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Dietary Trial Shows Benefits of a Low Emulsifier Diet for Crohn’s Disease

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Tue, 07/22/2025 - 12:07

WASHINGTON, DC — A low-emulsifier-containing diet led to a threefold increased likelihood of improvement in symptoms of Crohn’s disease compared with an emulsifier-containing diet in a randomized double-blind dietary trial involving 154 patients with mildly active disease living across the United Kingdom.

The findings were reported at Gut Microbiota for Health (GMFH) World Summit 2025 by Benoit Chassaing, PhD, of the Institut Pasteur, Paris, France, whose research leading up to the trial has demonstrated that food additive emulsifiers —ubiquitous in processed foods — alter microbiota composition and lead to microbiota encroachment into the mucus layer of the gut and subsequent chronic gut inflammation.

Patients in the ADDapt trial, which was also reported in an abstract earlier this year at the European Crohn’s and Colitis Organization (ECCO) 2025 Congress, had a Crohn’s disease activity index (CDAI) of 150-250 and evidence of inflammation (faecal calprotectin (FCP) ≥ 150 µg/g or endoscopy/radiology). All “had been exposed in their regular diets to emulsifiers,” said Chassaing, a co-investigator, during a GMFH session on “Dietary Drivers of Health and Disease.”

They were randomized to either a low-emulsifier diet or to a low-emulsifier diet followed by emulsifier “resupplementation” — a design meant to “account for the very strong placebo effect that is always observed with dietary studies,” he said.

All patients received dietary counseling, a smart phone app and barcode scan to support shopping, and weekly support. They also received supermarket foods for 25% of their needs that were either free of emulsifiers or contained emulsifiers, and they were provided three snacks per day that were emulsifier-free or contained carrageenan, carboxymethycellulse (CMC), and polysorbate-80 (P80) — dietary emulsifiers that are commonly added to processed foods to enhance texture and extend shelf-life.

In the intention-to-treat (ITT) analysis, 49% of patients in the intervention group reached the primary endpoint of a 70-point reduction or more in CDAI response after 8 weeks compared with 31% of those in the control group (P = .019), with an adjusted relative risk of response of 3.1 (P = .003), Chassaing shared at the GMFH meeting, convened by the American Gastroenterological Association and the European Society of Neurogastroenterology and Motility.

In the per-protocol analysis (n = 119), 61% and 47% of patients in the intervention and control groups, respectively, reached the primary outcome of CDAI response, with an adjusted relative risk of response of 3.0 (P = .018), he said.

Secondary endpoints included CDAI remission at 24 weeks, and according to the abstract for the ECCO Congress, in the ITT analysis, patients in the intervention group were more than twice as likely to experience remission.

Chassaing noted at the GMFH meeting that as part of the study, he and coinvestigators have been investigating the participants’ gut microbiota with metagenomic analyses. The study was led by Kevin Whelan, PhD, head of the Department of Nutritional Sciences at King’s College London, London, England.

 

Can Emulsifier-Sensitive Individuals Be Identified?

In murine model research 10 years ago, Chassaing showed that the administration of CMC and P80 results in microbiota encroachment into the mucus layer of the gut, alterations in microbiota composition — including an increase in bacteria that produce pro-inflammatory flagellin — and development of chronic inflammation.

Wild-type mice treated with these compounds developed metabolic disease, and mice that were modified to be predisposed to colitis had a higher incidence of robust colitis. Moreover, fecal transplantation from emulsifier-treated mice to germ-free mice reproduced these changes, “clearly suggesting that the microbiome itself is sufficient to drive chronic inflammation,” he said.

In recent years, in humans, analyses from the large French NutriNet-Sante prospective cohort study have shown associations between exposure to food additive emulsifiers and the risk for cardiovascular disease, the risk for cancer (overall, breast, and prostate), and the risk for type 2 diabetes.

But to explore causality and better understand the mechanisms of emulsifier-driven changes on the microbiota, Chassaing and his colleagues also launched the FRESH study (Functional Research on Emulsifier in Humans), a double-blind randomized controlled-feeding study of the emulsifier CMC. For 11 days, nine healthy patients consumed an emulsifier-free diet and 11 consumed an identical diet enriched with 15 g/d of CMC.

Patients on the CMC-containing diet had reduced microbiota diversity and depletions of an array of microbiota-related metabolites, but only a small subset had profound alterations in microbiota composition and increased microbiota encroachment into the mucus layer. “Some seemed to be resistant to CMC-induced microbiota encroachment, while some were highly susceptible,” Chassaing said.

The pilot study raised the question, he said, of whether there is an “infectivity component” — some kind of “sensitive” gut microbiota composition — that may be associated with dietary emulsifier-driven inflammation and disease.

In other murine research, Chassaing and his team found that germ-free mice colonized with Crohn’s disease-associated adherent-invasive E coli (AIEC) and subsequently given CMC or P80 developed chronic inflammation and metabolic dysregulation, “clearly demonstrating that you can convert resistant mice to sensitive mice just by adding one bacteria to the ecosystem,” he said. “The presence of AIEC alone was sufficient to drive the detrimental effects of dietary emulsifiers.”

(In vitro research with transcriptomic analysis then showed that the emulsifiers directly elicit AIEC virulence gene expression, Chassaing and his coauthors wrote in their 2020 paper, facilitating AIEC’s “penetration of the mucus layer and adherence to epithelial cells and resulting in activation of host pro-inflammatory signaling.”)

“We don’t think it’s solely the AIEC bacteria that will drive emulsifier sensitivity, though…we think it’s more complex,” Chassaing said at the meeting. Overall, the findings raise the question of whether emulsifier-sensitive individuals can be identified.

This, he said, is one of his most recent research questions. His lab has led the development of an in vitro microbiota model built to predict an individual’s sensitivity to emulsifiers. In a study published in April, the model recapitulated the differential CMC sensitivity observed in the earlier FRESH study, suggesting that an individual’s sensitivity to emulsifiers can indeed be predicted by examining their baseline microbiota.

 

Interpreting the Epidemiology

Chassaing’s research arch illustrates the synergy between epidemiological research, basic/translational research, and clinical interventional research that’s needed to understand the diet-microbiome intersection in inflammatory bowel disease, said Ashwin Ananthakrishnan, MBBS, MPH, AGAF, associate professor of medicine at Massachusetts General Hospital, Boston, in an interview at the meeting.

“It’s a good example of how to really span the spectrum, starting from the big picture and going deeper to understand mechanisms, and starting from mechanisms and expanding it out,” Ananthakrishnan said.

In his own talk about research on IBD, Ananthakrishnan said that epidemiological data have shown over the past 10-15 years that total dietary fiber is inversely associated with the risk for Crohn’s disease (with the strongest associations with fiber from fruits and vegetables). Studies have also shown that a higher intake of polyunsaturated fatty acids is associated with a lower risk for ulcerative colitis, whereas “an n-6-fatty acid-rich diet is associated with a higher risk of ulcerative colitis,” he said.

Dietary cohort studies, meanwhile, have shed light on the influence of dietary patterns — such as the Mediterranean diet and diets with high inflammatory potential—on IBD. A diet rich in ultra-processed foods has also been shown in a prospective cohort study to be associated with a higher risk for Crohn’s disease, with certain categories of ultra-processed foods (eg, breads and breakfast foods) having the strongest associations.

Such studies are limited in part, however, by inadequate assessment of potentially relevant variables such as emulsifiers, preservatives, and how the food is processed, he said.

And in interpreting the epidemiological research on fiber and IBD, for instance, one must appreciate that “there are a number of mechanisms by which fiber is impactful…there’s a big picture to look at,” Ananthakrishnan said. Fiber “can affect the microbiome, clearly, it can affect the gut barrier, and it can affect bile acids, and there are detailed translational studies in support of each of these.”

But there are other constituents of fruits and vegetables “that could potentially influence disease risk, such as AhR ligands and polyphenols,” he said. “And importantly, people not eating a lot of fiber may be eating a lot of ultra-processed foods.”

Most interventional studies of fiber have not shown a benefit of a high-fiber diet, Ananthakrishnan said, but there are multiple possible reasons and factors at play, including potential population differences (eg, in inflammatory status or baseline microbiota), shortcomings of the interventions, and potentially inaccurate outcomes.

Abigail Johnson, PhD, RDN, associate director of the Nutrition Coordinating Center, University of Minnesota Twin Cities, which supports dietary analysis, said during the session that the focus of dietary research is “moving toward understanding overall dietary patterns” as opposed to focusing more narrowly on vitamins, minerals, and macronutrients such as proteins, fats, and carbohydrates.

This is an improvement, though “we still don’t have good approaches for understanding [the contributions of] things like additives and emulsifiers, food preparation and cooking, and food processing,” said Johnson, assistant professor in the Division of Epidemiology and Community Health at University of Minnesota Twin Cities. “Perhaps by looking at things at the food level we can overcome some of these limitations.”

Ananthakrishnan reported being a consultant for Geneoscopy and receiving a research grant from Takeda. Chassaing did not report any financial disclosures. Johnson reported that she had no financial disclosures.

A version of this article appeared on Medscape.com.

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WASHINGTON, DC — A low-emulsifier-containing diet led to a threefold increased likelihood of improvement in symptoms of Crohn’s disease compared with an emulsifier-containing diet in a randomized double-blind dietary trial involving 154 patients with mildly active disease living across the United Kingdom.

The findings were reported at Gut Microbiota for Health (GMFH) World Summit 2025 by Benoit Chassaing, PhD, of the Institut Pasteur, Paris, France, whose research leading up to the trial has demonstrated that food additive emulsifiers —ubiquitous in processed foods — alter microbiota composition and lead to microbiota encroachment into the mucus layer of the gut and subsequent chronic gut inflammation.

Patients in the ADDapt trial, which was also reported in an abstract earlier this year at the European Crohn’s and Colitis Organization (ECCO) 2025 Congress, had a Crohn’s disease activity index (CDAI) of 150-250 and evidence of inflammation (faecal calprotectin (FCP) ≥ 150 µg/g or endoscopy/radiology). All “had been exposed in their regular diets to emulsifiers,” said Chassaing, a co-investigator, during a GMFH session on “Dietary Drivers of Health and Disease.”

They were randomized to either a low-emulsifier diet or to a low-emulsifier diet followed by emulsifier “resupplementation” — a design meant to “account for the very strong placebo effect that is always observed with dietary studies,” he said.

All patients received dietary counseling, a smart phone app and barcode scan to support shopping, and weekly support. They also received supermarket foods for 25% of their needs that were either free of emulsifiers or contained emulsifiers, and they were provided three snacks per day that were emulsifier-free or contained carrageenan, carboxymethycellulse (CMC), and polysorbate-80 (P80) — dietary emulsifiers that are commonly added to processed foods to enhance texture and extend shelf-life.

In the intention-to-treat (ITT) analysis, 49% of patients in the intervention group reached the primary endpoint of a 70-point reduction or more in CDAI response after 8 weeks compared with 31% of those in the control group (P = .019), with an adjusted relative risk of response of 3.1 (P = .003), Chassaing shared at the GMFH meeting, convened by the American Gastroenterological Association and the European Society of Neurogastroenterology and Motility.

In the per-protocol analysis (n = 119), 61% and 47% of patients in the intervention and control groups, respectively, reached the primary outcome of CDAI response, with an adjusted relative risk of response of 3.0 (P = .018), he said.

Secondary endpoints included CDAI remission at 24 weeks, and according to the abstract for the ECCO Congress, in the ITT analysis, patients in the intervention group were more than twice as likely to experience remission.

Chassaing noted at the GMFH meeting that as part of the study, he and coinvestigators have been investigating the participants’ gut microbiota with metagenomic analyses. The study was led by Kevin Whelan, PhD, head of the Department of Nutritional Sciences at King’s College London, London, England.

 

Can Emulsifier-Sensitive Individuals Be Identified?

In murine model research 10 years ago, Chassaing showed that the administration of CMC and P80 results in microbiota encroachment into the mucus layer of the gut, alterations in microbiota composition — including an increase in bacteria that produce pro-inflammatory flagellin — and development of chronic inflammation.

Wild-type mice treated with these compounds developed metabolic disease, and mice that were modified to be predisposed to colitis had a higher incidence of robust colitis. Moreover, fecal transplantation from emulsifier-treated mice to germ-free mice reproduced these changes, “clearly suggesting that the microbiome itself is sufficient to drive chronic inflammation,” he said.

In recent years, in humans, analyses from the large French NutriNet-Sante prospective cohort study have shown associations between exposure to food additive emulsifiers and the risk for cardiovascular disease, the risk for cancer (overall, breast, and prostate), and the risk for type 2 diabetes.

But to explore causality and better understand the mechanisms of emulsifier-driven changes on the microbiota, Chassaing and his colleagues also launched the FRESH study (Functional Research on Emulsifier in Humans), a double-blind randomized controlled-feeding study of the emulsifier CMC. For 11 days, nine healthy patients consumed an emulsifier-free diet and 11 consumed an identical diet enriched with 15 g/d of CMC.

Patients on the CMC-containing diet had reduced microbiota diversity and depletions of an array of microbiota-related metabolites, but only a small subset had profound alterations in microbiota composition and increased microbiota encroachment into the mucus layer. “Some seemed to be resistant to CMC-induced microbiota encroachment, while some were highly susceptible,” Chassaing said.

The pilot study raised the question, he said, of whether there is an “infectivity component” — some kind of “sensitive” gut microbiota composition — that may be associated with dietary emulsifier-driven inflammation and disease.

In other murine research, Chassaing and his team found that germ-free mice colonized with Crohn’s disease-associated adherent-invasive E coli (AIEC) and subsequently given CMC or P80 developed chronic inflammation and metabolic dysregulation, “clearly demonstrating that you can convert resistant mice to sensitive mice just by adding one bacteria to the ecosystem,” he said. “The presence of AIEC alone was sufficient to drive the detrimental effects of dietary emulsifiers.”

(In vitro research with transcriptomic analysis then showed that the emulsifiers directly elicit AIEC virulence gene expression, Chassaing and his coauthors wrote in their 2020 paper, facilitating AIEC’s “penetration of the mucus layer and adherence to epithelial cells and resulting in activation of host pro-inflammatory signaling.”)

“We don’t think it’s solely the AIEC bacteria that will drive emulsifier sensitivity, though…we think it’s more complex,” Chassaing said at the meeting. Overall, the findings raise the question of whether emulsifier-sensitive individuals can be identified.

This, he said, is one of his most recent research questions. His lab has led the development of an in vitro microbiota model built to predict an individual’s sensitivity to emulsifiers. In a study published in April, the model recapitulated the differential CMC sensitivity observed in the earlier FRESH study, suggesting that an individual’s sensitivity to emulsifiers can indeed be predicted by examining their baseline microbiota.

 

Interpreting the Epidemiology

Chassaing’s research arch illustrates the synergy between epidemiological research, basic/translational research, and clinical interventional research that’s needed to understand the diet-microbiome intersection in inflammatory bowel disease, said Ashwin Ananthakrishnan, MBBS, MPH, AGAF, associate professor of medicine at Massachusetts General Hospital, Boston, in an interview at the meeting.

“It’s a good example of how to really span the spectrum, starting from the big picture and going deeper to understand mechanisms, and starting from mechanisms and expanding it out,” Ananthakrishnan said.

In his own talk about research on IBD, Ananthakrishnan said that epidemiological data have shown over the past 10-15 years that total dietary fiber is inversely associated with the risk for Crohn’s disease (with the strongest associations with fiber from fruits and vegetables). Studies have also shown that a higher intake of polyunsaturated fatty acids is associated with a lower risk for ulcerative colitis, whereas “an n-6-fatty acid-rich diet is associated with a higher risk of ulcerative colitis,” he said.

Dietary cohort studies, meanwhile, have shed light on the influence of dietary patterns — such as the Mediterranean diet and diets with high inflammatory potential—on IBD. A diet rich in ultra-processed foods has also been shown in a prospective cohort study to be associated with a higher risk for Crohn’s disease, with certain categories of ultra-processed foods (eg, breads and breakfast foods) having the strongest associations.

Such studies are limited in part, however, by inadequate assessment of potentially relevant variables such as emulsifiers, preservatives, and how the food is processed, he said.

And in interpreting the epidemiological research on fiber and IBD, for instance, one must appreciate that “there are a number of mechanisms by which fiber is impactful…there’s a big picture to look at,” Ananthakrishnan said. Fiber “can affect the microbiome, clearly, it can affect the gut barrier, and it can affect bile acids, and there are detailed translational studies in support of each of these.”

But there are other constituents of fruits and vegetables “that could potentially influence disease risk, such as AhR ligands and polyphenols,” he said. “And importantly, people not eating a lot of fiber may be eating a lot of ultra-processed foods.”

Most interventional studies of fiber have not shown a benefit of a high-fiber diet, Ananthakrishnan said, but there are multiple possible reasons and factors at play, including potential population differences (eg, in inflammatory status or baseline microbiota), shortcomings of the interventions, and potentially inaccurate outcomes.

Abigail Johnson, PhD, RDN, associate director of the Nutrition Coordinating Center, University of Minnesota Twin Cities, which supports dietary analysis, said during the session that the focus of dietary research is “moving toward understanding overall dietary patterns” as opposed to focusing more narrowly on vitamins, minerals, and macronutrients such as proteins, fats, and carbohydrates.

This is an improvement, though “we still don’t have good approaches for understanding [the contributions of] things like additives and emulsifiers, food preparation and cooking, and food processing,” said Johnson, assistant professor in the Division of Epidemiology and Community Health at University of Minnesota Twin Cities. “Perhaps by looking at things at the food level we can overcome some of these limitations.”

Ananthakrishnan reported being a consultant for Geneoscopy and receiving a research grant from Takeda. Chassaing did not report any financial disclosures. Johnson reported that she had no financial disclosures.

A version of this article appeared on Medscape.com.

WASHINGTON, DC — A low-emulsifier-containing diet led to a threefold increased likelihood of improvement in symptoms of Crohn’s disease compared with an emulsifier-containing diet in a randomized double-blind dietary trial involving 154 patients with mildly active disease living across the United Kingdom.

The findings were reported at Gut Microbiota for Health (GMFH) World Summit 2025 by Benoit Chassaing, PhD, of the Institut Pasteur, Paris, France, whose research leading up to the trial has demonstrated that food additive emulsifiers —ubiquitous in processed foods — alter microbiota composition and lead to microbiota encroachment into the mucus layer of the gut and subsequent chronic gut inflammation.

Patients in the ADDapt trial, which was also reported in an abstract earlier this year at the European Crohn’s and Colitis Organization (ECCO) 2025 Congress, had a Crohn’s disease activity index (CDAI) of 150-250 and evidence of inflammation (faecal calprotectin (FCP) ≥ 150 µg/g or endoscopy/radiology). All “had been exposed in their regular diets to emulsifiers,” said Chassaing, a co-investigator, during a GMFH session on “Dietary Drivers of Health and Disease.”

They were randomized to either a low-emulsifier diet or to a low-emulsifier diet followed by emulsifier “resupplementation” — a design meant to “account for the very strong placebo effect that is always observed with dietary studies,” he said.

All patients received dietary counseling, a smart phone app and barcode scan to support shopping, and weekly support. They also received supermarket foods for 25% of their needs that were either free of emulsifiers or contained emulsifiers, and they were provided three snacks per day that were emulsifier-free or contained carrageenan, carboxymethycellulse (CMC), and polysorbate-80 (P80) — dietary emulsifiers that are commonly added to processed foods to enhance texture and extend shelf-life.

In the intention-to-treat (ITT) analysis, 49% of patients in the intervention group reached the primary endpoint of a 70-point reduction or more in CDAI response after 8 weeks compared with 31% of those in the control group (P = .019), with an adjusted relative risk of response of 3.1 (P = .003), Chassaing shared at the GMFH meeting, convened by the American Gastroenterological Association and the European Society of Neurogastroenterology and Motility.

In the per-protocol analysis (n = 119), 61% and 47% of patients in the intervention and control groups, respectively, reached the primary outcome of CDAI response, with an adjusted relative risk of response of 3.0 (P = .018), he said.

Secondary endpoints included CDAI remission at 24 weeks, and according to the abstract for the ECCO Congress, in the ITT analysis, patients in the intervention group were more than twice as likely to experience remission.

Chassaing noted at the GMFH meeting that as part of the study, he and coinvestigators have been investigating the participants’ gut microbiota with metagenomic analyses. The study was led by Kevin Whelan, PhD, head of the Department of Nutritional Sciences at King’s College London, London, England.

 

Can Emulsifier-Sensitive Individuals Be Identified?

In murine model research 10 years ago, Chassaing showed that the administration of CMC and P80 results in microbiota encroachment into the mucus layer of the gut, alterations in microbiota composition — including an increase in bacteria that produce pro-inflammatory flagellin — and development of chronic inflammation.

Wild-type mice treated with these compounds developed metabolic disease, and mice that were modified to be predisposed to colitis had a higher incidence of robust colitis. Moreover, fecal transplantation from emulsifier-treated mice to germ-free mice reproduced these changes, “clearly suggesting that the microbiome itself is sufficient to drive chronic inflammation,” he said.

In recent years, in humans, analyses from the large French NutriNet-Sante prospective cohort study have shown associations between exposure to food additive emulsifiers and the risk for cardiovascular disease, the risk for cancer (overall, breast, and prostate), and the risk for type 2 diabetes.

But to explore causality and better understand the mechanisms of emulsifier-driven changes on the microbiota, Chassaing and his colleagues also launched the FRESH study (Functional Research on Emulsifier in Humans), a double-blind randomized controlled-feeding study of the emulsifier CMC. For 11 days, nine healthy patients consumed an emulsifier-free diet and 11 consumed an identical diet enriched with 15 g/d of CMC.

Patients on the CMC-containing diet had reduced microbiota diversity and depletions of an array of microbiota-related metabolites, but only a small subset had profound alterations in microbiota composition and increased microbiota encroachment into the mucus layer. “Some seemed to be resistant to CMC-induced microbiota encroachment, while some were highly susceptible,” Chassaing said.

The pilot study raised the question, he said, of whether there is an “infectivity component” — some kind of “sensitive” gut microbiota composition — that may be associated with dietary emulsifier-driven inflammation and disease.

In other murine research, Chassaing and his team found that germ-free mice colonized with Crohn’s disease-associated adherent-invasive E coli (AIEC) and subsequently given CMC or P80 developed chronic inflammation and metabolic dysregulation, “clearly demonstrating that you can convert resistant mice to sensitive mice just by adding one bacteria to the ecosystem,” he said. “The presence of AIEC alone was sufficient to drive the detrimental effects of dietary emulsifiers.”

(In vitro research with transcriptomic analysis then showed that the emulsifiers directly elicit AIEC virulence gene expression, Chassaing and his coauthors wrote in their 2020 paper, facilitating AIEC’s “penetration of the mucus layer and adherence to epithelial cells and resulting in activation of host pro-inflammatory signaling.”)

