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New Guideline on EoE Reflects Over a Decade of Advances in Diagnosis and Management
according to a new clinical guideline from the American College of Gastroenterology (ACG).
As an update to the 2013 version, the guideline covers paradigm-shifting changes in EoE knowledge about risk factors, pathogenesis, validated outcome metrics, new nomenclature, and pediatric-specific considerations.
“There have been multiple advances across diagnosis, treatment, monitoring, and other aspects of EoE management in the decade since the last ACG guidelines and in the 5 years since the last AGA [American Gastroenterological Association] guidelines, including new drug approvals globally for EoE,” said lead author Evan Dellon, MD, AGAF, professor of gastroenterology and hepatology and director of the Center for Esophageal Diseases and Swallowing at the University of North Carolina School of Medicine, Chapel Hill.
“The guidelines aimed to provide practical and evidence-based recommendations that could be implemented in daily practice, as well as to provide advice on a number of aspects of diagnosis and management of EoE where there might not be a definitive evidence base, but where clinical questions commonly arise,” he said.
The update was published online in The American Journal of Gastroenterology.
EoE Diagnosis
EoE is a chronic allergen-induced, type 2 immune-mediated disease of the esophagus, which is characterized by symptoms of esophageal dysfunction (such as dysphagia and food impaction) and an eosinophilic predominant infiltrate in the esophagus, the authors wrote.
A diagnosis should be based on the presence of esophageal dysfunction symptoms and at least 15 eosinophils per high-power field on esophageal biopsy, particularly after ruling out non-EoE disorders. A critical change from the 2013 guideline eliminates the requirement of a PPI trial for diagnosis.
Endoscopic evaluation is critical for diagnosis, assessing treatment response, and long-term monitoring, the authors wrote. The guideline advises using the EoE endoscopic reference score (EREFS) to characterize endoscopic findings, a recommendation that was also endorsed in 2022 guidelines by the American Society for Gastrointestinal Endoscopy. EREFS classifies five key EoE features, including edema, rings, exudates, furrows, and strictures, by severity.
To assess for histologic features of EoE, at least six esophageal biopsies should be taken from at least two esophageal levels (such as proximal/mid and distal halves), specifically targeted in areas of furrows or exudates.
In addition, peak eosinophil counts should be quantified on esophageal biopsies from every endoscopy performed for EoE, which will help with subsequent management and monitoring.
As new research expands on the role of mast cells, T cells, basophils, NK cells, and fibroblasts in EoE, the authors postulate that using the EoE histologic scoring system may become more relevant in the future, particularly around findings such as persistent basal zone hyperplasia or lamina propria fibrosis as drivers of ongoing symptoms when eosinophil counts decline.
A Better Understanding of Pathogenesis
“While EoE is considered a relatively new disease, there has been a concerted effort by researchers and clinicians to work together, in partnership with patients, to better understand the basic disease pathogenesis and develop the best treatment approaches,” said Marc Rothenberg, MD, PhD, director of allergy and immunology at Cincinnati Children’s Hospital Medical Center, Ohio. Rothenberg wasn’t involved with the update.
“A lot of progress has been made since the initial thought that esophageal eosinophilia was a ramification of acid reflux disease,” said Rothenberg, the founding director and a principal investigator of the Consortium of Eosinophilic Gastrointestinal Disease Researchers.
“We now understand that the esophagus is an immune-responsive organ and that food allergies can be manifested as EoE. Investment in science is paying off as the basic disease pathoetiology has been uncovered, and this has led to successful strategies for disease intervention, including precision therapy.”
When treating EoE, the goals include improving patient symptoms and quality of life, improving endoscopic and histologic findings, normalizing growth and development in children, maintaining nutrition, and preventing complications such as food impaction or perforation.
This means addressing both the inflammatory and fibrostenotic aspects of the disease, the authors wrote. Pharmacologic or dietary therapies can treat the inflammatory component and may lead to esophageal improvements, whereas esophageal dilation can treat strictures and luminal narrowing. Notably, treatment choices should be individualized based on disease characteristics and patient preferences.
In general, PPIs are suggested as treatment, even beyond reflux symptoms. In EoE, PPIs can decrease eotaxin-3 cytokines that recruit eosinophils to the esophagus, improve esophageal barrier function, and maintain esophageal epithelial transcriptional homeostasis. Although potassium-competitive acid blocker medications have been studied in EoE, data remains limited. H2 receptor blockers don’t appear to be effective for EoE.
Swallowed topical corticosteroids have shown histologic efficacy, the authors reported, particularly in recent phase 3 trials of budesonide oral suspension (BOS) and budesonide orodispersible tablet (BOT). BOS was approved for EoE by the Food and Drug Administration (FDA) in 2024, and BOT was approved for EoE by the European Medicines Agency in 2018.
In terms of dietary elimination, a range of options appear to be effective for patients, including the six-food elimination diet, which has been studied most. However, less restrictive or step-up approaches (such as four-food elimination or one-food elimination of milk) may be better for patients, the authors wrote. Ultimately, the “optimal” choice is one that patients and families can adhere to and have the resources to complete.
In addition, they noted that allergy test-directed elimination diets aren’t currently recommended because EoE has delayed hypersensitivity, so skin prick, patch, or serum Ig allergy tests tend to have limited success in predicting EoE food triggers.
In terms of biologic treatments, dupilumab is recommended for ages 12 years or older who don’t respond to PPI therapy, as well as suggested for ages 1-11 years based on previous clinical trial data. The FDA approved the use of dupilumab for ages 1-11 years in February 2024.
In this update, the authors declined to make recommendations about other biologics such as cendakimab, benralizumab, lirentelimab, mepolizumab, or reslizumab. They also advised against using omaluzumab as a treatment for EoE.
“This new 2025 guideline summarizes and synthesizes key studies in support of proton pump inhibitors, topical steroids, dietary therapy, and biologics for EoE. Additionally, the guidelines are clinically relevant in providing practical suggestions (such as medication dosing) and expert opinions on key concepts in managing EoE,” said Joy Weiling Chang, MD, assistant professor of gastroenterology at the University of Michigan, Ann Arbor, who specializes in patient-physician preferences and decision-making in EoE care.
“It’s an exciting time to take care of patients with EoE with many new therapies, but the rapidly evolving options can be overwhelming,” said Chang, who wasn’t involved with the update. “Since there are no clinical effectiveness studies between the various treatments, and therapies can differ so much (with delivery and daily use, monitoring, cost), electing EoE treatment is an ideal opportunity for shared decision-making. Equipped with these clinical guidelines, clinicians can be empowered to elicit and consider patient preferences and values in the management of this chronic disease.”
The authors received no specific funding for this update. Dellon and Rothenberg reported receiving research funding and consultant roles with numerous pharmaceutical companies and organizations. Chang reported no relevant disclosures.
A version of this article appeared on Medscape.com.
according to a new clinical guideline from the American College of Gastroenterology (ACG).
As an update to the 2013 version, the guideline covers paradigm-shifting changes in EoE knowledge about risk factors, pathogenesis, validated outcome metrics, new nomenclature, and pediatric-specific considerations.
“There have been multiple advances across diagnosis, treatment, monitoring, and other aspects of EoE management in the decade since the last ACG guidelines and in the 5 years since the last AGA [American Gastroenterological Association] guidelines, including new drug approvals globally for EoE,” said lead author Evan Dellon, MD, AGAF, professor of gastroenterology and hepatology and director of the Center for Esophageal Diseases and Swallowing at the University of North Carolina School of Medicine, Chapel Hill.
“The guidelines aimed to provide practical and evidence-based recommendations that could be implemented in daily practice, as well as to provide advice on a number of aspects of diagnosis and management of EoE where there might not be a definitive evidence base, but where clinical questions commonly arise,” he said.
The update was published online in The American Journal of Gastroenterology.
EoE Diagnosis
EoE is a chronic allergen-induced, type 2 immune-mediated disease of the esophagus, which is characterized by symptoms of esophageal dysfunction (such as dysphagia and food impaction) and an eosinophilic predominant infiltrate in the esophagus, the authors wrote.
A diagnosis should be based on the presence of esophageal dysfunction symptoms and at least 15 eosinophils per high-power field on esophageal biopsy, particularly after ruling out non-EoE disorders. A critical change from the 2013 guideline eliminates the requirement of a PPI trial for diagnosis.
Endoscopic evaluation is critical for diagnosis, assessing treatment response, and long-term monitoring, the authors wrote. The guideline advises using the EoE endoscopic reference score (EREFS) to characterize endoscopic findings, a recommendation that was also endorsed in 2022 guidelines by the American Society for Gastrointestinal Endoscopy. EREFS classifies five key EoE features, including edema, rings, exudates, furrows, and strictures, by severity.
To assess for histologic features of EoE, at least six esophageal biopsies should be taken from at least two esophageal levels (such as proximal/mid and distal halves), specifically targeted in areas of furrows or exudates.
In addition, peak eosinophil counts should be quantified on esophageal biopsies from every endoscopy performed for EoE, which will help with subsequent management and monitoring.
As new research expands on the role of mast cells, T cells, basophils, NK cells, and fibroblasts in EoE, the authors postulate that using the EoE histologic scoring system may become more relevant in the future, particularly around findings such as persistent basal zone hyperplasia or lamina propria fibrosis as drivers of ongoing symptoms when eosinophil counts decline.
A Better Understanding of Pathogenesis
“While EoE is considered a relatively new disease, there has been a concerted effort by researchers and clinicians to work together, in partnership with patients, to better understand the basic disease pathogenesis and develop the best treatment approaches,” said Marc Rothenberg, MD, PhD, director of allergy and immunology at Cincinnati Children’s Hospital Medical Center, Ohio. Rothenberg wasn’t involved with the update.
“A lot of progress has been made since the initial thought that esophageal eosinophilia was a ramification of acid reflux disease,” said Rothenberg, the founding director and a principal investigator of the Consortium of Eosinophilic Gastrointestinal Disease Researchers.
“We now understand that the esophagus is an immune-responsive organ and that food allergies can be manifested as EoE. Investment in science is paying off as the basic disease pathoetiology has been uncovered, and this has led to successful strategies for disease intervention, including precision therapy.”
When treating EoE, the goals include improving patient symptoms and quality of life, improving endoscopic and histologic findings, normalizing growth and development in children, maintaining nutrition, and preventing complications such as food impaction or perforation.
This means addressing both the inflammatory and fibrostenotic aspects of the disease, the authors wrote. Pharmacologic or dietary therapies can treat the inflammatory component and may lead to esophageal improvements, whereas esophageal dilation can treat strictures and luminal narrowing. Notably, treatment choices should be individualized based on disease characteristics and patient preferences.
In general, PPIs are suggested as treatment, even beyond reflux symptoms. In EoE, PPIs can decrease eotaxin-3 cytokines that recruit eosinophils to the esophagus, improve esophageal barrier function, and maintain esophageal epithelial transcriptional homeostasis. Although potassium-competitive acid blocker medications have been studied in EoE, data remains limited. H2 receptor blockers don’t appear to be effective for EoE.
Swallowed topical corticosteroids have shown histologic efficacy, the authors reported, particularly in recent phase 3 trials of budesonide oral suspension (BOS) and budesonide orodispersible tablet (BOT). BOS was approved for EoE by the Food and Drug Administration (FDA) in 2024, and BOT was approved for EoE by the European Medicines Agency in 2018.
In terms of dietary elimination, a range of options appear to be effective for patients, including the six-food elimination diet, which has been studied most. However, less restrictive or step-up approaches (such as four-food elimination or one-food elimination of milk) may be better for patients, the authors wrote. Ultimately, the “optimal” choice is one that patients and families can adhere to and have the resources to complete.
In addition, they noted that allergy test-directed elimination diets aren’t currently recommended because EoE has delayed hypersensitivity, so skin prick, patch, or serum Ig allergy tests tend to have limited success in predicting EoE food triggers.
In terms of biologic treatments, dupilumab is recommended for ages 12 years or older who don’t respond to PPI therapy, as well as suggested for ages 1-11 years based on previous clinical trial data. The FDA approved the use of dupilumab for ages 1-11 years in February 2024.
In this update, the authors declined to make recommendations about other biologics such as cendakimab, benralizumab, lirentelimab, mepolizumab, or reslizumab. They also advised against using omaluzumab as a treatment for EoE.
“This new 2025 guideline summarizes and synthesizes key studies in support of proton pump inhibitors, topical steroids, dietary therapy, and biologics for EoE. Additionally, the guidelines are clinically relevant in providing practical suggestions (such as medication dosing) and expert opinions on key concepts in managing EoE,” said Joy Weiling Chang, MD, assistant professor of gastroenterology at the University of Michigan, Ann Arbor, who specializes in patient-physician preferences and decision-making in EoE care.
“It’s an exciting time to take care of patients with EoE with many new therapies, but the rapidly evolving options can be overwhelming,” said Chang, who wasn’t involved with the update. “Since there are no clinical effectiveness studies between the various treatments, and therapies can differ so much (with delivery and daily use, monitoring, cost), electing EoE treatment is an ideal opportunity for shared decision-making. Equipped with these clinical guidelines, clinicians can be empowered to elicit and consider patient preferences and values in the management of this chronic disease.”
The authors received no specific funding for this update. Dellon and Rothenberg reported receiving research funding and consultant roles with numerous pharmaceutical companies and organizations. Chang reported no relevant disclosures.
A version of this article appeared on Medscape.com.
according to a new clinical guideline from the American College of Gastroenterology (ACG).
As an update to the 2013 version, the guideline covers paradigm-shifting changes in EoE knowledge about risk factors, pathogenesis, validated outcome metrics, new nomenclature, and pediatric-specific considerations.
“There have been multiple advances across diagnosis, treatment, monitoring, and other aspects of EoE management in the decade since the last ACG guidelines and in the 5 years since the last AGA [American Gastroenterological Association] guidelines, including new drug approvals globally for EoE,” said lead author Evan Dellon, MD, AGAF, professor of gastroenterology and hepatology and director of the Center for Esophageal Diseases and Swallowing at the University of North Carolina School of Medicine, Chapel Hill.
“The guidelines aimed to provide practical and evidence-based recommendations that could be implemented in daily practice, as well as to provide advice on a number of aspects of diagnosis and management of EoE where there might not be a definitive evidence base, but where clinical questions commonly arise,” he said.
The update was published online in The American Journal of Gastroenterology.
EoE Diagnosis
EoE is a chronic allergen-induced, type 2 immune-mediated disease of the esophagus, which is characterized by symptoms of esophageal dysfunction (such as dysphagia and food impaction) and an eosinophilic predominant infiltrate in the esophagus, the authors wrote.
A diagnosis should be based on the presence of esophageal dysfunction symptoms and at least 15 eosinophils per high-power field on esophageal biopsy, particularly after ruling out non-EoE disorders. A critical change from the 2013 guideline eliminates the requirement of a PPI trial for diagnosis.
Endoscopic evaluation is critical for diagnosis, assessing treatment response, and long-term monitoring, the authors wrote. The guideline advises using the EoE endoscopic reference score (EREFS) to characterize endoscopic findings, a recommendation that was also endorsed in 2022 guidelines by the American Society for Gastrointestinal Endoscopy. EREFS classifies five key EoE features, including edema, rings, exudates, furrows, and strictures, by severity.
To assess for histologic features of EoE, at least six esophageal biopsies should be taken from at least two esophageal levels (such as proximal/mid and distal halves), specifically targeted in areas of furrows or exudates.
In addition, peak eosinophil counts should be quantified on esophageal biopsies from every endoscopy performed for EoE, which will help with subsequent management and monitoring.
As new research expands on the role of mast cells, T cells, basophils, NK cells, and fibroblasts in EoE, the authors postulate that using the EoE histologic scoring system may become more relevant in the future, particularly around findings such as persistent basal zone hyperplasia or lamina propria fibrosis as drivers of ongoing symptoms when eosinophil counts decline.
A Better Understanding of Pathogenesis
“While EoE is considered a relatively new disease, there has been a concerted effort by researchers and clinicians to work together, in partnership with patients, to better understand the basic disease pathogenesis and develop the best treatment approaches,” said Marc Rothenberg, MD, PhD, director of allergy and immunology at Cincinnati Children’s Hospital Medical Center, Ohio. Rothenberg wasn’t involved with the update.
“A lot of progress has been made since the initial thought that esophageal eosinophilia was a ramification of acid reflux disease,” said Rothenberg, the founding director and a principal investigator of the Consortium of Eosinophilic Gastrointestinal Disease Researchers.
“We now understand that the esophagus is an immune-responsive organ and that food allergies can be manifested as EoE. Investment in science is paying off as the basic disease pathoetiology has been uncovered, and this has led to successful strategies for disease intervention, including precision therapy.”
When treating EoE, the goals include improving patient symptoms and quality of life, improving endoscopic and histologic findings, normalizing growth and development in children, maintaining nutrition, and preventing complications such as food impaction or perforation.
This means addressing both the inflammatory and fibrostenotic aspects of the disease, the authors wrote. Pharmacologic or dietary therapies can treat the inflammatory component and may lead to esophageal improvements, whereas esophageal dilation can treat strictures and luminal narrowing. Notably, treatment choices should be individualized based on disease characteristics and patient preferences.
In general, PPIs are suggested as treatment, even beyond reflux symptoms. In EoE, PPIs can decrease eotaxin-3 cytokines that recruit eosinophils to the esophagus, improve esophageal barrier function, and maintain esophageal epithelial transcriptional homeostasis. Although potassium-competitive acid blocker medications have been studied in EoE, data remains limited. H2 receptor blockers don’t appear to be effective for EoE.
Swallowed topical corticosteroids have shown histologic efficacy, the authors reported, particularly in recent phase 3 trials of budesonide oral suspension (BOS) and budesonide orodispersible tablet (BOT). BOS was approved for EoE by the Food and Drug Administration (FDA) in 2024, and BOT was approved for EoE by the European Medicines Agency in 2018.
In terms of dietary elimination, a range of options appear to be effective for patients, including the six-food elimination diet, which has been studied most. However, less restrictive or step-up approaches (such as four-food elimination or one-food elimination of milk) may be better for patients, the authors wrote. Ultimately, the “optimal” choice is one that patients and families can adhere to and have the resources to complete.
In addition, they noted that allergy test-directed elimination diets aren’t currently recommended because EoE has delayed hypersensitivity, so skin prick, patch, or serum Ig allergy tests tend to have limited success in predicting EoE food triggers.
In terms of biologic treatments, dupilumab is recommended for ages 12 years or older who don’t respond to PPI therapy, as well as suggested for ages 1-11 years based on previous clinical trial data. The FDA approved the use of dupilumab for ages 1-11 years in February 2024.
In this update, the authors declined to make recommendations about other biologics such as cendakimab, benralizumab, lirentelimab, mepolizumab, or reslizumab. They also advised against using omaluzumab as a treatment for EoE.
“This new 2025 guideline summarizes and synthesizes key studies in support of proton pump inhibitors, topical steroids, dietary therapy, and biologics for EoE. Additionally, the guidelines are clinically relevant in providing practical suggestions (such as medication dosing) and expert opinions on key concepts in managing EoE,” said Joy Weiling Chang, MD, assistant professor of gastroenterology at the University of Michigan, Ann Arbor, who specializes in patient-physician preferences and decision-making in EoE care.
