IBD & Intestinal Disorders

TOPLINE:

Healthier sleep is associated with lower odds of developing a wide range of gastrointestinal conditions, regardless of genetic susceptibility, new research revealed.

METHODOLOGY:

• Due to the widespread prevalence of sleep issues and a growing burden of digestive diseases globally, researchers investigated the association between sleep quality and digestive disorders in a prospective cohort study of 410,586 people in the UK Biobank.
• Five individual sleep behaviors were assessed: sleep duration, insomnia, snoring, daytime sleepiness, and chronotype.
• A healthy sleep was defined as a morning chronotype, 7-8 hours of sleep duration, no self-reported snoring, never or rare insomnia, and a low frequency of daytime sleepiness, for a score of 5/5.
• The study investigators tracked the development of 16 digestive diseases over a mean period of 13.2 years.
• As well as looking at healthy sleep scores, researchers considered genetic susceptibility to gastrointestinal conditions.

TAKEAWAY:

• Participants with a healthy sleep score had 28% lower odds of developing any digestive disease (hazard ratio [HR], 0.72; 95% CI, 0.69-0.75) than those with a sleep score of 0/1.
• Of the 16 digestive diseases looked at, the reduction of risk was highest for irritable bowel syndrome at 50% (HR, 0.50; 95% CI, 0.45-0.57).
• A healthy sleep score was also associated with 37% reduced odds for metabolic dysfunction–associated steatotic liver disease (formerly known as nonalcoholic fatty liver disease; HR, 0.63; 95% CI, 0.55-0.71), 35% lower chance for peptic ulcer (HR, 0.65; 95% CI, 0.058-0.74), 34% reduced chance for dyspepsia (HR, 0.66; 95% CI, 0.58-0.75), and a 25% lower risk for diverticulosis (HR, 0.75; 95% CI, 0.71-0.80).
• High genetic risk and poor sleep scores were also associated with increased odds (53% to > 200%) of developing digestive diseases.
• However, healthy sleep reduced the risk for digestive diseases regardless of genetic susceptibility.

IN PRACTICE:

“Our findings underscore the potential holistic impact of different sleep behaviors in mitigating the risk of digestive diseases in clinical practice,” wrote Shiyi Yu, MD, of Guangdong Provincial People’s Hospital, Guangzhou, Guangdong, China, and colleagues.

Poor sleep can also change our gut microbiome, Dr. Yu told this news organization. If you don’t sleep well, the repair of the gut lining cannot be finished during the night.

SOURCE:

The study was presented at the Digestive Disease Week® (DDW), 2024, annual meeting.

DISCLOSURES:

Dr. Yu had no relevant financial disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

Healthier sleep is associated with lower odds of developing a wide range of gastrointestinal conditions, regardless of genetic susceptibility, new research revealed.

METHODOLOGY:

• Due to the widespread prevalence of sleep issues and a growing burden of digestive diseases globally, researchers investigated the association between sleep quality and digestive disorders in a prospective cohort study of 410,586 people in the UK Biobank.
• Five individual sleep behaviors were assessed: sleep duration, insomnia, snoring, daytime sleepiness, and chronotype.
• A healthy sleep was defined as a morning chronotype, 7-8 hours of sleep duration, no self-reported snoring, never or rare insomnia, and a low frequency of daytime sleepiness, for a score of 5/5.
• The study investigators tracked the development of 16 digestive diseases over a mean period of 13.2 years.
• As well as looking at healthy sleep scores, researchers considered genetic susceptibility to gastrointestinal conditions.

TAKEAWAY:

• Participants with a healthy sleep score had 28% lower odds of developing any digestive disease (hazard ratio [HR], 0.72; 95% CI, 0.69-0.75) than those with a sleep score of 0/1.
• Of the 16 digestive diseases looked at, the reduction of risk was highest for irritable bowel syndrome at 50% (HR, 0.50; 95% CI, 0.45-0.57).
• A healthy sleep score was also associated with 37% reduced odds for metabolic dysfunction–associated steatotic liver disease (formerly known as nonalcoholic fatty liver disease; HR, 0.63; 95% CI, 0.55-0.71), 35% lower chance for peptic ulcer (HR, 0.65; 95% CI, 0.058-0.74), 34% reduced chance for dyspepsia (HR, 0.66; 95% CI, 0.58-0.75), and a 25% lower risk for diverticulosis (HR, 0.75; 95% CI, 0.71-0.80).
• High genetic risk and poor sleep scores were also associated with increased odds (53% to > 200%) of developing digestive diseases.
• However, healthy sleep reduced the risk for digestive diseases regardless of genetic susceptibility.

IN PRACTICE:

“Our findings underscore the potential holistic impact of different sleep behaviors in mitigating the risk of digestive diseases in clinical practice,” wrote Shiyi Yu, MD, of Guangdong Provincial People’s Hospital, Guangzhou, Guangdong, China, and colleagues.

Poor sleep can also change our gut microbiome, Dr. Yu told this news organization. If you don’t sleep well, the repair of the gut lining cannot be finished during the night.

SOURCE:

The study was presented at the Digestive Disease Week® (DDW), 2024, annual meeting.

DISCLOSURES:

Dr. Yu had no relevant financial disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

Healthier sleep is associated with lower odds of developing a wide range of gastrointestinal conditions, regardless of genetic susceptibility, new research revealed.

METHODOLOGY:

• Due to the widespread prevalence of sleep issues and a growing burden of digestive diseases globally, researchers investigated the association between sleep quality and digestive disorders in a prospective cohort study of 410,586 people in the UK Biobank.
• Five individual sleep behaviors were assessed: sleep duration, insomnia, snoring, daytime sleepiness, and chronotype.
• A healthy sleep was defined as a morning chronotype, 7-8 hours of sleep duration, no self-reported snoring, never or rare insomnia, and a low frequency of daytime sleepiness, for a score of 5/5.
• The study investigators tracked the development of 16 digestive diseases over a mean period of 13.2 years.
• As well as looking at healthy sleep scores, researchers considered genetic susceptibility to gastrointestinal conditions.

TAKEAWAY:

• Participants with a healthy sleep score had 28% lower odds of developing any digestive disease (hazard ratio [HR], 0.72; 95% CI, 0.69-0.75) than those with a sleep score of 0/1.
• Of the 16 digestive diseases looked at, the reduction of risk was highest for irritable bowel syndrome at 50% (HR, 0.50; 95% CI, 0.45-0.57).
• A healthy sleep score was also associated with 37% reduced odds for metabolic dysfunction–associated steatotic liver disease (formerly known as nonalcoholic fatty liver disease; HR, 0.63; 95% CI, 0.55-0.71), 35% lower chance for peptic ulcer (HR, 0.65; 95% CI, 0.058-0.74), 34% reduced chance for dyspepsia (HR, 0.66; 95% CI, 0.58-0.75), and a 25% lower risk for diverticulosis (HR, 0.75; 95% CI, 0.71-0.80).
• High genetic risk and poor sleep scores were also associated with increased odds (53% to > 200%) of developing digestive diseases.
• However, healthy sleep reduced the risk for digestive diseases regardless of genetic susceptibility.

IN PRACTICE:

“Our findings underscore the potential holistic impact of different sleep behaviors in mitigating the risk of digestive diseases in clinical practice,” wrote Shiyi Yu, MD, of Guangdong Provincial People’s Hospital, Guangzhou, Guangdong, China, and colleagues.

Poor sleep can also change our gut microbiome, Dr. Yu told this news organization. If you don’t sleep well, the repair of the gut lining cannot be finished during the night.

SOURCE:

The study was presented at the Digestive Disease Week® (DDW), 2024, annual meeting.

DISCLOSURES:

Dr. Yu had no relevant financial disclosures.

A version of this article appeared on Medscape.com.

WASHINGTON — Guselkumab (Tremfya, Janssen/Johnson & Johnson) was superior to placebo for maintenance therapy in people with moderately to severely active ulcerative colitis (UC), according to the results of the phase 3 Quasar Maintenance Study.

The primary outcome of clinical remission at 44 weeks was greater with either of two dose regimens of guselkumab than with placebo, David Rubin, MD, AGAF, reported as part of his presentation (Abstract 759) at the annual Digestive Disease Week® (DDW).

Guselkumab is not the only biologic approved or in development for UC, but it is unique because of its dual action. It is an interleukin (IL)-23p19 subunit inhibitor that blocks IL-23 and also binds to the CD64 receptor on cells that produce IL-23.

Dr. Rubin, who is chief of the Section of Gastroenterology, Hepatology and Nutrition at University of Chicago Medicine, Chicago, said he was unsure at the beginning of the trial if this dual activity “might have any value.”

Targeting both the IL-23 circulating in the tissue and the receptor remains to be proven, “but nonetheless seems reasonable,” he said.

The study included 568 people, about 42% of whom had an inadequate response or were intolerant to prior advanced therapy, and 42.5% of whom had failed two or more advanced therapy classes.

Clinical responders from two prior guselkumab induction studies were enrolled in this randomized withdrawal, double-blind maintenance trial. At either 12 weeks or 24 weeks of induction, patients were randomly assigned to subcutaneous 200-mg guselkumab every 4 weeks (n = 190), 100-mg guselkumab every 8 weeks (n = 188), or placebo (n = 190). The placebo group served as a guselkumab withdrawal group.

Participants had a mean age of 41 years and a mean disease duration of 7.8 years. The 40% using oral corticosteroids were tapered off during the study.

A total of 45.2% of the 100-mg guselkumab group and 50.0% of the 200-mg guselkumab group met the primary outcome of clinical remission at week 44 compared with 18.9% with placebo.

“It was interesting to note that the 200 mg every 4 weeks was similar in efficacy at week 44 to the 100 mg every 8 weeks. It’s much less medicine, but you get similar results,” Dr. Rubin said.
 

Secondary Outcomes Also Superior

“The bottom line is not only did it work, but it worked when you look at some secondary endpoints, including endoscopic remission, where the bowel is completely healed,” Dr. Rubin said in an interview.

Overall, 34% of all participants who received guselkumab achieved this outcome, “which is a very high rate,” he said. “We haven’t seen a Mayo score of zero — meaning endoscopic remission — at that rate with any of our other therapies currently.”

Among the participants who achieved clinical remission, 69% of them also showed complete remission on endoscopy.

Other secondary outcomes significantly better at week 44 vs placebo included corticosteroid-free clinical remission, maintenance of clinical remission, clinical response, symptomatic remission, endoscopic improvement, histo-endoscopic mucosal improvement, endoscopic normalization, Inflammatory Bowel Disease Questionnaire remission, and fatigue response.

“It was a great study. I think it’s very promising data,” said session co-moderator Ashwin N. Ananthakrishnan, MBBS, MPH, AGAF, director of the Crohn’s and Colitis Center at Massachusetts General Hospital in Boston.

“As we get more data from these more selective interleukins, we’ll get a better sense of how that plays out” vs other similar agents in development, he added.
 

IL-23 Target Seems Safe

One or more adverse events were reported by 70% of the higher-dose guselkumab group, 65% of the lower-dose guselkumab group, and 68% of the placebo group.

The most common adverse events in a combined 200-mg and 100-mg guselkumab group were lower than in the placebo group: 11.2% vs 14.1% reported COVID-19, 11.2% vs 29.7% reported exacerbation of UC, and 6.1% vs 6.8% experienced arthralgia, respectively.

No cases of active tuberculosis, opportunistic infection, anaphylaxis, serum sickness, Hy’s law, or serious hepatic issues were reported. One patient had clear cell renal carcinoma, another had rectal adenocarcinoma, and one hemorrhagic stroke was reported in the treatment groups. No patients died during the trial.

A higher proportion of people in the placebo group (13.7%) discontinued the study than those in the 100-mg guselkumab group (10.6%) and the 200-mg guselkumab group (11.6%).