“We don’t think it’s solely the AIEC bacteria that will drive emulsifier sensitivity, though…we think it’s more complex,” Chassaing said at the meeting. Overall, the findings raise the question of whether emulsifier-sensitive individuals can be identified.

This, he said, is one of his most recent research questions. His lab has led the development of an in vitro microbiota model built to predict an individual’s sensitivity to emulsifiers. In a study published in April, the model recapitulated the differential CMC sensitivity observed in the earlier FRESH study, suggesting that an individual’s sensitivity to emulsifiers can indeed be predicted by examining their baseline microbiota.

 

Interpreting the Epidemiology

Chassaing’s research arch illustrates the synergy between epidemiological research, basic/translational research, and clinical interventional research that’s needed to understand the diet-microbiome intersection in inflammatory bowel disease, said Ashwin Ananthakrishnan, MBBS, MPH, AGAF, associate professor of medicine at Massachusetts General Hospital, Boston, in an interview at the meeting.

“It’s a good example of how to really span the spectrum, starting from the big picture and going deeper to understand mechanisms, and starting from mechanisms and expanding it out,” Ananthakrishnan said.

In his own talk about research on IBD, Ananthakrishnan said that epidemiological data have shown over the past 10-15 years that total dietary fiber is inversely associated with the risk for Crohn’s disease (with the strongest associations with fiber from fruits and vegetables). Studies have also shown that a higher intake of polyunsaturated fatty acids is associated with a lower risk for ulcerative colitis, whereas “an n-6-fatty acid-rich diet is associated with a higher risk of ulcerative colitis,” he said.

Dietary cohort studies, meanwhile, have shed light on the influence of dietary patterns — such as the Mediterranean diet and diets with high inflammatory potential—on IBD. A diet rich in ultra-processed foods has also been shown in a prospective cohort study to be associated with a higher risk for Crohn’s disease, with certain categories of ultra-processed foods (eg, breads and breakfast foods) having the strongest associations.

Such studies are limited in part, however, by inadequate assessment of potentially relevant variables such as emulsifiers, preservatives, and how the food is processed, he said.

And in interpreting the epidemiological research on fiber and IBD, for instance, one must appreciate that “there are a number of mechanisms by which fiber is impactful…there’s a big picture to look at,” Ananthakrishnan said. Fiber “can affect the microbiome, clearly, it can affect the gut barrier, and it can affect bile acids, and there are detailed translational studies in support of each of these.”

But there are other constituents of fruits and vegetables “that could potentially influence disease risk, such as AhR ligands and polyphenols,” he said. “And importantly, people not eating a lot of fiber may be eating a lot of ultra-processed foods.”

Most interventional studies of fiber have not shown a benefit of a high-fiber diet, Ananthakrishnan said, but there are multiple possible reasons and factors at play, including potential population differences (eg, in inflammatory status or baseline microbiota), shortcomings of the interventions, and potentially inaccurate outcomes.

Abigail Johnson, PhD, RDN, associate director of the Nutrition Coordinating Center, University of Minnesota Twin Cities, which supports dietary analysis, said during the session that the focus of dietary research is “moving toward understanding overall dietary patterns” as opposed to focusing more narrowly on vitamins, minerals, and macronutrients such as proteins, fats, and carbohydrates.

This is an improvement, though “we still don’t have good approaches for understanding [the contributions of] things like additives and emulsifiers, food preparation and cooking, and food processing,” said Johnson, assistant professor in the Division of Epidemiology and Community Health at University of Minnesota Twin Cities. “Perhaps by looking at things at the food level we can overcome some of these limitations.”

Ananthakrishnan reported being a consultant for Geneoscopy and receiving a research grant from Takeda. Chassaing did not report any financial disclosures. Johnson reported that she had no financial disclosures.

A version of this article appeared on Medscape.com.

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Does Tofacitinib Worsen Postoperative Complications in Acute Severe Ulcerative Colitis?

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A head-to-head comparison of the JAK inhibitor drug tofacitinib and chimeric monoclonal antibody infliximab in the treatment of acute severe ulcerative colitis (ASUC) shows that, contrary to concerns, tofacitinib is not associated with worse postoperative complications and in fact may reduce the risk of the need for colectomy.

“Tofacitinib has shown efficacy in managing ASUC, but concerns about postoperative complications have limited its adoption,” reported the authors in research published in Clinical Gastroenterology and Hepatology.“This study shows that tofacitinib is safe and doesn’t impair wound healing or lead to more infections if the patient needs an urgent colectomy, which is unfortunately common in this population,” senior author Jeffrey A. Berinstein, MD, of the Division of Gastroenterology and Hepatology, Michigan Medicine, Ann Arbor, Michigan, told GI & Hepatology News. 

Dr. Jeffrey A. Berinstein



Recent treatment advances for UC have provided significant benefits in reducing the severity of symptoms; however, about a quarter of patients go on to experience flares, with fecal urgency, rectal bleeding, and severe abdominal pain of ASUC potentially requiring hospitalization.

The standard of care for those patients is rapid induction with intravenous (IV) corticosteroids; however, up to 30% of patients don’t respond to those interventions, and even with subsequent treatment of cyclosporine and infliximab helping to reduce the risk for an urgent colectomy, patients often don’t respond, and ultimately, up to a third of patients with ASUC end up having to receive a colectomy.

While JAK inhibitor therapies, including tofacitinib and upadacitinib, have recently emerged as potentially important treatment options in such cases, showing reductions in the risk for colectomy, concerns about the drugs’ downstream biologic effects have given many clinicians reservations about their use.

“Anecdotally, gastroenterologists and surgeons have expressed concern about JAK inhibitors leading to poor wound healing, as well as increasing both intraoperative and postoperative complications, despite limited data to support these claims,” the authors wrote.

To better understand those possible risks, first author Charlotte Larson, MD, of the Department of Internal Medicine, Michigan Medicine, and colleagues conducted a multicenter, retrospective, case-control study of 109 patients hospitalized with ASUC at two centers in the US and 14 in France.

Of the patients, 41 were treated with tofacitinib and 68 with infliximab prior to colectomy. 

Among patients treated with tofacitinib, five (12.2%) received infliximab and four (9.8%) received cyclosporine rescue immediately prior to receiving tofacitinib during the index admission. In the infliximab group, one (1.5%) received rescue cyclosporine.

In a univariate analysis, the tofacitinib-treated patients showed significantly lower overall rates of postoperative complications than infliximab-treated patients (31.7% vs 64.7%; odds ratio [OR], 0.33; P = .006).

The tofacitinib-treated group also had lower rates of serious postoperative complications (12% vs 28.9; OR, 0.20; P = .016).

After adjusting for multivariate factors including age, inflammatory burden, nutrition status, 90-day cumulative corticosteroid exposure and open surgery, there was a trend favoring tofacitinib but no statistically significant difference between the two treatments in terms of serious postoperative complications (P = .061). 

However, a significantly lower rate of overall postoperative complications with tofacitinib was observed after the adjustment (odds ratio, 0.38; P = .023).

Importantly, a subanalysis showed that the 63.4% of tofacitinib-treated patients receiving the standard FDA-approved induction dose of 10 mg twice daily did indeed have significantly lower rates than infliximab-treated patients in terms of serious postoperative complications (OR, .10; P = .031), as well as overall postoperative complications (OR, 0.23; P = .003), whereas neither of the outcomes were significantly improved among the 36.6% of patients who received the higher-intensity thrice-daily tofacitinib dose (P = .3 and P = .4, respectively).

Further complicating the matter, in a previous case-control study that the research team conducted, it was the off-label, 10 mg thrice-daily dose of tofacitinib that performed favorably and was associated with a significantly lower risk for colectomy than the twice-daily dose (hazard ratio 0.28; P = .018); the twice-daily dose was not protective.

Berinstein added that a hypothesis for the benefits overall, with either dose, is that tofacitinib’s anti-inflammatory properties are key.

“We believe that lowering inflammation as much as possible, with the colon less inflamed, could be providing the benefit in lowering complications rate in surgery,” he explained.

Regarding the dosing, “it’s a careful trade-off,” Berinstein added. “Obviously, we want to avoid the need for a colectomy in the first place, as it is a life-changing surgery, but we don’t want to increase the risk of infections.” 

In other findings, the tofacitinib group had no increased risk for postoperative venous thrombotic embolisms (VTEs), which is important as tofacitinib exposure has previously been associated with an increased risk for VTEs independent of other prothrombotic factors common to patients with ASUC, including decreased ambulation, active inflammation, corticosteroid use, and major colorectal surgery.

“This observed absence of an increased VTE risk may alleviate some of the hypothetical postoperative safety concern attributed to JAK inhibitor therapy in this high-risk population,” the authors wrote.

Overall, the results underscore that “providers should feel comfortable using this medication if they need it and if they think it’s most likely to help their patients avoid colectomy,” Berinstein said.

“They should not give pause over concerns of postoperative complications because we didn’t show that,” he said.

Dr. Joseph D. Feuerstein



Commenting on the study, Joseph D. Feuerstein, MD, AGAF, of the Department of Medicine and Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, noted that, in general, in patients with ASUC who fail on IV steroids, “the main treatments are infliximab, cyclosporine, or a JAK inhibitor like tofacitinib or upadacitinib, [and] knowing that if someone needs surgery, the complication rates are similar and that pre-operative use is okay is reassuring.”

Regarding the protective effect observed with some circumstances, “I don’t put too much weight into that,” he noted. “[One] could speculate that it is somehow related to faster half-life of the drug, and it might not sit around as long,” he said.

Feuerstein added that “the study design being retrospective is a limitation, but this is the best data we have to date.”

Berinstein and Feuerstein had no disclosures to report.

A version of this article appeared on Medscape.com . 

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A head-to-head comparison of the JAK inhibitor drug tofacitinib and chimeric monoclonal antibody infliximab in the treatment of acute severe ulcerative colitis (ASUC) shows that, contrary to concerns, tofacitinib is not associated with worse postoperative complications and in fact may reduce the risk of the need for colectomy.

“Tofacitinib has shown efficacy in managing ASUC, but concerns about postoperative complications have limited its adoption,” reported the authors in research published in Clinical Gastroenterology and Hepatology.“This study shows that tofacitinib is safe and doesn’t impair wound healing or lead to more infections if the patient needs an urgent colectomy, which is unfortunately common in this population,” senior author Jeffrey A. Berinstein, MD, of the Division of Gastroenterology and Hepatology, Michigan Medicine, Ann Arbor, Michigan, told GI & Hepatology News. 

Dr. Jeffrey A. Berinstein



Recent treatment advances for UC have provided significant benefits in reducing the severity of symptoms; however, about a quarter of patients go on to experience flares, with fecal urgency, rectal bleeding, and severe abdominal pain of ASUC potentially requiring hospitalization.

The standard of care for those patients is rapid induction with intravenous (IV) corticosteroids; however, up to 30% of patients don’t respond to those interventions, and even with subsequent treatment of cyclosporine and infliximab helping to reduce the risk for an urgent colectomy, patients often don’t respond, and ultimately, up to a third of patients with ASUC end up having to receive a colectomy.

While JAK inhibitor therapies, including tofacitinib and upadacitinib, have recently emerged as potentially important treatment options in such cases, showing reductions in the risk for colectomy, concerns about the drugs’ downstream biologic effects have given many clinicians reservations about their use.

“Anecdotally, gastroenterologists and surgeons have expressed concern about JAK inhibitors leading to poor wound healing, as well as increasing both intraoperative and postoperative complications, despite limited data to support these claims,” the authors wrote.

To better understand those possible risks, first author Charlotte Larson, MD, of the Department of Internal Medicine, Michigan Medicine, and colleagues conducted a multicenter, retrospective, case-control study of 109 patients hospitalized with ASUC at two centers in the US and 14 in France.

Of the patients, 41 were treated with tofacitinib and 68 with infliximab prior to colectomy. 

Among patients treated with tofacitinib, five (12.2%) received infliximab and four (9.8%) received cyclosporine rescue immediately prior to receiving tofacitinib during the index admission. In the infliximab group, one (1.5%) received rescue cyclosporine.

In a univariate analysis, the tofacitinib-treated patients showed significantly lower overall rates of postoperative complications than infliximab-treated patients (31.7% vs 64.7%; odds ratio [OR], 0.33; P = .006).

The tofacitinib-treated group also had lower rates of serious postoperative complications (12% vs 28.9; OR, 0.20; P = .016).

After adjusting for multivariate factors including age, inflammatory burden, nutrition status, 90-day cumulative corticosteroid exposure and open surgery, there was a trend favoring tofacitinib but no statistically significant difference between the two treatments in terms of serious postoperative complications (P = .061). 

However, a significantly lower rate of overall postoperative complications with tofacitinib was observed after the adjustment (odds ratio, 0.38; P = .023).

Importantly, a subanalysis showed that the 63.4% of tofacitinib-treated patients receiving the standard FDA-approved induction dose of 10 mg twice daily did indeed have significantly lower rates than infliximab-treated patients in terms of serious postoperative complications (OR, .10; P = .031), as well as overall postoperative complications (OR, 0.23; P = .003), whereas neither of the outcomes were significantly improved among the 36.6% of patients who received the higher-intensity thrice-daily tofacitinib dose (P = .3 and P = .4, respectively).

Further complicating the matter, in a previous case-control study that the research team conducted, it was the off-label, 10 mg thrice-daily dose of tofacitinib that performed favorably and was associated with a significantly lower risk for colectomy than the twice-daily dose (hazard ratio 0.28; P = .018); the twice-daily dose was not protective.

Berinstein added that a hypothesis for the benefits overall, with either dose, is that tofacitinib’s anti-inflammatory properties are key.

“We believe that lowering inflammation as much as possible, with the colon less inflamed, could be providing the benefit in lowering complications rate in surgery,” he explained.

Regarding the dosing, “it’s a careful trade-off,” Berinstein added. “Obviously, we want to avoid the need for a colectomy in the first place, as it is a life-changing surgery, but we don’t want to increase the risk of infections.” 

In other findings, the tofacitinib group had no increased risk for postoperative venous thrombotic embolisms (VTEs), which is important as tofacitinib exposure has previously been associated with an increased risk for VTEs independent of other prothrombotic factors common to patients with ASUC, including decreased ambulation, active inflammation, corticosteroid use, and major colorectal surgery.

“This observed absence of an increased VTE risk may alleviate some of the hypothetical postoperative safety concern attributed to JAK inhibitor therapy in this high-risk population,” the authors wrote.

Overall, the results underscore that “providers should feel comfortable using this medication if they need it and if they think it’s most likely to help their patients avoid colectomy,” Berinstein said.

“They should not give pause over concerns of postoperative complications because we didn’t show that,” he said.

Dr. Joseph D. Feuerstein



Commenting on the study, Joseph D. Feuerstein, MD, AGAF, of the Department of Medicine and Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, noted that, in general, in patients with ASUC who fail on IV steroids, “the main treatments are infliximab, cyclosporine, or a JAK inhibitor like tofacitinib or upadacitinib, [and] knowing that if someone needs surgery, the complication rates are similar and that pre-operative use is okay is reassuring.”

Regarding the protective effect observed with some circumstances, “I don’t put too much weight into that,” he noted. “[One] could speculate that it is somehow related to faster half-life of the drug, and it might not sit around as long,” he said.

Feuerstein added that “the study design being retrospective is a limitation, but this is the best data we have to date.”

Berinstein and Feuerstein had no disclosures to report.

A version of this article appeared on Medscape.com . 

A head-to-head comparison of the JAK inhibitor drug tofacitinib and chimeric monoclonal antibody infliximab in the treatment of acute severe ulcerative colitis (ASUC) shows that, contrary to concerns, tofacitinib is not associated with worse postoperative complications and in fact may reduce the risk of the need for colectomy.

“Tofacitinib has shown efficacy in managing ASUC, but concerns about postoperative complications have limited its adoption,” reported the authors in research published in Clinical Gastroenterology and Hepatology.“This study shows that tofacitinib is safe and doesn’t impair wound healing or lead to more infections if the patient needs an urgent colectomy, which is unfortunately common in this population,” senior author Jeffrey A. Berinstein, MD, of the Division of Gastroenterology and Hepatology, Michigan Medicine, Ann Arbor, Michigan, told GI & Hepatology News. 

Dr. Jeffrey A. Berinstein



Recent treatment advances for UC have provided significant benefits in reducing the severity of symptoms; however, about a quarter of patients go on to experience flares, with fecal urgency, rectal bleeding, and severe abdominal pain of ASUC potentially requiring hospitalization.

The standard of care for those patients is rapid induction with intravenous (IV) corticosteroids; however, up to 30% of patients don’t respond to those interventions, and even with subsequent treatment of cyclosporine and infliximab helping to reduce the risk for an urgent colectomy, patients often don’t respond, and ultimately, up to a third of patients with ASUC end up having to receive a colectomy.

While JAK inhibitor therapies, including tofacitinib and upadacitinib, have recently emerged as potentially important treatment options in such cases, showing reductions in the risk for colectomy, concerns about the drugs’ downstream biologic effects have given many clinicians reservations about their use.

“Anecdotally, gastroenterologists and surgeons have expressed concern about JAK inhibitors leading to poor wound healing, as well as increasing both intraoperative and postoperative complications, despite limited data to support these claims,” the authors wrote.

To better understand those possible risks, first author Charlotte Larson, MD, of the Department of Internal Medicine, Michigan Medicine, and colleagues conducted a multicenter, retrospective, case-control study of 109 patients hospitalized with ASUC at two centers in the US and 14 in France.

Of the patients, 41 were treated with tofacitinib and 68 with infliximab prior to colectomy. 

Among patients treated with tofacitinib, five (12.2%) received infliximab and four (9.8%) received cyclosporine rescue immediately prior to receiving tofacitinib during the index admission. In the infliximab group, one (1.5%) received rescue cyclosporine.

In a univariate analysis, the tofacitinib-treated patients showed significantly lower overall rates of postoperative complications than infliximab-treated patients (31.7% vs 64.7%; odds ratio [OR], 0.33; P = .006).

The tofacitinib-treated group also had lower rates of serious postoperative complications (12% vs 28.9; OR, 0.20; P = .016).

After adjusting for multivariate factors including age, inflammatory burden, nutrition status, 90-day cumulative corticosteroid exposure and open surgery, there was a trend favoring tofacitinib but no statistically significant difference between the two treatments in terms of serious postoperative complications (P = .061). 

However, a significantly lower rate of overall postoperative complications with tofacitinib was observed after the adjustment (odds ratio, 0.38; P = .023).

Importantly, a subanalysis showed that the 63.4% of tofacitinib-treated patients receiving the standard FDA-approved induction dose of 10 mg twice daily did indeed have significantly lower rates than infliximab-treated patients in terms of serious postoperative complications (OR, .10; P = .031), as well as overall postoperative complications (OR, 0.23; P = .003), whereas neither of the outcomes were significantly improved among the 36.6% of patients who received the higher-intensity thrice-daily tofacitinib dose (P = .3 and P = .4, respectively).

Further complicating the matter, in a previous case-control study that the research team conducted, it was the off-label, 10 mg thrice-daily dose of tofacitinib that performed favorably and was associated with a significantly lower risk for colectomy than the twice-daily dose (hazard ratio 0.28; P = .018); the twice-daily dose was not protective.

Berinstein added that a hypothesis for the benefits overall, with either dose, is that tofacitinib’s anti-inflammatory properties are key.

“We believe that lowering inflammation as much as possible, with the colon less inflamed, could be providing the benefit in lowering complications rate in surgery,” he explained.

Regarding the dosing, “it’s a careful trade-off,” Berinstein added. “Obviously, we want to avoid the need for a colectomy in the first place, as it is a life-changing surgery, but we don’t want to increase the risk of infections.” 

In other findings, the tofacitinib group had no increased risk for postoperative venous thrombotic embolisms (VTEs), which is important as tofacitinib exposure has previously been associated with an increased risk for VTEs independent of other prothrombotic factors common to patients with ASUC, including decreased ambulation, active inflammation, corticosteroid use, and major colorectal surgery.

“This observed absence of an increased VTE risk may alleviate some of the hypothetical postoperative safety concern attributed to JAK inhibitor therapy in this high-risk population,” the authors wrote.

Overall, the results underscore that “providers should feel comfortable using this medication if they need it and if they think it’s most likely to help their patients avoid colectomy,” Berinstein said.

“They should not give pause over concerns of postoperative complications because we didn’t show that,” he said.

Dr. Joseph D. Feuerstein



Commenting on the study, Joseph D. Feuerstein, MD, AGAF, of the Department of Medicine and Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, noted that, in general, in patients with ASUC who fail on IV steroids, “the main treatments are infliximab, cyclosporine, or a JAK inhibitor like tofacitinib or upadacitinib, [and] knowing that if someone needs surgery, the complication rates are similar and that pre-operative use is okay is reassuring.”

Regarding the protective effect observed with some circumstances, “I don’t put too much weight into that,” he noted. “[One] could speculate that it is somehow related to faster half-life of the drug, and it might not sit around as long,” he said.

Feuerstein added that “the study design being retrospective is a limitation, but this is the best data we have to date.”

Berinstein and Feuerstein had no disclosures to report.

A version of this article appeared on Medscape.com . 

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Endoscopic Lifting Agents: AGA Issues New Clinical Practice Update

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The American Gastroenterological Association (AGA) has released a comprehensive clinical practice update on lifting agents for endoscopic surgery.

Published in Clinical Gastroenterology and Hepatology, the commentary reviews available agents and provides clinically relevant commentary on their indications and use — with the caveat that it is not a formal systematic review but rather empirical advice for endoscopists. No formal rating of the quality of evidence or strength of recommendations was performed.

Led by Tobias Zuchelli, MD, a clinical associate professor at Michigan State University and a gastroenterologist at the Henry Ford Health System in Detroit, the expert panel noted that endoscopists are increasingly resecting precancerous lesions and early cancers of the gastrointestinal tract.

“Although new endoscopic procedures have been developed, there had not been much in terms of high-quality guidance on lifting agents,” panelist Amit V. Patel, MD, a professor of medicine at Duke University and director of Endoscopy at Durham Veterans Affairs Medical Center in Durham, North Carolina, told GI & Hepatology News. “With our better understanding and use of techniques, this commentary was timely. It summarizes the available data on the topic and includes our clinical experiences.”

Dr. Amit V. Patel



Filling that knowledge gap, the document reviews in detail the timing and methods of agent injection according to procedure type, including the dynamic needle approach, the empirical merits of different agents such as saline (with or without blue contrast) and viscous agents, as well as lift-enhancing assistive devices — for example, the ERBEJET 2 high-pressure water jet, an adjustable hydrosurgical device to facilitate lifting. A chart provides an at-a-glance summary of agents and their pros and cons.

“The feedback from gastroenterologists so far has been quite positive on social media and on GI channels,” Patel said.