“It’s an exciting time to take care of patients with EoE with many new therapies, but the rapidly evolving options can be overwhelming,” said Chang, who wasn’t involved with the update. “Since there are no clinical effectiveness studies between the various treatments, and therapies can differ so much (with delivery and daily use, monitoring, cost), electing EoE treatment is an ideal opportunity for shared decision-making. Equipped with these clinical guidelines, clinicians can be empowered to elicit and consider patient preferences and values in the management of this chronic disease.”
The authors received no specific funding for this update. Dellon and Rothenberg reported receiving research funding and consultant roles with numerous pharmaceutical companies and organizations. Chang reported no relevant disclosures.
A version of this article appeared on Medscape.com.
FROM THE AMERICAN JOURNAL OF GASTROENTEROLOGY
Quality, Not Type, of Diet Linked to Microbiome Health
new research suggested.
For example, red meat was a strong driver of omnivore microbiomes, with corresponding signature microbes that are negatively correlated with host cardiometabolic health.
In contrast, the signature microbes found in vegans’ gut microbiomes were correlated with favorable cardiometabolic markers and were enriched in omnivores who ate more plant-based foods.
“From the viewpoint of the impact of diet on the gut microbiome, what seems to be more important is the diversity of healthy plant-based foods that are consumed,” principal author Nicola Segata, PhD, University of Trento in Italy, said in an interview. “Whether this comes within a vegan or an omnivore diet is less crucial, as long as there is no specific overconsumption of unhealthy food categories, such as red meat.”
Excluding broad categories of foods also can have consequences, he added. “For example, we saw that the exclusion of dairy fermented foods is associated with decreased presence of potentially probiotic microbes that are constitutive of such foods. Avoiding meat or dairy products does not necessarily have a positive effect if it does not come with a variety of quality plant-based products.”
The study was published online in Nature Microbiology.
Diet Tied to Microbial Signature
The researchers analyzed biological samples from 21,561 individuals across five multi-national cohorts to map how differences in diet patterns (omnivore, vegetarian, and vegan) are reflected in gut microbiomes.
They found that the three diet patterns are highly distinguishable by their microbial profiles and that each diet has corresponding unique signature microbes, including those tied to digestion of specific types of food and sometimes those derived from food itself.
The microbiomes of omnivores had an increased presence of bacteria associated with meat digestion, such as Alistipes putredinis, which is involved in protein fermentation. Omnivores also had more bacteria associated with both inflammatory bowel disease and increased colon cancer risk, such as Ruminococcus torques and Bilophila wadsworthia.
The microbiomes of vegans had an abundance of bacteria involved in fiber fermentation, such as several species of Bacteroides and Firmicutes phyla, which help produce short-chain fatty acids. These compounds have beneficial effects on gut health by reducing inflammation and helping to maintain a better homeostatic balance between an individual’s metabolism and immune system.
The main difference between vegetarians and vegans was the presence in vegetarians’ microbiomes of Streptococcus thermophilus, a bacterium found mainly in dairy products and used in the production of yogurt.
Dietary factors within each diet pattern, such as the amount of plant-based food, shape the microbiome more than the type of diet and are important for gut health, according to the authors. For example, by eating more plant-based foods, people with an omnivorous diet can bring the proportion of beneficial signature microbes in their microbiomes more in line with the levels in people who are vegan or vegetarian.
“Since our data showed that omnivores on average ingest significantly fewer healthy plant-based foods than vegetarians or vegans, optimizing the quality of omnivore diets by increasing dietary plant diversity could lead to better gut health,” they wrote.
The ultimate goal, Segata said, is “a precision nutrition approach that recommends foods based on the configuration of the microbiome of patients and of the aspects of the microbiome one wants to enhance. We are not there yet, but it is nonetheless important to know which foods are usually boosting which types of members of the gut microbiome.”
His team is currently analyzing changes in the gut microbiome induced by diet changes among thousands of participants in various cohorts.
“This is one of the next steps toward unraveling causality along the diet-microbiome-health axis, together with the cultivation of specific microbiome members of interest for potential prebiotic and probiotic strategies,” he said.
Conventional Dietary Advice for Now
The findings are consistent with those of previous studies, Jack Gilbert, MD, director of the Microbiome and Metagenomics Center at the University of California, San Diego, and president of Applied Microbiology International, Cambridge, England, said in an interview.
“Future research needs to focus on whether the gut microbial signature can predict those that develop cardiovascular disease in each cohort — ie, the n-of-1 studies, whereby a vegan develops cardiovascular disease, or a carnivore does not,” said Gilbert, who was not involved in the study.
With more data, he said, “we can also start examining these trends over time to understand what might be going on with these ‘oddballs.’ ”
“There is not much you can do with the ‘eat a healthy balanced diet’ routine,” he noted. “If I got a microbiome signature, I could potentially tell you what to eat to optimize your blood glucose trends and your lipid panels but not to handle long-term disease risk, yet. So sticking with the guideline-recommended dietary advice seems best, until we can provide more nuanced advice for the patient.
“Importantly, I would also like to see time-resolved data,” he added. “Signatures can fluctuate over time, even over days, and so collecting a few weeks of stool samples would help us to better align the microbiome signatures to clinical endpoints.”
Segata is a consultant to and receives options from ZOE. Gilbert is a member of the scientific advisory boards of Holobiome, BiomeSense, EcoBiomics Canadian Research Program, MASTER EU, Sun Genomics, and Oath; the editorial advisory board for The Scientist; and the external advisory board for the Binational Early Asthma & Microbiome Study. He is also an adviser for Bened Life.
A version of this article appeared on Medscape.com.
new research suggested.
For example, red meat was a strong driver of omnivore microbiomes, with corresponding signature microbes that are negatively correlated with host cardiometabolic health.
In contrast, the signature microbes found in vegans’ gut microbiomes were correlated with favorable cardiometabolic markers and were enriched in omnivores who ate more plant-based foods.
“From the viewpoint of the impact of diet on the gut microbiome, what seems to be more important is the diversity of healthy plant-based foods that are consumed,” principal author Nicola Segata, PhD, University of Trento in Italy, said in an interview. “Whether this comes within a vegan or an omnivore diet is less crucial, as long as there is no specific overconsumption of unhealthy food categories, such as red meat.”
Excluding broad categories of foods also can have consequences, he added. “For example, we saw that the exclusion of dairy fermented foods is associated with decreased presence of potentially probiotic microbes that are constitutive of such foods. Avoiding meat or dairy products does not necessarily have a positive effect if it does not come with a variety of quality plant-based products.”
The study was published online in Nature Microbiology.
Diet Tied to Microbial Signature
The researchers analyzed biological samples from 21,561 individuals across five multi-national cohorts to map how differences in diet patterns (omnivore, vegetarian, and vegan) are reflected in gut microbiomes.
They found that the three diet patterns are highly distinguishable by their microbial profiles and that each diet has corresponding unique signature microbes, including those tied to digestion of specific types of food and sometimes those derived from food itself.
The microbiomes of omnivores had an increased presence of bacteria associated with meat digestion, such as Alistipes putredinis, which is involved in protein fermentation. Omnivores also had more bacteria associated with both inflammatory bowel disease and increased colon cancer risk, such as Ruminococcus torques and Bilophila wadsworthia.
The microbiomes of vegans had an abundance of bacteria involved in fiber fermentation, such as several species of Bacteroides and Firmicutes phyla, which help produce short-chain fatty acids. These compounds have beneficial effects on gut health by reducing inflammation and helping to maintain a better homeostatic balance between an individual’s metabolism and immune system.
The main difference between vegetarians and vegans was the presence in vegetarians’ microbiomes of Streptococcus thermophilus, a bacterium found mainly in dairy products and used in the production of yogurt.
Dietary factors within each diet pattern, such as the amount of plant-based food, shape the microbiome more than the type of diet and are important for gut health, according to the authors. For example, by eating more plant-based foods, people with an omnivorous diet can bring the proportion of beneficial signature microbes in their microbiomes more in line with the levels in people who are vegan or vegetarian.
“Since our data showed that omnivores on average ingest significantly fewer healthy plant-based foods than vegetarians or vegans, optimizing the quality of omnivore diets by increasing dietary plant diversity could lead to better gut health,” they wrote.
The ultimate goal, Segata said, is “a precision nutrition approach that recommends foods based on the configuration of the microbiome of patients and of the aspects of the microbiome one wants to enhance. We are not there yet, but it is nonetheless important to know which foods are usually boosting which types of members of the gut microbiome.”
His team is currently analyzing changes in the gut microbiome induced by diet changes among thousands of participants in various cohorts.
“This is one of the next steps toward unraveling causality along the diet-microbiome-health axis, together with the cultivation of specific microbiome members of interest for potential prebiotic and probiotic strategies,” he said.
Conventional Dietary Advice for Now
The findings are consistent with those of previous studies, Jack Gilbert, MD, director of the Microbiome and Metagenomics Center at the University of California, San Diego, and president of Applied Microbiology International, Cambridge, England, said in an interview.
“Future research needs to focus on whether the gut microbial signature can predict those that develop cardiovascular disease in each cohort — ie, the n-of-1 studies, whereby a vegan develops cardiovascular disease, or a carnivore does not,” said Gilbert, who was not involved in the study.
With more data, he said, “we can also start examining these trends over time to understand what might be going on with these ‘oddballs.’ ”
“There is not much you can do with the ‘eat a healthy balanced diet’ routine,” he noted. “If I got a microbiome signature, I could potentially tell you what to eat to optimize your blood glucose trends and your lipid panels but not to handle long-term disease risk, yet. So sticking with the guideline-recommended dietary advice seems best, until we can provide more nuanced advice for the patient.
“Importantly, I would also like to see time-resolved data,” he added. “Signatures can fluctuate over time, even over days, and so collecting a few weeks of stool samples would help us to better align the microbiome signatures to clinical endpoints.”
Segata is a consultant to and receives options from ZOE. Gilbert is a member of the scientific advisory boards of Holobiome, BiomeSense, EcoBiomics Canadian Research Program, MASTER EU, Sun Genomics, and Oath; the editorial advisory board for The Scientist; and the external advisory board for the Binational Early Asthma & Microbiome Study. He is also an adviser for Bened Life.
A version of this article appeared on Medscape.com.
new research suggested.
For example, red meat was a strong driver of omnivore microbiomes, with corresponding signature microbes that are negatively correlated with host cardiometabolic health.
In contrast, the signature microbes found in vegans’ gut microbiomes were correlated with favorable cardiometabolic markers and were enriched in omnivores who ate more plant-based foods.
“From the viewpoint of the impact of diet on the gut microbiome, what seems to be more important is the diversity of healthy plant-based foods that are consumed,” principal author Nicola Segata, PhD, University of Trento in Italy, said in an interview. “Whether this comes within a vegan or an omnivore diet is less crucial, as long as there is no specific overconsumption of unhealthy food categories, such as red meat.”
Excluding broad categories of foods also can have consequences, he added. “For example, we saw that the exclusion of dairy fermented foods is associated with decreased presence of potentially probiotic microbes that are constitutive of such foods. Avoiding meat or dairy products does not necessarily have a positive effect if it does not come with a variety of quality plant-based products.”
The study was published online in Nature Microbiology.
Diet Tied to Microbial Signature
The researchers analyzed biological samples from 21,561 individuals across five multi-national cohorts to map how differences in diet patterns (omnivore, vegetarian, and vegan) are reflected in gut microbiomes.
They found that the three diet patterns are highly distinguishable by their microbial profiles and that each diet has corresponding unique signature microbes, including those tied to digestion of specific types of food and sometimes those derived from food itself.
The microbiomes of omnivores had an increased presence of bacteria associated with meat digestion, such as Alistipes putredinis, which is involved in protein fermentation. Omnivores also had more bacteria associated with both inflammatory bowel disease and increased colon cancer risk, such as Ruminococcus torques and Bilophila wadsworthia.
The microbiomes of vegans had an abundance of bacteria involved in fiber fermentation, such as several species of Bacteroides and Firmicutes phyla, which help produce short-chain fatty acids. These compounds have beneficial effects on gut health by reducing inflammation and helping to maintain a better homeostatic balance between an individual’s metabolism and immune system.
The main difference between vegetarians and vegans was the presence in vegetarians’ microbiomes of Streptococcus thermophilus, a bacterium found mainly in dairy products and used in the production of yogurt.
Dietary factors within each diet pattern, such as the amount of plant-based food, shape the microbiome more than the type of diet and are important for gut health, according to the authors. For example, by eating more plant-based foods, people with an omnivorous diet can bring the proportion of beneficial signature microbes in their microbiomes more in line with the levels in people who are vegan or vegetarian.
“Since our data showed that omnivores on average ingest significantly fewer healthy plant-based foods than vegetarians or vegans, optimizing the quality of omnivore diets by increasing dietary plant diversity could lead to better gut health,” they wrote.
The ultimate goal, Segata said, is “a precision nutrition approach that recommends foods based on the configuration of the microbiome of patients and of the aspects of the microbiome one wants to enhance. We are not there yet, but it is nonetheless important to know which foods are usually boosting which types of members of the gut microbiome.”
His team is currently analyzing changes in the gut microbiome induced by diet changes among thousands of participants in various cohorts.
“This is one of the next steps toward unraveling causality along the diet-microbiome-health axis, together with the cultivation of specific microbiome members of interest for potential prebiotic and probiotic strategies,” he said.
Conventional Dietary Advice for Now
The findings are consistent with those of previous studies, Jack Gilbert, MD, director of the Microbiome and Metagenomics Center at the University of California, San Diego, and president of Applied Microbiology International, Cambridge, England, said in an interview.
“Future research needs to focus on whether the gut microbial signature can predict those that develop cardiovascular disease in each cohort — ie, the n-of-1 studies, whereby a vegan develops cardiovascular disease, or a carnivore does not,” said Gilbert, who was not involved in the study.
With more data, he said, “we can also start examining these trends over time to understand what might be going on with these ‘oddballs.’ ”
“There is not much you can do with the ‘eat a healthy balanced diet’ routine,” he noted. “If I got a microbiome signature, I could potentially tell you what to eat to optimize your blood glucose trends and your lipid panels but not to handle long-term disease risk, yet. So sticking with the guideline-recommended dietary advice seems best, until we can provide more nuanced advice for the patient.
“Importantly, I would also like to see time-resolved data,” he added. “Signatures can fluctuate over time, even over days, and so collecting a few weeks of stool samples would help us to better align the microbiome signatures to clinical endpoints.”
Segata is a consultant to and receives options from ZOE. Gilbert is a member of the scientific advisory boards of Holobiome, BiomeSense, EcoBiomics Canadian Research Program, MASTER EU, Sun Genomics, and Oath; the editorial advisory board for The Scientist; and the external advisory board for the Binational Early Asthma & Microbiome Study. He is also an adviser for Bened Life.
A version of this article appeared on Medscape.com.
FROM NATURE MICROBIOLOGY
Managing GI and Liver Conditions During Pregnancy: New Guidance from AGA
according to a clinical practice update (CPU) from the American Gastroenterological Association.
Notably, procedures, medications, or other interventions intended to improve maternal health shouldn’t be withheld solely because the patient is pregnant, the authors wrote. Instead, treatments should be personalized based on a risk-benefit assessment.
“Pregnancy causes significant physiological changes that can affect the GI tract and liver function. Some common conditions — such as nausea, vomiting, gastroesophageal reflux disease (GERD), and constipation — may be exacerbated, and underlying GI or liver diseases can behave differently during pregnancy,” said lead author Shivangi Kothari, MD, associate professor of medicine and associate director of endoscopy at the University of Rochester Medical Center and Strong Memorial Hospital, both in Rochester, New York.
“These conditions can pose significant risks to both the mother and fetus, and their management requires a specialized, updated approach,” she said. “This clinical practice update stresses the need for coordinated, multidisciplinary care among obstetricians, gastroenterologists, hepatologists, and maternal-and-fetal medicine experts to ensure optimal outcomes, particularly in complex or high-risk cases.”
The update was published online in Gastroenterology.
Pregnancy-Related Concerns
The best path to optimal outcomes is to start early, the authors wrote. Before pregnancy, patients should consider preconception and contraceptive care counseling with a multidisciplinary team that can address GI and liver issues, especially among reproductive-age people who want to become pregnant.
Once pregnant, though, patients shouldn’t be deterred from receiving procedures, medications, or interventions just because they’re pregnant, the authors wrote. Instead, taking an individual approach will help clinicians decide what to do based on the risks and benefits.
At the beginning of pregnancy, early treatment of nausea and vomiting can reduce progression to hyperemesis gravidarum, the authors wrote. Stepwise treatment can include vitamin B6, doxylamine, hydration, and adequate nutrition, followed by ondansetron, metoclopramide, promethazine, and intravenous glucocorticoids in moderate to severe cases.
Constipation may also pose a problem because of hormonal, physiological, and medication-related changes. Treatment options can include dietary fiber, lactulose, and polyethylene glycol-based laxatives.
Patients with certain conditions — such as complex inflammatory bowel disease (IBD), advanced cirrhosis, or liver transplant — should work with a multidisciplinary team to coordinate birth, preferably in a tertiary care center, the authors wrote.
For patients with IBD, clinical remission helps to improve pregnancy outcomes, including before conception, during pregnancy, and throughout the postpartum period. Biologic agents should be used during pregnancy and postpartum, though methotrexate, thalidomide, and ozanimod should be stopped at least 6 months before conception.
For patients with chronic hepatitis B, serum hepatitis B virus DNA and liver biochemical levels should be tested. Patients with a serum level > 200,000 IU/mL during the third trimester should be considered for treatment with tenofovir disoproxil fumarate.
For patients on immunosuppressive therapy for chronic liver diseases or after liver transplantation, therapy should continue at the lowest effective dose. However, mycophenolate mofetil shouldn’t be administered during pregnancy.
Intrahepatic cholestasis of pregnancy may be diagnosed during the second or third trimester based on pruritus and a serum bile acid level > 10 μmol/L. Treatment should include oral ursodeoxycholic acid, with a total daily dose of 10-15 mg/kg.
Other pregnancy-related liver diseases — such as pre-eclampsia; hemolysis, elevated liver enzymes, and low platelets syndrome; and acute fatty liver of pregnancy — require careful birth planning and evaluation for possible liver transplantation. For certain high-risk patients, daily aspirin should start at week 12 of gestation.
In addition, elective endoscopic procedures should wait until after birth, and nonemergent but necessary procedures should be performed during the second trimester. Patients with cirrhosis should undergo evaluation for esophageal varices, and upper endoscopy should happen during the second trimester to guide beta-blocker therapy or endoscopic variceal litigation.
Endoscopic retrograde cholangiopancreatography can be performed for urgent indications, such as choledocholithiasis, cholangitis, and some gallstone pancreatitis cases, ideally during the second trimester.
Cholecystectomy is considered safe during pregnancy, with a laparoscopic approach as the standard of care regardless of trimester, though the second trimester is ideal.
