Commentary

The use of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) has increased over the past several years and has become a cornerstone in both diabetes and weight loss management, particularly because of its unique combination of glucose control, weight reduction potential, and cardiac and metabolic benefits. However, increased use of these agents presents a dilemma in gastrointestinal endoscopy as it pertains to their safety and management during the periprocedural period.

This review explores management of GLP-1 RAs in the periprocedural setting for endoscopic procedures based on current evidence and guidelines, highlighting gaps and future directions.

 

Pharmacology and Mechanisms of Action

GLP-1 RAs have several mechanisms of action that make them relevant in gastrointestinal endoscopy. These medications modulate glucose control via enhancement of glucose-dependent insulin secretion and reduction of postprandial glucagon, which promotes satiety and delays gastric emptying. This delay in gastric emptying mediated by vagal pathways has been postulated to increase gastric residuals, posing a risk for aspiration during anesthesia.¹

It is important to also consider the pharmacokinetics of GLP-1 RAs, as some have shorter half-lives on the order of several hours, like exenatide, while others, like semaglutide, are dosed weekly. Additionally, common side effects of GLP-1 RAs include nausea, vomiting, bloating, and early satiety, which pose challenges for patients undergoing endoscopic procedures. 

 

Current Guidelines

Various societies have published guidelines on the periprocedural use of GLP-1 RAs. The American Society of Anesthesiologist (ASA) in 2023 presented early recommendations to hold GLP-1 RAs either day of procedure or week prior depending on pharmacokinetics, because of the risk of delayed gastric emptying and increased potential for aspiration.² Soon thereafter, a multi-gastroenterology society guideline was released stating more data is needed to decide if GLP-1 RAs need to be held prior to endoscopic procedures.³

In early 2024, the American Gastroenterological Association (AGA) published a rapid clinical update that advocated for a more individualized approach, particularly in light of limited overall data for GLP-1 RAs and endoscopic procedures.⁴ In asymptomatic patients who follow typical fasting protocols for procedures, it is generally safe to proceed with endoscopy without holding GLP-1 RAs. In symptomatic patients (nausea, abdominal distension, etc), the AGA advises additional precautions, including performing transabdominal ultrasound if feasible to assess retained gastric contents. The AGA also suggests placing a patient on a clear liquid diet the day prior to the procedure — rather than holding GLP-1 RAs — as another reasonable strategy.

The guidelines continue to evolve with newer multi-society guidelines establishing best practices. While initially in 2023 the ASA did recommend holding these medications prior to endoscopy, the initial guidance was based on expert opinion with limited evidence. Newer multi-society guidance published jointly by the ASA along with various gastroenterology societies, including the AGA in December 2024, takes a more nuanced approach.⁵

The newer guidelines include two main recommendations:

1. Periprocedural management of GLP-1 RAs should be a joint decision among the procedural, anesthesia, and prescribing team balancing metabolic needs vs patient risks.

• In a low-risk patient, one that is asymptomatic and on standard dosing, among other factors, the guidance states that GLP-1 RAs can be continued.
• In higher-risk patients, the original guidance of holding a day or a week prior to endoscopic procedures should be followed.

2. Periprocedural management of GLP-1 RAs should attempt to minimize the aspiration risks loosely associated with delayed gastric emptying.

• Consider a 24-hour clear liquid diet a day prior to the procedure and transabdominal ultrasound to check gastric contents.
• It is acknowledged that this guidance is based on limited evidence and will be evolving as new medications and data are released.

Recent Clinical Studies

Although there is very little data to guide clinicians, several recent studies have been published that can direct clinical decision-making as guidelines continue to be refined and updated.

A multicenter trial of approximately 800 patients undergoing upper endoscopy found a significant difference in rates of retained gastric contents between those that underwent endoscopy who did and did not follow the ASA guidance on periprocedural management of GLP-1 RAs (12.7% vs 4.4%; P < .0001). However, there were no significant differences in rates of aborted procedures or unplanned intubations.

Furthermore, a multivariable analysis was performed controlling for GLP-1 RA type and other factors, which found the likelihood of gastric retention increased by 36% for every 1% increase in hemoglobin A1c. This study suggests that a more individualized approach to holding GLP-1 RA would be applicable rather than a universal periprocedural hold.⁶

More recently, a single-center study of nearly 600 patients undergoing upper endoscopy showed that while there were slightly increased rates of retained gastric contents (OR 3.80; P = .003) and aborted procedures (1.3% vs 0%; P = .02), the rates of adverse anesthesia events (hypoxia, etc) were similar between the groups and no cases of pulmonary aspiration were noted.7

One single-center study of 57 patients evaluated the safety of GLP-1 RAs in those undergoing endoscopic sleeve gastrectomy. GLP-1 RAs were continued on all patients, but all adhered to a liquid only diet for at least 24 hours prior to the procedure. There were no instances of retained gastric solids, aspiration, or hypoxia. This study suggests that with a 24-hour clear liquid diet and routine NPO recommendations prior to endoscopy, it would be safe to continue GLP-1 RAs. This study provides rationale for the AGA recommendation for a clear liquid diet 24 hours prior to endoscopic procedures for those on GLP-1 RAs.⁸

A study looking at those who underwent emergency surgery and endoscopy with claims data of use of GLP-1 RAs found an overall incidence of postoperative respiratory complications of 3.5% for those with GLP-1 RAs fill history vs 4.0% for those without (P = .12). Approximately 800 of the 24,000 patients identified had undergone endoscopic procedures for GI bleeding or food impaction. The study overall showed that preoperative use of GLP-1 RAs in patients undergoing surgery or endoscopy, evaluated as a combined group, was not associated with an increased risk of pulmonary complications.⁹

Lastly, a systematic review and meta-analysis that included 15 studies that quantified gastric emptying using various methods, including gastric emptying scintigraphy and acetaminophen absorption test, found that there was a quantifiable delay in gastric emptying of about 36 minutes, compared to placebo (P < .01), in patients using GLP-1 RAs. However, compared to standard periprocedural fasting, this delay is clinically insignificant and standard fasting protocols would still be appropriate for patients on GLP-1 RAs.¹⁰

These studies taken together suggest that while GLP-1 RAs can mildly increase the likelihood of retained gastric contents, there is no statistically significant increase in the risk of aspiration or other anesthesia complications. Furthermore, while decreased gastric emptying is a known effect of GLP-1 RAs, this effect may not be clinically significant in the context of standard periprocedural fasting protocols particularly when combined with a 24-hour clear liquid diet. These findings support at a minimum a more patient-specific strategy for periprocedural management of GLP-1 RAs.

 

Clinical Implications

These most recent studies, as well as prior studies and guidelines by various societies lead to a dilemma among endoscopists on proper patient counseling on GLP-1 RAs use before endoscopic procedures. Clinicians must balance the metabolic benefits of GLP-1 RAs with potential endoscopic complications and risks.

Holding therapy theoretically decreases aspiration risk and pulmonary complications, though evidence remains low to support this. Holding medication, however, affects glycemic control leading to potential rebound hyperglycemia which may impact and delay plans for endoscopy. With growing indications for the use of GLP-1 RAs, a more tailored patient-centered treatment plan may be required, especially with consideration of procedure indication and comorbidities.

Currently, practice patterns at different institutions vary widely, making standardization much more difficult. Some centers have opted to follow ASA guidelines of holding these medications up to 1 week prior to procedures, while others have continued therapy with no pre-procedural adjustments. This leaves endoscopists to deal with the downstream effects of inconvenience to patients, care delays, and financial considerations if procedures are postponed related to GLP-1 RAs use.

 

Future Directions

Future studies are needed to make further evidence-based recommendations. Studies should focus on stratifying risks and recommendations based on procedure type (EGD, colonoscopy, etc). More widespread implementation of gastric ultrasound can assist in real-time decision-making, albeit this would require expertise and dedicated time within the pre-procedural workflow. Randomized controlled trials comparing outcomes of patients who continue GLP-1 RAs vs those who discontinue stratified by baseline risk will be instrumental for making concrete guidelines that provide clarity on periprocedural management of GLP-1 RAs.

Conclusion

The periprocedural management of GLP-1 RAs remains a controversial topic that presents unique challenges in endoscopy. Several guidelines have been released by various stakeholders including anesthesiologists, gastroenterologists, and other prescribing providers. Clinical data remains limited with no robust evidence available to suggest that gastric emptying delays caused by GLP-1 RAs prior to endoscopic procedures significantly increases risk of aspiration, pulmonary complications, or other comorbidities. Evolving multi-society guidelines will be important to establish more consistent practices with reassessment of the data as new studies emerge. A multidisciplinary, individualized patient approach may be the best strategy for managing GLP-1 RAs for patients undergoing endoscopic procedures.

Dr. Sekar and Dr. Asamoah are based in the department of gastroenterology at MedStar Georgetown University Hospital, Washington, D.C. Dr. Sekar reports no conflicts of interest in regard to this article. Dr. Asamoah serves on the Johnson & Johnson advisory board for inflammatory bowel disease–related therapies.

References

1. Halim MA et al. Glucagon-Like Peptide-1 Inhibits Prandial Gastrointestinal Motility Through Myenteric Neuronal Mechanisms in Humans. J Clin Endocrinol Metab. 2018 Feb. doi: 10.1210/jc.2017-02006.

2. American Society of Anesthesiologists. American Society of Anesthesiologists releases consensus-based guidance on preoperative use of GLP-1 receptor agonists. 2023 Jun 20. www.asahq.org/about-asa/newsroom/news-releases/2023/06/american-society-of-anesthesiologists-consensus-based-guidance-on-preoperative

3. American Gastroenterological Association. GI multi-society statement regarding GLP-1 agonists and endoscopy. 2023 Jul 25. gastro.org/news/gi-multi-society-statement-regarding-glp-1-agonists-and-endoscopy/.

4. Hashash JG et al. AGA Rapid Clinical Practice Update on the Management of Patients Taking GLP-1 Receptor Agonists Prior to Endoscopy: Communication. Clin Gastroenterol Hepatol. 2024 Apr. doi: 10.1016/j.cgh.2023.11.002.

5. Kindel TL et al; American Gastroenterological Association; American Society for Metabolic and Bariatric Surgery; American Society of Anesthesiologists; International Society of Perioperative Care of Patients with Obesity; Society of American Gastrointestinal and Endoscopic Surgeons. Multi-society Clinical Practice Guidance for the Safe Use of Glucagon-like Peptide-1 Receptor Agonists in the Perioperative Period. Clin Gastroenterol Hepatol. 2024 Oct. doi: 10.1016/j.cgh.2024.10.003.

6. Phan J et al. Glucagon-Like Peptide Receptor Agonists Use Before Endoscopy Is Associated With Low Retained Gastric Contents: A Multicenter Cross-Sectional Analysis. Am J Gastroenterol. 2025 Mar. doi: 10.14309/ajg.0000000000002969.

7. Panchal S et al. Endoscopy and Anesthesia Outcomes Associated With Glucagon-like Peptide-1 Receptor Agonist use in Patients Undergoing Outpatient Upper Endoscopy. Gastrointest Endosc. 2025 Aug. doi:10.1016/j.gie.2025.01.004.

8. Maselli DB et al. Safe Continuation of glucagon-like Peptide 1 Receptor Agonists at Endoscopy: A Case Series of 57 Adults Undergoing Endoscopic Sleeve Gastroplasty. Obes Surg. 2024 Jul. doi: 10.1007/s11695-024-07278-2.

9. Dixit AA et al. Preoperative GLP-1 Receptor Agonist Use and Risk of Postoperative Respiratory Complications. JAMA. 2024 Apr. doi: 10.1001/jama.2024.5003.

10. Hiramoto B et al. Quantified Metrics of Gastric Emptying Delay by Glucagon-Like Peptide-1 Agonists: A systematic review and meta-analysis with insights for periprocedural management. Am J Gastroenterol. 2024 Jun. doi: 10.14309/ajg.0000000000002820.

The use of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) has increased over the past several years and has become a cornerstone in both diabetes and weight loss management, particularly because of its unique combination of glucose control, weight reduction potential, and cardiac and metabolic benefits. However, increased use of these agents presents a dilemma in gastrointestinal endoscopy as it pertains to their safety and management during the periprocedural period.

This review explores management of GLP-1 RAs in the periprocedural setting for endoscopic procedures based on current evidence and guidelines, highlighting gaps and future directions.

 

Pharmacology and Mechanisms of Action

GLP-1 RAs have several mechanisms of action that make them relevant in gastrointestinal endoscopy. These medications modulate glucose control via enhancement of glucose-dependent insulin secretion and reduction of postprandial glucagon, which promotes satiety and delays gastric emptying. This delay in gastric emptying mediated by vagal pathways has been postulated to increase gastric residuals, posing a risk for aspiration during anesthesia.¹

It is important to also consider the pharmacokinetics of GLP-1 RAs, as some have shorter half-lives on the order of several hours, like exenatide, while others, like semaglutide, are dosed weekly. Additionally, common side effects of GLP-1 RAs include nausea, vomiting, bloating, and early satiety, which pose challenges for patients undergoing endoscopic procedures. 

 

Current Guidelines

Various societies have published guidelines on the periprocedural use of GLP-1 RAs. The American Society of Anesthesiologist (ASA) in 2023 presented early recommendations to hold GLP-1 RAs either day of procedure or week prior depending on pharmacokinetics, because of the risk of delayed gastric emptying and increased potential for aspiration.² Soon thereafter, a multi-gastroenterology society guideline was released stating more data is needed to decide if GLP-1 RAs need to be held prior to endoscopic procedures.³

In early 2024, the American Gastroenterological Association (AGA) published a rapid clinical update that advocated for a more individualized approach, particularly in light of limited overall data for GLP-1 RAs and endoscopic procedures.⁴ In asymptomatic patients who follow typical fasting protocols for procedures, it is generally safe to proceed with endoscopy without holding GLP-1 RAs. In symptomatic patients (nausea, abdominal distension, etc), the AGA advises additional precautions, including performing transabdominal ultrasound if feasible to assess retained gastric contents. The AGA also suggests placing a patient on a clear liquid diet the day prior to the procedure — rather than holding GLP-1 RAs — as another reasonable strategy.

The guidelines continue to evolve with newer multi-society guidelines establishing best practices. While initially in 2023 the ASA did recommend holding these medications prior to endoscopy, the initial guidance was based on expert opinion with limited evidence. Newer multi-society guidance published jointly by the ASA along with various gastroenterology societies, including the AGA in December 2024, takes a more nuanced approach.⁵

The newer guidelines include two main recommendations:

1. Periprocedural management of GLP-1 RAs should be a joint decision among the procedural, anesthesia, and prescribing team balancing metabolic needs vs patient risks.

• In a low-risk patient, one that is asymptomatic and on standard dosing, among other factors, the guidance states that GLP-1 RAs can be continued.
• In higher-risk patients, the original guidance of holding a day or a week prior to endoscopic procedures should be followed.

2. Periprocedural management of GLP-1 RAs should attempt to minimize the aspiration risks loosely associated with delayed gastric emptying.

• Consider a 24-hour clear liquid diet a day prior to the procedure and transabdominal ultrasound to check gastric contents.
• It is acknowledged that this guidance is based on limited evidence and will be evolving as new medications and data are released.

Recent Clinical Studies

Although there is very little data to guide clinicians, several recent studies have been published that can direct clinical decision-making as guidelines continue to be refined and updated.

A multicenter trial of approximately 800 patients undergoing upper endoscopy found a significant difference in rates of retained gastric contents between those that underwent endoscopy who did and did not follow the ASA guidance on periprocedural management of GLP-1 RAs (12.7% vs 4.4%; P < .0001). However, there were no significant differences in rates of aborted procedures or unplanned intubations.

