath that.”
 

When It’s Time to Find a Physician Coach

Wondering whether coaching is right for you? Consider these symptoms:

• You need help setting boundaries at work.
• You feel like you’re sacrificing your own well-being for your job.
• You’re using maladaptive strategies to cope with the stress at work.
• You’ve reached a point where you are considering leaving the field.

If you’re interested in finding a physician coach, there are several places to begin your search, word of mouth being one of them. “Conferences and social media can also expose you to coaches,” suggested Dr. Esparaz. There are different methods and approaches to coaching. So, as you research, “make sure the coach you choose has techniques and a framework that fit what you’re after.” 

Dr. Austin warned that it is an unregulated industry, so buyer beware. To ensure you’re getting an accredited physician coach, look for people who have obtained an International Coach Federation (ICF) accreditation. These coaches will hold an associate certified coach credential, which requires at least 60 hours of coaching-specific training approved by the ICF, in addition to other assessments and education. 

Ensure that the coach you choose is within your budget. “There are some people charging astronomical rates out there,” Dr. Austin said. “If you’re burned out or struggling, it can be easy to reach for your credit card.”

Dr. Austin also cautioned doctors seeking a coach to avoid promises that sound too good to be true. Some coaching can have a gaslighting quality to it, she warned, “suggesting it can allow you to endure any environment.” But positive self-talk alone won’t cure an abusive or discriminatory situation. “If a client describes a toxic work environment,” the coach has an “ethical imperative” to help that person protect themselves. 
 

A Side Gig or a New Career Path

After Dr. Austin’s experience with her coach, she made the choice to continue as an emergency physician part-time while starting her own coaching business. “It’s important for me personally to keep in touch with what’s happening on the ground, but I have no judgment for anyone who chooses to leave clinical practice to become a coach.”

When Dr. Senesie looks back on her own struggles as a clinician, she recognizes the state of burnout she was in 10 years ago. “I knew there was an issue, but I didn’t have the mindset to find a way to make it work,” she said. “I left the field when I was at my depths of burnout, which is generally not the best way to go about it.” 

Guidance might have allowed her to take into account other avenues and helped her remain in the field, said Dr. Senesie. She has since learned that “there are many ways to practice medicine, and the way we’ve gone about it traditionally has worked for some, but not necessarily for everyone.” 

There may be more possibilities than you think. By helping you assess your path and make meaningful changes, a physician coach might be the key to remaining in the field you love.

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

When Andrea Austin, MD, an emergency medicine specialist, left the military in 2020, she knew the adjustment to civilian life and practice might be difficult. To help smooth the transition, she reached out to a physician mentor who also had a professional coaching certificate. After a conversation, Dr. Austin signed up for 6 months of career coaching. 

It was time well spent, according to Dr. Austin, who today is a coach herself. “It was really the first time I had the ability to choose what I wanted to do, and that required a mindset shift,” she explains. “A big part of coaching is helping physicians discover their agency so that they can make the best career choices.” 

courtesy Dr. Andrea Austin

Physicians have long lacked the coaching resources typically made available to corporate executives. But that’s changing. In today’s high-pressure environment, where doctors are burning out at a rapid pace, coaching can sometimes be an avenue to staying in the field, especially if that coach is a fellow physician who understands what you’re facing. 

With a physician shortage that the Association of American Medical Colleges expects to hit 86,000 in the next decade or so, coaching could be a stone worth turning over. A 2024 report in JAMA Network Open found that coaching provided by physician peers led to a significant reduction in interpersonal disengagement and burnout. 

“What I think is exciting about coaching is that it allows you to better understand yourself and know your strengths and weaknesses,” said Dr. Austin. “It might seem simple, but many ‘soft skills’ aren’t considered mainstream in medicine. Coaching allows us to understand them and ourselves better.” 
 

Why Are Doctors Using Coaches?

Although it’s hard to put a number on how many physicians are turning to coaches, the number of coaches available for doctors is growing rapidly. The American Medical Women’s Association maintains a database of physician coaches. According to deputy director Jodi Godfrey, MS, RDN, the number of members who have added coaching to their skill set has tripled in the past 4 years. “Many cite burnout as the reason they sought coaching support, and then they decided to go on to get certified in coaching.”

courtesy Michael Hanlon

The pandemic is one reason physician coaching has grown, said Elizabeth Esparaz, MD, an ophthalmologist and physician coach. “Since the pandemic, the word ‘burnout’ is thrown around a good deal.” And the causes are clear. “Doctors are facing longer hours, they must make split-second decisions, they’re multitasking, and they have less support staff.”