Pregnancy-Related Updates in Practice
Ultimately, clinicians should familiarize themselves with the best practice advice to feel comfortable when counseling and managing pregnancy-related concerns, especially high-risk patients, said Eugenia Shmidt, MD, assistant professor of gastroenterology, hepatology, and nutrition, and founder of the IBD Preconception and Pregnancy Planning Clinic at the University of Minnesota, Minneapolis.
“Half of all patients with GI and liver disease are women, and oftentimes, they don’t have appropriate guidance regarding reproductive health in the context of their disease,” she said. “There exists a very large knowledge gap in this area, particularly because most clinical trials exclude pregnant people.”
Most importantly, the advice statements can guide practitioners on how to help pregnant patients make informed reproductive decisions, she added.
“This CPU makes it clear that preconception counseling and multidisciplinary care are key in optimizing reproductive health, regardless of the underlying GI or liver disease,” Shmidt said. “GI practitioners should be counseling women well in advance of pregnancy and recruiting all relevant stakeholders as early as possible, even prior to conception. This way, pregnancy care is not reactive, but instead proactive.”
The authors received no specific funding for this update. Kothari and Shmidt reported no relevant disclosures.
A version of this article appeared on Medscape.com.
according to a clinical practice update (CPU) from the American Gastroenterological Association.
Notably, procedures, medications, or other interventions intended to improve maternal health shouldn’t be withheld solely because the patient is pregnant, the authors wrote. Instead, treatments should be personalized based on a risk-benefit assessment.
“Pregnancy causes significant physiological changes that can affect the GI tract and liver function. Some common conditions — such as nausea, vomiting, gastroesophageal reflux disease (GERD), and constipation — may be exacerbated, and underlying GI or liver diseases can behave differently during pregnancy,” said lead author Shivangi Kothari, MD, associate professor of medicine and associate director of endoscopy at the University of Rochester Medical Center and Strong Memorial Hospital, both in Rochester, New York.
“These conditions can pose significant risks to both the mother and fetus, and their management requires a specialized, updated approach,” she said. “This clinical practice update stresses the need for coordinated, multidisciplinary care among obstetricians, gastroenterologists, hepatologists, and maternal-and-fetal medicine experts to ensure optimal outcomes, particularly in complex or high-risk cases.”
The update was published online in Gastroenterology.
Pregnancy-Related Concerns
The best path to optimal outcomes is to start early, the authors wrote. Before pregnancy, patients should consider preconception and contraceptive care counseling with a multidisciplinary team that can address GI and liver issues, especially among reproductive-age people who want to become pregnant.
Once pregnant, though, patients shouldn’t be deterred from receiving procedures, medications, or interventions just because they’re pregnant, the authors wrote. Instead, taking an individual approach will help clinicians decide what to do based on the risks and benefits.
At the beginning of pregnancy, early treatment of nausea and vomiting can reduce progression to hyperemesis gravidarum, the authors wrote. Stepwise treatment can include vitamin B6, doxylamine, hydration, and adequate nutrition, followed by ondansetron, metoclopramide, promethazine, and intravenous glucocorticoids in moderate to severe cases.
Constipation may also pose a problem because of hormonal, physiological, and medication-related changes. Treatment options can include dietary fiber, lactulose, and polyethylene glycol-based laxatives.
Patients with certain conditions — such as complex inflammatory bowel disease (IBD), advanced cirrhosis, or liver transplant — should work with a multidisciplinary team to coordinate birth, preferably in a tertiary care center, the authors wrote.
For patients with IBD, clinical remission helps to improve pregnancy outcomes, including before conception, during pregnancy, and throughout the postpartum period. Biologic agents should be used during pregnancy and postpartum, though methotrexate, thalidomide, and ozanimod should be stopped at least 6 months before conception.
For patients with chronic hepatitis B, serum hepatitis B virus DNA and liver biochemical levels should be tested. Patients with a serum level > 200,000 IU/mL during the third trimester should be considered for treatment with tenofovir disoproxil fumarate.
For patients on immunosuppressive therapy for chronic liver diseases or after liver transplantation, therapy should continue at the lowest effective dose. However, mycophenolate mofetil shouldn’t be administered during pregnancy.
Intrahepatic cholestasis of pregnancy may be diagnosed during the second or third trimester based on pruritus and a serum bile acid level > 10 μmol/L. Treatment should include oral ursodeoxycholic acid, with a total daily dose of 10-15 mg/kg.
Other pregnancy-related liver diseases — such as pre-eclampsia; hemolysis, elevated liver enzymes, and low platelets syndrome; and acute fatty liver of pregnancy — require careful birth planning and evaluation for possible liver transplantation. For certain high-risk patients, daily aspirin should start at week 12 of gestation.
In addition, elective endoscopic procedures should wait until after birth, and nonemergent but necessary procedures should be performed during the second trimester. Patients with cirrhosis should undergo evaluation for esophageal varices, and upper endoscopy should happen during the second trimester to guide beta-blocker therapy or endoscopic variceal litigation.
Endoscopic retrograde cholangiopancreatography can be performed for urgent indications, such as choledocholithiasis, cholangitis, and some gallstone pancreatitis cases, ideally during the second trimester.
Cholecystectomy is considered safe during pregnancy, with a laparoscopic approach as the standard of care regardless of trimester, though the second trimester is ideal.
Pregnancy-Related Updates in Practice
Ultimately, clinicians should familiarize themselves with the best practice advice to feel comfortable when counseling and managing pregnancy-related concerns, especially high-risk patients, said Eugenia Shmidt, MD, assistant professor of gastroenterology, hepatology, and nutrition, and founder of the IBD Preconception and Pregnancy Planning Clinic at the University of Minnesota, Minneapolis.
“Half of all patients with GI and liver disease are women, and oftentimes, they don’t have appropriate guidance regarding reproductive health in the context of their disease,” she said. “There exists a very large knowledge gap in this area, particularly because most clinical trials exclude pregnant people.”
Most importantly, the advice statements can guide practitioners on how to help pregnant patients make informed reproductive decisions, she added.
“This CPU makes it clear that preconception counseling and multidisciplinary care are key in optimizing reproductive health, regardless of the underlying GI or liver disease,” Shmidt said. “GI practitioners should be counseling women well in advance of pregnancy and recruiting all relevant stakeholders as early as possible, even prior to conception. This way, pregnancy care is not reactive, but instead proactive.”
The authors received no specific funding for this update. Kothari and Shmidt reported no relevant disclosures.
A version of this article appeared on Medscape.com.
according to a clinical practice update (CPU) from the American Gastroenterological Association.
Notably, procedures, medications, or other interventions intended to improve maternal health shouldn’t be withheld solely because the patient is pregnant, the authors wrote. Instead, treatments should be personalized based on a risk-benefit assessment.
“Pregnancy causes significant physiological changes that can affect the GI tract and liver function. Some common conditions — such as nausea, vomiting, gastroesophageal reflux disease (GERD), and constipation — may be exacerbated, and underlying GI or liver diseases can behave differently during pregnancy,” said lead author Shivangi Kothari, MD, associate professor of medicine and associate director of endoscopy at the University of Rochester Medical Center and Strong Memorial Hospital, both in Rochester, New York.
“These conditions can pose significant risks to both the mother and fetus, and their management requires a specialized, updated approach,” she said. “This clinical practice update stresses the need for coordinated, multidisciplinary care among obstetricians, gastroenterologists, hepatologists, and maternal-and-fetal medicine experts to ensure optimal outcomes, particularly in complex or high-risk cases.”
The update was published online in Gastroenterology.
Pregnancy-Related Concerns
The best path to optimal outcomes is to start early, the authors wrote. Before pregnancy, patients should consider preconception and contraceptive care counseling with a multidisciplinary team that can address GI and liver issues, especially among reproductive-age people who want to become pregnant.
Once pregnant, though, patients shouldn’t be deterred from receiving procedures, medications, or interventions just because they’re pregnant, the authors wrote. Instead, taking an individual approach will help clinicians decide what to do based on the risks and benefits.
At the beginning of pregnancy, early treatment of nausea and vomiting can reduce progression to hyperemesis gravidarum, the authors wrote. Stepwise treatment can include vitamin B6, doxylamine, hydration, and adequate nutrition, followed by ondansetron, metoclopramide, promethazine, and intravenous glucocorticoids in moderate to severe cases.
Constipation may also pose a problem because of hormonal, physiological, and medication-related changes. Treatment options can include dietary fiber, lactulose, and polyethylene glycol-based laxatives.
Patients with certain conditions — such as complex inflammatory bowel disease (IBD), advanced cirrhosis, or liver transplant — should work with a multidisciplinary team to coordinate birth, preferably in a tertiary care center, the authors wrote.
For patients with IBD, clinical remission helps to improve pregnancy outcomes, including before conception, during pregnancy, and throughout the postpartum period. Biologic agents should be used during pregnancy and postpartum, though methotrexate, thalidomide, and ozanimod should be stopped at least 6 months before conception.
For patients with chronic hepatitis B, serum hepatitis B virus DNA and liver biochemical levels should be tested. Patients with a serum level > 200,000 IU/mL during the third trimester should be considered for treatment with tenofovir disoproxil fumarate.
For patients on immunosuppressive therapy for chronic liver diseases or after liver transplantation, therapy should continue at the lowest effective dose. However, mycophenolate mofetil shouldn’t be administered during pregnancy.
Intrahepatic cholestasis of pregnancy may be diagnosed during the second or third trimester based on pruritus and a serum bile acid level > 10 μmol/L. Treatment should include oral ursodeoxycholic acid, with a total daily dose of 10-15 mg/kg.
Other pregnancy-related liver diseases — such as pre-eclampsia; hemolysis, elevated liver enzymes, and low platelets syndrome; and acute fatty liver of pregnancy — require careful birth planning and evaluation for possible liver transplantation. For certain high-risk patients, daily aspirin should start at week 12 of gestation.
In addition, elective endoscopic procedures should wait until after birth, and nonemergent but necessary procedures should be performed during the second trimester. Patients with cirrhosis should undergo evaluation for esophageal varices, and upper endoscopy should happen during the second trimester to guide beta-blocker therapy or endoscopic variceal litigation.
Endoscopic retrograde cholangiopancreatography can be performed for urgent indications, such as choledocholithiasis, cholangitis, and some gallstone pancreatitis cases, ideally during the second trimester.
Cholecystectomy is considered safe during pregnancy, with a laparoscopic approach as the standard of care regardless of trimester, though the second trimester is ideal.
Pregnancy-Related Updates in Practice
Ultimately, clinicians should familiarize themselves with the best practice advice to feel comfortable when counseling and managing pregnancy-related concerns, especially high-risk patients, said Eugenia Shmidt, MD, assistant professor of gastroenterology, hepatology, and nutrition, and founder of the IBD Preconception and Pregnancy Planning Clinic at the University of Minnesota, Minneapolis.
“Half of all patients with GI and liver disease are women, and oftentimes, they don’t have appropriate guidance regarding reproductive health in the context of their disease,” she said. “There exists a very large knowledge gap in this area, particularly because most clinical trials exclude pregnant people.”
Most importantly, the advice statements can guide practitioners on how to help pregnant patients make informed reproductive decisions, she added.
“This CPU makes it clear that preconception counseling and multidisciplinary care are key in optimizing reproductive health, regardless of the underlying GI or liver disease,” Shmidt said. “GI practitioners should be counseling women well in advance of pregnancy and recruiting all relevant stakeholders as early as possible, even prior to conception. This way, pregnancy care is not reactive, but instead proactive.”
The authors received no specific funding for this update. Kothari and Shmidt reported no relevant disclosures.
A version of this article appeared on Medscape.com.
FROM GASTROENTEROLOGY
Obesity Linked with Malignant Progression of Barrett’s Esophagus
A dose-response relationship exists between body mass index (BMI) and esophageal adenocarcinoma (EAC) or high-grade dysplasia (HGD), the authors found.
“Obesity has been implicated in the pathogenesis of many reflux-related esophageal disorders such as gastroesophageal reflux disease (GERD), BE, and EAC,” said senior author Leo Alexandre, MRCP, PhD, a clinical associate professor and member of the Norwich Epidemiology Centre at the University of East Anglia and gastroenterologist with the Norfolk & Norwich University Hospital NHS Foundation Trust, both in Norwich, England.
“Guidelines advocate obesity as a criterion for targeted screening for BE in patients with chronic reflux symptoms,” he said. “While obesity is a recognized risk factor for both BE and EAC, it’s been unclear whether obesity is a risk factor for malignant progression.”
The study was published in Clinical Gastroenterology and Hepatology.
Analyzing Risk
BE, which is the only recognized precursor lesion to EAC, is associated with a 30-fold increase in the incidence of the aggressive cancer. Typically, malignant progression occurs when nondysplastic BE epithelium progresses to low-grade dysplasia (LGD) and then HGD, followed by invasive adenocarcinoma.
Current guidelines suggest that patients with BE undergo endoscopic surveillance for early detection of adenocarcinoma. However, clinical risk factors could help with risk stratification and a personalized approach to long-term BE management, the authors wrote.
Alexandre and colleagues reviewed case-control or cohort studies that reported on the effect of BMI on the progression of nondysplastic BE or LGD to EAC, HGD, or esophageal cancer (EC). Then they estimated the dose-response relationship with a two-stage dose-response meta-analysis.
Overall, 20 observational studies reported data on 38,565 adult patients, including 1684 patients who were diagnosed with EAC, HGD, or EC. The studies enrolled patients between 1976 and 2019 and were published between 2005 and 2022. Most were based in Europe or the United States, and 74.4% of participants were men.
Among 12 cohort studies with 19,223 patients who had baseline nondysplastic BE or LGD, 816 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .03%.
Among eight cohort studies with 6647 male patients who had baseline nondysplastic BE or LGD, 555 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .02%.
In addition, among 1992 female patients with baseline nondysplastic BE or LGD, 110 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .01%, which wasn’t a significant difference compared with the progression rate among male patients.
Based on meta-analyses, obesity was associated with a 4% increase in the risk for malignant progression among patients with BE (unadjusted odds ratio, 1.04; 95% CI, 1.00-1.07; P < .001).
Notably, each 5 unit increase in BMI was associated with a 6% increase in the risk of developing HGD or EAC (adjusted odds ratio, 1.06; 95% CI, 1.02-1.10; P < .001).
“Although the exact mechanisms by which obesity promotes esophageal carcinogenesis is not fully understood, several possible mechanisms may explain it,” Alexandre said. “The most obvious pathologic link is via GERD, with the mechanical effect of visceral obesity promoting the GERD directly, and the sequence of Barrett’s dysplasia to cancer indirectly. In addition, it has been demonstrated in experimental studies that gastric acid and bile acid drive malignant changes in esophageal epithelium through stimulation of proliferation, inhibition of apoptosis, and generation of free radicals.”
Considering Risk
This study highlights the importance of recognizing the association between obesity and cancer risks, said Prateek Sharma, MD, professor of medicine and director of gastrointestinal training at the University of Kansas School of Medicine, Kansas City, Kansas.
Sharma, who wasn’t involved with this study, coauthored an American Gastroenterological Association technical review on the management of BE.
“Obesity is a known risk factor for esophageal adenocarcinoma and may be a modifiable risk factor,” he said. “Showing that BMI is related to neoplastic progression in Barrett’s esophagus may impact surveillance intervals.”
Future research should look at additional obesity-related factors, such as visceral obesity and malignant progression of BE, as well as whether diet, lifestyle, and bariatric interventions can reduce the risk for progression.
“The next steps also include plugging BMI into risk scores and risk stratification models to enable targeted surveillance among high-risk groups,” Sharma said.
One of the study coauthors received funding as a National Institute for Health Research Academic clinical fellow. No other funding sources were declared. Alexandre and Sharma reported no relevant disclosures.
A version of this article appeared on Medscape.com.
A dose-response relationship exists between body mass index (BMI) and esophageal adenocarcinoma (EAC) or high-grade dysplasia (HGD), the authors found.
“Obesity has been implicated in the pathogenesis of many reflux-related esophageal disorders such as gastroesophageal reflux disease (GERD), BE, and EAC,” said senior author Leo Alexandre, MRCP, PhD, a clinical associate professor and member of the Norwich Epidemiology Centre at the University of East Anglia and gastroenterologist with the Norfolk & Norwich University Hospital NHS Foundation Trust, both in Norwich, England.
“Guidelines advocate obesity as a criterion for targeted screening for BE in patients with chronic reflux symptoms,” he said. “While obesity is a recognized risk factor for both BE and EAC, it’s been unclear whether obesity is a risk factor for malignant progression.”
The study was published in Clinical Gastroenterology and Hepatology.
Analyzing Risk
BE, which is the only recognized precursor lesion to EAC, is associated with a 30-fold increase in the incidence of the aggressive cancer. Typically, malignant progression occurs when nondysplastic BE epithelium progresses to low-grade dysplasia (LGD) and then HGD, followed by invasive adenocarcinoma.
Current guidelines suggest that patients with BE undergo endoscopic surveillance for early detection of adenocarcinoma. However, clinical risk factors could help with risk stratification and a personalized approach to long-term BE management, the authors wrote.
Alexandre and colleagues reviewed case-control or cohort studies that reported on the effect of BMI on the progression of nondysplastic BE or LGD to EAC, HGD, or esophageal cancer (EC). Then they estimated the dose-response relationship with a two-stage dose-response meta-analysis.
Overall, 20 observational studies reported data on 38,565 adult patients, including 1684 patients who were diagnosed with EAC, HGD, or EC. The studies enrolled patients between 1976 and 2019 and were published between 2005 and 2022. Most were based in Europe or the United States, and 74.4% of participants were men.
Among 12 cohort studies with 19,223 patients who had baseline nondysplastic BE or LGD, 816 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .03%.
Among eight cohort studies with 6647 male patients who had baseline nondysplastic BE or LGD, 555 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .02%.
In addition, among 1992 female patients with baseline nondysplastic BE or LGD, 110 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .01%, which wasn’t a significant difference compared with the progression rate among male patients.
Based on meta-analyses, obesity was associated with a 4% increase in the risk for malignant progression among patients with BE (unadjusted odds ratio, 1.04; 95% CI, 1.00-1.07; P < .001).
Notably, each 5 unit increase in BMI was associated with a 6% increase in the risk of developing HGD or EAC (adjusted odds ratio, 1.06; 95% CI, 1.02-1.10; P < .001).
“Although the exact mechanisms by which obesity promotes esophageal carcinogenesis is not fully understood, several possible mechanisms may explain it,” Alexandre said. “The most obvious pathologic link is via GERD, with the mechanical effect of visceral obesity promoting the GERD directly, and the sequence of Barrett’s dysplasia to cancer indirectly. In addition, it has been demonstrated in experimental studies that gastric acid and bile acid drive malignant changes in esophageal epithelium through stimulation of proliferation, inhibition of apoptosis, and generation of free radicals.”
Considering Risk
This study highlights the importance of recognizing the association between obesity and cancer risks, said Prateek Sharma, MD, professor of medicine and director of gastrointestinal training at the University of Kansas School of Medicine, Kansas City, Kansas.
Sharma, who wasn’t involved with this study, coauthored an American Gastroenterological Association technical review on the management of BE.
“Obesity is a known risk factor for esophageal adenocarcinoma and may be a modifiable risk factor,” he said. “Showing that BMI is related to neoplastic progression in Barrett’s esophagus may impact surveillance intervals.”