Endoscopic resection has evolved from snare polypectomy to endoscopic mucosal resection (EMR) and now, endoscopic submucosal dissection (ESD). The primary benefit of submucosal lifting is the creation of a separating submucosal cushion between the lesion and muscularis propria (MP), which reduces the risk for immediate or delayed perforation of the muscle. Adding a contrast agent also demarcates lesion margins and stains the submucosa, which is fundamental to ESD and allows for assessment of MP injury during EMR.

For decades, homemade solutions were used to lift lesions before removal, with the sentinel agent being normal saline, later mixed with a blue contrast agent, usually indigo carmine or methylene blue. The authors noted that some endoscopists performing ESD start the submucosal injection and incision using a prepackaged viscous solution. “The endoscopist may continue with the viscous fluid or transition to saline or another less expensive solution,” they wrote.

Saline tends to dissipate more quickly than viscous solutions, however. In 2015, the polymer compound SIC-8000 became the first FDA-approved submucosal injection agent. Since then, several other fluids have come on the market, although homemade agents remain available.

Among the update’s recommendations, the fluid selected for EMR should be determined by lesion size, predicted histology, and endoscopist preference. Based on the US Multi-Society Task Force (USMSTF) on Colorectal Cancer, submucosal injection is optional for nonpedunculated colorectal lesions (NPCRLs) of intermediate size (10-19 mm).

Cold snare polypectomy without submucosal injection was later found to be non-inferior to other resection methods utilizing submucosal injection for NPCRLs ≤ 15 mm. 

The update noted that the USMSTF considers EMR first-line therapy for most NPCRLs ≥ 20 mm and advocates viscous solutions as preferred, while the use of lifting agents for pedunculated polyps is generally at the discretion of the endoscopist.

For Patel, the main “clinical pearls” in the update are adding a contrast agent to normal saline, using a viscous agent for cold EMR, and manipulating the injection needle first tangentially and then dynamically toward the lumen to maximize separation of the lesion.

In terms of the ideal, an optimal lifting solution would be readily available, inexpensive, and premixed, providing a sustained submucosal cushion. “However, this ideal solution currently does not exist. Injection fluids should, therefore, be selected based on planned resection method, predicted histology, local expertise and preferences, and cost,” the panelists wrote.

Added Patel, “A lot of the agents out there check most of these boxes, but we’re hoping for further development toward the ideal.”

Offering a nonparticipant’s perspective on the overview, Wasseem Skef, MD, a gastroenterologist at UTHealth Houston, found the update very useful. “It always helps to have the literature summarized,” he told GI & Hepatology News. “It’s a pretty balanced review that pulls together the various options but allows people to stick to their preferred practice.”

Dr. Wasseem Skef



In his practice, the lifting agent selected depends on the type of resection. “Viscous agents are generally more popular for EMR-type resections,” Skef said. One unanswered question, he noted, is whether adding a hemostatic agent would be superior to a viscous agent alone. “But overall, this is a nice summary of available agents. Gastroenterologists should consider these different options if doing procedures like EMR.”

This review was sponsored by the AGA Institute. 

Zuchelli is a consultant for Boston Scientific. Patel consults for Medpace, Renexxion, and Sanofi. Skef reported having no relevant disclosures.

A version of this article appeared on Medscape.com . 

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The American Gastroenterological Association (AGA) has released a comprehensive clinical practice update on lifting agents for endoscopic surgery.

Published in Clinical Gastroenterology and Hepatology, the commentary reviews available agents and provides clinically relevant commentary on their indications and use — with the caveat that it is not a formal systematic review but rather empirical advice for endoscopists. No formal rating of the quality of evidence or strength of recommendations was performed.

Led by Tobias Zuchelli, MD, a clinical associate professor at Michigan State University and a gastroenterologist at the Henry Ford Health System in Detroit, the expert panel noted that endoscopists are increasingly resecting precancerous lesions and early cancers of the gastrointestinal tract.

“Although new endoscopic procedures have been developed, there had not been much in terms of high-quality guidance on lifting agents,” panelist Amit V. Patel, MD, a professor of medicine at Duke University and director of Endoscopy at Durham Veterans Affairs Medical Center in Durham, North Carolina, told GI & Hepatology News. “With our better understanding and use of techniques, this commentary was timely. It summarizes the available data on the topic and includes our clinical experiences.”

Dr. Amit V. Patel



Filling that knowledge gap, the document reviews in detail the timing and methods of agent injection according to procedure type, including the dynamic needle approach, the empirical merits of different agents such as saline (with or without blue contrast) and viscous agents, as well as lift-enhancing assistive devices — for example, the ERBEJET 2 high-pressure water jet, an adjustable hydrosurgical device to facilitate lifting. A chart provides an at-a-glance summary of agents and their pros and cons.

“The feedback from gastroenterologists so far has been quite positive on social media and on GI channels,” Patel said.

Endoscopic resection has evolved from snare polypectomy to endoscopic mucosal resection (EMR) and now, endoscopic submucosal dissection (ESD). The primary benefit of submucosal lifting is the creation of a separating submucosal cushion between the lesion and muscularis propria (MP), which reduces the risk for immediate or delayed perforation of the muscle. Adding a contrast agent also demarcates lesion margins and stains the submucosa, which is fundamental to ESD and allows for assessment of MP injury during EMR.

For decades, homemade solutions were used to lift lesions before removal, with the sentinel agent being normal saline, later mixed with a blue contrast agent, usually indigo carmine or methylene blue. The authors noted that some endoscopists performing ESD start the submucosal injection and incision using a prepackaged viscous solution. “The endoscopist may continue with the viscous fluid or transition to saline or another less expensive solution,” they wrote.

Saline tends to dissipate more quickly than viscous solutions, however. In 2015, the polymer compound SIC-8000 became the first FDA-approved submucosal injection agent. Since then, several other fluids have come on the market, although homemade agents remain available.

Among the update’s recommendations, the fluid selected for EMR should be determined by lesion size, predicted histology, and endoscopist preference. Based on the US Multi-Society Task Force (USMSTF) on Colorectal Cancer, submucosal injection is optional for nonpedunculated colorectal lesions (NPCRLs) of intermediate size (10-19 mm).

Cold snare polypectomy without submucosal injection was later found to be non-inferior to other resection methods utilizing submucosal injection for NPCRLs ≤ 15 mm. 

The update noted that the USMSTF considers EMR first-line therapy for most NPCRLs ≥ 20 mm and advocates viscous solutions as preferred, while the use of lifting agents for pedunculated polyps is generally at the discretion of the endoscopist.

For Patel, the main “clinical pearls” in the update are adding a contrast agent to normal saline, using a viscous agent for cold EMR, and manipulating the injection needle first tangentially and then dynamically toward the lumen to maximize separation of the lesion.

In terms of the ideal, an optimal lifting solution would be readily available, inexpensive, and premixed, providing a sustained submucosal cushion. “However, this ideal solution currently does not exist. Injection fluids should, therefore, be selected based on planned resection method, predicted histology, local expertise and preferences, and cost,” the panelists wrote.

Added Patel, “A lot of the agents out there check most of these boxes, but we’re hoping for further development toward the ideal.”

Offering a nonparticipant’s perspective on the overview, Wasseem Skef, MD, a gastroenterologist at UTHealth Houston, found the update very useful. “It always helps to have the literature summarized,” he told GI & Hepatology News. “It’s a pretty balanced review that pulls together the various options but allows people to stick to their preferred practice.”

Dr. Wasseem Skef



In his practice, the lifting agent selected depends on the type of resection. “Viscous agents are generally more popular for EMR-type resections,” Skef said. One unanswered question, he noted, is whether adding a hemostatic agent would be superior to a viscous agent alone. “But overall, this is a nice summary of available agents. Gastroenterologists should consider these different options if doing procedures like EMR.”

This review was sponsored by the AGA Institute. 

Zuchelli is a consultant for Boston Scientific. Patel consults for Medpace, Renexxion, and Sanofi. Skef reported having no relevant disclosures.

A version of this article appeared on Medscape.com . 

The American Gastroenterological Association (AGA) has released a comprehensive clinical practice update on lifting agents for endoscopic surgery.

Published in Clinical Gastroenterology and Hepatology, the commentary reviews available agents and provides clinically relevant commentary on their indications and use — with the caveat that it is not a formal systematic review but rather empirical advice for endoscopists. No formal rating of the quality of evidence or strength of recommendations was performed.

Led by Tobias Zuchelli, MD, a clinical associate professor at Michigan State University and a gastroenterologist at the Henry Ford Health System in Detroit, the expert panel noted that endoscopists are increasingly resecting precancerous lesions and early cancers of the gastrointestinal tract.

“Although new endoscopic procedures have been developed, there had not been much in terms of high-quality guidance on lifting agents,” panelist Amit V. Patel, MD, a professor of medicine at Duke University and director of Endoscopy at Durham Veterans Affairs Medical Center in Durham, North Carolina, told GI & Hepatology News. “With our better understanding and use of techniques, this commentary was timely. It summarizes the available data on the topic and includes our clinical experiences.”

Dr. Amit V. Patel



Filling that knowledge gap, the document reviews in detail the timing and methods of agent injection according to procedure type, including the dynamic needle approach, the empirical merits of different agents such as saline (with or without blue contrast) and viscous agents, as well as lift-enhancing assistive devices — for example, the ERBEJET 2 high-pressure water jet, an adjustable hydrosurgical device to facilitate lifting. A chart provides an at-a-glance summary of agents and their pros and cons.

“The feedback from gastroenterologists so far has been quite positive on social media and on GI channels,” Patel said.

Endoscopic resection has evolved from snare polypectomy to endoscopic mucosal resection (EMR) and now, endoscopic submucosal dissection (ESD). The primary benefit of submucosal lifting is the creation of a separating submucosal cushion between the lesion and muscularis propria (MP), which reduces the risk for immediate or delayed perforation of the muscle. Adding a contrast agent also demarcates lesion margins and stains the submucosa, which is fundamental to ESD and allows for assessment of MP injury during EMR.

For decades, homemade solutions were used to lift lesions before removal, with the sentinel agent being normal saline, later mixed with a blue contrast agent, usually indigo carmine or methylene blue. The authors noted that some endoscopists performing ESD start the submucosal injection and incision using a prepackaged viscous solution. “The endoscopist may continue with the viscous fluid or transition to saline or another less expensive solution,” they wrote.

Saline tends to dissipate more quickly than viscous solutions, however. In 2015, the polymer compound SIC-8000 became the first FDA-approved submucosal injection agent. Since then, several other fluids have come on the market, although homemade agents remain available.

Among the update’s recommendations, the fluid selected for EMR should be determined by lesion size, predicted histology, and endoscopist preference. Based on the US Multi-Society Task Force (USMSTF) on Colorectal Cancer, submucosal injection is optional for nonpedunculated colorectal lesions (NPCRLs) of intermediate size (10-19 mm).

Cold snare polypectomy without submucosal injection was later found to be non-inferior to other resection methods utilizing submucosal injection for NPCRLs ≤ 15 mm. 

The update noted that the USMSTF considers EMR first-line therapy for most NPCRLs ≥ 20 mm and advocates viscous solutions as preferred, while the use of lifting agents for pedunculated polyps is generally at the discretion of the endoscopist.

For Patel, the main “clinical pearls” in the update are adding a contrast agent to normal saline, using a viscous agent for cold EMR, and manipulating the injection needle first tangentially and then dynamically toward the lumen to maximize separation of the lesion.

In terms of the ideal, an optimal lifting solution would be readily available, inexpensive, and premixed, providing a sustained submucosal cushion. “However, this ideal solution currently does not exist. Injection fluids should, therefore, be selected based on planned resection method, predicted histology, local expertise and preferences, and cost,” the panelists wrote.

Added Patel, “A lot of the agents out there check most of these boxes, but we’re hoping for further development toward the ideal.”

Offering a nonparticipant’s perspective on the overview, Wasseem Skef, MD, a gastroenterologist at UTHealth Houston, found the update very useful. “It always helps to have the literature summarized,” he told GI & Hepatology News. “It’s a pretty balanced review that pulls together the various options but allows people to stick to their preferred practice.”

Dr. Wasseem Skef



In his practice, the lifting agent selected depends on the type of resection. “Viscous agents are generally more popular for EMR-type resections,” Skef said. One unanswered question, he noted, is whether adding a hemostatic agent would be superior to a viscous agent alone. “But overall, this is a nice summary of available agents. Gastroenterologists should consider these different options if doing procedures like EMR.”

This review was sponsored by the AGA Institute. 

Zuchelli is a consultant for Boston Scientific. Patel consults for Medpace, Renexxion, and Sanofi. Skef reported having no relevant disclosures.

A version of this article appeared on Medscape.com . 

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IBS, Chronic Idiopathic Constipation Surged During Pandemic

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The prevalence of irritable bowel syndrome (IBS) and chronic idiopathic constipation among US adults rose significantly during the COVID-19 pandemic, with a near doubling of the national rate of IBS over 2 years, a study has found.

The uptick is probably due to not only the direct impact of SARS-CoV-2 infection on the gastrointestinal tract but also to the psychological stress associated with pandemic life, the study team said. 

“COVID infection itself can definitely cause gastrointestinal symptoms like diarrhea, nausea, and abdominal pain — and for some people, those symptoms can linger and lead to chronic conditions like IBS,” Christopher V. Almario, MD, MSHPM, lead author and gastroenterologist at Cedars-Sinai Medical Center, Los Angeles, California, told GI & Hepatology News

Dr. Christopher V. Almario



“But the stress of living through the pandemic — lockdowns, fear, isolation — also likely played a major role as well in the increased prevalence of digestive disorders. Both the infection itself and the psychological toll of the pandemic can disrupt the gut-brain axis and trigger chronic digestive disorders like IBS,” Almario said. 

The study was published in Neurogastroenterology & Motility.

 

Growing Burden of Gut Disorders 

Disorders of gut-brain interaction (DGBIs) are a heterogeneous group of conditions in which gastrointestinal symptoms occur without any detectable structural or biochemical abnormalities in the digestive tract. They include IBS, functional dyspepsia, and chronic idiopathic constipation, among others. 

DGBIs are highly prevalent. Research has shown that nearly 40% of people in the US meet Rome IV criteria for at least one DGBI. 

Almario and colleagues assessed trends in prevalence of these conditions during the COVID-19 pandemic. Starting in May 2020 through May 2022, they conducted a series of online surveys with more than 160,000 adults aged 18 or older using validated Rome IV diagnostic questionnaires. 

Results showed that during the pandemic, IBS prevalence rose from 6.1% in May 2020 to 11.0% by May 2022, an increase of 0.188% per month (adjusted P < .001). 

Chronic idiopathic constipation showed a smaller but statistically significant increase, from 6.0% to 6.4% (0.056% per month; adjusted P < .001). 

Within the IBS subtypes, mixed-type IBS showed the largest relative increase (0.085% per month), followed by IBS with constipation (0.041% per month) and IBS with diarrhea (0.037% per month). 

There were no significant changes in the prevalence of other DGBIs, such as functional bloating, functional diarrhea, or functional dyspepsia, during the study period. 

Almario told GI & Hepatology News only about 9% of those surveyed reported a positive COVID test at the time of the surveys, but that figure probably underrepresents actual infections, especially in the early months of the pandemic. “Most of the survey responses came in during the earlier phases of the pandemic, and the percentage reporting a positive test increased over time,” he explained. 

Almario also noted that this study did not directly compare digestive disorder rates between infected and uninfected individuals. However, a separate study by the Cedars-Sinai team currently undergoing peer review addresses that question more directly. “That study, along with several other studies, show that having COVID increases the risk of developing conditions like IBS and functional dyspepsia,” Almario said. 

Taken together, the findings “underscore the increasing healthcare and economic burden of DGBI in the post-pandemic era, emphasizing the need for targeted efforts to effectively diagnose and manage these complex conditions,” they wrote. 

“This will be especially challenging for healthcare systems to address, given the existing shortage of primary care physicians and gastroenterologists — clinicians who primarily manage individuals with DGBI,” they noted. 

Support for this study was received from Ironwood Pharmaceuticals and Salix Pharmaceuticals in the form of institutional research grants to Cedars-Sinai. Almario has consulted for Exact Sciences, Greenspace Labs, Owlstone Medical, Salix Pharmaceuticals, and Universal DX.

A version of this article appeared on Medscape.com.

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The prevalence of irritable bowel syndrome (IBS) and chronic idiopathic constipation among US adults rose significantly during the COVID-19 pandemic, with a near doubling of the national rate of IBS over 2 years, a study has found.

The uptick is probably due to not only the direct impact of SARS-CoV-2 infection on the gastrointestinal tract but also to the psychological stress associated with pandemic life, the study team said. 

“COVID infection itself can definitely cause gastrointestinal symptoms like diarrhea, nausea, and abdominal pain — and for some people, those symptoms can linger and lead to chronic conditions like IBS,” Christopher V. Almario, MD, MSHPM, lead author and gastroenterologist at Cedars-Sinai Medical Center, Los Angeles, California, told GI & Hepatology News

Dr. Christopher V. Almario



“But the stress of living through the pandemic — lockdowns, fear, isolation — also likely played a major role as well in the increased prevalence of digestive disorders. Both the infection itself and the psychological toll of the pandemic can disrupt the gut-brain axis and trigger chronic digestive disorders like IBS,” Almario said. 

The study was published in Neurogastroenterology & Motility.

 

Growing Burden of Gut Disorders 

Disorders of gut-brain interaction (DGBIs) are a heterogeneous group of conditions in which gastrointestinal symptoms occur without any detectable structural or biochemical abnormalities in the digestive tract. They include IBS, functional dyspepsia, and chronic idiopathic constipation, among others. 

DGBIs are highly prevalent. Research has shown that nearly 40% of people in the US meet Rome IV criteria for at least one DGBI. 

Almario and colleagues assessed trends in prevalence of these conditions during the COVID-19 pandemic. Starting in May 2020 through May 2022, they conducted a series of online surveys with more than 160,000 adults aged 18 or older using validated Rome IV diagnostic questionnaires. 

Results showed that during the pandemic, IBS prevalence rose from 6.1% in May 2020 to 11.0% by May 2022, an increase of 0.188% per month (adjusted P < .001). 

Chronic idiopathic constipation showed a smaller but statistically significant increase, from 6.0% to 6.4% (0.056% per month; adjusted P < .001). 

Within the IBS subtypes, mixed-type IBS showed the largest relative increase (0.085% per month), followed by IBS with constipation (0.041% per month) and IBS with diarrhea (0.037% per month). 

There were no significant changes in the prevalence of other DGBIs, such as functional bloating, functional diarrhea, or functional dyspepsia, during the study period. 

Almario told GI & Hepatology News only about 9% of those surveyed reported a positive COVID test at the time of the surveys, but that figure probably underrepresents actual infections, especially in the early months of the pandemic. “Most of the survey responses came in during the earlier phases of the pandemic, and the percentage reporting a positive test increased over time,” he explained. 

Almario also noted that this study did not directly compare digestive disorder rates between infected and uninfected individuals. However, a separate study by the Cedars-Sinai team currently undergoing peer review addresses that question more directly. “That study, along with several other studies, show that having COVID increases the risk of developing conditions like IBS and functional dyspepsia,” Almario said. 

Taken together, the findings “underscore the increasing healthcare and economic burden of DGBI in the post-pandemic era, emphasizing the need for targeted efforts to effectively diagnose and manage these complex conditions,” they wrote. 

“This will be especially challenging for healthcare systems to address, given the existing shortage of primary care physicians and gastroenterologists — clinicians who primarily manage individuals with DGBI,” they noted. 

Support for this study was received from Ironwood Pharmaceuticals and Salix Pharmaceuticals in the form of institutional research grants to Cedars-Sinai. Almario has consulted for Exact Sciences, Greenspace Labs, Owlstone Medical, Salix Pharmaceuticals, and Universal DX.

A version of this article appeared on Medscape.com.

The prevalence of irritable bowel syndrome (IBS) and chronic idiopathic constipation among US adults rose significantly during the COVID-19 pandemic, with a near doubling of the national rate of IBS over 2 years, a study has found.

The uptick is probably due to not only the direct impact of SARS-CoV-2 infection on the gastrointestinal tract but also to the psychological stress associated with pandemic life, the study team said. 

“COVID infection itself can definitely cause gastrointestinal symptoms like diarrhea, nausea, and abdominal pain — and for some people, those symptoms can linger and lead to chronic conditions like IBS,” Christopher V. Almario, MD, MSHPM, lead author and gastroenterologist at Cedars-Sinai Medical Center, Los Angeles, California, told GI & Hepatology News

Dr. Christopher V. Almario



“But the stress of living through the pandemic — lockdowns, fear, isolation — also likely played a major role as well in the increased prevalence of digestive disorders. Both the infection itself and the psychological toll of the pandemic can disrupt the gut-brain axis and trigger chronic digestive disorders like IBS,” Almario said. 

The study was published in Neurogastroenterology & Motility.

 

Growing Burden of Gut Disorders 

Disorders of gut-brain interaction (DGBIs) are a heterogeneous group of conditions in which gastrointestinal symptoms occur without any detectable structural or biochemical abnormalities in the digestive tract. They include IBS, functional dyspepsia, and chronic idiopathic constipation, among others. 

DGBIs are highly prevalent. Research has shown that nearly 40% of people in the US meet Rome IV criteria for at least one DGBI. 

Almario and colleagues assessed trends in prevalence of these conditions during the COVID-19 pandemic. Starting in May 2020 through May 2022, they conducted a series of online surveys with more than 160,000 adults aged 18 or older using validated Rome IV diagnostic questionnaires. 

Results showed that during the pandemic, IBS prevalence rose from 6.1% in May 2020 to 11.0% by May 2022, an increase of 0.188% per month (adjusted P < .001). 

Chronic idiopathic constipation showed a smaller but statistically significant increase, from 6.0% to 6.4% (0.056% per month; adjusted P < .001). 

Within the IBS subtypes, mixed-type IBS showed the largest relative increase (0.085% per month), followed by IBS with constipation (0.041% per month) and IBS with diarrhea (0.037% per month). 

There were no significant changes in the prevalence of other DGBIs, such as functional bloating, functional diarrhea, or functional dyspepsia, during the study period. 

Almario told GI & Hepatology News only about 9% of those surveyed reported a positive COVID test at the time of the surveys, but that figure probably underrepresents actual infections, especially in the early months of the pandemic. “Most of the survey responses came in during the earlier phases of the pandemic, and the percentage reporting a positive test increased over time,” he explained. 

Almario also noted that this study did not directly compare digestive disorder rates between infected and uninfected individuals. However, a separate study by the Cedars-Sinai team currently undergoing peer review addresses that question more directly. “That study, along with several other studies, show that having COVID increases the risk of developing conditions like IBS and functional dyspepsia,” Almario said. 