Furthermore, a multivariable analysis was performed controlling for GLP-1 RA type and other factors, which found the likelihood of gastric retention increased by 36% for every 1% increase in hemoglobin A1c. This study suggests that a more individualized approach to holding GLP-1 RA would be applicable rather than a universal periprocedural hold.⁶

More recently, a single-center study of nearly 600 patients undergoing upper endoscopy showed that while there were slightly increased rates of retained gastric contents (OR 3.80; P = .003) and aborted procedures (1.3% vs 0%; P = .02), the rates of adverse anesthesia events (hypoxia, etc) were similar between the groups and no cases of pulmonary aspiration were noted.7

One single-center study of 57 patients evaluated the safety of GLP-1 RAs in those undergoing endoscopic sleeve gastrectomy. GLP-1 RAs were continued on all patients, but all adhered to a liquid only diet for at least 24 hours prior to the procedure. There were no instances of retained gastric solids, aspiration, or hypoxia. This study suggests that with a 24-hour clear liquid diet and routine NPO recommendations prior to endoscopy, it would be safe to continue GLP-1 RAs. This study provides rationale for the AGA recommendation for a clear liquid diet 24 hours prior to endoscopic procedures for those on GLP-1 RAs.⁸

A study looking at those who underwent emergency surgery and endoscopy with claims data of use of GLP-1 RAs found an overall incidence of postoperative respiratory complications of 3.5% for those with GLP-1 RAs fill history vs 4.0% for those without (P = .12). Approximately 800 of the 24,000 patients identified had undergone endoscopic procedures for GI bleeding or food impaction. The study overall showed that preoperative use of GLP-1 RAs in patients undergoing surgery or endoscopy, evaluated as a combined group, was not associated with an increased risk of pulmonary complications.⁹

Lastly, a systematic review and meta-analysis that included 15 studies that quantified gastric emptying using various methods, including gastric emptying scintigraphy and acetaminophen absorption test, found that there was a quantifiable delay in gastric emptying of about 36 minutes, compared to placebo (P < .01), in patients using GLP-1 RAs. However, compared to standard periprocedural fasting, this delay is clinically insignificant and standard fasting protocols would still be appropriate for patients on GLP-1 RAs.¹⁰

These studies taken together suggest that while GLP-1 RAs can mildly increase the likelihood of retained gastric contents, there is no statistically significant increase in the risk of aspiration or other anesthesia complications. Furthermore, while decreased gastric emptying is a known effect of GLP-1 RAs, this effect may not be clinically significant in the context of standard periprocedural fasting protocols particularly when combined with a 24-hour clear liquid diet. These findings support at a minimum a more patient-specific strategy for periprocedural management of GLP-1 RAs.

 

Clinical Implications

These most recent studies, as well as prior studies and guidelines by various societies lead to a dilemma among endoscopists on proper patient counseling on GLP-1 RAs use before endoscopic procedures. Clinicians must balance the metabolic benefits of GLP-1 RAs with potential endoscopic complications and risks.

Holding therapy theoretically decreases aspiration risk and pulmonary complications, though evidence remains low to support this. Holding medication, however, affects glycemic control leading to potential rebound hyperglycemia which may impact and delay plans for endoscopy. With growing indications for the use of GLP-1 RAs, a more tailored patient-centered treatment plan may be required, especially with consideration of procedure indication and comorbidities.

Currently, practice patterns at different institutions vary widely, making standardization much more difficult. Some centers have opted to follow ASA guidelines of holding these medications up to 1 week prior to procedures, while others have continued therapy with no pre-procedural adjustments. This leaves endoscopists to deal with the downstream effects of inconvenience to patients, care delays, and financial considerations if procedures are postponed related to GLP-1 RAs use.

 

Future Directions

Future studies are needed to make further evidence-based recommendations. Studies should focus on stratifying risks and recommendations based on procedure type (EGD, colonoscopy, etc). More widespread implementation of gastric ultrasound can assist in real-time decision-making, albeit this would require expertise and dedicated time within the pre-procedural workflow. Randomized controlled trials comparing outcomes of patients who continue GLP-1 RAs vs those who discontinue stratified by baseline risk will be instrumental for making concrete guidelines that provide clarity on periprocedural management of GLP-1 RAs.

Conclusion

The periprocedural management of GLP-1 RAs remains a controversial topic that presents unique challenges in endoscopy. Several guidelines have been released by various stakeholders including anesthesiologists, gastroenterologists, and other prescribing providers. Clinical data remains limited with no robust evidence available to suggest that gastric emptying delays caused by GLP-1 RAs prior to endoscopic procedures significantly increases risk of aspiration, pulmonary complications, or other comorbidities. Evolving multi-society guidelines will be important to establish more consistent practices with reassessment of the data as new studies emerge. A multidisciplinary, individualized patient approach may be the best strategy for managing GLP-1 RAs for patients undergoing endoscopic procedures.

Dr. Sekar and Dr. Asamoah are based in the department of gastroenterology at MedStar Georgetown University Hospital, Washington, D.C. Dr. Sekar reports no conflicts of interest in regard to this article. Dr. Asamoah serves on the Johnson & Johnson advisory board for inflammatory bowel disease–related therapies.

References

1. Halim MA et al. Glucagon-Like Peptide-1 Inhibits Prandial Gastrointestinal Motility Through Myenteric Neuronal Mechanisms in Humans. J Clin Endocrinol Metab. 2018 Feb. doi: 10.1210/jc.2017-02006.

2. American Society of Anesthesiologists. American Society of Anesthesiologists releases consensus-based guidance on preoperative use of GLP-1 receptor agonists. 2023 Jun 20. www.asahq.org/about-asa/newsroom/news-releases/2023/06/american-society-of-anesthesiologists-consensus-based-guidance-on-preoperative

3. American Gastroenterological Association. GI multi-society statement regarding GLP-1 agonists and endoscopy. 2023 Jul 25. gastro.org/news/gi-multi-society-statement-regarding-glp-1-agonists-and-endoscopy/.

4. Hashash JG et al. AGA Rapid Clinical Practice Update on the Management of Patients Taking GLP-1 Receptor Agonists Prior to Endoscopy: Communication. Clin Gastroenterol Hepatol. 2024 Apr. doi: 10.1016/j.cgh.2023.11.002.

5. Kindel TL et al; American Gastroenterological Association; American Society for Metabolic and Bariatric Surgery; American Society of Anesthesiologists; International Society of Perioperative Care of Patients with Obesity; Society of American Gastrointestinal and Endoscopic Surgeons. Multi-society Clinical Practice Guidance for the Safe Use of Glucagon-like Peptide-1 Receptor Agonists in the Perioperative Period. Clin Gastroenterol Hepatol. 2024 Oct. doi: 10.1016/j.cgh.2024.10.003.

6. Phan J et al. Glucagon-Like Peptide Receptor Agonists Use Before Endoscopy Is Associated With Low Retained Gastric Contents: A Multicenter Cross-Sectional Analysis. Am J Gastroenterol. 2025 Mar. doi: 10.14309/ajg.0000000000002969.

7. Panchal S et al. Endoscopy and Anesthesia Outcomes Associated With Glucagon-like Peptide-1 Receptor Agonist use in Patients Undergoing Outpatient Upper Endoscopy. Gastrointest Endosc. 2025 Aug. doi:10.1016/j.gie.2025.01.004.

8. Maselli DB et al. Safe Continuation of glucagon-like Peptide 1 Receptor Agonists at Endoscopy: A Case Series of 57 Adults Undergoing Endoscopic Sleeve Gastroplasty. Obes Surg. 2024 Jul. doi: 10.1007/s11695-024-07278-2.

9. Dixit AA et al. Preoperative GLP-1 Receptor Agonist Use and Risk of Postoperative Respiratory Complications. JAMA. 2024 Apr. doi: 10.1001/jama.2024.5003.

10. Hiramoto B et al. Quantified Metrics of Gastric Emptying Delay by Glucagon-Like Peptide-1 Agonists: A systematic review and meta-analysis with insights for periprocedural management. Am J Gastroenterol. 2024 Jun. doi: 10.14309/ajg.0000000000002820.

The use of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) has increased over the past several years and has become a cornerstone in both diabetes and weight loss management, particularly because of its unique combination of glucose control, weight reduction potential, and cardiac and metabolic benefits. However, increased use of these agents presents a dilemma in gastrointestinal endoscopy as it pertains to their safety and management during the periprocedural period.

This review explores management of GLP-1 RAs in the periprocedural setting for endoscopic procedures based on current evidence and guidelines, highlighting gaps and future directions.

 

Pharmacology and Mechanisms of Action

GLP-1 RAs have several mechanisms of action that make them relevant in gastrointestinal endoscopy. These medications modulate glucose control via enhancement of glucose-dependent insulin secretion and reduction of postprandial glucagon, which promotes satiety and delays gastric emptying. This delay in gastric emptying mediated by vagal pathways has been postulated to increase gastric residuals, posing a risk for aspiration during anesthesia.¹

It is important to also consider the pharmacokinetics of GLP-1 RAs, as some have shorter half-lives on the order of several hours, like exenatide, while others, like semaglutide, are dosed weekly. Additionally, common side effects of GLP-1 RAs include nausea, vomiting, bloating, and early satiety, which pose challenges for patients undergoing endoscopic procedures. 

 

Current Guidelines

Various societies have published guidelines on the periprocedural use of GLP-1 RAs. The American Society of Anesthesiologist (ASA) in 2023 presented early recommendations to hold GLP-1 RAs either day of procedure or week prior depending on pharmacokinetics, because of the risk of delayed gastric emptying and increased potential for aspiration.² Soon thereafter, a multi-gastroenterology society guideline was released stating more data is needed to decide if GLP-1 RAs need to be held prior to endoscopic procedures.³

In early 2024, the American Gastroenterological Association (AGA) published a rapid clinical update that advocated for a more individualized approach, particularly in light of limited overall data for GLP-1 RAs and endoscopic procedures.⁴ In asymptomatic patients who follow typical fasting protocols for procedures, it is generally safe to proceed with endoscopy without holding GLP-1 RAs. In symptomatic patients (nausea, abdominal distension, etc), the AGA advises additional precautions, including performing transabdominal ultrasound if feasible to assess retained gastric contents. The AGA also suggests placing a patient on a clear liquid diet the day prior to the procedure — rather than holding GLP-1 RAs — as another reasonable strategy.

The guidelines continue to evolve with newer multi-society guidelines establishing best practices. While initially in 2023 the ASA did recommend holding these medications prior to endoscopy, the initial guidance was based on expert opinion with limited evidence. Newer multi-society guidance published jointly by the ASA along with various gastroenterology societies, including the AGA in December 2024, takes a more nuanced approach.⁵

The newer guidelines include two main recommendations:

1. Periprocedural management of GLP-1 RAs should be a joint decision among the procedural, anesthesia, and prescribing team balancing metabolic needs vs patient risks.

• In a low-risk patient, one that is asymptomatic and on standard dosing, among other factors, the guidance states that GLP-1 RAs can be continued.
• In higher-risk patients, the original guidance of holding a day or a week prior to endoscopic procedures should be followed.

2. Periprocedural management of GLP-1 RAs should attempt to minimize the aspiration risks loosely associated with delayed gastric emptying.

• Consider a 24-hour clear liquid diet a day prior to the procedure and transabdominal ultrasound to check gastric contents.
• It is acknowledged that this guidance is based on limited evidence and will be evolving as new medications and data are released.

Recent Clinical Studies

Although there is very little data to guide clinicians, several recent studies have been published that can direct clinical decision-making as guidelines continue to be refined and updated.

A multicenter trial of approximately 800 patients undergoing upper endoscopy found a significant difference in rates of retained gastric contents between those that underwent endoscopy who did and did not follow the ASA guidance on periprocedural management of GLP-1 RAs (12.7% vs 4.4%; P < .0001). However, there were no significant differences in rates of aborted procedures or unplanned intubations.

Furthermore, a multivariable analysis was performed controlling for GLP-1 RA type and other factors, which found the likelihood of gastric retention increased by 36% for every 1% increase in hemoglobin A1c. This study suggests that a more individualized approach to holding GLP-1 RA would be applicable rather than a universal periprocedural hold.⁶

More recently, a single-center study of nearly 600 patients undergoing upper endoscopy showed that while there were slightly increased rates of retained gastric contents (OR 3.80; P = .003) and aborted procedures (1.3% vs 0%; P = .02), the rates of adverse anesthesia events (hypoxia, etc) were similar between the groups and no cases of pulmonary aspiration were noted.7

One single-center study of 57 patients evaluated the safety of GLP-1 RAs in those undergoing endoscopic sleeve gastrectomy. GLP-1 RAs were continued on all patients, but all adhered to a liquid only diet for at least 24 hours prior to the procedure. There were no instances of retained gastric solids, aspiration, or hypoxia. This study suggests that with a 24-hour clear liquid diet and routine NPO recommendations prior to endoscopy, it would be safe to continue GLP-1 RAs. This study provides rationale for the AGA recommendation for a clear liquid diet 24 hours prior to endoscopic procedures for those on GLP-1 RAs.⁸

A study looking at those who underwent emergency surgery and endoscopy with claims data of use of GLP-1 RAs found an overall incidence of postoperative respiratory complications of 3.5% for those with GLP-1 RAs fill history vs 4.0% for those without (P = .12). Approximately 800 of the 24,000 patients identified had undergone endoscopic procedures for GI bleeding or food impaction. The study overall showed that preoperative use of GLP-1 RAs in patients undergoing surgery or endoscopy, evaluated as a combined group, was not associated with an increased risk of pulmonary complications.⁹

Lastly, a systematic review and meta-analysis that included 15 studies that quantified gastric emptying using various methods, including gastric emptying scintigraphy and acetaminophen absorption test, found that there was a quantifiable delay in gastric emptying of about 36 minutes, compared to placebo (P < .01), in patients using GLP-1 RAs. However, compared to standard periprocedural fasting, this delay is clinically insignificant and standard fasting protocols would still be appropriate for patients on GLP-1 RAs.¹⁰

These studies taken together suggest that while GLP-1 RAs can mildly increase the likelihood of retained gastric contents, there is no statistically significant increase in the risk of aspiration or other anesthesia complications. Furthermore, while decreased gastric emptying is a known effect of GLP-1 RAs, this effect may not be clinically significant in the context of standard periprocedural fasting protocols particularly when combined with a 24-hour clear liquid diet. These findings support at a minimum a more patient-specific strategy for periprocedural management of GLP-1 RAs.

 

Clinical Implications

These most recent studies, as well as prior studies and guidelines by various societies lead to a dilemma among endoscopists on proper patient counseling on GLP-1 RAs use before endoscopic procedures. Clinicians must balance the metabolic benefits of GLP-1 RAs with potential endoscopic complications and risks.

Holding therapy theoretically decreases aspiration risk and pulmonary complications, though evidence remains low to support this. Holding medication, however, affects glycemic control leading to potential rebound hyperglycemia which may impact and delay plans for endoscopy. With growing indications for the use of GLP-1 RAs, a more tailored patient-centered treatment plan may be required, especially with consideration of procedure indication and comorbidities.

Currently, practice patterns at different institutions vary widely, making standardization much more difficult. Some centers have opted to follow ASA guidelines of holding these medications up to 1 week prior to procedures, while others have continued therapy with no pre-procedural adjustments. This leaves endoscopists to deal with the downstream effects of inconvenience to patients, care delays, and financial considerations if procedures are postponed related to GLP-1 RAs use.

 

Future Directions

Future studies are needed to make further evidence-based recommendations. Studies should focus on stratifying risks and recommendations based on procedure type (EGD, colonoscopy, etc). More widespread implementation of gastric ultrasound can assist in real-time decision-making, albeit this would require expertise and dedicated time within the pre-procedural workflow. Randomized controlled trials comparing outcomes of patients who continue GLP-1 RAs vs those who discontinue stratified by baseline risk will be instrumental for making concrete guidelines that provide clarity on periprocedural management of GLP-1 RAs.

Conclusion

The periprocedural management of GLP-1 RAs remains a controversial topic that presents unique challenges in endoscopy. Several guidelines have been released by various stakeholders including anesthesiologists, gastroenterologists, and other prescribing providers. Clinical data remains limited with no robust evidence available to suggest that gastric emptying delays caused by GLP-1 RAs prior to endoscopic procedures significantly increases risk of aspiration, pulmonary complications, or other comorbidities. Evolving multi-society guidelines will be important to establish more consistent practices with reassessment of the data as new studies emerge. A multidisciplinary, individualized patient approach may be the best strategy for managing GLP-1 RAs for patients undergoing endoscopic procedures.

Dr. Sekar and Dr. Asamoah are based in the department of gastroenterology at MedStar Georgetown University Hospital, Washington, D.C. Dr. Sekar reports no conflicts of interest in regard to this article. Dr. Asamoah serves on the Johnson & Johnson advisory board for inflammatory bowel disease–related therapies.

References

1. Halim MA et al. Glucagon-Like Peptide-1 Inhibits Prandial Gastrointestinal Motility Through Myenteric Neuronal Mechanisms in Humans. J Clin Endocrinol Metab. 2018 Feb. doi: 10.1210/jc.2017-02006.

2. American Society of Anesthesiologists. American Society of Anesthesiologists releases consensus-based guidance on preoperative use of GLP-1 receptor agonists. 2023 Jun 20. www.asahq.org/about-asa/newsroom/news-releases/2023/06/american-society-of-anesthesiologists-consensus-based-guidance-on-preoperative

3. American Gastroenterological Association. GI multi-society statement regarding GLP-1 agonists and endoscopy. 2023 Jul 25. gastro.org/news/gi-multi-society-statement-regarding-glp-1-agonists-and-endoscopy/.

