Neil Osterweil

CHICAGO – An analysis of posts on TikTok about cirrhosis finds that approximately 40% of these posts include misinformation, according to a study presented at the annual Digestive Disease Week® (DDW).

TikTok’s short video format is increasingly becoming a major source for news and information, especially for adolescents and young adults. In 2022 the technology news website The Verge reported that about 10% of all U.S. adults regularly get news from TikTok, including an estimated 26% of adults under 30.

“Our study highlights the alarming prevalence of misinformation related to liver disease and cirrhosis on the TikTok platform. This misinformation can potentially lead to harm and poor health outcomes for individuals seeking accurate information about their conditions,” wrote the study authors in their abstract.

The study, which was led by Macklin Loveland, MD, an internal medicine resident at the University of Arizona, Tucson, found that, among 2,223 TikTok posts related to liver disease or cirrhosis as of November 2022, 60.3% were found to have accurate medical information, but the remaining 39.7% contained misinformation.

Some of the misinformation offered highly dubious and potentially dangerous advice, such as “Reishi mushrooms can reverse liver damage,” when in fact there is evidence to suggest that reishi mushrooms, especially in powder form, may be toxic to the liver and may even cause fatal fulminant hepatitis.

In an interview, Dr. Loveland said that much of the good information about liver disease on TikTok seems to come from patients with cirrhosis or other liver diseases who post videos chronicling their experiences, whereas bad information seems to come from people who are trying to pitch a product such as “natural” or “alternative” medicine.

“People who have real-life, firsthand experiences with cirrhosis have a really nice platform to talk about their disease process and share information with other people with similar disease processes, and the majority of them are accurate,” he said. “Where the inaccuracies come in are when people are trying to profit off a product or sell a dietary supplement, and then things go by the wayside.”

It’s important for TikTok users to understand the intentions of other users, he said, and expressed the hope that content mediators within TikTok would help to keep misinformation at bay.

Skyler B. Johnson, MD, assistant professor of radiation oncology at the University of Utah Huntsman Cancer Institute, Salt Lake City, has studied misinformation about cancer on social media, and as he and colleagues reported in the Journal of the National Cancer Institute, of 200 articles on cancer posted on social media sites, 32.5% contained misinformation and 30.5% contained harmful information.

In an interview, Dr. Johnson, who was not involved in the study by Dr. Loveland and colleagues, offered advice for colleagues about countering misinformation.

“What we’re trying to do, as part of our research group, is encourage physicians to take an active role in addressing misinformation with their patients and also in their social networking interactions,” he said. “When I see a new patient with a new diagnosis of cancer, I warn them that they’re going to encounter things online that may or may not be true.”

He noted that, often when physicians instruct patients not to go online to research their disease, the first thing the vast majority of patients do after leaving the office is to jump online.

Instead, Dr. Johnson recommended inoculating patients against misinformation – not to discourage them from going online, but to inform them about the myriad good and bad information sources, and steer them toward trustworthy sites such as government agencies (the National Institutes of Health, Centers for Disease Control and Prevention, etc), academic medical center sites, or select nonprofit organizations, foundations, and medical associations.

“But at the end of the day, even those you have to be somewhat vigilant about, because there are some unscrupulous providers who exploit even those sites,” he added.
 

Study details

Dr. Loveland and colleagues used the TikTok search engine to look for posts containing the terms “cirrhosis” and “liver disease,” and watched all such videos that turned up in the search from beginning to end. They classified each post as either educational in intent or whether it depicted a firsthand experience with liver disease.

They determined whether each post was accurate or erroneous according to guidelines from the American Association for the Study of Liver Disease, American College of Gastroenterology, and American Gastroenterological Association. They also recorded the number of likes, comments, and the number of times that each video was shared.

Accurate posts were viewed and liked significantly more often than inaccurate ones, and accurate posts had significantly more comments that faulty posts.

However, both accurate and inaccurate posts were shared a similar number of times, suggesting that bad-quality information can metastasize just as easily as good information can be disseminated.

Dr. Loveland and colleagues echoed the recommendations of Dr. Johnson, stating that “health care provides should be aware of the potential for misinformation on social media and should strive to provide their patients with accurate and evidence-based information to inform their health care decisions.”

The study was internally funded. Dr. Loveland and Dr. Johnson reported having no conflicts of interest to disclose.

DDW is sponsored by the American Association for the Study of Liver Diseases, the AGA, the American Society for Gastrointestinal Endoscopy, and The Society for Surgery of the Alimentary Tract.

CHICAGO – An analysis of posts on TikTok about cirrhosis finds that approximately 40% of these posts include misinformation, according to a study presented at the annual Digestive Disease Week® (DDW).

TikTok’s short video format is increasingly becoming a major source for news and information, especially for adolescents and young adults. In 2022 the technology news website The Verge reported that about 10% of all U.S. adults regularly get news from TikTok, including an estimated 26% of adults under 30.

“Our study highlights the alarming prevalence of misinformation related to liver disease and cirrhosis on the TikTok platform. This misinformation can potentially lead to harm and poor health outcomes for individuals seeking accurate information about their conditions,” wrote the study authors in their abstract.

The study, which was led by Macklin Loveland, MD, an internal medicine resident at the University of Arizona, Tucson, found that, among 2,223 TikTok posts related to liver disease or cirrhosis as of November 2022, 60.3% were found to have accurate medical information, but the remaining 39.7% contained misinformation.

Some of the misinformation offered highly dubious and potentially dangerous advice, such as “Reishi mushrooms can reverse liver damage,” when in fact there is evidence to suggest that reishi mushrooms, especially in powder form, may be toxic to the liver and may even cause fatal fulminant hepatitis.

In an interview, Dr. Loveland said that much of the good information about liver disease on TikTok seems to come from patients with cirrhosis or other liver diseases who post videos chronicling their experiences, whereas bad information seems to come from people who are trying to pitch a product such as “natural” or “alternative” medicine.

“People who have real-life, firsthand experiences with cirrhosis have a really nice platform to talk about their disease process and share information with other people with similar disease processes, and the majority of them are accurate,” he said. “Where the inaccuracies come in are when people are trying to profit off a product or sell a dietary supplement, and then things go by the wayside.”

It’s important for TikTok users to understand the intentions of other users, he said, and expressed the hope that content mediators within TikTok would help to keep misinformation at bay.

Skyler B. Johnson, MD, assistant professor of radiation oncology at the University of Utah Huntsman Cancer Institute, Salt Lake City, has studied misinformation about cancer on social media, and as he and colleagues reported in the Journal of the National Cancer Institute, of 200 articles on cancer posted on social media sites, 32.5% contained misinformation and 30.5% contained harmful information.

In an interview, Dr. Johnson, who was not involved in the study by Dr. Loveland and colleagues, offered advice for colleagues about countering misinformation.

“What we’re trying to do, as part of our research group, is encourage physicians to take an active role in addressing misinformation with their patients and also in their social networking interactions,” he said. “When I see a new patient with a new diagnosis of cancer, I warn them that they’re going to encounter things online that may or may not be true.”

He noted that, often when physicians instruct patients not to go online to research their disease, the first thing the vast majority of patients do after leaving the office is to jump online.

Instead, Dr. Johnson recommended inoculating patients against misinformation – not to discourage them from going online, but to inform them about the myriad good and bad information sources, and steer them toward trustworthy sites such as government agencies (the National Institutes of Health, Centers for Disease Control and Prevention, etc), academic medical center sites, or select nonprofit organizations, foundations, and medical associations.

“But at the end of the day, even those you have to be somewhat vigilant about, because there are some unscrupulous providers who exploit even those sites,” he added.
 

Study details

Dr. Loveland and colleagues used the TikTok search engine to look for posts containing the terms “cirrhosis” and “liver disease,” and watched all such videos that turned up in the search from beginning to end. They classified each post as either educational in intent or whether it depicted a firsthand experience with liver disease.

They determined whether each post was accurate or erroneous according to guidelines from the American Association for the Study of Liver Disease, American College of Gastroenterology, and American Gastroenterological Association. They also recorded the number of likes, comments, and the number of times that each video was shared.

Accurate posts were viewed and liked significantly more often than inaccurate ones, and accurate posts had significantly more comments that faulty posts.

However, both accurate and inaccurate posts were shared a similar number of times, suggesting that bad-quality information can metastasize just as easily as good information can be disseminated.

Dr. Loveland and colleagues echoed the recommendations of Dr. Johnson, stating that “health care provides should be aware of the potential for misinformation on social media and should strive to provide their patients with accurate and evidence-based information to inform their health care decisions.”

The study was internally funded. Dr. Loveland and Dr. Johnson reported having no conflicts of interest to disclose.

DDW is sponsored by the American Association for the Study of Liver Diseases, the AGA, the American Society for Gastrointestinal Endoscopy, and The Society for Surgery of the Alimentary Tract.

CHICAGO – An analysis of posts on TikTok about cirrhosis finds that approximately 40% of these posts include misinformation, according to a study presented at the annual Digestive Disease Week® (DDW).

TikTok’s short video format is increasingly becoming a major source for news and information, especially for adolescents and young adults. In 2022 the technology news website The Verge reported that about 10% of all U.S. adults regularly get news from TikTok, including an estimated 26% of adults under 30.

“Our study highlights the alarming prevalence of misinformation related to liver disease and cirrhosis on the TikTok platform. This misinformation can potentially lead to harm and poor health outcomes for individuals seeking accurate information about their conditions,” wrote the study authors in their abstract.

The study, which was led by Macklin Loveland, MD, an internal medicine resident at the University of Arizona, Tucson, found that, among 2,223 TikTok posts related to liver disease or cirrhosis as of November 2022, 60.3% were found to have accurate medical information, but the remaining 39.7% contained misinformation.

Some of the misinformation offered highly dubious and potentially dangerous advice, such as “Reishi mushrooms can reverse liver damage,” when in fact there is evidence to suggest that reishi mushrooms, especially in powder form, may be toxic to the liver and may even cause fatal fulminant hepatitis.

In an interview, Dr. Loveland said that much of the good information about liver disease on TikTok seems to come from patients with cirrhosis or other liver diseases who post videos chronicling their experiences, whereas bad information seems to come from people who are trying to pitch a product such as “natural” or “alternative” medicine.

“People who have real-life, firsthand experiences with cirrhosis have a really nice platform to talk about their disease process and share information with other people with similar disease processes, and the majority of them are accurate,” he said. “Where the inaccuracies come in are when people are trying to profit off a product or sell a dietary supplement, and then things go by the wayside.”

It’s important for TikTok users to understand the intentions of other users, he said, and expressed the hope that content mediators within TikTok would help to keep misinformation at bay.

Skyler B. Johnson, MD, assistant professor of radiation oncology at the University of Utah Huntsman Cancer Institute, Salt Lake City, has studied misinformation about cancer on social media, and as he and colleagues reported in the Journal of the National Cancer Institute, of 200 articles on cancer posted on social media sites, 32.5% contained misinformation and 30.5% contained harmful information.

In an interview, Dr. Johnson, who was not involved in the study by Dr. Loveland and colleagues, offered advice for colleagues about countering misinformation.

“What we’re trying to do, as part of our research group, is encourage physicians to take an active role in addressing misinformation with their patients and also in their social networking interactions,” he said. “When I see a new patient with a new diagnosis of cancer, I warn them that they’re going to encounter things online that may or may not be true.”

He noted that, often when physicians instruct patients not to go online to research their disease, the first thing the vast majority of patients do after leaving the office is to jump online.

Instead, Dr. Johnson recommended inoculating patients against misinformation – not to discourage them from going online, but to inform them about the myriad good and bad information sources, and steer them toward trustworthy sites such as government agencies (the National Institutes of Health, Centers for Disease Control and Prevention, etc), academic medical center sites, or select nonprofit organizations, foundations, and medical associations.

“But at the end of the day, even those you have to be somewhat vigilant about, because there are some unscrupulous providers who exploit even those sites,” he added.
 

Study details

Dr. Loveland and colleagues used the TikTok search engine to look for posts containing the terms “cirrhosis” and “liver disease,” and watched all such videos that turned up in the search from beginning to end. They classified each post as either educational in intent or whether it depicted a firsthand experience with liver disease.

They determined whether each post was accurate or erroneous according to guidelines from the American Association for the Study of Liver Disease, American College of Gastroenterology, and American Gastroenterological Association. They also recorded the number of likes, comments, and the number of times that each video was shared.

Accurate posts were viewed and liked significantly more often than inaccurate ones, and accurate posts had significantly more comments that faulty posts.

However, both accurate and inaccurate posts were shared a similar number of times, suggesting that bad-quality information can metastasize just as easily as good information can be disseminated.

Dr. Loveland and colleagues echoed the recommendations of Dr. Johnson, stating that “health care provides should be aware of the potential for misinformation on social media and should strive to provide their patients with accurate and evidence-based information to inform their health care decisions.”

The study was internally funded. Dr. Loveland and Dr. Johnson reported having no conflicts of interest to disclose.

DDW is sponsored by the American Association for the Study of Liver Diseases, the AGA, the American Society for Gastrointestinal Endoscopy, and The Society for Surgery of the Alimentary Tract.

CHICAGO – Preoperative clinical diagnoses of pancreatic cystic neoplasms (PCNs) are frequently found to be in error when patients go to surgery as recommended under international guidelines, data from a retrospective study show.

An analysis of all pancreatic resections performed for presumed PCN at the Verona Pancreas Institute, Italy, from 2011 through 2020 showed a high degree of discrepancy between the preoperative clinical diagnosis and the final postoperative pathology, with some lesions being misdiagnosed in nearly two-thirds of cases, reported Anna Burelli, MD, of the department of general and pancreatic surgery at the University of Verona.

“Diagnostic errors are still common for resected PCNs. Morphological and clinical information alone still poorly frame actual targets for surgery, and hopefully the development of new reliable biomarkers will represent the next evolution in pancreatic cystic neoplasm management,” she said in an oral abstract session at the annual Digestive Disease Week^® (DDW).

Diagnostic errors are significant issues in care of patients with PCN, because clinicians must balance the need for prompt, definitive treatment when necessary with the need for avoiding the significant morbidity of pancreatic resection for patients with lesions that turn out to be nonmalignant.

The investigators define “misdiagnosis” as a discrepancy between the preoperative clinical diagnosis and the postoperative pathology, and “mismatch” as a discrepancy between the preoperative suspicion of malignant or benign disease and the final pathology.
 

Checkered history

In previous cases series from Massachusetts General Hospital in Boston (2010) and the Verona Pancreas Institute (2012) – both experienced, high-volume centers – PCN misdiagnosis rates were 30% and 21%, respectively, and results from the current study show that things haven’t changed much since then, Dr. Burelli said.

PCNs are divided into neoplastic and nonneoplastic categories, with mucin-producing subtypes considered to be precancerous lesions that require accurate diagnosis and close monitoring.

Examples of neoplastic PCNs are intraductal papillary mucinous neoplasms (IPMNs) of the main pancreatic duct or side branch and mucinous cystadenomas. In contrast, serous cystadenomas, considered nonneoplastic, are mostly benign lesions discovered incidentally during abdominal imaging for another indication. It is very difficult, however, to distinguish between the two PCN subtypes clinically.

For example, Dr. Burelli showed images from a patient who received a preoperative diagnosis of mixed IPMN that was in fact found to be chronic pancreatitis on postoperative pathology.

Dr. Burelli noted that AGA and joint European guidelines for management of PCNs have been updated over the past decade, with the latest AGA iteration in 2015.

A 2017 study evaluating the 2015 AGA guidelines for management of asymptomatic PCNs found that following the guidelines in a large multicenter cohort “would have resulted in 60 % fewer patients being referred for surgical resection, and accurately recommended surveillance in 95% of patients with asymptomatic PCNs.”

Misdiagnosis and mismatch common

In the current study, Dr. Burelli and colleagues reviewed all pancreatic resections performed for PCNs at their center from 2011 through 2020.

Of 601 patients included in the retrospective study, 301 underwent endoscopic ultrasound (EUS).

The investigators identified misdiagnosis in 19% of cases and mismatch in 34%, and there was no significant improvement in diagnostic accuracy among the 50% of patients who underwent EUS.

The most frequently misdiagnosed lesions were cystic neuroendocrine tumors, in 61% of cases. The least misdiagnosed lesions were pseudopapillary tumors, in 6% of cases.

Many of the diagnostic errors were clinically important. For example, seven cases presumed to be serous cystic neoplasms (an almost always benign lesion) were found on final pathology to have a different, malignant histology.

Mismatch examples included 50 IPMNs with high-risk stigmata that were presumed to be malignant before surgery but were nonmalignant on final pathology, and 38 IPMNs without high-risk stigmata which were thought on clinical examination to be benign but turned out to be malignant on final pathology.

“Our results are in line with the current literature,” Dr. Burelli said, citing a recent meta-analysis showing that among 3,292 patients who underwent resection for mucinous cystic neoplasms (MCNs), the pooled rate of malignancy was 16.1%, yet the 2012 International Association of Pancreatology guidelines recommend surgery for all fit patients with MCNs, and joint European evidence-based guidelines from 2018 recommend surgery for MCNs 40 mm or larger, those with mural nodules, and for patients who are symptomatic.

The 16.1% pooled malignancy rate suggests “that there is space for surveillance in most cases of MCNs,” she said.

In addition, morphologic and clinical evaluation for IPMN with high-risk stigmata have been shown to have low specificity and low sensitivity, “so should guideline recommendations be revised?” Dr. Burelli said.

She pointed to a recent multi-institutional study in Gastroenterology showing that real-time next-generation sequencing of pancreatic cyst fluid “is sensitive and specific for various pancreatic cyst types and advanced neoplasia arising from mucinous cysts, but also reveals the diversity of genomic alterations seen in pancreatic cysts and their clinical significance.”

“This is not the future; this is the present,” she concluded.

Invited discussant R. Matthew Walsh, MD, a surgeon specializing in pancreatic and cancer surgery at the Cleveland Clinic, complimented the contributions of her group.

“The patient that you showed with chronic pancreatitis could have very well benefited from the operation regardless of the diagnosis if they were symptomatic,” he said, addressing Dr. Burelli. “So what is the group that is the regrettable surgical patients, and where are you aiming your studies? Is it really the 24% with high-risk features in IPMN that have low-grade dysplasia, or is it the 58% who we’re not sure why they were operated on because they didn’t have high-grade features who had low-grade dysplasia?”

She replied that “the goal here is to avoid surgery for benign entities, and we know that the only true benign entities are serous cystic neoplasms, and all the others have a malignant potential, but we think at Verona Pancreas Institute there is no reason to operate on low-grade dysplasia free patients. This is what we really would like to avoid.”

Dr. Walsh also asked, given their finding that EUS did not appear to offer a benefit to patients or change decision making, which patients should still get EUS.

“I think that only patients in which the diagnosis is uncertain or in which there are some worrisome features or high-risk stigmata should undergo EUS before surgery, and also to continue follow-up,” Dr. Burelli said. “I don’t think that the conclusion is that EUS is not useful, but it’s not useful in all.”