“In general, we have accepted that the IL-23 target seems to be a very safe one,” Dr. Rubin said.

A leading theory is that unlike some interleukins, IL-23 is only expressed where the body has inflammation; therefore, targeting IL-23 does not affect other areas, he explained.

If approved by the Food and Drug Administration, it would expand the official indications for guselkumab, which was approved in 2020 for psoriatic arthritis and in 2017 for plaque psoriasis.

The study was supported by Janssen Research & Development, LLC. Dr. Rubin is a consultant for Janssen. Dr. Ananthakrishnan had no relevant disclosures.

A version of this article appeared on Medscape.com.

WASHINGTON — Guselkumab (Tremfya, Janssen/Johnson & Johnson) was superior to placebo for maintenance therapy in people with moderately to severely active ulcerative colitis (UC), according to the results of the phase 3 Quasar Maintenance Study.

The primary outcome of clinical remission at 44 weeks was greater with either of two dose regimens of guselkumab than with placebo, David Rubin, MD, AGAF, reported as part of his presentation (Abstract 759) at the annual Digestive Disease Week® (DDW).

Guselkumab is not the only biologic approved or in development for UC, but it is unique because of its dual action. It is an interleukin (IL)-23p19 subunit inhibitor that blocks IL-23 and also binds to the CD64 receptor on cells that produce IL-23.

Dr. Rubin, who is chief of the Section of Gastroenterology, Hepatology and Nutrition at University of Chicago Medicine, Chicago, said he was unsure at the beginning of the trial if this dual activity “might have any value.”

Targeting both the IL-23 circulating in the tissue and the receptor remains to be proven, “but nonetheless seems reasonable,” he said.

The study included 568 people, about 42% of whom had an inadequate response or were intolerant to prior advanced therapy, and 42.5% of whom had failed two or more advanced therapy classes.

Clinical responders from two prior guselkumab induction studies were enrolled in this randomized withdrawal, double-blind maintenance trial. At either 12 weeks or 24 weeks of induction, patients were randomly assigned to subcutaneous 200-mg guselkumab every 4 weeks (n = 190), 100-mg guselkumab every 8 weeks (n = 188), or placebo (n = 190). The placebo group served as a guselkumab withdrawal group.

Participants had a mean age of 41 years and a mean disease duration of 7.8 years. The 40% using oral corticosteroids were tapered off during the study.

A total of 45.2% of the 100-mg guselkumab group and 50.0% of the 200-mg guselkumab group met the primary outcome of clinical remission at week 44 compared with 18.9% with placebo.

“It was interesting to note that the 200 mg every 4 weeks was similar in efficacy at week 44 to the 100 mg every 8 weeks. It’s much less medicine, but you get similar results,” Dr. Rubin said.
 

Secondary Outcomes Also Superior

“The bottom line is not only did it work, but it worked when you look at some secondary endpoints, including endoscopic remission, where the bowel is completely healed,” Dr. Rubin said in an interview.

Overall, 34% of all participants who received guselkumab achieved this outcome, “which is a very high rate,” he said. “We haven’t seen a Mayo score of zero — meaning endoscopic remission — at that rate with any of our other therapies currently.”

Among the participants who achieved clinical remission, 69% of them also showed complete remission on endoscopy.

Other secondary outcomes significantly better at week 44 vs placebo included corticosteroid-free clinical remission, maintenance of clinical remission, clinical response, symptomatic remission, endoscopic improvement, histo-endoscopic mucosal improvement, endoscopic normalization, Inflammatory Bowel Disease Questionnaire remission, and fatigue response.

“It was a great study. I think it’s very promising data,” said session co-moderator Ashwin N. Ananthakrishnan, MBBS, MPH, AGAF, director of the Crohn’s and Colitis Center at Massachusetts General Hospital in Boston.

“As we get more data from these more selective interleukins, we’ll get a better sense of how that plays out” vs other similar agents in development, he added.
 

IL-23 Target Seems Safe

One or more adverse events were reported by 70% of the higher-dose guselkumab group, 65% of the lower-dose guselkumab group, and 68% of the placebo group.

The most common adverse events in a combined 200-mg and 100-mg guselkumab group were lower than in the placebo group: 11.2% vs 14.1% reported COVID-19, 11.2% vs 29.7% reported exacerbation of UC, and 6.1% vs 6.8% experienced arthralgia, respectively.

No cases of active tuberculosis, opportunistic infection, anaphylaxis, serum sickness, Hy’s law, or serious hepatic issues were reported. One patient had clear cell renal carcinoma, another had rectal adenocarcinoma, and one hemorrhagic stroke was reported in the treatment groups. No patients died during the trial.

A higher proportion of people in the placebo group (13.7%) discontinued the study than those in the 100-mg guselkumab group (10.6%) and the 200-mg guselkumab group (11.6%).

“In general, we have accepted that the IL-23 target seems to be a very safe one,” Dr. Rubin said.

A leading theory is that unlike some interleukins, IL-23 is only expressed where the body has inflammation; therefore, targeting IL-23 does not affect other areas, he explained.

If approved by the Food and Drug Administration, it would expand the official indications for guselkumab, which was approved in 2020 for psoriatic arthritis and in 2017 for plaque psoriasis.

The study was supported by Janssen Research & Development, LLC. Dr. Rubin is a consultant for Janssen. Dr. Ananthakrishnan had no relevant disclosures.

A version of this article appeared on Medscape.com.

WASHINGTON — Guselkumab (Tremfya, Janssen/Johnson & Johnson) was superior to placebo for maintenance therapy in people with moderately to severely active ulcerative colitis (UC), according to the results of the phase 3 Quasar Maintenance Study.

The primary outcome of clinical remission at 44 weeks was greater with either of two dose regimens of guselkumab than with placebo, David Rubin, MD, AGAF, reported as part of his presentation (Abstract 759) at the annual Digestive Disease Week® (DDW).

Guselkumab is not the only biologic approved or in development for UC, but it is unique because of its dual action. It is an interleukin (IL)-23p19 subunit inhibitor that blocks IL-23 and also binds to the CD64 receptor on cells that produce IL-23.

Dr. Rubin, who is chief of the Section of Gastroenterology, Hepatology and Nutrition at University of Chicago Medicine, Chicago, said he was unsure at the beginning of the trial if this dual activity “might have any value.”

Targeting both the IL-23 circulating in the tissue and the receptor remains to be proven, “but nonetheless seems reasonable,” he said.

The study included 568 people, about 42% of whom had an inadequate response or were intolerant to prior advanced therapy, and 42.5% of whom had failed two or more advanced therapy classes.

Clinical responders from two prior guselkumab induction studies were enrolled in this randomized withdrawal, double-blind maintenance trial. At either 12 weeks or 24 weeks of induction, patients were randomly assigned to subcutaneous 200-mg guselkumab every 4 weeks (n = 190), 100-mg guselkumab every 8 weeks (n = 188), or placebo (n = 190). The placebo group served as a guselkumab withdrawal group.

Participants had a mean age of 41 years and a mean disease duration of 7.8 years. The 40% using oral corticosteroids were tapered off during the study.

A total of 45.2% of the 100-mg guselkumab group and 50.0% of the 200-mg guselkumab group met the primary outcome of clinical remission at week 44 compared with 18.9% with placebo.

“It was interesting to note that the 200 mg every 4 weeks was similar in efficacy at week 44 to the 100 mg every 8 weeks. It’s much less medicine, but you get similar results,” Dr. Rubin said.
 

Secondary Outcomes Also Superior

“The bottom line is not only did it work, but it worked when you look at some secondary endpoints, including endoscopic remission, where the bowel is completely healed,” Dr. Rubin said in an interview.

Overall, 34% of all participants who received guselkumab achieved this outcome, “which is a very high rate,” he said. “We haven’t seen a Mayo score of zero — meaning endoscopic remission — at that rate with any of our other therapies currently.”

Among the participants who achieved clinical remission, 69% of them also showed complete remission on endoscopy.

Other secondary outcomes significantly better at week 44 vs placebo included corticosteroid-free clinical remission, maintenance of clinical remission, clinical response, symptomatic remission, endoscopic improvement, histo-endoscopic mucosal improvement, endoscopic normalization, Inflammatory Bowel Disease Questionnaire remission, and fatigue response.

“It was a great study. I think it’s very promising data,” said session co-moderator Ashwin N. Ananthakrishnan, MBBS, MPH, AGAF, director of the Crohn’s and Colitis Center at Massachusetts General Hospital in Boston.

“As we get more data from these more selective interleukins, we’ll get a better sense of how that plays out” vs other similar agents in development, he added.
 

IL-23 Target Seems Safe

One or more adverse events were reported by 70% of the higher-dose guselkumab group, 65% of the lower-dose guselkumab group, and 68% of the placebo group.

The most common adverse events in a combined 200-mg and 100-mg guselkumab group were lower than in the placebo group: 11.2% vs 14.1% reported COVID-19, 11.2% vs 29.7% reported exacerbation of UC, and 6.1% vs 6.8% experienced arthralgia, respectively.

No cases of active tuberculosis, opportunistic infection, anaphylaxis, serum sickness, Hy’s law, or serious hepatic issues were reported. One patient had clear cell renal carcinoma, another had rectal adenocarcinoma, and one hemorrhagic stroke was reported in the treatment groups. No patients died during the trial.

A higher proportion of people in the placebo group (13.7%) discontinued the study than those in the 100-mg guselkumab group (10.6%) and the 200-mg guselkumab group (11.6%).

“In general, we have accepted that the IL-23 target seems to be a very safe one,” Dr. Rubin said.

A leading theory is that unlike some interleukins, IL-23 is only expressed where the body has inflammation; therefore, targeting IL-23 does not affect other areas, he explained.

If approved by the Food and Drug Administration, it would expand the official indications for guselkumab, which was approved in 2020 for psoriatic arthritis and in 2017 for plaque psoriasis.

The study was supported by Janssen Research & Development, LLC. Dr. Rubin is a consultant for Janssen. Dr. Ananthakrishnan had no relevant disclosures.

A version of this article appeared on Medscape.com.

WASHINGTON — Statin use may contribute to a significant reduction in the risk of new primary sclerosing cholangitis (PSC) among patients with inflammatory bowel disease (IBD), according to a study presented at Digestive Disease Week^® (DDW) 2024.

Statin use was associated with an 86% risk reduction, and only .09% of IBD patients who took statins developed PSC.

“We all take care of patients with liver disease, and we know what a significant burden PSC is. These patients have a significantly elevated risk of enhanced fibrosis and cirrhosis, multiple cancers, and cholangitis and sepsis,” said lead author Chiraag Kulkarni, MD, a gastroenterology fellow at Stanford (California) University Medical School.

“Despite this, we have to date no proven effective medical care for PSC,” he said. “However, over the last decade, there is growing evidence that statins may be beneficial in liver disease, and we see this evidence base stretching from basic science to clinical data.”

Dr. Kulkarni pointed to numerous studies that indicate statins may slow disease progression in steatotic liver disease, viral hepatitis, and cirrhosis. But could statins prevent the onset of PSC?

Because PSC incidence is low, Dr. Kulkarni and colleagues focused on a patient population with higher prevalence — those with IBD, who have an overall lifetime risk of 2% to 7%. The research team followed patients from the date of IBD diagnosis.

Among 33,813 patients with IBD in a national dataset from 2018 onward, 8813 used statins. Statin users tended to be older than non–statin users.

Overall, 181 patients developed new onset PSC during a median follow-up of about 45 months after initial IBD diagnosis. Only eight statin users (.09%) developed PSC, compared with 173 patients (.69%) in the control group.