4. Hashash JG et al. AGA Rapid Clinical Practice Update on the Management of Patients Taking GLP-1 Receptor Agonists Prior to Endoscopy: Communication. Clin Gastroenterol Hepatol. 2024 Apr. doi: 10.1016/j.cgh.2023.11.002.

5. Kindel TL et al; American Gastroenterological Association; American Society for Metabolic and Bariatric Surgery; American Society of Anesthesiologists; International Society of Perioperative Care of Patients with Obesity; Society of American Gastrointestinal and Endoscopic Surgeons. Multi-society Clinical Practice Guidance for the Safe Use of Glucagon-like Peptide-1 Receptor Agonists in the Perioperative Period. Clin Gastroenterol Hepatol. 2024 Oct. doi: 10.1016/j.cgh.2024.10.003.

6. Phan J et al. Glucagon-Like Peptide Receptor Agonists Use Before Endoscopy Is Associated With Low Retained Gastric Contents: A Multicenter Cross-Sectional Analysis. Am J Gastroenterol. 2025 Mar. doi: 10.14309/ajg.0000000000002969.

7. Panchal S et al. Endoscopy and Anesthesia Outcomes Associated With Glucagon-like Peptide-1 Receptor Agonist use in Patients Undergoing Outpatient Upper Endoscopy. Gastrointest Endosc. 2025 Aug. doi:10.1016/j.gie.2025.01.004.

8. Maselli DB et al. Safe Continuation of glucagon-like Peptide 1 Receptor Agonists at Endoscopy: A Case Series of 57 Adults Undergoing Endoscopic Sleeve Gastroplasty. Obes Surg. 2024 Jul. doi: 10.1007/s11695-024-07278-2.

9. Dixit AA et al. Preoperative GLP-1 Receptor Agonist Use and Risk of Postoperative Respiratory Complications. JAMA. 2024 Apr. doi: 10.1001/jama.2024.5003.

10. Hiramoto B et al. Quantified Metrics of Gastric Emptying Delay by Glucagon-Like Peptide-1 Agonists: A systematic review and meta-analysis with insights for periprocedural management. Am J Gastroenterol. 2024 Jun. doi: 10.14309/ajg.0000000000002820.

The better part of valor is discretion.

Henry IV, Part 1 by William Shakespeare¹

This is the second part of an exploration of the phenomenon of stolen valor, where individuals claim military exploits or acts of heroism that are either fabricated or exaggerated, and/or awards and medals they did not earn.² In June, I focused on the unsettling story of Sarah Cavanaugh, a young US Department of Veterans Affairs (VA) social worker who posed as a decorated, heroic, and seriously wounded Marine veteran for years. Cavanaugh’s manipulative masquerade allowed her to receive coveted spots in veteran recovery programs, thousands of dollars in fraudulent donations, the leadership of a local Veterans of Foreign Wars post, and eventually a federal conviction and prison sentence.³ The first column focused on the legal history of stolen valor; this editorial analyzes the clinical import and ethical impact of the behavior of military imposters. Military imposters are the culprits who steal valor.

It would be easy and perhaps reassuring to assume that stolen valor has emerged as another deplorable example of a national culture in which the betrayal of trust in human beings and loss of faith in institutions and aspirations has reached a nadir. Ironically, stolen valor is inextricably linked to the founding of the United States. When General George Washington inaugurated the American military tradition of awarding decorations to honor the bravery and sacrifices of the patriot Army, he anticipated military imposters. He tried to deter stolen valor through the threat of chastisement: “Should any who are not entitled to these honors have the insolence to assume the badges of them, they shall be severely punished,” Washington warned.⁴

It is plausible to think such despicable conduct occurs only as the ugly side of the beauty of our unparalleled national freedom, but this is a mistake. Cases of stolen valor have been reported in many countries around the world, with some of the most infamous found in the United Kingdom.⁵

While many brazen military imposters like Cavanaugh never serve, there is a small subset who honorably wore a uniform yet embellish their service record with secret missions and meritorious gallantry that purportedly earned them high rank and even higher awards. A most puzzling and disturbing example of this group is an allegation that surfaced when celebrated Navy SEAL Chris Kyle declared in American Sniper that he had won 3 additional combat awards for combat valor in addition to the Silver Star and 3 Bronze Stars actually listed in his service record.⁶

The fact that for centuries stolen valor has plagued multiple nations suggests, at least to this psychiatrically trained mind, that something deeper and darker in human nature than profit alone drives military imposters. Philosopher Verna Gehring has distilled these less tangible motivations into the concept of virtue imposters. According to Gehring, military phonies are a notorious exemplar: “The military phony adopts a past not her own, acts of courage she did not perform—she impersonates the heroic character and virtues she does not possess.”⁷ There could be no more apposite depiction of Cavanaugh, other military imposters, or a legion of other offenders of honor. ⁸

As with Cavanaugh, financial gain is a byproduct of the machinations of military imposters and is usually secondary to the pursuit of nonmaterial rewards such as power, influence, admiration, emulation, empathy, and charity. Gehring contends, and I agree, that virtue imposters are more pernicious and culpable than the plethora of more prosaic scammers and swindlers who use deceit primarily as a means of economic exploitation: “The virtue impostor by contrast plays on people’s better natures—their generosity, humility, and their need for heroes.”⁷

Military imposters cause real and lasting harm. Every veteran who exaggerates claims or scams the VA unjustly steals human and monetary resources from other deserving veterans whose integrity would not permit them to break the rules.⁹ Yet, even more harmful is the potential damage to therapeutic relationships: federal practitioners may become skeptical of a veteran’s history even when there is little to no grounds for suspicion. Veterans, in turn, may experience a breach of trust and betrayal not only from health care professionals and VA leaders but from their brothers and sisters in arms. On an ever-wider scale, every military impostor who is exposed may diminish the respect and honor all veterans have earned. 

It is clear, then, why a small group of former service members has adopted the cause of uncovering military imposters and adroitly using the media to identify signs of stolen valor.¹⁰ Yet deception mars even these mostly well-intentioned campaigns, as some more zealous stolen valor hunters may make allegations that turn out to be false.¹¹ Nevertheless, 500 years ago and in a very different context Shakespeare was, right on the mark: the better part of valor is discretion in describing one’s achievements, in relying on the veracity of our veteran’s narratives, and when there are sound reasons to do so verifying the truth of what our patients, friends, and even family tell us about their time in the military.¹

The better part of valor is discretion.

Henry IV, Part 1 by William Shakespeare¹

This is the second part of an exploration of the phenomenon of stolen valor, where individuals claim military exploits or acts of heroism that are either fabricated or exaggerated, and/or awards and medals they did not earn.² In June, I focused on the unsettling story of Sarah Cavanaugh, a young US Department of Veterans Affairs (VA) social worker who posed as a decorated, heroic, and seriously wounded Marine veteran for years. Cavanaugh’s manipulative masquerade allowed her to receive coveted spots in veteran recovery programs, thousands of dollars in fraudulent donations, the leadership of a local Veterans of Foreign Wars post, and eventually a federal conviction and prison sentence.³ The first column focused on the legal history of stolen valor; this editorial analyzes the clinical import and ethical impact of the behavior of military imposters. Military imposters are the culprits who steal valor.

It would be easy and perhaps reassuring to assume that stolen valor has emerged as another deplorable example of a national culture in which the betrayal of trust in human beings and loss of faith in institutions and aspirations has reached a nadir. Ironically, stolen valor is inextricably linked to the founding of the United States. When General George Washington inaugurated the American military tradition of awarding decorations to honor the bravery and sacrifices of the patriot Army, he anticipated military imposters. He tried to deter stolen valor through the threat of chastisement: “Should any who are not entitled to these honors have the insolence to assume the badges of them, they shall be severely punished,” Washington warned.⁴

It is plausible to think such despicable conduct occurs only as the ugly side of the beauty of our unparalleled national freedom, but this is a mistake. Cases of stolen valor have been reported in many countries around the world, with some of the most infamous found in the United Kingdom.⁵

While many brazen military imposters like Cavanaugh never serve, there is a small subset who honorably wore a uniform yet embellish their service record with secret missions and meritorious gallantry that purportedly earned them high rank and even higher awards. A most puzzling and disturbing example of this group is an allegation that surfaced when celebrated Navy SEAL Chris Kyle declared in American Sniper that he had won 3 additional combat awards for combat valor in addition to the Silver Star and 3 Bronze Stars actually listed in his service record.⁶

The fact that for centuries stolen valor has plagued multiple nations suggests, at least to this psychiatrically trained mind, that something deeper and darker in human nature than profit alone drives military imposters. Philosopher Verna Gehring has distilled these less tangible motivations into the concept of virtue imposters. According to Gehring, military phonies are a notorious exemplar: “The military phony adopts a past not her own, acts of courage she did not perform—she impersonates the heroic character and virtues she does not possess.”⁷ There could be no more apposite depiction of Cavanaugh, other military imposters, or a legion of other offenders of honor. ⁸

As with Cavanaugh, financial gain is a byproduct of the machinations of military imposters and is usually secondary to the pursuit of nonmaterial rewards such as power, influence, admiration, emulation, empathy, and charity. Gehring contends, and I agree, that virtue imposters are more pernicious and culpable than the plethora of more prosaic scammers and swindlers who use deceit primarily as a means of economic exploitation: “The virtue impostor by contrast plays on people’s better natures—their generosity, humility, and their need for heroes.”⁷

Military imposters cause real and lasting harm. Every veteran who exaggerates claims or scams the VA unjustly steals human and monetary resources from other deserving veterans whose integrity would not permit them to break the rules.⁹ Yet, even more harmful is the potential damage to therapeutic relationships: federal practitioners may become skeptical of a veteran’s history even when there is little to no grounds for suspicion. Veterans, in turn, may experience a breach of trust and betrayal not only from health care professionals and VA leaders but from their brothers and sisters in arms. On an ever-wider scale, every military impostor who is exposed may diminish the respect and honor all veterans have earned. 

It is clear, then, why a small group of former service members has adopted the cause of uncovering military imposters and adroitly using the media to identify signs of stolen valor.¹⁰ Yet deception mars even these mostly well-intentioned campaigns, as some more zealous stolen valor hunters may make allegations that turn out to be false.¹¹ Nevertheless, 500 years ago and in a very different context Shakespeare was, right on the mark: the better part of valor is discretion in describing one’s achievements, in relying on the veracity of our veteran’s narratives, and when there are sound reasons to do so verifying the truth of what our patients, friends, and even family tell us about their time in the military.¹

The better part of valor is discretion.

Henry IV, Part 1 by William Shakespeare¹

This is the second part of an exploration of the phenomenon of stolen valor, where individuals claim military exploits or acts of heroism that are either fabricated or exaggerated, and/or awards and medals they did not earn.² In June, I focused on the unsettling story of Sarah Cavanaugh, a young US Department of Veterans Affairs (VA) social worker who posed as a decorated, heroic, and seriously wounded Marine veteran for years. Cavanaugh’s manipulative masquerade allowed her to receive coveted spots in veteran recovery programs, thousands of dollars in fraudulent donations, the leadership of a local Veterans of Foreign Wars post, and eventually a federal conviction and prison sentence.³ The first column focused on the legal history of stolen valor; this editorial analyzes the clinical import and ethical impact of the behavior of military imposters. Military imposters are the culprits who steal valor.

It would be easy and perhaps reassuring to assume that stolen valor has emerged as another deplorable example of a national culture in which the betrayal of trust in human beings and loss of faith in institutions and aspirations has reached a nadir. Ironically, stolen valor is inextricably linked to the founding of the United States. When General George Washington inaugurated the American military tradition of awarding decorations to honor the bravery and sacrifices of the patriot Army, he anticipated military imposters. He tried to deter stolen valor through the threat of chastisement: “Should any who are not entitled to these honors have the insolence to assume the badges of them, they shall be severely punished,” Washington warned.⁴

It is plausible to think such despicable conduct occurs only as the ugly side of the beauty of our unparalleled national freedom, but this is a mistake. Cases of stolen valor have been reported in many countries around the world, with some of the most infamous found in the United Kingdom.⁵

While many brazen military imposters like Cavanaugh never serve, there is a small subset who honorably wore a uniform yet embellish their service record with secret missions and meritorious gallantry that purportedly earned them high rank and even higher awards. A most puzzling and disturbing example of this group is an allegation that surfaced when celebrated Navy SEAL Chris Kyle declared in American Sniper that he had won 3 additional combat awards for combat valor in addition to the Silver Star and 3 Bronze Stars actually listed in his service record.⁶

The fact that for centuries stolen valor has plagued multiple nations suggests, at least to this psychiatrically trained mind, that something deeper and darker in human nature than profit alone drives military imposters. Philosopher Verna Gehring has distilled these less tangible motivations into the concept of virtue imposters. According to Gehring, military phonies are a notorious exemplar: “The military phony adopts a past not her own, acts of courage she did not perform—she impersonates the heroic character and virtues she does not possess.”⁷ There could be no more apposite depiction of Cavanaugh, other military imposters, or a legion of other offenders of honor. ⁸

As with Cavanaugh, financial gain is a byproduct of the machinations of military imposters and is usually secondary to the pursuit of nonmaterial rewards such as power, influence, admiration, emulation, empathy, and charity. Gehring contends, and I agree, that virtue imposters are more pernicious and culpable than the plethora of more prosaic scammers and swindlers who use deceit primarily as a means of economic exploitation: “The virtue impostor by contrast plays on people’s better natures—their generosity, humility, and their need for heroes.”⁷

Military imposters cause real and lasting harm. Every veteran who exaggerates claims or scams the VA unjustly steals human and monetary resources from other deserving veterans whose integrity would not permit them to break the rules.⁹ Yet, even more harmful is the potential damage to therapeutic relationships: federal practitioners may become skeptical of a veteran’s history even when there is little to no grounds for suspicion. Veterans, in turn, may experience a breach of trust and betrayal not only from health care professionals and VA leaders but from their brothers and sisters in arms. On an ever-wider scale, every military impostor who is exposed may diminish the respect and honor all veterans have earned. 

It is clear, then, why a small group of former service members has adopted the cause of uncovering military imposters and adroitly using the media to identify signs of stolen valor.¹⁰ Yet deception mars even these mostly well-intentioned campaigns, as some more zealous stolen valor hunters may make allegations that turn out to be false.¹¹ Nevertheless, 500 years ago and in a very different context Shakespeare was, right on the mark: the better part of valor is discretion in describing one’s achievements, in relying on the veracity of our veteran’s narratives, and when there are sound reasons to do so verifying the truth of what our patients, friends, and even family tell us about their time in the military.¹

This transcript has been edited for clarity.

New guidelines have lowered the age to begin screening for colon cancer to 45 years old. Although this change is positive, we’re still seeing advanced cancer in younger patients who haven’t been screened in time. 

Once diagnosed, these patients undergo surgery and chemotherapy and often return to us asking, “What can I do now to help myself?” 

Two recent studies highlight interventions that are simple, affordable, and actionable today: exercise and aspirin. Let’s take a closer look at the results.

 

Exercise’s Risk Reduction Potential

The idea that exercise reduces cancer recurrence and mortality is supported by observational data. The mechanistic effects behind this have been ascribed to metabolic growth factors, inflammatory changes, immune function changes, and perhaps even positive impact on sleep. 

A study just published in The New England Journal of Medicine examined structured exercise after adjuvant chemotherapy for colon cancer. The phase 3 randomized CHALLENGE trial, mostly conducted at Canadian and Australian centers, recruited patients with resected stage II or III colon cancer (9.8% and 90.2%, respectively) who had completed adjuvant chemotherapy. Patients with recurrences within a year of diagnosis were excluded, as they were more likely to have highly aggressive, biologically active disease. 

Patients were randomized to receive healthcare education materials alone or in conjunction with a structured exercise program over a 3-year follow-up period. 

The exercise intervention, delivered in person or virtually, focused on increasing recreational aerobic activity over baseline by at least 10 metabolic equivalent task (MET). An increment of 10 MET hours per week is not too vigorous. It is essentially the equivalent of adding about 45-60 minutes of brisk walking or 25-30 minutes of jogging 3-4 times a week.

Patients were asked to increase MET over the first 6 months and then maintain or further increase the amount over the next 2.5 years. They were permitted to structure their own exercise program by choosing the type, frequency, intensity, and duration of aerobic exercise. 

The primary endpoint was disease-free survival, with secondary endpoints assessing overall survival, patient-reported outcomes, and other outcomes. Although designed to detect differences at 3 years, follow-up was also performed out to 5 and 8 years.

At a median follow-up of 7.9 years, exercise reduced the relative risk of disease recurrence, new primary cancer, or death by 28% (P = .02). This benefit persisted — and even strengthened — over time, with disease-free survival increasing by 6.4 and 7.1 percentage points at 5 and 8 years, respectively. 