Taken together, the findings “underscore the increasing healthcare and economic burden of DGBI in the post-pandemic era, emphasizing the need for targeted efforts to effectively diagnose and manage these complex conditions,” they wrote. 

“This will be especially challenging for healthcare systems to address, given the existing shortage of primary care physicians and gastroenterologists — clinicians who primarily manage individuals with DGBI,” they noted. 

Support for this study was received from Ironwood Pharmaceuticals and Salix Pharmaceuticals in the form of institutional research grants to Cedars-Sinai. Almario has consulted for Exact Sciences, Greenspace Labs, Owlstone Medical, Salix Pharmaceuticals, and Universal DX.

A version of this article appeared on Medscape.com.

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How Common Meds Can Secretly Wreck Your Patients’ Microbiome

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Thu, 07/10/2025 - 09:31

Effective ways to combat harmful viruses, bacteria, fungi, and parasitic worms have driven major advances in medicine and contributed to a significant increase in human life expectancy over the past century. However, as knowledge about the role of these microorganisms in promoting and maintaining health deepens, there is a need for a new look at the impact of these treatments.

The list of drugs that can directly alter the gut microbiota is long. In addition to antibiotics, antivirals, antifungals, anthelmintics, proton pump inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), laxatives, oral antidiabetics, antidepressants, antipsychotics, statins, chemotherapeutics, and immunosuppressants can trigger dysbiosis.

2020 study published in Nature Communications, which analyzed the impact of common medications on the composition and metabolic function of the gut bacteria, showed that of the 41 classes of medications, researchers found that 19 were associated with changes in the microbiome, most notably antibiotics, proton pump inhibitors, laxatives, and metformin.

“There are still no protocols aimed at preserving the microbiota during pharmacological treatment. Future research should identify biomarkers of drug-induced dysbiosis and potentially adapt live biotherapeutics to counteract it,” said Maria Júlia Segantini, MD, a coloproctologist at the University of São Paulo, Brazil.

 

Known Facts

Antibiotics, antivirals, antifungals, and anthelmintics eliminate pathogens but can also disrupt the microbiota across the gut, skin, mouth, lungs, and genitourinary tract.

“This ecosystem is part of the innate immune system and helps to balance inflammation and homeostasis. Loss of microbial diversity alters interspecies interactions and changes nutrient availability, which can undermine the ability to fend off pathogens,” said Segantini, noting the role of microbiota in vitamin K and B-complex production.

“The microbiome may lose its ability to prevent pathogens from taking hold. This is due to the loss of microbial diversity, changes in interactions between species, and the availability of nutrients,” she added.

Antibiotics, as is well known, eliminate bacterial species indiscriminately, reduce the presence of beneficial bacteria in the gut, and, therefore, favor the growth of opportunistic pathogenic microorganisms. However, in addition to their direct effects on microorganisms, different medications can alter the intestinal microbiota through various mechanisms linked to their specific actions. Here are some examples:

Proton pump inhibitors: These can facilitate the translocation of bacteria from the mouth to the intestine and affect the metabolic functions of the intestinal microbiota. “In users of these medications, there may be an enrichment of pathways related to carbohydrate metabolism, such as glycolysis and pyruvate metabolism, indicating possible changes in intestinal metabolism,” Segantini explained.

NSAIDs: NSAIDs can modify the function and composition of the intestinal microbiota, favor the growth of pathogenic species, and reduce the diversity of preexisting bacteria by reducing the presence of beneficial commensal bacteria, such as Lactobacillus and Bifidobacterium. “This is due to changes in the permeability of the intestinal wall, due to the inhibition of prostaglandins that help maintain the integrity of the intestinal barrier, enteropathy induced by NSAIDs, and drug interactions,” said Segantini.

Laxatives: Accelerated intestinal transit using laxatives impairs the quality of the microbiota and alters bile acid. Osmotic agents, such as lactulose and polyethylene glycol, may decrease resistance to infection.

“Studies in animal models indicate that polyethylene glycol can increase the proportion of Bacteroides and reduce the abundance of Bacteroidales bacteria, with lasting repercussions on the intestinal microbiota. Stimulant laxatives, in addition to causing an acceleration of the evacuation flow, can lead to a decrease in the production of short-chain fatty acids, which are important for intestinal health,” Segantini explained.

Chemotherapeutics: Chemotherapeutic agents can significantly influence the intestinal microbiota and affect its composition, diversity, and functionality, which in turn can affect the efficacy of treatment and the occurrence of adverse effects. “5-fluorouracil led to a decrease in the abundance of beneficial anaerobic genera, such as Blautia, and an increase in opportunistic pathogens, such as Staphylococcus and Escherichia coli, during chemotherapy. In addition, it can lead to an increase in the abundance of Bacteroidetes and Proteobacteria while reducing Firmicutes and Actinobacteria. These changes can affect the function of the intestinal barrier and the immune response. Other problems related to chemotherapy-induced dysbiosis are the adverse effects themselves, such as diarrhea and mucositis,” said Segantini.

Statins: Animal studies suggest that treatment with statins, including atorvastatin, may alter the composition of the gut microbiota. “These changes include the reduction of beneficial bacteria, such as Akkermansia muciniphila, and the increase in intestinal pathogens, resulting in intestinal dysbiosis. The use of statins can affect the diversity of the intestinal microbiota, although the results vary according to the type of statin and the clinical context.”

“Statins can activate intestinal nuclear receptors, such as pregnane X receptors, which modulate the expression of genes involved in bile metabolism and the inflammatory response. This activation can contribute to changes in the intestinal microbiota and associated metabolic processes. Although statins play a fundamental role in reducing cardiovascular risk, their interactions with the intestinal microbiota can influence the efficacy of treatment and the profile of adverse effects,” said Segantini.

Immunosuppressants: The use of immunosuppressants, such as corticosteroids, tacrolimus, and mycophenolate, has been associated with changes in the composition of the intestinal microbiota. “Immunosuppressant-induced dysbiosis can compromise the intestinal barrier, increase permeability, and facilitate bacterial translocation. This can result in opportunistic infections by pathogens and post-transplant complications, such as graft rejection and post-transplant diabetes,” Segantini stated.

“Alteration of the gut microbiota by immunosuppressants may influence the host’s immune response. For example, tacrolimus has been associated with an increase in the abundance of AllobaculumBacteroides, and Lactobacillus, in addition to elevated levels of regulatory T cells in the colonic mucosa and circulation, suggesting a role in modulating gut immunity,” she said.

Antipsychotics: Antipsychotics can affect gut microbiota in several ways, influencing bacterial composition and diversity, which may contribute to adverse metabolic and gastrointestinal effects.

“Olanzapine, for example, has been shown in rodent studies to increase the abundance of Firmicutes and reduce that of Bacteroidetes, resulting in a higher Firmicutes/Bacteroidetes ratio, which is associated with weight gain and dyslipidemia,” said Segantini.

She stated that risperidone increased the abundance of Firmicutes and decreased that of Bacteroidetes in animal models, correlating with weight gain and reduced basal metabolic rate. “Fecal transfer from risperidone-treated mice to naive mice resulted in decreased metabolic rate, suggesting that the gut microbiota would mediate these effects.”

Treatment with aripiprazole increased microbial diversity and the abundance of ClostridiumPeptoclostridiumIntestinibacter, and Christensenellaceae, in addition to promoting increased intestinal permeability in animal models.

“Therefore, the use of these medications can lead to metabolic changes, such as weight gain, hyperglycemia, dyslipidemia, and hypertension. This is due to a decrease in the production of short-chain fatty acids, which are important for maintaining the integrity of the intestinal barrier. Another change frequently observed in clinical practice is constipation induced by these medications. This functional change can also generate changes in the intestinal microbiota,” she said.

Oral antidiabetic agents: Oral antidiabetic agents influence the intestinal microbiota in different ways, depending on the therapeutic class. However, not all drug interactions in the microbiome are harmful. Liraglutide, a GLP-1 receptor agonist, promotes the growth of beneficial bacteria associated with metabolism.

“Exenatide, another GLP-1 agonist, has varied effects and can increase both beneficial and inflammatory bacteria,” explained Álvaro Delgado, MD, a gastroenterologist at Hospital Alemão Oswaldo Cruz in São Paulo, Brazil.

“In humans, an increase in bacteria such as Faecalibacterium prausnitzii has been observed, with positive effects. However, more studies are needed to evaluate the clinical impacts,” he said, and that, in animal models, these changes caused by GLP-1 agonists are linked to metabolic changes, such as greater glucose tolerance.

Metformin has been linked to increased abundance of A muciniphila, a beneficial bacterium that degrades mucin and produces short-chain fatty acids. “These bacteria are associated with improved insulin sensitivity and reduced inflammation,” he said.

Segantini stated that studies in mice have shown that vildagliptin also plays a positive role in altering the composition of the intestinal microbiota, increasing the abundance of Lactobacillus and Roseburia, and reducing Oscillibacter. “This same beneficial effect is seen with the use of sitagliptin,” she said.

Studies in animal models have also indicated that empagliflozin and dapagliflozin increase the populations of short-chain fatty acid-producing bacteria, such as Bacteroides and Odoribacter, and reduce the populations of lipopolysaccharide-producing bacteria, such as Oscillibacter.

“There are still not many studies regarding the use of sulfonylureas on the intestinal microbiota, so their action on the microbiota is still controversial,” said Segantini.

Antivirals: Antiviral treatment can influence gut microbiota in complex ways, depending on the type of infection and medication used.

“Although many studies focus on the effects of viral infection on the microbiota, there is evidence that antiviral treatment can also restore the healthy composition of the microbiota, promoting additional benefits to gut and immune health,” said Segantini.

In mice with chronic hepatitis B, entecavir restored the alpha diversity of the gut microbiota, which was reduced due to infection. In addition, the recovery of beneficial bacteria, such as Akkermansia and Blautia, was observed, which was associated with the protection of the intestinal barrier and reduction of hepatic inflammation.

Studies have indicated that tenofovir may aid in the recovery of intestinal dysbiosis induced by chronic hepatitis B virus infection and promote the restoration of a healthy microbial composition.

“Specifically, an increase in Collinsella and Bifidobacterium, bacteria associated with the production of short-chain fatty acids and modulation of the immune response, was observed,” said Segantini.

The use of antiretrovirals, such as lopinavir and ritonavir, has been associated with changes in the composition of the intestinal microbiota in patients living with HIV.

“A decrease in Lachnospira, Butyricicoccus, Oscillospira, and Prevotella, bacteria that produce short-chain fatty acids that are important in intestinal health and in modulating the immune response, was observed.”

Antifungals: As a side effect, antifungals also eliminate commensal fungi, which “share intestinal niches with microbiota bacteria, balancing their immunological functions. When modified, they culminate in dysbiosis, worsening of inflammatory pathologies — such as colitis and allergic diseases — and can increase bacterial translocation,” said Segantini. 

For example, fluconazole reduces the abundance of Candida spp. while promoting the growth of fungi such as AspergillusWallemia, and Epicoccum.

“A relative increase in Firmicutes and Proteobacteria and a decrease in Bacteroidetes, Deferribacteres, Patescibacteria, and Tenericutes were also observed,” she explained.

Anthelmintics: These also affect the intestinal bacterial and fungal microbiota and alter the modulation of the immune response, in addition to having specific effects depending on the type of drug used.

 

Clinical Advice

Symptoms of dysbiosis include abdominal distension, flatulence, constipation or diarrhea, pain, fatigue, and mood swings. “The diagnosis is made based on the clinical picture, since tests such as small intestinal bacterial overgrowth, which indicate metabolites of bacteria associated with dysbiosis, specific stool tests, and microbiota mapping with GI-MAP [Gastrointestinal Microbial Assay Plus], for example, are expensive, difficult to access, and often inconclusive for diagnosis and for assessing the cause of the microbiota alteration,” explained Fernando Seefelder Flaquer, MD, a gastroenterologist at Albert Einstein Israelite Hospital in São Paulo.

When caused by medication, dysbiosis tends to be reversed naturally after discontinuation of the drug. “However, in medications with a high chance of altering the microbiota, probiotics can be used as prevention,” said Flaquer.

“To avoid problems, it is important to use antibiotics with caution and prefer, when possible, those with a reduced spectrum,” advised Delgado.

“Supplementation with probiotics and prebiotics can help maintain the balance of the microbiota, but it should be evaluated on a case-by-case basis, as its indications are still restricted at present.”

Currently, dysbiosis management relies on nutritional support and lifestyle modifications. “Physical exercise, management of psychological changes, and use of probiotics and prebiotics. In specific cases, individualized treatment may even require the administration of some types of antibiotics,” explained Segantini.

Although fecal microbiota transplantation (FMT) has been widely discussed and increasingly studied, it should still be approached with caution. While promising, FMT remains experimental for most conditions, and its use outside research settings should be carefully considered, particularly in patients who are immunocompromised or have compromised intestinal barriers.

“Currently, the treatment has stood out as promising for cases of recurrent Clostridioides difficile infection, being the only consolidated clinical indication,” said Segantini.

 

Science Hype

The interest in gut microbiome research has undoubtedly driven important scientific advances, but it also risks exaggeration. While the field holds enormous promise, much of the research remains in its early stages.

“The indiscriminate use of probiotics and reliance on microbiota analysis tests for personalized probiotic prescriptions are growing concerns,” Delgado warned. “We need to bridge the gap between basic science and clinical application. When that translation happens, it could revolutionize care for many diseases.”

Flaquer emphasized a broader issue: “There has been an overvaluation of dysbiosis and microbiota-focused treatments as cure-alls for a wide range of conditions — often subjective or lacking solid scientific correlation — such as depression, anxiety, fatigue, cancer, and even autism.”

With ongoing advances in microbiome research, understanding the impact of this complex ecosystem on human health has become essential across all medical specialties. In pediatrics, for instance, microbiota plays a critical role in immune and metabolic development, particularly in preventing conditions such as allergies and obesity.

In digestive surgery, preoperative use of probiotics has been shown to reduce complications and enhance postoperative recovery. Neurological research has highlighted the gut-brain axis as a potential factor in the development of neurodegenerative diseases. In gynecology, regulating the vaginal microbiota is key to preventing infections and complications during pregnancy.

“Given the connections between the microbiota and both intestinal and systemic diseases, every medical specialist should understand how it relates to the conditions they treat daily,” concluded Flaquer.

This story was translated from Medscape’s Portuguese edition.

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Effective ways to combat harmful viruses, bacteria, fungi, and parasitic worms have driven major advances in medicine and contributed to a significant increase in human life expectancy over the past century. However, as knowledge about the role of these microorganisms in promoting and maintaining health deepens, there is a need for a new look at the impact of these treatments.

The list of drugs that can directly alter the gut microbiota is long. In addition to antibiotics, antivirals, antifungals, anthelmintics, proton pump inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), laxatives, oral antidiabetics, antidepressants, antipsychotics, statins, chemotherapeutics, and immunosuppressants can trigger dysbiosis.

2020 study published in Nature Communications, which analyzed the impact of common medications on the composition and metabolic function of the gut bacteria, showed that of the 41 classes of medications, researchers found that 19 were associated with changes in the microbiome, most notably antibiotics, proton pump inhibitors, laxatives, and metformin.

“There are still no protocols aimed at preserving the microbiota during pharmacological treatment. Future research should identify biomarkers of drug-induced dysbiosis and potentially adapt live biotherapeutics to counteract it,” said Maria Júlia Segantini, MD, a coloproctologist at the University of São Paulo, Brazil.

 

Known Facts

Antibiotics, antivirals, antifungals, and anthelmintics eliminate pathogens but can also disrupt the microbiota across the gut, skin, mouth, lungs, and genitourinary tract.

“This ecosystem is part of the innate immune system and helps to balance inflammation and homeostasis. Loss of microbial diversity alters interspecies interactions and changes nutrient availability, which can undermine the ability to fend off pathogens,” said Segantini, noting the role of microbiota in vitamin K and B-complex production.

“The microbiome may lose its ability to prevent pathogens from taking hold. This is due to the loss of microbial diversity, changes in interactions between species, and the availability of nutrients,” she added.

Antibiotics, as is well known, eliminate bacterial species indiscriminately, reduce the presence of beneficial bacteria in the gut, and, therefore, favor the growth of opportunistic pathogenic microorganisms. However, in addition to their direct effects on microorganisms, different medications can alter the intestinal microbiota through various mechanisms linked to their specific actions. Here are some examples:

Proton pump inhibitors: These can facilitate the translocation of bacteria from the mouth to the intestine and affect the metabolic functions of the intestinal microbiota. “In users of these medications, there may be an enrichment of pathways related to carbohydrate metabolism, such as glycolysis and pyruvate metabolism, indicating possible changes in intestinal metabolism,” Segantini explained.

NSAIDs: NSAIDs can modify the function and composition of the intestinal microbiota, favor the growth of pathogenic species, and reduce the diversity of preexisting bacteria by reducing the presence of beneficial commensal bacteria, such as Lactobacillus and Bifidobacterium. “This is due to changes in the permeability of the intestinal wall, due to the inhibition of prostaglandins that help maintain the integrity of the intestinal barrier, enteropathy induced by NSAIDs, and drug interactions,” said Segantini.

Laxatives: Accelerated intestinal transit using laxatives impairs the quality of the microbiota and alters bile acid. Osmotic agents, such as lactulose and polyethylene glycol, may decrease resistance to infection.

“Studies in animal models indicate that polyethylene glycol can increase the proportion of Bacteroides and reduce the abundance of Bacteroidales bacteria, with lasting repercussions on the intestinal microbiota. Stimulant laxatives, in addition to causing an acceleration of the evacuation flow, can lead to a decrease in the production of short-chain fatty acids, which are important for intestinal health,” Segantini explained.

Chemotherapeutics: Chemotherapeutic agents can significantly influence the intestinal microbiota and affect its composition, diversity, and functionality, which in turn can affect the efficacy of treatment and the occurrence of adverse effects. “5-fluorouracil led to a decrease in the abundance of beneficial anaerobic genera, such as Blautia, and an increase in opportunistic pathogens, such as Staphylococcus and Escherichia coli, during chemotherapy. In addition, it can lead to an increase in the abundance of Bacteroidetes and Proteobacteria while reducing Firmicutes and Actinobacteria. These changes can affect the function of the intestinal barrier and the immune response. Other problems related to chemotherapy-induced dysbiosis are the adverse effects themselves, such as diarrhea and mucositis,” said Segantini.

Statins: Animal studies suggest that treatment with statins, including atorvastatin, may alter the composition of the gut microbiota. “These changes include the reduction of beneficial bacteria, such as Akkermansia muciniphila, and the increase in intestinal pathogens, resulting in intestinal dysbiosis. The use of statins can affect the diversity of the intestinal microbiota, although the results vary according to the type of statin and the clinical context.”

“Statins can activate intestinal nuclear receptors, such as pregnane X receptors, which modulate the expression of genes involved in bile metabolism and the inflammatory response. This activation can contribute to changes in the intestinal microbiota and associated metabolic processes. Although statins play a fundamental role in reducing cardiovascular risk, their interactions with the intestinal microbiota can influence the efficacy of treatment and the profile of adverse effects,” said Segantini.

Immunosuppressants: The use of immunosuppressants, such as corticosteroids, tacrolimus, and mycophenolate, has been associated with changes in the composition of the intestinal microbiota. “Immunosuppressant-induced dysbiosis can compromise the intestinal barrier, increase permeability, and facilitate bacterial translocation. This can result in opportunistic infections by pathogens and post-transplant complications, such as graft rejection and post-transplant diabetes,” Segantini stated.

“Alteration of the gut microbiota by immunosuppressants may influence the host’s immune response. For example, tacrolimus has been associated with an increase in the abundance of AllobaculumBacteroides, and Lactobacillus, in addition to elevated levels of regulatory T cells in the colonic mucosa and circulation, suggesting a role in modulating gut immunity,” she said.

Antipsychotics: Antipsychotics can affect gut microbiota in several ways, influencing bacterial composition and diversity, which may contribute to adverse metabolic and gastrointestinal effects.

“Olanzapine, for example, has been shown in rodent studies to increase the abundance of Firmicutes and reduce that of Bacteroidetes, resulting in a higher Firmicutes/Bacteroidetes ratio, which is associated with weight gain and dyslipidemia,” said Segantini.

She stated that risperidone increased the abundance of Firmicutes and decreased that of Bacteroidetes in animal models, correlating with weight gain and reduced basal metabolic rate. “Fecal transfer from risperidone-treated mice to naive mice resulted in decreased metabolic rate, suggesting that the gut microbiota would mediate these effects.”

Treatment with aripiprazole increased microbial diversity and the abundance of ClostridiumPeptoclostridiumIntestinibacter, and Christensenellaceae, in addition to promoting increased intestinal permeability in animal models.

“Therefore, the use of these medications can lead to metabolic changes, such as weight gain, hyperglycemia, dyslipidemia, and hypertension. This is due to a decrease in the production of short-chain fatty acids, which are important for maintaining the integrity of the intestinal barrier. Another change frequently observed in clinical practice is constipation induced by these medications. This functional change can also generate changes in the intestinal microbiota,” she said.

Oral antidiabetic agents: Oral antidiabetic agents influence the intestinal microbiota in different ways, depending on the therapeutic class. However, not all drug interactions in the microbiome are harmful. Liraglutide, a GLP-1 receptor agonist, promotes the growth of beneficial bacteria associated with metabolism.

“Exenatide, another GLP-1 agonist, has varied effects and can increase both beneficial and inflammatory bacteria,” explained Álvaro Delgado, MD, a gastroenterologist at Hospital Alemão Oswaldo Cruz in São Paulo, Brazil.

“In humans, an increase in bacteria such as Faecalibacterium prausnitzii has been observed, with positive effects. However, more studies are needed to evaluate the clinical impacts,” he said, and that, in animal models, these changes caused by GLP-1 agonists are linked to metabolic changes, such as greater glucose tolerance.

Metformin has been linked to increased abundance of A muciniphila, a beneficial bacterium that degrades mucin and produces short-chain fatty acids. “These bacteria are associated with improved insulin sensitivity and reduced inflammation,” he said.

Segantini stated that studies in mice have shown that vildagliptin also plays a positive role in altering the composition of the intestinal microbiota, increasing the abundance of Lactobacillus and Roseburia, and reducing Oscillibacter. “This same beneficial effect is seen with the use of sitagliptin,” she said.

Studies in animal models have also indicated that empagliflozin and dapagliflozin increase the populations of short-chain fatty acid-producing bacteria, such as Bacteroides and Odoribacter, and reduce the populations of lipopolysaccharide-producing bacteria, such as Oscillibacter.

“There are still not many studies regarding the use of sulfonylureas on the intestinal microbiota, so their action on the microbiota is still controversial,” said Segantini.

Antivirals: Antiviral treatment can influence gut microbiota in complex ways, depending on the type of infection and medication used.