In a propensity score-matched analysis, statin therapy was associated with a significantly lower risk of developing PSC (HR .14, P < .001). The associated E-value was 5.5, which suggested a robust finding and unlikely to be due to non-visible confounding.

The findings were consistent across secondary and sensitivity analyses, including by age, duration of statin use, and type of statin. For instance, for patients under age 50 where PSC is more likely to occur, statins were associated with a 90% reduction in PSC risk.

“We take away two things from this. First, it’s suggested that a protective effect occurs at ages where PSC is most likely to occur,” Dr. Kulkarni said. “Second, in combination with our propensity score-matched analysis, the results we are observing are not due to a survival bias, where the patients who survive to an age where statins are prescribed simply have a biologically different predilection for developing PSC.”

Statins also protected against PSC in both ulcerative colitis (HR .21) and Crohn’s disease (HR .15), as well as both women (HR .16) and men (HR .22).

Given the uncertainty about the optimal duration of statin therapy for a protective effect, Dr. Kulkarni and colleagues looked at a lag time of 12 months. They found statins were associated with an 84% risk reduction (HR .16), which was similar to the primary analysis.

The study was limited by the inability to capture dosage data or medication adherence. The findings raised several questions, Dr. Kulkarni said, such as the underlying mechanisms and clinical implications. For instance, the underlying mechanisms appear to be related to the pleiotropic effect of statins, modulation of gut inflammation, and alterations in bile acid profiles.

“This is really fascinating and interesting. I wonder about this as a primary prevention strategy in those who have normal cholesterol. Could this work or not?” said Gyongyi Szabo, MD, AGAF, chief academic officer at Beth Israel Deaconess Medical Center, Boston, who was a moderator for the Liver & Biliary Section Distinguished Abstract Plenary Session.

Beth Israel Deaconess Medical Center

WASHINGTON — Statin use may contribute to a significant reduction in the risk of new primary sclerosing cholangitis (PSC) among patients with inflammatory bowel disease (IBD), according to a study presented at Digestive Disease Week^® (DDW) 2024.

Statin use was associated with an 86% risk reduction, and only .09% of IBD patients who took statins developed PSC.

“We all take care of patients with liver disease, and we know what a significant burden PSC is. These patients have a significantly elevated risk of enhanced fibrosis and cirrhosis, multiple cancers, and cholangitis and sepsis,” said lead author Chiraag Kulkarni, MD, a gastroenterology fellow at Stanford (California) University Medical School.

“Despite this, we have to date no proven effective medical care for PSC,” he said. “However, over the last decade, there is growing evidence that statins may be beneficial in liver disease, and we see this evidence base stretching from basic science to clinical data.”

Dr. Kulkarni pointed to numerous studies that indicate statins may slow disease progression in steatotic liver disease, viral hepatitis, and cirrhosis. But could statins prevent the onset of PSC?

Because PSC incidence is low, Dr. Kulkarni and colleagues focused on a patient population with higher prevalence — those with IBD, who have an overall lifetime risk of 2% to 7%. The research team followed patients from the date of IBD diagnosis.

Among 33,813 patients with IBD in a national dataset from 2018 onward, 8813 used statins. Statin users tended to be older than non–statin users.

Overall, 181 patients developed new onset PSC during a median follow-up of about 45 months after initial IBD diagnosis. Only eight statin users (.09%) developed PSC, compared with 173 patients (.69%) in the control group.

In a propensity score-matched analysis, statin therapy was associated with a significantly lower risk of developing PSC (HR .14, P < .001). The associated E-value was 5.5, which suggested a robust finding and unlikely to be due to non-visible confounding.

The findings were consistent across secondary and sensitivity analyses, including by age, duration of statin use, and type of statin. For instance, for patients under age 50 where PSC is more likely to occur, statins were associated with a 90% reduction in PSC risk.

“We take away two things from this. First, it’s suggested that a protective effect occurs at ages where PSC is most likely to occur,” Dr. Kulkarni said. “Second, in combination with our propensity score-matched analysis, the results we are observing are not due to a survival bias, where the patients who survive to an age where statins are prescribed simply have a biologically different predilection for developing PSC.”

Statins also protected against PSC in both ulcerative colitis (HR .21) and Crohn’s disease (HR .15), as well as both women (HR .16) and men (HR .22).

Given the uncertainty about the optimal duration of statin therapy for a protective effect, Dr. Kulkarni and colleagues looked at a lag time of 12 months. They found statins were associated with an 84% risk reduction (HR .16), which was similar to the primary analysis.

The study was limited by the inability to capture dosage data or medication adherence. The findings raised several questions, Dr. Kulkarni said, such as the underlying mechanisms and clinical implications. For instance, the underlying mechanisms appear to be related to the pleiotropic effect of statins, modulation of gut inflammation, and alterations in bile acid profiles.

“This is really fascinating and interesting. I wonder about this as a primary prevention strategy in those who have normal cholesterol. Could this work or not?” said Gyongyi Szabo, MD, AGAF, chief academic officer at Beth Israel Deaconess Medical Center, Boston, who was a moderator for the Liver & Biliary Section Distinguished Abstract Plenary Session.

Beth Israel Deaconess Medical Center

WASHINGTON — Statin use may contribute to a significant reduction in the risk of new primary sclerosing cholangitis (PSC) among patients with inflammatory bowel disease (IBD), according to a study presented at Digestive Disease Week^® (DDW) 2024.

Statin use was associated with an 86% risk reduction, and only .09% of IBD patients who took statins developed PSC.

“We all take care of patients with liver disease, and we know what a significant burden PSC is. These patients have a significantly elevated risk of enhanced fibrosis and cirrhosis, multiple cancers, and cholangitis and sepsis,” said lead author Chiraag Kulkarni, MD, a gastroenterology fellow at Stanford (California) University Medical School.

“Despite this, we have to date no proven effective medical care for PSC,” he said. “However, over the last decade, there is growing evidence that statins may be beneficial in liver disease, and we see this evidence base stretching from basic science to clinical data.”

Dr. Kulkarni pointed to numerous studies that indicate statins may slow disease progression in steatotic liver disease, viral hepatitis, and cirrhosis. But could statins prevent the onset of PSC?

Because PSC incidence is low, Dr. Kulkarni and colleagues focused on a patient population with higher prevalence — those with IBD, who have an overall lifetime risk of 2% to 7%. The research team followed patients from the date of IBD diagnosis.

Among 33,813 patients with IBD in a national dataset from 2018 onward, 8813 used statins. Statin users tended to be older than non–statin users.

Overall, 181 patients developed new onset PSC during a median follow-up of about 45 months after initial IBD diagnosis. Only eight statin users (.09%) developed PSC, compared with 173 patients (.69%) in the control group.

In a propensity score-matched analysis, statin therapy was associated with a significantly lower risk of developing PSC (HR .14, P < .001). The associated E-value was 5.5, which suggested a robust finding and unlikely to be due to non-visible confounding.

The findings were consistent across secondary and sensitivity analyses, including by age, duration of statin use, and type of statin. For instance, for patients under age 50 where PSC is more likely to occur, statins were associated with a 90% reduction in PSC risk.

“We take away two things from this. First, it’s suggested that a protective effect occurs at ages where PSC is most likely to occur,” Dr. Kulkarni said. “Second, in combination with our propensity score-matched analysis, the results we are observing are not due to a survival bias, where the patients who survive to an age where statins are prescribed simply have a biologically different predilection for developing PSC.”

Statins also protected against PSC in both ulcerative colitis (HR .21) and Crohn’s disease (HR .15), as well as both women (HR .16) and men (HR .22).

Given the uncertainty about the optimal duration of statin therapy for a protective effect, Dr. Kulkarni and colleagues looked at a lag time of 12 months. They found statins were associated with an 84% risk reduction (HR .16), which was similar to the primary analysis.

The study was limited by the inability to capture dosage data or medication adherence. The findings raised several questions, Dr. Kulkarni said, such as the underlying mechanisms and clinical implications. For instance, the underlying mechanisms appear to be related to the pleiotropic effect of statins, modulation of gut inflammation, and alterations in bile acid profiles.

“This is really fascinating and interesting. I wonder about this as a primary prevention strategy in those who have normal cholesterol. Could this work or not?” said Gyongyi Szabo, MD, AGAF, chief academic officer at Beth Israel Deaconess Medical Center, Boston, who was a moderator for the Liver & Biliary Section Distinguished Abstract Plenary Session.

Beth Israel Deaconess Medical Center

WASHINGTON — The selective interleukin (IL)–23p29 monoclonal antibody mirikizumab demonstrated safety and efficacy in people with moderate to severe Crohn’s disease compared with placebo up to 52 weeks, according to results of the phase 3 randomized, double blind, treat-through VIVID-1 study. 

Bruce E. Sands, MD, AGAF, chief of gastroenterology at the Icahn School of Medicine at Mount Sinai in New York, reported the findings in a poster (Abstract Su1801) at the annual Digestive Disease Week^® (DDW).

The FDA approved mirikizumab (Omvoh, Eli Lilly) to treat moderate to severe ulcerative colitis in October 2023. 

Dr. Sands and a team of US and international collaborators studied 1065 adults with Crohn’s disease or fistulizing Crohn’s disease for 3 months or more, with a mean duration of more than 7 years. At baseline, participants had a Simple Endoscopic Score for Crohn’s Disease (SES-CD) of 7 or more and reported an inadequate response, lost response, or intolerance to other therapy.

A total of 579 people were randomly assigned to mirikizumab and another 199 to placebo. Another 287 patients received ustekinumab; though they were not included in this current analysis, the findings were presented separately at DDW 2024. 

Mean age of study participants was 30 years, and men comprised 57%-59% of the groups. Nearly half (49%) of each group previously failed biologic therapy. 

A primary composite endpoint was clinical response at 12 weeks according to patient reported outcome and endoscopic response at 52 weeks measured with the SES-CD. A second primary endpoint was clinical response at 12 weeks by patient reported outcome combined with clinical remission on Crohn’s Disease Activity Index (CDAI) at 52 weeks.

Researchers also tracked 12 major secondary endpoints for mirikizumab vs placebo, including clinical response, endoscopic response, and clinical remission at week 12 and week 52. 
 

Efficacy Findings

A higher percentage of participants in the mirikizumab group achieved 12-week secondary endpoints compared with placebo. In the treatment group, 32.5% reached endoscopic response vs 12.6% in the placebo group, a statistically significant difference (P < .000001). In addition, 17.6% achieved endoscopic remission in the treatment group vs 7.0% in the placebo group at 12 weeks (P < .000213).

The “treat-through” results at 52 weeks revealed that a higher proportion of the group taking mirikizumab met the co-primary endpoints compared with placebo. A total of 48.4% in the mirikizumab group vs 9.0% in the placebo group achieved endoscopic response (P < .000001). Similarly, a higher proportion met clinical remission on the CDAI, 54.1% in the treatment group vs 19.6% in the placebo group (P < .000001).

Overall, 38% of mirikizumab-treated patients vs 9% of the placebo group reached a composite endpoint of patient reported clinical response at week 12 and endoscopic response by SES-CD at week 52 (P < .000001).

Dr. Sands and colleagues also combined clinical response reported by patients at 12 weeks with CDAI findings for clinical remission at week 52. A total of 45.4% in the treatment group met the combined endpoint compared with 19.6% of the placebo group (P < .000001). 

In an additional analysis, the researchers looked at this composite endpoint in patients in both groups who had failed or not failed a prior biologic for a total of 43.4% vs 12.4%, and 47.3% vs 26.5%, respectively.

“Mirikizumab demonstrated statistically significant and clinically meaningful improvements” in the study co-primary endpoints and secondary endpoints compared with placebo, the researchers concluded. 
 

Safety Findings

Safety outcomes during the 52-week study were “consistent with the known safety profile” of mirikizumab, the researchers noted. 