Musculoskeletal adverse events were slightly higher in the exercise group compared with the health education group (18.5% vs 11.5%, respectively), but only 10% were directly attributed to the exercise. 

There are considerations when interpreting these results. First, there was an attrition over time for compliance and training. It would be interesting to see whether that impacted the results. Second, it’s unclear whether patient pedigree or a genomic pathway may predispose to a benefit here for the exercise group. 

But overall, this phase 3 trial provides class 1 evidence supporting exercise as a low-cost, high-impact intervention to reduce cancer recurrence.

 

Adjuvant Aspirin in Colon Cancer Subset

That’s a perfect segue into another recent study looking at the effects of adjuvant aspirin on the prevention of recurrence.

The ALASCCA trial— conducted across centers in Sweden, Denmark, Finland, and Norway — assessed patients with stage I-III rectal cancer or stage II-III colon cancer. It focused on a subset of patients with an oncogenic abnormality called PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha). 

PIK3CA occurs in approximately a third of colon cancers and is associated with significant chemotherapy resistance and a higher rate of disease progression. 

Of the included patients, 1103 (37%) had alterations in the PIK3CA pathway. Researchers randomized patients to receive either 160 mg of aspirin or placebo daily for 3 years, starting within 3 months of surgery. 

Among patients with PIK3CA mutations, aspirin dramatically reduced the risk for time to recurrence by nearly 50% at 3 years (P = .044). Adverse events associated with aspirin were minimal, including one case each of gastrointestinal bleeding, hematoma, and allergic reaction. 

There is no evidence that higher aspirin doses provide greater prevention of colorectal cancer recurrence. The 160-mg use in the current study is fairly normal, roughly equivalent to two low-dose (81-mg) aspirin tablets. 

Now, it’s worth noting that the use of aspirin for the primary prevention of cardiovascular disease was initially recommended by the US Preventive Services Task Force in 2016. This recommendation was then recanted in 2022, when the same group reported limited net benefit to this approach. 

 

Two Proactive Actions

These studies highlight 2 interventions — exercise and aspirin — that are low cost, accessible, and appeal to patients eager to help prevent their cancer from recurring. 

Exercise is broadly beneficial and can be recommended immediately. 

For aspirin, patients should work with their oncologist to determine their PIK3CA mutation status, as this subgroup appears to benefit the most. 

These findings offer patients meaningful, proactive interventions they can apply to support their recovery and reduce the risk of recurrence. Hopefully these new findings will help guide your clinical conversations.

Johnson is a regular contributor to Medscape. He is professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, and a past president of the American College of Gastroenterology. His primary focus is the clinical practice of gastroenterology. He has published extensively in the internal medicine/gastroenterology literature, with principal research interests in esophageal and colon disease, and more recently in sleep and microbiome effects on gastrointestinal health and disease. He disclosed that he is an adviser for ISOThrive. 

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

New guidelines have lowered the age to begin screening for colon cancer to 45 years old. Although this change is positive, we’re still seeing advanced cancer in younger patients who haven’t been screened in time. 

Once diagnosed, these patients undergo surgery and chemotherapy and often return to us asking, “What can I do now to help myself?” 

Two recent studies highlight interventions that are simple, affordable, and actionable today: exercise and aspirin. Let’s take a closer look at the results.

 

Exercise’s Risk Reduction Potential

The idea that exercise reduces cancer recurrence and mortality is supported by observational data. The mechanistic effects behind this have been ascribed to metabolic growth factors, inflammatory changes, immune function changes, and perhaps even positive impact on sleep. 

A study just published in The New England Journal of Medicine examined structured exercise after adjuvant chemotherapy for colon cancer. The phase 3 randomized CHALLENGE trial, mostly conducted at Canadian and Australian centers, recruited patients with resected stage II or III colon cancer (9.8% and 90.2%, respectively) who had completed adjuvant chemotherapy. Patients with recurrences within a year of diagnosis were excluded, as they were more likely to have highly aggressive, biologically active disease. 

Patients were randomized to receive healthcare education materials alone or in conjunction with a structured exercise program over a 3-year follow-up period. 

The exercise intervention, delivered in person or virtually, focused on increasing recreational aerobic activity over baseline by at least 10 metabolic equivalent task (MET). An increment of 10 MET hours per week is not too vigorous. It is essentially the equivalent of adding about 45-60 minutes of brisk walking or 25-30 minutes of jogging 3-4 times a week.

Patients were asked to increase MET over the first 6 months and then maintain or further increase the amount over the next 2.5 years. They were permitted to structure their own exercise program by choosing the type, frequency, intensity, and duration of aerobic exercise. 

The primary endpoint was disease-free survival, with secondary endpoints assessing overall survival, patient-reported outcomes, and other outcomes. Although designed to detect differences at 3 years, follow-up was also performed out to 5 and 8 years.

At a median follow-up of 7.9 years, exercise reduced the relative risk of disease recurrence, new primary cancer, or death by 28% (P = .02). This benefit persisted — and even strengthened — over time, with disease-free survival increasing by 6.4 and 7.1 percentage points at 5 and 8 years, respectively. 

Musculoskeletal adverse events were slightly higher in the exercise group compared with the health education group (18.5% vs 11.5%, respectively), but only 10% were directly attributed to the exercise. 

There are considerations when interpreting these results. First, there was an attrition over time for compliance and training. It would be interesting to see whether that impacted the results. Second, it’s unclear whether patient pedigree or a genomic pathway may predispose to a benefit here for the exercise group. 

But overall, this phase 3 trial provides class 1 evidence supporting exercise as a low-cost, high-impact intervention to reduce cancer recurrence.

 

Adjuvant Aspirin in Colon Cancer Subset

That’s a perfect segue into another recent study looking at the effects of adjuvant aspirin on the prevention of recurrence.

The ALASCCA trial— conducted across centers in Sweden, Denmark, Finland, and Norway — assessed patients with stage I-III rectal cancer or stage II-III colon cancer. It focused on a subset of patients with an oncogenic abnormality called PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha). 

PIK3CA occurs in approximately a third of colon cancers and is associated with significant chemotherapy resistance and a higher rate of disease progression. 

Of the included patients, 1103 (37%) had alterations in the PIK3CA pathway. Researchers randomized patients to receive either 160 mg of aspirin or placebo daily for 3 years, starting within 3 months of surgery. 

Among patients with PIK3CA mutations, aspirin dramatically reduced the risk for time to recurrence by nearly 50% at 3 years (P = .044). Adverse events associated with aspirin were minimal, including one case each of gastrointestinal bleeding, hematoma, and allergic reaction. 

There is no evidence that higher aspirin doses provide greater prevention of colorectal cancer recurrence. The 160-mg use in the current study is fairly normal, roughly equivalent to two low-dose (81-mg) aspirin tablets. 

Now, it’s worth noting that the use of aspirin for the primary prevention of cardiovascular disease was initially recommended by the US Preventive Services Task Force in 2016. This recommendation was then recanted in 2022, when the same group reported limited net benefit to this approach. 

 

Two Proactive Actions

These studies highlight 2 interventions — exercise and aspirin — that are low cost, accessible, and appeal to patients eager to help prevent their cancer from recurring. 

Exercise is broadly beneficial and can be recommended immediately. 

For aspirin, patients should work with their oncologist to determine their PIK3CA mutation status, as this subgroup appears to benefit the most. 

These findings offer patients meaningful, proactive interventions they can apply to support their recovery and reduce the risk of recurrence. Hopefully these new findings will help guide your clinical conversations.

Johnson is a regular contributor to Medscape. He is professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, and a past president of the American College of Gastroenterology. His primary focus is the clinical practice of gastroenterology. He has published extensively in the internal medicine/gastroenterology literature, with principal research interests in esophageal and colon disease, and more recently in sleep and microbiome effects on gastrointestinal health and disease. He disclosed that he is an adviser for ISOThrive. 

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

New guidelines have lowered the age to begin screening for colon cancer to 45 years old. Although this change is positive, we’re still seeing advanced cancer in younger patients who haven’t been screened in time. 

Once diagnosed, these patients undergo surgery and chemotherapy and often return to us asking, “What can I do now to help myself?” 

Two recent studies highlight interventions that are simple, affordable, and actionable today: exercise and aspirin. Let’s take a closer look at the results.

 

Exercise’s Risk Reduction Potential

The idea that exercise reduces cancer recurrence and mortality is supported by observational data. The mechanistic effects behind this have been ascribed to metabolic growth factors, inflammatory changes, immune function changes, and perhaps even positive impact on sleep. 

A study just published in The New England Journal of Medicine examined structured exercise after adjuvant chemotherapy for colon cancer. The phase 3 randomized CHALLENGE trial, mostly conducted at Canadian and Australian centers, recruited patients with resected stage II or III colon cancer (9.8% and 90.2%, respectively) who had completed adjuvant chemotherapy. Patients with recurrences within a year of diagnosis were excluded, as they were more likely to have highly aggressive, biologically active disease. 

Patients were randomized to receive healthcare education materials alone or in conjunction with a structured exercise program over a 3-year follow-up period. 

The exercise intervention, delivered in person or virtually, focused on increasing recreational aerobic activity over baseline by at least 10 metabolic equivalent task (MET). An increment of 10 MET hours per week is not too vigorous. It is essentially the equivalent of adding about 45-60 minutes of brisk walking or 25-30 minutes of jogging 3-4 times a week.

Patients were asked to increase MET over the first 6 months and then maintain or further increase the amount over the next 2.5 years. They were permitted to structure their own exercise program by choosing the type, frequency, intensity, and duration of aerobic exercise. 

The primary endpoint was disease-free survival, with secondary endpoints assessing overall survival, patient-reported outcomes, and other outcomes. Although designed to detect differences at 3 years, follow-up was also performed out to 5 and 8 years.

At a median follow-up of 7.9 years, exercise reduced the relative risk of disease recurrence, new primary cancer, or death by 28% (P = .02). This benefit persisted — and even strengthened — over time, with disease-free survival increasing by 6.4 and 7.1 percentage points at 5 and 8 years, respectively. 

Musculoskeletal adverse events were slightly higher in the exercise group compared with the health education group (18.5% vs 11.5%, respectively), but only 10% were directly attributed to the exercise. 

There are considerations when interpreting these results. First, there was an attrition over time for compliance and training. It would be interesting to see whether that impacted the results. Second, it’s unclear whether patient pedigree or a genomic pathway may predispose to a benefit here for the exercise group. 

But overall, this phase 3 trial provides class 1 evidence supporting exercise as a low-cost, high-impact intervention to reduce cancer recurrence.

 

Adjuvant Aspirin in Colon Cancer Subset

That’s a perfect segue into another recent study looking at the effects of adjuvant aspirin on the prevention of recurrence.

The ALASCCA trial— conducted across centers in Sweden, Denmark, Finland, and Norway — assessed patients with stage I-III rectal cancer or stage II-III colon cancer. It focused on a subset of patients with an oncogenic abnormality called PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha). 

PIK3CA occurs in approximately a third of colon cancers and is associated with significant chemotherapy resistance and a higher rate of disease progression. 

Of the included patients, 1103 (37%) had alterations in the PIK3CA pathway. Researchers randomized patients to receive either 160 mg of aspirin or placebo daily for 3 years, starting within 3 months of surgery. 

Among patients with PIK3CA mutations, aspirin dramatically reduced the risk for time to recurrence by nearly 50% at 3 years (P = .044). Adverse events associated with aspirin were minimal, including one case each of gastrointestinal bleeding, hematoma, and allergic reaction. 

There is no evidence that higher aspirin doses provide greater prevention of colorectal cancer recurrence. The 160-mg use in the current study is fairly normal, roughly equivalent to two low-dose (81-mg) aspirin tablets. 

Now, it’s worth noting that the use of aspirin for the primary prevention of cardiovascular disease was initially recommended by the US Preventive Services Task Force in 2016. This recommendation was then recanted in 2022, when the same group reported limited net benefit to this approach. 

 

Two Proactive Actions

These studies highlight 2 interventions — exercise and aspirin — that are low cost, accessible, and appeal to patients eager to help prevent their cancer from recurring. 

Exercise is broadly beneficial and can be recommended immediately. 

For aspirin, patients should work with their oncologist to determine their PIK3CA mutation status, as this subgroup appears to benefit the most. 

These findings offer patients meaningful, proactive interventions they can apply to support their recovery and reduce the risk of recurrence. Hopefully these new findings will help guide your clinical conversations.

Johnson is a regular contributor to Medscape. He is professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, and a past president of the American College of Gastroenterology. His primary focus is the clinical practice of gastroenterology. He has published extensively in the internal medicine/gastroenterology literature, with principal research interests in esophageal and colon disease, and more recently in sleep and microbiome effects on gastrointestinal health and disease. He disclosed that he is an adviser for ISOThrive. 

A version of this article appeared on Medscape.com.

Endometrial cancer is a common type of gynecologic cancer, and its incidence is rising steadily in the United States and globally. Most cases are endometrioid adenocarcinomas, arising from the inner lining of the uterus — the endometrium. While many patients are diagnosed early because of noticeable symptoms like abnormal bleeding, trends in both incidence and mortality are concerning, especially given the persistent racial and socioeconomic disparities in outcomes.

In addition to being the most common uterine malignancy, endometrial cancer is at the forefront of precision oncology in gynecology. The traditional classification systems based on histology and hormone dependence are now being augmented by molecular subtyping that better informs prognosis and treatment. As diagnostic tools, genetic testing, and therapeutic strategies advance, the management of endometrial cancer is becoming increasingly personalized. 

Here are five things to know about endometrial cancer:

1. Endometrial cancer is one of the few cancers with increasing mortality.

Endometrial cancer accounts for the majority of uterine cancers in the United States with an overall lifetime risk for women of about 1 in 40. Since the mid-2000s, incidence rates have risen steadily, by > 1% per year, reflecting both lifestyle and environmental factors. Importantly, the disease tends to be diagnosed at an early stage due to the presence of warning signs like postmenopausal bleeding, which contributes to relatively favorable survival outcomes when caught early.

However, mortality trends continue to evolve. From 1999 to 2013, death rates from endometrial cancer in the US declined slightly, but since 2013, they have increased sharply — by > 8% annually — according to recent data. This upward trend in mortality disproportionately affects non-Hispanic Black women, who experience the highest mortality rate (4.7 per 100,000) among all racial and ethnic groups. This disparity is likely caused by a complex interplay of factors, including delays in diagnosis, more aggressive tumor biology, and inequities in access to care. Addressing these disparities remains a key priority in improving outcomes.

 

2. Risk factors go beyond hormones and age.

Risk factors for endometrial cancer include prolonged exposure to unopposed estrogen, which can result from estrogen-only hormone replacement therapy, higher BMI, and early menarche or late menopause. Nulliparity (having never been pregnant) and older age also increase risk, as does tamoxifen use — a medication commonly prescribed for breast cancer prevention. These factors cumulatively increase endometrial proliferation and the potential for atypical cellular changes. Endometrial hyperplasia, a known precursor to cancer, is often linked to these hormonal imbalances and may require surveillance or treatment.

Beyond estrogen’s influence, a growing body of research is uncovering additional risk contributors. Women with polycystic ovary syndrome (PCOS), metabolic syndrome, or diabetes face elevated risk of developing endometrial cancer. Genetic syndromes, particularly Lynch and Cowden syndromes, are associated with significantly increased lifetime risks of endometrial cancer. Environmental exposures, such as the use of hair relaxers, are being investigated as emerging risk factors. Additionally, race remains a risk marker, with Black women not only experiencing higher mortality but also more aggressive subtypes of the disease. These complex, overlapping risks highlight the importance of individualized risk assessment and early intervention strategies.

 

3. Postmenopausal bleeding is the hallmark symptom — but not the only one.

In endometrial cancer, the majority of cases are diagnosed at an early stage, largely because of the hallmark symptom of postmenopausal bleeding. In addition to bleeding, patients may present with vaginal discharge, pyometra, and even pain and abdominal distension in advanced disease. Any bleeding in a postmenopausal woman should prompt evaluation, as it may signal endometrial hyperplasia or carcinoma. In premenopausal women, irregular or heavy menstrual bleeding may raise suspicion, particularly when accompanied by risk factors such as PCOS.

The diagnostic workup for suspected endometrial cancer in women, particularly those presenting with postmenopausal bleeding, begins with a focused clinical assessment and frequently includes transvaginal ultrasound (TVUS) to evaluate the endometrium. While TVUS can aid in identifying structural abnormalities or suggest malignancy, endometrial sampling is warranted in all postmenopausal women with abnormal bleeding, regardless of endometrial thickness. Office-based biopsy is the preferred initial approach due to its convenience and diagnostic yield; however, if the sample is nondiagnostic or technically difficult to obtain, hysteroscopy with directed biopsy or dilation and curettage should be pursued.