For example, large, microcystic lesions can be readily identified radiographically, but other, more complex cases may still require EUS to help nail down or refine a diagnosis, she said.

The study was internally funded. Dr. Burelli and Dr. Walsh reported having no conflicts of interest.

DDW is sponsored by the American Association for the Study of Liver Diseases, the American Gastroenterological Association, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – Preoperative clinical diagnoses of pancreatic cystic neoplasms (PCNs) are frequently found to be in error when patients go to surgery as recommended under international guidelines, data from a retrospective study show.

An analysis of all pancreatic resections performed for presumed PCN at the Verona Pancreas Institute, Italy, from 2011 through 2020 showed a high degree of discrepancy between the preoperative clinical diagnosis and the final postoperative pathology, with some lesions being misdiagnosed in nearly two-thirds of cases, reported Anna Burelli, MD, of the department of general and pancreatic surgery at the University of Verona.

“Diagnostic errors are still common for resected PCNs. Morphological and clinical information alone still poorly frame actual targets for surgery, and hopefully the development of new reliable biomarkers will represent the next evolution in pancreatic cystic neoplasm management,” she said in an oral abstract session at the annual Digestive Disease Week^® (DDW).

Diagnostic errors are significant issues in care of patients with PCN, because clinicians must balance the need for prompt, definitive treatment when necessary with the need for avoiding the significant morbidity of pancreatic resection for patients with lesions that turn out to be nonmalignant.

The investigators define “misdiagnosis” as a discrepancy between the preoperative clinical diagnosis and the postoperative pathology, and “mismatch” as a discrepancy between the preoperative suspicion of malignant or benign disease and the final pathology.
 

Checkered history

In previous cases series from Massachusetts General Hospital in Boston (2010) and the Verona Pancreas Institute (2012) – both experienced, high-volume centers – PCN misdiagnosis rates were 30% and 21%, respectively, and results from the current study show that things haven’t changed much since then, Dr. Burelli said.

PCNs are divided into neoplastic and nonneoplastic categories, with mucin-producing subtypes considered to be precancerous lesions that require accurate diagnosis and close monitoring.

Examples of neoplastic PCNs are intraductal papillary mucinous neoplasms (IPMNs) of the main pancreatic duct or side branch and mucinous cystadenomas. In contrast, serous cystadenomas, considered nonneoplastic, are mostly benign lesions discovered incidentally during abdominal imaging for another indication. It is very difficult, however, to distinguish between the two PCN subtypes clinically.

For example, Dr. Burelli showed images from a patient who received a preoperative diagnosis of mixed IPMN that was in fact found to be chronic pancreatitis on postoperative pathology.

Dr. Burelli noted that AGA and joint European guidelines for management of PCNs have been updated over the past decade, with the latest AGA iteration in 2015.

A 2017 study evaluating the 2015 AGA guidelines for management of asymptomatic PCNs found that following the guidelines in a large multicenter cohort “would have resulted in 60 % fewer patients being referred for surgical resection, and accurately recommended surveillance in 95% of patients with asymptomatic PCNs.”

Misdiagnosis and mismatch common

In the current study, Dr. Burelli and colleagues reviewed all pancreatic resections performed for PCNs at their center from 2011 through 2020.

Of 601 patients included in the retrospective study, 301 underwent endoscopic ultrasound (EUS).

The investigators identified misdiagnosis in 19% of cases and mismatch in 34%, and there was no significant improvement in diagnostic accuracy among the 50% of patients who underwent EUS.

The most frequently misdiagnosed lesions were cystic neuroendocrine tumors, in 61% of cases. The least misdiagnosed lesions were pseudopapillary tumors, in 6% of cases.

Many of the diagnostic errors were clinically important. For example, seven cases presumed to be serous cystic neoplasms (an almost always benign lesion) were found on final pathology to have a different, malignant histology.

Mismatch examples included 50 IPMNs with high-risk stigmata that were presumed to be malignant before surgery but were nonmalignant on final pathology, and 38 IPMNs without high-risk stigmata which were thought on clinical examination to be benign but turned out to be malignant on final pathology.

“Our results are in line with the current literature,” Dr. Burelli said, citing a recent meta-analysis showing that among 3,292 patients who underwent resection for mucinous cystic neoplasms (MCNs), the pooled rate of malignancy was 16.1%, yet the 2012 International Association of Pancreatology guidelines recommend surgery for all fit patients with MCNs, and joint European evidence-based guidelines from 2018 recommend surgery for MCNs 40 mm or larger, those with mural nodules, and for patients who are symptomatic.

The 16.1% pooled malignancy rate suggests “that there is space for surveillance in most cases of MCNs,” she said.

In addition, morphologic and clinical evaluation for IPMN with high-risk stigmata have been shown to have low specificity and low sensitivity, “so should guideline recommendations be revised?” Dr. Burelli said.

She pointed to a recent multi-institutional study in Gastroenterology showing that real-time next-generation sequencing of pancreatic cyst fluid “is sensitive and specific for various pancreatic cyst types and advanced neoplasia arising from mucinous cysts, but also reveals the diversity of genomic alterations seen in pancreatic cysts and their clinical significance.”

“This is not the future; this is the present,” she concluded.

Invited discussant R. Matthew Walsh, MD, a surgeon specializing in pancreatic and cancer surgery at the Cleveland Clinic, complimented the contributions of her group.

“The patient that you showed with chronic pancreatitis could have very well benefited from the operation regardless of the diagnosis if they were symptomatic,” he said, addressing Dr. Burelli. “So what is the group that is the regrettable surgical patients, and where are you aiming your studies? Is it really the 24% with high-risk features in IPMN that have low-grade dysplasia, or is it the 58% who we’re not sure why they were operated on because they didn’t have high-grade features who had low-grade dysplasia?”

She replied that “the goal here is to avoid surgery for benign entities, and we know that the only true benign entities are serous cystic neoplasms, and all the others have a malignant potential, but we think at Verona Pancreas Institute there is no reason to operate on low-grade dysplasia free patients. This is what we really would like to avoid.”

Dr. Walsh also asked, given their finding that EUS did not appear to offer a benefit to patients or change decision making, which patients should still get EUS.

“I think that only patients in which the diagnosis is uncertain or in which there are some worrisome features or high-risk stigmata should undergo EUS before surgery, and also to continue follow-up,” Dr. Burelli said. “I don’t think that the conclusion is that EUS is not useful, but it’s not useful in all.”

For example, large, microcystic lesions can be readily identified radiographically, but other, more complex cases may still require EUS to help nail down or refine a diagnosis, she said.

The study was internally funded. Dr. Burelli and Dr. Walsh reported having no conflicts of interest.

DDW is sponsored by the American Association for the Study of Liver Diseases, the American Gastroenterological Association, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – Preoperative clinical diagnoses of pancreatic cystic neoplasms (PCNs) are frequently found to be in error when patients go to surgery as recommended under international guidelines, data from a retrospective study show.

An analysis of all pancreatic resections performed for presumed PCN at the Verona Pancreas Institute, Italy, from 2011 through 2020 showed a high degree of discrepancy between the preoperative clinical diagnosis and the final postoperative pathology, with some lesions being misdiagnosed in nearly two-thirds of cases, reported Anna Burelli, MD, of the department of general and pancreatic surgery at the University of Verona.

“Diagnostic errors are still common for resected PCNs. Morphological and clinical information alone still poorly frame actual targets for surgery, and hopefully the development of new reliable biomarkers will represent the next evolution in pancreatic cystic neoplasm management,” she said in an oral abstract session at the annual Digestive Disease Week^® (DDW).

Diagnostic errors are significant issues in care of patients with PCN, because clinicians must balance the need for prompt, definitive treatment when necessary with the need for avoiding the significant morbidity of pancreatic resection for patients with lesions that turn out to be nonmalignant.

The investigators define “misdiagnosis” as a discrepancy between the preoperative clinical diagnosis and the postoperative pathology, and “mismatch” as a discrepancy between the preoperative suspicion of malignant or benign disease and the final pathology.
 

Checkered history

In previous cases series from Massachusetts General Hospital in Boston (2010) and the Verona Pancreas Institute (2012) – both experienced, high-volume centers – PCN misdiagnosis rates were 30% and 21%, respectively, and results from the current study show that things haven’t changed much since then, Dr. Burelli said.

PCNs are divided into neoplastic and nonneoplastic categories, with mucin-producing subtypes considered to be precancerous lesions that require accurate diagnosis and close monitoring.

Examples of neoplastic PCNs are intraductal papillary mucinous neoplasms (IPMNs) of the main pancreatic duct or side branch and mucinous cystadenomas. In contrast, serous cystadenomas, considered nonneoplastic, are mostly benign lesions discovered incidentally during abdominal imaging for another indication. It is very difficult, however, to distinguish between the two PCN subtypes clinically.

For example, Dr. Burelli showed images from a patient who received a preoperative diagnosis of mixed IPMN that was in fact found to be chronic pancreatitis on postoperative pathology.

Dr. Burelli noted that AGA and joint European guidelines for management of PCNs have been updated over the past decade, with the latest AGA iteration in 2015.

A 2017 study evaluating the 2015 AGA guidelines for management of asymptomatic PCNs found that following the guidelines in a large multicenter cohort “would have resulted in 60 % fewer patients being referred for surgical resection, and accurately recommended surveillance in 95% of patients with asymptomatic PCNs.”

Misdiagnosis and mismatch common

In the current study, Dr. Burelli and colleagues reviewed all pancreatic resections performed for PCNs at their center from 2011 through 2020.

Of 601 patients included in the retrospective study, 301 underwent endoscopic ultrasound (EUS).

The investigators identified misdiagnosis in 19% of cases and mismatch in 34%, and there was no significant improvement in diagnostic accuracy among the 50% of patients who underwent EUS.

The most frequently misdiagnosed lesions were cystic neuroendocrine tumors, in 61% of cases. The least misdiagnosed lesions were pseudopapillary tumors, in 6% of cases.

Many of the diagnostic errors were clinically important. For example, seven cases presumed to be serous cystic neoplasms (an almost always benign lesion) were found on final pathology to have a different, malignant histology.

Mismatch examples included 50 IPMNs with high-risk stigmata that were presumed to be malignant before surgery but were nonmalignant on final pathology, and 38 IPMNs without high-risk stigmata which were thought on clinical examination to be benign but turned out to be malignant on final pathology.

“Our results are in line with the current literature,” Dr. Burelli said, citing a recent meta-analysis showing that among 3,292 patients who underwent resection for mucinous cystic neoplasms (MCNs), the pooled rate of malignancy was 16.1%, yet the 2012 International Association of Pancreatology guidelines recommend surgery for all fit patients with MCNs, and joint European evidence-based guidelines from 2018 recommend surgery for MCNs 40 mm or larger, those with mural nodules, and for patients who are symptomatic.

The 16.1% pooled malignancy rate suggests “that there is space for surveillance in most cases of MCNs,” she said.

In addition, morphologic and clinical evaluation for IPMN with high-risk stigmata have been shown to have low specificity and low sensitivity, “so should guideline recommendations be revised?” Dr. Burelli said.

She pointed to a recent multi-institutional study in Gastroenterology showing that real-time next-generation sequencing of pancreatic cyst fluid “is sensitive and specific for various pancreatic cyst types and advanced neoplasia arising from mucinous cysts, but also reveals the diversity of genomic alterations seen in pancreatic cysts and their clinical significance.”

“This is not the future; this is the present,” she concluded.

Invited discussant R. Matthew Walsh, MD, a surgeon specializing in pancreatic and cancer surgery at the Cleveland Clinic, complimented the contributions of her group.

“The patient that you showed with chronic pancreatitis could have very well benefited from the operation regardless of the diagnosis if they were symptomatic,” he said, addressing Dr. Burelli. “So what is the group that is the regrettable surgical patients, and where are you aiming your studies? Is it really the 24% with high-risk features in IPMN that have low-grade dysplasia, or is it the 58% who we’re not sure why they were operated on because they didn’t have high-grade features who had low-grade dysplasia?”

She replied that “the goal here is to avoid surgery for benign entities, and we know that the only true benign entities are serous cystic neoplasms, and all the others have a malignant potential, but we think at Verona Pancreas Institute there is no reason to operate on low-grade dysplasia free patients. This is what we really would like to avoid.”

Dr. Walsh also asked, given their finding that EUS did not appear to offer a benefit to patients or change decision making, which patients should still get EUS.

“I think that only patients in which the diagnosis is uncertain or in which there are some worrisome features or high-risk stigmata should undergo EUS before surgery, and also to continue follow-up,” Dr. Burelli said. “I don’t think that the conclusion is that EUS is not useful, but it’s not useful in all.”

For example, large, microcystic lesions can be readily identified radiographically, but other, more complex cases may still require EUS to help nail down or refine a diagnosis, she said.

The study was internally funded. Dr. Burelli and Dr. Walsh reported having no conflicts of interest.

DDW is sponsored by the American Association for the Study of Liver Diseases, the American Gastroenterological Association, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – New data from an ongoing study shows that regular meat consumption is associated with inflammatory bowel disease (IBD) flares, specifically for patients with ulcerative colitis.

The data, which was presented on May 7 in Chicago at the annual Digestive Disease Week® meeting, is based on an analysis of data from the PREdiCCt study (Prognostic Effect of Environmental Factors in Crohn’s and Colitis) in which diets of patients with IBD were tracked over 2-3 months with 2-year follow-ups. While the study itself includes nearly 3,000 patients from the United Kingdom who are in clinical remission, this analysis included 497 patients with Crohn’s disease and 520 with ulcerative colitis.

The highest level of patient-reported meat consumption was associated with doubled risk for hard flares – defined as an increase in symptoms plus elevation in c-reactive protein (CRP) and fecal calprotection (FCAL) plus a change in IBD therapy – in patients with ulcerative colitis, said study author Charlie W Lees, PhD, FRCP(Ed), Western General Hospital and University of Edinburgh.

Investigators also evaluated the occurrence of soft flares, which was defined as a negative response to the question, “Do you think your disease has been well controlled in the past month or since you last logged on to the portal?”

After a median follow-up of 1,481.5 days, hard flares occurred at a rate of 5.6% per year, but it did not differ by IBD subtype. However, soft flares accumulated rapidly. Hard flares with baseline FCAL levels in the 50-250 mcg/g range, as well as FCAL levels above 250 mcg, were associated with flares.

The mean baseline total protein intake was 91.9 g per day of which 35.8 g came from animal sources. The hazard ratio for the highest vs. lowest quartile of meat intake in the ulcerative colitis group was 2.08. They found no associations between hard flares with intake of total dietary fiber, N-6 polyunsaturated acids, or ultraprocessed foods, which Dr. Lees found surprising.

“Perhaps most intriguingly, when we look at ultraprocessed food intake, no difference in Crohn’s disease, and no difference in ulcerative colitis,” Dr. Lees said.

The finding is in contradiction to a study reported at the Crohn’s & Colitis Congress this year that found additives in ultraprocessed foods appear to have deleterious effects on intestinal microbiota, while others may exert their influence through mechanisms, such as endoplasmic stress.

However, the new data are consistent with a previously reported association between meat consumption and ulcerative colitis development, and suggests that reducing meat consumption could help to reduce the risk of flare in patients with ulcerative colitis.

PREdiCCt is designed to examine dietary, environmental, genetic, and microbiotic factors that are associated with disease flares in patients with Crohn’s disease and ulcerative colitis. Investigators are evaluating potential contributions to disease flares from total animal protein intake, dietary fiber, N-6 polyunsaturated fatty acids, dietary emulsifiers, and ultraprocessed foods, and total bacterial gene count in stool samples. They aim to examine data from 2,500 microbiome samples currently being sequenced at the Wellcome Sanger Institute in Hinxton, England, to determine whether the association between meat and ulcerative colitis flares could be related, as they hypothesize, to diet-induced alterations in the gut microbiome.

The research is preliminary with many unanswered questions, said Russell D. Cohen, MD, director of the inflammatory bowel disease center at the University of Chicago.

“I think he still has to evaluate a lot of the data that he has already collected because, are you talking about meat? Are you talking about poultry? Are you talking about fish? It is interesting, but it still needs to be evaluated further before we make any conclusive decisions,” he said. Dr. Cohen was not involved in the research.

He said the presumed effect of meat consumption on disease exacerbation appeared to take years, “which is a little surprising. If you really thought that IBD was due to something in diet, you would see the response right away, so it doesn’t follow timewise. Why does it takes 5 years? It should be within 5 weeks or 5 days.”

Dr. Lees disclosed relationships with Abbvie, Takeda, Pfizer, Galapagos, and BDD Pharma, among others.

DDW is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – New data from an ongoing study shows that regular meat consumption is associated with inflammatory bowel disease (IBD) flares, specifically for patients with ulcerative colitis.

The data, which was presented on May 7 in Chicago at the annual Digestive Disease Week® meeting, is based on an analysis of data from the PREdiCCt study (Prognostic Effect of Environmental Factors in Crohn’s and Colitis) in which diets of patients with IBD were tracked over 2-3 months with 2-year follow-ups. While the study itself includes nearly 3,000 patients from the United Kingdom who are in clinical remission, this analysis included 497 patients with Crohn’s disease and 520 with ulcerative colitis.

The highest level of patient-reported meat consumption was associated with doubled risk for hard flares – defined as an increase in symptoms plus elevation in c-reactive protein (CRP) and fecal calprotection (FCAL) plus a change in IBD therapy – in patients with ulcerative colitis, said study author Charlie W Lees, PhD, FRCP(Ed), Western General Hospital and University of Edinburgh.

Investigators also evaluated the occurrence of soft flares, which was defined as a negative response to the question, “Do you think your disease has been well controlled in the past month or since you last logged on to the portal?”

After a median follow-up of 1,481.5 days, hard flares occurred at a rate of 5.6% per year, but it did not differ by IBD subtype. However, soft flares accumulated rapidly. Hard flares with baseline FCAL levels in the 50-250 mcg/g range, as well as FCAL levels above 250 mcg, were associated with flares.

The mean baseline total protein intake was 91.9 g per day of which 35.8 g came from animal sources. The hazard ratio for the highest vs. lowest quartile of meat intake in the ulcerative colitis group was 2.08. They found no associations between hard flares with intake of total dietary fiber, N-6 polyunsaturated acids, or ultraprocessed foods, which Dr. Lees found surprising.

“Perhaps most intriguingly, when we look at ultraprocessed food intake, no difference in Crohn’s disease, and no difference in ulcerative colitis,” Dr. Lees said.

The finding is in contradiction to a study reported at the Crohn’s & Colitis Congress this year that found additives in ultraprocessed foods appear to have deleterious effects on intestinal microbiota, while others may exert their influence through mechanisms, such as endoplasmic stress.

However, the new data are consistent with a previously reported association between meat consumption and ulcerative colitis development, and suggests that reducing meat consumption could help to reduce the risk of flare in patients with ulcerative colitis.