Among her coaching clients, Dr. Austin has noticed other common struggles: fears of litigation, time scarcity with patients, declining reimbursement that hasn’t kept up with inflation, and loss of autonomy because of the corporatization of healthcare. 

Coaching, Dr. Esparaz believes, can be an antidote to many of these issues. “Coaches help doctors see their strengths and find better ways of applying them,” she said. “We help them move forward, and also see their blind spots.”
 

Clarity, Goals, and Making the Right Choices

Physician coaching comes in a variety of flavors — some one on one, and others in the form of group sessions. All, however, serve the purpose of helping physicians gain career clarity. “Sometimes clients realize their job may not be working for them, but that there are things they can do to change that without having to leave the field,” said Jattu Senesie, MD, a former ob.gyn. who is now a physician coach. 

Dr. Esparaz works with doctors to establish SMART goals: specific, measurable, attainable, realistic, and time based. She gave the example of learning how to set boundaries. “If a physician is asked to create a presentation for work, I encourage them to ask for compensation or administrative time before committing to unpaid tasks.”

Another big issue: charting. It’s increasingly burdensome, and many doctors find it encroaching on their home lives. “If we can identify a problem like that, we can come up with a strategy for mitigating it,” Dr. Esparaz said. This might include setting a goal of getting 80% of charting completed immediately after the patient encounter on the busiest clinic day of the week. The client tests the experiment and then revisits it with the coach to discuss what worked and what didn’t, refining the process until it has freed up the physician’s home life. 

courtesy Dr. Jattu Senesie

The younger generation of doctors often struggles with career choices, too, because it’s the first time they are without structure, said Dr. Senesie. There’s med school and residency, which puts a framework around every move a doctor makes. But once they become attending physicians, the choices are endless. “Coaching can help them find a new structure and systems that will allow them to thrive.”

Although mentoring has been a well-embraced concept for decades, it “hits a wall,” at some point in terms of what it can offer, Dr. Austin said. That’s where coaching can take over. “There’s a point where a mentor cannot help someone self-actualize. As a coach, you don’t need to know everything about a doctor’s life, but you can help them learn to ask themselves the right questions to solve problems.”
 

Should You Stay or Should You Go?

Dr. Austin’s approach begins with the premise that healthcare today is challenging and dysfunctional — but doctors still have agency. She has worked with clients on the verge of leaving the field and helped them find their way back. 

“They have a light bulb moment and open up to the idea that they have much to give still,” she said. “We take an inventory to help them better communicate their needs and make changes, and I help them connect to their values. Sometimes that exercise allows them to reframe their current work environment.” 

Not every doctor who goes through coaching remains in the field. But “that’s the exception, not the rule,” Dr. Austin said. And that’s okay. “If that’s the outcome, coaching probably helped them get to that point faster, and with an informed decision.” 

Dr. Senesie has been coaching for about a decade, and in that time, she’s seen a shift that goes beyond figuring out career goals. “Doctors are more aware of the need for well-being today. The pandemic made it impossible to ignore what doesn’t work for us. When I work with clients, we look for ways to make the job more tenable.” 

According to Dr. Senesie, younger doctors are looking for that balance at the outset. “They want to be physicians, but they also want a life,” she said. “It’s a challenge for them because in addition to that mindset, they’re also coming out with more debt than older generations. They want out from underneath that.”
 

When It’s Time to Find a Physician Coach

Wondering whether coaching is right for you? Consider these symptoms:

• You need help setting boundaries at work.
• You feel like you’re sacrificing your own well-being for your job.
• You’re using maladaptive strategies to cope with the stress at work.
• You’ve reached a point where you are considering leaving the field.

If you’re interested in finding a physician coach, there are several places to begin your search, word of mouth being one of them. “Conferences and social media can also expose you to coaches,” suggested Dr. Esparaz. There are different methods and approaches to coaching. So, as you research, “make sure the coach you choose has techniques and a framework that fit what you’re after.” 

Dr. Austin warned that it is an unregulated industry, so buyer beware. To ensure you’re getting an accredited physician coach, look for people who have obtained an International Coach Federation (ICF) accreditation. These coaches will hold an associate certified coach credential, which requires at least 60 hours of coaching-specific training approved by the ICF, in addition to other assessments and education. 

Ensure that the coach you choose is within your budget. “There are some people charging astronomical rates out there,” Dr. Austin said. “If you’re burned out or struggling, it can be easy to reach for your credit card.”