 

4. Classification systems are evolving to include molecular subtypes.

Historically, endometrial cancers were classified using the World Health Organization system based on histology and by hormone dependence: Type 1 (estrogen-dependent, typically endometrioid and low grade) and Type 2 (non-estrogen dependent, often serous and high grade). Type 1 cancers tend to have a better prognosis and slower progression, while Type 2 cancers are more aggressive and require intensive treatment. While helpful, this binary classification does not fully capture the biological diversity or treatment responsiveness of the disease.

The field is now moving toward molecular classification, which offers a more nuanced understanding. The four main molecular subtypes include: polymerase epsilon (POLE)-mutant, mismatch repair (MMR)-deficient, p53-abnormal, and no specific molecular profile (NSMP). These groups differ in prognosis and therapeutic implications. POLE-mutant tumors with extremely high mutational burdens generally have excellent outcomes and may not require aggressive adjuvant therapy. In contrast, p53-abnormal tumors are associated with chromosomal instability, TP53 mutations, and poor outcomes, necessitating more aggressive multimodal treatment. MMR-deficient tumors are particularly responsive to immunotherapy. These molecular distinctions are changing how clinicians approach risk stratification and management in patients with endometrial cancer.

 

5. Treatment is increasingly personalized — and immunotherapy is expanding.

The cornerstone of treatment for early-stage endometrial cancer is surgical: total hysterectomy with bilateral salpingo-oophorectomy, often with sentinel node mapping or lymphadenectomy. Adjuvant therapy depends on factors such as stage, grade, histology, and molecular subtype. Fertility-sparing management with progestin therapy is an option for highly selected patients with early-stage, low-grade tumors. Clinical guidelines recommend that fertility desires be addressed prior to initiating treatment, as standard surgical management typically results in loss of reproductive capacity.

For advanced or recurrent disease, treatment becomes more complex and increasingly individualized. Chemotherapy, often with carboplatin and paclitaxel, is standard for stage III/IV and recurrent disease. Molecular findings now guide additional therapy: For instance, MMR-deficient tumors may respond to checkpoint inhibitors. As targeted agents and combination regimens continue to emerge, treatment of endometrial is increasingly focused on precision medicine.

Markman is professor of medical oncology and therapeutics research and President of Medicine & Science at City of Hope in Atlanta and Chicago. He has disclosed relevant financial relationships with AstraZeneca, GSK and Myriad.

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

Endometrial cancer is a common type of gynecologic cancer, and its incidence is rising steadily in the United States and globally. Most cases are endometrioid adenocarcinomas, arising from the inner lining of the uterus — the endometrium. While many patients are diagnosed early because of noticeable symptoms like abnormal bleeding, trends in both incidence and mortality are concerning, especially given the persistent racial and socioeconomic disparities in outcomes.

In addition to being the most common uterine malignancy, endometrial cancer is at the forefront of precision oncology in gynecology. The traditional classification systems based on histology and hormone dependence are now being augmented by molecular subtyping that better informs prognosis and treatment. As diagnostic tools, genetic testing, and therapeutic strategies advance, the management of endometrial cancer is becoming increasingly personalized. 

Here are five things to know about endometrial cancer:

1. Endometrial cancer is one of the few cancers with increasing mortality.

Endometrial cancer accounts for the majority of uterine cancers in the United States with an overall lifetime risk for women of about 1 in 40. Since the mid-2000s, incidence rates have risen steadily, by > 1% per year, reflecting both lifestyle and environmental factors. Importantly, the disease tends to be diagnosed at an early stage due to the presence of warning signs like postmenopausal bleeding, which contributes to relatively favorable survival outcomes when caught early.

However, mortality trends continue to evolve. From 1999 to 2013, death rates from endometrial cancer in the US declined slightly, but since 2013, they have increased sharply — by > 8% annually — according to recent data. This upward trend in mortality disproportionately affects non-Hispanic Black women, who experience the highest mortality rate (4.7 per 100,000) among all racial and ethnic groups. This disparity is likely caused by a complex interplay of factors, including delays in diagnosis, more aggressive tumor biology, and inequities in access to care. Addressing these disparities remains a key priority in improving outcomes.

 

2. Risk factors go beyond hormones and age.

Risk factors for endometrial cancer include prolonged exposure to unopposed estrogen, which can result from estrogen-only hormone replacement therapy, higher BMI, and early menarche or late menopause. Nulliparity (having never been pregnant) and older age also increase risk, as does tamoxifen use — a medication commonly prescribed for breast cancer prevention. These factors cumulatively increase endometrial proliferation and the potential for atypical cellular changes. Endometrial hyperplasia, a known precursor to cancer, is often linked to these hormonal imbalances and may require surveillance or treatment.

Beyond estrogen’s influence, a growing body of research is uncovering additional risk contributors. Women with polycystic ovary syndrome (PCOS), metabolic syndrome, or diabetes face elevated risk of developing endometrial cancer. Genetic syndromes, particularly Lynch and Cowden syndromes, are associated with significantly increased lifetime risks of endometrial cancer. Environmental exposures, such as the use of hair relaxers, are being investigated as emerging risk factors. Additionally, race remains a risk marker, with Black women not only experiencing higher mortality but also more aggressive subtypes of the disease. These complex, overlapping risks highlight the importance of individualized risk assessment and early intervention strategies.

 

3. Postmenopausal bleeding is the hallmark symptom — but not the only one.

In endometrial cancer, the majority of cases are diagnosed at an early stage, largely because of the hallmark symptom of postmenopausal bleeding. In addition to bleeding, patients may present with vaginal discharge, pyometra, and even pain and abdominal distension in advanced disease. Any bleeding in a postmenopausal woman should prompt evaluation, as it may signal endometrial hyperplasia or carcinoma. In premenopausal women, irregular or heavy menstrual bleeding may raise suspicion, particularly when accompanied by risk factors such as PCOS.

The diagnostic workup for suspected endometrial cancer in women, particularly those presenting with postmenopausal bleeding, begins with a focused clinical assessment and frequently includes transvaginal ultrasound (TVUS) to evaluate the endometrium. While TVUS can aid in identifying structural abnormalities or suggest malignancy, endometrial sampling is warranted in all postmenopausal women with abnormal bleeding, regardless of endometrial thickness. Office-based biopsy is the preferred initial approach due to its convenience and diagnostic yield; however, if the sample is nondiagnostic or technically difficult to obtain, hysteroscopy with directed biopsy or dilation and curettage should be pursued.

 

4. Classification systems are evolving to include molecular subtypes.

Historically, endometrial cancers were classified using the World Health Organization system based on histology and by hormone dependence: Type 1 (estrogen-dependent, typically endometrioid and low grade) and Type 2 (non-estrogen dependent, often serous and high grade). Type 1 cancers tend to have a better prognosis and slower progression, while Type 2 cancers are more aggressive and require intensive treatment. While helpful, this binary classification does not fully capture the biological diversity or treatment responsiveness of the disease.

The field is now moving toward molecular classification, which offers a more nuanced understanding. The four main molecular subtypes include: polymerase epsilon (POLE)-mutant, mismatch repair (MMR)-deficient, p53-abnormal, and no specific molecular profile (NSMP). These groups differ in prognosis and therapeutic implications. POLE-mutant tumors with extremely high mutational burdens generally have excellent outcomes and may not require aggressive adjuvant therapy. In contrast, p53-abnormal tumors are associated with chromosomal instability, TP53 mutations, and poor outcomes, necessitating more aggressive multimodal treatment. MMR-deficient tumors are particularly responsive to immunotherapy. These molecular distinctions are changing how clinicians approach risk stratification and management in patients with endometrial cancer.

 

5. Treatment is increasingly personalized — and immunotherapy is expanding.

The cornerstone of treatment for early-stage endometrial cancer is surgical: total hysterectomy with bilateral salpingo-oophorectomy, often with sentinel node mapping or lymphadenectomy. Adjuvant therapy depends on factors such as stage, grade, histology, and molecular subtype. Fertility-sparing management with progestin therapy is an option for highly selected patients with early-stage, low-grade tumors. Clinical guidelines recommend that fertility desires be addressed prior to initiating treatment, as standard surgical management typically results in loss of reproductive capacity.

For advanced or recurrent disease, treatment becomes more complex and increasingly individualized. Chemotherapy, often with carboplatin and paclitaxel, is standard for stage III/IV and recurrent disease. Molecular findings now guide additional therapy: For instance, MMR-deficient tumors may respond to checkpoint inhibitors. As targeted agents and combination regimens continue to emerge, treatment of endometrial is increasingly focused on precision medicine.

Markman is professor of medical oncology and therapeutics research and President of Medicine & Science at City of Hope in Atlanta and Chicago. He has disclosed relevant financial relationships with AstraZeneca, GSK and Myriad.

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

Endometrial cancer is a common type of gynecologic cancer, and its incidence is rising steadily in the United States and globally. Most cases are endometrioid adenocarcinomas, arising from the inner lining of the uterus — the endometrium. While many patients are diagnosed early because of noticeable symptoms like abnormal bleeding, trends in both incidence and mortality are concerning, especially given the persistent racial and socioeconomic disparities in outcomes.

In addition to being the most common uterine malignancy, endometrial cancer is at the forefront of precision oncology in gynecology. The traditional classification systems based on histology and hormone dependence are now being augmented by molecular subtyping that better informs prognosis and treatment. As diagnostic tools, genetic testing, and therapeutic strategies advance, the management of endometrial cancer is becoming increasingly personalized. 

Here are five things to know about endometrial cancer:

1. Endometrial cancer is one of the few cancers with increasing mortality.

Endometrial cancer accounts for the majority of uterine cancers in the United States with an overall lifetime risk for women of about 1 in 40. Since the mid-2000s, incidence rates have risen steadily, by > 1% per year, reflecting both lifestyle and environmental factors. Importantly, the disease tends to be diagnosed at an early stage due to the presence of warning signs like postmenopausal bleeding, which contributes to relatively favorable survival outcomes when caught early.

However, mortality trends continue to evolve. From 1999 to 2013, death rates from endometrial cancer in the US declined slightly, but since 2013, they have increased sharply — by > 8% annually — according to recent data. This upward trend in mortality disproportionately affects non-Hispanic Black women, who experience the highest mortality rate (4.7 per 100,000) among all racial and ethnic groups. This disparity is likely caused by a complex interplay of factors, including delays in diagnosis, more aggressive tumor biology, and inequities in access to care. Addressing these disparities remains a key priority in improving outcomes.

 

2. Risk factors go beyond hormones and age.

Risk factors for endometrial cancer include prolonged exposure to unopposed estrogen, which can result from estrogen-only hormone replacement therapy, higher BMI, and early menarche or late menopause. Nulliparity (having never been pregnant) and older age also increase risk, as does tamoxifen use — a medication commonly prescribed for breast cancer prevention. These factors cumulatively increase endometrial proliferation and the potential for atypical cellular changes. Endometrial hyperplasia, a known precursor to cancer, is often linked to these hormonal imbalances and may require surveillance or treatment.

Beyond estrogen’s influence, a growing body of research is uncovering additional risk contributors. Women with polycystic ovary syndrome (PCOS), metabolic syndrome, or diabetes face elevated risk of developing endometrial cancer. Genetic syndromes, particularly Lynch and Cowden syndromes, are associated with significantly increased lifetime risks of endometrial cancer. Environmental exposures, such as the use of hair relaxers, are being investigated as emerging risk factors. Additionally, race remains a risk marker, with Black women not only experiencing higher mortality but also more aggressive subtypes of the disease. These complex, overlapping risks highlight the importance of individualized risk assessment and early intervention strategies.

 

3. Postmenopausal bleeding is the hallmark symptom — but not the only one.

In endometrial cancer, the majority of cases are diagnosed at an early stage, largely because of the hallmark symptom of postmenopausal bleeding. In addition to bleeding, patients may present with vaginal discharge, pyometra, and even pain and abdominal distension in advanced disease. Any bleeding in a postmenopausal woman should prompt evaluation, as it may signal endometrial hyperplasia or carcinoma. In premenopausal women, irregular or heavy menstrual bleeding may raise suspicion, particularly when accompanied by risk factors such as PCOS.

The diagnostic workup for suspected endometrial cancer in women, particularly those presenting with postmenopausal bleeding, begins with a focused clinical assessment and frequently includes transvaginal ultrasound (TVUS) to evaluate the endometrium. While TVUS can aid in identifying structural abnormalities or suggest malignancy, endometrial sampling is warranted in all postmenopausal women with abnormal bleeding, regardless of endometrial thickness. Office-based biopsy is the preferred initial approach due to its convenience and diagnostic yield; however, if the sample is nondiagnostic or technically difficult to obtain, hysteroscopy with directed biopsy or dilation and curettage should be pursued.

 

4. Classification systems are evolving to include molecular subtypes.

Historically, endometrial cancers were classified using the World Health Organization system based on histology and by hormone dependence: Type 1 (estrogen-dependent, typically endometrioid and low grade) and Type 2 (non-estrogen dependent, often serous and high grade). Type 1 cancers tend to have a better prognosis and slower progression, while Type 2 cancers are more aggressive and require intensive treatment. While helpful, this binary classification does not fully capture the biological diversity or treatment responsiveness of the disease.

The field is now moving toward molecular classification, which offers a more nuanced understanding. The four main molecular subtypes include: polymerase epsilon (POLE)-mutant, mismatch repair (MMR)-deficient, p53-abnormal, and no specific molecular profile (NSMP). These groups differ in prognosis and therapeutic implications. POLE-mutant tumors with extremely high mutational burdens generally have excellent outcomes and may not require aggressive adjuvant therapy. In contrast, p53-abnormal tumors are associated with chromosomal instability, TP53 mutations, and poor outcomes, necessitating more aggressive multimodal treatment. MMR-deficient tumors are particularly responsive to immunotherapy. These molecular distinctions are changing how clinicians approach risk stratification and management in patients with endometrial cancer.

 

5. Treatment is increasingly personalized — and immunotherapy is expanding.

The cornerstone of treatment for early-stage endometrial cancer is surgical: total hysterectomy with bilateral salpingo-oophorectomy, often with sentinel node mapping or lymphadenectomy. Adjuvant therapy depends on factors such as stage, grade, histology, and molecular subtype. Fertility-sparing management with progestin therapy is an option for highly selected patients with early-stage, low-grade tumors. Clinical guidelines recommend that fertility desires be addressed prior to initiating treatment, as standard surgical management typically results in loss of reproductive capacity.

For advanced or recurrent disease, treatment becomes more complex and increasingly individualized. Chemotherapy, often with carboplatin and paclitaxel, is standard for stage III/IV and recurrent disease. Molecular findings now guide additional therapy: For instance, MMR-deficient tumors may respond to checkpoint inhibitors. As targeted agents and combination regimens continue to emerge, treatment of endometrial is increasingly focused on precision medicine.

Markman is professor of medical oncology and therapeutics research and President of Medicine & Science at City of Hope in Atlanta and Chicago. He has disclosed relevant financial relationships with AstraZeneca, GSK and Myriad.

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

The umbrella term skin of color (SOC) includes individuals identifying as Black/African, Hispanic, Asian, Native American, Middle Eastern, and Mediterranean as well as multiracial groups. While the Fitzpatrick skin typing system is not an accurate proxy for describing skin tone, SOC populations typically correspond to Fitzpatrick skin types IV to VI, and clinical researchers often report the Fitzpatrick skin type of their study populations.¹

Over the past several decades, the underrepresentation of diverse skin tones in educational resources has limited clinical training.² For example, only 10.3% of conditions featured in contemporary dermatology textbooks are shown in darker skin tones.³ This educational resource gap has spurred a transformative movement toward inclusivity in dermatologic education, research, and clinical practice. Notable examples include VisualDx⁴ and Dermatology for Skin of Color.⁵ In addition, Cutis began publishing the Dx Across the Skin Color Spectrum fact sheet series in 2022 to highlight differences in how cutaneous conditions manifest in various skin tones (https://www.mdedge.com/cutis/dx-across-skin-color-spectrum).

These resources play a critical role in advancing dermatologic knowledge, ensuring that dermatologists and other health care professionals are well equipped to diagnose and treat dermatologic conditions in SOC populations with accuracy and cultural humility. These innovations also have enhanced our understanding of how common dermatologic conditions manifest and respond to treatment in SOC populations. Herein, we highlight advances in diagnostic and therapeutic approaches for the most common concerns among SOC populations in the United States, including acne vulgaris, atopic dermatitis (AD), seborrheic dermatitis (SD), melasma, postinflammatory hyperpigmentation, psoriasis, and seborrheic keratosis.