PREdiCCt is designed to examine dietary, environmental, genetic, and microbiotic factors that are associated with disease flares in patients with Crohn’s disease and ulcerative colitis. Investigators are evaluating potential contributions to disease flares from total animal protein intake, dietary fiber, N-6 polyunsaturated fatty acids, dietary emulsifiers, and ultraprocessed foods, and total bacterial gene count in stool samples. They aim to examine data from 2,500 microbiome samples currently being sequenced at the Wellcome Sanger Institute in Hinxton, England, to determine whether the association between meat and ulcerative colitis flares could be related, as they hypothesize, to diet-induced alterations in the gut microbiome.

The research is preliminary with many unanswered questions, said Russell D. Cohen, MD, director of the inflammatory bowel disease center at the University of Chicago.

“I think he still has to evaluate a lot of the data that he has already collected because, are you talking about meat? Are you talking about poultry? Are you talking about fish? It is interesting, but it still needs to be evaluated further before we make any conclusive decisions,” he said. Dr. Cohen was not involved in the research.

He said the presumed effect of meat consumption on disease exacerbation appeared to take years, “which is a little surprising. If you really thought that IBD was due to something in diet, you would see the response right away, so it doesn’t follow timewise. Why does it takes 5 years? It should be within 5 weeks or 5 days.”

Dr. Lees disclosed relationships with Abbvie, Takeda, Pfizer, Galapagos, and BDD Pharma, among others.

DDW is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – New data from an ongoing study shows that regular meat consumption is associated with inflammatory bowel disease (IBD) flares, specifically for patients with ulcerative colitis.

The data, which was presented on May 7 in Chicago at the annual Digestive Disease Week® meeting, is based on an analysis of data from the PREdiCCt study (Prognostic Effect of Environmental Factors in Crohn’s and Colitis) in which diets of patients with IBD were tracked over 2-3 months with 2-year follow-ups. While the study itself includes nearly 3,000 patients from the United Kingdom who are in clinical remission, this analysis included 497 patients with Crohn’s disease and 520 with ulcerative colitis.

The highest level of patient-reported meat consumption was associated with doubled risk for hard flares – defined as an increase in symptoms plus elevation in c-reactive protein (CRP) and fecal calprotection (FCAL) plus a change in IBD therapy – in patients with ulcerative colitis, said study author Charlie W Lees, PhD, FRCP(Ed), Western General Hospital and University of Edinburgh.

Investigators also evaluated the occurrence of soft flares, which was defined as a negative response to the question, “Do you think your disease has been well controlled in the past month or since you last logged on to the portal?”

After a median follow-up of 1,481.5 days, hard flares occurred at a rate of 5.6% per year, but it did not differ by IBD subtype. However, soft flares accumulated rapidly. Hard flares with baseline FCAL levels in the 50-250 mcg/g range, as well as FCAL levels above 250 mcg, were associated with flares.

The mean baseline total protein intake was 91.9 g per day of which 35.8 g came from animal sources. The hazard ratio for the highest vs. lowest quartile of meat intake in the ulcerative colitis group was 2.08. They found no associations between hard flares with intake of total dietary fiber, N-6 polyunsaturated acids, or ultraprocessed foods, which Dr. Lees found surprising.

“Perhaps most intriguingly, when we look at ultraprocessed food intake, no difference in Crohn’s disease, and no difference in ulcerative colitis,” Dr. Lees said.

The finding is in contradiction to a study reported at the Crohn’s & Colitis Congress this year that found additives in ultraprocessed foods appear to have deleterious effects on intestinal microbiota, while others may exert their influence through mechanisms, such as endoplasmic stress.

However, the new data are consistent with a previously reported association between meat consumption and ulcerative colitis development, and suggests that reducing meat consumption could help to reduce the risk of flare in patients with ulcerative colitis.

PREdiCCt is designed to examine dietary, environmental, genetic, and microbiotic factors that are associated with disease flares in patients with Crohn’s disease and ulcerative colitis. Investigators are evaluating potential contributions to disease flares from total animal protein intake, dietary fiber, N-6 polyunsaturated fatty acids, dietary emulsifiers, and ultraprocessed foods, and total bacterial gene count in stool samples. They aim to examine data from 2,500 microbiome samples currently being sequenced at the Wellcome Sanger Institute in Hinxton, England, to determine whether the association between meat and ulcerative colitis flares could be related, as they hypothesize, to diet-induced alterations in the gut microbiome.

The research is preliminary with many unanswered questions, said Russell D. Cohen, MD, director of the inflammatory bowel disease center at the University of Chicago.

“I think he still has to evaluate a lot of the data that he has already collected because, are you talking about meat? Are you talking about poultry? Are you talking about fish? It is interesting, but it still needs to be evaluated further before we make any conclusive decisions,” he said. Dr. Cohen was not involved in the research.

He said the presumed effect of meat consumption on disease exacerbation appeared to take years, “which is a little surprising. If you really thought that IBD was due to something in diet, you would see the response right away, so it doesn’t follow timewise. Why does it takes 5 years? It should be within 5 weeks or 5 days.”

Dr. Lees disclosed relationships with Abbvie, Takeda, Pfizer, Galapagos, and BDD Pharma, among others.

DDW is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

Are there clinically significant differences between axial spondyloarthritis with psoriasis and psoriatic arthritis with axial symptoms? Does it matter?

It all depends on whom you ask, but right now the evidence seems to be tipping in favor of the “splitters” who cite evidence supporting their contention that axial spondyloarthritis (axSpA)/ankylosing spondylitis (AS) with psoriasis and psoriatic arthritis (PsA) with axial symptoms are distinct clinical entities that require more precise diagnosis and treatment.

“Lumpers,” in contrast, argue that they are different points on the same clinical spectrum.

The debate is not just of academic interest, but has real consequences for patients, say specialists on both sides of the aisle.
 

Overlapping features, different presentations

“Axial SpA and axPsA have overlapping features but also meaningful differences in genetics, clinical presentation, imaging, and immunophenotype. Efforts are underway to develop classification criteria for axPsA to aid research efforts as well as clinical diagnosis and management,” Philip J. Mease, MD, director of rheumatology research at Swedish Medical Center/Providence–St. Joseph Health in Seattle, and colleagues contend.

In an editorial published in the International Journal of Rheumatic Diseases, Dr. Mease and colleagues noted that, although HLA-B*27 is a genetic risk factor for both axPsA and axSpA, some HLA-B alleles are significantly associated with axPsA, whereas other alleles are associated with axSpA.

In addition, while genes in the interleukin-23 and IL-17 pathway are associated with increased risk for axSpA, genes in the IL-13 pathway have been identified as risk markers for axPsA, they noted.
 

Two cohorts better than one?

Dafna Gladman, MD, professor of medicine at the University of Toronto and senior scientist at the Schroeder Arthritis Institute at Toronto Western Hospital, and colleagues have a unique perspective on the similarities and differences between the disease entities.

Her group’s research uses data on cohorts of patients treated in two separate clinics at Toronto Western Hospital: one for patients with PsA, and one for patients with axial spondyloarthritis, including those with ankylosing spondylitis, nonradiographic axSpA, and spondylitis associated with inflammatory bowel disease.

“Our work has shown that there are differences, and one of the reasons that it’s now important is that the anti–IL-23 medications, both the IL-12/23 inhibitor ustekinumab [Stelara] and the IL-23 inhibitor guselkumab [Tremfya] work for psoriatic arthritis, whereas IL-23 did not work in ankylosing spondylitis, so that provided further impetus to look into the distinction between the two groups,” Dr. Gladman said in an interview.

Dr. Gladman and colleagues published a study in Rheumatology in which they compared clinical presentations and features of patients with AS with or without psoriasis with patients with axPsA.

They found that patients with AS with or without psoriasis tended to be younger, had a higher proportion of males to females, and were more likely to be positive for HLA-B*27. Patients with AS also had more back pain at presentation, worse axial disease activity scores, worse global assessments by physicians, and higher grades of sacroiliitis, and they were more likely to be taking biologic agents.

“What that showed, right off the top, that whether we’re looking at the total group or we’re looking specifically at those patients who have psoriasis or don’t have psoriasis, they are different from those with psoriatic arthritis with axial disease,” she said.

They concluded that “axPsA seems to be a distinct entity.”
 

Two clinics, same presentation

Because the aforementioned study included all patients with PsA with or without peripheral disease, the investigators decided to filter out some of the background noise and conduct a second study in which they compared patients who presented to the two clinics with the same presentation, either with spinal disease and psoriasis to the spondylitis clinic, or with psoriasis and isolated axial disease to the PsA clinic.

The results, published in Annals of the Rheumatic Diseases, showed that just 2.03% of patients with PsA had isolated axial disease, and an additional 29.38% had axial and peripheral disease.

In this study, “you can see that even in that group there are distinct differences. The patients that are labeled psoriatic spondylitis are different from those that are labeled ankylosing spondylitis with psoriasis,” Dr. Gladman said.

Isolated axial disease in patients with PsA was associated with HLA-B*27 positivity and lower Health Assessment Questionnaire scores. In addition, patients who were HLA-B*27 positive also had a nearly eightfold higher risk for developing peripheral disease over time.

Patients with isolated axial PsA were significantly more likely to be diagnosed at an older age (mean, 37.44 vs. 29.65 years), had higher Psoriasis Area Severity Index scores and a higher likelihood of having psoriatic nail lesions than patients with AS with isolated axial disease and psoriasis.

In contrast, patients with isolated axSpA with psoriasis were more likely to have inflammatory back pain, spinal pain, joint pain/swelling, and areas of localized tenderness, and they had greater severity of morning stiffness.

Dr. Gladman noted that, although AS and PsA are associated with the same gene that encodes for the IL-23 receptor, each condition is associated with a different single-nucleotide polymorphism.

Same disease, different flavors?

But as Mark Twain said, it is difference of opinion that makes horse races, and some specialists in rheumatology say that axSpA amd axPsA are just two sides of the same coin.

Pramod Rathod

“There are always different schools of thought. I believe that they are not different diseases, but a spectrum of diseases,” said Shailendra Singh, MD, a rheumatologist at Unity Health Medical Center in Searcy, Ark., and past president of the Arkansas Rheumatology Association.

In an interview, Dr. Singh said that the spectrum ranges from diseases with primarily axial involvement, such as AS, to those with primarily peripheral involvement, such as reactive arthritis.

He pointed out that these conditions have overlapping symptoms, including enthesitis, dactylitis, and uveitis, and inflammatory arthritis.

Daniel Wendling, MD, PhD, from the Centre Hospitalier Régional Universitaire de Besançon (France), Université de Franche-Comté, and colleagues agreed.

“The criteria currently available for both SpA [ASAS (Assessment of Spondyloarthritis International Society) criteria] and PsA [CASPAR (Classification for Psoriatic Arthritis) criteria] are classification criteria, not diagnostic criteria. They are not very stringent and are not exclusive. Thus, the same patient can easily be classified simultaneously in both entities, making the distinction between axSpA with psoriasis and axPsA theoretical,” they wrote in an editorial published in Joint Bone Spine.

They cited as an example of the allegedly fuzzy criteria a prospective study conducted by the investigators in Bath, England, in which modified New York criteria for AS were met by 24% of patients with AS, and CASPAR criteria for PsA were met by an equal number of patients with AS.
 

Therapeutic implications

Dr. Wendling and colleagues acknowledge the differences cited in studies by Dr. Gladman, Dr. Mease, and others between patients with axPsA and those with axSpA, but argue that the differences are not that great and not so clear.

“It should also be emphasized that, although some differences between axPsA and axSpA reach statistical significance, they are mostly at the margin, with low odd ratios,” they wrote.

“It is also important to consider the variability in the definition of axPsA, sometimes simply ‘physician reported’ and elsewhere based on the modified New York radiographic criteria; the latter are only present late in the course of the disease, and this may induce bias,” they continued.

Dr. Singh agreed that, as noted by Dr. Gladman, some patients will respond to anti–IL-17, anti–IL-23, and anti–IL-12/23 agents, whereas others will have better responses with tumor necrosis factor (TNF) inhibitors, and still others, such as those with peripheral involvement in the hands and feet may fare better with nonbiologic disease-modifying antirheumatic drugs such as methotrexate.
 

Answers to come?

Dr. Gladman noted that the information available to date about the efficacy of IL-23 inhibition in axPsA is based on a post hoc analysis of the PSUMMIT 1 and 2 controlled trials in PsA, and is not definitive.

The randomized, controlled STAR trial, currently recruiting patients, is designed to see whether guselkumab can reduce axial symptoms and inflammation in patients with active axPsA.

“What I say is, there is a rationale for [anti–IL-23] to work in psoriatic arthritis, and not work in ankylosing spondylitis,” she said.

In contrast, IL-17 inhibitors, anti-TNF agents, and Janus kinase inhibitors show efficacy against both axPsA and AS. Rituximab is ineffective against PsA, but has shown efficacy against AS, especially in patients with neurologic complications from anti-TNF agents.

“There may be other medications that would work more specifically in axial psoriatic arthritis that don’t work in ankylosing spondylitis, but at least recognizing that there may be some differences, and that therefore a correct diagnosis should be obtained, might be important,” she said.

Ideally, the picture will become clearer with results from the ongoing Axial Involvement in Psoriatic Arthritis cohort, a joint project of ASAS and the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. The multinational, cross-sectional study is designed “to systematically evaluate clinical and imaging manifestations indicative of axial involvement in patients with PsA and to develop classification criteria and a unified nomenclature for axial involvement in PsA that would allow defining a homogeneous subgroup of patients for research.”

Stay tuned.

Dr. Gladman’s research is supported by a grant from the Krembil Foundation. Dr. Singh disclosed research support from various companies. Funding sources and conflict of interest disclosures from other works cited are contained in their respective references.

Are there clinically significant differences between axial spondyloarthritis with psoriasis and psoriatic arthritis with axial symptoms? Does it matter?

It all depends on whom you ask, but right now the evidence seems to be tipping in favor of the “splitters” who cite evidence supporting their contention that axial spondyloarthritis (axSpA)/ankylosing spondylitis (AS) with psoriasis and psoriatic arthritis (PsA) with axial symptoms are distinct clinical entities that require more precise diagnosis and treatment.

“Lumpers,” in contrast, argue that they are different points on the same clinical spectrum.

The debate is not just of academic interest, but has real consequences for patients, say specialists on both sides of the aisle.
 

Overlapping features, different presentations

“Axial SpA and axPsA have overlapping features but also meaningful differences in genetics, clinical presentation, imaging, and immunophenotype. Efforts are underway to develop classification criteria for axPsA to aid research efforts as well as clinical diagnosis and management,” Philip J. Mease, MD, director of rheumatology research at Swedish Medical Center/Providence–St. Joseph Health in Seattle, and colleagues contend.

In an editorial published in the International Journal of Rheumatic Diseases, Dr. Mease and colleagues noted that, although HLA-B*27 is a genetic risk factor for both axPsA and axSpA, some HLA-B alleles are significantly associated with axPsA, whereas other alleles are associated with axSpA.

In addition, while genes in the interleukin-23 and IL-17 pathway are associated with increased risk for axSpA, genes in the IL-13 pathway have been identified as risk markers for axPsA, they noted.
 

Two cohorts better than one?

Dafna Gladman, MD, professor of medicine at the University of Toronto and senior scientist at the Schroeder Arthritis Institute at Toronto Western Hospital, and colleagues have a unique perspective on the similarities and differences between the disease entities.

Her group’s research uses data on cohorts of patients treated in two separate clinics at Toronto Western Hospital: one for patients with PsA, and one for patients with axial spondyloarthritis, including those with ankylosing spondylitis, nonradiographic axSpA, and spondylitis associated with inflammatory bowel disease.

“Our work has shown that there are differences, and one of the reasons that it’s now important is that the anti–IL-23 medications, both the IL-12/23 inhibitor ustekinumab [Stelara] and the IL-23 inhibitor guselkumab [Tremfya] work for psoriatic arthritis, whereas IL-23 did not work in ankylosing spondylitis, so that provided further impetus to look into the distinction between the two groups,” Dr. Gladman said in an interview.

Dr. Gladman and colleagues published a study in Rheumatology in which they compared clinical presentations and features of patients with AS with or without psoriasis with patients with axPsA.

They found that patients with AS with or without psoriasis tended to be younger, had a higher proportion of males to females, and were more likely to be positive for HLA-B*27. Patients with AS also had more back pain at presentation, worse axial disease activity scores, worse global assessments by physicians, and higher grades of sacroiliitis, and they were more likely to be taking biologic agents.

“What that showed, right off the top, that whether we’re looking at the total group or we’re looking specifically at those patients who have psoriasis or don’t have psoriasis, they are different from those with psoriatic arthritis with axial disease,” she said.

They concluded that “axPsA seems to be a distinct entity.”
 

Two clinics, same presentation

Because the aforementioned study included all patients with PsA with or without peripheral disease, the investigators decided to filter out some of the background noise and conduct a second study in which they compared patients who presented to the two clinics with the same presentation, either with spinal disease and psoriasis to the spondylitis clinic, or with psoriasis and isolated axial disease to the PsA clinic.

The results, published in Annals of the Rheumatic Diseases, showed that just 2.03% of patients with PsA had isolated axial disease, and an additional 29.38% had axial and peripheral disease.

In this study, “you can see that even in that group there are distinct differences. The patients that are labeled psoriatic spondylitis are different from those that are labeled ankylosing spondylitis with psoriasis,” Dr. Gladman said.

Isolated axial disease in patients with PsA was associated with HLA-B*27 positivity and lower Health Assessment Questionnaire scores. In addition, patients who were HLA-B*27 positive also had a nearly eightfold higher risk for developing peripheral disease over time.

Patients with isolated axial PsA were significantly more likely to be diagnosed at an older age (mean, 37.44 vs. 29.65 years), had higher Psoriasis Area Severity Index scores and a higher likelihood of having psoriatic nail lesions than patients with AS with isolated axial disease and psoriasis.

In contrast, patients with isolated axSpA with psoriasis were more likely to have inflammatory back pain, spinal pain, joint pain/swelling, and areas of localized tenderness, and they had greater severity of morning stiffness.

Dr. Gladman noted that, although AS and PsA are associated with the same gene that encodes for the IL-23 receptor, each condition is associated with a different single-nucleotide polymorphism.

Same disease, different flavors?

But as Mark Twain said, it is difference of opinion that makes horse races, and some specialists in rheumatology say that axSpA amd axPsA are just two sides of the same coin.

Pramod Rathod

“There are always different schools of thought. I believe that they are not different diseases, but a spectrum of diseases,” said Shailendra Singh, MD, a rheumatologist at Unity Health Medical Center in Searcy, Ark., and past president of the Arkansas Rheumatology Association.

In an interview, Dr. Singh said that the spectrum ranges from diseases with primarily axial involvement, such as AS, to those with primarily peripheral involvement, such as reactive arthritis.

He pointed out that these conditions have overlapping symptoms, including enthesitis, dactylitis, and uveitis, and inflammatory arthritis.