Dr. Austin also cautioned doctors seeking a coach to avoid promises that sound too good to be true. Some coaching can have a gaslighting quality to it, she warned, “suggesting it can allow you to endure any environment.” But positive self-talk alone won’t cure an abusive or discriminatory situation. “If a client describes a toxic work environment,” the coach has an “ethical imperative” to help that person protect themselves. 
 

A Side Gig or a New Career Path

After Dr. Austin’s experience with her coach, she made the choice to continue as an emergency physician part-time while starting her own coaching business. “It’s important for me personally to keep in touch with what’s happening on the ground, but I have no judgment for anyone who chooses to leave clinical practice to become a coach.”

When Dr. Senesie looks back on her own struggles as a clinician, she recognizes the state of burnout she was in 10 years ago. “I knew there was an issue, but I didn’t have the mindset to find a way to make it work,” she said. “I left the field when I was at my depths of burnout, which is generally not the best way to go about it.” 

Guidance might have allowed her to take into account other avenues and helped her remain in the field, said Dr. Senesie. She has since learned that “there are many ways to practice medicine, and the way we’ve gone about it traditionally has worked for some, but not necessarily for everyone.” 

There may be more possibilities than you think. By helping you assess your path and make meaningful changes, a physician coach might be the key to remaining in the field you love.

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

When Andrea Austin, MD, an emergency medicine specialist, left the military in 2020, she knew the adjustment to civilian life and practice might be difficult. To help smooth the transition, she reached out to a physician mentor who also had a professional coaching certificate. After a conversation, Dr. Austin signed up for 6 months of career coaching. 

It was time well spent, according to Dr. Austin, who today is a coach herself. “It was really the first time I had the ability to choose what I wanted to do, and that required a mindset shift,” she explains. “A big part of coaching is helping physicians discover their agency so that they can make the best career choices.” 

courtesy Dr. Andrea Austin

Physicians have long lacked the coaching resources typically made available to corporate executives. But that’s changing. In today’s high-pressure environment, where doctors are burning out at a rapid pace, coaching can sometimes be an avenue to staying in the field, especially if that coach is a fellow physician who understands what you’re facing. 

With a physician shortage that the Association of American Medical Colleges expects to hit 86,000 in the next decade or so, coaching could be a stone worth turning over. A 2024 report in JAMA Network Open found that coaching provided by physician peers led to a significant reduction in interpersonal disengagement and burnout. 

“What I think is exciting about coaching is that it allows you to better understand yourself and know your strengths and weaknesses,” said Dr. Austin. “It might seem simple, but many ‘soft skills’ aren’t considered mainstream in medicine. Coaching allows us to understand them and ourselves better.” 
 

Why Are Doctors Using Coaches?

Although it’s hard to put a number on how many physicians are turning to coaches, the number of coaches available for doctors is growing rapidly. The American Medical Women’s Association maintains a database of physician coaches. According to deputy director Jodi Godfrey, MS, RDN, the number of members who have added coaching to their skill set has tripled in the past 4 years. “Many cite burnout as the reason they sought coaching support, and then they decided to go on to get certified in coaching.”

courtesy Michael Hanlon

The pandemic is one reason physician coaching has grown, said Elizabeth Esparaz, MD, an ophthalmologist and physician coach. “Since the pandemic, the word ‘burnout’ is thrown around a good deal.” And the causes are clear. “Doctors are facing longer hours, they must make split-second decisions, they’re multitasking, and they have less support staff.”

Among her coaching clients, Dr. Austin has noticed other common struggles: fears of litigation, time scarcity with patients, declining reimbursement that hasn’t kept up with inflation, and loss of autonomy because of the corporatization of healthcare. 

Coaching, Dr. Esparaz believes, can be an antidote to many of these issues. “Coaches help doctors see their strengths and find better ways of applying them,” she said. “We help them move forward, and also see their blind spots.”
 

Clarity, Goals, and Making the Right Choices

Physician coaching comes in a variety of flavors — some one on one, and others in the form of group sessions. All, however, serve the purpose of helping physicians gain career clarity. “Sometimes clients realize their job may not be working for them, but that there are things they can do to change that without having to leave the field,” said Jattu Senesie, MD, a former ob.gyn. who is now a physician coach. 

Dr. Esparaz works with doctors to establish SMART goals: specific, measurable, attainable, realistic, and time based. She gave the example of learning how to set boundaries. “If a physician is asked to create a presentation for work, I encourage them to ask for compensation or administrative time before committing to unpaid tasks.”