Treatment-emergent adverse events occurred in 78.6% of mirikizumab participants vs 73.0% of the placebo group. The most common were COVID-19, anemia, and arthralgia. Serious adverse events were reported in 10.3% of the mirikizumab group vs 17.1% of the placebo group. There were seven opportunistic infections in the treatment group, including herpes zoster and Candida, compared with none in the placebo group. 

One person in the placebo cohort died of a pulmonary embolism; there were no deaths in the mirikizumab group. 

People randomly assigned to placebo without a response at 12 weeks were switched over to mirikizumab. However, the findings from this group between 12 and 52 weeks were excluded from the 1-year data presented at DDW 2024, including one death from worsening Crohn’s disease during that time.

Mirikizumab looked particularly robust in this study, and it may turn out to be a critically important option for our patients, said Jordan Axelrad, MD, MPH, co-director of the Inflammatory Bowel Disease Center at NYU Langone Health in New York City. Dr. Axelrad was not involved in this study. 

Of importance, effect sizes were similar for “bio-naive and previously biologic-exposed patients,” he added. 

These data “really underscore that therapies targeting IL-23 may be clinically useful for Crohn’s disease patients with prior biologic failure, representing a significant departure from our previous experience with other biologic classes,” Dr. Axelrad said.

The study was funded by Eli Lilly and Company. Dr. Sands is a consultant and receives grant funding from Lilly. Dr. Axelrad had no relevant disclosures. 

A version of this article appeared on Medscape.com.

WASHINGTON — The selective interleukin (IL)–23p29 monoclonal antibody mirikizumab demonstrated safety and efficacy in people with moderate to severe Crohn’s disease compared with placebo up to 52 weeks, according to results of the phase 3 randomized, double blind, treat-through VIVID-1 study. 

Bruce E. Sands, MD, AGAF, chief of gastroenterology at the Icahn School of Medicine at Mount Sinai in New York, reported the findings in a poster (Abstract Su1801) at the annual Digestive Disease Week^® (DDW).

The FDA approved mirikizumab (Omvoh, Eli Lilly) to treat moderate to severe ulcerative colitis in October 2023. 

Dr. Sands and a team of US and international collaborators studied 1065 adults with Crohn’s disease or fistulizing Crohn’s disease for 3 months or more, with a mean duration of more than 7 years. At baseline, participants had a Simple Endoscopic Score for Crohn’s Disease (SES-CD) of 7 or more and reported an inadequate response, lost response, or intolerance to other therapy.

A total of 579 people were randomly assigned to mirikizumab and another 199 to placebo. Another 287 patients received ustekinumab; though they were not included in this current analysis, the findings were presented separately at DDW 2024. 

Mean age of study participants was 30 years, and men comprised 57%-59% of the groups. Nearly half (49%) of each group previously failed biologic therapy. 

A primary composite endpoint was clinical response at 12 weeks according to patient reported outcome and endoscopic response at 52 weeks measured with the SES-CD. A second primary endpoint was clinical response at 12 weeks by patient reported outcome combined with clinical remission on Crohn’s Disease Activity Index (CDAI) at 52 weeks.

Researchers also tracked 12 major secondary endpoints for mirikizumab vs placebo, including clinical response, endoscopic response, and clinical remission at week 12 and week 52. 
 

Efficacy Findings

A higher percentage of participants in the mirikizumab group achieved 12-week secondary endpoints compared with placebo. In the treatment group, 32.5% reached endoscopic response vs 12.6% in the placebo group, a statistically significant difference (P < .000001). In addition, 17.6% achieved endoscopic remission in the treatment group vs 7.0% in the placebo group at 12 weeks (P < .000213).

The “treat-through” results at 52 weeks revealed that a higher proportion of the group taking mirikizumab met the co-primary endpoints compared with placebo. A total of 48.4% in the mirikizumab group vs 9.0% in the placebo group achieved endoscopic response (P < .000001). Similarly, a higher proportion met clinical remission on the CDAI, 54.1% in the treatment group vs 19.6% in the placebo group (P < .000001).

Overall, 38% of mirikizumab-treated patients vs 9% of the placebo group reached a composite endpoint of patient reported clinical response at week 12 and endoscopic response by SES-CD at week 52 (P < .000001).

Dr. Sands and colleagues also combined clinical response reported by patients at 12 weeks with CDAI findings for clinical remission at week 52. A total of 45.4% in the treatment group met the combined endpoint compared with 19.6% of the placebo group (P < .000001). 

In an additional analysis, the researchers looked at this composite endpoint in patients in both groups who had failed or not failed a prior biologic for a total of 43.4% vs 12.4%, and 47.3% vs 26.5%, respectively.

“Mirikizumab demonstrated statistically significant and clinically meaningful improvements” in the study co-primary endpoints and secondary endpoints compared with placebo, the researchers concluded. 
 

Safety Findings

Safety outcomes during the 52-week study were “consistent with the known safety profile” of mirikizumab, the researchers noted. 

Treatment-emergent adverse events occurred in 78.6% of mirikizumab participants vs 73.0% of the placebo group. The most common were COVID-19, anemia, and arthralgia. Serious adverse events were reported in 10.3% of the mirikizumab group vs 17.1% of the placebo group. There were seven opportunistic infections in the treatment group, including herpes zoster and Candida, compared with none in the placebo group. 

One person in the placebo cohort died of a pulmonary embolism; there were no deaths in the mirikizumab group. 

People randomly assigned to placebo without a response at 12 weeks were switched over to mirikizumab. However, the findings from this group between 12 and 52 weeks were excluded from the 1-year data presented at DDW 2024, including one death from worsening Crohn’s disease during that time.

Mirikizumab looked particularly robust in this study, and it may turn out to be a critically important option for our patients, said Jordan Axelrad, MD, MPH, co-director of the Inflammatory Bowel Disease Center at NYU Langone Health in New York City. Dr. Axelrad was not involved in this study. 

Of importance, effect sizes were similar for “bio-naive and previously biologic-exposed patients,” he added. 

These data “really underscore that therapies targeting IL-23 may be clinically useful for Crohn’s disease patients with prior biologic failure, representing a significant departure from our previous experience with other biologic classes,” Dr. Axelrad said.

The study was funded by Eli Lilly and Company. Dr. Sands is a consultant and receives grant funding from Lilly. Dr. Axelrad had no relevant disclosures. 

A version of this article appeared on Medscape.com.

WASHINGTON — The selective interleukin (IL)–23p29 monoclonal antibody mirikizumab demonstrated safety and efficacy in people with moderate to severe Crohn’s disease compared with placebo up to 52 weeks, according to results of the phase 3 randomized, double blind, treat-through VIVID-1 study. 

Bruce E. Sands, MD, AGAF, chief of gastroenterology at the Icahn School of Medicine at Mount Sinai in New York, reported the findings in a poster (Abstract Su1801) at the annual Digestive Disease Week^® (DDW).

The FDA approved mirikizumab (Omvoh, Eli Lilly) to treat moderate to severe ulcerative colitis in October 2023. 

Dr. Sands and a team of US and international collaborators studied 1065 adults with Crohn’s disease or fistulizing Crohn’s disease for 3 months or more, with a mean duration of more than 7 years. At baseline, participants had a Simple Endoscopic Score for Crohn’s Disease (SES-CD) of 7 or more and reported an inadequate response, lost response, or intolerance to other therapy.

A total of 579 people were randomly assigned to mirikizumab and another 199 to placebo. Another 287 patients received ustekinumab; though they were not included in this current analysis, the findings were presented separately at DDW 2024. 

Mean age of study participants was 30 years, and men comprised 57%-59% of the groups. Nearly half (49%) of each group previously failed biologic therapy. 

A primary composite endpoint was clinical response at 12 weeks according to patient reported outcome and endoscopic response at 52 weeks measured with the SES-CD. A second primary endpoint was clinical response at 12 weeks by patient reported outcome combined with clinical remission on Crohn’s Disease Activity Index (CDAI) at 52 weeks.

Researchers also tracked 12 major secondary endpoints for mirikizumab vs placebo, including clinical response, endoscopic response, and clinical remission at week 12 and week 52. 
 

Efficacy Findings

A higher percentage of participants in the mirikizumab group achieved 12-week secondary endpoints compared with placebo. In the treatment group, 32.5% reached endoscopic response vs 12.6% in the placebo group, a statistically significant difference (P < .000001). In addition, 17.6% achieved endoscopic remission in the treatment group vs 7.0% in the placebo group at 12 weeks (P < .000213).

The “treat-through” results at 52 weeks revealed that a higher proportion of the group taking mirikizumab met the co-primary endpoints compared with placebo. A total of 48.4% in the mirikizumab group vs 9.0% in the placebo group achieved endoscopic response (P < .000001). Similarly, a higher proportion met clinical remission on the CDAI, 54.1% in the treatment group vs 19.6% in the placebo group (P < .000001).

Overall, 38% of mirikizumab-treated patients vs 9% of the placebo group reached a composite endpoint of patient reported clinical response at week 12 and endoscopic response by SES-CD at week 52 (P < .000001).

Dr. Sands and colleagues also combined clinical response reported by patients at 12 weeks with CDAI findings for clinical remission at week 52. A total of 45.4% in the treatment group met the combined endpoint compared with 19.6% of the placebo group (P < .000001). 

In an additional analysis, the researchers looked at this composite endpoint in patients in both groups who had failed or not failed a prior biologic for a total of 43.4% vs 12.4%, and 47.3% vs 26.5%, respectively.

“Mirikizumab demonstrated statistically significant and clinically meaningful improvements” in the study co-primary endpoints and secondary endpoints compared with placebo, the researchers concluded. 
 

Safety Findings

Safety outcomes during the 52-week study were “consistent with the known safety profile” of mirikizumab, the researchers noted. 

Treatment-emergent adverse events occurred in 78.6% of mirikizumab participants vs 73.0% of the placebo group. The most common were COVID-19, anemia, and arthralgia. Serious adverse events were reported in 10.3% of the mirikizumab group vs 17.1% of the placebo group. There were seven opportunistic infections in the treatment group, including herpes zoster and Candida, compared with none in the placebo group. 

One person in the placebo cohort died of a pulmonary embolism; there were no deaths in the mirikizumab group. 

People randomly assigned to placebo without a response at 12 weeks were switched over to mirikizumab. However, the findings from this group between 12 and 52 weeks were excluded from the 1-year data presented at DDW 2024, including one death from worsening Crohn’s disease during that time.

Mirikizumab looked particularly robust in this study, and it may turn out to be a critically important option for our patients, said Jordan Axelrad, MD, MPH, co-director of the Inflammatory Bowel Disease Center at NYU Langone Health in New York City. Dr. Axelrad was not involved in this study. 

Of importance, effect sizes were similar for “bio-naive and previously biologic-exposed patients,” he added. 

These data “really underscore that therapies targeting IL-23 may be clinically useful for Crohn’s disease patients with prior biologic failure, representing a significant departure from our previous experience with other biologic classes,” Dr. Axelrad said.

The study was funded by Eli Lilly and Company. Dr. Sands is a consultant and receives grant funding from Lilly. Dr. Axelrad had no relevant disclosures. 

A version of this article appeared on Medscape.com.

WASHINGTON — As part of a quality improvement initiative, gastroenterologists at the University of Texas Health Science Center reduced endoscopic waste by using a single tool rather than multiple tools during colonoscopies, according to a study presented at Digestive Disease Week^® (DDW).

After discussing environmentally conscious practices during regular meetings, the odds of gastroenterologists using a single tool — either biopsy forceps or a snare — compared with multiple disposable tools was three times higher.

“The burden of waste is massive, with GI being the third-largest waste generator in healthcare. The number of procedures is increasing, which just means more waste, and we have to look at ways to reduce it,” said lead author Prateek Harne, MD, a gastroenterology fellow at the University of Texas Health Science Center.