Daniel Wendling, MD, PhD, from the Centre Hospitalier Régional Universitaire de Besançon (France), Université de Franche-Comté, and colleagues agreed.

“The criteria currently available for both SpA [ASAS (Assessment of Spondyloarthritis International Society) criteria] and PsA [CASPAR (Classification for Psoriatic Arthritis) criteria] are classification criteria, not diagnostic criteria. They are not very stringent and are not exclusive. Thus, the same patient can easily be classified simultaneously in both entities, making the distinction between axSpA with psoriasis and axPsA theoretical,” they wrote in an editorial published in Joint Bone Spine.

They cited as an example of the allegedly fuzzy criteria a prospective study conducted by the investigators in Bath, England, in which modified New York criteria for AS were met by 24% of patients with AS, and CASPAR criteria for PsA were met by an equal number of patients with AS.
 

Therapeutic implications

Dr. Wendling and colleagues acknowledge the differences cited in studies by Dr. Gladman, Dr. Mease, and others between patients with axPsA and those with axSpA, but argue that the differences are not that great and not so clear.

“It should also be emphasized that, although some differences between axPsA and axSpA reach statistical significance, they are mostly at the margin, with low odd ratios,” they wrote.

“It is also important to consider the variability in the definition of axPsA, sometimes simply ‘physician reported’ and elsewhere based on the modified New York radiographic criteria; the latter are only present late in the course of the disease, and this may induce bias,” they continued.

Dr. Singh agreed that, as noted by Dr. Gladman, some patients will respond to anti–IL-17, anti–IL-23, and anti–IL-12/23 agents, whereas others will have better responses with tumor necrosis factor (TNF) inhibitors, and still others, such as those with peripheral involvement in the hands and feet may fare better with nonbiologic disease-modifying antirheumatic drugs such as methotrexate.
 

Answers to come?

Dr. Gladman noted that the information available to date about the efficacy of IL-23 inhibition in axPsA is based on a post hoc analysis of the PSUMMIT 1 and 2 controlled trials in PsA, and is not definitive.

The randomized, controlled STAR trial, currently recruiting patients, is designed to see whether guselkumab can reduce axial symptoms and inflammation in patients with active axPsA.

“What I say is, there is a rationale for [anti–IL-23] to work in psoriatic arthritis, and not work in ankylosing spondylitis,” she said.

In contrast, IL-17 inhibitors, anti-TNF agents, and Janus kinase inhibitors show efficacy against both axPsA and AS. Rituximab is ineffective against PsA, but has shown efficacy against AS, especially in patients with neurologic complications from anti-TNF agents.

“There may be other medications that would work more specifically in axial psoriatic arthritis that don’t work in ankylosing spondylitis, but at least recognizing that there may be some differences, and that therefore a correct diagnosis should be obtained, might be important,” she said.

Ideally, the picture will become clearer with results from the ongoing Axial Involvement in Psoriatic Arthritis cohort, a joint project of ASAS and the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. The multinational, cross-sectional study is designed “to systematically evaluate clinical and imaging manifestations indicative of axial involvement in patients with PsA and to develop classification criteria and a unified nomenclature for axial involvement in PsA that would allow defining a homogeneous subgroup of patients for research.”

Stay tuned.

Dr. Gladman’s research is supported by a grant from the Krembil Foundation. Dr. Singh disclosed research support from various companies. Funding sources and conflict of interest disclosures from other works cited are contained in their respective references.

Are there clinically significant differences between axial spondyloarthritis with psoriasis and psoriatic arthritis with axial symptoms? Does it matter?

It all depends on whom you ask, but right now the evidence seems to be tipping in favor of the “splitters” who cite evidence supporting their contention that axial spondyloarthritis (axSpA)/ankylosing spondylitis (AS) with psoriasis and psoriatic arthritis (PsA) with axial symptoms are distinct clinical entities that require more precise diagnosis and treatment.

“Lumpers,” in contrast, argue that they are different points on the same clinical spectrum.

The debate is not just of academic interest, but has real consequences for patients, say specialists on both sides of the aisle.
 

Overlapping features, different presentations

“Axial SpA and axPsA have overlapping features but also meaningful differences in genetics, clinical presentation, imaging, and immunophenotype. Efforts are underway to develop classification criteria for axPsA to aid research efforts as well as clinical diagnosis and management,” Philip J. Mease, MD, director of rheumatology research at Swedish Medical Center/Providence–St. Joseph Health in Seattle, and colleagues contend.

In an editorial published in the International Journal of Rheumatic Diseases, Dr. Mease and colleagues noted that, although HLA-B*27 is a genetic risk factor for both axPsA and axSpA, some HLA-B alleles are significantly associated with axPsA, whereas other alleles are associated with axSpA.

In addition, while genes in the interleukin-23 and IL-17 pathway are associated with increased risk for axSpA, genes in the IL-13 pathway have been identified as risk markers for axPsA, they noted.
 

Two cohorts better than one?

Dafna Gladman, MD, professor of medicine at the University of Toronto and senior scientist at the Schroeder Arthritis Institute at Toronto Western Hospital, and colleagues have a unique perspective on the similarities and differences between the disease entities.

Her group’s research uses data on cohorts of patients treated in two separate clinics at Toronto Western Hospital: one for patients with PsA, and one for patients with axial spondyloarthritis, including those with ankylosing spondylitis, nonradiographic axSpA, and spondylitis associated with inflammatory bowel disease.

“Our work has shown that there are differences, and one of the reasons that it’s now important is that the anti–IL-23 medications, both the IL-12/23 inhibitor ustekinumab [Stelara] and the IL-23 inhibitor guselkumab [Tremfya] work for psoriatic arthritis, whereas IL-23 did not work in ankylosing spondylitis, so that provided further impetus to look into the distinction between the two groups,” Dr. Gladman said in an interview.

Dr. Gladman and colleagues published a study in Rheumatology in which they compared clinical presentations and features of patients with AS with or without psoriasis with patients with axPsA.

They found that patients with AS with or without psoriasis tended to be younger, had a higher proportion of males to females, and were more likely to be positive for HLA-B*27. Patients with AS also had more back pain at presentation, worse axial disease activity scores, worse global assessments by physicians, and higher grades of sacroiliitis, and they were more likely to be taking biologic agents.

“What that showed, right off the top, that whether we’re looking at the total group or we’re looking specifically at those patients who have psoriasis or don’t have psoriasis, they are different from those with psoriatic arthritis with axial disease,” she said.

They concluded that “axPsA seems to be a distinct entity.”
 

Two clinics, same presentation

Because the aforementioned study included all patients with PsA with or without peripheral disease, the investigators decided to filter out some of the background noise and conduct a second study in which they compared patients who presented to the two clinics with the same presentation, either with spinal disease and psoriasis to the spondylitis clinic, or with psoriasis and isolated axial disease to the PsA clinic.

The results, published in Annals of the Rheumatic Diseases, showed that just 2.03% of patients with PsA had isolated axial disease, and an additional 29.38% had axial and peripheral disease.

In this study, “you can see that even in that group there are distinct differences. The patients that are labeled psoriatic spondylitis are different from those that are labeled ankylosing spondylitis with psoriasis,” Dr. Gladman said.

Isolated axial disease in patients with PsA was associated with HLA-B*27 positivity and lower Health Assessment Questionnaire scores. In addition, patients who were HLA-B*27 positive also had a nearly eightfold higher risk for developing peripheral disease over time.

Patients with isolated axial PsA were significantly more likely to be diagnosed at an older age (mean, 37.44 vs. 29.65 years), had higher Psoriasis Area Severity Index scores and a higher likelihood of having psoriatic nail lesions than patients with AS with isolated axial disease and psoriasis.

In contrast, patients with isolated axSpA with psoriasis were more likely to have inflammatory back pain, spinal pain, joint pain/swelling, and areas of localized tenderness, and they had greater severity of morning stiffness.

Dr. Gladman noted that, although AS and PsA are associated with the same gene that encodes for the IL-23 receptor, each condition is associated with a different single-nucleotide polymorphism.

Same disease, different flavors?

But as Mark Twain said, it is difference of opinion that makes horse races, and some specialists in rheumatology say that axSpA amd axPsA are just two sides of the same coin.

Pramod Rathod

“There are always different schools of thought. I believe that they are not different diseases, but a spectrum of diseases,” said Shailendra Singh, MD, a rheumatologist at Unity Health Medical Center in Searcy, Ark., and past president of the Arkansas Rheumatology Association.

In an interview, Dr. Singh said that the spectrum ranges from diseases with primarily axial involvement, such as AS, to those with primarily peripheral involvement, such as reactive arthritis.

He pointed out that these conditions have overlapping symptoms, including enthesitis, dactylitis, and uveitis, and inflammatory arthritis.

Daniel Wendling, MD, PhD, from the Centre Hospitalier Régional Universitaire de Besançon (France), Université de Franche-Comté, and colleagues agreed.

“The criteria currently available for both SpA [ASAS (Assessment of Spondyloarthritis International Society) criteria] and PsA [CASPAR (Classification for Psoriatic Arthritis) criteria] are classification criteria, not diagnostic criteria. They are not very stringent and are not exclusive. Thus, the same patient can easily be classified simultaneously in both entities, making the distinction between axSpA with psoriasis and axPsA theoretical,” they wrote in an editorial published in Joint Bone Spine.

They cited as an example of the allegedly fuzzy criteria a prospective study conducted by the investigators in Bath, England, in which modified New York criteria for AS were met by 24% of patients with AS, and CASPAR criteria for PsA were met by an equal number of patients with AS.
 

Therapeutic implications

Dr. Wendling and colleagues acknowledge the differences cited in studies by Dr. Gladman, Dr. Mease, and others between patients with axPsA and those with axSpA, but argue that the differences are not that great and not so clear.

“It should also be emphasized that, although some differences between axPsA and axSpA reach statistical significance, they are mostly at the margin, with low odd ratios,” they wrote.

“It is also important to consider the variability in the definition of axPsA, sometimes simply ‘physician reported’ and elsewhere based on the modified New York radiographic criteria; the latter are only present late in the course of the disease, and this may induce bias,” they continued.

Dr. Singh agreed that, as noted by Dr. Gladman, some patients will respond to anti–IL-17, anti–IL-23, and anti–IL-12/23 agents, whereas others will have better responses with tumor necrosis factor (TNF) inhibitors, and still others, such as those with peripheral involvement in the hands and feet may fare better with nonbiologic disease-modifying antirheumatic drugs such as methotrexate.
 

Answers to come?

Dr. Gladman noted that the information available to date about the efficacy of IL-23 inhibition in axPsA is based on a post hoc analysis of the PSUMMIT 1 and 2 controlled trials in PsA, and is not definitive.

The randomized, controlled STAR trial, currently recruiting patients, is designed to see whether guselkumab can reduce axial symptoms and inflammation in patients with active axPsA.

“What I say is, there is a rationale for [anti–IL-23] to work in psoriatic arthritis, and not work in ankylosing spondylitis,” she said.

In contrast, IL-17 inhibitors, anti-TNF agents, and Janus kinase inhibitors show efficacy against both axPsA and AS. Rituximab is ineffective against PsA, but has shown efficacy against AS, especially in patients with neurologic complications from anti-TNF agents.

“There may be other medications that would work more specifically in axial psoriatic arthritis that don’t work in ankylosing spondylitis, but at least recognizing that there may be some differences, and that therefore a correct diagnosis should be obtained, might be important,” she said.

Ideally, the picture will become clearer with results from the ongoing Axial Involvement in Psoriatic Arthritis cohort, a joint project of ASAS and the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis. The multinational, cross-sectional study is designed “to systematically evaluate clinical and imaging manifestations indicative of axial involvement in patients with PsA and to develop classification criteria and a unified nomenclature for axial involvement in PsA that would allow defining a homogeneous subgroup of patients for research.”

Stay tuned.

Dr. Gladman’s research is supported by a grant from the Krembil Foundation. Dr. Singh disclosed research support from various companies. Funding sources and conflict of interest disclosures from other works cited are contained in their respective references.

CHICAGO – It’s been 125 years since the founding of the American Gastroenterological Association (AGA). It’s gone from a small organization in which gastroenterology wasn’t even a known medical specialty, to an organization that grants millions of dollars in research funding each year.

University of California San Diego

Congratulating the organization on its 125th anniversary, AGA president John M. Carethers, MD, AGAF, reflected on its history and outlined many accomplishments and challenges. He spoke with optimism about gastroenterology’s future during his presidential address on May 8 at the annual Digestive Disease Week® (DDW) meeting in Chicago.

“I congratulate the AGA on its quasquicentennial, or 125th anniversary,” said Dr. Carethers, who is distinguished professor of medicine and vice chancellor for health sciences at the University of California, San Diego.

The AGA was founded in 1897 by Detroit-based physician Charles Aaron, MD. His passion was gastroenterology, but at that point, it wasn’t an established medical discipline. Dr. Aaron, Max Einhorn, MD, and 8 other colleagues formed the American Gastroenterological Association. Today, with nearly 16,000 members, the organization has become a driving force in improving the care of patients with gastrointestinal conditions.

Among AGA’s accomplishments since its founding: In 1940, the American Board of Internal Medicine certified gastroenterology as a subspecialty. Three years later, the first issue of Gastroenterology, the AGA’s flagship journal, was published. And, in 1971, the very first Digestive Disease Week® meeting took place.

In terms of medical advances that have been made since those early years, the list is vast: From the description of ileitis in 1932 by Burril B. Crohn, MD, in 1932 to the discovery of the hepatitis B surface antigen in 1965 and the more recent discovery of germline mutations in DNA mismatch repair genes as a cause of Lynch syndrome.

Dr. Carethers outlined goals for the future, including building a leadership team that is “reflective of our practice here in the United States,” Dr. Carethers said. Creating a culturally and gender diverse leadership team will only strengthen the organization and the practice of gastroenterology. The AGA’s first female president, Sarah Jordan, MD, was named in 1942, and since then, the AGA has been led by women and men from different ethnic backgrounds, including himself, who is AGA’s first president of African American heritage.

The AGA has committed to a number of diversity and equity objectives, including the AGA Equity Project, an initiative launched in 2020 whose goal is to achieve equity and eradicate disparities in digestive diseases with a focus on justice and equity, research and funding, workforce and leadership, recognition of the achievements of people of color, unconscious bias, and engagement with early career members.

“I am not only excited about the diversity and equity objectives within our specialty ... but also the innovation and things to come for our specialty,” Dr. Carethers said.

Securing funding for early-stage innovations in medicine can be difficult across medical disciplines, including gastroenterology. So, last year, the AGA, with Varia Ventures, launched the GI Opportunity Fund 1 to support early-stage GI-based companies. The goal is to raise $25 million for the initial fund. Through the AGA’s Center for GI Innovation and Technology and the AGA Tech Summit, early-stage companies may have new funding opportunities.

And, through the AGA Research Foundation, the organization will continue to support clinical research. Last year, $2.6 million in grants were awarded to investigators.

Dr. Carethers is a board director at Avantor, a life sciences supply company.

The meeting is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – It’s been 125 years since the founding of the American Gastroenterological Association (AGA). It’s gone from a small organization in which gastroenterology wasn’t even a known medical specialty, to an organization that grants millions of dollars in research funding each year.

University of California San Diego

Congratulating the organization on its 125th anniversary, AGA president John M. Carethers, MD, AGAF, reflected on its history and outlined many accomplishments and challenges. He spoke with optimism about gastroenterology’s future during his presidential address on May 8 at the annual Digestive Disease Week® (DDW) meeting in Chicago.

“I congratulate the AGA on its quasquicentennial, or 125th anniversary,” said Dr. Carethers, who is distinguished professor of medicine and vice chancellor for health sciences at the University of California, San Diego.

The AGA was founded in 1897 by Detroit-based physician Charles Aaron, MD. His passion was gastroenterology, but at that point, it wasn’t an established medical discipline. Dr. Aaron, Max Einhorn, MD, and 8 other colleagues formed the American Gastroenterological Association. Today, with nearly 16,000 members, the organization has become a driving force in improving the care of patients with gastrointestinal conditions.

Among AGA’s accomplishments since its founding: In 1940, the American Board of Internal Medicine certified gastroenterology as a subspecialty. Three years later, the first issue of Gastroenterology, the AGA’s flagship journal, was published. And, in 1971, the very first Digestive Disease Week® meeting took place.

In terms of medical advances that have been made since those early years, the list is vast: From the description of ileitis in 1932 by Burril B. Crohn, MD, in 1932 to the discovery of the hepatitis B surface antigen in 1965 and the more recent discovery of germline mutations in DNA mismatch repair genes as a cause of Lynch syndrome.

Dr. Carethers outlined goals for the future, including building a leadership team that is “reflective of our practice here in the United States,” Dr. Carethers said. Creating a culturally and gender diverse leadership team will only strengthen the organization and the practice of gastroenterology. The AGA’s first female president, Sarah Jordan, MD, was named in 1942, and since then, the AGA has been led by women and men from different ethnic backgrounds, including himself, who is AGA’s first president of African American heritage.

The AGA has committed to a number of diversity and equity objectives, including the AGA Equity Project, an initiative launched in 2020 whose goal is to achieve equity and eradicate disparities in digestive diseases with a focus on justice and equity, research and funding, workforce and leadership, recognition of the achievements of people of color, unconscious bias, and engagement with early career members.

“I am not only excited about the diversity and equity objectives within our specialty ... but also the innovation and things to come for our specialty,” Dr. Carethers said.

Securing funding for early-stage innovations in medicine can be difficult across medical disciplines, including gastroenterology. So, last year, the AGA, with Varia Ventures, launched the GI Opportunity Fund 1 to support early-stage GI-based companies. The goal is to raise $25 million for the initial fund. Through the AGA’s Center for GI Innovation and Technology and the AGA Tech Summit, early-stage companies may have new funding opportunities.

And, through the AGA Research Foundation, the organization will continue to support clinical research. Last year, $2.6 million in grants were awarded to investigators.

Dr. Carethers is a board director at Avantor, a life sciences supply company.

The meeting is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – It’s been 125 years since the founding of the American Gastroenterological Association (AGA). It’s gone from a small organization in which gastroenterology wasn’t even a known medical specialty, to an organization that grants millions of dollars in research funding each year.

University of California San Diego

Congratulating the organization on its 125th anniversary, AGA president John M. Carethers, MD, AGAF, reflected on its history and outlined many accomplishments and challenges. He spoke with optimism about gastroenterology’s future during his presidential address on May 8 at the annual Digestive Disease Week® (DDW) meeting in Chicago.

“I congratulate the AGA on its quasquicentennial, or 125th anniversary,” said Dr. Carethers, who is distinguished professor of medicine and vice chancellor for health sciences at the University of California, San Diego.

The AGA was founded in 1897 by Detroit-based physician Charles Aaron, MD. His passion was gastroenterology, but at that point, it wasn’t an established medical discipline. Dr. Aaron, Max Einhorn, MD, and 8 other colleagues formed the American Gastroenterological Association. Today, with nearly 16,000 members, the organization has become a driving force in improving the care of patients with gastrointestinal conditions.