Future research should look at additional obesity-related factors, such as visceral obesity and malignant progression of BE, as well as whether diet, lifestyle, and bariatric interventions can reduce the risk for progression.
“The next steps also include plugging BMI into risk scores and risk stratification models to enable targeted surveillance among high-risk groups,” Sharma said.
One of the study coauthors received funding as a National Institute for Health Research Academic clinical fellow. No other funding sources were declared. Alexandre and Sharma reported no relevant disclosures.
A version of this article appeared on Medscape.com.
A dose-response relationship exists between body mass index (BMI) and esophageal adenocarcinoma (EAC) or high-grade dysplasia (HGD), the authors found.
“Obesity has been implicated in the pathogenesis of many reflux-related esophageal disorders such as gastroesophageal reflux disease (GERD), BE, and EAC,” said senior author Leo Alexandre, MRCP, PhD, a clinical associate professor and member of the Norwich Epidemiology Centre at the University of East Anglia and gastroenterologist with the Norfolk & Norwich University Hospital NHS Foundation Trust, both in Norwich, England.
“Guidelines advocate obesity as a criterion for targeted screening for BE in patients with chronic reflux symptoms,” he said. “While obesity is a recognized risk factor for both BE and EAC, it’s been unclear whether obesity is a risk factor for malignant progression.”
The study was published in Clinical Gastroenterology and Hepatology.
Analyzing Risk
BE, which is the only recognized precursor lesion to EAC, is associated with a 30-fold increase in the incidence of the aggressive cancer. Typically, malignant progression occurs when nondysplastic BE epithelium progresses to low-grade dysplasia (LGD) and then HGD, followed by invasive adenocarcinoma.
Current guidelines suggest that patients with BE undergo endoscopic surveillance for early detection of adenocarcinoma. However, clinical risk factors could help with risk stratification and a personalized approach to long-term BE management, the authors wrote.
Alexandre and colleagues reviewed case-control or cohort studies that reported on the effect of BMI on the progression of nondysplastic BE or LGD to EAC, HGD, or esophageal cancer (EC). Then they estimated the dose-response relationship with a two-stage dose-response meta-analysis.
Overall, 20 observational studies reported data on 38,565 adult patients, including 1684 patients who were diagnosed with EAC, HGD, or EC. The studies enrolled patients between 1976 and 2019 and were published between 2005 and 2022. Most were based in Europe or the United States, and 74.4% of participants were men.
Among 12 cohort studies with 19,223 patients who had baseline nondysplastic BE or LGD, 816 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .03%.
Among eight cohort studies with 6647 male patients who had baseline nondysplastic BE or LGD, 555 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .02%.
In addition, among 1992 female patients with baseline nondysplastic BE or LGD, 110 progressed to EAC, HGD, or EC. The pooled annual rate of progression was .01%, which wasn’t a significant difference compared with the progression rate among male patients.
Based on meta-analyses, obesity was associated with a 4% increase in the risk for malignant progression among patients with BE (unadjusted odds ratio, 1.04; 95% CI, 1.00-1.07; P < .001).
Notably, each 5 unit increase in BMI was associated with a 6% increase in the risk of developing HGD or EAC (adjusted odds ratio, 1.06; 95% CI, 1.02-1.10; P < .001).
“Although the exact mechanisms by which obesity promotes esophageal carcinogenesis is not fully understood, several possible mechanisms may explain it,” Alexandre said. “The most obvious pathologic link is via GERD, with the mechanical effect of visceral obesity promoting the GERD directly, and the sequence of Barrett’s dysplasia to cancer indirectly. In addition, it has been demonstrated in experimental studies that gastric acid and bile acid drive malignant changes in esophageal epithelium through stimulation of proliferation, inhibition of apoptosis, and generation of free radicals.”
Considering Risk
This study highlights the importance of recognizing the association between obesity and cancer risks, said Prateek Sharma, MD, professor of medicine and director of gastrointestinal training at the University of Kansas School of Medicine, Kansas City, Kansas.
Sharma, who wasn’t involved with this study, coauthored an American Gastroenterological Association technical review on the management of BE.
“Obesity is a known risk factor for esophageal adenocarcinoma and may be a modifiable risk factor,” he said. “Showing that BMI is related to neoplastic progression in Barrett’s esophagus may impact surveillance intervals.”
Future research should look at additional obesity-related factors, such as visceral obesity and malignant progression of BE, as well as whether diet, lifestyle, and bariatric interventions can reduce the risk for progression.
“The next steps also include plugging BMI into risk scores and risk stratification models to enable targeted surveillance among high-risk groups,” Sharma said.
One of the study coauthors received funding as a National Institute for Health Research Academic clinical fellow. No other funding sources were declared. Alexandre and Sharma reported no relevant disclosures.
A version of this article appeared on Medscape.com.
FROM CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
AGA Clinical Practice Update: P-CABs Can Help When PPI Therapy Fails
, according to a recent clinical practice update from the American Gastroenterological Association (AGA).
However, P-CABs are recommended in place of proton pump inhibitors (PPIs) for most patients with Helicobacter pylori and other conditions where patients haven’t responded to PPIs.
“P-CABs are a newer medication class now available in the US, associated with more rapid, potent, and prolonged gastric acid inhibition than PPI formulations,” said lead author Amit Patel, MD, a gastroenterologist at the Duke University School of Medicine and Durham Veterans Affairs Medical Center, Durham, North Carolina.
“P-CABs have potentially significant clinical benefits in the management of Helicobacter pylori infection and GERD, particularly more severe erosive esophagitis,” he said. “Emerging data are affording additional insights into the clinical benefits of P-CABs in settings such as on-demand therapy for reflux-associated symptoms, bleeding gastroduodenal ulcers, and endoscopic eradication therapy for Barrett’s esophagus.”
The update was published in Gastroenterology .
P-CAB Developments
For most patients, PPIs and histamine-2 receptor antagonists remain the primary way to inhibit gastric acid secretion for common upper gastrointestinal conditions, the authors wrote. However, P-CABs such as vonoprazan and tegoprazan may provide relief when PPIs have limitations.
Unlike PPIs, P-CABs are considered acid-stable, don’t require premeal dosing, aren’t prodrugs, and don’t require conversion to an active form to provide pharmacologic effects. They tend to have longer half-lives and more rapid onset. Serum gastrin levels typically remain higher with P-CABs.
In terms of safety, randomized trial data indicate that P-CABs are generally well tolerated and have short-term and medium-term safety similar to PPIs. Due to potent acid suppression, enteric infection risks remain higher, though long-term safety data is needed, the authors wrote.
Overall, P-CABs appear to be equally as potent or more potent than PPIs, though more potent acid inhibition isn’t necessarily associated with better outcomes, the authors wrote. For most foregut acid-related disorders — such as heartburn and prevention of nonsteroidal anti-inflammatory drug–associated ulcers — P-CABs can help when patients fail PPI therapy.
In general, though, nonclinical factors related to cost, barriers to obtaining medication, and limited long-term safety data may outweigh the advantages of P-CABs, especially if clinical superiority isn’t yet known, the authors wrote.
For GERD, clinicians generally shouldn’t use P-CABs as first-line therapy for patients with uninvestigated heartburn symptoms or nonerosive reflux disease. However, P-CABs should be used for those with documented acid-related reflux who fail therapy with twice-daily PPIs. They may also be appropriate for on-demand heartburn therapy, although more evidence is needed.
For erosive esophagitis, P-CABs generally shouldn’t be used for milder cases but can be considered for patients with more severe cases that haven’t responded to PPIs, including refractory esophagitis.
For H pylori, P-CABs should be used in place of PPIs for eradication regimens, including among patients with clarithromycin-resistant strains. In contrast with most of the other indications in the update, the short-term duration of H pylori treatment reduced the authors’ concerns about P-CAB costs and safety.
For peptic ulcer disease, P-CABs generally shouldn’t be used as first-line treatment or prophylaxis. However, the rapid onset and potent acid inhibition could be useful for patients with bleeding gastroduodenal ulcers and high-risk stigmata.
“Emerging data will allow refinements in the populations and clinical settings for which P-CABs at various doses may be considered and advised — and may reveal more clinical scenarios in which they can provide meaningful benefit,” Patel said. “Further investigations, including additional populations and novel indicators, as well as evaluating long-term safety data and cost-effectiveness, are warranted, as P-CABs are incorporated more broadly into clinical practice worldwide.”
The authors received no specific funding for this update. Patel reported no relevant disclosures.
A version of this article appeared on Medscape.com.
, according to a recent clinical practice update from the American Gastroenterological Association (AGA).
However, P-CABs are recommended in place of proton pump inhibitors (PPIs) for most patients with Helicobacter pylori and other conditions where patients haven’t responded to PPIs.
“P-CABs are a newer medication class now available in the US, associated with more rapid, potent, and prolonged gastric acid inhibition than PPI formulations,” said lead author Amit Patel, MD, a gastroenterologist at the Duke University School of Medicine and Durham Veterans Affairs Medical Center, Durham, North Carolina.
“P-CABs have potentially significant clinical benefits in the management of Helicobacter pylori infection and GERD, particularly more severe erosive esophagitis,” he said. “Emerging data are affording additional insights into the clinical benefits of P-CABs in settings such as on-demand therapy for reflux-associated symptoms, bleeding gastroduodenal ulcers, and endoscopic eradication therapy for Barrett’s esophagus.”
The update was published in Gastroenterology .
P-CAB Developments
For most patients, PPIs and histamine-2 receptor antagonists remain the primary way to inhibit gastric acid secretion for common upper gastrointestinal conditions, the authors wrote. However, P-CABs such as vonoprazan and tegoprazan may provide relief when PPIs have limitations.
Unlike PPIs, P-CABs are considered acid-stable, don’t require premeal dosing, aren’t prodrugs, and don’t require conversion to an active form to provide pharmacologic effects. They tend to have longer half-lives and more rapid onset. Serum gastrin levels typically remain higher with P-CABs.
In terms of safety, randomized trial data indicate that P-CABs are generally well tolerated and have short-term and medium-term safety similar to PPIs. Due to potent acid suppression, enteric infection risks remain higher, though long-term safety data is needed, the authors wrote.
Overall, P-CABs appear to be equally as potent or more potent than PPIs, though more potent acid inhibition isn’t necessarily associated with better outcomes, the authors wrote. For most foregut acid-related disorders — such as heartburn and prevention of nonsteroidal anti-inflammatory drug–associated ulcers — P-CABs can help when patients fail PPI therapy.
In general, though, nonclinical factors related to cost, barriers to obtaining medication, and limited long-term safety data may outweigh the advantages of P-CABs, especially if clinical superiority isn’t yet known, the authors wrote.
For GERD, clinicians generally shouldn’t use P-CABs as first-line therapy for patients with uninvestigated heartburn symptoms or nonerosive reflux disease. However, P-CABs should be used for those with documented acid-related reflux who fail therapy with twice-daily PPIs. They may also be appropriate for on-demand heartburn therapy, although more evidence is needed.
For erosive esophagitis, P-CABs generally shouldn’t be used for milder cases but can be considered for patients with more severe cases that haven’t responded to PPIs, including refractory esophagitis.
For H pylori, P-CABs should be used in place of PPIs for eradication regimens, including among patients with clarithromycin-resistant strains. In contrast with most of the other indications in the update, the short-term duration of H pylori treatment reduced the authors’ concerns about P-CAB costs and safety.
For peptic ulcer disease, P-CABs generally shouldn’t be used as first-line treatment or prophylaxis. However, the rapid onset and potent acid inhibition could be useful for patients with bleeding gastroduodenal ulcers and high-risk stigmata.
“Emerging data will allow refinements in the populations and clinical settings for which P-CABs at various doses may be considered and advised — and may reveal more clinical scenarios in which they can provide meaningful benefit,” Patel said. “Further investigations, including additional populations and novel indicators, as well as evaluating long-term safety data and cost-effectiveness, are warranted, as P-CABs are incorporated more broadly into clinical practice worldwide.”
The authors received no specific funding for this update. Patel reported no relevant disclosures.
A version of this article appeared on Medscape.com.
, according to a recent clinical practice update from the American Gastroenterological Association (AGA).
However, P-CABs are recommended in place of proton pump inhibitors (PPIs) for most patients with Helicobacter pylori and other conditions where patients haven’t responded to PPIs.
“P-CABs are a newer medication class now available in the US, associated with more rapid, potent, and prolonged gastric acid inhibition than PPI formulations,” said lead author Amit Patel, MD, a gastroenterologist at the Duke University School of Medicine and Durham Veterans Affairs Medical Center, Durham, North Carolina.
“P-CABs have potentially significant clinical benefits in the management of Helicobacter pylori infection and GERD, particularly more severe erosive esophagitis,” he said. “Emerging data are affording additional insights into the clinical benefits of P-CABs in settings such as on-demand therapy for reflux-associated symptoms, bleeding gastroduodenal ulcers, and endoscopic eradication therapy for Barrett’s esophagus.”
The update was published in Gastroenterology .
P-CAB Developments
For most patients, PPIs and histamine-2 receptor antagonists remain the primary way to inhibit gastric acid secretion for common upper gastrointestinal conditions, the authors wrote. However, P-CABs such as vonoprazan and tegoprazan may provide relief when PPIs have limitations.
Unlike PPIs, P-CABs are considered acid-stable, don’t require premeal dosing, aren’t prodrugs, and don’t require conversion to an active form to provide pharmacologic effects. They tend to have longer half-lives and more rapid onset. Serum gastrin levels typically remain higher with P-CABs.
In terms of safety, randomized trial data indicate that P-CABs are generally well tolerated and have short-term and medium-term safety similar to PPIs. Due to potent acid suppression, enteric infection risks remain higher, though long-term safety data is needed, the authors wrote.
Overall, P-CABs appear to be equally as potent or more potent than PPIs, though more potent acid inhibition isn’t necessarily associated with better outcomes, the authors wrote. For most foregut acid-related disorders — such as heartburn and prevention of nonsteroidal anti-inflammatory drug–associated ulcers — P-CABs can help when patients fail PPI therapy.
In general, though, nonclinical factors related to cost, barriers to obtaining medication, and limited long-term safety data may outweigh the advantages of P-CABs, especially if clinical superiority isn’t yet known, the authors wrote.
For GERD, clinicians generally shouldn’t use P-CABs as first-line therapy for patients with uninvestigated heartburn symptoms or nonerosive reflux disease. However, P-CABs should be used for those with documented acid-related reflux who fail therapy with twice-daily PPIs. They may also be appropriate for on-demand heartburn therapy, although more evidence is needed.
For erosive esophagitis, P-CABs generally shouldn’t be used for milder cases but can be considered for patients with more severe cases that haven’t responded to PPIs, including refractory esophagitis.
For H pylori, P-CABs should be used in place of PPIs for eradication regimens, including among patients with clarithromycin-resistant strains. In contrast with most of the other indications in the update, the short-term duration of H pylori treatment reduced the authors’ concerns about P-CAB costs and safety.
For peptic ulcer disease, P-CABs generally shouldn’t be used as first-line treatment or prophylaxis. However, the rapid onset and potent acid inhibition could be useful for patients with bleeding gastroduodenal ulcers and high-risk stigmata.
“Emerging data will allow refinements in the populations and clinical settings for which P-CABs at various doses may be considered and advised — and may reveal more clinical scenarios in which they can provide meaningful benefit,” Patel said. “Further investigations, including additional populations and novel indicators, as well as evaluating long-term safety data and cost-effectiveness, are warranted, as P-CABs are incorporated more broadly into clinical practice worldwide.”
The authors received no specific funding for this update. Patel reported no relevant disclosures.
A version of this article appeared on Medscape.com.
FROM GASTROENTEROLOGY
Treating GERD: Lifestyle Modifications vs Medication
Dear colleagues,
Gastroesophageal reflux disease (GERD) is a common reason for referral to gastroenterology. It affects a broad cross-section of our population and is often managed through a combination of lifestyle modifications and proton pump inhibitors (PPIs). However,
While PPIs are highly effective, concerns about their potential side effects frequently make headlines. Moreover, the financial burden of lifelong PPI use is a growing consideration. In this issue of Perspectives, Dr. Brijesh B. Patel and Dr. Juan D. Gomez Cifuentes explore these questions. Dr. Gomez Cifuentes highlights the benefits of lifestyle changes and identifies which strategies have proved most effective in his practice. Dr. Patel examines the ubiquitous use of PPIs and the challenges of sustaining adherence to lifestyle modifications. We hope these discussions will spark new ideas for managing GERD in your own practice.
We also welcome your thoughts on this topic — join the conversation on X at @AGA_GIHN.
Gyanprakash A. Ketwaroo, MD, MSc, is associate professor of medicine, Yale University, New Haven, and chief of endoscopy at West Haven VA Medical Center, both in Connecticut. He is an associate editor for GI & Hepatology News.
Do Lifestyle Changes Still Apply in the Treatment of GERD?
BY JUAN D. GOMEZ CIFUENTES, MD
Lifestyle changes are an essential part of managing gastroesophageal reflux disease (GERD). Increasingly, patients are asking about non-medication approaches to control their symptoms. These lifestyle modifications can be categorized into four main areas: 1) Weight loss, the cornerstone intervention, with significant symptom improvement observed after losing as little as 1.7 BMI points. 2) Dietary modifications, which includes both the traditional avoidance of trigger foods and the newer focus on a diet low in simple carbohydrates. 3) Bedtime adjustments, strategies that include elevating the head of the bed, sleeping on the left side, using anti-reflux pillows, and avoiding late-night meals. 4) Tobacco cessation, a key measure for reducing GERD symptoms and promoting overall health. I routinely discuss these changes with my patients, as they not only help manage GERD but also foster healthy habits and have a positive impact beyond the gastrointestinal tract.
Weight loss is the most impactful lifestyle intervention for GERD. Research shows a clear linear improvement in symptoms with weight reduction. Traditionally, losing 10% of body weight is a widely accepted goal, extrapolated from other obesity-associated conditions. A reduction in 3.5 points of BMI led to significant symptom improvement in landmark studies but also a modest reduction of 1.7 BMI points has been shown to provide symptom relief.1 Abdominal circumference is another key metric used to track progress, as central obesity rather than BMI alone is strongly linked with GERD. Goals are typically set at less than 40 inches for men and 35 inches for women. Patients using GLP-1 agonists should be informed that these medications may temporarily worsen GERD symptoms due to delayed gastric emptying, however in the long-term these symptoms are expected to improve once significant weight loss is achieved.