“Although many studies focus on the effects of viral infection on the microbiota, there is evidence that antiviral treatment can also restore the healthy composition of the microbiota, promoting additional benefits to gut and immune health,” said Segantini.

In mice with chronic hepatitis B, entecavir restored the alpha diversity of the gut microbiota, which was reduced due to infection. In addition, the recovery of beneficial bacteria, such as Akkermansia and Blautia, was observed, which was associated with the protection of the intestinal barrier and reduction of hepatic inflammation.

Studies have indicated that tenofovir may aid in the recovery of intestinal dysbiosis induced by chronic hepatitis B virus infection and promote the restoration of a healthy microbial composition.

“Specifically, an increase in Collinsella and Bifidobacterium, bacteria associated with the production of short-chain fatty acids and modulation of the immune response, was observed,” said Segantini.

The use of antiretrovirals, such as lopinavir and ritonavir, has been associated with changes in the composition of the intestinal microbiota in patients living with HIV.

“A decrease in Lachnospira, Butyricicoccus, Oscillospira, and Prevotella, bacteria that produce short-chain fatty acids that are important in intestinal health and in modulating the immune response, was observed.”

Antifungals: As a side effect, antifungals also eliminate commensal fungi, which “share intestinal niches with microbiota bacteria, balancing their immunological functions. When modified, they culminate in dysbiosis, worsening of inflammatory pathologies — such as colitis and allergic diseases — and can increase bacterial translocation,” said Segantini. 

For example, fluconazole reduces the abundance of Candida spp. while promoting the growth of fungi such as AspergillusWallemia, and Epicoccum.

“A relative increase in Firmicutes and Proteobacteria and a decrease in Bacteroidetes, Deferribacteres, Patescibacteria, and Tenericutes were also observed,” she explained.

Anthelmintics: These also affect the intestinal bacterial and fungal microbiota and alter the modulation of the immune response, in addition to having specific effects depending on the type of drug used.

 

Clinical Advice

Symptoms of dysbiosis include abdominal distension, flatulence, constipation or diarrhea, pain, fatigue, and mood swings. “The diagnosis is made based on the clinical picture, since tests such as small intestinal bacterial overgrowth, which indicate metabolites of bacteria associated with dysbiosis, specific stool tests, and microbiota mapping with GI-MAP [Gastrointestinal Microbial Assay Plus], for example, are expensive, difficult to access, and often inconclusive for diagnosis and for assessing the cause of the microbiota alteration,” explained Fernando Seefelder Flaquer, MD, a gastroenterologist at Albert Einstein Israelite Hospital in São Paulo.

When caused by medication, dysbiosis tends to be reversed naturally after discontinuation of the drug. “However, in medications with a high chance of altering the microbiota, probiotics can be used as prevention,” said Flaquer.

“To avoid problems, it is important to use antibiotics with caution and prefer, when possible, those with a reduced spectrum,” advised Delgado.

“Supplementation with probiotics and prebiotics can help maintain the balance of the microbiota, but it should be evaluated on a case-by-case basis, as its indications are still restricted at present.”

Currently, dysbiosis management relies on nutritional support and lifestyle modifications. “Physical exercise, management of psychological changes, and use of probiotics and prebiotics. In specific cases, individualized treatment may even require the administration of some types of antibiotics,” explained Segantini.

Although fecal microbiota transplantation (FMT) has been widely discussed and increasingly studied, it should still be approached with caution. While promising, FMT remains experimental for most conditions, and its use outside research settings should be carefully considered, particularly in patients who are immunocompromised or have compromised intestinal barriers.

“Currently, the treatment has stood out as promising for cases of recurrent Clostridioides difficile infection, being the only consolidated clinical indication,” said Segantini.

 

Science Hype

The interest in gut microbiome research has undoubtedly driven important scientific advances, but it also risks exaggeration. While the field holds enormous promise, much of the research remains in its early stages.

“The indiscriminate use of probiotics and reliance on microbiota analysis tests for personalized probiotic prescriptions are growing concerns,” Delgado warned. “We need to bridge the gap between basic science and clinical application. When that translation happens, it could revolutionize care for many diseases.”

Flaquer emphasized a broader issue: “There has been an overvaluation of dysbiosis and microbiota-focused treatments as cure-alls for a wide range of conditions — often subjective or lacking solid scientific correlation — such as depression, anxiety, fatigue, cancer, and even autism.”

With ongoing advances in microbiome research, understanding the impact of this complex ecosystem on human health has become essential across all medical specialties. In pediatrics, for instance, microbiota plays a critical role in immune and metabolic development, particularly in preventing conditions such as allergies and obesity.

In digestive surgery, preoperative use of probiotics has been shown to reduce complications and enhance postoperative recovery. Neurological research has highlighted the gut-brain axis as a potential factor in the development of neurodegenerative diseases. In gynecology, regulating the vaginal microbiota is key to preventing infections and complications during pregnancy.

“Given the connections between the microbiota and both intestinal and systemic diseases, every medical specialist should understand how it relates to the conditions they treat daily,” concluded Flaquer.

This story was translated from Medscape’s Portuguese edition.

Effective ways to combat harmful viruses, bacteria, fungi, and parasitic worms have driven major advances in medicine and contributed to a significant increase in human life expectancy over the past century. However, as knowledge about the role of these microorganisms in promoting and maintaining health deepens, there is a need for a new look at the impact of these treatments.

The list of drugs that can directly alter the gut microbiota is long. In addition to antibiotics, antivirals, antifungals, anthelmintics, proton pump inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), laxatives, oral antidiabetics, antidepressants, antipsychotics, statins, chemotherapeutics, and immunosuppressants can trigger dysbiosis.

2020 study published in Nature Communications, which analyzed the impact of common medications on the composition and metabolic function of the gut bacteria, showed that of the 41 classes of medications, researchers found that 19 were associated with changes in the microbiome, most notably antibiotics, proton pump inhibitors, laxatives, and metformin.

“There are still no protocols aimed at preserving the microbiota during pharmacological treatment. Future research should identify biomarkers of drug-induced dysbiosis and potentially adapt live biotherapeutics to counteract it,” said Maria Júlia Segantini, MD, a coloproctologist at the University of São Paulo, Brazil.

 

Known Facts

Antibiotics, antivirals, antifungals, and anthelmintics eliminate pathogens but can also disrupt the microbiota across the gut, skin, mouth, lungs, and genitourinary tract.

“This ecosystem is part of the innate immune system and helps to balance inflammation and homeostasis. Loss of microbial diversity alters interspecies interactions and changes nutrient availability, which can undermine the ability to fend off pathogens,” said Segantini, noting the role of microbiota in vitamin K and B-complex production.

“The microbiome may lose its ability to prevent pathogens from taking hold. This is due to the loss of microbial diversity, changes in interactions between species, and the availability of nutrients,” she added.

Antibiotics, as is well known, eliminate bacterial species indiscriminately, reduce the presence of beneficial bacteria in the gut, and, therefore, favor the growth of opportunistic pathogenic microorganisms. However, in addition to their direct effects on microorganisms, different medications can alter the intestinal microbiota through various mechanisms linked to their specific actions. Here are some examples:

Proton pump inhibitors: These can facilitate the translocation of bacteria from the mouth to the intestine and affect the metabolic functions of the intestinal microbiota. “In users of these medications, there may be an enrichment of pathways related to carbohydrate metabolism, such as glycolysis and pyruvate metabolism, indicating possible changes in intestinal metabolism,” Segantini explained.

NSAIDs: NSAIDs can modify the function and composition of the intestinal microbiota, favor the growth of pathogenic species, and reduce the diversity of preexisting bacteria by reducing the presence of beneficial commensal bacteria, such as Lactobacillus and Bifidobacterium. “This is due to changes in the permeability of the intestinal wall, due to the inhibition of prostaglandins that help maintain the integrity of the intestinal barrier, enteropathy induced by NSAIDs, and drug interactions,” said Segantini.

Laxatives: Accelerated intestinal transit using laxatives impairs the quality of the microbiota and alters bile acid. Osmotic agents, such as lactulose and polyethylene glycol, may decrease resistance to infection.

“Studies in animal models indicate that polyethylene glycol can increase the proportion of Bacteroides and reduce the abundance of Bacteroidales bacteria, with lasting repercussions on the intestinal microbiota. Stimulant laxatives, in addition to causing an acceleration of the evacuation flow, can lead to a decrease in the production of short-chain fatty acids, which are important for intestinal health,” Segantini explained.

Chemotherapeutics: Chemotherapeutic agents can significantly influence the intestinal microbiota and affect its composition, diversity, and functionality, which in turn can affect the efficacy of treatment and the occurrence of adverse effects. “5-fluorouracil led to a decrease in the abundance of beneficial anaerobic genera, such as Blautia, and an increase in opportunistic pathogens, such as Staphylococcus and Escherichia coli, during chemotherapy. In addition, it can lead to an increase in the abundance of Bacteroidetes and Proteobacteria while reducing Firmicutes and Actinobacteria. These changes can affect the function of the intestinal barrier and the immune response. Other problems related to chemotherapy-induced dysbiosis are the adverse effects themselves, such as diarrhea and mucositis,” said Segantini.

Statins: Animal studies suggest that treatment with statins, including atorvastatin, may alter the composition of the gut microbiota. “These changes include the reduction of beneficial bacteria, such as Akkermansia muciniphila, and the increase in intestinal pathogens, resulting in intestinal dysbiosis. The use of statins can affect the diversity of the intestinal microbiota, although the results vary according to the type of statin and the clinical context.”

“Statins can activate intestinal nuclear receptors, such as pregnane X receptors, which modulate the expression of genes involved in bile metabolism and the inflammatory response. This activation can contribute to changes in the intestinal microbiota and associated metabolic processes. Although statins play a fundamental role in reducing cardiovascular risk, their interactions with the intestinal microbiota can influence the efficacy of treatment and the profile of adverse effects,” said Segantini.

Immunosuppressants: The use of immunosuppressants, such as corticosteroids, tacrolimus, and mycophenolate, has been associated with changes in the composition of the intestinal microbiota. “Immunosuppressant-induced dysbiosis can compromise the intestinal barrier, increase permeability, and facilitate bacterial translocation. This can result in opportunistic infections by pathogens and post-transplant complications, such as graft rejection and post-transplant diabetes,” Segantini stated.

“Alteration of the gut microbiota by immunosuppressants may influence the host’s immune response. For example, tacrolimus has been associated with an increase in the abundance of AllobaculumBacteroides, and Lactobacillus, in addition to elevated levels of regulatory T cells in the colonic mucosa and circulation, suggesting a role in modulating gut immunity,” she said.

Antipsychotics: Antipsychotics can affect gut microbiota in several ways, influencing bacterial composition and diversity, which may contribute to adverse metabolic and gastrointestinal effects.

“Olanzapine, for example, has been shown in rodent studies to increase the abundance of Firmicutes and reduce that of Bacteroidetes, resulting in a higher Firmicutes/Bacteroidetes ratio, which is associated with weight gain and dyslipidemia,” said Segantini.

She stated that risperidone increased the abundance of Firmicutes and decreased that of Bacteroidetes in animal models, correlating with weight gain and reduced basal metabolic rate. “Fecal transfer from risperidone-treated mice to naive mice resulted in decreased metabolic rate, suggesting that the gut microbiota would mediate these effects.”

Treatment with aripiprazole increased microbial diversity and the abundance of ClostridiumPeptoclostridiumIntestinibacter, and Christensenellaceae, in addition to promoting increased intestinal permeability in animal models.

“Therefore, the use of these medications can lead to metabolic changes, such as weight gain, hyperglycemia, dyslipidemia, and hypertension. This is due to a decrease in the production of short-chain fatty acids, which are important for maintaining the integrity of the intestinal barrier. Another change frequently observed in clinical practice is constipation induced by these medications. This functional change can also generate changes in the intestinal microbiota,” she said.

Oral antidiabetic agents: Oral antidiabetic agents influence the intestinal microbiota in different ways, depending on the therapeutic class. However, not all drug interactions in the microbiome are harmful. Liraglutide, a GLP-1 receptor agonist, promotes the growth of beneficial bacteria associated with metabolism.

“Exenatide, another GLP-1 agonist, has varied effects and can increase both beneficial and inflammatory bacteria,” explained Álvaro Delgado, MD, a gastroenterologist at Hospital Alemão Oswaldo Cruz in São Paulo, Brazil.

“In humans, an increase in bacteria such as Faecalibacterium prausnitzii has been observed, with positive effects. However, more studies are needed to evaluate the clinical impacts,” he said, and that, in animal models, these changes caused by GLP-1 agonists are linked to metabolic changes, such as greater glucose tolerance.

Metformin has been linked to increased abundance of A muciniphila, a beneficial bacterium that degrades mucin and produces short-chain fatty acids. “These bacteria are associated with improved insulin sensitivity and reduced inflammation,” he said.

Segantini stated that studies in mice have shown that vildagliptin also plays a positive role in altering the composition of the intestinal microbiota, increasing the abundance of Lactobacillus and Roseburia, and reducing Oscillibacter. “This same beneficial effect is seen with the use of sitagliptin,” she said.

Studies in animal models have also indicated that empagliflozin and dapagliflozin increase the populations of short-chain fatty acid-producing bacteria, such as Bacteroides and Odoribacter, and reduce the populations of lipopolysaccharide-producing bacteria, such as Oscillibacter.

“There are still not many studies regarding the use of sulfonylureas on the intestinal microbiota, so their action on the microbiota is still controversial,” said Segantini.

Antivirals: Antiviral treatment can influence gut microbiota in complex ways, depending on the type of infection and medication used.

“Although many studies focus on the effects of viral infection on the microbiota, there is evidence that antiviral treatment can also restore the healthy composition of the microbiota, promoting additional benefits to gut and immune health,” said Segantini.

In mice with chronic hepatitis B, entecavir restored the alpha diversity of the gut microbiota, which was reduced due to infection. In addition, the recovery of beneficial bacteria, such as Akkermansia and Blautia, was observed, which was associated with the protection of the intestinal barrier and reduction of hepatic inflammation.

Studies have indicated that tenofovir may aid in the recovery of intestinal dysbiosis induced by chronic hepatitis B virus infection and promote the restoration of a healthy microbial composition.

“Specifically, an increase in Collinsella and Bifidobacterium, bacteria associated with the production of short-chain fatty acids and modulation of the immune response, was observed,” said Segantini.

The use of antiretrovirals, such as lopinavir and ritonavir, has been associated with changes in the composition of the intestinal microbiota in patients living with HIV.

“A decrease in Lachnospira, Butyricicoccus, Oscillospira, and Prevotella, bacteria that produce short-chain fatty acids that are important in intestinal health and in modulating the immune response, was observed.”

Antifungals: As a side effect, antifungals also eliminate commensal fungi, which “share intestinal niches with microbiota bacteria, balancing their immunological functions. When modified, they culminate in dysbiosis, worsening of inflammatory pathologies — such as colitis and allergic diseases — and can increase bacterial translocation,” said Segantini. 

For example, fluconazole reduces the abundance of Candida spp. while promoting the growth of fungi such as AspergillusWallemia, and Epicoccum.

“A relative increase in Firmicutes and Proteobacteria and a decrease in Bacteroidetes, Deferribacteres, Patescibacteria, and Tenericutes were also observed,” she explained.

Anthelmintics: These also affect the intestinal bacterial and fungal microbiota and alter the modulation of the immune response, in addition to having specific effects depending on the type of drug used.

 

Clinical Advice

Symptoms of dysbiosis include abdominal distension, flatulence, constipation or diarrhea, pain, fatigue, and mood swings. “The diagnosis is made based on the clinical picture, since tests such as small intestinal bacterial overgrowth, which indicate metabolites of bacteria associated with dysbiosis, specific stool tests, and microbiota mapping with GI-MAP [Gastrointestinal Microbial Assay Plus], for example, are expensive, difficult to access, and often inconclusive for diagnosis and for assessing the cause of the microbiota alteration,” explained Fernando Seefelder Flaquer, MD, a gastroenterologist at Albert Einstein Israelite Hospital in São Paulo.

When caused by medication, dysbiosis tends to be reversed naturally after discontinuation of the drug. “However, in medications with a high chance of altering the microbiota, probiotics can be used as prevention,” said Flaquer.

“To avoid problems, it is important to use antibiotics with caution and prefer, when possible, those with a reduced spectrum,” advised Delgado.

“Supplementation with probiotics and prebiotics can help maintain the balance of the microbiota, but it should be evaluated on a case-by-case basis, as its indications are still restricted at present.”

Currently, dysbiosis management relies on nutritional support and lifestyle modifications. “Physical exercise, management of psychological changes, and use of probiotics and prebiotics. In specific cases, individualized treatment may even require the administration of some types of antibiotics,” explained Segantini.

Although fecal microbiota transplantation (FMT) has been widely discussed and increasingly studied, it should still be approached with caution. While promising, FMT remains experimental for most conditions, and its use outside research settings should be carefully considered, particularly in patients who are immunocompromised or have compromised intestinal barriers.

“Currently, the treatment has stood out as promising for cases of recurrent Clostridioides difficile infection, being the only consolidated clinical indication,” said Segantini.

 

Science Hype

The interest in gut microbiome research has undoubtedly driven important scientific advances, but it also risks exaggeration. While the field holds enormous promise, much of the research remains in its early stages.

“The indiscriminate use of probiotics and reliance on microbiota analysis tests for personalized probiotic prescriptions are growing concerns,” Delgado warned. “We need to bridge the gap between basic science and clinical application. When that translation happens, it could revolutionize care for many diseases.”

Flaquer emphasized a broader issue: “There has been an overvaluation of dysbiosis and microbiota-focused treatments as cure-alls for a wide range of conditions — often subjective or lacking solid scientific correlation — such as depression, anxiety, fatigue, cancer, and even autism.”

With ongoing advances in microbiome research, understanding the impact of this complex ecosystem on human health has become essential across all medical specialties. In pediatrics, for instance, microbiota plays a critical role in immune and metabolic development, particularly in preventing conditions such as allergies and obesity.

In digestive surgery, preoperative use of probiotics has been shown to reduce complications and enhance postoperative recovery. Neurological research has highlighted the gut-brain axis as a potential factor in the development of neurodegenerative diseases. In gynecology, regulating the vaginal microbiota is key to preventing infections and complications during pregnancy.

“Given the connections between the microbiota and both intestinal and systemic diseases, every medical specialist should understand how it relates to the conditions they treat daily,” concluded Flaquer.

This story was translated from Medscape’s Portuguese edition.

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Sclerosing Mesenteritis: What GIs Need to Know About This Rare Disease

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AGA has issued an updated pragmatic review on sclerosing mesenteritis (SM). Published in Clinical Gastroenterology and Hepatology, the update evaluates available evidence for diagnosis and treatment and examines opportunities for future research in SM, previously known by such names as misty mesentery, mesenteric panniculitis, and inflammatory pseudotumor.

Led by Mark T. Worthington, MD, AGAF, a professor of medicine in the Division of Gastroenterology and Hepatology at the University of Virginia in Charlottesville, Virginia, an expert AGA panel described SM as an uncommon benign idiopathic autoimmune disease of the mesenteric fat. Although of poorly understood etiology, gastroenterologists need to be prepared to diagnose it.

“CT radiologists increasingly are reporting SM and related lesions, such as misty mesentery,” Worthington told GI & Hepatology News. “We are also seeing new SM cases caused by immune checkpoint inhibitors in cancer treatment, and the oncologists ask us to manage this because it interferes with the treatment of the underlying malignancy. Those are often readily treated because we catch them so early.” Metabolic syndrome and associated conditions increase the risk for SM, as does aging.

The recent changes are intended to help clinicians predict disease activity and the need for other testing or treatment. “For instance, most cases are indolent and do not require aggressive treatment — often no treatment at all — but for those that are aggressive, we want the clinician to be able to identify those and make sure the treatment is appropriate. The aggressive cases may warrant tertiary referral,” Worthington said. “A secondary cancer is a possibility in this condition, so drawing from the SM radiology studies, we try to help the clinician decide who needs other testing, such as PET-CT or biopsy, and who can be monitored.”

As many as 60% of cases are asymptomatic, requiring no treatment. Abdominal pain is the most frequent symptom and its location on clinical examination should correspond to the SM lesion on imaging. Treatment involves anti-inflammatory medications tailored to disease severity and clinical response.

No biopsy is not necessary if the lesion meets three of the five CT criteria reported by B. Coulier and has no features of more aggressive disease or malignancy. Although some have suggested that SM may be a paraneoplastic syndrome, current evidence does not support this. SM needs to be differentiated from other diagnoses such as non-Hodgkin’s lymphoma, peritoneal carcinomatosis, and mesenteric fibromatosis.

“There are now CT guidelines for who actually has SM, who needs a biopsy or a PET-CT to rule-out malignancy, and who doesn’t,” said Worthington. “Radiologists do not always use the Coulier criteria for diagnosis, but often they will with encouragement. From this review, a GI clinician should be able to identify SM on CT.”

Epidemiologically, retrospective CT studies have reported a frequency of 0.6%-1.1%, the panelists noted. And while demographic data are limited, a large early case series reported that SM patients had a mean age of 55 years and more likely to be men and of White race.

Patients with SM do not have a higher prevalence of autoimmunity in general, but may have increased rates of metabolic syndrome, obesity, coronary artery disease, and urolithiasis, the panelists noted.

The update allows room for differences in clinical judgment. “For instance, a longer or more frequent CT surveillance interval can be justified depending on the patient’s findings, and no one should feel locked in by these recommendations,” Worthington said.

 

Medical Therapy

Although there is no surgical cure, pharmacologic options are many. These include prednisone, tamoxifen, colchicine, azathioprine, thalidomide, cyclophosphamide, and methotrexate, as well as the biologics rituximab, infliximab and ustekinumab. Current corticosteroid-based therapies often require months to achieve a clinical response, however.

Bowel obstruction is managed nonoperatively when feasible, but medically refractory disease may require surgical bypass.

Offering his perspective on the guidance but not involved in its formulation, Gastroenterologist Stephen B. Hanauer, MD, AGAF, a professor of medicine at Northwestern Medicine in Chicago, said, “The most useful component of the practical review is the algorithm for diagnosis and determination when biopsy or follow-up imaging is reasonable in the absence of evidence.” He stressed that the recommendations are pragmatic rather than evidence-based “as there are no controlled trials and the presentation is heterogeneous.”

Dr. Stephen B. Hanauer



Hanauer added that none of the recommended treatments have been shown to impact reduction on imaging. “Hence, all of the treatments are empiric without biological or imaging endpoints.”

In his experience, patients with inflammatory features are the best candidates for immune-directed therapies as reduction in inflammatory markers is a potential endpoint, although no therapies have demonstrated an effect on imaging or progression. “As an IBD doctor, I favor steroids and azathioprine or anti-TNF directed therapy, but again, there is no evidence beyond reports of symptomatic improvement.” 