Among AGA’s accomplishments since its founding: In 1940, the American Board of Internal Medicine certified gastroenterology as a subspecialty. Three years later, the first issue of Gastroenterology, the AGA’s flagship journal, was published. And, in 1971, the very first Digestive Disease Week® meeting took place.

In terms of medical advances that have been made since those early years, the list is vast: From the description of ileitis in 1932 by Burril B. Crohn, MD, in 1932 to the discovery of the hepatitis B surface antigen in 1965 and the more recent discovery of germline mutations in DNA mismatch repair genes as a cause of Lynch syndrome.

Dr. Carethers outlined goals for the future, including building a leadership team that is “reflective of our practice here in the United States,” Dr. Carethers said. Creating a culturally and gender diverse leadership team will only strengthen the organization and the practice of gastroenterology. The AGA’s first female president, Sarah Jordan, MD, was named in 1942, and since then, the AGA has been led by women and men from different ethnic backgrounds, including himself, who is AGA’s first president of African American heritage.

The AGA has committed to a number of diversity and equity objectives, including the AGA Equity Project, an initiative launched in 2020 whose goal is to achieve equity and eradicate disparities in digestive diseases with a focus on justice and equity, research and funding, workforce and leadership, recognition of the achievements of people of color, unconscious bias, and engagement with early career members.

“I am not only excited about the diversity and equity objectives within our specialty ... but also the innovation and things to come for our specialty,” Dr. Carethers said.

Securing funding for early-stage innovations in medicine can be difficult across medical disciplines, including gastroenterology. So, last year, the AGA, with Varia Ventures, launched the GI Opportunity Fund 1 to support early-stage GI-based companies. The goal is to raise $25 million for the initial fund. Through the AGA’s Center for GI Innovation and Technology and the AGA Tech Summit, early-stage companies may have new funding opportunities.

And, through the AGA Research Foundation, the organization will continue to support clinical research. Last year, $2.6 million in grants were awarded to investigators.

Dr. Carethers is a board director at Avantor, a life sciences supply company.

The meeting is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

To see the harmful effects of climate change firsthand, you need look no farther than the nearest pulmonary clinic.

The causes and effects are unmistakable: pollen storms leading to allergy sufferers flooding into allergists’ offices; rising air pollution levels increasing risk for obstructive airway diseases, cardiopulmonary complications, and non–small cell lung cancer; melting snowpacks and atmospheric rivers inundating neighborhoods and leaving moldy debris and incipient fungal infections in their wake.

“The reason why we think climate change is going to change the type of disease patterns and the severity of illness that we see in patients with respiratory diseases is that it changes a lot of the environment as well as the exposures,” said Bathmapriya Balakrishnan, BMedSci, BMBS, from the section of Pulmonary, Critical Care, and Sleep Medicine in the department of medicine at West Virginia University, Morgantown.

“What we’re going to see is not just new diseases but also exacerbation of chronic diseases, things like asthma [and] COPD. And there’s also concern that patients who are otherwise healthy, because they now have more exposures that are due to climate change, can then develop these diseases,” she said in an interview.

Ms. Balakrishnan is the lead author of a comprehensive, evidence-based review focused on the effects of climate change and air pollution across the spectrum of pulmonary disorders. The review is published online ahead of print in the journal Chest.

“As pulmonologists, understanding and improving awareness of the adverse effects of climate change and air pollution are crucial steps. To inform health care providers of evidence-based methods and improve patient counselling, further research regarding measures that limit exposure is needed. Empowering patients with resources to monitor air quality and minimize exposure is a key preventative measure for decreasing morbidity and mortality while improving quality of  life,” Ms. Balakrishnan and colleagues write.

Similarly, in a statement on the effects of climate change on respiratory health, the American Public Health Association succinctly summarized the problem: “Warmer temperatures lead to an increase in pollutants and allergens. Poor air quality leads to reduced lung function, increased risk of asthma complications, heart attacks, heart failure, and death. Air pollution and allergens are the main exposures affecting lung and heart health in this changing climate.”
 

Early spring

Stanley Fineman, MD, MBA, a past president of the American College of Allergy, Asthma, & Immunology and an allergist in private practice in Atlanta, has seen firsthand how global warming and an earlier start to spring allergy season is affecting his patients.

“The season, at least in our area metro Atlanta, started earlier and has been lasting longer. The pollen counts are very high,” he told this news organization.

“In February we started seeing pollen counts over 1,000 [grams per cubic meter], which is unheard of, and in March about half the days we counted levels that were over 1,000, which is also unheard of. In April it was over 1,000 almost half the days.”

Dr. Fineman and colleagues both in Atlanta and across the country have reported sharp increases in the proportion of new adult patients and in existing patients who have experienced exacerbation of previously mild disease.

“Probably what’s happened is that they may have had some allergic sensitivity that resulted in milder manifestations, but this year they’re getting major manifestations,” Dr. Fineman said.

In a 2014 article in the journal European Respiratory Review, Gennaro D’Amato, MD, from High Speciality Hospital Antonio Cardarelli, Naples, Italy, and colleagues outlined the main effects of climate on pollen levels: “1) an increase in plant growth and faster plant growth; 2) an increase in the amount of pollen produced by each plant; 3) an increase in the amount of allergenic proteins contained in pollen; 4) an increase in the start time of plant growth and, therefore, the start of pollen production; 5) an earlier and longer pollen season; 6) change in the geospatial distribution of pollen, that is plant ranges and long-distance atmospheric transport moving polewards,” they write.
 

Bad air

In addition to pollen, the ambient air in many places is increasingly becoming saturated with bioallergenic proteins such as bacteria, viruses, animal dander, insects, molds, and plant species, Ms. Balakrishnan and colleagues noted, adding that “atmospheric levels of carbon dioxide have also been found to increase pollen productivity. These changes result in greater over-the-counter medication use, emergency department visits, and outpatient visits for respiratory illnesses.”

The rash of violent storms that has washed over much of the United States in recent months is also likely to increase the incidence of so-called “thunderstorm asthma,” caused when large quantities of respirable particulate matter are released before or during a thunderstorm.

Air pollution from the burning of carbon-based fuels and from wildfires sparked by hotter and drier conditions increase airborne particulate matter that can seriously exacerbate asthma, COPD, and other obstructive airway conditions.

In addition, as previously reported by Medscape, exposure to particulate matter has been implicated as a possible cause of non–small cell lung cancer in persons who have never smoked.
 

Critical care challenges

Among the myriad other effects of climate change postulated in evidence enumerated by Ms. Balakrishnan and colleagues are chest infections and pleural diseases, such as aspergillosis infections that occur after catastrophic flooding; increased incidence of Mycobacterium avium complex infections and hypersensitivity pneumonitis; increased demands on critical care specialists from natural disasters; pollution-induced cardiac arrest; and heat prostration and heat stroke from increasingly prevalent heat waves.

The reviewers also examined evidence suggesting links between climate change and pulmonary hypertension, interstitial lung disease, sleep disorders, and occupational pulmonary disorders.
 

Power to the patients

“Pulmonologists should counsel patients on ways to minimize outdoor and indoor pollution, using tight-fitting respirators and home air-purifying systems without encroaching on patients’ beliefs and choices,” the authors advise.

“Empowering patients with resources to monitor air quality daily, in inclement weather, and during disasters would help minimize exposure and thus improve overall health. The pulmonologist can play an important role in emphasizing the impact of climate change on pulmonary disorders during patient care encounters,” they write.

Ms. Balakrishan adds that another important mitigation measure that can be taken today is education.

“In medical school we don’t really learn about the impact of climate change – at least in my generation of physicians, climate change or global warming weren’t part of the medical curriculum – but now I think that there’s a lot of advocacy work being done by medical students who actually want more education on climate change and its effects on pulmonary diseases,” she said.

The study by Ms. Balakrishnan and colleagues was unfunded. Ms. Balakrishnan reports no relevant financial relationships. Co-author Mary-Beth Scholand, MD, has received personal fees from serving on advisory boards and speakers bureaus for Genentech, Boehringer Ingelheim, Veracyte, and United Therapeutics. Co-author Sean Callahan, MD, has received personal fees for serving on advisory boards for Gilead and Boehringer Ingelheim. Dr. Fineman reports no relevant financial relationships.

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

To see the harmful effects of climate change firsthand, you need look no farther than the nearest pulmonary clinic.

The causes and effects are unmistakable: pollen storms leading to allergy sufferers flooding into allergists’ offices; rising air pollution levels increasing risk for obstructive airway diseases, cardiopulmonary complications, and non–small cell lung cancer; melting snowpacks and atmospheric rivers inundating neighborhoods and leaving moldy debris and incipient fungal infections in their wake.

“The reason why we think climate change is going to change the type of disease patterns and the severity of illness that we see in patients with respiratory diseases is that it changes a lot of the environment as well as the exposures,” said Bathmapriya Balakrishnan, BMedSci, BMBS, from the section of Pulmonary, Critical Care, and Sleep Medicine in the department of medicine at West Virginia University, Morgantown.

“What we’re going to see is not just new diseases but also exacerbation of chronic diseases, things like asthma [and] COPD. And there’s also concern that patients who are otherwise healthy, because they now have more exposures that are due to climate change, can then develop these diseases,” she said in an interview.

Ms. Balakrishnan is the lead author of a comprehensive, evidence-based review focused on the effects of climate change and air pollution across the spectrum of pulmonary disorders. The review is published online ahead of print in the journal Chest.

“As pulmonologists, understanding and improving awareness of the adverse effects of climate change and air pollution are crucial steps. To inform health care providers of evidence-based methods and improve patient counselling, further research regarding measures that limit exposure is needed. Empowering patients with resources to monitor air quality and minimize exposure is a key preventative measure for decreasing morbidity and mortality while improving quality of  life,” Ms. Balakrishnan and colleagues write.

Similarly, in a statement on the effects of climate change on respiratory health, the American Public Health Association succinctly summarized the problem: “Warmer temperatures lead to an increase in pollutants and allergens. Poor air quality leads to reduced lung function, increased risk of asthma complications, heart attacks, heart failure, and death. Air pollution and allergens are the main exposures affecting lung and heart health in this changing climate.”
 

Early spring

Stanley Fineman, MD, MBA, a past president of the American College of Allergy, Asthma, & Immunology and an allergist in private practice in Atlanta, has seen firsthand how global warming and an earlier start to spring allergy season is affecting his patients.

“The season, at least in our area metro Atlanta, started earlier and has been lasting longer. The pollen counts are very high,” he told this news organization.

“In February we started seeing pollen counts over 1,000 [grams per cubic meter], which is unheard of, and in March about half the days we counted levels that were over 1,000, which is also unheard of. In April it was over 1,000 almost half the days.”

Dr. Fineman and colleagues both in Atlanta and across the country have reported sharp increases in the proportion of new adult patients and in existing patients who have experienced exacerbation of previously mild disease.

“Probably what’s happened is that they may have had some allergic sensitivity that resulted in milder manifestations, but this year they’re getting major manifestations,” Dr. Fineman said.

In a 2014 article in the journal European Respiratory Review, Gennaro D’Amato, MD, from High Speciality Hospital Antonio Cardarelli, Naples, Italy, and colleagues outlined the main effects of climate on pollen levels: “1) an increase in plant growth and faster plant growth; 2) an increase in the amount of pollen produced by each plant; 3) an increase in the amount of allergenic proteins contained in pollen; 4) an increase in the start time of plant growth and, therefore, the start of pollen production; 5) an earlier and longer pollen season; 6) change in the geospatial distribution of pollen, that is plant ranges and long-distance atmospheric transport moving polewards,” they write.
 

Bad air

In addition to pollen, the ambient air in many places is increasingly becoming saturated with bioallergenic proteins such as bacteria, viruses, animal dander, insects, molds, and plant species, Ms. Balakrishnan and colleagues noted, adding that “atmospheric levels of carbon dioxide have also been found to increase pollen productivity. These changes result in greater over-the-counter medication use, emergency department visits, and outpatient visits for respiratory illnesses.”

The rash of violent storms that has washed over much of the United States in recent months is also likely to increase the incidence of so-called “thunderstorm asthma,” caused when large quantities of respirable particulate matter are released before or during a thunderstorm.

Air pollution from the burning of carbon-based fuels and from wildfires sparked by hotter and drier conditions increase airborne particulate matter that can seriously exacerbate asthma, COPD, and other obstructive airway conditions.

In addition, as previously reported by Medscape, exposure to particulate matter has been implicated as a possible cause of non–small cell lung cancer in persons who have never smoked.
 

Critical care challenges

Among the myriad other effects of climate change postulated in evidence enumerated by Ms. Balakrishnan and colleagues are chest infections and pleural diseases, such as aspergillosis infections that occur after catastrophic flooding; increased incidence of Mycobacterium avium complex infections and hypersensitivity pneumonitis; increased demands on critical care specialists from natural disasters; pollution-induced cardiac arrest; and heat prostration and heat stroke from increasingly prevalent heat waves.

The reviewers also examined evidence suggesting links between climate change and pulmonary hypertension, interstitial lung disease, sleep disorders, and occupational pulmonary disorders.
 

Power to the patients

“Pulmonologists should counsel patients on ways to minimize outdoor and indoor pollution, using tight-fitting respirators and home air-purifying systems without encroaching on patients’ beliefs and choices,” the authors advise.

“Empowering patients with resources to monitor air quality daily, in inclement weather, and during disasters would help minimize exposure and thus improve overall health. The pulmonologist can play an important role in emphasizing the impact of climate change on pulmonary disorders during patient care encounters,” they write.

Ms. Balakrishan adds that another important mitigation measure that can be taken today is education.

“In medical school we don’t really learn about the impact of climate change – at least in my generation of physicians, climate change or global warming weren’t part of the medical curriculum – but now I think that there’s a lot of advocacy work being done by medical students who actually want more education on climate change and its effects on pulmonary diseases,” she said.

The study by Ms. Balakrishnan and colleagues was unfunded. Ms. Balakrishnan reports no relevant financial relationships. Co-author Mary-Beth Scholand, MD, has received personal fees from serving on advisory boards and speakers bureaus for Genentech, Boehringer Ingelheim, Veracyte, and United Therapeutics. Co-author Sean Callahan, MD, has received personal fees for serving on advisory boards for Gilead and Boehringer Ingelheim. Dr. Fineman reports no relevant financial relationships.

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

To see the harmful effects of climate change firsthand, you need look no farther than the nearest pulmonary clinic.

The causes and effects are unmistakable: pollen storms leading to allergy sufferers flooding into allergists’ offices; rising air pollution levels increasing risk for obstructive airway diseases, cardiopulmonary complications, and non–small cell lung cancer; melting snowpacks and atmospheric rivers inundating neighborhoods and leaving moldy debris and incipient fungal infections in their wake.

“The reason why we think climate change is going to change the type of disease patterns and the severity of illness that we see in patients with respiratory diseases is that it changes a lot of the environment as well as the exposures,” said Bathmapriya Balakrishnan, BMedSci, BMBS, from the section of Pulmonary, Critical Care, and Sleep Medicine in the department of medicine at West Virginia University, Morgantown.

“What we’re going to see is not just new diseases but also exacerbation of chronic diseases, things like asthma [and] COPD. And there’s also concern that patients who are otherwise healthy, because they now have more exposures that are due to climate change, can then develop these diseases,” she said in an interview.

Ms. Balakrishnan is the lead author of a comprehensive, evidence-based review focused on the effects of climate change and air pollution across the spectrum of pulmonary disorders. The review is published online ahead of print in the journal Chest.

“As pulmonologists, understanding and improving awareness of the adverse effects of climate change and air pollution are crucial steps. To inform health care providers of evidence-based methods and improve patient counselling, further research regarding measures that limit exposure is needed. Empowering patients with resources to monitor air quality and minimize exposure is a key preventative measure for decreasing morbidity and mortality while improving quality of  life,” Ms. Balakrishnan and colleagues write.

Similarly, in a statement on the effects of climate change on respiratory health, the American Public Health Association succinctly summarized the problem: “Warmer temperatures lead to an increase in pollutants and allergens. Poor air quality leads to reduced lung function, increased risk of asthma complications, heart attacks, heart failure, and death. Air pollution and allergens are the main exposures affecting lung and heart health in this changing climate.”
 

Early spring

Stanley Fineman, MD, MBA, a past president of the American College of Allergy, Asthma, & Immunology and an allergist in private practice in Atlanta, has seen firsthand how global warming and an earlier start to spring allergy season is affecting his patients.

“The season, at least in our area metro Atlanta, started earlier and has been lasting longer. The pollen counts are very high,” he told this news organization.

“In February we started seeing pollen counts over 1,000 [grams per cubic meter], which is unheard of, and in March about half the days we counted levels that were over 1,000, which is also unheard of. In April it was over 1,000 almost half the days.”

Dr. Fineman and colleagues both in Atlanta and across the country have reported sharp increases in the proportion of new adult patients and in existing patients who have experienced exacerbation of previously mild disease.

“Probably what’s happened is that they may have had some allergic sensitivity that resulted in milder manifestations, but this year they’re getting major manifestations,” Dr. Fineman said.

In a 2014 article in the journal European Respiratory Review, Gennaro D’Amato, MD, from High Speciality Hospital Antonio Cardarelli, Naples, Italy, and colleagues outlined the main effects of climate on pollen levels: “1) an increase in plant growth and faster plant growth; 2) an increase in the amount of pollen produced by each plant; 3) an increase in the amount of allergenic proteins contained in pollen; 4) an increase in the start time of plant growth and, therefore, the start of pollen production; 5) an earlier and longer pollen season; 6) change in the geospatial distribution of pollen, that is plant ranges and long-distance atmospheric transport moving polewards,” they write.
 

Bad air

In addition to pollen, the ambient air in many places is increasingly becoming saturated with bioallergenic proteins such as bacteria, viruses, animal dander, insects, molds, and plant species, Ms. Balakrishnan and colleagues noted, adding that “atmospheric levels of carbon dioxide have also been found to increase pollen productivity. These changes result in greater over-the-counter medication use, emergency department visits, and outpatient visits for respiratory illnesses.”

The rash of violent storms that has washed over much of the United States in recent months is also likely to increase the incidence of so-called “thunderstorm asthma,” caused when large quantities of respirable particulate matter are released before or during a thunderstorm.

Air pollution from the burning of carbon-based fuels and from wildfires sparked by hotter and drier conditions increase airborne particulate matter that can seriously exacerbate asthma, COPD, and other obstructive airway conditions.

In addition, as previously reported by Medscape, exposure to particulate matter has been implicated as a possible cause of non–small cell lung cancer in persons who have never smoked.
 

Critical care challenges

Among the myriad other effects of climate change postulated in evidence enumerated by Ms. Balakrishnan and colleagues are chest infections and pleural diseases, such as aspergillosis infections that occur after catastrophic flooding; increased incidence of Mycobacterium avium complex infections and hypersensitivity pneumonitis; increased demands on critical care specialists from natural disasters; pollution-induced cardiac arrest; and heat prostration and heat stroke from increasingly prevalent heat waves.