Food triggers vary among individuals, with common culprits including fatty meals, spicy foods, chocolate, tomato sauce, citrus fruits, and carbonated beverages. Patients tend to overemphasize diet elimination based on triggers and engage in strict diets. Patients are frequently afraid of these foods causing direct damage to the esophageal mucosa but the hypothesis is that these triggers worsen GERD by increasing transient relaxations of the lower esophageal sphincter. The evidence behind this and diet elimination based on triggers has always been weak. In my practice, I encourage patients to follow a diet low in simple carbohydrates. Simple carbohydrates are present in highly processed food, the average western diet contains ~140 g/day. In a trial, a diet low in simple sugars (monosaccharides and disaccharides < 62 g/day) without reducing total daily calories, objectively improved total acid exposure time in pH study.2
Thanks to gravity, nocturnal GERD symptoms are the culprit of many restless nights in these patients. I recommend avoiding food 3 hours before lying down. Since the stomach empties approximately 90% of its contents after 4 hours, waiting longer is not recommended and may result in hunger, making it harder to fall asleep. Sleeping on the left side, which takes advantage of the gastric anatomy, has proved to objectively decrease nocturnal acid exposure time, though some patients may find it challenging to maintain this position all night.3
Elevating the head of the bed is another effective intervention, but it must involve raising the upper body from the waist. Patients should avoid stacking ordinary pillows as this will only elevate the neck and place the body in an unnatural position for sleeping. The most effective strategies are putting blocks/bricks under the feet of the bed, using a bed wedge between the mattress and the box spring or using an adjustable bed frame. There are two types of pillows that have been shown to improve nocturnal GERD symptoms. The classic wedge pillows and the more expensive Medcline reflux relief system®. The Medcline pillow has a dual mechanism that elevates the upper body but also keeps the body on the left side position.4
Tobacco cessation is strongly recommended. Tobacco worsens GERD symptoms by reducing the lower esophageal sphincter pressure and decreasing saliva production which is one of the key components of the normal esophageal acid barrier. Moreover, it is a known risk factor for esophageal cancer. Alcohol has a variety of negative health impacts and decreasing alcohol intake is advised; however, the link between alcohol and GERD symptoms is less robust, especially in patients with low occasional consumption.
In summary, lifestyle modifications play a pivotal role in managing GERD symptoms, offering patients effective, non-pharmacologic strategies to complement medical treatments. Weight loss remains the cornerstone, with even modest reductions in BMI showing significant symptom relief. Dietary adjustments, particularly adopting a low-simple-carbohydrate diet, provide an evidence-based approach. Various bedtime interventions are available to improve nocturnal GERD symptoms. Finally, tobacco cessation is essential, not only for GERD symptom relief but also for overall health. By integrating these lifestyle changes into their routine, patients can improve GERD symptoms while building healthy habits.
Dr. Gomez Cifuentes is vice-chair in the section of gastroenterology at Presbyterian Healthcare Services, Albuquerque, New Mexico. He declares no conflicts of interest.
References
1. Ness-Jensen E et al. Lifestyle Intervention in Gastroesophageal Reflux Disease. Clin Gastroenterol Hepatol. 2016 Feb;14(2):175-82.e1-3. doi: 10.1016/j.cgh.2015.04.176.
2. Gu C et al. The Effects of Modifying Amount and Type of Dietary Carbohydrate on Esophageal Acid Exposure Time and Esophageal Reflux Symptoms: A Randomized Controlled Trial. Am J Gastroenterol. 2022 Oct 1;117(10):1655-1667. doi: 10.14309/ajg.0000000000001889.
3. Schuitenmaker JM et al. Associations Between Sleep Position and Nocturnal Gastroesophageal Reflux: A Study Using Concurrent Monitoring of Sleep Position and Esophageal pH and Impedance. Am J Gastroenterol. 2022 Feb 1;117(2):346-351. doi: 10.14309/ajg.0000000000001588.
4. Person E et al. A Novel Sleep Positioning Device Reduces Gastroesophageal Reflux: A Randomized Controlled Trial. J Clin Gastroenterol. 2015 Sep;49(8):655-9. doi: 10.1097/MCG.0000000000000359.
Medical Therapy Is the Cornerstone of Effective GERD Treatment
BY BRIJESH B. PATEL, MD
Today, I saw Mr. S in the office for gastroesophageal reflux disease (GERD). He has been on a trial of proton pump inhibitors (PPIs) and has implemented several lifestyle modifications to manage his reflux. He shared his frustrations, saying, “Doctor, I’ve tried changing my diet, sleeping in a recliner, and adjusting the timing of my meals. I’m practically not enjoying food anymore, and these lifestyle changes have affected my quality of life. Despite all this, I still wake up in the middle of the night with a ‘horrible taste’ in my mouth, and it’s ruining my sleep.”
Later that day, during a discussion with my trainees, one posed an important question: “What about lifestyle measures in the treatment of GERD?” This is a common query in both clinical and academic settings. GERD, with a prevalence estimated at ~20%, is often underreported as many patients begin self-medicating with over-the-counter acid suppressive therapies before seeking medical care. For gastroenterologists, PPIs, histamine-2 receptor antagonists (H2RAs), and now potassium-competitive acid blockers (PCABs) form the cornerstone of GERD management.
When I lecture medical students, residents, and fellows about GERD, I emphasize a standard approach: initiating an 8- to 12-week trial of PPIs followed by reassessment. I also stress the importance of combining medical therapy with lifestyle measures. However, the question remains: How adherent are our patients to these lifestyle changes? Similarly, how effectively are trainees integrating the value of lifestyle modifications into their practice? As an academic gastroenterologist, I can teach the theory, but is it being translated into real-world patient care?
The advent of PPIs has been a game changer for managing GERD symptoms and preventing disease progression. PPIs are the backbone of treatment in both gastroenterology and primary care, and they have profoundly improved patients’ quality of life. Most of my patients who present with GERD — whether due to uncontrolled reflux or acid exposure — have already been on a trial of PPIs before seeing me. My role often involves optimizing their timing of PPI administration, addressing incorrect usage, and reinforcing the importance of adherence. In some cases, I incorporate H2RAs as adjunctive therapy for patients who fail to respond adequately to PPIs, particularly when objective disease activity is confirmed through pH studies. These studies also highlight how challenging it is for many patients to maintain a refluxogenic-free lifestyle.
Lifestyle modifications should supplement and support GERD management. Regardless of medical specialty, lifestyle measures should be the first line of treatment. However, adherence and effectiveness vary widely. In reality, achieving sustained weight loss, meal timing adjustments, and dietary modifications (e.g., eliminating trigger foods like red wine, chocolate, coffee, and tomato-based sauces) is a significant challenge for patients. While these measures can reduce the need for PPIs in some cases, they are rarely sufficient as standalone treatments. Until lifestyle modifications are consistently and sustainably incorporated into daily routines, acid-suppressive therapy will remain the mainstay of GERD management.
Turning to newer therapies, PCABs are now FDA-approved for treating GERD. Early efficacy data suggest that PCABs are non-inferior to PPIs, with promising results in managing LA Class C and D esophagitis and maintaining symptom-free days. However, like PPIs, PCABs are associated with potential adverse effects, including C. difficile colitis, impacts on bone health, renal impairment, and mineral deficiencies. While these risks must be carefully discussed with patients, the benefits of medical therapy far outweigh the risks, especially for those with erosive esophagitis, Barrett’s esophagus, or a high-risk profile for esophageal cancer. In such cases, medical therapies provide superior disease control compared to lifestyle measures, supported by both subjective and objective data.
Managing GERD requires a multipronged approach. Relying solely on lifestyle measures rarely provides complete benefit, as restrictive dietary regimens are difficult to sustain long term. Like many, I can maintain a restrictive diet temporarily but find it unsustainable over time. Conversely, adherence to daily or twice-daily medications tends to be much higher than compliance with multi-level lifestyle changes (e.g., restrictive diets, weight loss, and trigger-food avoidance).
Our therapeutic arsenal for GERD continues to expand, enabling more effective management of patients with uncontrolled acid reflux. While I will continue to counsel patients and educate trainees on the value of lifestyle modifications, I emphasize the importance of adherence to timely medical therapy — whether with PPIs, H2RAs, or PCABs — as the cornerstone of effective GERD treatment.
Dr. Patel is associate program director in the division of digestive diseases & nutrition, at USF Health, Tampa, Fla. He declares no conflicts of interest.
Dear colleagues,
Gastroesophageal reflux disease (GERD) is a common reason for referral to gastroenterology. It affects a broad cross-section of our population and is often managed through a combination of lifestyle modifications and proton pump inhibitors (PPIs). However,
While PPIs are highly effective, concerns about their potential side effects frequently make headlines. Moreover, the financial burden of lifelong PPI use is a growing consideration. In this issue of Perspectives, Dr. Brijesh B. Patel and Dr. Juan D. Gomez Cifuentes explore these questions. Dr. Gomez Cifuentes highlights the benefits of lifestyle changes and identifies which strategies have proved most effective in his practice. Dr. Patel examines the ubiquitous use of PPIs and the challenges of sustaining adherence to lifestyle modifications. We hope these discussions will spark new ideas for managing GERD in your own practice.
We also welcome your thoughts on this topic — join the conversation on X at @AGA_GIHN.
Gyanprakash A. Ketwaroo, MD, MSc, is associate professor of medicine, Yale University, New Haven, and chief of endoscopy at West Haven VA Medical Center, both in Connecticut. He is an associate editor for GI & Hepatology News.
Do Lifestyle Changes Still Apply in the Treatment of GERD?
BY JUAN D. GOMEZ CIFUENTES, MD
Lifestyle changes are an essential part of managing gastroesophageal reflux disease (GERD). Increasingly, patients are asking about non-medication approaches to control their symptoms. These lifestyle modifications can be categorized into four main areas: 1) Weight loss, the cornerstone intervention, with significant symptom improvement observed after losing as little as 1.7 BMI points. 2) Dietary modifications, which includes both the traditional avoidance of trigger foods and the newer focus on a diet low in simple carbohydrates. 3) Bedtime adjustments, strategies that include elevating the head of the bed, sleeping on the left side, using anti-reflux pillows, and avoiding late-night meals. 4) Tobacco cessation, a key measure for reducing GERD symptoms and promoting overall health. I routinely discuss these changes with my patients, as they not only help manage GERD but also foster healthy habits and have a positive impact beyond the gastrointestinal tract.
Weight loss is the most impactful lifestyle intervention for GERD. Research shows a clear linear improvement in symptoms with weight reduction. Traditionally, losing 10% of body weight is a widely accepted goal, extrapolated from other obesity-associated conditions. A reduction in 3.5 points of BMI led to significant symptom improvement in landmark studies but also a modest reduction of 1.7 BMI points has been shown to provide symptom relief.1 Abdominal circumference is another key metric used to track progress, as central obesity rather than BMI alone is strongly linked with GERD. Goals are typically set at less than 40 inches for men and 35 inches for women. Patients using GLP-1 agonists should be informed that these medications may temporarily worsen GERD symptoms due to delayed gastric emptying, however in the long-term these symptoms are expected to improve once significant weight loss is achieved.
Food triggers vary among individuals, with common culprits including fatty meals, spicy foods, chocolate, tomato sauce, citrus fruits, and carbonated beverages. Patients tend to overemphasize diet elimination based on triggers and engage in strict diets. Patients are frequently afraid of these foods causing direct damage to the esophageal mucosa but the hypothesis is that these triggers worsen GERD by increasing transient relaxations of the lower esophageal sphincter. The evidence behind this and diet elimination based on triggers has always been weak. In my practice, I encourage patients to follow a diet low in simple carbohydrates. Simple carbohydrates are present in highly processed food, the average western diet contains ~140 g/day. In a trial, a diet low in simple sugars (monosaccharides and disaccharides < 62 g/day) without reducing total daily calories, objectively improved total acid exposure time in pH study.2
Thanks to gravity, nocturnal GERD symptoms are the culprit of many restless nights in these patients. I recommend avoiding food 3 hours before lying down. Since the stomach empties approximately 90% of its contents after 4 hours, waiting longer is not recommended and may result in hunger, making it harder to fall asleep. Sleeping on the left side, which takes advantage of the gastric anatomy, has proved to objectively decrease nocturnal acid exposure time, though some patients may find it challenging to maintain this position all night.3
Elevating the head of the bed is another effective intervention, but it must involve raising the upper body from the waist. Patients should avoid stacking ordinary pillows as this will only elevate the neck and place the body in an unnatural position for sleeping. The most effective strategies are putting blocks/bricks under the feet of the bed, using a bed wedge between the mattress and the box spring or using an adjustable bed frame. There are two types of pillows that have been shown to improve nocturnal GERD symptoms. The classic wedge pillows and the more expensive Medcline reflux relief system®. The Medcline pillow has a dual mechanism that elevates the upper body but also keeps the body on the left side position.4
Tobacco cessation is strongly recommended. Tobacco worsens GERD symptoms by reducing the lower esophageal sphincter pressure and decreasing saliva production which is one of the key components of the normal esophageal acid barrier. Moreover, it is a known risk factor for esophageal cancer. Alcohol has a variety of negative health impacts and decreasing alcohol intake is advised; however, the link between alcohol and GERD symptoms is less robust, especially in patients with low occasional consumption.
In summary, lifestyle modifications play a pivotal role in managing GERD symptoms, offering patients effective, non-pharmacologic strategies to complement medical treatments. Weight loss remains the cornerstone, with even modest reductions in BMI showing significant symptom relief. Dietary adjustments, particularly adopting a low-simple-carbohydrate diet, provide an evidence-based approach. Various bedtime interventions are available to improve nocturnal GERD symptoms. Finally, tobacco cessation is essential, not only for GERD symptom relief but also for overall health. By integrating these lifestyle changes into their routine, patients can improve GERD symptoms while building healthy habits.
Dr. Gomez Cifuentes is vice-chair in the section of gastroenterology at Presbyterian Healthcare Services, Albuquerque, New Mexico. He declares no conflicts of interest.
References
1. Ness-Jensen E et al. Lifestyle Intervention in Gastroesophageal Reflux Disease. Clin Gastroenterol Hepatol. 2016 Feb;14(2):175-82.e1-3. doi: 10.1016/j.cgh.2015.04.176.
2. Gu C et al. The Effects of Modifying Amount and Type of Dietary Carbohydrate on Esophageal Acid Exposure Time and Esophageal Reflux Symptoms: A Randomized Controlled Trial. Am J Gastroenterol. 2022 Oct 1;117(10):1655-1667. doi: 10.14309/ajg.0000000000001889.
3. Schuitenmaker JM et al. Associations Between Sleep Position and Nocturnal Gastroesophageal Reflux: A Study Using Concurrent Monitoring of Sleep Position and Esophageal pH and Impedance. Am J Gastroenterol. 2022 Feb 1;117(2):346-351. doi: 10.14309/ajg.0000000000001588.
4. Person E et al. A Novel Sleep Positioning Device Reduces Gastroesophageal Reflux: A Randomized Controlled Trial. J Clin Gastroenterol. 2015 Sep;49(8):655-9. doi: 10.1097/MCG.0000000000000359.
Medical Therapy Is the Cornerstone of Effective GERD Treatment
BY BRIJESH B. PATEL, MD
Today, I saw Mr. S in the office for gastroesophageal reflux disease (GERD). He has been on a trial of proton pump inhibitors (PPIs) and has implemented several lifestyle modifications to manage his reflux. He shared his frustrations, saying, “Doctor, I’ve tried changing my diet, sleeping in a recliner, and adjusting the timing of my meals. I’m practically not enjoying food anymore, and these lifestyle changes have affected my quality of life. Despite all this, I still wake up in the middle of the night with a ‘horrible taste’ in my mouth, and it’s ruining my sleep.”
Later that day, during a discussion with my trainees, one posed an important question: “What about lifestyle measures in the treatment of GERD?” This is a common query in both clinical and academic settings. GERD, with a prevalence estimated at ~20%, is often underreported as many patients begin self-medicating with over-the-counter acid suppressive therapies before seeking medical care. For gastroenterologists, PPIs, histamine-2 receptor antagonists (H2RAs), and now potassium-competitive acid blockers (PCABs) form the cornerstone of GERD management.
When I lecture medical students, residents, and fellows about GERD, I emphasize a standard approach: initiating an 8- to 12-week trial of PPIs followed by reassessment. I also stress the importance of combining medical therapy with lifestyle measures. However, the question remains: How adherent are our patients to these lifestyle changes? Similarly, how effectively are trainees integrating the value of lifestyle modifications into their practice? As an academic gastroenterologist, I can teach the theory, but is it being translated into real-world patient care?
The advent of PPIs has been a game changer for managing GERD symptoms and preventing disease progression. PPIs are the backbone of treatment in both gastroenterology and primary care, and they have profoundly improved patients’ quality of life. Most of my patients who present with GERD — whether due to uncontrolled reflux or acid exposure — have already been on a trial of PPIs before seeing me. My role often involves optimizing their timing of PPI administration, addressing incorrect usage, and reinforcing the importance of adherence. In some cases, I incorporate H2RAs as adjunctive therapy for patients who fail to respond adequately to PPIs, particularly when objective disease activity is confirmed through pH studies. These studies also highlight how challenging it is for many patients to maintain a refluxogenic-free lifestyle.
Lifestyle modifications should supplement and support GERD management. Regardless of medical specialty, lifestyle measures should be the first line of treatment. However, adherence and effectiveness vary widely. In reality, achieving sustained weight loss, meal timing adjustments, and dietary modifications (e.g., eliminating trigger foods like red wine, chocolate, coffee, and tomato-based sauces) is a significant challenge for patients. While these measures can reduce the need for PPIs in some cases, they are rarely sufficient as standalone treatments. Until lifestyle modifications are consistently and sustainably incorporated into daily routines, acid-suppressive therapy will remain the mainstay of GERD management.
Turning to newer therapies, PCABs are now FDA-approved for treating GERD. Early efficacy data suggest that PCABs are non-inferior to PPIs, with promising results in managing LA Class C and D esophagitis and maintaining symptom-free days. However, like PPIs, PCABs are associated with potential adverse effects, including C. difficile colitis, impacts on bone health, renal impairment, and mineral deficiencies. While these risks must be carefully discussed with patients, the benefits of medical therapy far outweigh the risks, especially for those with erosive esophagitis, Barrett’s esophagus, or a high-risk profile for esophageal cancer. In such cases, medical therapies provide superior disease control compared to lifestyle measures, supported by both subjective and objective data.
Managing GERD requires a multipronged approach. Relying solely on lifestyle measures rarely provides complete benefit, as restrictive dietary regimens are difficult to sustain long term. Like many, I can maintain a restrictive diet temporarily but find it unsustainable over time. Conversely, adherence to daily or twice-daily medications tends to be much higher than compliance with multi-level lifestyle changes (e.g., restrictive diets, weight loss, and trigger-food avoidance).
Our therapeutic arsenal for GERD continues to expand, enabling more effective management of patients with uncontrolled acid reflux. While I will continue to counsel patients and educate trainees on the value of lifestyle modifications, I emphasize the importance of adherence to timely medical therapy — whether with PPIs, H2RAs, or PCABs — as the cornerstone of effective GERD treatment.
Dr. Patel is associate program director in the division of digestive diseases & nutrition, at USF Health, Tampa, Fla. He declares no conflicts of interest.
Dear colleagues,
Gastroesophageal reflux disease (GERD) is a common reason for referral to gastroenterology. It affects a broad cross-section of our population and is often managed through a combination of lifestyle modifications and proton pump inhibitors (PPIs). However,
While PPIs are highly effective, concerns about their potential side effects frequently make headlines. Moreover, the financial burden of lifelong PPI use is a growing consideration. In this issue of Perspectives, Dr. Brijesh B. Patel and Dr. Juan D. Gomez Cifuentes explore these questions. Dr. Gomez Cifuentes highlights the benefits of lifestyle changes and identifies which strategies have proved most effective in his practice. Dr. Patel examines the ubiquitous use of PPIs and the challenges of sustaining adherence to lifestyle modifications. We hope these discussions will spark new ideas for managing GERD in your own practice.