Chief Concerns Common Among SOC Populations in the United States

Acne Vulgaris—In patients with SOC, acne frequently results in pigmentary changes and scarring that can manifest as both hypertrophic and keloidal scars.⁶ Clinical evidence from randomized controlled studies supports the use of topical dapsone gel as a safe and effective frontline treatment for acne in patients with SOC.^7,8 Notably, the US Food and Drug Administration–approved 1726-nm laser with a contact-cooling sapphire window has demonstrated safety and efficacy in the management of acne across Fitzpatrick skin types II to VI.^9-11 To manage atrophic acne scars, cutting-edge laser and radiofrequency devices including erbium-doped yttrium aluminum garnet, fractional CO₂, and picosecond lasers have been effectively employed in SOC populations. When these energy-based treatments are combined with cooling systems, they substantially reduce the risk for thermal damage in darker skin tones.^12,13

Atopic Dermatitis—While epidemiologic data indicate that Black patients experience a higher prevalence (19.3%) of AD than Asian (17.8%), White (16.1%), or Hispanic (7.8%) groups in the United States, this disparity may be influenced by factors such as access to care and environmental stressors, which require further study.^14-16 The pathogenesis of AD involves a complex interaction between skin barrier dysfunction, immune dysregulation, and environmental triggers, with patients with SOC exhibiting distinct endotypes.^14,17 For example, East Asian individuals have elevated T_H17-related cytokines and a blended T_H17/T_H2 AD-psoriasis endotype,^14,18 while Black individuals have greater T_H2 skewing and filaggrin variations and higher serum IgE levels.¹⁷ Diagnostic advancements, including a modified Eczema Area and Severity Index using grayscale rather than erythema-based assessments for patients with SOC as well as a novel SOC dermatology atlas that includes AD have increased equity in disease evaluation.^19,20 Recent clinical trials support the efficacy of topical crisaborole, topical ruxolitinib, and biologics such as dupilumab, tralokinumab, lebrikizumab, and fezakinumab for AD in SOC populations, with dupilumab also improving postinflammatory hyperpigmentation.^20-22

Seborrheic Dermatitis—Seborrheic dermatitis is common in patients with SOC, though its manifestations vary by racial/ethnic background.²³ In Black patients, petaloid SD is more prevalent and can resemble secondary syphilis, making accurate diagnosis essential to rule out potential mimickers.²⁴ Effective treatments remain limited, as current therapies often fail to address both the underlying yeast-driven inflammation and the resulting pigmentary changes that commonly affect SOC populations.²⁵ Roflumilast foam 0.3%, a phosphodiesterase 4 inhibitor, has emerged as a promising option, offering both anti-inflammatory benefits and improvements in pigmentary alterations—making it particularly valuable for treatment of SD in patients with SOC.²⁶

Melasma—Melasma is more prevalent in women with darker skin types, particularly those of African descent and those from East and Southeast Asia or Latin America.^27,28 Standard treatments including hydroquinone, retinoids, azelaic acid, kojic acid, ascorbic acid, arbutin, alpha hydroxy acids, niacinamide, and the Kligman formula (5% hydroquinone, 0.1% tretinoin, and 0.1% dexamethasone) remain therapeutic foundations in patients with SOC.²⁹ Newer alternatives that are effective in SOC populations include topical metformin 30%30; topical isobutylamido thiazolyl resorcinol or thiamidol31; and tranexamic acid cream 5%, which has comparable efficacy to hydroquinone 4% with fewer adverse effects.³² Laser therapies such as the 675-nm and 1064-nm Q-switched neodymium-doped yttrium aluminum garnet lasers, offer effective pigment reduction and are safe in darker skin tones.^33,34

Postinflammatory Hyperpigmentation—Postinflammatory hyperpigmentation, often triggered by acne in SOC populations,²³ manifests as brown, tan, or gray discoloration and is managed using similar topical agents as melasma, with the 1927-nm laser providing an additional treatment option for patients with SOC.^27,35,36

Psoriasis—In patients with SOC, psoriasis often manifests with thicker plaques, increased scaling, and greater body surface area involvement, leading to considerable quality-of-life implications.³⁷ Although prevalence is highest in White populations (3.6%), Asian (2.5%) and Hispanic/Latino (1.9%) patients experience increased disease severity, potentially explaining why psoriasis is among the top chief complaints for these racial/ ethnic groups in the United States.^23,38 Greater diversity in clinical trials has improved our understanding of the efficacy of biologics for psoriasis in SOC populations. The VISIBLE trial—the first SOC-exclusive psoriasis trial—demonstrated a Psoriasis Area and Severity Index 90 response in 57.1% (44/77) of participants receiving guselkumab vs 3.8% (1/26) of participants receiving placebo by week 16 (P<.001).³⁹ Other biologics such as risankizumab, secukinumab, and brodalumab also have shown efficacy in SOC populations.^40-42 Additionally, topical therapies such as calcipotriene-betamethasone dipropionate cream/aerosol foam and halobetasol propionatetazarotene lotion have proven effective, with minimal adverse effects and low discontinuation rates in patients with SOC.^43-46

Seborrheic Keratosis—In SOC, seborrheic keratosis (SK) often appears as a variant known as dermatosis papulosa nigra (DPN), manifesting as small, benign, hyperpigmented papules, particularly on the face and neck.⁴⁷ Dermatosis papulosa nigra is common in Black, Hispanic, and some Asian populations, with variations in color and distribution among different racial/ethnic groups.⁴⁸ For example, in Korean populations, SKs commonly affect males, and in contrast to the dark brown color common in White populations, SKs in Korean patients often appear lighter brown or sometimes pink.⁴⁹ In contrast to the verrucous and stuck-on appearance often seen in White populations, South Asian populations more often have variants including pedunculated SKs, flat SKs, and stucco keratoses.⁵⁰ High-resolution dermoscopy improves differentiation from malignant lesions; however, a sudden SK eruption in any population warrants evaluation for underlying malignancy. Cryotherapy, though effective for removal of SKs, can cause pigmentary changes in SOC populations, making laser therapy and electrosurgery preferable for these patients due to the lower risk for pigmentary sequela. If hyperpigmentation occurs, topical treatments such as hydroquinone, tretinoin, or azelaic acid can help. New laser technologies and hydrogen-peroxide–based therapies offer safer and more effective removal options while minimizing pigmentary risks in SOC populations.^47,50 While DPNs are common in patients with darker skin tones, there are limited data on optimal treatment frequency, insurance coverage, and efficacy. This literature gap hinders our understanding of treatment accessibility and economic impact on our patients.⁵¹

Final Thoughts

Innovations such as standardized scoring systems and customized therapeutic strategies for conditions including acne, pigmentary disorders, and atopic dermatitis have markedly enhanced patient care and outcomes for the most common chief concerns in SOC populations. In addition, population-specific advancements have addressed unique diagnostic and therapeutic developments in Black, Asian/Pacific Islander, and Hispanic groups, from the nuanced presentations of atopic and seborrheic dermatitis in Black patients, to those of psoriasis in Asian/Pacific Islander and Hispanic populations. Finally, updated epidemiologic studies are essential to capture the current and evolving dermatologic concerns pertinent to patients with SOC, ensuring that future clinical and research efforts align with the unique needs of these populations.

The umbrella term skin of color (SOC) includes individuals identifying as Black/African, Hispanic, Asian, Native American, Middle Eastern, and Mediterranean as well as multiracial groups. While the Fitzpatrick skin typing system is not an accurate proxy for describing skin tone, SOC populations typically correspond to Fitzpatrick skin types IV to VI, and clinical researchers often report the Fitzpatrick skin type of their study populations.¹

Over the past several decades, the underrepresentation of diverse skin tones in educational resources has limited clinical training.² For example, only 10.3% of conditions featured in contemporary dermatology textbooks are shown in darker skin tones.³ This educational resource gap has spurred a transformative movement toward inclusivity in dermatologic education, research, and clinical practice. Notable examples include VisualDx⁴ and Dermatology for Skin of Color.⁵ In addition, Cutis began publishing the Dx Across the Skin Color Spectrum fact sheet series in 2022 to highlight differences in how cutaneous conditions manifest in various skin tones (https://www.mdedge.com/cutis/dx-across-skin-color-spectrum).

These resources play a critical role in advancing dermatologic knowledge, ensuring that dermatologists and other health care professionals are well equipped to diagnose and treat dermatologic conditions in SOC populations with accuracy and cultural humility. These innovations also have enhanced our understanding of how common dermatologic conditions manifest and respond to treatment in SOC populations. Herein, we highlight advances in diagnostic and therapeutic approaches for the most common concerns among SOC populations in the United States, including acne vulgaris, atopic dermatitis (AD), seborrheic dermatitis (SD), melasma, postinflammatory hyperpigmentation, psoriasis, and seborrheic keratosis.

Chief Concerns Common Among SOC Populations in the United States

Acne Vulgaris—In patients with SOC, acne frequently results in pigmentary changes and scarring that can manifest as both hypertrophic and keloidal scars.⁶ Clinical evidence from randomized controlled studies supports the use of topical dapsone gel as a safe and effective frontline treatment for acne in patients with SOC.^7,8 Notably, the US Food and Drug Administration–approved 1726-nm laser with a contact-cooling sapphire window has demonstrated safety and efficacy in the management of acne across Fitzpatrick skin types II to VI.^9-11 To manage atrophic acne scars, cutting-edge laser and radiofrequency devices including erbium-doped yttrium aluminum garnet, fractional CO₂, and picosecond lasers have been effectively employed in SOC populations. When these energy-based treatments are combined with cooling systems, they substantially reduce the risk for thermal damage in darker skin tones.^12,13

Atopic Dermatitis—While epidemiologic data indicate that Black patients experience a higher prevalence (19.3%) of AD than Asian (17.8%), White (16.1%), or Hispanic (7.8%) groups in the United States, this disparity may be influenced by factors such as access to care and environmental stressors, which require further study.^14-16 The pathogenesis of AD involves a complex interaction between skin barrier dysfunction, immune dysregulation, and environmental triggers, with patients with SOC exhibiting distinct endotypes.^14,17 For example, East Asian individuals have elevated T_H17-related cytokines and a blended T_H17/T_H2 AD-psoriasis endotype,^14,18 while Black individuals have greater T_H2 skewing and filaggrin variations and higher serum IgE levels.¹⁷ Diagnostic advancements, including a modified Eczema Area and Severity Index using grayscale rather than erythema-based assessments for patients with SOC as well as a novel SOC dermatology atlas that includes AD have increased equity in disease evaluation.^19,20 Recent clinical trials support the efficacy of topical crisaborole, topical ruxolitinib, and biologics such as dupilumab, tralokinumab, lebrikizumab, and fezakinumab for AD in SOC populations, with dupilumab also improving postinflammatory hyperpigmentation.^20-22

Seborrheic Dermatitis—Seborrheic dermatitis is common in patients with SOC, though its manifestations vary by racial/ethnic background.²³ In Black patients, petaloid SD is more prevalent and can resemble secondary syphilis, making accurate diagnosis essential to rule out potential mimickers.²⁴ Effective treatments remain limited, as current therapies often fail to address both the underlying yeast-driven inflammation and the resulting pigmentary changes that commonly affect SOC populations.²⁵ Roflumilast foam 0.3%, a phosphodiesterase 4 inhibitor, has emerged as a promising option, offering both anti-inflammatory benefits and improvements in pigmentary alterations—making it particularly valuable for treatment of SD in patients with SOC.²⁶

Melasma—Melasma is more prevalent in women with darker skin types, particularly those of African descent and those from East and Southeast Asia or Latin America.^27,28 Standard treatments including hydroquinone, retinoids, azelaic acid, kojic acid, ascorbic acid, arbutin, alpha hydroxy acids, niacinamide, and the Kligman formula (5% hydroquinone, 0.1% tretinoin, and 0.1% dexamethasone) remain therapeutic foundations in patients with SOC.²⁹ Newer alternatives that are effective in SOC populations include topical metformin 30%30; topical isobutylamido thiazolyl resorcinol or thiamidol31; and tranexamic acid cream 5%, which has comparable efficacy to hydroquinone 4% with fewer adverse effects.³² Laser therapies such as the 675-nm and 1064-nm Q-switched neodymium-doped yttrium aluminum garnet lasers, offer effective pigment reduction and are safe in darker skin tones.^33,34

Postinflammatory Hyperpigmentation—Postinflammatory hyperpigmentation, often triggered by acne in SOC populations,²³ manifests as brown, tan, or gray discoloration and is managed using similar topical agents as melasma, with the 1927-nm laser providing an additional treatment option for patients with SOC.^27,35,36

Psoriasis—In patients with SOC, psoriasis often manifests with thicker plaques, increased scaling, and greater body surface area involvement, leading to considerable quality-of-life implications.³⁷ Although prevalence is highest in White populations (3.6%), Asian (2.5%) and Hispanic/Latino (1.9%) patients experience increased disease severity, potentially explaining why psoriasis is among the top chief complaints for these racial/ ethnic groups in the United States.^23,38 Greater diversity in clinical trials has improved our understanding of the efficacy of biologics for psoriasis in SOC populations. The VISIBLE trial—the first SOC-exclusive psoriasis trial—demonstrated a Psoriasis Area and Severity Index 90 response in 57.1% (44/77) of participants receiving guselkumab vs 3.8% (1/26) of participants receiving placebo by week 16 (P<.001).³⁹ Other biologics such as risankizumab, secukinumab, and brodalumab also have shown efficacy in SOC populations.^40-42 Additionally, topical therapies such as calcipotriene-betamethasone dipropionate cream/aerosol foam and halobetasol propionatetazarotene lotion have proven effective, with minimal adverse effects and low discontinuation rates in patients with SOC.^43-46

Seborrheic Keratosis—In SOC, seborrheic keratosis (SK) often appears as a variant known as dermatosis papulosa nigra (DPN), manifesting as small, benign, hyperpigmented papules, particularly on the face and neck.⁴⁷ Dermatosis papulosa nigra is common in Black, Hispanic, and some Asian populations, with variations in color and distribution among different racial/ethnic groups.⁴⁸ For example, in Korean populations, SKs commonly affect males, and in contrast to the dark brown color common in White populations, SKs in Korean patients often appear lighter brown or sometimes pink.⁴⁹ In contrast to the verrucous and stuck-on appearance often seen in White populations, South Asian populations more often have variants including pedunculated SKs, flat SKs, and stucco keratoses.⁵⁰ High-resolution dermoscopy improves differentiation from malignant lesions; however, a sudden SK eruption in any population warrants evaluation for underlying malignancy. Cryotherapy, though effective for removal of SKs, can cause pigmentary changes in SOC populations, making laser therapy and electrosurgery preferable for these patients due to the lower risk for pigmentary sequela. If hyperpigmentation occurs, topical treatments such as hydroquinone, tretinoin, or azelaic acid can help. New laser technologies and hydrogen-peroxide–based therapies offer safer and more effective removal options while minimizing pigmentary risks in SOC populations.^47,50 While DPNs are common in patients with darker skin tones, there are limited data on optimal treatment frequency, insurance coverage, and efficacy. This literature gap hinders our understanding of treatment accessibility and economic impact on our patients.⁵¹

Final Thoughts

Innovations such as standardized scoring systems and customized therapeutic strategies for conditions including acne, pigmentary disorders, and atopic dermatitis have markedly enhanced patient care and outcomes for the most common chief concerns in SOC populations. In addition, population-specific advancements have addressed unique diagnostic and therapeutic developments in Black, Asian/Pacific Islander, and Hispanic groups, from the nuanced presentations of atopic and seborrheic dermatitis in Black patients, to those of psoriasis in Asian/Pacific Islander and Hispanic populations. Finally, updated epidemiologic studies are essential to capture the current and evolving dermatologic concerns pertinent to patients with SOC, ensuring that future clinical and research efforts align with the unique needs of these populations.

The umbrella term skin of color (SOC) includes individuals identifying as Black/African, Hispanic, Asian, Native American, Middle Eastern, and Mediterranean as well as multiracial groups. While the Fitzpatrick skin typing system is not an accurate proxy for describing skin tone, SOC populations typically correspond to Fitzpatrick skin types IV to VI, and clinical researchers often report the Fitzpatrick skin type of their study populations.¹

Over the past several decades, the underrepresentation of diverse skin tones in educational resources has limited clinical training.² For example, only 10.3% of conditions featured in contemporary dermatology textbooks are shown in darker skin tones.³ This educational resource gap has spurred a transformative movement toward inclusivity in dermatologic education, research, and clinical practice. Notable examples include VisualDx⁴ and Dermatology for Skin of Color.⁵ In addition, Cutis began publishing the Dx Across the Skin Color Spectrum fact sheet series in 2022 to highlight differences in how cutaneous conditions manifest in various skin tones (https://www.mdedge.com/cutis/dx-across-skin-color-spectrum).