Worthington and colleagues agreed that treatment protocols have developed empirically. “Future investigation for symptomatic SM should focus on the nature of the inflammatory response, including causative cytokines and other proinflammatory mediators, the goal being targeted therapy with fewer side effects and a more rapid clinical response,” they wrote.

Currently, said Worthington, the biggest gaps remain in treatment. “Even the best studies are small and anecdotal, and we do not know the cytokine or other proinflammatory mediators.”

This guidance was supported by the AGA. Worthington reported renumeration from TriCity Surgery Center, Prescott, Ariz. Hanauer had no conflicts of interest relevant to their comments.

A version of this article appeared on Medscape.com.

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AGA has issued an updated pragmatic review on sclerosing mesenteritis (SM). Published in Clinical Gastroenterology and Hepatology, the update evaluates available evidence for diagnosis and treatment and examines opportunities for future research in SM, previously known by such names as misty mesentery, mesenteric panniculitis, and inflammatory pseudotumor.

Led by Mark T. Worthington, MD, AGAF, a professor of medicine in the Division of Gastroenterology and Hepatology at the University of Virginia in Charlottesville, Virginia, an expert AGA panel described SM as an uncommon benign idiopathic autoimmune disease of the mesenteric fat. Although of poorly understood etiology, gastroenterologists need to be prepared to diagnose it.

“CT radiologists increasingly are reporting SM and related lesions, such as misty mesentery,” Worthington told GI & Hepatology News. “We are also seeing new SM cases caused by immune checkpoint inhibitors in cancer treatment, and the oncologists ask us to manage this because it interferes with the treatment of the underlying malignancy. Those are often readily treated because we catch them so early.” Metabolic syndrome and associated conditions increase the risk for SM, as does aging.

The recent changes are intended to help clinicians predict disease activity and the need for other testing or treatment. “For instance, most cases are indolent and do not require aggressive treatment — often no treatment at all — but for those that are aggressive, we want the clinician to be able to identify those and make sure the treatment is appropriate. The aggressive cases may warrant tertiary referral,” Worthington said. “A secondary cancer is a possibility in this condition, so drawing from the SM radiology studies, we try to help the clinician decide who needs other testing, such as PET-CT or biopsy, and who can be monitored.”

As many as 60% of cases are asymptomatic, requiring no treatment. Abdominal pain is the most frequent symptom and its location on clinical examination should correspond to the SM lesion on imaging. Treatment involves anti-inflammatory medications tailored to disease severity and clinical response.

No biopsy is not necessary if the lesion meets three of the five CT criteria reported by B. Coulier and has no features of more aggressive disease or malignancy. Although some have suggested that SM may be a paraneoplastic syndrome, current evidence does not support this. SM needs to be differentiated from other diagnoses such as non-Hodgkin’s lymphoma, peritoneal carcinomatosis, and mesenteric fibromatosis.

“There are now CT guidelines for who actually has SM, who needs a biopsy or a PET-CT to rule-out malignancy, and who doesn’t,” said Worthington. “Radiologists do not always use the Coulier criteria for diagnosis, but often they will with encouragement. From this review, a GI clinician should be able to identify SM on CT.”

Epidemiologically, retrospective CT studies have reported a frequency of 0.6%-1.1%, the panelists noted. And while demographic data are limited, a large early case series reported that SM patients had a mean age of 55 years and more likely to be men and of White race.

Patients with SM do not have a higher prevalence of autoimmunity in general, but may have increased rates of metabolic syndrome, obesity, coronary artery disease, and urolithiasis, the panelists noted.

The update allows room for differences in clinical judgment. “For instance, a longer or more frequent CT surveillance interval can be justified depending on the patient’s findings, and no one should feel locked in by these recommendations,” Worthington said.

 

Medical Therapy

Although there is no surgical cure, pharmacologic options are many. These include prednisone, tamoxifen, colchicine, azathioprine, thalidomide, cyclophosphamide, and methotrexate, as well as the biologics rituximab, infliximab and ustekinumab. Current corticosteroid-based therapies often require months to achieve a clinical response, however.

Bowel obstruction is managed nonoperatively when feasible, but medically refractory disease may require surgical bypass.

Offering his perspective on the guidance but not involved in its formulation, Gastroenterologist Stephen B. Hanauer, MD, AGAF, a professor of medicine at Northwestern Medicine in Chicago, said, “The most useful component of the practical review is the algorithm for diagnosis and determination when biopsy or follow-up imaging is reasonable in the absence of evidence.” He stressed that the recommendations are pragmatic rather than evidence-based “as there are no controlled trials and the presentation is heterogeneous.”

Dr. Stephen B. Hanauer



Hanauer added that none of the recommended treatments have been shown to impact reduction on imaging. “Hence, all of the treatments are empiric without biological or imaging endpoints.”

In his experience, patients with inflammatory features are the best candidates for immune-directed therapies as reduction in inflammatory markers is a potential endpoint, although no therapies have demonstrated an effect on imaging or progression. “As an IBD doctor, I favor steroids and azathioprine or anti-TNF directed therapy, but again, there is no evidence beyond reports of symptomatic improvement.” 

Worthington and colleagues agreed that treatment protocols have developed empirically. “Future investigation for symptomatic SM should focus on the nature of the inflammatory response, including causative cytokines and other proinflammatory mediators, the goal being targeted therapy with fewer side effects and a more rapid clinical response,” they wrote.

Currently, said Worthington, the biggest gaps remain in treatment. “Even the best studies are small and anecdotal, and we do not know the cytokine or other proinflammatory mediators.”

This guidance was supported by the AGA. Worthington reported renumeration from TriCity Surgery Center, Prescott, Ariz. Hanauer had no conflicts of interest relevant to their comments.

A version of this article appeared on Medscape.com.

AGA has issued an updated pragmatic review on sclerosing mesenteritis (SM). Published in Clinical Gastroenterology and Hepatology, the update evaluates available evidence for diagnosis and treatment and examines opportunities for future research in SM, previously known by such names as misty mesentery, mesenteric panniculitis, and inflammatory pseudotumor.

Led by Mark T. Worthington, MD, AGAF, a professor of medicine in the Division of Gastroenterology and Hepatology at the University of Virginia in Charlottesville, Virginia, an expert AGA panel described SM as an uncommon benign idiopathic autoimmune disease of the mesenteric fat. Although of poorly understood etiology, gastroenterologists need to be prepared to diagnose it.

“CT radiologists increasingly are reporting SM and related lesions, such as misty mesentery,” Worthington told GI & Hepatology News. “We are also seeing new SM cases caused by immune checkpoint inhibitors in cancer treatment, and the oncologists ask us to manage this because it interferes with the treatment of the underlying malignancy. Those are often readily treated because we catch them so early.” Metabolic syndrome and associated conditions increase the risk for SM, as does aging.

The recent changes are intended to help clinicians predict disease activity and the need for other testing or treatment. “For instance, most cases are indolent and do not require aggressive treatment — often no treatment at all — but for those that are aggressive, we want the clinician to be able to identify those and make sure the treatment is appropriate. The aggressive cases may warrant tertiary referral,” Worthington said. “A secondary cancer is a possibility in this condition, so drawing from the SM radiology studies, we try to help the clinician decide who needs other testing, such as PET-CT or biopsy, and who can be monitored.”

As many as 60% of cases are asymptomatic, requiring no treatment. Abdominal pain is the most frequent symptom and its location on clinical examination should correspond to the SM lesion on imaging. Treatment involves anti-inflammatory medications tailored to disease severity and clinical response.

No biopsy is not necessary if the lesion meets three of the five CT criteria reported by B. Coulier and has no features of more aggressive disease or malignancy. Although some have suggested that SM may be a paraneoplastic syndrome, current evidence does not support this. SM needs to be differentiated from other diagnoses such as non-Hodgkin’s lymphoma, peritoneal carcinomatosis, and mesenteric fibromatosis.

“There are now CT guidelines for who actually has SM, who needs a biopsy or a PET-CT to rule-out malignancy, and who doesn’t,” said Worthington. “Radiologists do not always use the Coulier criteria for diagnosis, but often they will with encouragement. From this review, a GI clinician should be able to identify SM on CT.”

Epidemiologically, retrospective CT studies have reported a frequency of 0.6%-1.1%, the panelists noted. And while demographic data are limited, a large early case series reported that SM patients had a mean age of 55 years and more likely to be men and of White race.

Patients with SM do not have a higher prevalence of autoimmunity in general, but may have increased rates of metabolic syndrome, obesity, coronary artery disease, and urolithiasis, the panelists noted.

The update allows room for differences in clinical judgment. “For instance, a longer or more frequent CT surveillance interval can be justified depending on the patient’s findings, and no one should feel locked in by these recommendations,” Worthington said.

 

Medical Therapy

Although there is no surgical cure, pharmacologic options are many. These include prednisone, tamoxifen, colchicine, azathioprine, thalidomide, cyclophosphamide, and methotrexate, as well as the biologics rituximab, infliximab and ustekinumab. Current corticosteroid-based therapies often require months to achieve a clinical response, however.

Bowel obstruction is managed nonoperatively when feasible, but medically refractory disease may require surgical bypass.

Offering his perspective on the guidance but not involved in its formulation, Gastroenterologist Stephen B. Hanauer, MD, AGAF, a professor of medicine at Northwestern Medicine in Chicago, said, “The most useful component of the practical review is the algorithm for diagnosis and determination when biopsy or follow-up imaging is reasonable in the absence of evidence.” He stressed that the recommendations are pragmatic rather than evidence-based “as there are no controlled trials and the presentation is heterogeneous.”

Dr. Stephen B. Hanauer



Hanauer added that none of the recommended treatments have been shown to impact reduction on imaging. “Hence, all of the treatments are empiric without biological or imaging endpoints.”

In his experience, patients with inflammatory features are the best candidates for immune-directed therapies as reduction in inflammatory markers is a potential endpoint, although no therapies have demonstrated an effect on imaging or progression. “As an IBD doctor, I favor steroids and azathioprine or anti-TNF directed therapy, but again, there is no evidence beyond reports of symptomatic improvement.” 

Worthington and colleagues agreed that treatment protocols have developed empirically. “Future investigation for symptomatic SM should focus on the nature of the inflammatory response, including causative cytokines and other proinflammatory mediators, the goal being targeted therapy with fewer side effects and a more rapid clinical response,” they wrote.

Currently, said Worthington, the biggest gaps remain in treatment. “Even the best studies are small and anecdotal, and we do not know the cytokine or other proinflammatory mediators.”

This guidance was supported by the AGA. Worthington reported renumeration from TriCity Surgery Center, Prescott, Ariz. Hanauer had no conflicts of interest relevant to their comments.

A version of this article appeared on Medscape.com.

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Antibiotics Pre-Appendectomy Don’t Lower Perforation Risk, But Reduce Infections

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Antibiotic treatment while awaiting appendectomy does not lower risk for appendiceal perforation in patients with uncomplicated acute appendicitis, according to a new study.

While the percentage of surgical site infections (SSIs) was small for both groups, patients who received antibiotics during the waiting period had lower rates of these infections.

The trial — titled PERFECT-Antibiotics — was a substudy embedded in a larger PERFECT clinical trial, which aimed to determine whether an in-hospital delay of appendectomy resulted in increased risk for appendiceal perforation when compared to emergent surgery.

The trial “concluded that appendectomy does not need to be performed promptly in acute uncomplicated appendicitis and can be scheduled within 24 hours without increasing complications,” senior author Panu Mentula, MD, of the Department of Gastroenterological Surgery, Helsinki University Hospital, Helsinki, Finland, and colleagues wrote in the study. “The next question is whether preoperatively started antibiotic treatment reduces the risk of appendiceal perforations.”

The findings were published online in JAMA Surgery on May 14, 2025.

 

Trial Design

PERFECT-Antibiotics was an open-label, randomized trial conducted at two hospitals in Finland and one hospital in Norway. Researchers enrolled 1774 individuals diagnosed with acute uncomplicated appendicitis, diagnosed clinically or via imaging. Patients were placed in one of two groups: The antibiotic group received intravenous (IV) cefuroxime (1500 mg) and metronidazole (500 mg) every 8 hours until surgery, while the nonantibiotic group waited for surgery without antibiotics.

All patients received one dose of IV cefuroxime (1500 mg) and metronidazole (500 mg) during anesthesia induction. The primary outcome was perforated appendicitis and secondary outcomes included complication rate and SSIs within 30 days of follow-up.

The median age of patients was 35 years (interquartile range [IQR], 28-46 years), and 55% of patients were men. Patients waited a median time of 9 hours (IQR, 4.3-15.5) from study randomization to undergoing surgery.

 

No Difference in Appendiceal Perforation

Of the 888 patients in the preoperative antibiotic group, 26.2% received one dose, 38.7% received two doses, 22.6% received three doses, and 11.8% received four or more doses of antibiotics, including the antibiotic dose given during anesthesia. A total of 74 patients (8.3%) in this group had a perforated appendix.

Of the 886 patients not given preoperative antibiotics, 79 (8.9%) had a perforated appendix, which met the predetermined noninferiority threshold.

The groups had similar complication rates over the 30-day follow-up, though SSIs were lower in the antibiotic group (1.6%) than the no antibiotic group (3.2%).

The researchers estimated that the number needed to treat for antibiotic therapy was 63 for SSIs, 83 for intra-abdominal SSI, and 125 for reintervention.

“Although longer preoperative antibiotic treatment resulted in slightly lower rate of postoperative infectious complications, the actual difference was very small and probably clinically not significant to justify longer preoperative antibiotic treatment,” Mentula and colleagues wrote.

 

Lower Infection Rates With Antibiotics

Commenting on the study for GI & Hepatology News, Theodore Pappas, MD, professor of surgery at Duke University School of Medicine in Durham, North Carolina, placed greater importance on these secondary outcomes.

Intra-abdominal infections, a subset of SSIs, were more than twice as common in the no-antibiotic group (1.9%) than in the antibiotic group (0.7%; P = .02). Positive blood cultures were also more common in the no-antibiotic group than the antibiotic group (P = .02).

While the authors qualified these results, “the reality was it was better to use antibiotics,” he said.

There was also a “big overlap between the two groups,” he said, which may have muted differences between the two groups. For example, one fourth of patients in the antibiotic group received only one dose of antibiotics, the same treatment regimen as the no-antibiotic group.

“Although protocol required prophylaxis in all patients in the induction of anesthesia, some clinicians thought that it was unnecessary, because antibiotics had already been given only a couple of hours ago” in patients in the antibiotic group, Mentula told GI & Hepatology News. She did not think that would affect the study’s results.

The PERFECT trial and the antibiotics subtrial answer two important questions that have been asked for years, Pappas continued: Whether appendectomy for uncomplicated acute appendicitis needs to be performed emergently and if antibiotics administered while waiting for surgery improve outcomes.

“Basically, the study shows that you probably should keep them on antibiotics while you’re waiting,” he said.

The study was funded by Finnish Medical Foundation, the Mary and Georg Ehrnrooth Foundation, the Biomedicum Helsinki Foundation, and The Norwegian Surveillance Programme for Antimicrobial Resistance and research funds from the Finnish government. Mentula received grants from the Finnish government during the conduct of the study and personal fees from Pfizer outside the submitted work. Pappas reported no relevant disclosures.

A version of this article appeared on Medscape.com.

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Antibiotic treatment while awaiting appendectomy does not lower risk for appendiceal perforation in patients with uncomplicated acute appendicitis, according to a new study.

While the percentage of surgical site infections (SSIs) was small for both groups, patients who received antibiotics during the waiting period had lower rates of these infections.

The trial — titled PERFECT-Antibiotics — was a substudy embedded in a larger PERFECT clinical trial, which aimed to determine whether an in-hospital delay of appendectomy resulted in increased risk for appendiceal perforation when compared to emergent surgery.

The trial “concluded that appendectomy does not need to be performed promptly in acute uncomplicated appendicitis and can be scheduled within 24 hours without increasing complications,” senior author Panu Mentula, MD, of the Department of Gastroenterological Surgery, Helsinki University Hospital, Helsinki, Finland, and colleagues wrote in the study. “The next question is whether preoperatively started antibiotic treatment reduces the risk of appendiceal perforations.”

The findings were published online in JAMA Surgery on May 14, 2025.

 

Trial Design

PERFECT-Antibiotics was an open-label, randomized trial conducted at two hospitals in Finland and one hospital in Norway. Researchers enrolled 1774 individuals diagnosed with acute uncomplicated appendicitis, diagnosed clinically or via imaging. Patients were placed in one of two groups: The antibiotic group received intravenous (IV) cefuroxime (1500 mg) and metronidazole (500 mg) every 8 hours until surgery, while the nonantibiotic group waited for surgery without antibiotics.

All patients received one dose of IV cefuroxime (1500 mg) and metronidazole (500 mg) during anesthesia induction. The primary outcome was perforated appendicitis and secondary outcomes included complication rate and SSIs within 30 days of follow-up.

The median age of patients was 35 years (interquartile range [IQR], 28-46 years), and 55% of patients were men. Patients waited a median time of 9 hours (IQR, 4.3-15.5) from study randomization to undergoing surgery.

 

No Difference in Appendiceal Perforation

Of the 888 patients in the preoperative antibiotic group, 26.2% received one dose, 38.7% received two doses, 22.6% received three doses, and 11.8% received four or more doses of antibiotics, including the antibiotic dose given during anesthesia. A total of 74 patients (8.3%) in this group had a perforated appendix.

Of the 886 patients not given preoperative antibiotics, 79 (8.9%) had a perforated appendix, which met the predetermined noninferiority threshold.

The groups had similar complication rates over the 30-day follow-up, though SSIs were lower in the antibiotic group (1.6%) than the no antibiotic group (3.2%).

The researchers estimated that the number needed to treat for antibiotic therapy was 63 for SSIs, 83 for intra-abdominal SSI, and 125 for reintervention.

“Although longer preoperative antibiotic treatment resulted in slightly lower rate of postoperative infectious complications, the actual difference was very small and probably clinically not significant to justify longer preoperative antibiotic treatment,” Mentula and colleagues wrote.

 

Lower Infection Rates With Antibiotics

Commenting on the study for GI & Hepatology News, Theodore Pappas, MD, professor of surgery at Duke University School of Medicine in Durham, North Carolina, placed greater importance on these secondary outcomes.

Intra-abdominal infections, a subset of SSIs, were more than twice as common in the no-antibiotic group (1.9%) than in the antibiotic group (0.7%; P = .02). Positive blood cultures were also more common in the no-antibiotic group than the antibiotic group (P = .02).

While the authors qualified these results, “the reality was it was better to use antibiotics,” he said.

There was also a “big overlap between the two groups,” he said, which may have muted differences between the two groups. For example, one fourth of patients in the antibiotic group received only one dose of antibiotics, the same treatment regimen as the no-antibiotic group.

“Although protocol required prophylaxis in all patients in the induction of anesthesia, some clinicians thought that it was unnecessary, because antibiotics had already been given only a couple of hours ago” in patients in the antibiotic group, Mentula told GI & Hepatology News. She did not think that would affect the study’s results.

The PERFECT trial and the antibiotics subtrial answer two important questions that have been asked for years, Pappas continued: Whether appendectomy for uncomplicated acute appendicitis needs to be performed emergently and if antibiotics administered while waiting for surgery improve outcomes.

“Basically, the study shows that you probably should keep them on antibiotics while you’re waiting,” he said.

The study was funded by Finnish Medical Foundation, the Mary and Georg Ehrnrooth Foundation, the Biomedicum Helsinki Foundation, and The Norwegian Surveillance Programme for Antimicrobial Resistance and research funds from the Finnish government. Mentula received grants from the Finnish government during the conduct of the study and personal fees from Pfizer outside the submitted work. Pappas reported no relevant disclosures.

A version of this article appeared on Medscape.com.

Antibiotic treatment while awaiting appendectomy does not lower risk for appendiceal perforation in patients with uncomplicated acute appendicitis, according to a new study.

While the percentage of surgical site infections (SSIs) was small for both groups, patients who received antibiotics during the waiting period had lower rates of these infections.

The trial — titled PERFECT-Antibiotics — was a substudy embedded in a larger PERFECT clinical trial, which aimed to determine whether an in-hospital delay of appendectomy resulted in increased risk for appendiceal perforation when compared to emergent surgery.

The trial “concluded that appendectomy does not need to be performed promptly in acute uncomplicated appendicitis and can be scheduled within 24 hours without increasing complications,” senior author Panu Mentula, MD, of the Department of Gastroenterological Surgery, Helsinki University Hospital, Helsinki, Finland, and colleagues wrote in the study. “The next question is whether preoperatively started antibiotic treatment reduces the risk of appendiceal perforations.”

The findings were published online in JAMA Surgery on May 14, 2025.

 

Trial Design

PERFECT-Antibiotics was an open-label, randomized trial conducted at two hospitals in Finland and one hospital in Norway. Researchers enrolled 1774 individuals diagnosed with acute uncomplicated appendicitis, diagnosed clinically or via imaging. Patients were placed in one of two groups: The antibiotic group received intravenous (IV) cefuroxime (1500 mg) and metronidazole (500 mg) every 8 hours until surgery, while the nonantibiotic group waited for surgery without antibiotics.

All patients received one dose of IV cefuroxime (1500 mg) and metronidazole (500 mg) during anesthesia induction. The primary outcome was perforated appendicitis and secondary outcomes included complication rate and SSIs within 30 days of follow-up.

The median age of patients was 35 years (interquartile range [IQR], 28-46 years), and 55% of patients were men. Patients waited a median time of 9 hours (IQR, 4.3-15.5) from study randomization to undergoing surgery.

 

No Difference in Appendiceal Perforation

Of the 888 patients in the preoperative antibiotic group, 26.2% received one dose, 38.7% received two doses, 22.6% received three doses, and 11.8% received four or more doses of antibiotics, including the antibiotic dose given during anesthesia. A total of 74 patients (8.3%) in this group had a perforated appendix.

Of the 886 patients not given preoperative antibiotics, 79 (8.9%) had a perforated appendix, which met the predetermined noninferiority threshold.

The groups had similar complication rates over the 30-day follow-up, though SSIs were lower in the antibiotic group (1.6%) than the no antibiotic group (3.2%).

The researchers estimated that the number needed to treat for antibiotic therapy was 63 for SSIs, 83 for intra-abdominal SSI, and 125 for reintervention.

“Although longer preoperative antibiotic treatment resulted in slightly lower rate of postoperative infectious complications, the actual difference was very small and probably clinically not significant to justify longer preoperative antibiotic treatment,” Mentula and colleagues wrote.

 

Lower Infection Rates With Antibiotics

Commenting on the study for GI & Hepatology News, Theodore Pappas, MD, professor of surgery at Duke University School of Medicine in Durham, North Carolina, placed greater importance on these secondary outcomes.