We also welcome your thoughts on this topic — join the conversation on X at @AGA_GIHN.
Gyanprakash A. Ketwaroo, MD, MSc, is associate professor of medicine, Yale University, New Haven, and chief of endoscopy at West Haven VA Medical Center, both in Connecticut. He is an associate editor for GI & Hepatology News.
Do Lifestyle Changes Still Apply in the Treatment of GERD?
BY JUAN D. GOMEZ CIFUENTES, MD
Lifestyle changes are an essential part of managing gastroesophageal reflux disease (GERD). Increasingly, patients are asking about non-medication approaches to control their symptoms. These lifestyle modifications can be categorized into four main areas: 1) Weight loss, the cornerstone intervention, with significant symptom improvement observed after losing as little as 1.7 BMI points. 2) Dietary modifications, which includes both the traditional avoidance of trigger foods and the newer focus on a diet low in simple carbohydrates. 3) Bedtime adjustments, strategies that include elevating the head of the bed, sleeping on the left side, using anti-reflux pillows, and avoiding late-night meals. 4) Tobacco cessation, a key measure for reducing GERD symptoms and promoting overall health. I routinely discuss these changes with my patients, as they not only help manage GERD but also foster healthy habits and have a positive impact beyond the gastrointestinal tract.
Weight loss is the most impactful lifestyle intervention for GERD. Research shows a clear linear improvement in symptoms with weight reduction. Traditionally, losing 10% of body weight is a widely accepted goal, extrapolated from other obesity-associated conditions. A reduction in 3.5 points of BMI led to significant symptom improvement in landmark studies but also a modest reduction of 1.7 BMI points has been shown to provide symptom relief.1 Abdominal circumference is another key metric used to track progress, as central obesity rather than BMI alone is strongly linked with GERD. Goals are typically set at less than 40 inches for men and 35 inches for women. Patients using GLP-1 agonists should be informed that these medications may temporarily worsen GERD symptoms due to delayed gastric emptying, however in the long-term these symptoms are expected to improve once significant weight loss is achieved.
Food triggers vary among individuals, with common culprits including fatty meals, spicy foods, chocolate, tomato sauce, citrus fruits, and carbonated beverages. Patients tend to overemphasize diet elimination based on triggers and engage in strict diets. Patients are frequently afraid of these foods causing direct damage to the esophageal mucosa but the hypothesis is that these triggers worsen GERD by increasing transient relaxations of the lower esophageal sphincter. The evidence behind this and diet elimination based on triggers has always been weak. In my practice, I encourage patients to follow a diet low in simple carbohydrates. Simple carbohydrates are present in highly processed food, the average western diet contains ~140 g/day. In a trial, a diet low in simple sugars (monosaccharides and disaccharides < 62 g/day) without reducing total daily calories, objectively improved total acid exposure time in pH study.2
Thanks to gravity, nocturnal GERD symptoms are the culprit of many restless nights in these patients. I recommend avoiding food 3 hours before lying down. Since the stomach empties approximately 90% of its contents after 4 hours, waiting longer is not recommended and may result in hunger, making it harder to fall asleep. Sleeping on the left side, which takes advantage of the gastric anatomy, has proved to objectively decrease nocturnal acid exposure time, though some patients may find it challenging to maintain this position all night.3
Elevating the head of the bed is another effective intervention, but it must involve raising the upper body from the waist. Patients should avoid stacking ordinary pillows as this will only elevate the neck and place the body in an unnatural position for sleeping. The most effective strategies are putting blocks/bricks under the feet of the bed, using a bed wedge between the mattress and the box spring or using an adjustable bed frame. There are two types of pillows that have been shown to improve nocturnal GERD symptoms. The classic wedge pillows and the more expensive Medcline reflux relief system®. The Medcline pillow has a dual mechanism that elevates the upper body but also keeps the body on the left side position.4
Tobacco cessation is strongly recommended. Tobacco worsens GERD symptoms by reducing the lower esophageal sphincter pressure and decreasing saliva production which is one of the key components of the normal esophageal acid barrier. Moreover, it is a known risk factor for esophageal cancer. Alcohol has a variety of negative health impacts and decreasing alcohol intake is advised; however, the link between alcohol and GERD symptoms is less robust, especially in patients with low occasional consumption.
In summary, lifestyle modifications play a pivotal role in managing GERD symptoms, offering patients effective, non-pharmacologic strategies to complement medical treatments. Weight loss remains the cornerstone, with even modest reductions in BMI showing significant symptom relief. Dietary adjustments, particularly adopting a low-simple-carbohydrate diet, provide an evidence-based approach. Various bedtime interventions are available to improve nocturnal GERD symptoms. Finally, tobacco cessation is essential, not only for GERD symptom relief but also for overall health. By integrating these lifestyle changes into their routine, patients can improve GERD symptoms while building healthy habits.
Dr. Gomez Cifuentes is vice-chair in the section of gastroenterology at Presbyterian Healthcare Services, Albuquerque, New Mexico. He declares no conflicts of interest.
References
1. Ness-Jensen E et al. Lifestyle Intervention in Gastroesophageal Reflux Disease. Clin Gastroenterol Hepatol. 2016 Feb;14(2):175-82.e1-3. doi: 10.1016/j.cgh.2015.04.176.
2. Gu C et al. The Effects of Modifying Amount and Type of Dietary Carbohydrate on Esophageal Acid Exposure Time and Esophageal Reflux Symptoms: A Randomized Controlled Trial. Am J Gastroenterol. 2022 Oct 1;117(10):1655-1667. doi: 10.14309/ajg.0000000000001889.
3. Schuitenmaker JM et al. Associations Between Sleep Position and Nocturnal Gastroesophageal Reflux: A Study Using Concurrent Monitoring of Sleep Position and Esophageal pH and Impedance. Am J Gastroenterol. 2022 Feb 1;117(2):346-351. doi: 10.14309/ajg.0000000000001588.
4. Person E et al. A Novel Sleep Positioning Device Reduces Gastroesophageal Reflux: A Randomized Controlled Trial. J Clin Gastroenterol. 2015 Sep;49(8):655-9. doi: 10.1097/MCG.0000000000000359.
Medical Therapy Is the Cornerstone of Effective GERD Treatment
BY BRIJESH B. PATEL, MD
Today, I saw Mr. S in the office for gastroesophageal reflux disease (GERD). He has been on a trial of proton pump inhibitors (PPIs) and has implemented several lifestyle modifications to manage his reflux. He shared his frustrations, saying, “Doctor, I’ve tried changing my diet, sleeping in a recliner, and adjusting the timing of my meals. I’m practically not enjoying food anymore, and these lifestyle changes have affected my quality of life. Despite all this, I still wake up in the middle of the night with a ‘horrible taste’ in my mouth, and it’s ruining my sleep.”
Later that day, during a discussion with my trainees, one posed an important question: “What about lifestyle measures in the treatment of GERD?” This is a common query in both clinical and academic settings. GERD, with a prevalence estimated at ~20%, is often underreported as many patients begin self-medicating with over-the-counter acid suppressive therapies before seeking medical care. For gastroenterologists, PPIs, histamine-2 receptor antagonists (H2RAs), and now potassium-competitive acid blockers (PCABs) form the cornerstone of GERD management.
When I lecture medical students, residents, and fellows about GERD, I emphasize a standard approach: initiating an 8- to 12-week trial of PPIs followed by reassessment. I also stress the importance of combining medical therapy with lifestyle measures. However, the question remains: How adherent are our patients to these lifestyle changes? Similarly, how effectively are trainees integrating the value of lifestyle modifications into their practice? As an academic gastroenterologist, I can teach the theory, but is it being translated into real-world patient care?
The advent of PPIs has been a game changer for managing GERD symptoms and preventing disease progression. PPIs are the backbone of treatment in both gastroenterology and primary care, and they have profoundly improved patients’ quality of life. Most of my patients who present with GERD — whether due to uncontrolled reflux or acid exposure — have already been on a trial of PPIs before seeing me. My role often involves optimizing their timing of PPI administration, addressing incorrect usage, and reinforcing the importance of adherence. In some cases, I incorporate H2RAs as adjunctive therapy for patients who fail to respond adequately to PPIs, particularly when objective disease activity is confirmed through pH studies. These studies also highlight how challenging it is for many patients to maintain a refluxogenic-free lifestyle.
Lifestyle modifications should supplement and support GERD management. Regardless of medical specialty, lifestyle measures should be the first line of treatment. However, adherence and effectiveness vary widely. In reality, achieving sustained weight loss, meal timing adjustments, and dietary modifications (e.g., eliminating trigger foods like red wine, chocolate, coffee, and tomato-based sauces) is a significant challenge for patients. While these measures can reduce the need for PPIs in some cases, they are rarely sufficient as standalone treatments. Until lifestyle modifications are consistently and sustainably incorporated into daily routines, acid-suppressive therapy will remain the mainstay of GERD management.
Turning to newer therapies, PCABs are now FDA-approved for treating GERD. Early efficacy data suggest that PCABs are non-inferior to PPIs, with promising results in managing LA Class C and D esophagitis and maintaining symptom-free days. However, like PPIs, PCABs are associated with potential adverse effects, including C. difficile colitis, impacts on bone health, renal impairment, and mineral deficiencies. While these risks must be carefully discussed with patients, the benefits of medical therapy far outweigh the risks, especially for those with erosive esophagitis, Barrett’s esophagus, or a high-risk profile for esophageal cancer. In such cases, medical therapies provide superior disease control compared to lifestyle measures, supported by both subjective and objective data.
Managing GERD requires a multipronged approach. Relying solely on lifestyle measures rarely provides complete benefit, as restrictive dietary regimens are difficult to sustain long term. Like many, I can maintain a restrictive diet temporarily but find it unsustainable over time. Conversely, adherence to daily or twice-daily medications tends to be much higher than compliance with multi-level lifestyle changes (e.g., restrictive diets, weight loss, and trigger-food avoidance).
Our therapeutic arsenal for GERD continues to expand, enabling more effective management of patients with uncontrolled acid reflux. While I will continue to counsel patients and educate trainees on the value of lifestyle modifications, I emphasize the importance of adherence to timely medical therapy — whether with PPIs, H2RAs, or PCABs — as the cornerstone of effective GERD treatment.
Dr. Patel is associate program director in the division of digestive diseases & nutrition, at USF Health, Tampa, Fla. He declares no conflicts of interest.
PPI-Responsive Disease a Subtype of EoE Rather Than GERD
, according to comparative proteomic analyses.
Notably, after PPI therapy, the protein profiles of responsive patients reverted and appeared similar to non-EoE patients, whereas the profiles of nonresponsive patients remained largely unchanged.
“Identifying protein biomarkers associated with PPI response may help distinguish EoE phenotypes and guide therapy selections,” said senior author Walter Chan, MD, AGAF, associate professor of medicine in the Division of Gastroenterology, Hepatology, and Endoscopy at Harvard Medical School and director of the center for gastrointestinal motility at Brigham and Women’s Hospital, Boston.
“These findings may provide the framework for developing protein biomarkers to assess response to therapy and monitor disease activity,” he added.
The study was published online in Gastroenterology.
Comparative Proteomic Analyses
Chan and colleagues conducted a prospective exploratory pilot study to identify the differences in esophageal protein profiles among PPI-responsive-EoE (PPI-R-EoE), PPI-nonresponsive-EoE (PPI-NR-EoE), and non-EoE controls using SOMAscan, a proteomics platform that allows simultaneous detection of 1305 human proteins.
The research team prospectively enrolled patients undergoing endoscopy for esophageal symptoms or for EoE follow-up, obtaining clinically indicated biopsies as well as extra samples from the midesophagus.
Patients who were diagnosed with EoE (at 15 or greater eosinophils per high-power field, or eos/hpf) were treated with 20 mg of omeprazole twice daily for 8 weeks, followed by repeat biopsies to assess treatment response.
Patients with histologic remission (fewer than 15 eos/hpf) were classified as PPI-R-EoE, whereas those with persistently active disease were classified as PPI-NR-EoE. Patients without EoE served as controls and were categorized as having erosive esophagitis (EE) or no esophagitis.
Overall, the study enrolled 32 patients, including 15 with PPI-R-EoE, eight with PPI-NR-EoE, three with EE, and six with no esophagitis. The demographics, symptoms, and endoscopic findings were similar between the PPI-R-EoE and PPI-NR-EoE patients.
At the index endoscopy, the PPI-R-EoE and PPI-NR-EoE patients had similar esophageal protein profiles, with only 20 proteins differentially expressed at a relaxed cutoff of P < .1. An analysis of the 20 proteins predicted lower expression of six proteins that may be associated with gastrointestinal inflammation in nonresponsive patients, including STAT1, STAT3, CFB, interleukin (IL)-17RA, TNFRSF1A, and SERPINA3.
In addition, 136 proteins — including 15 with corrected P < .05 — clearly discriminated PPI-R-EoE patients from non-EoE controls, and 255 proteins — including 249 with P < .05 — discriminated PPI-NR-EoE patients from controls. Both types of EoE patients had proteins associated with enhanced inflammation and vasculogenesis, as well as down-regulation of CRISP3 and DSG1 and upregulation of TNFAIP6.
The comparative analyses also showed that the follow-up biopsies of PPI-R-EoE patients had protein profiles that resembled non-EoE controls after PPI therapy.
“This further supports the hypothesis that despite the PPI response, PPI-R-EoE represents a subtype of EoE rather than gastroesophageal reflux disease (GERD),” Chan said.
Future EoE Considerations
Although most expressed proteins appeared similar between PPI-responsive and nonresponsive patients before treatment, a few proteins differed related to gastrointestinal inflammation, the study authors wrote, including some previously implicated in IL4 and IL13 inflammatory pathways.
“Further study of these proteins may provide insights into the EoE pathogenic pathway, explore their potential to predict PPI response at diagnosis, and identify possible therapeutic targets,” they wrote.
The authors pointed to the small study size as the primary limitation, noting that the pilot study was intended to explore the feasibility of using SomaScan to assess esophageal protein profiles in different EoE phenotypes. In the future, larger studies with more expansive candidate proteins could help characterize the differences and better identify specific proteins and pathways in EoE, they wrote.
“The takeaway is that PPI responsiveness does not distinguish EoE from GERD but rather PPI is a primary therapy for EoE independent of GERD,” said Marc Rothenberg, MD, director of allergy and immunology and director of the Cincinnati Center for Eosinophilic Disorders at Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio.
Rothenberg, who wasn’t involved with this study, has conducted transcriptome analyses of PPI-R-EoE, which showed PPI-reversible allergic inflammation.
“PPI-R-EoE and PPI-NR-EoE look the same at the molecular level,” he said. “After therapy, PPI-R-EoE normalizes, as per its definition.”
This study was supported by the Campaign Urging Research for Eosinophilic Disease Foundation Grant, the Kenneth and Louise Goldberg Junior Faculty Award, and a National Institutes of Health award. Chan declared advisory board positions with several pharmaceutical companies and Rothenberg reported no relevant disclosures.
A version of this article appeared on Medscape.com.
, according to comparative proteomic analyses.
Notably, after PPI therapy, the protein profiles of responsive patients reverted and appeared similar to non-EoE patients, whereas the profiles of nonresponsive patients remained largely unchanged.
“Identifying protein biomarkers associated with PPI response may help distinguish EoE phenotypes and guide therapy selections,” said senior author Walter Chan, MD, AGAF, associate professor of medicine in the Division of Gastroenterology, Hepatology, and Endoscopy at Harvard Medical School and director of the center for gastrointestinal motility at Brigham and Women’s Hospital, Boston.
“These findings may provide the framework for developing protein biomarkers to assess response to therapy and monitor disease activity,” he added.
The study was published online in Gastroenterology.
Comparative Proteomic Analyses
Chan and colleagues conducted a prospective exploratory pilot study to identify the differences in esophageal protein profiles among PPI-responsive-EoE (PPI-R-EoE), PPI-nonresponsive-EoE (PPI-NR-EoE), and non-EoE controls using SOMAscan, a proteomics platform that allows simultaneous detection of 1305 human proteins.
The research team prospectively enrolled patients undergoing endoscopy for esophageal symptoms or for EoE follow-up, obtaining clinically indicated biopsies as well as extra samples from the midesophagus.
Patients who were diagnosed with EoE (at 15 or greater eosinophils per high-power field, or eos/hpf) were treated with 20 mg of omeprazole twice daily for 8 weeks, followed by repeat biopsies to assess treatment response.
Patients with histologic remission (fewer than 15 eos/hpf) were classified as PPI-R-EoE, whereas those with persistently active disease were classified as PPI-NR-EoE. Patients without EoE served as controls and were categorized as having erosive esophagitis (EE) or no esophagitis.
Overall, the study enrolled 32 patients, including 15 with PPI-R-EoE, eight with PPI-NR-EoE, three with EE, and six with no esophagitis. The demographics, symptoms, and endoscopic findings were similar between the PPI-R-EoE and PPI-NR-EoE patients.
At the index endoscopy, the PPI-R-EoE and PPI-NR-EoE patients had similar esophageal protein profiles, with only 20 proteins differentially expressed at a relaxed cutoff of P < .1. An analysis of the 20 proteins predicted lower expression of six proteins that may be associated with gastrointestinal inflammation in nonresponsive patients, including STAT1, STAT3, CFB, interleukin (IL)-17RA, TNFRSF1A, and SERPINA3.
In addition, 136 proteins — including 15 with corrected P < .05 — clearly discriminated PPI-R-EoE patients from non-EoE controls, and 255 proteins — including 249 with P < .05 — discriminated PPI-NR-EoE patients from controls. Both types of EoE patients had proteins associated with enhanced inflammation and vasculogenesis, as well as down-regulation of CRISP3 and DSG1 and upregulation of TNFAIP6.
The comparative analyses also showed that the follow-up biopsies of PPI-R-EoE patients had protein profiles that resembled non-EoE controls after PPI therapy.
“This further supports the hypothesis that despite the PPI response, PPI-R-EoE represents a subtype of EoE rather than gastroesophageal reflux disease (GERD),” Chan said.
Future EoE Considerations
Although most expressed proteins appeared similar between PPI-responsive and nonresponsive patients before treatment, a few proteins differed related to gastrointestinal inflammation, the study authors wrote, including some previously implicated in IL4 and IL13 inflammatory pathways.
“Further study of these proteins may provide insights into the EoE pathogenic pathway, explore their potential to predict PPI response at diagnosis, and identify possible therapeutic targets,” they wrote.
The authors pointed to the small study size as the primary limitation, noting that the pilot study was intended to explore the feasibility of using SomaScan to assess esophageal protein profiles in different EoE phenotypes. In the future, larger studies with more expansive candidate proteins could help characterize the differences and better identify specific proteins and pathways in EoE, they wrote.
“The takeaway is that PPI responsiveness does not distinguish EoE from GERD but rather PPI is a primary therapy for EoE independent of GERD,” said Marc Rothenberg, MD, director of allergy and immunology and director of the Cincinnati Center for Eosinophilic Disorders at Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio.