These resources play a critical role in advancing dermatologic knowledge, ensuring that dermatologists and other health care professionals are well equipped to diagnose and treat dermatologic conditions in SOC populations with accuracy and cultural humility. These innovations also have enhanced our understanding of how common dermatologic conditions manifest and respond to treatment in SOC populations. Herein, we highlight advances in diagnostic and therapeutic approaches for the most common concerns among SOC populations in the United States, including acne vulgaris, atopic dermatitis (AD), seborrheic dermatitis (SD), melasma, postinflammatory hyperpigmentation, psoriasis, and seborrheic keratosis.

Chief Concerns Common Among SOC Populations in the United States

Acne Vulgaris—In patients with SOC, acne frequently results in pigmentary changes and scarring that can manifest as both hypertrophic and keloidal scars.⁶ Clinical evidence from randomized controlled studies supports the use of topical dapsone gel as a safe and effective frontline treatment for acne in patients with SOC.^7,8 Notably, the US Food and Drug Administration–approved 1726-nm laser with a contact-cooling sapphire window has demonstrated safety and efficacy in the management of acne across Fitzpatrick skin types II to VI.^9-11 To manage atrophic acne scars, cutting-edge laser and radiofrequency devices including erbium-doped yttrium aluminum garnet, fractional CO₂, and picosecond lasers have been effectively employed in SOC populations. When these energy-based treatments are combined with cooling systems, they substantially reduce the risk for thermal damage in darker skin tones.^12,13

Atopic Dermatitis—While epidemiologic data indicate that Black patients experience a higher prevalence (19.3%) of AD than Asian (17.8%), White (16.1%), or Hispanic (7.8%) groups in the United States, this disparity may be influenced by factors such as access to care and environmental stressors, which require further study.^14-16 The pathogenesis of AD involves a complex interaction between skin barrier dysfunction, immune dysregulation, and environmental triggers, with patients with SOC exhibiting distinct endotypes.^14,17 For example, East Asian individuals have elevated T_H17-related cytokines and a blended T_H17/T_H2 AD-psoriasis endotype,^14,18 while Black individuals have greater T_H2 skewing and filaggrin variations and higher serum IgE levels.¹⁷ Diagnostic advancements, including a modified Eczema Area and Severity Index using grayscale rather than erythema-based assessments for patients with SOC as well as a novel SOC dermatology atlas that includes AD have increased equity in disease evaluation.^19,20 Recent clinical trials support the efficacy of topical crisaborole, topical ruxolitinib, and biologics such as dupilumab, tralokinumab, lebrikizumab, and fezakinumab for AD in SOC populations, with dupilumab also improving postinflammatory hyperpigmentation.^20-22

Seborrheic Dermatitis—Seborrheic dermatitis is common in patients with SOC, though its manifestations vary by racial/ethnic background.²³ In Black patients, petaloid SD is more prevalent and can resemble secondary syphilis, making accurate diagnosis essential to rule out potential mimickers.²⁴ Effective treatments remain limited, as current therapies often fail to address both the underlying yeast-driven inflammation and the resulting pigmentary changes that commonly affect SOC populations.²⁵ Roflumilast foam 0.3%, a phosphodiesterase 4 inhibitor, has emerged as a promising option, offering both anti-inflammatory benefits and improvements in pigmentary alterations—making it particularly valuable for treatment of SD in patients with SOC.²⁶

Melasma—Melasma is more prevalent in women with darker skin types, particularly those of African descent and those from East and Southeast Asia or Latin America.^27,28 Standard treatments including hydroquinone, retinoids, azelaic acid, kojic acid, ascorbic acid, arbutin, alpha hydroxy acids, niacinamide, and the Kligman formula (5% hydroquinone, 0.1% tretinoin, and 0.1% dexamethasone) remain therapeutic foundations in patients with SOC.²⁹ Newer alternatives that are effective in SOC populations include topical metformin 30%30; topical isobutylamido thiazolyl resorcinol or thiamidol31; and tranexamic acid cream 5%, which has comparable efficacy to hydroquinone 4% with fewer adverse effects.³² Laser therapies such as the 675-nm and 1064-nm Q-switched neodymium-doped yttrium aluminum garnet lasers, offer effective pigment reduction and are safe in darker skin tones.^33,34

Postinflammatory Hyperpigmentation—Postinflammatory hyperpigmentation, often triggered by acne in SOC populations,²³ manifests as brown, tan, or gray discoloration and is managed using similar topical agents as melasma, with the 1927-nm laser providing an additional treatment option for patients with SOC.^27,35,36

Psoriasis—In patients with SOC, psoriasis often manifests with thicker plaques, increased scaling, and greater body surface area involvement, leading to considerable quality-of-life implications.³⁷ Although prevalence is highest in White populations (3.6%), Asian (2.5%) and Hispanic/Latino (1.9%) patients experience increased disease severity, potentially explaining why psoriasis is among the top chief complaints for these racial/ ethnic groups in the United States.^23,38 Greater diversity in clinical trials has improved our understanding of the efficacy of biologics for psoriasis in SOC populations. The VISIBLE trial—the first SOC-exclusive psoriasis trial—demonstrated a Psoriasis Area and Severity Index 90 response in 57.1% (44/77) of participants receiving guselkumab vs 3.8% (1/26) of participants receiving placebo by week 16 (P<.001).³⁹ Other biologics such as risankizumab, secukinumab, and brodalumab also have shown efficacy in SOC populations.^40-42 Additionally, topical therapies such as calcipotriene-betamethasone dipropionate cream/aerosol foam and halobetasol propionatetazarotene lotion have proven effective, with minimal adverse effects and low discontinuation rates in patients with SOC.^43-46

Seborrheic Keratosis—In SOC, seborrheic keratosis (SK) often appears as a variant known as dermatosis papulosa nigra (DPN), manifesting as small, benign, hyperpigmented papules, particularly on the face and neck.⁴⁷ Dermatosis papulosa nigra is common in Black, Hispanic, and some Asian populations, with variations in color and distribution among different racial/ethnic groups.⁴⁸ For example, in Korean populations, SKs commonly affect males, and in contrast to the dark brown color common in White populations, SKs in Korean patients often appear lighter brown or sometimes pink.⁴⁹ In contrast to the verrucous and stuck-on appearance often seen in White populations, South Asian populations more often have variants including pedunculated SKs, flat SKs, and stucco keratoses.⁵⁰ High-resolution dermoscopy improves differentiation from malignant lesions; however, a sudden SK eruption in any population warrants evaluation for underlying malignancy. Cryotherapy, though effective for removal of SKs, can cause pigmentary changes in SOC populations, making laser therapy and electrosurgery preferable for these patients due to the lower risk for pigmentary sequela. If hyperpigmentation occurs, topical treatments such as hydroquinone, tretinoin, or azelaic acid can help. New laser technologies and hydrogen-peroxide–based therapies offer safer and more effective removal options while minimizing pigmentary risks in SOC populations.^47,50 While DPNs are common in patients with darker skin tones, there are limited data on optimal treatment frequency, insurance coverage, and efficacy. This literature gap hinders our understanding of treatment accessibility and economic impact on our patients.⁵¹

Final Thoughts

Innovations such as standardized scoring systems and customized therapeutic strategies for conditions including acne, pigmentary disorders, and atopic dermatitis have markedly enhanced patient care and outcomes for the most common chief concerns in SOC populations. In addition, population-specific advancements have addressed unique diagnostic and therapeutic developments in Black, Asian/Pacific Islander, and Hispanic groups, from the nuanced presentations of atopic and seborrheic dermatitis in Black patients, to those of psoriasis in Asian/Pacific Islander and Hispanic populations. Finally, updated epidemiologic studies are essential to capture the current and evolving dermatologic concerns pertinent to patients with SOC, ensuring that future clinical and research efforts align with the unique needs of these populations.

In our June issue, I highlighted the potentially seismic clinical implications of the U.S. Supreme Court’s then-pending decision in the Kennedy vs. Braidwood Management, Inc., case. That ruling, recently released at the conclusion of the Court’s term, ultimately affirmed the Affordable Care Act’s mandate requiring insurers to cover certain preventive services, including colorectal cancer screening tests, without cost-sharing.

In doing so, however, the court determined that members of the U.S. Preventive Services Task Force (USPSTF), which recommends these services, are “inferior officers” appropriately appointed by the Secretary of Health and Human Services (HHS), rather than needing Senate confirmation. Thus, the decision reinforced the HHS Secretary’s authority to oversee and potentially influence USPSTF recommendations in the future. While the decision represented a victory in upholding a key provision of the ACA, it also signaled a potential threat to the scientific independence of the body charged with making those preventive care recommendations in a scientifically rigorous, unbiased manner. 

As anticipated, the HHS Secretary responded to the Supreme Court’s ruling by abruptly canceling the USPSTF’s scheduled July meeting. This decision, coupled with his recent disbanding of the entire 17-member Advisory Committee on Immunization Practices — the group responsible for shaping evidence-based vaccine policy — has raised serious concerns across the healthcare field. On July 9th, AGA joined a coalition of 104 health organizations in submitting a letter to the Chair and Ranking Members of the Senate Committee on Health, Education, Labor and Pensions and the House Committee on Energy and Commerce, urging them to protect the integrity of the USPSTF.

The fight to protect science-based health policy is far from over — effective advocacy necessitates that clinicians use their professional platforms to push back against the politicization of science – not only for the integrity of the medical profession, but for the health and future of the patients we serve. At a time when medical misinformation runs rampant, undermining the independence of scientific bodies risks sowing confusion, eroding public trust, and compromising patient care for years to come.

Megan A. Adams, MD, JD, MSc 

Editor in Chief

In our June issue, I highlighted the potentially seismic clinical implications of the U.S. Supreme Court’s then-pending decision in the Kennedy vs. Braidwood Management, Inc., case. That ruling, recently released at the conclusion of the Court’s term, ultimately affirmed the Affordable Care Act’s mandate requiring insurers to cover certain preventive services, including colorectal cancer screening tests, without cost-sharing.

In doing so, however, the court determined that members of the U.S. Preventive Services Task Force (USPSTF), which recommends these services, are “inferior officers” appropriately appointed by the Secretary of Health and Human Services (HHS), rather than needing Senate confirmation. Thus, the decision reinforced the HHS Secretary’s authority to oversee and potentially influence USPSTF recommendations in the future. While the decision represented a victory in upholding a key provision of the ACA, it also signaled a potential threat to the scientific independence of the body charged with making those preventive care recommendations in a scientifically rigorous, unbiased manner. 

As anticipated, the HHS Secretary responded to the Supreme Court’s ruling by abruptly canceling the USPSTF’s scheduled July meeting. This decision, coupled with his recent disbanding of the entire 17-member Advisory Committee on Immunization Practices — the group responsible for shaping evidence-based vaccine policy — has raised serious concerns across the healthcare field. On July 9th, AGA joined a coalition of 104 health organizations in submitting a letter to the Chair and Ranking Members of the Senate Committee on Health, Education, Labor and Pensions and the House Committee on Energy and Commerce, urging them to protect the integrity of the USPSTF.

The fight to protect science-based health policy is far from over — effective advocacy necessitates that clinicians use their professional platforms to push back against the politicization of science – not only for the integrity of the medical profession, but for the health and future of the patients we serve. At a time when medical misinformation runs rampant, undermining the independence of scientific bodies risks sowing confusion, eroding public trust, and compromising patient care for years to come.

Megan A. Adams, MD, JD, MSc 

Editor in Chief

In our June issue, I highlighted the potentially seismic clinical implications of the U.S. Supreme Court’s then-pending decision in the Kennedy vs. Braidwood Management, Inc., case. That ruling, recently released at the conclusion of the Court’s term, ultimately affirmed the Affordable Care Act’s mandate requiring insurers to cover certain preventive services, including colorectal cancer screening tests, without cost-sharing.

In doing so, however, the court determined that members of the U.S. Preventive Services Task Force (USPSTF), which recommends these services, are “inferior officers” appropriately appointed by the Secretary of Health and Human Services (HHS), rather than needing Senate confirmation. Thus, the decision reinforced the HHS Secretary’s authority to oversee and potentially influence USPSTF recommendations in the future. While the decision represented a victory in upholding a key provision of the ACA, it also signaled a potential threat to the scientific independence of the body charged with making those preventive care recommendations in a scientifically rigorous, unbiased manner. 

As anticipated, the HHS Secretary responded to the Supreme Court’s ruling by abruptly canceling the USPSTF’s scheduled July meeting. This decision, coupled with his recent disbanding of the entire 17-member Advisory Committee on Immunization Practices — the group responsible for shaping evidence-based vaccine policy — has raised serious concerns across the healthcare field. On July 9th, AGA joined a coalition of 104 health organizations in submitting a letter to the Chair and Ranking Members of the Senate Committee on Health, Education, Labor and Pensions and the House Committee on Energy and Commerce, urging them to protect the integrity of the USPSTF.

The fight to protect science-based health policy is far from over — effective advocacy necessitates that clinicians use their professional platforms to push back against the politicization of science – not only for the integrity of the medical profession, but for the health and future of the patients we serve. At a time when medical misinformation runs rampant, undermining the independence of scientific bodies risks sowing confusion, eroding public trust, and compromising patient care for years to come.

Megan A. Adams, MD, JD, MSc 

Editor in Chief

How did I develop a strong interest in acne and rosacea? Interest on a personal level was with me throughout my adolescence and post-teen years as I suffered with very severe facial acne from ages 13 through 23 (1967-1977). I was sometimes called “pizza face” in high school, and biweekly trips to a dermatology office that always had a packed waiting room were of little help that I could appreciate visibly. Six straight years of extractions, intralesional injections, draining of fluctuant cysts, UVC light treatments, oral tetracycline, irritating topical formulations of benzoyl peroxide and tretinoin, and topical sulfacetamide-sulfur products resulted in minimal improvement. However, maybe all of this did something to what was happening underneath the skin surface, as I have no residual acne scars. I do recall vividly that I walked the halls in high school and college consistently affected by a very red face from the topical agents and smelling like rotten eggs from the topical sulfur application. I fortunately handled it well emotionally and socially, for which I am very thankful. Many people affected with acne do not.

In dermatology, I have always had a strong interest in pathophysiology and therapeutics, rooted I am sure in my background as a pharmacist. Although I was always interested in acne therapy, I was fully captivated by a presentation given by Dr. Jim Leyden many years ago at a small meeting in Myrtle Beach, South Carolina. He brought the subject of acne to life in a way that more than grabbed my complete attention and ignited an interest in learning everything I could about it. Over time, I was fortunate enough to work alongside Dr. Leyden and many other household names in acne at meetings and publications to further education on one of the most common disease states seen in ambulatory dermatology practices worldwide. The rest is history, leading to almost 4 decades of work in acne on many levels in dermatology, all being efforts that I am grateful for.

What I have observed to date is that we have had few revolutionary advances in acne therapy, the major one being oral isotretinoin, which was first brought to market in 1982. We are still utilizing many of the same therapeutic agents that I used back when I was treated for acne. A few new topical compounds have emerged, such as dapsone and clascoterone, and a narrow-spectrum tetracycline agent, sarecycline, also was developed. These agents do represent important advances with some specific benefits. There have been many major improvements in drug delivery formulations, including several vehicle technologies that allow augmented skin tolerability, increased efficacy, and improved stability, allowing for combination therapy products containing 2 or 3 active ingredients. A recent example is the first triple-combination topical acne therapy with excellent supporting data on speed of onset, efficacy, and safety.¹

Technological advances also have aided in the development of modified- or extended-release formulations of oral antibiotics, such as doxycycline and minocycline, which allow for reduced adverse effects and lower daily dosages. Lidose formulations of isotretinoin have circumvented the need for concurrent ingestion of a high-fat meal to facilitate its absorption in the gastrointestinal tract (as required with conventional formulations). Many hours also have been spent on delivery devices and vehicles such as pumps, foams, and aqueous-based gels. Let us not forget the efforts and myriad products directed at skin care, cosmeceuticals, and physical devices (lasers and lights) for acne. Regardless of the above, we have not seen the monumental therapeutic and research revolution for acne that we have experienced more recently with biologic agents, Janus kinase inhibitors, and other modes of action for many common disease states such as atopic dermatitis, psoriasis, alopecia areata, vitiligo, hidradenitis suppurativa, prurigo nodularis, and chronic spontaneous urticaria.