Overall, the healthcare industry generates 8.5% of U.S. greenhouse emissions, with more than 70% coming from used instruments and supplies, he said. GI endoscopy generates 85,000 metric tons of carbon dioxide waste annually. That waste stems from high case volumes, patient travel, the decontamination process, and single-use devices.

After seeing the waste at his institution, Dr. Harne wondered how to reduce single-use device and nonrenewable waste, particularly the tools used during polypectomies. He and colleagues decided to focus on single-tool use and collected data about the tools used during screening colonoscopies for 8 weeks before an intervention.

As part of the intervention, Dr. Harne and colleagues discussed green endoscopy initiatives supported by North American gastrointestinal societies during a journal club meeting with gastroenterology faculty. They also discussed potential strategies to reduce waste in day-to-day practice during a monthly business meeting, particularly focused on being mindful of using tools during polypectomies. The meetings occurred 3 days apart.

Then Dr. Harne and colleagues collected data regarding tool use during screening colonoscopies, looking at the number and type of instruments used. Before the meetings, 210 patients underwent colonoscopies, including 34% that required no intervention, 32% that required one tool, and 33% that required multiple tools.

After the meetings, 112 patients underwent colonoscopies, including 34% that required no tools, 49% that used one tool, and 17% that used multiple tools. This represented a 17% increase in the use of one tool (P < .01) and a 16% decrease in the use of multiple tools (P < .01). The odds of using a single tool compared with multiple tools was 2.98, and there was a statistically significant increase in uptake of snare for polypectomy.

The study was limited by being at a single center, having a small sample size, and using a short-term assessment. At the same time, the findings show potential for a low-cost solution through open discussion with gastroenterologists.

“Sir Isaac Newton had two holes for two different sized cats in his home, but all of his cats ended up using the bigger hole,” Dr. Harne said in his conclusion. “Maybe we can do the same for polypectomies and use only the tools that we need.”

In an interview, Dr. Harne noted he spoke with the janitorial staff at his institution to learn more about endoscopy unit waste, including how much is recycled, how much is incinerated, and who handles the waste. He recognized the work being done in Europe to understand and reduce endoscopic waste and hopes U.S. groups begin to implement more measures.

“Gastroenterologists and their teams need to be more cognizant of the impact we have on the environment,” Dr. Harne said. “As our study shows, if providers are aware that they can and should use fewer tools to get the same results, it can lead to a statistically significant impact, just with a friendly reminder to reduce use.”

After the presentation, Dr. Harne discussed other shifts with conference attendees, such as not opening or unwrapping tools until needed during a procedure.

“Small changes could have big impacts. Everything that we do in QI [quality improvement] is meant to help patients and the environment,” said Amanda Krouse, MD, a research fellow at the University of California, San Diego, who was a moderator of the DDW session on GI fellow–directed QI projects.

In an interview, Alana Persaud, MD, an endoscopy fellow at Geisinger Medical Center in Danville, Pennsylvania, also a moderator of the session, said: “Ultimately, the medical services we’re providing are for the longevity of our patients, but at the same time, we don’t want it to be to the detriment of the environment, so paying attention to green endoscopy when we can preserve and use more discretion with our devices is worth it so we can all thrive together.”

Dr. Harne did not have any disclosures.

WASHINGTON — As part of a quality improvement initiative, gastroenterologists at the University of Texas Health Science Center reduced endoscopic waste by using a single tool rather than multiple tools during colonoscopies, according to a study presented at Digestive Disease Week^® (DDW).

After discussing environmentally conscious practices during regular meetings, the odds of gastroenterologists using a single tool — either biopsy forceps or a snare — compared with multiple disposable tools was three times higher.

“The burden of waste is massive, with GI being the third-largest waste generator in healthcare. The number of procedures is increasing, which just means more waste, and we have to look at ways to reduce it,” said lead author Prateek Harne, MD, a gastroenterology fellow at the University of Texas Health Science Center.

Overall, the healthcare industry generates 8.5% of U.S. greenhouse emissions, with more than 70% coming from used instruments and supplies, he said. GI endoscopy generates 85,000 metric tons of carbon dioxide waste annually. That waste stems from high case volumes, patient travel, the decontamination process, and single-use devices.

After seeing the waste at his institution, Dr. Harne wondered how to reduce single-use device and nonrenewable waste, particularly the tools used during polypectomies. He and colleagues decided to focus on single-tool use and collected data about the tools used during screening colonoscopies for 8 weeks before an intervention.

As part of the intervention, Dr. Harne and colleagues discussed green endoscopy initiatives supported by North American gastrointestinal societies during a journal club meeting with gastroenterology faculty. They also discussed potential strategies to reduce waste in day-to-day practice during a monthly business meeting, particularly focused on being mindful of using tools during polypectomies. The meetings occurred 3 days apart.

Then Dr. Harne and colleagues collected data regarding tool use during screening colonoscopies, looking at the number and type of instruments used. Before the meetings, 210 patients underwent colonoscopies, including 34% that required no intervention, 32% that required one tool, and 33% that required multiple tools.

After the meetings, 112 patients underwent colonoscopies, including 34% that required no tools, 49% that used one tool, and 17% that used multiple tools. This represented a 17% increase in the use of one tool (P < .01) and a 16% decrease in the use of multiple tools (P < .01). The odds of using a single tool compared with multiple tools was 2.98, and there was a statistically significant increase in uptake of snare for polypectomy.

The study was limited by being at a single center, having a small sample size, and using a short-term assessment. At the same time, the findings show potential for a low-cost solution through open discussion with gastroenterologists.

“Sir Isaac Newton had two holes for two different sized cats in his home, but all of his cats ended up using the bigger hole,” Dr. Harne said in his conclusion. “Maybe we can do the same for polypectomies and use only the tools that we need.”

In an interview, Dr. Harne noted he spoke with the janitorial staff at his institution to learn more about endoscopy unit waste, including how much is recycled, how much is incinerated, and who handles the waste. He recognized the work being done in Europe to understand and reduce endoscopic waste and hopes U.S. groups begin to implement more measures.

“Gastroenterologists and their teams need to be more cognizant of the impact we have on the environment,” Dr. Harne said. “As our study shows, if providers are aware that they can and should use fewer tools to get the same results, it can lead to a statistically significant impact, just with a friendly reminder to reduce use.”

After the presentation, Dr. Harne discussed other shifts with conference attendees, such as not opening or unwrapping tools until needed during a procedure.

“Small changes could have big impacts. Everything that we do in QI [quality improvement] is meant to help patients and the environment,” said Amanda Krouse, MD, a research fellow at the University of California, San Diego, who was a moderator of the DDW session on GI fellow–directed QI projects.

In an interview, Alana Persaud, MD, an endoscopy fellow at Geisinger Medical Center in Danville, Pennsylvania, also a moderator of the session, said: “Ultimately, the medical services we’re providing are for the longevity of our patients, but at the same time, we don’t want it to be to the detriment of the environment, so paying attention to green endoscopy when we can preserve and use more discretion with our devices is worth it so we can all thrive together.”

Dr. Harne did not have any disclosures.

WASHINGTON — As part of a quality improvement initiative, gastroenterologists at the University of Texas Health Science Center reduced endoscopic waste by using a single tool rather than multiple tools during colonoscopies, according to a study presented at Digestive Disease Week^® (DDW).

After discussing environmentally conscious practices during regular meetings, the odds of gastroenterologists using a single tool — either biopsy forceps or a snare — compared with multiple disposable tools was three times higher.

“The burden of waste is massive, with GI being the third-largest waste generator in healthcare. The number of procedures is increasing, which just means more waste, and we have to look at ways to reduce it,” said lead author Prateek Harne, MD, a gastroenterology fellow at the University of Texas Health Science Center.

Overall, the healthcare industry generates 8.5% of U.S. greenhouse emissions, with more than 70% coming from used instruments and supplies, he said. GI endoscopy generates 85,000 metric tons of carbon dioxide waste annually. That waste stems from high case volumes, patient travel, the decontamination process, and single-use devices.

After seeing the waste at his institution, Dr. Harne wondered how to reduce single-use device and nonrenewable waste, particularly the tools used during polypectomies. He and colleagues decided to focus on single-tool use and collected data about the tools used during screening colonoscopies for 8 weeks before an intervention.

As part of the intervention, Dr. Harne and colleagues discussed green endoscopy initiatives supported by North American gastrointestinal societies during a journal club meeting with gastroenterology faculty. They also discussed potential strategies to reduce waste in day-to-day practice during a monthly business meeting, particularly focused on being mindful of using tools during polypectomies. The meetings occurred 3 days apart.

Then Dr. Harne and colleagues collected data regarding tool use during screening colonoscopies, looking at the number and type of instruments used. Before the meetings, 210 patients underwent colonoscopies, including 34% that required no intervention, 32% that required one tool, and 33% that required multiple tools.

After the meetings, 112 patients underwent colonoscopies, including 34% that required no tools, 49% that used one tool, and 17% that used multiple tools. This represented a 17% increase in the use of one tool (P < .01) and a 16% decrease in the use of multiple tools (P < .01). The odds of using a single tool compared with multiple tools was 2.98, and there was a statistically significant increase in uptake of snare for polypectomy.

The study was limited by being at a single center, having a small sample size, and using a short-term assessment. At the same time, the findings show potential for a low-cost solution through open discussion with gastroenterologists.

“Sir Isaac Newton had two holes for two different sized cats in his home, but all of his cats ended up using the bigger hole,” Dr. Harne said in his conclusion. “Maybe we can do the same for polypectomies and use only the tools that we need.”

In an interview, Dr. Harne noted he spoke with the janitorial staff at his institution to learn more about endoscopy unit waste, including how much is recycled, how much is incinerated, and who handles the waste. He recognized the work being done in Europe to understand and reduce endoscopic waste and hopes U.S. groups begin to implement more measures.

“Gastroenterologists and their teams need to be more cognizant of the impact we have on the environment,” Dr. Harne said. “As our study shows, if providers are aware that they can and should use fewer tools to get the same results, it can lead to a statistically significant impact, just with a friendly reminder to reduce use.”

After the presentation, Dr. Harne discussed other shifts with conference attendees, such as not opening or unwrapping tools until needed during a procedure.

“Small changes could have big impacts. Everything that we do in QI [quality improvement] is meant to help patients and the environment,” said Amanda Krouse, MD, a research fellow at the University of California, San Diego, who was a moderator of the DDW session on GI fellow–directed QI projects.

In an interview, Alana Persaud, MD, an endoscopy fellow at Geisinger Medical Center in Danville, Pennsylvania, also a moderator of the session, said: “Ultimately, the medical services we’re providing are for the longevity of our patients, but at the same time, we don’t want it to be to the detriment of the environment, so paying attention to green endoscopy when we can preserve and use more discretion with our devices is worth it so we can all thrive together.”

Dr. Harne did not have any disclosures.

Genetic predisposition likely directs intestinal disease location in pediatric Crohn’s disease (CD) — whether colon-predominant (C-CD) or small-bowel-predominant (SB-CD), a small analysis in Cellular and Molecular Gastroenterology and Hepatology suggests.

Richard Kellermayer, MD, PhD, professor of pediatrics in the Section of Pediatric Gastroenterology, Hepatology and Nutrition at Baylor College of Medicine in Houston, Texas, and colleagues compared the genetic makeup of patients based on their Crohn’s disease location — predominantly in the small bowel (L4) or predominantly in the colon (L2 and/or L3). They then generated bipartite networks of susceptibility genes to study the polygenic background of the disease subtypes. They hypothesize that such networks may govern where a patient develops Crohn’s disease.