Rothenberg, who wasn’t involved with this study, has conducted transcriptome analyses of PPI-R-EoE, which showed PPI-reversible allergic inflammation.
“PPI-R-EoE and PPI-NR-EoE look the same at the molecular level,” he said. “After therapy, PPI-R-EoE normalizes, as per its definition.”
This study was supported by the Campaign Urging Research for Eosinophilic Disease Foundation Grant, the Kenneth and Louise Goldberg Junior Faculty Award, and a National Institutes of Health award. Chan declared advisory board positions with several pharmaceutical companies and Rothenberg reported no relevant disclosures.
A version of this article appeared on Medscape.com.
, according to comparative proteomic analyses.
Notably, after PPI therapy, the protein profiles of responsive patients reverted and appeared similar to non-EoE patients, whereas the profiles of nonresponsive patients remained largely unchanged.
“Identifying protein biomarkers associated with PPI response may help distinguish EoE phenotypes and guide therapy selections,” said senior author Walter Chan, MD, AGAF, associate professor of medicine in the Division of Gastroenterology, Hepatology, and Endoscopy at Harvard Medical School and director of the center for gastrointestinal motility at Brigham and Women’s Hospital, Boston.
“These findings may provide the framework for developing protein biomarkers to assess response to therapy and monitor disease activity,” he added.
The study was published online in Gastroenterology.
Comparative Proteomic Analyses
Chan and colleagues conducted a prospective exploratory pilot study to identify the differences in esophageal protein profiles among PPI-responsive-EoE (PPI-R-EoE), PPI-nonresponsive-EoE (PPI-NR-EoE), and non-EoE controls using SOMAscan, a proteomics platform that allows simultaneous detection of 1305 human proteins.
The research team prospectively enrolled patients undergoing endoscopy for esophageal symptoms or for EoE follow-up, obtaining clinically indicated biopsies as well as extra samples from the midesophagus.
Patients who were diagnosed with EoE (at 15 or greater eosinophils per high-power field, or eos/hpf) were treated with 20 mg of omeprazole twice daily for 8 weeks, followed by repeat biopsies to assess treatment response.
Patients with histologic remission (fewer than 15 eos/hpf) were classified as PPI-R-EoE, whereas those with persistently active disease were classified as PPI-NR-EoE. Patients without EoE served as controls and were categorized as having erosive esophagitis (EE) or no esophagitis.
Overall, the study enrolled 32 patients, including 15 with PPI-R-EoE, eight with PPI-NR-EoE, three with EE, and six with no esophagitis. The demographics, symptoms, and endoscopic findings were similar between the PPI-R-EoE and PPI-NR-EoE patients.
At the index endoscopy, the PPI-R-EoE and PPI-NR-EoE patients had similar esophageal protein profiles, with only 20 proteins differentially expressed at a relaxed cutoff of P < .1. An analysis of the 20 proteins predicted lower expression of six proteins that may be associated with gastrointestinal inflammation in nonresponsive patients, including STAT1, STAT3, CFB, interleukin (IL)-17RA, TNFRSF1A, and SERPINA3.
In addition, 136 proteins — including 15 with corrected P < .05 — clearly discriminated PPI-R-EoE patients from non-EoE controls, and 255 proteins — including 249 with P < .05 — discriminated PPI-NR-EoE patients from controls. Both types of EoE patients had proteins associated with enhanced inflammation and vasculogenesis, as well as down-regulation of CRISP3 and DSG1 and upregulation of TNFAIP6.
The comparative analyses also showed that the follow-up biopsies of PPI-R-EoE patients had protein profiles that resembled non-EoE controls after PPI therapy.
“This further supports the hypothesis that despite the PPI response, PPI-R-EoE represents a subtype of EoE rather than gastroesophageal reflux disease (GERD),” Chan said.
Future EoE Considerations
Although most expressed proteins appeared similar between PPI-responsive and nonresponsive patients before treatment, a few proteins differed related to gastrointestinal inflammation, the study authors wrote, including some previously implicated in IL4 and IL13 inflammatory pathways.
“Further study of these proteins may provide insights into the EoE pathogenic pathway, explore their potential to predict PPI response at diagnosis, and identify possible therapeutic targets,” they wrote.
The authors pointed to the small study size as the primary limitation, noting that the pilot study was intended to explore the feasibility of using SomaScan to assess esophageal protein profiles in different EoE phenotypes. In the future, larger studies with more expansive candidate proteins could help characterize the differences and better identify specific proteins and pathways in EoE, they wrote.
“The takeaway is that PPI responsiveness does not distinguish EoE from GERD but rather PPI is a primary therapy for EoE independent of GERD,” said Marc Rothenberg, MD, director of allergy and immunology and director of the Cincinnati Center for Eosinophilic Disorders at Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio.
Rothenberg, who wasn’t involved with this study, has conducted transcriptome analyses of PPI-R-EoE, which showed PPI-reversible allergic inflammation.
“PPI-R-EoE and PPI-NR-EoE look the same at the molecular level,” he said. “After therapy, PPI-R-EoE normalizes, as per its definition.”
This study was supported by the Campaign Urging Research for Eosinophilic Disease Foundation Grant, the Kenneth and Louise Goldberg Junior Faculty Award, and a National Institutes of Health award. Chan declared advisory board positions with several pharmaceutical companies and Rothenberg reported no relevant disclosures.
A version of this article appeared on Medscape.com.
Biomarkers Predict Villous Atrophy in Potential Celiac Disease Patients
according to investigators.
Given that PCD patients present with positive serology and intact duodenal architecture, these findings may provide a much-needed tool for identifying patients who are more likely to benefit from early dietary interventions, lead author Renata Auricchio, MD, PhD, of the University of Naples Federico II, Italy, and colleagues reported.
“PCD offers the unique opportunity to observe the progression of gluten-induced tissue damage in celiac disease,” the investigators wrote in Gastroenterology. “These patients recognize gluten and produce specific autoantibodies, but have not developed intestinal damage.”
The study included 31 children with asymptomatic PCD who were eating a gluten-containing diet. Serum samples from each child were analyzed for the relative abundance of 92 inflammation-linked proteins using a proximity extension immunoassay. Statistical analyses, including partial least squares discriminant and linear discriminant analyses, were then applied to identify which proteins were associated with the development of VA.
After a mean follow-up period of 5.85 years, 14 participants developed VA (ie, celiac disease), while the remaining 17 remained asymptomatic.
Panel analysis revealed that specific inflammatory proteins, including interleukin (IL)–20, IL-2, sirtuin 2 (SIRT2), leukemia inhibitory factor (LIF), IL-22 receptor subunit a1, cystatin D (CST5), IL-17 receptor A, IL-15 receptor subunit a (RA), CUB domain–containing protein 1 (CDCP1), and IL-14, were 1.23- to 1.76-fold higher in children who developed VA. Among these, seven proteins — CDCP1, IL-2, LIF, IL10RA, SIRT2, CST5, and IL-4 — were able to significantly distinguish between symptomatic and asymptomatic cases in a linear discriminant model. This panel of seven proteins achieved a predictive accuracy of 96.8% in identifying children at risk of VA.
Additionally, bioinformatics pathway analysis confirmed that the broader set of proteins is involved in the positive regulation of JAK-STAT signaling (involving IL-22 receptor subunit a1, IL-4, IL-20, IL10RA, LIF, and IL-2), inflammatory responses (IL-4, IL-20, LIF, and IL-2), and processes such as tyrosine phosphorylation, leukocyte differentiation, IgG isotype switching, and protein phosphorylation regulation. These findings suggest that gluten-induced inflammation may already be active in early stages of the disease, including the initial phases of leukocyte differentiation, according to the investigators.
“Over a long follow-up on a gluten-containing diet, only 40% of these patients progressed to VA,” Dr. Auricchio and colleagues wrote. “Notably, 25%-30% of children with PCD even stop producing anti–tissue transglutaminase antibodies, and the others keep on producing autoantibodies but preserve a normal intestinal mucosa. Considering these data, the decision to address a patient with PCD on a gluten-free diet at time of diagnosis is quite critical.”
The researchers noted that this new model, with accuracy exceeding 95%, is well suited for routine use because of its practicality and reliability.
“Our previous model, based mainly on small intestinal mucosa features, moved a step toward the prediction of outcome but still required a mucosal biopsy, and the accuracy of prediction was not greater than 80%, which is somewhat uncertain for a lifelong clinical decision,” they wrote. In contrast, the present model “appears to be sufficient to immediately suggest a gluten-free diet in children with PCD, who are almost certainly committed to developing VA.”
The investigators called for long-term studies to validate their findings in other cohorts, including adult populations.This study was supported by the TIMID project and Inflammation in Human Early Life: Targeting Impacts on Life Course Health (INITIALISE) by the Horizon Europe Program of the European Union. The investigators disclosed no conflicts of interest.
Patients with positive celiac serologies but normal villous architecture on biopsy are considered to have potential celiac disease (PCD). While the prevalence of PCD is not well-established, it is estimated to be around 1%. This study by Auricchio and colleagues investigates seven serum proteomic biomarkers that could help predict whether asymptomatic patients with PCD are at risk of developing villous atrophy (VA).
The study also identifies specific inflammatory proteins present in PCD patients who are likely to develop VA. These biomarkers provide valuable insights into the pathogenesis of celiac disease and the development of VA in genetically predisposed individuals.
As celiac disease is increasingly diagnosed without biopsies, serum proteomic biomarkers could be crucial in identifying patients who may benefit from starting a gluten-free diet (GFD) earlier, potentially preventing complications. According to the European Society of Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) guidelines, children can be diagnosed with celiac disease if their tissue transglutaminase IgA level is 10 times the upper limit of normal, confirmed by a positive endomysial antibody test. However, this approach may lead to many patients committing to a lifelong GFD despite having only PCD, as biopsies may not have been performed. In this study, 60% of patients with PCD did not progress to VA, suggesting that biomarkers could help prevent unnecessary long-term GFD commitments.
Stephanie M. Moleski, MD, is the director of the Jefferson Celiac Center and associate professor in the division of gastroenterology at Thomas Jefferson University Hospital in Philadelphia. She reported no conflicts of interest.
Patients with positive celiac serologies but normal villous architecture on biopsy are considered to have potential celiac disease (PCD). While the prevalence of PCD is not well-established, it is estimated to be around 1%. This study by Auricchio and colleagues investigates seven serum proteomic biomarkers that could help predict whether asymptomatic patients with PCD are at risk of developing villous atrophy (VA).
The study also identifies specific inflammatory proteins present in PCD patients who are likely to develop VA. These biomarkers provide valuable insights into the pathogenesis of celiac disease and the development of VA in genetically predisposed individuals.
As celiac disease is increasingly diagnosed without biopsies, serum proteomic biomarkers could be crucial in identifying patients who may benefit from starting a gluten-free diet (GFD) earlier, potentially preventing complications. According to the European Society of Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) guidelines, children can be diagnosed with celiac disease if their tissue transglutaminase IgA level is 10 times the upper limit of normal, confirmed by a positive endomysial antibody test. However, this approach may lead to many patients committing to a lifelong GFD despite having only PCD, as biopsies may not have been performed. In this study, 60% of patients with PCD did not progress to VA, suggesting that biomarkers could help prevent unnecessary long-term GFD commitments.
Stephanie M. Moleski, MD, is the director of the Jefferson Celiac Center and associate professor in the division of gastroenterology at Thomas Jefferson University Hospital in Philadelphia. She reported no conflicts of interest.
Patients with positive celiac serologies but normal villous architecture on biopsy are considered to have potential celiac disease (PCD). While the prevalence of PCD is not well-established, it is estimated to be around 1%. This study by Auricchio and colleagues investigates seven serum proteomic biomarkers that could help predict whether asymptomatic patients with PCD are at risk of developing villous atrophy (VA).
The study also identifies specific inflammatory proteins present in PCD patients who are likely to develop VA. These biomarkers provide valuable insights into the pathogenesis of celiac disease and the development of VA in genetically predisposed individuals.
As celiac disease is increasingly diagnosed without biopsies, serum proteomic biomarkers could be crucial in identifying patients who may benefit from starting a gluten-free diet (GFD) earlier, potentially preventing complications. According to the European Society of Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) guidelines, children can be diagnosed with celiac disease if their tissue transglutaminase IgA level is 10 times the upper limit of normal, confirmed by a positive endomysial antibody test. However, this approach may lead to many patients committing to a lifelong GFD despite having only PCD, as biopsies may not have been performed. In this study, 60% of patients with PCD did not progress to VA, suggesting that biomarkers could help prevent unnecessary long-term GFD commitments.
Stephanie M. Moleski, MD, is the director of the Jefferson Celiac Center and associate professor in the division of gastroenterology at Thomas Jefferson University Hospital in Philadelphia. She reported no conflicts of interest.
according to investigators.
Given that PCD patients present with positive serology and intact duodenal architecture, these findings may provide a much-needed tool for identifying patients who are more likely to benefit from early dietary interventions, lead author Renata Auricchio, MD, PhD, of the University of Naples Federico II, Italy, and colleagues reported.
“PCD offers the unique opportunity to observe the progression of gluten-induced tissue damage in celiac disease,” the investigators wrote in Gastroenterology. “These patients recognize gluten and produce specific autoantibodies, but have not developed intestinal damage.”
The study included 31 children with asymptomatic PCD who were eating a gluten-containing diet. Serum samples from each child were analyzed for the relative abundance of 92 inflammation-linked proteins using a proximity extension immunoassay. Statistical analyses, including partial least squares discriminant and linear discriminant analyses, were then applied to identify which proteins were associated with the development of VA.
After a mean follow-up period of 5.85 years, 14 participants developed VA (ie, celiac disease), while the remaining 17 remained asymptomatic.
Panel analysis revealed that specific inflammatory proteins, including interleukin (IL)–20, IL-2, sirtuin 2 (SIRT2), leukemia inhibitory factor (LIF), IL-22 receptor subunit a1, cystatin D (CST5), IL-17 receptor A, IL-15 receptor subunit a (RA), CUB domain–containing protein 1 (CDCP1), and IL-14, were 1.23- to 1.76-fold higher in children who developed VA. Among these, seven proteins — CDCP1, IL-2, LIF, IL10RA, SIRT2, CST5, and IL-4 — were able to significantly distinguish between symptomatic and asymptomatic cases in a linear discriminant model. This panel of seven proteins achieved a predictive accuracy of 96.8% in identifying children at risk of VA.
Additionally, bioinformatics pathway analysis confirmed that the broader set of proteins is involved in the positive regulation of JAK-STAT signaling (involving IL-22 receptor subunit a1, IL-4, IL-20, IL10RA, LIF, and IL-2), inflammatory responses (IL-4, IL-20, LIF, and IL-2), and processes such as tyrosine phosphorylation, leukocyte differentiation, IgG isotype switching, and protein phosphorylation regulation. These findings suggest that gluten-induced inflammation may already be active in early stages of the disease, including the initial phases of leukocyte differentiation, according to the investigators.
“Over a long follow-up on a gluten-containing diet, only 40% of these patients progressed to VA,” Dr. Auricchio and colleagues wrote. “Notably, 25%-30% of children with PCD even stop producing anti–tissue transglutaminase antibodies, and the others keep on producing autoantibodies but preserve a normal intestinal mucosa. Considering these data, the decision to address a patient with PCD on a gluten-free diet at time of diagnosis is quite critical.”
The researchers noted that this new model, with accuracy exceeding 95%, is well suited for routine use because of its practicality and reliability.
“Our previous model, based mainly on small intestinal mucosa features, moved a step toward the prediction of outcome but still required a mucosal biopsy, and the accuracy of prediction was not greater than 80%, which is somewhat uncertain for a lifelong clinical decision,” they wrote. In contrast, the present model “appears to be sufficient to immediately suggest a gluten-free diet in children with PCD, who are almost certainly committed to developing VA.”
The investigators called for long-term studies to validate their findings in other cohorts, including adult populations.This study was supported by the TIMID project and Inflammation in Human Early Life: Targeting Impacts on Life Course Health (INITIALISE) by the Horizon Europe Program of the European Union. The investigators disclosed no conflicts of interest.
according to investigators.
Given that PCD patients present with positive serology and intact duodenal architecture, these findings may provide a much-needed tool for identifying patients who are more likely to benefit from early dietary interventions, lead author Renata Auricchio, MD, PhD, of the University of Naples Federico II, Italy, and colleagues reported.
“PCD offers the unique opportunity to observe the progression of gluten-induced tissue damage in celiac disease,” the investigators wrote in Gastroenterology. “These patients recognize gluten and produce specific autoantibodies, but have not developed intestinal damage.”
The study included 31 children with asymptomatic PCD who were eating a gluten-containing diet. Serum samples from each child were analyzed for the relative abundance of 92 inflammation-linked proteins using a proximity extension immunoassay. Statistical analyses, including partial least squares discriminant and linear discriminant analyses, were then applied to identify which proteins were associated with the development of VA.
After a mean follow-up period of 5.85 years, 14 participants developed VA (ie, celiac disease), while the remaining 17 remained asymptomatic.
Panel analysis revealed that specific inflammatory proteins, including interleukin (IL)–20, IL-2, sirtuin 2 (SIRT2), leukemia inhibitory factor (LIF), IL-22 receptor subunit a1, cystatin D (CST5), IL-17 receptor A, IL-15 receptor subunit a (RA), CUB domain–containing protein 1 (CDCP1), and IL-14, were 1.23- to 1.76-fold higher in children who developed VA. Among these, seven proteins — CDCP1, IL-2, LIF, IL10RA, SIRT2, CST5, and IL-4 — were able to significantly distinguish between symptomatic and asymptomatic cases in a linear discriminant model. This panel of seven proteins achieved a predictive accuracy of 96.8% in identifying children at risk of VA.
Additionally, bioinformatics pathway analysis confirmed that the broader set of proteins is involved in the positive regulation of JAK-STAT signaling (involving IL-22 receptor subunit a1, IL-4, IL-20, IL10RA, LIF, and IL-2), inflammatory responses (IL-4, IL-20, LIF, and IL-2), and processes such as tyrosine phosphorylation, leukocyte differentiation, IgG isotype switching, and protein phosphorylation regulation. These findings suggest that gluten-induced inflammation may already be active in early stages of the disease, including the initial phases of leukocyte differentiation, according to the investigators.
“Over a long follow-up on a gluten-containing diet, only 40% of these patients progressed to VA,” Dr. Auricchio and colleagues wrote. “Notably, 25%-30% of children with PCD even stop producing anti–tissue transglutaminase antibodies, and the others keep on producing autoantibodies but preserve a normal intestinal mucosa. Considering these data, the decision to address a patient with PCD on a gluten-free diet at time of diagnosis is quite critical.”
The researchers noted that this new model, with accuracy exceeding 95%, is well suited for routine use because of its practicality and reliability.
“Our previous model, based mainly on small intestinal mucosa features, moved a step toward the prediction of outcome but still required a mucosal biopsy, and the accuracy of prediction was not greater than 80%, which is somewhat uncertain for a lifelong clinical decision,” they wrote. In contrast, the present model “appears to be sufficient to immediately suggest a gluten-free diet in children with PCD, who are almost certainly committed to developing VA.”