Intra-abdominal infections, a subset of SSIs, were more than twice as common in the no-antibiotic group (1.9%) than in the antibiotic group (0.7%; P = .02). Positive blood cultures were also more common in the no-antibiotic group than the antibiotic group (P = .02).

While the authors qualified these results, “the reality was it was better to use antibiotics,” he said.

There was also a “big overlap between the two groups,” he said, which may have muted differences between the two groups. For example, one fourth of patients in the antibiotic group received only one dose of antibiotics, the same treatment regimen as the no-antibiotic group.

“Although protocol required prophylaxis in all patients in the induction of anesthesia, some clinicians thought that it was unnecessary, because antibiotics had already been given only a couple of hours ago” in patients in the antibiotic group, Mentula told GI & Hepatology News. She did not think that would affect the study’s results.

The PERFECT trial and the antibiotics subtrial answer two important questions that have been asked for years, Pappas continued: Whether appendectomy for uncomplicated acute appendicitis needs to be performed emergently and if antibiotics administered while waiting for surgery improve outcomes.

“Basically, the study shows that you probably should keep them on antibiotics while you’re waiting,” he said.

The study was funded by Finnish Medical Foundation, the Mary and Georg Ehrnrooth Foundation, the Biomedicum Helsinki Foundation, and The Norwegian Surveillance Programme for Antimicrobial Resistance and research funds from the Finnish government. Mentula received grants from the Finnish government during the conduct of the study and personal fees from Pfizer outside the submitted work. Pappas reported no relevant disclosures.

A version of this article appeared on Medscape.com.

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Gut Microbiome Changes in Chronic Pain — Test and Treat?

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A new study adds to what has been emerging in the literature — namely that there appear to be gut microbiome “signatures” for various pain conditions — suggesting that microbiome-based diagnostics and therapeutics may one day be routine for a broad range of pain conditions.

“There is now a whole list of pain conditions that appear to have these signatures, including postoperative pain, arthritis, neuropathy and migraine to name a few,” Robert Bonakdar, MD, director of pain management, Scripps Center for Integrative Medicine, San Diego, told GI & Hepatology News.

Fibromyalgia and complex regional pain syndrome (CRPS) are also on the list.

A team led by Amir Minerbi, MD, PhD, director of the Institute for Pain Medicine, Haifa, Israel, and colleagues published one of the first articles on gut changes in fibromyalgia. They noted that the gut microbiome could be utilized to determine which individuals had the condition and which did not — with about a 90% accuracy.

The team went on to show that transplanting gut microbiota from patients with fibromyalgia into germ-free mice was sufficient to induce pain-like behaviors in the animals — “effects that were reversed when healthy human microbiota were transplanted instead,” Minerbi told GI & Hepatology News.

Further, in a pilot clinical study, the researchers showed that transplanting microbiota from healthy donors led to a reduction in pain and other symptoms in women with treatment-resistant fibromyalgia.

Most recently, they found significant differences in the composition of the gut microbiome in a cohort of patients with CRPS from Israel, compared to matched pain-free control individuals.

Notably, two species — Dialister succinatiphilus and Phascolarctobacterium faecium – were enriched in patients with CRPS, while three species — Ligilactobacillus salivarius, Bifidobacterium dentium, and Bifidobacterium adolescentis – were increased in control samples, according to their report published last month in Anesthesiology.

“Importantly,” these findings were replicated in an independent cohort of patients with CRPS from Canada, “suggesting that the observed microbiome signature is robust and consistent across different environments,” Minerbi told GI & Hepatology News.

 

Causal Role? 

“These findings collectively suggest a causal role for the gut microbiome in at least some chronic pain conditions,” Minerbi said.

However, the co-authors of a linked editorial cautioned that it’s “unclear if D succinatiphilus or P faecium are functionally relevant to CRPS pathophysiology or if the bacteria increased in healthy control samples protect against CRPS development.”

Minerbi and colleagues also observed that fecal concentrations of all measured short chain fatty acids (SCFA) in patients with CRPS were lower on average compared to pain-free control individuals, of which butyric, hexanoic, and valeric acid showed significant depletion.

Additionally, plasma concentrations of acetic acid showed significant depletion in patients with CRPS vs control individuals, while propionate, butyrate, isobutyrate and 2-methyl-butyric acid showed a trend toward lower concentrations.

The quantification of SCFA in patient stool and serum is a “notable advance” in this study, Zulmary Manjarres, PhD; Ashley Plumb, PhD; and Katelyn Sadler, PhD; with the Center for Advanced Pain Studies at The University of Texas at Dallas, wrote in their editorial.

SCFA are produced by bacteria as a byproduct of dietary fiber fermentation and appropriate levels of these compounds are important to maintain low levels of inflammation in the colon and overall gut health, they explained.

This begs the question of whether administering probiotic bacteria — many of which are believed to exert health benefits through SCFA production — can be used to treat CRPS-associated pain. It’s something that needs to be studied, the editorialists wrote.

Yet, in their view, the “most notable achievement” of Minerbi and colleagues is the development of a machine learning model that accurately, specifically and sensitively categorized individuals as patients with CRPS or control individuals based on their fecal microbiome signature.

The model, trained on exact sequence variant data from the Israeli patients, achieved 89.5% accuracy, 90.0% sensitivity, and 88.9% specificity in distinguishing patients with CRPS from control individuals in the Canadian cohort.

Interestingly, in three patients with CRPS who underwent limb amputation and recovered from their pain, their gut microbiome signature remained unchanged, suggesting that microbiome alterations might precede or persist beyond symptomatic phases.

 

Test and Treat: Are We There Yet? 

The gut microbiome link to chronic pain syndromes is a hot area of research, but for now gut microbial testing followed by treatment aimed at “fixing” the microbiome remains largely experimental.

At this point, comprehensive gut-microbiome sequencing is not a routine, guideline-supported part of care for fibromyalgia or any chronic pain condition.

“Unfortunately, even for doctors interested in this area, we are not quite at the state of being able to diagnose and treat pain syndrome based on microbiome data,” Bonakdar told GI & Hepatology News.

He said there are many reasons for this including that this type of microbiome analysis is not commonly available at a routine lab. If patients do obtain testing, then the results are quite complex and may not translate to a diagnosis or a simple microbiome intervention.

“I think the closest option we have now is considering supplementing with commonly beneficial probiotic in pain conditions,” Bonakdar said.

One example is a preliminary fibromyalgia trial which found that supplementing with LactobacillusBifidobacterium, and Saccharomyces boulardii appeared to have benefit.

“Unfortunately, this is hit or miss as other trials such as one in low back pain did not find benefit,” Bonakdar said.

Addressing gut microbiome changes will become “more actionable when microbiome analysis is more commonplace as well as is the ability to tailor treatment to the abnormalities seen on testing in a real-world manner,” Bonakdar said.

“Until then, there is no harm in promoting an anti-inflammatory diet for our patients with pain which we know can improve components of the microbiome while also supporting pain management,” he concluded.

Minerbi, Bonakdar, and the editorial writers had no relevant disclosures.

A version of this article appeared on Medscape.com.

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A new study adds to what has been emerging in the literature — namely that there appear to be gut microbiome “signatures” for various pain conditions — suggesting that microbiome-based diagnostics and therapeutics may one day be routine for a broad range of pain conditions.

“There is now a whole list of pain conditions that appear to have these signatures, including postoperative pain, arthritis, neuropathy and migraine to name a few,” Robert Bonakdar, MD, director of pain management, Scripps Center for Integrative Medicine, San Diego, told GI & Hepatology News.

Fibromyalgia and complex regional pain syndrome (CRPS) are also on the list.

A team led by Amir Minerbi, MD, PhD, director of the Institute for Pain Medicine, Haifa, Israel, and colleagues published one of the first articles on gut changes in fibromyalgia. They noted that the gut microbiome could be utilized to determine which individuals had the condition and which did not — with about a 90% accuracy.

The team went on to show that transplanting gut microbiota from patients with fibromyalgia into germ-free mice was sufficient to induce pain-like behaviors in the animals — “effects that were reversed when healthy human microbiota were transplanted instead,” Minerbi told GI & Hepatology News.

Further, in a pilot clinical study, the researchers showed that transplanting microbiota from healthy donors led to a reduction in pain and other symptoms in women with treatment-resistant fibromyalgia.

Most recently, they found significant differences in the composition of the gut microbiome in a cohort of patients with CRPS from Israel, compared to matched pain-free control individuals.

Notably, two species — Dialister succinatiphilus and Phascolarctobacterium faecium – were enriched in patients with CRPS, while three species — Ligilactobacillus salivarius, Bifidobacterium dentium, and Bifidobacterium adolescentis – were increased in control samples, according to their report published last month in Anesthesiology.

“Importantly,” these findings were replicated in an independent cohort of patients with CRPS from Canada, “suggesting that the observed microbiome signature is robust and consistent across different environments,” Minerbi told GI & Hepatology News.

 

Causal Role? 

“These findings collectively suggest a causal role for the gut microbiome in at least some chronic pain conditions,” Minerbi said.

However, the co-authors of a linked editorial cautioned that it’s “unclear if D succinatiphilus or P faecium are functionally relevant to CRPS pathophysiology or if the bacteria increased in healthy control samples protect against CRPS development.”

Minerbi and colleagues also observed that fecal concentrations of all measured short chain fatty acids (SCFA) in patients with CRPS were lower on average compared to pain-free control individuals, of which butyric, hexanoic, and valeric acid showed significant depletion.

Additionally, plasma concentrations of acetic acid showed significant depletion in patients with CRPS vs control individuals, while propionate, butyrate, isobutyrate and 2-methyl-butyric acid showed a trend toward lower concentrations.

The quantification of SCFA in patient stool and serum is a “notable advance” in this study, Zulmary Manjarres, PhD; Ashley Plumb, PhD; and Katelyn Sadler, PhD; with the Center for Advanced Pain Studies at The University of Texas at Dallas, wrote in their editorial.

SCFA are produced by bacteria as a byproduct of dietary fiber fermentation and appropriate levels of these compounds are important to maintain low levels of inflammation in the colon and overall gut health, they explained.

This begs the question of whether administering probiotic bacteria — many of which are believed to exert health benefits through SCFA production — can be used to treat CRPS-associated pain. It’s something that needs to be studied, the editorialists wrote.

Yet, in their view, the “most notable achievement” of Minerbi and colleagues is the development of a machine learning model that accurately, specifically and sensitively categorized individuals as patients with CRPS or control individuals based on their fecal microbiome signature.

The model, trained on exact sequence variant data from the Israeli patients, achieved 89.5% accuracy, 90.0% sensitivity, and 88.9% specificity in distinguishing patients with CRPS from control individuals in the Canadian cohort.

Interestingly, in three patients with CRPS who underwent limb amputation and recovered from their pain, their gut microbiome signature remained unchanged, suggesting that microbiome alterations might precede or persist beyond symptomatic phases.

 

Test and Treat: Are We There Yet? 

The gut microbiome link to chronic pain syndromes is a hot area of research, but for now gut microbial testing followed by treatment aimed at “fixing” the microbiome remains largely experimental.

At this point, comprehensive gut-microbiome sequencing is not a routine, guideline-supported part of care for fibromyalgia or any chronic pain condition.

“Unfortunately, even for doctors interested in this area, we are not quite at the state of being able to diagnose and treat pain syndrome based on microbiome data,” Bonakdar told GI & Hepatology News.

He said there are many reasons for this including that this type of microbiome analysis is not commonly available at a routine lab. If patients do obtain testing, then the results are quite complex and may not translate to a diagnosis or a simple microbiome intervention.

“I think the closest option we have now is considering supplementing with commonly beneficial probiotic in pain conditions,” Bonakdar said.

One example is a preliminary fibromyalgia trial which found that supplementing with LactobacillusBifidobacterium, and Saccharomyces boulardii appeared to have benefit.

“Unfortunately, this is hit or miss as other trials such as one in low back pain did not find benefit,” Bonakdar said.

Addressing gut microbiome changes will become “more actionable when microbiome analysis is more commonplace as well as is the ability to tailor treatment to the abnormalities seen on testing in a real-world manner,” Bonakdar said.

“Until then, there is no harm in promoting an anti-inflammatory diet for our patients with pain which we know can improve components of the microbiome while also supporting pain management,” he concluded.

Minerbi, Bonakdar, and the editorial writers had no relevant disclosures.

A version of this article appeared on Medscape.com.

A new study adds to what has been emerging in the literature — namely that there appear to be gut microbiome “signatures” for various pain conditions — suggesting that microbiome-based diagnostics and therapeutics may one day be routine for a broad range of pain conditions.

“There is now a whole list of pain conditions that appear to have these signatures, including postoperative pain, arthritis, neuropathy and migraine to name a few,” Robert Bonakdar, MD, director of pain management, Scripps Center for Integrative Medicine, San Diego, told GI & Hepatology News.

Fibromyalgia and complex regional pain syndrome (CRPS) are also on the list.

A team led by Amir Minerbi, MD, PhD, director of the Institute for Pain Medicine, Haifa, Israel, and colleagues published one of the first articles on gut changes in fibromyalgia. They noted that the gut microbiome could be utilized to determine which individuals had the condition and which did not — with about a 90% accuracy.

The team went on to show that transplanting gut microbiota from patients with fibromyalgia into germ-free mice was sufficient to induce pain-like behaviors in the animals — “effects that were reversed when healthy human microbiota were transplanted instead,” Minerbi told GI & Hepatology News.

Further, in a pilot clinical study, the researchers showed that transplanting microbiota from healthy donors led to a reduction in pain and other symptoms in women with treatment-resistant fibromyalgia.

Most recently, they found significant differences in the composition of the gut microbiome in a cohort of patients with CRPS from Israel, compared to matched pain-free control individuals.

Notably, two species — Dialister succinatiphilus and Phascolarctobacterium faecium – were enriched in patients with CRPS, while three species — Ligilactobacillus salivarius, Bifidobacterium dentium, and Bifidobacterium adolescentis – were increased in control samples, according to their report published last month in Anesthesiology.

“Importantly,” these findings were replicated in an independent cohort of patients with CRPS from Canada, “suggesting that the observed microbiome signature is robust and consistent across different environments,” Minerbi told GI & Hepatology News.

 

Causal Role? 

“These findings collectively suggest a causal role for the gut microbiome in at least some chronic pain conditions,” Minerbi said.

However, the co-authors of a linked editorial cautioned that it’s “unclear if D succinatiphilus or P faecium are functionally relevant to CRPS pathophysiology or if the bacteria increased in healthy control samples protect against CRPS development.”

Minerbi and colleagues also observed that fecal concentrations of all measured short chain fatty acids (SCFA) in patients with CRPS were lower on average compared to pain-free control individuals, of which butyric, hexanoic, and valeric acid showed significant depletion.

Additionally, plasma concentrations of acetic acid showed significant depletion in patients with CRPS vs control individuals, while propionate, butyrate, isobutyrate and 2-methyl-butyric acid showed a trend toward lower concentrations.

The quantification of SCFA in patient stool and serum is a “notable advance” in this study, Zulmary Manjarres, PhD; Ashley Plumb, PhD; and Katelyn Sadler, PhD; with the Center for Advanced Pain Studies at The University of Texas at Dallas, wrote in their editorial.

SCFA are produced by bacteria as a byproduct of dietary fiber fermentation and appropriate levels of these compounds are important to maintain low levels of inflammation in the colon and overall gut health, they explained.

This begs the question of whether administering probiotic bacteria — many of which are believed to exert health benefits through SCFA production — can be used to treat CRPS-associated pain. It’s something that needs to be studied, the editorialists wrote.

Yet, in their view, the “most notable achievement” of Minerbi and colleagues is the development of a machine learning model that accurately, specifically and sensitively categorized individuals as patients with CRPS or control individuals based on their fecal microbiome signature.

The model, trained on exact sequence variant data from the Israeli patients, achieved 89.5% accuracy, 90.0% sensitivity, and 88.9% specificity in distinguishing patients with CRPS from control individuals in the Canadian cohort.

Interestingly, in three patients with CRPS who underwent limb amputation and recovered from their pain, their gut microbiome signature remained unchanged, suggesting that microbiome alterations might precede or persist beyond symptomatic phases.

 

Test and Treat: Are We There Yet? 

The gut microbiome link to chronic pain syndromes is a hot area of research, but for now gut microbial testing followed by treatment aimed at “fixing” the microbiome remains largely experimental.

At this point, comprehensive gut-microbiome sequencing is not a routine, guideline-supported part of care for fibromyalgia or any chronic pain condition.

“Unfortunately, even for doctors interested in this area, we are not quite at the state of being able to diagnose and treat pain syndrome based on microbiome data,” Bonakdar told GI & Hepatology News.

He said there are many reasons for this including that this type of microbiome analysis is not commonly available at a routine lab. If patients do obtain testing, then the results are quite complex and may not translate to a diagnosis or a simple microbiome intervention.

“I think the closest option we have now is considering supplementing with commonly beneficial probiotic in pain conditions,” Bonakdar said.

One example is a preliminary fibromyalgia trial which found that supplementing with LactobacillusBifidobacterium, and Saccharomyces boulardii appeared to have benefit.

“Unfortunately, this is hit or miss as other trials such as one in low back pain did not find benefit,” Bonakdar said.

Addressing gut microbiome changes will become “more actionable when microbiome analysis is more commonplace as well as is the ability to tailor treatment to the abnormalities seen on testing in a real-world manner,” Bonakdar said.

“Until then, there is no harm in promoting an anti-inflammatory diet for our patients with pain which we know can improve components of the microbiome while also supporting pain management,” he concluded.

Minerbi, Bonakdar, and the editorial writers had no relevant disclosures.

A version of this article appeared on Medscape.com.

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Journal Highlights: January-April 2025

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Below are some selections from what I am reading in the AGA journals, highlighting clinically applicable and possibly practice-changing expert reviews and studies.

Dr. Judy A. Trieu

Esophagus/Motility

Carlson DA, et al. A Standardized Approach to Performing and Interpreting Functional Lumen Imaging Probe Panometry for Esophageal Motility Disorders: The Dallas Consensus. Gastroenterology. 2025 Feb. doi: 10.1053/j.gastro.2025.01.234.

Parkman HP, et al; NIDDK Gastroparesis Clinical Research Consortium. Characterization of Patients with Symptoms of Gastroparesis Having Frequent Emergency Department Visits and Hospitalizations. Clin Gastroenterol Hepatol. 2025 Apr. doi: 10.1016/j.cgh.2025.01.033.

Dellon ES, et al. Long-term Safety and Efficacy of Budesonide Oral Suspension for Eosinophilic Esophagitis: A 4-Year, Phase 3, Open-Label Study. Clin Gastroenterol Hepatol. 2025 Feb. doi: 10.1016/j.cgh.2024.12.024.

Small Bowel

Hård Af Segerstad EM, et al; TEDDY Study Group. Early Dietary Fiber Intake Reduces Celiac Disease Risk in Genetically Prone Children: Insights From the TEDDY Study. Gastroenterology. 2025 Feb. doi: 10.1053/j.gastro.2025.01.241.

Colon

Shaukat A, et al. AGA Clinical Practice Update on Current Role of Blood Tests for Colorectal Cancer Screening: Commentary. Clin Gastroenterol Hepatol. 2025 Apr. doi: 10.1016/j.cgh.2025.04.003.

Bergman D, et al. Cholecystectomy is a Risk Factor for Microscopic Colitis: A Nationwide Population-based Matched Case Control Study. Clin Gastroenterol Hepatol. 2025 Mar. doi: 10.1016/j.cgh.2024.12.032.

Inflammatory Bowel Disease

Ben-Horin S, et al; Israeli IBD Research Nucleus (IIRN). Capsule Endoscopy-Guided Proactive Treat-to-Target Versus Continued Standard Care in Patients With Quiescent Crohn’s Disease: A Randomized Controlled Trial. Gastroenterology. 2025 Mar. doi: 10.1053/j.gastro.2025.02.031.

Pancreas

Guilabert L, et al; ERICA Consortium. Impact of Fluid Therapy in the Emergency Department in Acute Pancreatitis: a posthoc analysis of the WATERFALL Trial. Clin Gastroenterol Hepatol. 2025 Apr. doi: 10.1016/j.cgh.2025.01.038.

Hepatology

Rhee H, et al. Noncontrast Magnetic Resonance Imaging vs Ultrasonography for Hepatocellular Carcinoma Surveillance: A Randomized, Single-Center Trial. Gastroenterology. 2025 Jan. doi: 10.1053/j.gastro.2024.12.035.

Kronsten VT, et al. Hepatic Encephalopathy: When Lactulose and Rifaximin Are Not Working. Gastroenterology. 2025 Jan. doi: 10.1053/j.gastro.2025.01.010.

Edelson JC, et al. Accuracy and Safety of Endoscopic Ultrasound–Guided Liver Biopsy in Patients with Metabolic Dysfunction–Associated Liver Disease. Tech Innov Gastrointest Endosc. 2025 Apr. doi: 10.1016/j.tige.2025.250918.

Miscellaneous

Martin J, et al. Practical and Impactful Tips for Private Industry Collaborations with Gastroenterology Practices. Clin Gastroenterol Hepatol. 2025 Mar. doi: 10.1016/j.cgh.2025.01.021.

Tejada, Natalia et al. Glucagon-like Peptide-1 Receptor Agonists Are Not Associated With Increased Incidence of Pneumonia After Endoscopic Procedures. Tech Innov Gastrointest Endosc. 2025 Apr. doi: 10.1016/j.tige.2025.250925.

Lazaridis KN, et al. Microplastics and Nanoplastics and the Digestive System. Gastro Hep Adv. 2025 May. doi: 10.1016/j.gastha.2025.100694.



Dr. Trieu is assistant professor of medicine, interventional endoscopy, in the Division of Gastroenterology at Washington University in St. Louis School of Medicine, Missouri.

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Below are some selections from what I am reading in the AGA journals, highlighting clinically applicable and possibly practice-changing expert reviews and studies.

Dr. Judy A. Trieu

Esophagus/Motility

Carlson DA, et al. A Standardized Approach to Performing and Interpreting Functional Lumen Imaging Probe Panometry for Esophageal Motility Disorders: The Dallas Consensus. Gastroenterology. 2025 Feb. doi: 10.1053/j.gastro.2025.01.234.

Parkman HP, et al; NIDDK Gastroparesis Clinical Research Consortium. Characterization of Patients with Symptoms of Gastroparesis Having Frequent Emergency Department Visits and Hospitalizations. Clin Gastroenterol Hepatol. 2025 Apr. doi: 10.1016/j.cgh.2025.01.033.

Dellon ES, et al. Long-term Safety and Efficacy of Budesonide Oral Suspension for Eosinophilic Esophagitis: A 4-Year, Phase 3, Open-Label Study. Clin Gastroenterol Hepatol. 2025 Feb. doi: 10.1016/j.cgh.2024.12.024.