Baylor College of Medicine

According to current understanding, as Dr. Kellermayer told GI & Hepatology News, most autoimmune disorders, CD included, develop in people with a genetic predisposition after serial environmental insults between conception and young adulthood. “As opposed to single-gene-associated genetic disorders, autoimmune diseases are linked to several hundred genes in which subtle anomalies can work in concert to predispose someone to a certain disorder,” he said. “We hope our findings will guide the development of personalized treatments based on the disease location at diagnosis to advance precision medicine.”
 

CD cases

Eight cases of SB-CD and 11 of C-CD met the inclusion criteria. Mean age at CD diagnosis was about 11 years for both subtypes, while 36.3% of patients with C-CD were female vs 25% of those with SB-CD. Ethnicity was 72.2% White in the C-CD group and 87.5% in the SB-CD group.

As to the main ileocolonic locations according to the Paris Classification of pediatric inflammatory bowel disease, 54.5% in the C-CD group had involvement at L2 and 45.5% at L3. In SB-CD cases, 100% had disease at L4b, 37.5% at L4, and 50% at L1.

The researchers identified 115 single-nucleotide polymorphisms (SNPs) with a combined annotation-dependent depletion (CADD) score on Phil’s Read Editor (PHRED) of >10 that was associated with 97 genes. PHRED is a computer program measuring the quality of the identification of nucleobases generated by automated DNA sequencing and scores the deleteriousness of single-nucleotide variants. The identified genes in this study had a significantly (P < .01) different allele variation between C-CD and SB-CD.

Among the top 28 candidates was an SNP in the EFNA3 gene with a CADD score > 20 for differentiating between the two phenotypically distinct CD groups. Furthermore, the EFNA3 rs17723260 (predicted to be deleterious) was found to have a significantly lower allele frequency (4.5%) in C-CD compared with its allele frequency of 37.5% in SB-CD (chi square P = .0097).

“This finding indicates that EFNA3 might play a role in modulating colonic inflammation, in which a deleterious genetic defect might provide protection against colitis (and direct autoimmunity against the proximal small bowel) in the polygenic background of CD,” the investigators wrote.

EFNA3 has been linked to both CD and ulcerative colitis. Another four genes associated with the top five SNP candidates had already been connected with IBD or mammalian intestinal inflammation. 

According to the authors, the biomedical literature and mouse model findings “implicate the translational relevance of our candidate gene compendium for directing colon- vs small-bowel–predominant CD development.” They hope the findings will be replicated in larger CD cohorts differentiated by disease location. “Our work may set the nidus for CD subtype–based precision medicine by guiding individualized treatment strategies,” they wrote.

This study was supported by the ProKIIDS Network of the Crohn’s and Colitis Foundation and the Public Health Service. It was also supported by the Wagner, Frugoni, and Klaasmeyer families’ Gutsy Kids Fund and by the DR and GL Laws Fund. The authors disclosed no conflicts of interest.

Genetic predisposition likely directs intestinal disease location in pediatric Crohn’s disease (CD) — whether colon-predominant (C-CD) or small-bowel-predominant (SB-CD), a small analysis in Cellular and Molecular Gastroenterology and Hepatology suggests.

Richard Kellermayer, MD, PhD, professor of pediatrics in the Section of Pediatric Gastroenterology, Hepatology and Nutrition at Baylor College of Medicine in Houston, Texas, and colleagues compared the genetic makeup of patients based on their Crohn’s disease location — predominantly in the small bowel (L4) or predominantly in the colon (L2 and/or L3). They then generated bipartite networks of susceptibility genes to study the polygenic background of the disease subtypes. They hypothesize that such networks may govern where a patient develops Crohn’s disease.

Baylor College of Medicine

According to current understanding, as Dr. Kellermayer told GI & Hepatology News, most autoimmune disorders, CD included, develop in people with a genetic predisposition after serial environmental insults between conception and young adulthood. “As opposed to single-gene-associated genetic disorders, autoimmune diseases are linked to several hundred genes in which subtle anomalies can work in concert to predispose someone to a certain disorder,” he said. “We hope our findings will guide the development of personalized treatments based on the disease location at diagnosis to advance precision medicine.”
 

CD cases

Eight cases of SB-CD and 11 of C-CD met the inclusion criteria. Mean age at CD diagnosis was about 11 years for both subtypes, while 36.3% of patients with C-CD were female vs 25% of those with SB-CD. Ethnicity was 72.2% White in the C-CD group and 87.5% in the SB-CD group.

As to the main ileocolonic locations according to the Paris Classification of pediatric inflammatory bowel disease, 54.5% in the C-CD group had involvement at L2 and 45.5% at L3. In SB-CD cases, 100% had disease at L4b, 37.5% at L4, and 50% at L1.

The researchers identified 115 single-nucleotide polymorphisms (SNPs) with a combined annotation-dependent depletion (CADD) score on Phil’s Read Editor (PHRED) of >10 that was associated with 97 genes. PHRED is a computer program measuring the quality of the identification of nucleobases generated by automated DNA sequencing and scores the deleteriousness of single-nucleotide variants. The identified genes in this study had a significantly (P < .01) different allele variation between C-CD and SB-CD.

Among the top 28 candidates was an SNP in the EFNA3 gene with a CADD score > 20 for differentiating between the two phenotypically distinct CD groups. Furthermore, the EFNA3 rs17723260 (predicted to be deleterious) was found to have a significantly lower allele frequency (4.5%) in C-CD compared with its allele frequency of 37.5% in SB-CD (chi square P = .0097).

“This finding indicates that EFNA3 might play a role in modulating colonic inflammation, in which a deleterious genetic defect might provide protection against colitis (and direct autoimmunity against the proximal small bowel) in the polygenic background of CD,” the investigators wrote.

EFNA3 has been linked to both CD and ulcerative colitis. Another four genes associated with the top five SNP candidates had already been connected with IBD or mammalian intestinal inflammation. 

According to the authors, the biomedical literature and mouse model findings “implicate the translational relevance of our candidate gene compendium for directing colon- vs small-bowel–predominant CD development.” They hope the findings will be replicated in larger CD cohorts differentiated by disease location. “Our work may set the nidus for CD subtype–based precision medicine by guiding individualized treatment strategies,” they wrote.

This study was supported by the ProKIIDS Network of the Crohn’s and Colitis Foundation and the Public Health Service. It was also supported by the Wagner, Frugoni, and Klaasmeyer families’ Gutsy Kids Fund and by the DR and GL Laws Fund. The authors disclosed no conflicts of interest.

Genetic predisposition likely directs intestinal disease location in pediatric Crohn’s disease (CD) — whether colon-predominant (C-CD) or small-bowel-predominant (SB-CD), a small analysis in Cellular and Molecular Gastroenterology and Hepatology suggests.

Richard Kellermayer, MD, PhD, professor of pediatrics in the Section of Pediatric Gastroenterology, Hepatology and Nutrition at Baylor College of Medicine in Houston, Texas, and colleagues compared the genetic makeup of patients based on their Crohn’s disease location — predominantly in the small bowel (L4) or predominantly in the colon (L2 and/or L3). They then generated bipartite networks of susceptibility genes to study the polygenic background of the disease subtypes. They hypothesize that such networks may govern where a patient develops Crohn’s disease.

Baylor College of Medicine

According to current understanding, as Dr. Kellermayer told GI & Hepatology News, most autoimmune disorders, CD included, develop in people with a genetic predisposition after serial environmental insults between conception and young adulthood. “As opposed to single-gene-associated genetic disorders, autoimmune diseases are linked to several hundred genes in which subtle anomalies can work in concert to predispose someone to a certain disorder,” he said. “We hope our findings will guide the development of personalized treatments based on the disease location at diagnosis to advance precision medicine.”
 

CD cases

Eight cases of SB-CD and 11 of C-CD met the inclusion criteria. Mean age at CD diagnosis was about 11 years for both subtypes, while 36.3% of patients with C-CD were female vs 25% of those with SB-CD. Ethnicity was 72.2% White in the C-CD group and 87.5% in the SB-CD group.

As to the main ileocolonic locations according to the Paris Classification of pediatric inflammatory bowel disease, 54.5% in the C-CD group had involvement at L2 and 45.5% at L3. In SB-CD cases, 100% had disease at L4b, 37.5% at L4, and 50% at L1.

The researchers identified 115 single-nucleotide polymorphisms (SNPs) with a combined annotation-dependent depletion (CADD) score on Phil’s Read Editor (PHRED) of >10 that was associated with 97 genes. PHRED is a computer program measuring the quality of the identification of nucleobases generated by automated DNA sequencing and scores the deleteriousness of single-nucleotide variants. The identified genes in this study had a significantly (P < .01) different allele variation between C-CD and SB-CD.

Among the top 28 candidates was an SNP in the EFNA3 gene with a CADD score > 20 for differentiating between the two phenotypically distinct CD groups. Furthermore, the EFNA3 rs17723260 (predicted to be deleterious) was found to have a significantly lower allele frequency (4.5%) in C-CD compared with its allele frequency of 37.5% in SB-CD (chi square P = .0097).

“This finding indicates that EFNA3 might play a role in modulating colonic inflammation, in which a deleterious genetic defect might provide protection against colitis (and direct autoimmunity against the proximal small bowel) in the polygenic background of CD,” the investigators wrote.

EFNA3 has been linked to both CD and ulcerative colitis. Another four genes associated with the top five SNP candidates had already been connected with IBD or mammalian intestinal inflammation. 

According to the authors, the biomedical literature and mouse model findings “implicate the translational relevance of our candidate gene compendium for directing colon- vs small-bowel–predominant CD development.” They hope the findings will be replicated in larger CD cohorts differentiated by disease location. “Our work may set the nidus for CD subtype–based precision medicine by guiding individualized treatment strategies,” they wrote.

This study was supported by the ProKIIDS Network of the Crohn’s and Colitis Foundation and the Public Health Service. It was also supported by the Wagner, Frugoni, and Klaasmeyer families’ Gutsy Kids Fund and by the DR and GL Laws Fund. The authors disclosed no conflicts of interest.

A new two-measure metric seems to improve accuracy and statistical precision in assessing celiac disease (CeD) histology compared with either of two components alone, according to a study in Clinical Gastroenterology and Hepatology.

The new morphometric duodenal biopsy mucosal scale joins together villous height-to-crypt depth ratio (Vh:Cd) and intraepithelial lymphocytes (IEL) — each key CeD histological measures of the small intestine — in a scale called VCIEL.

The authors believe the VCIEL will enable a broader and more accurate measurement of mucosal health in CeD. It will be particularly useful for population analysis in clinical trials and could improve the powering of trial design. “Use of VCIEL may lead to better outcome measures for potential new therapeutic treatments benefiting patients,” wrote Jocelyn A. Silvester, MD, PhD, a pediatrician at Boston Children’s Hospital and an assistant professor at Harvard Medical School, and colleagues.

Boston Children’s Hospital

The Study

In the absence of a broadly accepted single measure of mucosal injury in CeD, the group assessed whether the composite metric could improve statistical precision for assessing histology.

Enter VCIEL, which combines the Vh:Cd and IEL for individual patients with equal weighting by converting each scale to a fraction of their standard deviation and summing the results.

The researchers applied the VCIEL formula in a reanalysis of four clinical gluten-challenge trials and compared the results for Vh:Cd and IEL separately with those for VCIEL for clinical significance (effect size) and statistical significance.

In reanalysis of the ALV003-1021 trial, for example, the researchers observed an effect size and P value (analysis of covariance) of 1.37 and .038 for a delta (difference) value of Vh:Cd 1.17 and .005 for IEL and 1.86 and .004 for VCIEL.