Unfortunately, the slow development of advances in treatments for acne has been compounded further by the widespread availability of generic equivalents of most topical and oral therapies along with several over-the- counter topical medications. The expanded skin care and cosmeceutical product world has further diluted the perceived value of topical prescription therapies for acne. The marked difficulty in achieving and sustaining total clearance of acne, with the exception of many individuals treated with oral isotretinoin, results in many patients searching for other options, often through sources beyond dermatology practices (eg, the internet). While some of these sources may provide valid suggestions, they often are not truly substantiated by valid clinical research and are not formally regulated by the US Food and Drug Administration.

All of the above, in addition to the barriers to medication coverage put in place by third-party organizations such as pharmacy benefit managers, have contributed to the extreme slowdown in the development of new prescription therapies for acne. What this leads me to believe is that until there is a true meeting of the minds of all stakeholders on policies that facilitate access to both established and newly available acne therapies, there will be an enduring diminished incentive to support the development of newer acne treatments that will continue to spiral progressively downward. Some research on acne will always continue, such as the search for an acne vaccine and cutaneous microbiome alterations that are in progress.^2,3 However, I do not see much happening in the foreseeable future. I am not inherently a pessimist or a “prophet of doom,” so I sincerely hope I am wrong.

How did I develop a strong interest in acne and rosacea? Interest on a personal level was with me throughout my adolescence and post-teen years as I suffered with very severe facial acne from ages 13 through 23 (1967-1977). I was sometimes called “pizza face” in high school, and biweekly trips to a dermatology office that always had a packed waiting room were of little help that I could appreciate visibly. Six straight years of extractions, intralesional injections, draining of fluctuant cysts, UVC light treatments, oral tetracycline, irritating topical formulations of benzoyl peroxide and tretinoin, and topical sulfacetamide-sulfur products resulted in minimal improvement. However, maybe all of this did something to what was happening underneath the skin surface, as I have no residual acne scars. I do recall vividly that I walked the halls in high school and college consistently affected by a very red face from the topical agents and smelling like rotten eggs from the topical sulfur application. I fortunately handled it well emotionally and socially, for which I am very thankful. Many people affected with acne do not.

In dermatology, I have always had a strong interest in pathophysiology and therapeutics, rooted I am sure in my background as a pharmacist. Although I was always interested in acne therapy, I was fully captivated by a presentation given by Dr. Jim Leyden many years ago at a small meeting in Myrtle Beach, South Carolina. He brought the subject of acne to life in a way that more than grabbed my complete attention and ignited an interest in learning everything I could about it. Over time, I was fortunate enough to work alongside Dr. Leyden and many other household names in acne at meetings and publications to further education on one of the most common disease states seen in ambulatory dermatology practices worldwide. The rest is history, leading to almost 4 decades of work in acne on many levels in dermatology, all being efforts that I am grateful for.

What I have observed to date is that we have had few revolutionary advances in acne therapy, the major one being oral isotretinoin, which was first brought to market in 1982. We are still utilizing many of the same therapeutic agents that I used back when I was treated for acne. A few new topical compounds have emerged, such as dapsone and clascoterone, and a narrow-spectrum tetracycline agent, sarecycline, also was developed. These agents do represent important advances with some specific benefits. There have been many major improvements in drug delivery formulations, including several vehicle technologies that allow augmented skin tolerability, increased efficacy, and improved stability, allowing for combination therapy products containing 2 or 3 active ingredients. A recent example is the first triple-combination topical acne therapy with excellent supporting data on speed of onset, efficacy, and safety.¹

Technological advances also have aided in the development of modified- or extended-release formulations of oral antibiotics, such as doxycycline and minocycline, which allow for reduced adverse effects and lower daily dosages. Lidose formulations of isotretinoin have circumvented the need for concurrent ingestion of a high-fat meal to facilitate its absorption in the gastrointestinal tract (as required with conventional formulations). Many hours also have been spent on delivery devices and vehicles such as pumps, foams, and aqueous-based gels. Let us not forget the efforts and myriad products directed at skin care, cosmeceuticals, and physical devices (lasers and lights) for acne. Regardless of the above, we have not seen the monumental therapeutic and research revolution for acne that we have experienced more recently with biologic agents, Janus kinase inhibitors, and other modes of action for many common disease states such as atopic dermatitis, psoriasis, alopecia areata, vitiligo, hidradenitis suppurativa, prurigo nodularis, and chronic spontaneous urticaria.

Unfortunately, the slow development of advances in treatments for acne has been compounded further by the widespread availability of generic equivalents of most topical and oral therapies along with several over-the- counter topical medications. The expanded skin care and cosmeceutical product world has further diluted the perceived value of topical prescription therapies for acne. The marked difficulty in achieving and sustaining total clearance of acne, with the exception of many individuals treated with oral isotretinoin, results in many patients searching for other options, often through sources beyond dermatology practices (eg, the internet). While some of these sources may provide valid suggestions, they often are not truly substantiated by valid clinical research and are not formally regulated by the US Food and Drug Administration.

All of the above, in addition to the barriers to medication coverage put in place by third-party organizations such as pharmacy benefit managers, have contributed to the extreme slowdown in the development of new prescription therapies for acne. What this leads me to believe is that until there is a true meeting of the minds of all stakeholders on policies that facilitate access to both established and newly available acne therapies, there will be an enduring diminished incentive to support the development of newer acne treatments that will continue to spiral progressively downward. Some research on acne will always continue, such as the search for an acne vaccine and cutaneous microbiome alterations that are in progress.^2,3 However, I do not see much happening in the foreseeable future. I am not inherently a pessimist or a “prophet of doom,” so I sincerely hope I am wrong.

How did I develop a strong interest in acne and rosacea? Interest on a personal level was with me throughout my adolescence and post-teen years as I suffered with very severe facial acne from ages 13 through 23 (1967-1977). I was sometimes called “pizza face” in high school, and biweekly trips to a dermatology office that always had a packed waiting room were of little help that I could appreciate visibly. Six straight years of extractions, intralesional injections, draining of fluctuant cysts, UVC light treatments, oral tetracycline, irritating topical formulations of benzoyl peroxide and tretinoin, and topical sulfacetamide-sulfur products resulted in minimal improvement. However, maybe all of this did something to what was happening underneath the skin surface, as I have no residual acne scars. I do recall vividly that I walked the halls in high school and college consistently affected by a very red face from the topical agents and smelling like rotten eggs from the topical sulfur application. I fortunately handled it well emotionally and socially, for which I am very thankful. Many people affected with acne do not.

In dermatology, I have always had a strong interest in pathophysiology and therapeutics, rooted I am sure in my background as a pharmacist. Although I was always interested in acne therapy, I was fully captivated by a presentation given by Dr. Jim Leyden many years ago at a small meeting in Myrtle Beach, South Carolina. He brought the subject of acne to life in a way that more than grabbed my complete attention and ignited an interest in learning everything I could about it. Over time, I was fortunate enough to work alongside Dr. Leyden and many other household names in acne at meetings and publications to further education on one of the most common disease states seen in ambulatory dermatology practices worldwide. The rest is history, leading to almost 4 decades of work in acne on many levels in dermatology, all being efforts that I am grateful for.

What I have observed to date is that we have had few revolutionary advances in acne therapy, the major one being oral isotretinoin, which was first brought to market in 1982. We are still utilizing many of the same therapeutic agents that I used back when I was treated for acne. A few new topical compounds have emerged, such as dapsone and clascoterone, and a narrow-spectrum tetracycline agent, sarecycline, also was developed. These agents do represent important advances with some specific benefits. There have been many major improvements in drug delivery formulations, including several vehicle technologies that allow augmented skin tolerability, increased efficacy, and improved stability, allowing for combination therapy products containing 2 or 3 active ingredients. A recent example is the first triple-combination topical acne therapy with excellent supporting data on speed of onset, efficacy, and safety.¹

Technological advances also have aided in the development of modified- or extended-release formulations of oral antibiotics, such as doxycycline and minocycline, which allow for reduced adverse effects and lower daily dosages. Lidose formulations of isotretinoin have circumvented the need for concurrent ingestion of a high-fat meal to facilitate its absorption in the gastrointestinal tract (as required with conventional formulations). Many hours also have been spent on delivery devices and vehicles such as pumps, foams, and aqueous-based gels. Let us not forget the efforts and myriad products directed at skin care, cosmeceuticals, and physical devices (lasers and lights) for acne. Regardless of the above, we have not seen the monumental therapeutic and research revolution for acne that we have experienced more recently with biologic agents, Janus kinase inhibitors, and other modes of action for many common disease states such as atopic dermatitis, psoriasis, alopecia areata, vitiligo, hidradenitis suppurativa, prurigo nodularis, and chronic spontaneous urticaria.

Unfortunately, the slow development of advances in treatments for acne has been compounded further by the widespread availability of generic equivalents of most topical and oral therapies along with several over-the- counter topical medications. The expanded skin care and cosmeceutical product world has further diluted the perceived value of topical prescription therapies for acne. The marked difficulty in achieving and sustaining total clearance of acne, with the exception of many individuals treated with oral isotretinoin, results in many patients searching for other options, often through sources beyond dermatology practices (eg, the internet). While some of these sources may provide valid suggestions, they often are not truly substantiated by valid clinical research and are not formally regulated by the US Food and Drug Administration.

All of the above, in addition to the barriers to medication coverage put in place by third-party organizations such as pharmacy benefit managers, have contributed to the extreme slowdown in the development of new prescription therapies for acne. What this leads me to believe is that until there is a true meeting of the minds of all stakeholders on policies that facilitate access to both established and newly available acne therapies, there will be an enduring diminished incentive to support the development of newer acne treatments that will continue to spiral progressively downward. Some research on acne will always continue, such as the search for an acne vaccine and cutaneous microbiome alterations that are in progress.^2,3 However, I do not see much happening in the foreseeable future. I am not inherently a pessimist or a “prophet of doom,” so I sincerely hope I am wrong.

Dear Friends,

Like many readers, I just returned from Digestive Disease Week® (DDW) in San Diego, California. For the first time in my early career, my experience was not just overwhelming and exhausting. Before, I wanted to do everything – lectures, posters, meetings with friends, prospective research collaborators, and more! This year, I acknowledged that instead of spreading myself thin and not fully engaging, I made a focused daily schedule mixed with productivity and social events, selecting only what was most important to me at this time in my career. This time, after DDW, instead of giving in to my inner introvert and holing myself in my house for a week to recover, I am invigorated by what I learned and the people I met. I can’t wait to see what’s to come next year!

In this issue’s “In Focus”, Dr. Evan Dellon describes his diagnostic approach, including a clear history, endoscopic evaluation with biopsy, and ruling out other causes of esophageal eosinophilia. He emphasizes that treatment should target both inflammation and fibrostenosis and reviews the guidelines and evidence behind first-line treatments, surveillance, and long-term maintenance.

In the second of a two-part series in the “Short Clinical Review” section, Dr. Christopher Vélez, Dr. Rosa L. Yu, and Dr. Jennifer Dimino discuss care for patients with disorders of brain-gut interaction from historically marginalized communities. They highlight ways to improve care for these patients in day-to-day clinical practice.

The transition from trainee to a practicing gastroenterologist may bring with it responsibilities of giving feedback to trainees and/or colleagues to improve. In the “Early Career” section, Dr. Michelle Baliss and Dr. Christine Hachem give practical tips on how best to deliver feedback, with a focus on creating time, building rapport, bidirectional communication, and more.

Lastly, in the “Finance/Legal” section, John S. Gardner, a financial advisor, guides trainees and early career gastroenterologists through estate planning – why it’s important, how to do it effectively, and long-term benefits to starting early.

If you are interested in contributing or have ideas for future TNG topics, please contact me (tjudy@wustl.edu) or Danielle Kiefer (dkiefer@gastro.org), Communications/Managing Editor of TNG.

Until next time, I leave you with a historical fun fact because we would not be where we are now without appreciating where we were: the first case of eosinophilic esophagitis was only first described in 1978 and became a distinct entity in the early 1990s.

Yours truly, 

Judy A. Trieu, MD, MPH

Editor-in-Chief

Assistant Professor of Medicine

Interventional Endoscopy, Division of Gastroenterology

Washington University School of Medicine in St. Louis

Dear Friends,

Like many readers, I just returned from Digestive Disease Week® (DDW) in San Diego, California. For the first time in my early career, my experience was not just overwhelming and exhausting. Before, I wanted to do everything – lectures, posters, meetings with friends, prospective research collaborators, and more! This year, I acknowledged that instead of spreading myself thin and not fully engaging, I made a focused daily schedule mixed with productivity and social events, selecting only what was most important to me at this time in my career. This time, after DDW, instead of giving in to my inner introvert and holing myself in my house for a week to recover, I am invigorated by what I learned and the people I met. I can’t wait to see what’s to come next year!

In this issue’s “In Focus”, Dr. Evan Dellon describes his diagnostic approach, including a clear history, endoscopic evaluation with biopsy, and ruling out other causes of esophageal eosinophilia. He emphasizes that treatment should target both inflammation and fibrostenosis and reviews the guidelines and evidence behind first-line treatments, surveillance, and long-term maintenance.

In the second of a two-part series in the “Short Clinical Review” section, Dr. Christopher Vélez, Dr. Rosa L. Yu, and Dr. Jennifer Dimino discuss care for patients with disorders of brain-gut interaction from historically marginalized communities. They highlight ways to improve care for these patients in day-to-day clinical practice.

The transition from trainee to a practicing gastroenterologist may bring with it responsibilities of giving feedback to trainees and/or colleagues to improve. In the “Early Career” section, Dr. Michelle Baliss and Dr. Christine Hachem give practical tips on how best to deliver feedback, with a focus on creating time, building rapport, bidirectional communication, and more.

Lastly, in the “Finance/Legal” section, John S. Gardner, a financial advisor, guides trainees and early career gastroenterologists through estate planning – why it’s important, how to do it effectively, and long-term benefits to starting early.

If you are interested in contributing or have ideas for future TNG topics, please contact me (tjudy@wustl.edu) or Danielle Kiefer (dkiefer@gastro.org), Communications/Managing Editor of TNG.

Until next time, I leave you with a historical fun fact because we would not be where we are now without appreciating where we were: the first case of eosinophilic esophagitis was only first described in 1978 and became a distinct entity in the early 1990s.

Yours truly, 

Judy A. Trieu, MD, MPH

Editor-in-Chief

Assistant Professor of Medicine

Interventional Endoscopy, Division of Gastroenterology

Washington University School of Medicine in St. Louis

Dear Friends,

Like many readers, I just returned from Digestive Disease Week® (DDW) in San Diego, California. For the first time in my early career, my experience was not just overwhelming and exhausting. Before, I wanted to do everything – lectures, posters, meetings with friends, prospective research collaborators, and more! This year, I acknowledged that instead of spreading myself thin and not fully engaging, I made a focused daily schedule mixed with productivity and social events, selecting only what was most important to me at this time in my career. This time, after DDW, instead of giving in to my inner introvert and holing myself in my house for a week to recover, I am invigorated by what I learned and the people I met. I can’t wait to see what’s to come next year!

In this issue’s “In Focus”, Dr. Evan Dellon describes his diagnostic approach, including a clear history, endoscopic evaluation with biopsy, and ruling out other causes of esophageal eosinophilia. He emphasizes that treatment should target both inflammation and fibrostenosis and reviews the guidelines and evidence behind first-line treatments, surveillance, and long-term maintenance.

In the second of a two-part series in the “Short Clinical Review” section, Dr. Christopher Vélez, Dr. Rosa L. Yu, and Dr. Jennifer Dimino discuss care for patients with disorders of brain-gut interaction from historically marginalized communities. They highlight ways to improve care for these patients in day-to-day clinical practice.

The transition from trainee to a practicing gastroenterologist may bring with it responsibilities of giving feedback to trainees and/or colleagues to improve. In the “Early Career” section, Dr. Michelle Baliss and Dr. Christine Hachem give practical tips on how best to deliver feedback, with a focus on creating time, building rapport, bidirectional communication, and more.

Lastly, in the “Finance/Legal” section, John S. Gardner, a financial advisor, guides trainees and early career gastroenterologists through estate planning – why it’s important, how to do it effectively, and long-term benefits to starting early.

If you are interested in contributing or have ideas for future TNG topics, please contact me (tjudy@wustl.edu) or Danielle Kiefer (dkiefer@gastro.org), Communications/Managing Editor of TNG.

Until next time, I leave you with a historical fun fact because we would not be where we are now without appreciating where we were: the first case of eosinophilic esophagitis was only first described in 1978 and became a distinct entity in the early 1990s.

Yours truly, 

Judy A. Trieu, MD, MPH

Editor-in-Chief

Assistant Professor of Medicine

Interventional Endoscopy, Division of Gastroenterology

Washington University School of Medicine in St. Louis