Another big issue: charting. It’s increasingly burdensome, and many doctors find it encroaching on their home lives. “If we can identify a problem like that, we can come up with a strategy for mitigating it,” Dr. Esparaz said. This might include setting a goal of getting 80% of charting completed immediately after the patient encounter on the busiest clinic day of the week. The client tests the experiment and then revisits it with the coach to discuss what worked and what didn’t, refining the process until it has freed up the physician’s home life. 

courtesy Dr. Jattu Senesie

The younger generation of doctors often struggles with career choices, too, because it’s the first time they are without structure, said Dr. Senesie. There’s med school and residency, which puts a framework around every move a doctor makes. But once they become attending physicians, the choices are endless. “Coaching can help them find a new structure and systems that will allow them to thrive.”

Although mentoring has been a well-embraced concept for decades, it “hits a wall,” at some point in terms of what it can offer, Dr. Austin said. That’s where coaching can take over. “There’s a point where a mentor cannot help someone self-actualize. As a coach, you don’t need to know everything about a doctor’s life, but you can help them learn to ask themselves the right questions to solve problems.”
 

Should You Stay or Should You Go?

Dr. Austin’s approach begins with the premise that healthcare today is challenging and dysfunctional — but doctors still have agency. She has worked with clients on the verge of leaving the field and helped them find their way back. 

“They have a light bulb moment and open up to the idea that they have much to give still,” she said. “We take an inventory to help them better communicate their needs and make changes, and I help them connect to their values. Sometimes that exercise allows them to reframe their current work environment.” 

Not every doctor who goes through coaching remains in the field. But “that’s the exception, not the rule,” Dr. Austin said. And that’s okay. “If that’s the outcome, coaching probably helped them get to that point faster, and with an informed decision.” 

Dr. Senesie has been coaching for about a decade, and in that time, she’s seen a shift that goes beyond figuring out career goals. “Doctors are more aware of the need for well-being today. The pandemic made it impossible to ignore what doesn’t work for us. When I work with clients, we look for ways to make the job more tenable.” 

According to Dr. Senesie, younger doctors are looking for that balance at the outset. “They want to be physicians, but they also want a life,” she said. “It’s a challenge for them because in addition to that mindset, they’re also coming out with more debt than older generations. They want out from underneath that.”
 

When It’s Time to Find a Physician Coach

Wondering whether coaching is right for you? Consider these symptoms:

• You need help setting boundaries at work.
• You feel like you’re sacrificing your own well-being for your job.
• You’re using maladaptive strategies to cope with the stress at work.
• You’ve reached a point where you are considering leaving the field.

If you’re interested in finding a physician coach, there are several places to begin your search, word of mouth being one of them. “Conferences and social media can also expose you to coaches,” suggested Dr. Esparaz. There are different methods and approaches to coaching. So, as you research, “make sure the coach you choose has techniques and a framework that fit what you’re after.” 

Dr. Austin warned that it is an unregulated industry, so buyer beware. To ensure you’re getting an accredited physician coach, look for people who have obtained an International Coach Federation (ICF) accreditation. These coaches will hold an associate certified coach credential, which requires at least 60 hours of coaching-specific training approved by the ICF, in addition to other assessments and education. 

Ensure that the coach you choose is within your budget. “There are some people charging astronomical rates out there,” Dr. Austin said. “If you’re burned out or struggling, it can be easy to reach for your credit card.”

Dr. Austin also cautioned doctors seeking a coach to avoid promises that sound too good to be true. Some coaching can have a gaslighting quality to it, she warned, “suggesting it can allow you to endure any environment.” But positive self-talk alone won’t cure an abusive or discriminatory situation. “If a client describes a toxic work environment,” the coach has an “ethical imperative” to help that person protect themselves. 
 

A Side Gig or a New Career Path

After Dr. Austin’s experience with her coach, she made the choice to continue as an emergency physician part-time while starting her own coaching business. “It’s important for me personally to keep in touch with what’s happening on the ground, but I have no judgment for anyone who chooses to leave clinical practice to become a coach.”

When Dr. Senesie looks back on her own struggles as a clinician, she recognizes the state of burnout she was in 10 years ago. “I knew there was an issue, but I didn’t have the mindset to find a way to make it work,” she said. “I left the field when I was at my depths of burnout, which is generally not the best way to go about it.” 

Guidance might have allowed her to take into account other avenues and helped her remain in the field, said Dr. Senesie. She has since learned that “there are many ways to practice medicine, and the way we’ve gone about it traditionally has worked for some, but not necessarily for everyone.” 

There may be more possibilities than you think. By helping you assess your path and make meaningful changes, a physician coach might be the key to remaining in the field you love.

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