For the similar gluten-challenge IMGX003-NCCIH-1721 trial, the corresponding delta results were .76 and .057 for Vh:Cd, .98 and .018 for IEL, and 1.14 and .007 for VCIEL. Comparable improvements with VCIEL over individual Vh:Cd and IEL were observed for other studies, including a nontherapeutic gluten challenge study.

In NCT03409796 trial data, the computation of VCIEL values showed an improved statistical significance relative to the component values of Vh:Cd and IEL by the within-group paired 2-tailed t test P values from baseline to day 15, particularly at a 10-g gluten challenge dose: Vh:Cd, IEL, VCIEL = .0050, .0031, and .0014, respectively.

Little correlation emerged between baseline values and changes with intervention for Vh:Cd and IEL on an individual patient basis.

The greater accuracy and statistical precision of the VCIEL scale are presumably due to averaging over some of the measurement uncertainty in individual patient and timepoint Vh:Cd and IEL values and creating a composite of different histologic properties, the authors noted.

This study was funded by ImmunogenX, Inc. First author Jack A. Syage is a cofounder and shareholder in ImmunogenX Inc. Dr. Silvester has served on an advisory board for Takeda Pharmaceuticals and has received research funding from Biomedal S.L., Cour Pharmaceuticals, and Glutenostics LLC. Several coauthors disclosed various financial ties to multiple private-sector pharmaceutical and biomedical companies, including ImmunogenX.

A new two-measure metric seems to improve accuracy and statistical precision in assessing celiac disease (CeD) histology compared with either of two components alone, according to a study in Clinical Gastroenterology and Hepatology.

The new morphometric duodenal biopsy mucosal scale joins together villous height-to-crypt depth ratio (Vh:Cd) and intraepithelial lymphocytes (IEL) — each key CeD histological measures of the small intestine — in a scale called VCIEL.

The authors believe the VCIEL will enable a broader and more accurate measurement of mucosal health in CeD. It will be particularly useful for population analysis in clinical trials and could improve the powering of trial design. “Use of VCIEL may lead to better outcome measures for potential new therapeutic treatments benefiting patients,” wrote Jocelyn A. Silvester, MD, PhD, a pediatrician at Boston Children’s Hospital and an assistant professor at Harvard Medical School, and colleagues.

Boston Children’s Hospital

The Study

In the absence of a broadly accepted single measure of mucosal injury in CeD, the group assessed whether the composite metric could improve statistical precision for assessing histology.

Enter VCIEL, which combines the Vh:Cd and IEL for individual patients with equal weighting by converting each scale to a fraction of their standard deviation and summing the results.

The researchers applied the VCIEL formula in a reanalysis of four clinical gluten-challenge trials and compared the results for Vh:Cd and IEL separately with those for VCIEL for clinical significance (effect size) and statistical significance.

In reanalysis of the ALV003-1021 trial, for example, the researchers observed an effect size and P value (analysis of covariance) of 1.37 and .038 for a delta (difference) value of Vh:Cd 1.17 and .005 for IEL and 1.86 and .004 for VCIEL.

For the similar gluten-challenge IMGX003-NCCIH-1721 trial, the corresponding delta results were .76 and .057 for Vh:Cd, .98 and .018 for IEL, and 1.14 and .007 for VCIEL. Comparable improvements with VCIEL over individual Vh:Cd and IEL were observed for other studies, including a nontherapeutic gluten challenge study.

In NCT03409796 trial data, the computation of VCIEL values showed an improved statistical significance relative to the component values of Vh:Cd and IEL by the within-group paired 2-tailed t test P values from baseline to day 15, particularly at a 10-g gluten challenge dose: Vh:Cd, IEL, VCIEL = .0050, .0031, and .0014, respectively.

Little correlation emerged between baseline values and changes with intervention for Vh:Cd and IEL on an individual patient basis.

The greater accuracy and statistical precision of the VCIEL scale are presumably due to averaging over some of the measurement uncertainty in individual patient and timepoint Vh:Cd and IEL values and creating a composite of different histologic properties, the authors noted.

This study was funded by ImmunogenX, Inc. First author Jack A. Syage is a cofounder and shareholder in ImmunogenX Inc. Dr. Silvester has served on an advisory board for Takeda Pharmaceuticals and has received research funding from Biomedal S.L., Cour Pharmaceuticals, and Glutenostics LLC. Several coauthors disclosed various financial ties to multiple private-sector pharmaceutical and biomedical companies, including ImmunogenX.

A new two-measure metric seems to improve accuracy and statistical precision in assessing celiac disease (CeD) histology compared with either of two components alone, according to a study in Clinical Gastroenterology and Hepatology.

The new morphometric duodenal biopsy mucosal scale joins together villous height-to-crypt depth ratio (Vh:Cd) and intraepithelial lymphocytes (IEL) — each key CeD histological measures of the small intestine — in a scale called VCIEL.

The authors believe the VCIEL will enable a broader and more accurate measurement of mucosal health in CeD. It will be particularly useful for population analysis in clinical trials and could improve the powering of trial design. “Use of VCIEL may lead to better outcome measures for potential new therapeutic treatments benefiting patients,” wrote Jocelyn A. Silvester, MD, PhD, a pediatrician at Boston Children’s Hospital and an assistant professor at Harvard Medical School, and colleagues.

Boston Children’s Hospital

The Study

In the absence of a broadly accepted single measure of mucosal injury in CeD, the group assessed whether the composite metric could improve statistical precision for assessing histology.

Enter VCIEL, which combines the Vh:Cd and IEL for individual patients with equal weighting by converting each scale to a fraction of their standard deviation and summing the results.

The researchers applied the VCIEL formula in a reanalysis of four clinical gluten-challenge trials and compared the results for Vh:Cd and IEL separately with those for VCIEL for clinical significance (effect size) and statistical significance.

In reanalysis of the ALV003-1021 trial, for example, the researchers observed an effect size and P value (analysis of covariance) of 1.37 and .038 for a delta (difference) value of Vh:Cd 1.17 and .005 for IEL and 1.86 and .004 for VCIEL.

For the similar gluten-challenge IMGX003-NCCIH-1721 trial, the corresponding delta results were .76 and .057 for Vh:Cd, .98 and .018 for IEL, and 1.14 and .007 for VCIEL. Comparable improvements with VCIEL over individual Vh:Cd and IEL were observed for other studies, including a nontherapeutic gluten challenge study.

In NCT03409796 trial data, the computation of VCIEL values showed an improved statistical significance relative to the component values of Vh:Cd and IEL by the within-group paired 2-tailed t test P values from baseline to day 15, particularly at a 10-g gluten challenge dose: Vh:Cd, IEL, VCIEL = .0050, .0031, and .0014, respectively.

Little correlation emerged between baseline values and changes with intervention for Vh:Cd and IEL on an individual patient basis.

The greater accuracy and statistical precision of the VCIEL scale are presumably due to averaging over some of the measurement uncertainty in individual patient and timepoint Vh:Cd and IEL values and creating a composite of different histologic properties, the authors noted.

This study was funded by ImmunogenX, Inc. First author Jack A. Syage is a cofounder and shareholder in ImmunogenX Inc. Dr. Silvester has served on an advisory board for Takeda Pharmaceuticals and has received research funding from Biomedal S.L., Cour Pharmaceuticals, and Glutenostics LLC. Several coauthors disclosed various financial ties to multiple private-sector pharmaceutical and biomedical companies, including ImmunogenX.

Have you ever wished you could access all of our Crohn’s disease resources in one place? We’ve compiled our Crohn’s disease clinical guidance, continuing education resources, patient education, and FAQs into one convenient toolkit.

Toolkit includes clinical guidance on:

• Role of biomarkers for the management of Crohn’s disease
• Medical management of moderate to severe luminal and perianal fistulizing Crohn’s disease
• Diet and nutritional therapies in patients with IBD

Check it out at www.gastro.org/toolkit.

Have you ever wished you could access all of our Crohn’s disease resources in one place? We’ve compiled our Crohn’s disease clinical guidance, continuing education resources, patient education, and FAQs into one convenient toolkit.

Toolkit includes clinical guidance on:

• Role of biomarkers for the management of Crohn’s disease
• Medical management of moderate to severe luminal and perianal fistulizing Crohn’s disease
• Diet and nutritional therapies in patients with IBD

Check it out at www.gastro.org/toolkit.

Have you ever wished you could access all of our Crohn’s disease resources in one place? We’ve compiled our Crohn’s disease clinical guidance, continuing education resources, patient education, and FAQs into one convenient toolkit.

Toolkit includes clinical guidance on:

• Role of biomarkers for the management of Crohn’s disease
• Medical management of moderate to severe luminal and perianal fistulizing Crohn’s disease
• Diet and nutritional therapies in patients with IBD

Check it out at www.gastro.org/toolkit.

Children who ate a high-quality diet at 1 year of age were at a 25% reduced risk of developing inflammatory bowel disease (IBD) in later life, prospective pooled data from two Scandinavian birth cohorts suggested.

It appears important to feed children a quality diet at a very young age, in particular one rich in vegetables and fish, since by age three, only dietary fish intake had any impact on IBD risk.

Ms. Guo

Although high intakes of these two food categories in very early life correlated with lower IBD risk, exposure to sugar-sweetened beverages (SSBs) was associated with an increased risk. “While non-causal explanations for our results cannot be ruled out, these novel findings are consistent with the hypothesis that early-life diet, possibly mediated through changes in the gut microbiome, may affect the risk of developing IBD,” wrote lead author Annie Guo, a PhD candidate in the Department of Pediatrics, University of Gothenburg, Sweden, and colleagues. The report was published in Gut.

“This is a population-based study investigating the risk for IBD, rather than the specific effect of diet,” Ms. Guo said in an interview. “Therefore, the results are not enough on their own to be translated into individual advice that can be applicable in the clinic. However, the study supports current dietary guidelines for small children, that is, the intake of sugar should be limited and a higher intake of fish and vegetables is beneficial for overall health.”
 

Two-Cohort Study

The investigators prospectively recorded food-group information on children (just under half were female) from the All Babies in Southeast Sweden and The Norwegian Mother, Father and Child Cohort Study to assess the diet quality using a Healthy Eating Index and intake frequency. Parents answered questions about their offspring’s diet at ages 12-18 months and 30-36 months. Quality of diet was measured by intake of meat, fish, fruit, vegetables, dairy, sweets, snacks, and drinks.

The Swedish cohort included 21,700 children born between October 1997 and October 1999, while the Norwegian analysis included 114,500 children, 95,200 mothers, and 75,200 fathers recruited from across Norway from 1999 to 2008. In 1,304,433 person-years of follow-up, the researchers tracked 81,280 participants from birth to childhood and adolescence, with median follow-ups in the two cohorts ranging from 1 year of age to 21.3 years (Sweden) and to 15.2 years of age (Norway). Of these children, 307 were diagnosed with IBD: Crohn’s disease (CD; n = 131); ulcerative colitis (UC; n = 97); and IBD unclassified (n = 79).

Adjusting for parental IBD history, sex, origin, education, and maternal comorbidities, the study found:

• Compared with low-quality diet, both medium- and high-quality diets at 1 year were associated with a roughly 25% reduced risk for IBD (pooled adjusted hazard ratio [aHR], 0.75 [95% CI, 0.58-0.98] and 0.75 [0.56-1.0], respectively).
• The pooled aHR per increase of category was 0.86 (95% CI, 0.74-0.99). The pooled aHR for IBD in 1-year-olds with high vs low fish intake was 0.70 (95% CI, 0.49-1.0), and this diet showed an association with a reduced risk for UC (pooled aHR, 0.46; 95% CI, 0.21-0.99). Higher vegetable intake at 1 year was also associated with a risk reduction in IBD (HR, 0.72; 95% CI, 0.55-0.95). It has been hypothesized that intake of vegetables and vegetable fibers may have programming effects on the immune system.
• AutoWith 72% of children reportedly consuming SSBs at age 1, pooled aHRs showed that some vs no intake of SSBs was associated with an increased risk for later IBD (pooled aHR, 1.42; 95% CI, 1.05-1.90).
• There were no obvious associations between overall IBD or CD/UC risk and meat, dairy, fruit, grains, potatoes, and foods high in sugar and/or fat. Diet at age 3 years was not associated with incident IBD (pooled aHR, 1.02; 95% CI, 0.76-1.37), suggesting that the risk impact of diet is greatest on very young and vulnerable microbiomes.