The reviewers also examined evidence suggesting links between climate change and pulmonary hypertension, interstitial lung disease, sleep disorders, and occupational pulmonary disorders.
 

Power to the patients

“Pulmonologists should counsel patients on ways to minimize outdoor and indoor pollution, using tight-fitting respirators and home air-purifying systems without encroaching on patients’ beliefs and choices,” the authors advise.

“Empowering patients with resources to monitor air quality daily, in inclement weather, and during disasters would help minimize exposure and thus improve overall health. The pulmonologist can play an important role in emphasizing the impact of climate change on pulmonary disorders during patient care encounters,” they write.

Ms. Balakrishan adds that another important mitigation measure that can be taken today is education.

“In medical school we don’t really learn about the impact of climate change – at least in my generation of physicians, climate change or global warming weren’t part of the medical curriculum – but now I think that there’s a lot of advocacy work being done by medical students who actually want more education on climate change and its effects on pulmonary diseases,” she said.

The study by Ms. Balakrishnan and colleagues was unfunded. Ms. Balakrishnan reports no relevant financial relationships. Co-author Mary-Beth Scholand, MD, has received personal fees from serving on advisory boards and speakers bureaus for Genentech, Boehringer Ingelheim, Veracyte, and United Therapeutics. Co-author Sean Callahan, MD, has received personal fees for serving on advisory boards for Gilead and Boehringer Ingelheim. Dr. Fineman reports no relevant financial relationships.

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

CHICAGO – Improving access to preventive health care services, such as colorectal cancer screening, for the poor and uninsured has led to better health outcomes, shows a study presented on May 6 in Chicago at the annual Digestive Disease Week®.

Researchers from the University of California, Los Angeles, reported that states with expanded Medicaid coverage had significantly higher rates of colorectal cancer (CRC) screening than states where officials refused federal support for Medicaid expansion.

Led by Megan R. McLeod, MD, an internal medicine resident at the University of California, Los Angeles, researchers compared CRC screening rates in states that did not adopt Medicaid expansion in 2021 with screening rates in states that invested Medicaid expansion into 1,284 Federally Qualified Health Centers, which are nonprofit health centers or clinics that serve medically underserved areas and populations. In this study, 76% of these centers were in states that accepted Medicaid expansion. The median colorectal cancer screening rate was 42.1% in Medicaid expansion states, compared with 36.5% in nonexpansion states

“The impact of being uninsured on CRC screening participation was profound in nonexpansion states,” said Dr. McLeod, who will be a UCLA gastroenterology fellow this year.

The study adds to a growing body of evidence that shows Medicaid expansion, which increases access to health care services to previously uninsured or underinsured patients, can improve health outcomes and may reduce racial and economic disparities.

For example, a 2019 study based on electronic health record data presented at the annual meeting of the American Society of Clinical Oncology showed that, after Medicaid expansion, racial differences in timely cancer treatment effectively disappeared. Before Medicaid expansion, Black patients were 4.8% less likely than White patients to receive timely cancer treatment, which is defined as treatment starting within 30 days of the diagnosis of an advanced or metastatic solid tumor. After Medicaid expansion, however, the difference between the racial groups dwindled to 0.8% and was no longer statistically significant.

Researchers at Weill Cornell Medical Center in New York reported in 2020 at the virtual annual meeting of the American Association for the Study of Liver Diseases that, 1 year after Medicaid expansion began on Jan. 1, 2014, the rate of liver-related mortality began to decline in 18 states with expanded coverage, whereas the rate of liver-related deaths continued to climb in 14 states that did not expand Medicaid.

The U.S. Health Resources and Services Administration funds Federally Qualified Health Centers (FQHC) that serve nearly 29 million patients throughout the country, including a large proportion whose care is covered by Medicaid. Among patients cared for in these centers, one in three have incomes below the federal poverty line, and one in five are uninsured.

Screening rates compared

Dr. McLeod and colleagues sought to determine whether Medicaid expansion would have an effect on CRC screening rates at these centers. The final analysis included 6,940,879 patients (between 50 and 74 years), of whom 1.7% were unhoused and 17.6% were uninsured.

Medicaid expansion status appeared to have a direct impact on whether screenings were even offered to patients. Centers in rural areas and those with a high proportion of uninsured patients were found to have significantly higher odds for doing fewer CRC screenings. In Medicaid expansion states, CRC screening rates were significantly lower for patients who were male, Black, Hispanic, had low income, were unhoused, or were uninsured.

In a Q&A that followed the presentation, Steven Itzkowitz, MD, director of the GI fellowship program at the Icahn School of Medicine at Mount Sinai, New York, suggested the type of CRC test patients are offered is directly related to Medicaid expansion status.

“In New York, before Cologuard (a colon and rectal cancer screening test) was covered by Medicaid, it wasn’t used very much, but once it got paid for by Medicaid, rates went up,” he said.

The study was internally supported. Dr. McLeod reported no conflicts of interest. Dr. Itzkowitz has been a consultant for Exact Sciences, the maker of Cologuard.

DDW is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – Improving access to preventive health care services, such as colorectal cancer screening, for the poor and uninsured has led to better health outcomes, shows a study presented on May 6 in Chicago at the annual Digestive Disease Week®.

Researchers from the University of California, Los Angeles, reported that states with expanded Medicaid coverage had significantly higher rates of colorectal cancer (CRC) screening than states where officials refused federal support for Medicaid expansion.

Led by Megan R. McLeod, MD, an internal medicine resident at the University of California, Los Angeles, researchers compared CRC screening rates in states that did not adopt Medicaid expansion in 2021 with screening rates in states that invested Medicaid expansion into 1,284 Federally Qualified Health Centers, which are nonprofit health centers or clinics that serve medically underserved areas and populations. In this study, 76% of these centers were in states that accepted Medicaid expansion. The median colorectal cancer screening rate was 42.1% in Medicaid expansion states, compared with 36.5% in nonexpansion states

“The impact of being uninsured on CRC screening participation was profound in nonexpansion states,” said Dr. McLeod, who will be a UCLA gastroenterology fellow this year.

The study adds to a growing body of evidence that shows Medicaid expansion, which increases access to health care services to previously uninsured or underinsured patients, can improve health outcomes and may reduce racial and economic disparities.

For example, a 2019 study based on electronic health record data presented at the annual meeting of the American Society of Clinical Oncology showed that, after Medicaid expansion, racial differences in timely cancer treatment effectively disappeared. Before Medicaid expansion, Black patients were 4.8% less likely than White patients to receive timely cancer treatment, which is defined as treatment starting within 30 days of the diagnosis of an advanced or metastatic solid tumor. After Medicaid expansion, however, the difference between the racial groups dwindled to 0.8% and was no longer statistically significant.

Researchers at Weill Cornell Medical Center in New York reported in 2020 at the virtual annual meeting of the American Association for the Study of Liver Diseases that, 1 year after Medicaid expansion began on Jan. 1, 2014, the rate of liver-related mortality began to decline in 18 states with expanded coverage, whereas the rate of liver-related deaths continued to climb in 14 states that did not expand Medicaid.

The U.S. Health Resources and Services Administration funds Federally Qualified Health Centers (FQHC) that serve nearly 29 million patients throughout the country, including a large proportion whose care is covered by Medicaid. Among patients cared for in these centers, one in three have incomes below the federal poverty line, and one in five are uninsured.

Screening rates compared

Dr. McLeod and colleagues sought to determine whether Medicaid expansion would have an effect on CRC screening rates at these centers. The final analysis included 6,940,879 patients (between 50 and 74 years), of whom 1.7% were unhoused and 17.6% were uninsured.

Medicaid expansion status appeared to have a direct impact on whether screenings were even offered to patients. Centers in rural areas and those with a high proportion of uninsured patients were found to have significantly higher odds for doing fewer CRC screenings. In Medicaid expansion states, CRC screening rates were significantly lower for patients who were male, Black, Hispanic, had low income, were unhoused, or were uninsured.

In a Q&A that followed the presentation, Steven Itzkowitz, MD, director of the GI fellowship program at the Icahn School of Medicine at Mount Sinai, New York, suggested the type of CRC test patients are offered is directly related to Medicaid expansion status.

“In New York, before Cologuard (a colon and rectal cancer screening test) was covered by Medicaid, it wasn’t used very much, but once it got paid for by Medicaid, rates went up,” he said.

The study was internally supported. Dr. McLeod reported no conflicts of interest. Dr. Itzkowitz has been a consultant for Exact Sciences, the maker of Cologuard.

DDW is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – Improving access to preventive health care services, such as colorectal cancer screening, for the poor and uninsured has led to better health outcomes, shows a study presented on May 6 in Chicago at the annual Digestive Disease Week®.

Researchers from the University of California, Los Angeles, reported that states with expanded Medicaid coverage had significantly higher rates of colorectal cancer (CRC) screening than states where officials refused federal support for Medicaid expansion.

Led by Megan R. McLeod, MD, an internal medicine resident at the University of California, Los Angeles, researchers compared CRC screening rates in states that did not adopt Medicaid expansion in 2021 with screening rates in states that invested Medicaid expansion into 1,284 Federally Qualified Health Centers, which are nonprofit health centers or clinics that serve medically underserved areas and populations. In this study, 76% of these centers were in states that accepted Medicaid expansion. The median colorectal cancer screening rate was 42.1% in Medicaid expansion states, compared with 36.5% in nonexpansion states

“The impact of being uninsured on CRC screening participation was profound in nonexpansion states,” said Dr. McLeod, who will be a UCLA gastroenterology fellow this year.

The study adds to a growing body of evidence that shows Medicaid expansion, which increases access to health care services to previously uninsured or underinsured patients, can improve health outcomes and may reduce racial and economic disparities.

For example, a 2019 study based on electronic health record data presented at the annual meeting of the American Society of Clinical Oncology showed that, after Medicaid expansion, racial differences in timely cancer treatment effectively disappeared. Before Medicaid expansion, Black patients were 4.8% less likely than White patients to receive timely cancer treatment, which is defined as treatment starting within 30 days of the diagnosis of an advanced or metastatic solid tumor. After Medicaid expansion, however, the difference between the racial groups dwindled to 0.8% and was no longer statistically significant.

Researchers at Weill Cornell Medical Center in New York reported in 2020 at the virtual annual meeting of the American Association for the Study of Liver Diseases that, 1 year after Medicaid expansion began on Jan. 1, 2014, the rate of liver-related mortality began to decline in 18 states with expanded coverage, whereas the rate of liver-related deaths continued to climb in 14 states that did not expand Medicaid.

The U.S. Health Resources and Services Administration funds Federally Qualified Health Centers (FQHC) that serve nearly 29 million patients throughout the country, including a large proportion whose care is covered by Medicaid. Among patients cared for in these centers, one in three have incomes below the federal poverty line, and one in five are uninsured.

Screening rates compared

Dr. McLeod and colleagues sought to determine whether Medicaid expansion would have an effect on CRC screening rates at these centers. The final analysis included 6,940,879 patients (between 50 and 74 years), of whom 1.7% were unhoused and 17.6% were uninsured.

Medicaid expansion status appeared to have a direct impact on whether screenings were even offered to patients. Centers in rural areas and those with a high proportion of uninsured patients were found to have significantly higher odds for doing fewer CRC screenings. In Medicaid expansion states, CRC screening rates were significantly lower for patients who were male, Black, Hispanic, had low income, were unhoused, or were uninsured.

In a Q&A that followed the presentation, Steven Itzkowitz, MD, director of the GI fellowship program at the Icahn School of Medicine at Mount Sinai, New York, suggested the type of CRC test patients are offered is directly related to Medicaid expansion status.

“In New York, before Cologuard (a colon and rectal cancer screening test) was covered by Medicaid, it wasn’t used very much, but once it got paid for by Medicaid, rates went up,” he said.

The study was internally supported. Dr. McLeod reported no conflicts of interest. Dr. Itzkowitz has been a consultant for Exact Sciences, the maker of Cologuard.

DDW is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

ORLANDO – Patients with hepatocellular carcinoma (HCC) who undergo surgery or thermal ablation with curative intent are at high risk for recurrence, but currently, no adjuvant therapy standard of care exists for these patients.

New findings signal a promising option for these patients. The combination of the immune checkpoint inhibitor atezolizumab (Tecentriq) and the angiogenesis inhibitor bevacizumab (Avastin) was associated with a significant improvement in recurrence-free survival, compared with active surveillance, and represents the first option to show efficacy in the adjuvant setting following surgical resection of HCCs for patients at high risk for recurrence.

The recurrence-free survival benefit corresponded to a 28% reduced risk of recurrence or death among patients who received the combination therapy in comparison with active surveillance. However, the overall survival data remain immature.

The data come from an interim analysis of the IMbrave050 trial, which was presented at the annual meeting of the American Association for Cancer Research.

“Atezolizumab plus bevacizumab may be a practice-changing adjuvant treatment options for patients with high-risk HCC,” said lead investigator Pierce Chow, MBBS, PhD, codirector of the National Cancer Centre Singapore Comprehensive Liver Cancer Clinic. He presented the results in an oral abstract session at the meeting. The combination “may also change clinical indications for surgical resection” because clinicians may be more likely to consider resection for patients at extremely high risk for recurrence if the risk of recurrence can be reduced with this combination.

In the previous IMbrave150 trial, the combination of atezolizumab and bevacizumab significantly improved outcomes for patients with high-risk and non–high-risk unresectable HCC, compared with the standard of care sorafenib (Nexavar).

In that trial, the median overall survival in the intention-to-treat population was 19.2 months for patients who received atezolizumab-bevacizumab versus 13.4 months for patients who received sorafenib (P = .0009).

The combination was also associated with improvements in progression-free survival and objective response rates, compared with sorafenib.

On the basis of these results, the IMbrave050 investigators explored whether the same benefits would occur for patients with resectable disease considered to be at high risk for recurrence owing to tumor size, vascular invasion, or poor tumor differentiation. The trial compared the combination for 334 patients with active surveillance, also for 334 patients, in the adjuvant setting.

Patients were considered good candidates for thermal ablation if they had a single tumor greater than 2 cm, but not larger than 5 cm in its longest dimension, or if they had four or fewer tumors, all of which were no larger than 5 cm. For all other patients, surgical resection was recommended.

The median age of the patients was 60. For about half of patients in each arm, the expression level of programmed death–ligand-1 (PD-L1) was 1% or higher.

After a median follow-up of 17.4 months, the 12-month recurrence-free survival rate, as assessed by independent review, was 78% for patients in the treatment arm, compared with 65% for patients who were assigned to active surveillance (hazard ratio, 0.72; P = .012). This finding was generally consistent across clinical subgroups, including groups based on age, sex, race/ethnicity, performance status, PD-L1 expression, number of high-risk features, Barcelona Clinic Liver Cancer stage, cancer etiology, procedure type, microvascular invasion, or tumor numbers and size.

Of 133 patients on active surveillance who experienced a protocol-defined recurrence event, 81 (61%) crossed over to the atezolizumab/bevacizumab arm.

The overall survival benefit of the combination therapy was less clear. Dr. Chow called the overall survival data “highly immature” at the time of data cutoff.

Overall, 47 patients died – 7 more in the combination arm (27 vs. 20). More specifically, 17 patients in the combination arm and 16 on active surveillance died from progressive disease; 6 patients in the treatment arm versus 1 on surveillance died from adverse events. The remaining deaths were attributed to other causes. Two deaths in the combination arm were considered treatment related, one from esophageal varices hemorrhage, and the other from ischemic stroke.

Dr. Chow said a number of deaths attributed to HCC recurrence was similar between the groups. There were three COVID-19–related deaths within 1 year of randomization, all in the combination arm.

As for adverse events, the safety of the combination was largely consistent with that reported in the IMbrave150 trial. Nearly all patients experienced at least one adverse event. Treatment-related grade 3 or 4 adverse events occurred in 34.9% of patients in the combination group, and serious treatment-related events occurred in 13.3%.

The most common adverse events of any grade were proteinuria, hypertension, decreased platelet count, increases in liver enzyme level, hypothyroidism, arthralgia, pruritus, rash, increase in serum bilirubin level, and fever.

Invited discussant Stephen L. Chan, MD, from the Chinese University of Hong Kong, said the study was “definitely” relevant to clinicians and addresses “a very important unmet need.”

Dr. Chan noted that he thinks this combination will “likely” be practice changing, given the improvement in recurrence-free survival, but “certainly we need more data to guide us in patient selection.”

The study was funded by F. Hoffman–La Roche. Dr. Chow has consulting for and has received honoraria and grant/research support from Roche and others. Dr. Chan has received honoraria from Roche and consulting fees and grant/research support from others.

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

ORLANDO – Patients with hepatocellular carcinoma (HCC) who undergo surgery or thermal ablation with curative intent are at high risk for recurrence, but currently, no adjuvant therapy standard of care exists for these patients.

New findings signal a promising option for these patients. The combination of the immune checkpoint inhibitor atezolizumab (Tecentriq) and the angiogenesis inhibitor bevacizumab (Avastin) was associated with a significant improvement in recurrence-free survival, compared with active surveillance, and represents the first option to show efficacy in the adjuvant setting following surgical resection of HCCs for patients at high risk for recurrence.

The recurrence-free survival benefit corresponded to a 28% reduced risk of recurrence or death among patients who received the combination therapy in comparison with active surveillance. However, the overall survival data remain immature.

The data come from an interim analysis of the IMbrave050 trial, which was presented at the annual meeting of the American Association for Cancer Research.

“Atezolizumab plus bevacizumab may be a practice-changing adjuvant treatment options for patients with high-risk HCC,” said lead investigator Pierce Chow, MBBS, PhD, codirector of the National Cancer Centre Singapore Comprehensive Liver Cancer Clinic. He presented the results in an oral abstract session at the meeting. The combination “may also change clinical indications for surgical resection” because clinicians may be more likely to consider resection for patients at extremely high risk for recurrence if the risk of recurrence can be reduced with this combination.

In the previous IMbrave150 trial, the combination of atezolizumab and bevacizumab significantly improved outcomes for patients with high-risk and non–high-risk unresectable HCC, compared with the standard of care sorafenib (Nexavar).

In that trial, the median overall survival in the intention-to-treat population was 19.2 months for patients who received atezolizumab-bevacizumab versus 13.4 months for patients who received sorafenib (P = .0009).

The combination was also associated with improvements in progression-free survival and objective response rates, compared with sorafenib.

On the basis of these results, the IMbrave050 investigators explored whether the same benefits would occur for patients with resectable disease considered to be at high risk for recurrence owing to tumor size, vascular invasion, or poor tumor differentiation. The trial compared the combination for 334 patients with active surveillance, also for 334 patients, in the adjuvant setting.

Patients were considered good candidates for thermal ablation if they had a single tumor greater than 2 cm, but not larger than 5 cm in its longest dimension, or if they had four or fewer tumors, all of which were no larger than 5 cm. For all other patients, surgical resection was recommended.