Small Bowel

Hård Af Segerstad EM, et al; TEDDY Study Group. Early Dietary Fiber Intake Reduces Celiac Disease Risk in Genetically Prone Children: Insights From the TEDDY Study. Gastroenterology. 2025 Feb. doi: 10.1053/j.gastro.2025.01.241.

Colon

Shaukat A, et al. AGA Clinical Practice Update on Current Role of Blood Tests for Colorectal Cancer Screening: Commentary. Clin Gastroenterol Hepatol. 2025 Apr. doi: 10.1016/j.cgh.2025.04.003.

Bergman D, et al. Cholecystectomy is a Risk Factor for Microscopic Colitis: A Nationwide Population-based Matched Case Control Study. Clin Gastroenterol Hepatol. 2025 Mar. doi: 10.1016/j.cgh.2024.12.032.

Inflammatory Bowel Disease

Ben-Horin S, et al; Israeli IBD Research Nucleus (IIRN). Capsule Endoscopy-Guided Proactive Treat-to-Target Versus Continued Standard Care in Patients With Quiescent Crohn’s Disease: A Randomized Controlled Trial. Gastroenterology. 2025 Mar. doi: 10.1053/j.gastro.2025.02.031.

Pancreas

Guilabert L, et al; ERICA Consortium. Impact of Fluid Therapy in the Emergency Department in Acute Pancreatitis: a posthoc analysis of the WATERFALL Trial. Clin Gastroenterol Hepatol. 2025 Apr. doi: 10.1016/j.cgh.2025.01.038.

Hepatology

Rhee H, et al. Noncontrast Magnetic Resonance Imaging vs Ultrasonography for Hepatocellular Carcinoma Surveillance: A Randomized, Single-Center Trial. Gastroenterology. 2025 Jan. doi: 10.1053/j.gastro.2024.12.035.

Kronsten VT, et al. Hepatic Encephalopathy: When Lactulose and Rifaximin Are Not Working. Gastroenterology. 2025 Jan. doi: 10.1053/j.gastro.2025.01.010.

Edelson JC, et al. Accuracy and Safety of Endoscopic Ultrasound–Guided Liver Biopsy in Patients with Metabolic Dysfunction–Associated Liver Disease. Tech Innov Gastrointest Endosc. 2025 Apr. doi: 10.1016/j.tige.2025.250918.

Miscellaneous

Martin J, et al. Practical and Impactful Tips for Private Industry Collaborations with Gastroenterology Practices. Clin Gastroenterol Hepatol. 2025 Mar. doi: 10.1016/j.cgh.2025.01.021.

Tejada, Natalia et al. Glucagon-like Peptide-1 Receptor Agonists Are Not Associated With Increased Incidence of Pneumonia After Endoscopic Procedures. Tech Innov Gastrointest Endosc. 2025 Apr. doi: 10.1016/j.tige.2025.250925.

Lazaridis KN, et al. Microplastics and Nanoplastics and the Digestive System. Gastro Hep Adv. 2025 May. doi: 10.1016/j.gastha.2025.100694.



Dr. Trieu is assistant professor of medicine, interventional endoscopy, in the Division of Gastroenterology at Washington University in St. Louis School of Medicine, Missouri.

Below are some selections from what I am reading in the AGA journals, highlighting clinically applicable and possibly practice-changing expert reviews and studies.

Dr. Judy A. Trieu

Esophagus/Motility

Carlson DA, et al. A Standardized Approach to Performing and Interpreting Functional Lumen Imaging Probe Panometry for Esophageal Motility Disorders: The Dallas Consensus. Gastroenterology. 2025 Feb. doi: 10.1053/j.gastro.2025.01.234.

Parkman HP, et al; NIDDK Gastroparesis Clinical Research Consortium. Characterization of Patients with Symptoms of Gastroparesis Having Frequent Emergency Department Visits and Hospitalizations. Clin Gastroenterol Hepatol. 2025 Apr. doi: 10.1016/j.cgh.2025.01.033.

Dellon ES, et al. Long-term Safety and Efficacy of Budesonide Oral Suspension for Eosinophilic Esophagitis: A 4-Year, Phase 3, Open-Label Study. Clin Gastroenterol Hepatol. 2025 Feb. doi: 10.1016/j.cgh.2024.12.024.

Small Bowel

Hård Af Segerstad EM, et al; TEDDY Study Group. Early Dietary Fiber Intake Reduces Celiac Disease Risk in Genetically Prone Children: Insights From the TEDDY Study. Gastroenterology. 2025 Feb. doi: 10.1053/j.gastro.2025.01.241.

Colon

Shaukat A, et al. AGA Clinical Practice Update on Current Role of Blood Tests for Colorectal Cancer Screening: Commentary. Clin Gastroenterol Hepatol. 2025 Apr. doi: 10.1016/j.cgh.2025.04.003.

Bergman D, et al. Cholecystectomy is a Risk Factor for Microscopic Colitis: A Nationwide Population-based Matched Case Control Study. Clin Gastroenterol Hepatol. 2025 Mar. doi: 10.1016/j.cgh.2024.12.032.

Inflammatory Bowel Disease

Ben-Horin S, et al; Israeli IBD Research Nucleus (IIRN). Capsule Endoscopy-Guided Proactive Treat-to-Target Versus Continued Standard Care in Patients With Quiescent Crohn’s Disease: A Randomized Controlled Trial. Gastroenterology. 2025 Mar. doi: 10.1053/j.gastro.2025.02.031.

Pancreas

Guilabert L, et al; ERICA Consortium. Impact of Fluid Therapy in the Emergency Department in Acute Pancreatitis: a posthoc analysis of the WATERFALL Trial. Clin Gastroenterol Hepatol. 2025 Apr. doi: 10.1016/j.cgh.2025.01.038.

Hepatology

Rhee H, et al. Noncontrast Magnetic Resonance Imaging vs Ultrasonography for Hepatocellular Carcinoma Surveillance: A Randomized, Single-Center Trial. Gastroenterology. 2025 Jan. doi: 10.1053/j.gastro.2024.12.035.

Kronsten VT, et al. Hepatic Encephalopathy: When Lactulose and Rifaximin Are Not Working. Gastroenterology. 2025 Jan. doi: 10.1053/j.gastro.2025.01.010.

Edelson JC, et al. Accuracy and Safety of Endoscopic Ultrasound–Guided Liver Biopsy in Patients with Metabolic Dysfunction–Associated Liver Disease. Tech Innov Gastrointest Endosc. 2025 Apr. doi: 10.1016/j.tige.2025.250918.

Miscellaneous

Martin J, et al. Practical and Impactful Tips for Private Industry Collaborations with Gastroenterology Practices. Clin Gastroenterol Hepatol. 2025 Mar. doi: 10.1016/j.cgh.2025.01.021.

Tejada, Natalia et al. Glucagon-like Peptide-1 Receptor Agonists Are Not Associated With Increased Incidence of Pneumonia After Endoscopic Procedures. Tech Innov Gastrointest Endosc. 2025 Apr. doi: 10.1016/j.tige.2025.250925.

Lazaridis KN, et al. Microplastics and Nanoplastics and the Digestive System. Gastro Hep Adv. 2025 May. doi: 10.1016/j.gastha.2025.100694.



Dr. Trieu is assistant professor of medicine, interventional endoscopy, in the Division of Gastroenterology at Washington University in St. Louis School of Medicine, Missouri.

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Video Capsule Endoscopy Aids Targeted Treatment in Quiescent Crohn’s

Aligning Monitoring Techniques with Therapeutic Targets
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Mon, 06/16/2025 - 10:31

A treat-to target (T2T) strategy based on video capsule endoscopy (VCE) identified Crohn’s disease (CD) patients in clinical remission but with small bowel inflammation, resulting in fewer clinical flares versus a treat-by-symptoms standard approach.

“A VCE-guided treat-to-target strategy for patients with CD in remission confers superior clinical outcomes compared with continued standard care,” investigators led by Shomron Ben-Horin, MD, director of gastroenterology at Sheba Medical Center in Ramat-Gan, Israel.

Published in Gastroenterology, the CURE-CD (Comprehensive Individualized Proactive Therapy of Crohn’s Disease), a prospective, temporally blinded, randomized controled trial, looked at 60 adult patients with quiescent CD involving the small bowel (either L1 or L3 iof the terminal ileum and upper colon).

The researchers defined quiescent disease as corticosteroid-free clinical remission with a Crohn’s Disease Activity Index (CDAI) of <50 for the past 3 months on a stable regimen.

Patients ingested a VCE at baseline and those with a Lewis inflammatory score (LS) of ≥350 were designated high risk (n = 40) and randomized to either T2T optimization (n = 20) or continuing standard care (n = 20). 

T2T was optimized with repeat VCE results every 6 months. Patients with LS <350 (“low risk”) continued standard care. The primary outcome was the rate of disease exacerbation, demonstrated by a CDAI increase of >70 points and a score >150, or hospitalization/surgery, in high-risk standard care vs T2T groups at 24 months.

Dr. Shomrom Ben-Horin



Treatment intensification in the high-risk group allocated to a proactive strategy comprised biologic dose escalation (n = 11 of 20), starting a biologic (n = 8 of 20), or swapping biologics (n = 1 of 20). 

The primary outcome, clinical flare by 24 months, occurred in 5 of 20 (25%) of high-risk treat-to-target patients vs 14 of 20 (70%) of the high-risk standard-care group (odds ratio [OR], .14; 95% confidence interval [CI], .04–.57, P = .006). 

Mucosal healing was significantly more common in the T2T group when determined by a cutoff LS < 350 (OR, 4.5, 95% CI, 1.7–17.4, nominal P value = .03), but not by the combined scores of total LS < 450 and highest-segment LS < 350. 

Among all patients continuing standard care (n = 40), baseline LS was numerically higher among relapsers vs nonrelapsers (450, 225–900 vs 225, 135–600, respectively, P = .07). 

As to safety, of 221 VCEs ingested, there was a single (.4%) temporary retention, which spontaneously resolved.

“VCE monitoring of CD was approved into government reimbursement in Israel last year, and I know several European countries are also considering the inclusion of this new indication for VCE in their payer reimbursement,” Ben-Horin told GI & Hepatology News. “Uptake in Israel is still baby-stepping. In our center it’s much more common to monitor T2T for small bowel patients, but this approach is still not widely applied.”

The authors cautioned that since the focus was the small bowel, the findings are not necessarily generalizable to patients with Crohn’s colitis.

The study was supported by the Leona M. & Harry B. Helmsley Charitable Trust, Medtronic (USA), AbbVie (Israel), and Takeda. The funders did not intervene in the design or interpretation of the study.

Ben-Horin reported advisory, consulting fees, research support, and/or stocks/options from several pharmaceutical firms. Several coauthors disclosed similar relations with private-sector companies.
 

Body
Mariangela Allocca

As treat-to-target (T2T) strategies continue to redefine inflammatory bowel disease (IBD) care, this randomized controlled trial by Ben-Horin et al. highlights the value of proactive video capsule endoscopy (VCE) monitoring in patients with quiescent small bowel Crohn’s disease (CD).

The study demonstrated that scheduled VCE every six months, used to guide treatment adjustments, significantly reduced clinical flares over 24 months compared to symptom-based standard care. While differences in mucosal healing between groups were less pronounced, the results underscore that monitoring objective inflammation, even in asymptomatic patients, can improve clinical outcomes.



In clinical practice, symptom-driven management remains common, often due to limited access to endoscopy or patient hesitancy toward invasive procedures. VCE offers a non-invasive, well-tolerated alternative that may improve patient adherence to disease monitoring, particularly in small bowel CD. This approach addresses a significant gap in care, as nearly half of IBD patients do not undergo objective disease assessment within a year of starting biologics.

 

Dr. Silvio Danese



Clinicians should consider integrating VCE into individualized T2T strategies, especially in settings where endoscopic access is constrained. Furthermore, adjunctive non-invasive tools such as intestinal ultrasound (IUS) with biomarkers could further support a non-invasive, patient-centered monitoring approach. As the definition of remission evolves toward more ambitious targets like transmural healing, the integration of cross-sectional imaging modalities such as IUS into routine monitoring protocols may become essential. Aligning monitoring techniques with evolving therapeutic targets and patient preferences will be key to optimizing long-term disease control in CD.

Mariangela Allocca, MD, PhD, is head of the IBD Center at IRCCS Hospital San Raffaele, and professor of gastroenterology at Vita-Salute San Raffaele University, both in Milan, Italy. Silvio Danese, MD, PhD, is professor of gastroenterology at Vita-Salute San Raffaele University and IRCCS San Raffaele Hospital, Milan. Both authors report consulting and/or speaking fees from multiple drug and device companies.

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Body
Mariangela Allocca

As treat-to-target (T2T) strategies continue to redefine inflammatory bowel disease (IBD) care, this randomized controlled trial by Ben-Horin et al. highlights the value of proactive video capsule endoscopy (VCE) monitoring in patients with quiescent small bowel Crohn’s disease (CD).

The study demonstrated that scheduled VCE every six months, used to guide treatment adjustments, significantly reduced clinical flares over 24 months compared to symptom-based standard care. While differences in mucosal healing between groups were less pronounced, the results underscore that monitoring objective inflammation, even in asymptomatic patients, can improve clinical outcomes.



In clinical practice, symptom-driven management remains common, often due to limited access to endoscopy or patient hesitancy toward invasive procedures. VCE offers a non-invasive, well-tolerated alternative that may improve patient adherence to disease monitoring, particularly in small bowel CD. This approach addresses a significant gap in care, as nearly half of IBD patients do not undergo objective disease assessment within a year of starting biologics.

 

Dr. Silvio Danese



Clinicians should consider integrating VCE into individualized T2T strategies, especially in settings where endoscopic access is constrained. Furthermore, adjunctive non-invasive tools such as intestinal ultrasound (IUS) with biomarkers could further support a non-invasive, patient-centered monitoring approach. As the definition of remission evolves toward more ambitious targets like transmural healing, the integration of cross-sectional imaging modalities such as IUS into routine monitoring protocols may become essential. Aligning monitoring techniques with evolving therapeutic targets and patient preferences will be key to optimizing long-term disease control in CD.

Mariangela Allocca, MD, PhD, is head of the IBD Center at IRCCS Hospital San Raffaele, and professor of gastroenterology at Vita-Salute San Raffaele University, both in Milan, Italy. Silvio Danese, MD, PhD, is professor of gastroenterology at Vita-Salute San Raffaele University and IRCCS San Raffaele Hospital, Milan. Both authors report consulting and/or speaking fees from multiple drug and device companies.

Body
Mariangela Allocca

As treat-to-target (T2T) strategies continue to redefine inflammatory bowel disease (IBD) care, this randomized controlled trial by Ben-Horin et al. highlights the value of proactive video capsule endoscopy (VCE) monitoring in patients with quiescent small bowel Crohn’s disease (CD).

The study demonstrated that scheduled VCE every six months, used to guide treatment adjustments, significantly reduced clinical flares over 24 months compared to symptom-based standard care. While differences in mucosal healing between groups were less pronounced, the results underscore that monitoring objective inflammation, even in asymptomatic patients, can improve clinical outcomes.



In clinical practice, symptom-driven management remains common, often due to limited access to endoscopy or patient hesitancy toward invasive procedures. VCE offers a non-invasive, well-tolerated alternative that may improve patient adherence to disease monitoring, particularly in small bowel CD. This approach addresses a significant gap in care, as nearly half of IBD patients do not undergo objective disease assessment within a year of starting biologics.

 

Dr. Silvio Danese



Clinicians should consider integrating VCE into individualized T2T strategies, especially in settings where endoscopic access is constrained. Furthermore, adjunctive non-invasive tools such as intestinal ultrasound (IUS) with biomarkers could further support a non-invasive, patient-centered monitoring approach. As the definition of remission evolves toward more ambitious targets like transmural healing, the integration of cross-sectional imaging modalities such as IUS into routine monitoring protocols may become essential. Aligning monitoring techniques with evolving therapeutic targets and patient preferences will be key to optimizing long-term disease control in CD.

Mariangela Allocca, MD, PhD, is head of the IBD Center at IRCCS Hospital San Raffaele, and professor of gastroenterology at Vita-Salute San Raffaele University, both in Milan, Italy. Silvio Danese, MD, PhD, is professor of gastroenterology at Vita-Salute San Raffaele University and IRCCS San Raffaele Hospital, Milan. Both authors report consulting and/or speaking fees from multiple drug and device companies.

Title
Aligning Monitoring Techniques with Therapeutic Targets
Aligning Monitoring Techniques with Therapeutic Targets

A treat-to target (T2T) strategy based on video capsule endoscopy (VCE) identified Crohn’s disease (CD) patients in clinical remission but with small bowel inflammation, resulting in fewer clinical flares versus a treat-by-symptoms standard approach.

“A VCE-guided treat-to-target strategy for patients with CD in remission confers superior clinical outcomes compared with continued standard care,” investigators led by Shomron Ben-Horin, MD, director of gastroenterology at Sheba Medical Center in Ramat-Gan, Israel.

Published in Gastroenterology, the CURE-CD (Comprehensive Individualized Proactive Therapy of Crohn’s Disease), a prospective, temporally blinded, randomized controled trial, looked at 60 adult patients with quiescent CD involving the small bowel (either L1 or L3 iof the terminal ileum and upper colon).

The researchers defined quiescent disease as corticosteroid-free clinical remission with a Crohn’s Disease Activity Index (CDAI) of <50 for the past 3 months on a stable regimen.

Patients ingested a VCE at baseline and those with a Lewis inflammatory score (LS) of ≥350 were designated high risk (n = 40) and randomized to either T2T optimization (n = 20) or continuing standard care (n = 20). 

T2T was optimized with repeat VCE results every 6 months. Patients with LS <350 (“low risk”) continued standard care. The primary outcome was the rate of disease exacerbation, demonstrated by a CDAI increase of >70 points and a score >150, or hospitalization/surgery, in high-risk standard care vs T2T groups at 24 months.

Dr. Shomrom Ben-Horin



Treatment intensification in the high-risk group allocated to a proactive strategy comprised biologic dose escalation (n = 11 of 20), starting a biologic (n = 8 of 20), or swapping biologics (n = 1 of 20). 

The primary outcome, clinical flare by 24 months, occurred in 5 of 20 (25%) of high-risk treat-to-target patients vs 14 of 20 (70%) of the high-risk standard-care group (odds ratio [OR], .14; 95% confidence interval [CI], .04–.57, P = .006). 

Mucosal healing was significantly more common in the T2T group when determined by a cutoff LS < 350 (OR, 4.5, 95% CI, 1.7–17.4, nominal P value = .03), but not by the combined scores of total LS < 450 and highest-segment LS < 350. 

Among all patients continuing standard care (n = 40), baseline LS was numerically higher among relapsers vs nonrelapsers (450, 225–900 vs 225, 135–600, respectively, P = .07). 

As to safety, of 221 VCEs ingested, there was a single (.4%) temporary retention, which spontaneously resolved.

“VCE monitoring of CD was approved into government reimbursement in Israel last year, and I know several European countries are also considering the inclusion of this new indication for VCE in their payer reimbursement,” Ben-Horin told GI & Hepatology News. “Uptake in Israel is still baby-stepping. In our center it’s much more common to monitor T2T for small bowel patients, but this approach is still not widely applied.”

The authors cautioned that since the focus was the small bowel, the findings are not necessarily generalizable to patients with Crohn’s colitis.

The study was supported by the Leona M. & Harry B. Helmsley Charitable Trust, Medtronic (USA), AbbVie (Israel), and Takeda. The funders did not intervene in the design or interpretation of the study.

Ben-Horin reported advisory, consulting fees, research support, and/or stocks/options from several pharmaceutical firms. Several coauthors disclosed similar relations with private-sector companies.
 

A treat-to target (T2T) strategy based on video capsule endoscopy (VCE) identified Crohn’s disease (CD) patients in clinical remission but with small bowel inflammation, resulting in fewer clinical flares versus a treat-by-symptoms standard approach.

“A VCE-guided treat-to-target strategy for patients with CD in remission confers superior clinical outcomes compared with continued standard care,” investigators led by Shomron Ben-Horin, MD, director of gastroenterology at Sheba Medical Center in Ramat-Gan, Israel.

Published in Gastroenterology, the CURE-CD (Comprehensive Individualized Proactive Therapy of Crohn’s Disease), a prospective, temporally blinded, randomized controled trial, looked at 60 adult patients with quiescent CD involving the small bowel (either L1 or L3 iof the terminal ileum and upper colon).

The researchers defined quiescent disease as corticosteroid-free clinical remission with a Crohn’s Disease Activity Index (CDAI) of <50 for the past 3 months on a stable regimen.

Patients ingested a VCE at baseline and those with a Lewis inflammatory score (LS) of ≥350 were designated high risk (n = 40) and randomized to either T2T optimization (n = 20) or continuing standard care (n = 20). 

T2T was optimized with repeat VCE results every 6 months. Patients with LS <350 (“low risk”) continued standard care. The primary outcome was the rate of disease exacerbation, demonstrated by a CDAI increase of >70 points and a score >150, or hospitalization/surgery, in high-risk standard care vs T2T groups at 24 months.

Dr. Shomrom Ben-Horin



Treatment intensification in the high-risk group allocated to a proactive strategy comprised biologic dose escalation (n = 11 of 20), starting a biologic (n = 8 of 20), or swapping biologics (n = 1 of 20). 

The primary outcome, clinical flare by 24 months, occurred in 5 of 20 (25%) of high-risk treat-to-target patients vs 14 of 20 (70%) of the high-risk standard-care group (odds ratio [OR], .14; 95% confidence interval [CI], .04–.57, P = .006). 

Mucosal healing was significantly more common in the T2T group when determined by a cutoff LS < 350 (OR, 4.5, 95% CI, 1.7–17.4, nominal P value = .03), but not by the combined scores of total LS < 450 and highest-segment LS < 350. 

Among all patients continuing standard care (n = 40), baseline LS was numerically higher among relapsers vs nonrelapsers (450, 225–900 vs 225, 135–600, respectively, P = .07). 

As to safety, of 221 VCEs ingested, there was a single (.4%) temporary retention, which spontaneously resolved.

“VCE monitoring of CD was approved into government reimbursement in Israel last year, and I know several European countries are also considering the inclusion of this new indication for VCE in their payer reimbursement,” Ben-Horin told GI & Hepatology News. “Uptake in Israel is still baby-stepping. In our center it’s much more common to monitor T2T for small bowel patients, but this approach is still not widely applied.”

The authors cautioned that since the focus was the small bowel, the findings are not necessarily generalizable to patients with Crohn’s colitis.

The study was supported by the Leona M. & Harry B. Helmsley Charitable Trust, Medtronic (USA), AbbVie (Israel), and Takeda. The funders did not intervene in the design or interpretation of the study.

Ben-Horin reported advisory, consulting fees, research support, and/or stocks/options from several pharmaceutical firms. Several coauthors disclosed similar relations with private-sector companies.
 

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