The investigators called for long-term studies to validate their findings in other cohorts, including adult populations.This study was supported by the TIMID project and Inflammation in Human Early Life: Targeting Impacts on Life Course Health (INITIALISE) by the Horizon Europe Program of the European Union. The investigators disclosed no conflicts of interest.
FROM GASTROENTEROLOGY
Journal Highlights: Sept.-Oct. 2024
Upper GI
Levinthal DJ et al. AGA Clinical Practice Update on Diagnosis and Management of Cyclic Vomiting Syndrome: Commentary. Gastroenterology. 2024 Sep. doi: 10.1053/j.gastro.2024.05.031.
Geeratragool T et al. Comparison of Vonoprazan Versus Intravenous Proton Pump Inhibitor for Prevention of High-Risk Peptic Ulcers Rebleeding After Successful Endoscopic Hemostasis: A Multicenter Randomized Noninferiority Trial. Gastroenterology. 2024 Sep. doi: 10.1053/j.gastro.2024.03.036.
Goodoory VC et al. Effect of Brain-Gut Behavioral Treatments on Abdominal Pain in Irritable Bowel Syndrome: Systematic Review and Network Meta-Analysis. Gastroenterology. 2024 Oct. doi: 10.1053/j.gastro.2024.05.010.
Kurlander JE et al; Gastrointestinal Bleeding Working Group. Prescribing of Proton Pump Inhibitors for Prevention of Upper Gastrointestinal Bleeding in US Outpatient Visits. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.01.047.
Oliva S et al. Crafting a Therapeutic Pyramid for Eosinophilic Esophagitis in the Age of Biologics. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.04.020.
Lower GI
Redd WD et al. Follow-Up Colonoscopy for Detection of Missed Colorectal Cancer After Diverticulitis. Clin Gastroenterol Hepatol. 2024 Oct. doi: 10.1016/j.cgh.2024.03.036.
Peyrin-Biroulet L et al. Upadacitinib Achieves Clinical and Endoscopic Outcomes in Crohn’s Disease Regardless of Prior Biologic Exposure. Clin Gastroenterol Hepatol. 2024 Oct. doi: 10.1016/j.cgh.2024.02.026.
Chang PW et al. ChatGPT4 Outperforms Endoscopists for Determination of Postcolonoscopy Rescreening and Surveillance Recommendations. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.04.022.
Liver
Wang L et al. Association of GLP-1 Receptor Agonists and Hepatocellular Carcinoma Incidence and Hepatic Decompensation in Patients With Type 2 Diabetes. Gastroenterology. 2024 Sep. doi: 10.1053/j.gastro.2024.04.029.
Bajaj JS et al. Serum Ammonia Levels Do Not Correlate With Overt Hepatic Encephalopathy Severity in Hospitalized Patients With Cirrhosis. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.02.015.
Endoscopy
Steinbrück I, et al. Cold Versus Hot Snare Endoscopic Resection of Large Nonpedunculated Colorectal Polyps: Randomized Controlled German CHRONICLE Trial. Gastroenterology. 2024 Sep. doi: 10.1053/j.gastro.2024.05.013.
Misc.
Kothari S et al. AGA Clinical Practice Update on Pregnancy-Related Gastrointestinal and Liver Disease: Expert Review. Gastroenterology. 2024 Oct. doi: 10.1053/j.gastro.2024.06.014.
Chavannes M et al. AGA Clinical Practice Update on the Role of Intestinal Ultrasound in Inflammatory Bowel Disease: Commentary. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.04.039.
Dr. Trieu is assistant professor of medicine, interventional endoscopy, in the Division of Gastroenterology at Washington University in St. Louis School of Medicine, Missouri.
Upper GI
Levinthal DJ et al. AGA Clinical Practice Update on Diagnosis and Management of Cyclic Vomiting Syndrome: Commentary. Gastroenterology. 2024 Sep. doi: 10.1053/j.gastro.2024.05.031.
Geeratragool T et al. Comparison of Vonoprazan Versus Intravenous Proton Pump Inhibitor for Prevention of High-Risk Peptic Ulcers Rebleeding After Successful Endoscopic Hemostasis: A Multicenter Randomized Noninferiority Trial. Gastroenterology. 2024 Sep. doi: 10.1053/j.gastro.2024.03.036.
Goodoory VC et al. Effect of Brain-Gut Behavioral Treatments on Abdominal Pain in Irritable Bowel Syndrome: Systematic Review and Network Meta-Analysis. Gastroenterology. 2024 Oct. doi: 10.1053/j.gastro.2024.05.010.
Kurlander JE et al; Gastrointestinal Bleeding Working Group. Prescribing of Proton Pump Inhibitors for Prevention of Upper Gastrointestinal Bleeding in US Outpatient Visits. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.01.047.
Oliva S et al. Crafting a Therapeutic Pyramid for Eosinophilic Esophagitis in the Age of Biologics. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.04.020.
Lower GI
Redd WD et al. Follow-Up Colonoscopy for Detection of Missed Colorectal Cancer After Diverticulitis. Clin Gastroenterol Hepatol. 2024 Oct. doi: 10.1016/j.cgh.2024.03.036.
Peyrin-Biroulet L et al. Upadacitinib Achieves Clinical and Endoscopic Outcomes in Crohn’s Disease Regardless of Prior Biologic Exposure. Clin Gastroenterol Hepatol. 2024 Oct. doi: 10.1016/j.cgh.2024.02.026.
Chang PW et al. ChatGPT4 Outperforms Endoscopists for Determination of Postcolonoscopy Rescreening and Surveillance Recommendations. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.04.022.
Liver
Wang L et al. Association of GLP-1 Receptor Agonists and Hepatocellular Carcinoma Incidence and Hepatic Decompensation in Patients With Type 2 Diabetes. Gastroenterology. 2024 Sep. doi: 10.1053/j.gastro.2024.04.029.
Bajaj JS et al. Serum Ammonia Levels Do Not Correlate With Overt Hepatic Encephalopathy Severity in Hospitalized Patients With Cirrhosis. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.02.015.
Endoscopy
Steinbrück I, et al. Cold Versus Hot Snare Endoscopic Resection of Large Nonpedunculated Colorectal Polyps: Randomized Controlled German CHRONICLE Trial. Gastroenterology. 2024 Sep. doi: 10.1053/j.gastro.2024.05.013.
Misc.
Kothari S et al. AGA Clinical Practice Update on Pregnancy-Related Gastrointestinal and Liver Disease: Expert Review. Gastroenterology. 2024 Oct. doi: 10.1053/j.gastro.2024.06.014.
Chavannes M et al. AGA Clinical Practice Update on the Role of Intestinal Ultrasound in Inflammatory Bowel Disease: Commentary. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.04.039.
Dr. Trieu is assistant professor of medicine, interventional endoscopy, in the Division of Gastroenterology at Washington University in St. Louis School of Medicine, Missouri.
Upper GI
Levinthal DJ et al. AGA Clinical Practice Update on Diagnosis and Management of Cyclic Vomiting Syndrome: Commentary. Gastroenterology. 2024 Sep. doi: 10.1053/j.gastro.2024.05.031.
Geeratragool T et al. Comparison of Vonoprazan Versus Intravenous Proton Pump Inhibitor for Prevention of High-Risk Peptic Ulcers Rebleeding After Successful Endoscopic Hemostasis: A Multicenter Randomized Noninferiority Trial. Gastroenterology. 2024 Sep. doi: 10.1053/j.gastro.2024.03.036.
Goodoory VC et al. Effect of Brain-Gut Behavioral Treatments on Abdominal Pain in Irritable Bowel Syndrome: Systematic Review and Network Meta-Analysis. Gastroenterology. 2024 Oct. doi: 10.1053/j.gastro.2024.05.010.
Kurlander JE et al; Gastrointestinal Bleeding Working Group. Prescribing of Proton Pump Inhibitors for Prevention of Upper Gastrointestinal Bleeding in US Outpatient Visits. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.01.047.
Oliva S et al. Crafting a Therapeutic Pyramid for Eosinophilic Esophagitis in the Age of Biologics. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.04.020.
Lower GI
Redd WD et al. Follow-Up Colonoscopy for Detection of Missed Colorectal Cancer After Diverticulitis. Clin Gastroenterol Hepatol. 2024 Oct. doi: 10.1016/j.cgh.2024.03.036.
Peyrin-Biroulet L et al. Upadacitinib Achieves Clinical and Endoscopic Outcomes in Crohn’s Disease Regardless of Prior Biologic Exposure. Clin Gastroenterol Hepatol. 2024 Oct. doi: 10.1016/j.cgh.2024.02.026.
Chang PW et al. ChatGPT4 Outperforms Endoscopists for Determination of Postcolonoscopy Rescreening and Surveillance Recommendations. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.04.022.
Liver
Wang L et al. Association of GLP-1 Receptor Agonists and Hepatocellular Carcinoma Incidence and Hepatic Decompensation in Patients With Type 2 Diabetes. Gastroenterology. 2024 Sep. doi: 10.1053/j.gastro.2024.04.029.
Bajaj JS et al. Serum Ammonia Levels Do Not Correlate With Overt Hepatic Encephalopathy Severity in Hospitalized Patients With Cirrhosis. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.02.015.
Endoscopy
Steinbrück I, et al. Cold Versus Hot Snare Endoscopic Resection of Large Nonpedunculated Colorectal Polyps: Randomized Controlled German CHRONICLE Trial. Gastroenterology. 2024 Sep. doi: 10.1053/j.gastro.2024.05.013.
Misc.
Kothari S et al. AGA Clinical Practice Update on Pregnancy-Related Gastrointestinal and Liver Disease: Expert Review. Gastroenterology. 2024 Oct. doi: 10.1053/j.gastro.2024.06.014.
Chavannes M et al. AGA Clinical Practice Update on the Role of Intestinal Ultrasound in Inflammatory Bowel Disease: Commentary. Clin Gastroenterol Hepatol. 2024 Sep. doi: 10.1016/j.cgh.2024.04.039.
Dr. Trieu is assistant professor of medicine, interventional endoscopy, in the Division of Gastroenterology at Washington University in St. Louis School of Medicine, Missouri.
Endoscopic Sleeve Gastroplasty Yields Durable Weight Loss at 10 Years
PHILADELPHIA —
“The procedure is dependable and safe and should be considered among individuals who have not attained their desired results through lifestyle medications and those who are not eligible for or choose not to undergo bariatric procedures,” said Ali Lahooti, with the Department of Gastroenterology and Hepatology, Weill Cornell Medical College, New York City. He presented his research at the annual meeting of the American College of Gastroenterology (ACG).
Obesity is a growing global health challenge. Lifestyle modification as a standalone therapy has limited effectiveness achieving weight loss. Pharmacotherapies are more efficacious, but they’re also associated with higher costs of and risk for side effects, leading to lower rates of compliance, Lahooti explained.
Bariatric surgery remains the most effective therapy for management of obesity and improvement of comorbid conditions, yet < 1% of candidates undergo a surgical intervention either because of access, cost, or fear of the procedure.
“Endoscopic treatments for obesity, such as ESG, can potentially fill this gap by combining durable weight loss with lower risk and costs,” Lahooti said.
He and his colleagues assessed outcomes out to 10 years in 404 patients (mean age, 45 years; 76% women; mean body mass index, 37.3) who underwent ESG between 2013 and 2024 at a single large tertiary hospital.
Out of the 404 patients, 397, 335, 249, and 110 patients were eligible for 1-, 3-, 5-, and 10-year follow-up, with complete follow-up rates of 85%, 66%, 79%, and 62%, respectively.
The primary outcome was weight loss at 10 years after ESG reported at percent total body weight loss (%TBWL).
At 10 years, mean %TBWL (the primary outcome) was 10.5% — with 53% of patients maintaining at least 5% TBWL and 42% maintaining at least 10% weight loss, Lahooti reported.
ESG had a favorable safety profile; 20% of patients experienced mild abdominal pain, constipation, heartburn, and nausea after the procedure that typically resolved within 2 weeks of the procedure.
“There were a total of three moderate adverse events — two perigastric leaks, one repaired endoscopically, and another that only required antibiotics,” Lahooti reported. There were no severe or fatal adverse events.
About 11% of patients had endoscopic revision via retightening or resuturing at 10 years, the study team noted in their conference abstract.
Bariatric Surgery Remains Gold Standard
Lahooti shared that in his experience, some patients will need a revision at “about 40 months,” but at the same time, he’s seen some patients at 10 years “and their sutures are still in place.”
Session comoderator Shivangi Kothari, MD, with the Center for Advanced Therapeutic Endoscopy, University of Rochester Medical Center in New York, congratulated Lahooti for providing “robust” long-term data on ESG and said, “there is a need for more studies like this.”
In an interview, Ann M. Rogers, MD, president of the American Society for Metabolic and Bariatric Surgery, noted that bariatric surgery remains the “gold standard for weight loss and metabolic improvements,” with studies showing “around 30%” TWBL at 10 years, compared with about 10% at 10 years in this study.
Another key caveat, said Rogers, is that there are practical barriers to ESG; insurance typically does not cover the procedure because they view it as “cosmetic.”
The study had no commercial funding. Lahooti and Rogers had no relevant disclosures.
A version of this article first appeared on Medscape.com.
PHILADELPHIA —
“The procedure is dependable and safe and should be considered among individuals who have not attained their desired results through lifestyle medications and those who are not eligible for or choose not to undergo bariatric procedures,” said Ali Lahooti, with the Department of Gastroenterology and Hepatology, Weill Cornell Medical College, New York City. He presented his research at the annual meeting of the American College of Gastroenterology (ACG).
Obesity is a growing global health challenge. Lifestyle modification as a standalone therapy has limited effectiveness achieving weight loss. Pharmacotherapies are more efficacious, but they’re also associated with higher costs of and risk for side effects, leading to lower rates of compliance, Lahooti explained.
Bariatric surgery remains the most effective therapy for management of obesity and improvement of comorbid conditions, yet < 1% of candidates undergo a surgical intervention either because of access, cost, or fear of the procedure.
“Endoscopic treatments for obesity, such as ESG, can potentially fill this gap by combining durable weight loss with lower risk and costs,” Lahooti said.
He and his colleagues assessed outcomes out to 10 years in 404 patients (mean age, 45 years; 76% women; mean body mass index, 37.3) who underwent ESG between 2013 and 2024 at a single large tertiary hospital.
Out of the 404 patients, 397, 335, 249, and 110 patients were eligible for 1-, 3-, 5-, and 10-year follow-up, with complete follow-up rates of 85%, 66%, 79%, and 62%, respectively.
The primary outcome was weight loss at 10 years after ESG reported at percent total body weight loss (%TBWL).
At 10 years, mean %TBWL (the primary outcome) was 10.5% — with 53% of patients maintaining at least 5% TBWL and 42% maintaining at least 10% weight loss, Lahooti reported.
ESG had a favorable safety profile; 20% of patients experienced mild abdominal pain, constipation, heartburn, and nausea after the procedure that typically resolved within 2 weeks of the procedure.
“There were a total of three moderate adverse events — two perigastric leaks, one repaired endoscopically, and another that only required antibiotics,” Lahooti reported. There were no severe or fatal adverse events.
About 11% of patients had endoscopic revision via retightening or resuturing at 10 years, the study team noted in their conference abstract.
Bariatric Surgery Remains Gold Standard
Lahooti shared that in his experience, some patients will need a revision at “about 40 months,” but at the same time, he’s seen some patients at 10 years “and their sutures are still in place.”
Session comoderator Shivangi Kothari, MD, with the Center for Advanced Therapeutic Endoscopy, University of Rochester Medical Center in New York, congratulated Lahooti for providing “robust” long-term data on ESG and said, “there is a need for more studies like this.”
In an interview, Ann M. Rogers, MD, president of the American Society for Metabolic and Bariatric Surgery, noted that bariatric surgery remains the “gold standard for weight loss and metabolic improvements,” with studies showing “around 30%” TWBL at 10 years, compared with about 10% at 10 years in this study.
Another key caveat, said Rogers, is that there are practical barriers to ESG; insurance typically does not cover the procedure because they view it as “cosmetic.”
The study had no commercial funding. Lahooti and Rogers had no relevant disclosures.
A version of this article first appeared on Medscape.com.
PHILADELPHIA —
“The procedure is dependable and safe and should be considered among individuals who have not attained their desired results through lifestyle medications and those who are not eligible for or choose not to undergo bariatric procedures,” said Ali Lahooti, with the Department of Gastroenterology and Hepatology, Weill Cornell Medical College, New York City. He presented his research at the annual meeting of the American College of Gastroenterology (ACG).
Obesity is a growing global health challenge. Lifestyle modification as a standalone therapy has limited effectiveness achieving weight loss. Pharmacotherapies are more efficacious, but they’re also associated with higher costs of and risk for side effects, leading to lower rates of compliance, Lahooti explained.
Bariatric surgery remains the most effective therapy for management of obesity and improvement of comorbid conditions, yet < 1% of candidates undergo a surgical intervention either because of access, cost, or fear of the procedure.
“Endoscopic treatments for obesity, such as ESG, can potentially fill this gap by combining durable weight loss with lower risk and costs,” Lahooti said.
He and his colleagues assessed outcomes out to 10 years in 404 patients (mean age, 45 years; 76% women; mean body mass index, 37.3) who underwent ESG between 2013 and 2024 at a single large tertiary hospital.
Out of the 404 patients, 397, 335, 249, and 110 patients were eligible for 1-, 3-, 5-, and 10-year follow-up, with complete follow-up rates of 85%, 66%, 79%, and 62%, respectively.
The primary outcome was weight loss at 10 years after ESG reported at percent total body weight loss (%TBWL).
At 10 years, mean %TBWL (the primary outcome) was 10.5% — with 53% of patients maintaining at least 5% TBWL and 42% maintaining at least 10% weight loss, Lahooti reported.
ESG had a favorable safety profile; 20% of patients experienced mild abdominal pain, constipation, heartburn, and nausea after the procedure that typically resolved within 2 weeks of the procedure.
“There were a total of three moderate adverse events — two perigastric leaks, one repaired endoscopically, and another that only required antibiotics,” Lahooti reported. There were no severe or fatal adverse events.
About 11% of patients had endoscopic revision via retightening or resuturing at 10 years, the study team noted in their conference abstract.
Bariatric Surgery Remains Gold Standard
Lahooti shared that in his experience, some patients will need a revision at “about 40 months,” but at the same time, he’s seen some patients at 10 years “and their sutures are still in place.”
Session comoderator Shivangi Kothari, MD, with the Center for Advanced Therapeutic Endoscopy, University of Rochester Medical Center in New York, congratulated Lahooti for providing “robust” long-term data on ESG and said, “there is a need for more studies like this.”
In an interview, Ann M. Rogers, MD, president of the American Society for Metabolic and Bariatric Surgery, noted that bariatric surgery remains the “gold standard for weight loss and metabolic improvements,” with studies showing “around 30%” TWBL at 10 years, compared with about 10% at 10 years in this study.
Another key caveat, said Rogers, is that there are practical barriers to ESG; insurance typically does not cover the procedure because they view it as “cosmetic.”
The study had no commercial funding. Lahooti and Rogers had no relevant disclosures.
A version of this article first appeared on Medscape.com.
FROM ACG 2024