The median age of the patients was 60. For about half of patients in each arm, the expression level of programmed death–ligand-1 (PD-L1) was 1% or higher.

After a median follow-up of 17.4 months, the 12-month recurrence-free survival rate, as assessed by independent review, was 78% for patients in the treatment arm, compared with 65% for patients who were assigned to active surveillance (hazard ratio, 0.72; P = .012). This finding was generally consistent across clinical subgroups, including groups based on age, sex, race/ethnicity, performance status, PD-L1 expression, number of high-risk features, Barcelona Clinic Liver Cancer stage, cancer etiology, procedure type, microvascular invasion, or tumor numbers and size.

Of 133 patients on active surveillance who experienced a protocol-defined recurrence event, 81 (61%) crossed over to the atezolizumab/bevacizumab arm.

The overall survival benefit of the combination therapy was less clear. Dr. Chow called the overall survival data “highly immature” at the time of data cutoff.

Overall, 47 patients died – 7 more in the combination arm (27 vs. 20). More specifically, 17 patients in the combination arm and 16 on active surveillance died from progressive disease; 6 patients in the treatment arm versus 1 on surveillance died from adverse events. The remaining deaths were attributed to other causes. Two deaths in the combination arm were considered treatment related, one from esophageal varices hemorrhage, and the other from ischemic stroke.

Dr. Chow said a number of deaths attributed to HCC recurrence was similar between the groups. There were three COVID-19–related deaths within 1 year of randomization, all in the combination arm.

As for adverse events, the safety of the combination was largely consistent with that reported in the IMbrave150 trial. Nearly all patients experienced at least one adverse event. Treatment-related grade 3 or 4 adverse events occurred in 34.9% of patients in the combination group, and serious treatment-related events occurred in 13.3%.

The most common adverse events of any grade were proteinuria, hypertension, decreased platelet count, increases in liver enzyme level, hypothyroidism, arthralgia, pruritus, rash, increase in serum bilirubin level, and fever.

Invited discussant Stephen L. Chan, MD, from the Chinese University of Hong Kong, said the study was “definitely” relevant to clinicians and addresses “a very important unmet need.”

Dr. Chan noted that he thinks this combination will “likely” be practice changing, given the improvement in recurrence-free survival, but “certainly we need more data to guide us in patient selection.”

The study was funded by F. Hoffman–La Roche. Dr. Chow has consulting for and has received honoraria and grant/research support from Roche and others. Dr. Chan has received honoraria from Roche and consulting fees and grant/research support from others.

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

ORLANDO – Patients with hepatocellular carcinoma (HCC) who undergo surgery or thermal ablation with curative intent are at high risk for recurrence, but currently, no adjuvant therapy standard of care exists for these patients.

New findings signal a promising option for these patients. The combination of the immune checkpoint inhibitor atezolizumab (Tecentriq) and the angiogenesis inhibitor bevacizumab (Avastin) was associated with a significant improvement in recurrence-free survival, compared with active surveillance, and represents the first option to show efficacy in the adjuvant setting following surgical resection of HCCs for patients at high risk for recurrence.

The recurrence-free survival benefit corresponded to a 28% reduced risk of recurrence or death among patients who received the combination therapy in comparison with active surveillance. However, the overall survival data remain immature.

The data come from an interim analysis of the IMbrave050 trial, which was presented at the annual meeting of the American Association for Cancer Research.

“Atezolizumab plus bevacizumab may be a practice-changing adjuvant treatment options for patients with high-risk HCC,” said lead investigator Pierce Chow, MBBS, PhD, codirector of the National Cancer Centre Singapore Comprehensive Liver Cancer Clinic. He presented the results in an oral abstract session at the meeting. The combination “may also change clinical indications for surgical resection” because clinicians may be more likely to consider resection for patients at extremely high risk for recurrence if the risk of recurrence can be reduced with this combination.

In the previous IMbrave150 trial, the combination of atezolizumab and bevacizumab significantly improved outcomes for patients with high-risk and non–high-risk unresectable HCC, compared with the standard of care sorafenib (Nexavar).

In that trial, the median overall survival in the intention-to-treat population was 19.2 months for patients who received atezolizumab-bevacizumab versus 13.4 months for patients who received sorafenib (P = .0009).

The combination was also associated with improvements in progression-free survival and objective response rates, compared with sorafenib.

On the basis of these results, the IMbrave050 investigators explored whether the same benefits would occur for patients with resectable disease considered to be at high risk for recurrence owing to tumor size, vascular invasion, or poor tumor differentiation. The trial compared the combination for 334 patients with active surveillance, also for 334 patients, in the adjuvant setting.

Patients were considered good candidates for thermal ablation if they had a single tumor greater than 2 cm, but not larger than 5 cm in its longest dimension, or if they had four or fewer tumors, all of which were no larger than 5 cm. For all other patients, surgical resection was recommended.

The median age of the patients was 60. For about half of patients in each arm, the expression level of programmed death–ligand-1 (PD-L1) was 1% or higher.

After a median follow-up of 17.4 months, the 12-month recurrence-free survival rate, as assessed by independent review, was 78% for patients in the treatment arm, compared with 65% for patients who were assigned to active surveillance (hazard ratio, 0.72; P = .012). This finding was generally consistent across clinical subgroups, including groups based on age, sex, race/ethnicity, performance status, PD-L1 expression, number of high-risk features, Barcelona Clinic Liver Cancer stage, cancer etiology, procedure type, microvascular invasion, or tumor numbers and size.

Of 133 patients on active surveillance who experienced a protocol-defined recurrence event, 81 (61%) crossed over to the atezolizumab/bevacizumab arm.

The overall survival benefit of the combination therapy was less clear. Dr. Chow called the overall survival data “highly immature” at the time of data cutoff.

Overall, 47 patients died – 7 more in the combination arm (27 vs. 20). More specifically, 17 patients in the combination arm and 16 on active surveillance died from progressive disease; 6 patients in the treatment arm versus 1 on surveillance died from adverse events. The remaining deaths were attributed to other causes. Two deaths in the combination arm were considered treatment related, one from esophageal varices hemorrhage, and the other from ischemic stroke.

Dr. Chow said a number of deaths attributed to HCC recurrence was similar between the groups. There were three COVID-19–related deaths within 1 year of randomization, all in the combination arm.

As for adverse events, the safety of the combination was largely consistent with that reported in the IMbrave150 trial. Nearly all patients experienced at least one adverse event. Treatment-related grade 3 or 4 adverse events occurred in 34.9% of patients in the combination group, and serious treatment-related events occurred in 13.3%.

The most common adverse events of any grade were proteinuria, hypertension, decreased platelet count, increases in liver enzyme level, hypothyroidism, arthralgia, pruritus, rash, increase in serum bilirubin level, and fever.

Invited discussant Stephen L. Chan, MD, from the Chinese University of Hong Kong, said the study was “definitely” relevant to clinicians and addresses “a very important unmet need.”

Dr. Chan noted that he thinks this combination will “likely” be practice changing, given the improvement in recurrence-free survival, but “certainly we need more data to guide us in patient selection.”

The study was funded by F. Hoffman–La Roche. Dr. Chow has consulting for and has received honoraria and grant/research support from Roche and others. Dr. Chan has received honoraria from Roche and consulting fees and grant/research support from others.

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

The combination of a patient-specific mRNA-based cancer vaccine (mRNA-4157/V940, Moderna and Merck) and the immune checkpoint inhibitor pembrolizumab significantly improved recurrence-free survival for patients with high-risk melanoma compared with pembrolizumab alone, according to the latest data from the KEYNOTE-942 trial.

This recurrence-free survival benefit corresponded to a 44% reduced risk of recurrence or death in patients who received the personalized vaccine plus pembrolizumab compared with the immunotherapy alone.

The randomized phase 2b trial is the first to show a positive result for a cancer vaccine in a randomized trial. The results, if confirmed in further studies, hold promise for treating other solid tumors with sensitivity to the programmed death-1 (PD-1) protein, investigators said.

“KEYNOTE-942 is the first randomized study to demonstrate improvement in recurrence-free survival in melanoma, or in any cancer in my view, with an individualized neoantigen vaccine approach,” trial investigator Jeffrey S. Weber, MD, PhD, of NYU Langone Perlmutter Cancer Center in New York, said during an oral abstract session at the annual meeting of the American Association for Cancer Research.

“I have every confidence that this strategy will be expanded to other histologies that are PD-1 sensitive, such as non–small cell lung cancer, renal cell cancer, hepatocellular cancer, gastroesophageal cancer, et cetera,” Dr. Weber said.

Invited discussant Margaret Callahan, MD, PhD, of Memorial Sloan Kettering Cancer Center in New York, called the results “exciting,” especially in light of previous results in cancer vaccine trials. “Despite hundreds of formulations and dozens of studies, cancer vaccines have been disappointing so far, and have largely failed to have a meaningful impact in oncology,” she said.
 

A promising personalized vaccine

The mRNA vaccine is individually tailored and encodes up to 34 patient-specific tumor neoantigens. The vaccine also acts as an adjuvant to strengthen the immune response.

Dr. Weber said that the “mRNA 4157 is what one would call an individualized neoantigen therapy. It will target an individual patient’s unique tumor mutations, and the revelation over the last 5-10 years, is that, for better or worse, virtually all the neoantigens are unique to an individual patient. There are very, very few true universal neoantigens, or at least universal neoantigens that could have clinical utility.”

The vaccines are developed from tumor biopsy tissues that then undergo whole exome and RNA sequencing to identify single nucleotide variants that are present in the tumor but not in normal tissue.

The findings are then fed into a computer algorithm that identifies potential neoepitope peptides that would bind well to the patient’s human leukocyte antigen (HLA) type and could evoke strong T-cell responses.

“Once they’re chosen, you concatenate the sequences together into a single-strand mRNA vaccine, it’s packaged with nanoparticles to encapsulate it, and there you have your mRNA vaccine,” Dr. Weber explained.

In the KEYNOTE-942 trial, the investigators randomly assigned patients with completely resected high-risk cutaneous melanoma on a 2:1 basis to receive mRNA-4157 via intramuscular injection every 3 weeks for a total of nine doses, plus intravenous pembrolizumab every 3 weeks for 18 cycles (107 patients) or pembrolizumab alone (50 patients). Median follow-up was 101 weeks in the combination group and 105 weeks in the pembrolizumab group.

Overall, the 18-month recurrence-free survival rates were 78.6% in the combination arm and 62.2% in the pembrolizumab arm. The recurrence-free survival rates corresponded to a 44% reduced risk of recurrence or death in patients who received the personalized vaccine plus pembrolizumab compared with those who received only pembrolizumab (hazard ratio [HR] for recurrence, 0.561; P =.0266).

Grade 3 or greater adverse events occurred in 25% of patients in the combination group and 18% of patients in the pembrolizumab group. The most common grade 3 event associated with the vaccine was fatigue. No grade 4 adverse events or deaths were associated with the vaccine, and the addition of the vaccine to pembrolizumab did not appear to increase risk for immune-mediated adverse events.

In a subanalysis, Dr. Weber and colleagues explored the relationship between tumor mutational burden and recurrence-free survival. Higher tumor mutational burden may mean more neoepitopes to target, which is helpful when developing personalized neoantigen vaccines, explained coinvestigator Ryan Sullivan, MD, associate director of the melanoma program at Mass General Cancer Center, Boston, who presented the subanalysis results.

The investigators performed whole exome and whole transcriptome sequencing of baseline tumor biopsy samples to determine the mutational burden of tumors and defined a high mutational burden as 10 or more mutations per megabase.

Overall, in the combination group, patients with a higher tumor mutational burden at baseline showed improved outcomes (HR, 0.652; 95% confidence interval [CI], 0.284-1.494), as did patients with a lower tumor mutational burden (HR, 0.586; 95% CI, 0.243-1.415).

The authors found the same was true for patients with high vs. low tumor inflammation scores (high: HR, 0.576; 95% CI, 0.209-1.591 vs. low: HR, 0.528; 95% CI, 0.253-1.101) and higher PD-L1 expression (PD-L1 positive: HR, 0.485; 95% CI, 0.226-1.039 vs. PD-L1 negative: HR, 0.162; 95% CI, 0.038-0.685).

The hazard ratios crossed 1, which suggest that the combination was similarly effective in all patient subsets, said Dr. Sullivan.

Dr. Callahan also highlighted that the P value was based on a one-side log-rank test, “a relatively low bar to jump over” and that there were slight imbalances in both PD-1 expression status and tumor mutational burden – both of which favored the vaccine group and may be associated with better recurrence-free survival.

The 16% difference in recurrence-free survival seen with the combination vs. pembrolizumab alone, if confirmed in further studies, “is clinically meaningful for high-risk patients,” said Dr. Callahan. “The authors are to be congratulated for presenting the first randomized study of a neoantigen vaccine with a clinical efficacy primary endpoint, and this is a trial that incorporates many of the lessons we’ve learned along the years.”

Dr. Sullivan also commented on the promising results. “The field of cancer vaccines is a wasteland of failed clinical trials after some initial promising data, so to have something like this where it does appear that this vaccine strategy works is good not only for patients with melanoma but for those people who have dedicated their lives to trying to develop cancer vaccines,” he said in an interview.

KEYNOTE-942 was funded by Moderna with collaboration from Merck. Dr. Weber has financial relationships with Merck, Moderna, and other companies. Dr. Sullivan has served as a paid consultant for Merck and has received research funding from the company. Dr. Callahan disclosed a consulting/advisory role with Moderna, Merck, and others.
 

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

The combination of a patient-specific mRNA-based cancer vaccine (mRNA-4157/V940, Moderna and Merck) and the immune checkpoint inhibitor pembrolizumab significantly improved recurrence-free survival for patients with high-risk melanoma compared with pembrolizumab alone, according to the latest data from the KEYNOTE-942 trial.

This recurrence-free survival benefit corresponded to a 44% reduced risk of recurrence or death in patients who received the personalized vaccine plus pembrolizumab compared with the immunotherapy alone.

The randomized phase 2b trial is the first to show a positive result for a cancer vaccine in a randomized trial. The results, if confirmed in further studies, hold promise for treating other solid tumors with sensitivity to the programmed death-1 (PD-1) protein, investigators said.

“KEYNOTE-942 is the first randomized study to demonstrate improvement in recurrence-free survival in melanoma, or in any cancer in my view, with an individualized neoantigen vaccine approach,” trial investigator Jeffrey S. Weber, MD, PhD, of NYU Langone Perlmutter Cancer Center in New York, said during an oral abstract session at the annual meeting of the American Association for Cancer Research.

“I have every confidence that this strategy will be expanded to other histologies that are PD-1 sensitive, such as non–small cell lung cancer, renal cell cancer, hepatocellular cancer, gastroesophageal cancer, et cetera,” Dr. Weber said.

Invited discussant Margaret Callahan, MD, PhD, of Memorial Sloan Kettering Cancer Center in New York, called the results “exciting,” especially in light of previous results in cancer vaccine trials. “Despite hundreds of formulations and dozens of studies, cancer vaccines have been disappointing so far, and have largely failed to have a meaningful impact in oncology,” she said.
 

A promising personalized vaccine

The mRNA vaccine is individually tailored and encodes up to 34 patient-specific tumor neoantigens. The vaccine also acts as an adjuvant to strengthen the immune response.

Dr. Weber said that the “mRNA 4157 is what one would call an individualized neoantigen therapy. It will target an individual patient’s unique tumor mutations, and the revelation over the last 5-10 years, is that, for better or worse, virtually all the neoantigens are unique to an individual patient. There are very, very few true universal neoantigens, or at least universal neoantigens that could have clinical utility.”

The vaccines are developed from tumor biopsy tissues that then undergo whole exome and RNA sequencing to identify single nucleotide variants that are present in the tumor but not in normal tissue.

The findings are then fed into a computer algorithm that identifies potential neoepitope peptides that would bind well to the patient’s human leukocyte antigen (HLA) type and could evoke strong T-cell responses.

“Once they’re chosen, you concatenate the sequences together into a single-strand mRNA vaccine, it’s packaged with nanoparticles to encapsulate it, and there you have your mRNA vaccine,” Dr. Weber explained.

In the KEYNOTE-942 trial, the investigators randomly assigned patients with completely resected high-risk cutaneous melanoma on a 2:1 basis to receive mRNA-4157 via intramuscular injection every 3 weeks for a total of nine doses, plus intravenous pembrolizumab every 3 weeks for 18 cycles (107 patients) or pembrolizumab alone (50 patients). Median follow-up was 101 weeks in the combination group and 105 weeks in the pembrolizumab group.

Overall, the 18-month recurrence-free survival rates were 78.6% in the combination arm and 62.2% in the pembrolizumab arm. The recurrence-free survival rates corresponded to a 44% reduced risk of recurrence or death in patients who received the personalized vaccine plus pembrolizumab compared with those who received only pembrolizumab (hazard ratio [HR] for recurrence, 0.561; P =.0266).

Grade 3 or greater adverse events occurred in 25% of patients in the combination group and 18% of patients in the pembrolizumab group. The most common grade 3 event associated with the vaccine was fatigue. No grade 4 adverse events or deaths were associated with the vaccine, and the addition of the vaccine to pembrolizumab did not appear to increase risk for immune-mediated adverse events.

In a subanalysis, Dr. Weber and colleagues explored the relationship between tumor mutational burden and recurrence-free survival. Higher tumor mutational burden may mean more neoepitopes to target, which is helpful when developing personalized neoantigen vaccines, explained coinvestigator Ryan Sullivan, MD, associate director of the melanoma program at Mass General Cancer Center, Boston, who presented the subanalysis results.

The investigators performed whole exome and whole transcriptome sequencing of baseline tumor biopsy samples to determine the mutational burden of tumors and defined a high mutational burden as 10 or more mutations per megabase.

Overall, in the combination group, patients with a higher tumor mutational burden at baseline showed improved outcomes (HR, 0.652; 95% confidence interval [CI], 0.284-1.494), as did patients with a lower tumor mutational burden (HR, 0.586; 95% CI, 0.243-1.415).

The authors found the same was true for patients with high vs. low tumor inflammation scores (high: HR, 0.576; 95% CI, 0.209-1.591 vs. low: HR, 0.528; 95% CI, 0.253-1.101) and higher PD-L1 expression (PD-L1 positive: HR, 0.485; 95% CI, 0.226-1.039 vs. PD-L1 negative: HR, 0.162; 95% CI, 0.038-0.685).

The hazard ratios crossed 1, which suggest that the combination was similarly effective in all patient subsets, said Dr. Sullivan.

Dr. Callahan also highlighted that the P value was based on a one-side log-rank test, “a relatively low bar to jump over” and that there were slight imbalances in both PD-1 expression status and tumor mutational burden – both of which favored the vaccine group and may be associated with better recurrence-free survival.

The 16% difference in recurrence-free survival seen with the combination vs. pembrolizumab alone, if confirmed in further studies, “is clinically meaningful for high-risk patients,” said Dr. Callahan. “The authors are to be congratulated for presenting the first randomized study of a neoantigen vaccine with a clinical efficacy primary endpoint, and this is a trial that incorporates many of the lessons we’ve learned along the years.”

Dr. Sullivan also commented on the promising results. “The field of cancer vaccines is a wasteland of failed clinical trials after some initial promising data, so to have something like this where it does appear that this vaccine strategy works is good not only for patients with melanoma but for those people who have dedicated their lives to trying to develop cancer vaccines,” he said in an interview.

KEYNOTE-942 was funded by Moderna with collaboration from Merck. Dr. Weber has financial relationships with Merck, Moderna, and other companies. Dr. Sullivan has served as a paid consultant for Merck and has received research funding from the company. Dr. Callahan disclosed a consulting/advisory role with Moderna, Merck, and others.
 

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

The combination of a patient-specific mRNA-based cancer vaccine (mRNA-4157/V940, Moderna and Merck) and the immune checkpoint inhibitor pembrolizumab significantly improved recurrence-free survival for patients with high-risk melanoma compared with pembrolizumab alone, according to the latest data from the KEYNOTE-942 trial.

This recurrence-free survival benefit corresponded to a 44% reduced risk of recurrence or death in patients who received the personalized vaccine plus pembrolizumab compared with the immunotherapy alone.

The randomized phase 2b trial is the first to show a positive result for a cancer vaccine in a randomized trial. The results, if confirmed in further studies, hold promise for treating other solid tumors with sensitivity to the programmed death-1 (PD-1) protein, investigators said.

“KEYNOTE-942 is the first randomized study to demonstrate improvement in recurrence-free survival in melanoma, or in any cancer in my view, with an individualized neoantigen vaccine approach,” trial investigator Jeffrey S. Weber, MD, PhD, of NYU Langone Perlmutter Cancer Center in New York, said during an oral abstract session at the annual meeting of the American Association for Cancer Research.

“I have every confidence that this strategy will be expanded to other histologies that are PD-1 sensitive, such as non–small cell lung cancer, renal cell cancer, hepatocellular cancer, gastroesophageal cancer, et cetera,” Dr. Weber said.

Invited discussant Margaret Callahan, MD, PhD, of Memorial Sloan Kettering Cancer Center in New York, called the results “exciting,” especially in light of previous results in cancer vaccine trials. “Despite hundreds of formulations and dozens of studies, cancer vaccines have been disappointing so far, and have largely failed to have a meaningful impact in oncology,” she said.
 

A promising personalized vaccine

The mRNA vaccine is individually tailored and encodes up to 34 patient-specific tumor neoantigens. The vaccine also acts as an adjuvant to strengthen the immune response.

Dr. Weber said that the “mRNA 4157 is what one would call an individualized neoantigen therapy. It will target an individual patient’s unique tumor mutations, and the revelation over the last 5-10 years, is that, for better or worse, virtually all the neoantigens are unique to an individual patient. There are very, very few true universal neoantigens, or at least universal neoantigens that could have clinical utility.”

The vaccines are developed from tumor biopsy tissues that then undergo whole exome and RNA sequencing to identify single nucleotide variants that are present in the tumor but not in normal tissue.

The findings are then fed into a computer algorithm that identifies potential neoepitope peptides that would bind well to the patient’s human leukocyte antigen (HLA) type and could evoke strong T-cell responses.

“Once they’re chosen, you concatenate the sequences together into a single-strand mRNA vaccine, it’s packaged with nanoparticles to encapsulate it, and there you have your mRNA vaccine,” Dr. Weber explained.

In the KEYNOTE-942 trial, the investigators randomly assigned patients with completely resected high-risk cutaneous melanoma on a 2:1 basis to receive mRNA-4157 via intramuscular injection every 3 weeks for a total of nine doses, plus intravenous pembrolizumab every 3 weeks for 18 cycles (107 patients) or pembrolizumab alone (50 patients). Median follow-up was 101 weeks in the combination group and 105 weeks in the pembrolizumab group.

Overall, the 18-month recurrence-free survival rates were 78.6% in the combination arm and 62.2% in the pembrolizumab arm. The recurrence-free survival rates corresponded to a 44% reduced risk of recurrence or death in patients who received the personalized vaccine plus pembrolizumab compared with those who received only pembrolizumab (hazard ratio [HR] for recurrence, 0.561; P =.0266).

Grade 3 or greater adverse events occurred in 25% of patients in the combination group and 18% of patients in the pembrolizumab group. The most common grade 3 event associated with the vaccine was fatigue. No grade 4 adverse events or deaths were associated with the vaccine, and the addition of the vaccine to pembrolizumab did not appear to increase risk for immune-mediated adverse events.

In a subanalysis, Dr. Weber and colleagues explored the relationship between tumor mutational burden and recurrence-free survival. Higher tumor mutational burden may mean more neoepitopes to target, which is helpful when developing personalized neoantigen vaccines, explained coinvestigator Ryan Sullivan, MD, associate director of the melanoma program at Mass General Cancer Center, Boston, who presented the subanalysis results.

The investigators performed whole exome and whole transcriptome sequencing of baseline tumor biopsy samples to determine the mutational burden of tumors and defined a high mutational burden as 10 or more mutations per megabase.

Overall, in the combination group, patients with a higher tumor mutational burden at baseline showed improved outcomes (HR, 0.652; 95% confidence interval [CI], 0.284-1.494), as did patients with a lower tumor mutational burden (HR, 0.586; 95% CI, 0.243-1.415).

The authors found the same was true for patients with high vs. low tumor inflammation scores (high: HR, 0.576; 95% CI, 0.209-1.591 vs. low: HR, 0.528; 95% CI, 0.253-1.101) and higher PD-L1 expression (PD-L1 positive: HR, 0.485; 95% CI, 0.226-1.039 vs. PD-L1 negative: HR, 0.162; 95% CI, 0.038-0.685).

The hazard ratios crossed 1, which suggest that the combination was similarly effective in all patient subsets, said Dr. Sullivan.

Dr. Callahan also highlighted that the P value was based on a one-side log-rank test, “a relatively low bar to jump over” and that there were slight imbalances in both PD-1 expression status and tumor mutational burden – both of which favored the vaccine group and may be associated with better recurrence-free survival.

The 16% difference in recurrence-free survival seen with the combination vs. pembrolizumab alone, if confirmed in further studies, “is clinically meaningful for high-risk patients,” said Dr. Callahan. “The authors are to be congratulated for presenting the first randomized study of a neoantigen vaccine with a clinical efficacy primary endpoint, and this is a trial that incorporates many of the lessons we’ve learned along the years.”

Dr. Sullivan also commented on the promising results. “The field of cancer vaccines is a wasteland of failed clinical trials after some initial promising data, so to have something like this where it does appear that this vaccine strategy works is good not only for patients with melanoma but for those people who have dedicated their lives to trying to develop cancer vaccines,” he said in an interview.

KEYNOTE-942 was funded by Moderna with collaboration from Merck. Dr. Weber has financial relationships with Merck, Moderna, and other companies. Dr. Sullivan has served as a paid consultant for Merck and has received research funding from the company. Dr. Callahan disclosed a consulting/advisory role with Moderna, Merck, and others.
 

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

Non-Hispanic persons of African ancestry typically have worse clinical outcomes from colorectal cancer (CRC) than individuals of other heritages, a disparity attributed to many factors, including socioeconomic, environmental, and genetic influences, as well as less access to care.

Results from a new genomic study provide greater clarity regarding the genetic piece of the puzzle: Persons of African background tend to have fewer targetable alterations, compared with patients of other races.

The findings were presented in a briefing and scientific poster session at the annual meeting of the American Association for Cancer Research.

Overall, the numbers to date show a clear trend: The incidence of and mortality from CRC are higher among Black patients than other populations. However, the extent to which genetic difference plays a role in these disparities remains unclear.

In the current study, researchers from Memorial Sloan Kettering (MSK) Cancer Center in New York explored how germline and somatic genomic alterations differ among patients of African ancestry, in comparison with those of European and other heritage, and how those differences might influence CRC outcomes.

Lead author Henry Walch, MS, a computational biologist at MSK, and colleagues compared genomic profiles among nearly 3,800 patients with CRC who were treated at MSK from 2014 to 2022. Patients in the study were classified by genetic ancestry as European (3,201 patients), African (236 patients), East Asian (253 patients), and South Asian (89 patients).

Tumor and normal tissues from the patients underwent next-generation DNA sequencing with a panel that covers 505 cancer-associated genes.

An analysis of overall survival by genetic ancestry confirmed findings from other studies: Overall survival was significantly worse among patients of African ancestry than among those of other groups (median 45.7 vs. 67.1 months).

The investigators used a precision oncology knowledge base (OncoKB) to assign levels of therapeutic actionability for each genomic alteration that was identified. The highest assigned value was for drugs that have been approved by the U.S. Food and Drug Administration and that target FDA-recognized biomarkers. The lowest value was assigned to biomarkers for which there was “compelling biological evidence” that the particular biomarker predicted response to a drug.

The team found that the percentage of patients who qualified for immunotherapy on the basis of microsatellite instability or high tumor mutational burden was significantly lower among patients of African heritage, compared with those of European heritage (13.5% vs. 20.4%; P = .008).

Compared with those of European ancestry, patients of African ancestry had significantly fewer actionable alterations (5.6% vs. 11.2%; P = .01). This difference was largely driven by the lack of targetable BRAF mutations (1.8% vs. 5.0%).

Mutations in APC, the most frequently altered gene in CRC, are typically associated with cancer outcomes, but the authors found that overall survival was similar for patients of African heritage regardless of whether they had altered or wild-type APC (median overall survival, 45.0 months for altered APC vs. 45.9 months for wild-type APC; P = .91). However, a significant association between APC status and overall survival was observed for patients of European ancestry (median, 64.6 months for altered APC vs. 45.6 months for wild-type APC; P < .0001).

Analyses that accounted for sex, age, primary tumor location, and stage at diagnosis also showed an association between APC status and overall survival for patients of European heritage (hazard ratio, 0.64), but not for patients of African heritage (HR, 0.74, P = .492).

Mr. Walch noted that a limitation of the study is that information regarding comprehensive treatment, environmental exposures, lifestyle, and socioeconomic factors was not available for the analysis but that these elements likely play an important role in patient outcomes.

“This is a complex problem involving many unseen factors, and the genomic landscape is a piece of a much larger puzzle,” said Mr. Walch. He noted that future studies will incorporate these factors into the models “with the ultimate goal of identifying opportunities to intervene and improve outcomes.”

Briefing moderator Lisa Newman, MD, MPH, of Weill Cornell Medicine and New York–Presbyterian, in New York, commented that Mr. Walch presented “some very compelling data that demonstrate the importance of including individuals from diverse backgrounds into [cancer] research.”

The study was funded in part by a Chris4Life Early Career Investigator Award Grant from the Colorectal Cancer Alliance for Francisco Sanchez-Vega, PhD, senior author of the study. Dr. Sanchez-Vega was also supported by an AACR-Minority and Minority-serving Institution Faculty Scholar in Cancer Research Award. Mr. Walch and Dr. Newman have disclosed no relevant financial relationships.

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

Non-Hispanic persons of African ancestry typically have worse clinical outcomes from colorectal cancer (CRC) than individuals of other heritages, a disparity attributed to many factors, including socioeconomic, environmental, and genetic influences, as well as less access to care.

Results from a new genomic study provide greater clarity regarding the genetic piece of the puzzle: Persons of African background tend to have fewer targetable alterations, compared with patients of other races.

The findings were presented in a briefing and scientific poster session at the annual meeting of the American Association for Cancer Research.

Overall, the numbers to date show a clear trend: The incidence of and mortality from CRC are higher among Black patients than other populations. However, the extent to which genetic difference plays a role in these disparities remains unclear.

In the current study, researchers from Memorial Sloan Kettering (MSK) Cancer Center in New York explored how germline and somatic genomic alterations differ among patients of African ancestry, in comparison with those of European and other heritage, and how those differences might influence CRC outcomes.

Lead author Henry Walch, MS, a computational biologist at MSK, and colleagues compared genomic profiles among nearly 3,800 patients with CRC who were treated at MSK from 2014 to 2022. Patients in the study were classified by genetic ancestry as European (3,201 patients), African (236 patients), East Asian (253 patients), and South Asian (89 patients).

Tumor and normal tissues from the patients underwent next-generation DNA sequencing with a panel that covers 505 cancer-associated genes.

An analysis of overall survival by genetic ancestry confirmed findings from other studies: Overall survival was significantly worse among patients of African ancestry than among those of other groups (median 45.7 vs. 67.1 months).

The investigators used a precision oncology knowledge base (OncoKB) to assign levels of therapeutic actionability for each genomic alteration that was identified. The highest assigned value was for drugs that have been approved by the U.S. Food and Drug Administration and that target FDA-recognized biomarkers. The lowest value was assigned to biomarkers for which there was “compelling biological evidence” that the particular biomarker predicted response to a drug.

The team found that the percentage of patients who qualified for immunotherapy on the basis of microsatellite instability or high tumor mutational burden was significantly lower among patients of African heritage, compared with those of European heritage (13.5% vs. 20.4%; P = .008).

Compared with those of European ancestry, patients of African ancestry had significantly fewer actionable alterations (5.6% vs. 11.2%; P = .01). This difference was largely driven by the lack of targetable BRAF mutations (1.8% vs. 5.0%).

Mutations in APC, the most frequently altered gene in CRC, are typically associated with cancer outcomes, but the authors found that overall survival was similar for patients of African heritage regardless of whether they had altered or wild-type APC (median overall survival, 45.0 months for altered APC vs. 45.9 months for wild-type APC; P = .91). However, a significant association between APC status and overall survival was observed for patients of European ancestry (median, 64.6 months for altered APC vs. 45.6 months for wild-type APC; P < .0001).

Analyses that accounted for sex, age, primary tumor location, and stage at diagnosis also showed an association between APC status and overall survival for patients of European heritage (hazard ratio, 0.64), but not for patients of African heritage (HR, 0.74, P = .492).

Mr. Walch noted that a limitation of the study is that information regarding comprehensive treatment, environmental exposures, lifestyle, and socioeconomic factors was not available for the analysis but that these elements likely play an important role in patient outcomes.

“This is a complex problem involving many unseen factors, and the genomic landscape is a piece of a much larger puzzle,” said Mr. Walch. He noted that future studies will incorporate these factors into the models “with the ultimate goal of identifying opportunities to intervene and improve outcomes.”

Briefing moderator Lisa Newman, MD, MPH, of Weill Cornell Medicine and New York–Presbyterian, in New York, commented that Mr. Walch presented “some very compelling data that demonstrate the importance of including individuals from diverse backgrounds into [cancer] research.”

The study was funded in part by a Chris4Life Early Career Investigator Award Grant from the Colorectal Cancer Alliance for Francisco Sanchez-Vega, PhD, senior author of the study. Dr. Sanchez-Vega was also supported by an AACR-Minority and Minority-serving Institution Faculty Scholar in Cancer Research Award. Mr. Walch and Dr. Newman have disclosed no relevant financial relationships.

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

Non-Hispanic persons of African ancestry typically have worse clinical outcomes from colorectal cancer (CRC) than individuals of other heritages, a disparity attributed to many factors, including socioeconomic, environmental, and genetic influences, as well as less access to care.

Results from a new genomic study provide greater clarity regarding the genetic piece of the puzzle: Persons of African background tend to have fewer targetable alterations, compared with patients of other races.

The findings were presented in a briefing and scientific poster session at the annual meeting of the American Association for Cancer Research.

Overall, the numbers to date show a clear trend: The incidence of and mortality from CRC are higher among Black patients than other populations. However, the extent to which genetic difference plays a role in these disparities remains unclear.

In the current study, researchers from Memorial Sloan Kettering (MSK) Cancer Center in New York explored how germline and somatic genomic alterations differ among patients of African ancestry, in comparison with those of European and other heritage, and how those differences might influence CRC outcomes.

Lead author Henry Walch, MS, a computational biologist at MSK, and colleagues compared genomic profiles among nearly 3,800 patients with CRC who were treated at MSK from 2014 to 2022. Patients in the study were classified by genetic ancestry as European (3,201 patients), African (236 patients), East Asian (253 patients), and South Asian (89 patients).

Tumor and normal tissues from the patients underwent next-generation DNA sequencing with a panel that covers 505 cancer-associated genes.

An analysis of overall survival by genetic ancestry confirmed findings from other studies: Overall survival was significantly worse among patients of African ancestry than among those of other groups (median 45.7 vs. 67.1 months).

The investigators used a precision oncology knowledge base (OncoKB) to assign levels of therapeutic actionability for each genomic alteration that was identified. The highest assigned value was for drugs that have been approved by the U.S. Food and Drug Administration and that target FDA-recognized biomarkers. The lowest value was assigned to biomarkers for which there was “compelling biological evidence” that the particular biomarker predicted response to a drug.

The team found that the percentage of patients who qualified for immunotherapy on the basis of microsatellite instability or high tumor mutational burden was significantly lower among patients of African heritage, compared with those of European heritage (13.5% vs. 20.4%; P = .008).

Compared with those of European ancestry, patients of African ancestry had significantly fewer actionable alterations (5.6% vs. 11.2%; P = .01). This difference was largely driven by the lack of targetable BRAF mutations (1.8% vs. 5.0%).

Mutations in APC, the most frequently altered gene in CRC, are typically associated with cancer outcomes, but the authors found that overall survival was similar for patients of African heritage regardless of whether they had altered or wild-type APC (median overall survival, 45.0 months for altered APC vs. 45.9 months for wild-type APC; P = .91). However, a significant association between APC status and overall survival was observed for patients of European ancestry (median, 64.6 months for altered APC vs. 45.6 months for wild-type APC; P < .0001).

Analyses that accounted for sex, age, primary tumor location, and stage at diagnosis also showed an association between APC status and overall survival for patients of European heritage (hazard ratio, 0.64), but not for patients of African heritage (HR, 0.74, P = .492).

Mr. Walch noted that a limitation of the study is that information regarding comprehensive treatment, environmental exposures, lifestyle, and socioeconomic factors was not available for the analysis but that these elements likely play an important role in patient outcomes.

“This is a complex problem involving many unseen factors, and the genomic landscape is a piece of a much larger puzzle,” said Mr. Walch. He noted that future studies will incorporate these factors into the models “with the ultimate goal of identifying opportunities to intervene and improve outcomes.”

Briefing moderator Lisa Newman, MD, MPH, of Weill Cornell Medicine and New York–Presbyterian, in New York, commented that Mr. Walch presented “some very compelling data that demonstrate the importance of including individuals from diverse backgrounds into [cancer] research.”

The study was funded in part by a Chris4Life Early Career Investigator Award Grant from the Colorectal Cancer Alliance for Francisco Sanchez-Vega, PhD, senior author of the study. Dr. Sanchez-Vega was also supported by an AACR-Minority and Minority-serving Institution Faculty Scholar in Cancer Research Award. Mr. Walch and Dr. Newman have disclosed no relevant financial relationships.

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