Ms. Guo noted that a Swedish national survey among 4-year-olds found a mean SSB consumption of 187 g/d with a mean frequency of once daily. The most desired changes in food habits are a lower intake of soft drinks, sweets, crisps, cakes, and biscuits and an increase in the intake of fruits and vegetables. A similar Norwegian survey among 2-year-olds showed that SSBs were consumed by 36% of all children with a mean intake of 40 g/d.

The exact mechanism by which sugar affects the intestinal microbiota is not established. “However, what we do know is that an excessive intake of sugar can disrupt the balance of the gut microbiome,” Ms. Guo said. “And if the child has a high intake of foods with high in sugar, that also increases the chances that the child’s overall diet has a lower intake of other foods that contribute to a diverse microbiome such as fruits and vegetables.”

An ‘Elegant’ Study

In an accompanying editorial, gastroenterologist Ashwin N. Ananthakrishnan, MBBS, MPH, AGAF, of Mass General Brigham and the Mass General Research Institute, Boston, cautioned that accurately measuring food intake in very young children is difficult, and dietary questionnaires in this study did not address food additives and emulsifiers common in commercial baby food, which may play a role in the pathogenesis of IBD.

Mass General Brigham

Another study limitation is that the dietary questionnaire used has not been qualitatively or quantitatively validated against other more conventional methods, said Dr. Ananthakrishnan, who was not involved in the research.

Nevertheless, he called the study “elegant” and expanding of the data on the importance of this period in IBD development. “Although in the present study there was no association between diet at 3 years and development of IBD (in contrast to the association observed for dietary intake at 1 year), other prospective cohorts of adult-onset IBD have demonstrated an inverse association between vegetable or fish intake and reduced risk for CD while sugar-sweetened beverages have been linked to a higher risk for IBD.”

As to the question of recommending early preventive diet for IBD, “thus far, data on the impact of diet very early in childhood, outside of breastfeeding, on the risk for IBD has been lacking,” Dr. Ananthakrishnan said in an interview. “This important study highlights that diet as early as 1 year can modify subsequent risk for IBD. This raises the intriguing possibility of whether early changes in diet could be used, particularly in those at higher risk, to reduce or even prevent future development of IBD. Of course, more works needs to be done to define modifiability of diet as a risk factor, but this is an important supportive data.”

In his editorial, Dr. Ananthakrishnan stated that despite the absence of gold-standard interventional data demonstrating a benefit of dietary interventions, “in my opinion, it may still be reasonable to suggest such interventions to motivate individuals who incorporate several of the dietary patterns associated with lower risk for IBD from this and other studies. This includes ensuring adequate dietary fiber, particularly from fruits and vegetables, intake of fish, minimizing sugar-sweetened beverages and preferring fresh over processed and ultra-processed foods and snacks.” According to the study authors, their novel findings support further research on the role of childhood diet in the prevention of IBD.

The All Babies in Southeast Sweden Study is supported by Barndiabetesfonden (Swedish Child Diabetes Foundation), the Swedish Council for Working Life and Social Research, the Swedish Research Council, the Medical Research Council of Southeast Sweden, the JDRF Wallenberg Foundation, ALF and LFoU grants from Region Östergötland and Linköping University, and the Joanna Cocozza Foundation.

The Norwegian Mother, Father and Child Cohort Study is supported by the Norwegian Ministry of Health and Care Services and the Ministry of Education and Research.

Ms. Guo received grants from the Swedish Society for Medical Research and the Henning and Johan Throne-Holst Foundation to conduct this study. Co-author Karl Mårild has received funding from the Swedish Society for Medical Research, the Swedish Research Council, and ALF, Sweden’s medical research and education co-ordinating body. The authors declared no competing interests. Dr. Ananthakrishnan is supported by the National Institutes of Health, the Leona M. and Harry B. Helmsley Charitable Trust, and the Chleck Family Foundation. He has served on the scientific advisory board for Geneoscopy.

Children who ate a high-quality diet at 1 year of age were at a 25% reduced risk of developing inflammatory bowel disease (IBD) in later life, prospective pooled data from two Scandinavian birth cohorts suggested.

It appears important to feed children a quality diet at a very young age, in particular one rich in vegetables and fish, since by age three, only dietary fish intake had any impact on IBD risk.

Ms. Guo

Although high intakes of these two food categories in very early life correlated with lower IBD risk, exposure to sugar-sweetened beverages (SSBs) was associated with an increased risk. “While non-causal explanations for our results cannot be ruled out, these novel findings are consistent with the hypothesis that early-life diet, possibly mediated through changes in the gut microbiome, may affect the risk of developing IBD,” wrote lead author Annie Guo, a PhD candidate in the Department of Pediatrics, University of Gothenburg, Sweden, and colleagues. The report was published in Gut.

“This is a population-based study investigating the risk for IBD, rather than the specific effect of diet,” Ms. Guo said in an interview. “Therefore, the results are not enough on their own to be translated into individual advice that can be applicable in the clinic. However, the study supports current dietary guidelines for small children, that is, the intake of sugar should be limited and a higher intake of fish and vegetables is beneficial for overall health.”
 

Two-Cohort Study

The investigators prospectively recorded food-group information on children (just under half were female) from the All Babies in Southeast Sweden and The Norwegian Mother, Father and Child Cohort Study to assess the diet quality using a Healthy Eating Index and intake frequency. Parents answered questions about their offspring’s diet at ages 12-18 months and 30-36 months. Quality of diet was measured by intake of meat, fish, fruit, vegetables, dairy, sweets, snacks, and drinks.

The Swedish cohort included 21,700 children born between October 1997 and October 1999, while the Norwegian analysis included 114,500 children, 95,200 mothers, and 75,200 fathers recruited from across Norway from 1999 to 2008. In 1,304,433 person-years of follow-up, the researchers tracked 81,280 participants from birth to childhood and adolescence, with median follow-ups in the two cohorts ranging from 1 year of age to 21.3 years (Sweden) and to 15.2 years of age (Norway). Of these children, 307 were diagnosed with IBD: Crohn’s disease (CD; n = 131); ulcerative colitis (UC; n = 97); and IBD unclassified (n = 79).

Adjusting for parental IBD history, sex, origin, education, and maternal comorbidities, the study found:

• Compared with low-quality diet, both medium- and high-quality diets at 1 year were associated with a roughly 25% reduced risk for IBD (pooled adjusted hazard ratio [aHR], 0.75 [95% CI, 0.58-0.98] and 0.75 [0.56-1.0], respectively).
• The pooled aHR per increase of category was 0.86 (95% CI, 0.74-0.99). The pooled aHR for IBD in 1-year-olds with high vs low fish intake was 0.70 (95% CI, 0.49-1.0), and this diet showed an association with a reduced risk for UC (pooled aHR, 0.46; 95% CI, 0.21-0.99). Higher vegetable intake at 1 year was also associated with a risk reduction in IBD (HR, 0.72; 95% CI, 0.55-0.95). It has been hypothesized that intake of vegetables and vegetable fibers may have programming effects on the immune system.
• AutoWith 72% of children reportedly consuming SSBs at age 1, pooled aHRs showed that some vs no intake of SSBs was associated with an increased risk for later IBD (pooled aHR, 1.42; 95% CI, 1.05-1.90).
• There were no obvious associations between overall IBD or CD/UC risk and meat, dairy, fruit, grains, potatoes, and foods high in sugar and/or fat. Diet at age 3 years was not associated with incident IBD (pooled aHR, 1.02; 95% CI, 0.76-1.37), suggesting that the risk impact of diet is greatest on very young and vulnerable microbiomes.

Ms. Guo noted that a Swedish national survey among 4-year-olds found a mean SSB consumption of 187 g/d with a mean frequency of once daily. The most desired changes in food habits are a lower intake of soft drinks, sweets, crisps, cakes, and biscuits and an increase in the intake of fruits and vegetables. A similar Norwegian survey among 2-year-olds showed that SSBs were consumed by 36% of all children with a mean intake of 40 g/d.

The exact mechanism by which sugar affects the intestinal microbiota is not established. “However, what we do know is that an excessive intake of sugar can disrupt the balance of the gut microbiome,” Ms. Guo said. “And if the child has a high intake of foods with high in sugar, that also increases the chances that the child’s overall diet has a lower intake of other foods that contribute to a diverse microbiome such as fruits and vegetables.”

An ‘Elegant’ Study

In an accompanying editorial, gastroenterologist Ashwin N. Ananthakrishnan, MBBS, MPH, AGAF, of Mass General Brigham and the Mass General Research Institute, Boston, cautioned that accurately measuring food intake in very young children is difficult, and dietary questionnaires in this study did not address food additives and emulsifiers common in commercial baby food, which may play a role in the pathogenesis of IBD.

Mass General Brigham

Another study limitation is that the dietary questionnaire used has not been qualitatively or quantitatively validated against other more conventional methods, said Dr. Ananthakrishnan, who was not involved in the research.

Nevertheless, he called the study “elegant” and expanding of the data on the importance of this period in IBD development. “Although in the present study there was no association between diet at 3 years and development of IBD (in contrast to the association observed for dietary intake at 1 year), other prospective cohorts of adult-onset IBD have demonstrated an inverse association between vegetable or fish intake and reduced risk for CD while sugar-sweetened beverages have been linked to a higher risk for IBD.”

As to the question of recommending early preventive diet for IBD, “thus far, data on the impact of diet very early in childhood, outside of breastfeeding, on the risk for IBD has been lacking,” Dr. Ananthakrishnan said in an interview. “This important study highlights that diet as early as 1 year can modify subsequent risk for IBD. This raises the intriguing possibility of whether early changes in diet could be used, particularly in those at higher risk, to reduce or even prevent future development of IBD. Of course, more works needs to be done to define modifiability of diet as a risk factor, but this is an important supportive data.”

In his editorial, Dr. Ananthakrishnan stated that despite the absence of gold-standard interventional data demonstrating a benefit of dietary interventions, “in my opinion, it may still be reasonable to suggest such interventions to motivate individuals who incorporate several of the dietary patterns associated with lower risk for IBD from this and other studies. This includes ensuring adequate dietary fiber, particularly from fruits and vegetables, intake of fish, minimizing sugar-sweetened beverages and preferring fresh over processed and ultra-processed foods and snacks.” According to the study authors, their novel findings support further research on the role of childhood diet in the prevention of IBD.

The All Babies in Southeast Sweden Study is supported by Barndiabetesfonden (Swedish Child Diabetes Foundation), the Swedish Council for Working Life and Social Research, the Swedish Research Council, the Medical Research Council of Southeast Sweden, the JDRF Wallenberg Foundation, ALF and LFoU grants from Region Östergötland and Linköping University, and the Joanna Cocozza Foundation.

The Norwegian Mother, Father and Child Cohort Study is supported by the Norwegian Ministry of Health and Care Services and the Ministry of Education and Research.

Ms. Guo received grants from the Swedish Society for Medical Research and the Henning and Johan Throne-Holst Foundation to conduct this study. Co-author Karl Mårild has received funding from the Swedish Society for Medical Research, the Swedish Research Council, and ALF, Sweden’s medical research and education co-ordinating body. The authors declared no competing interests. Dr. Ananthakrishnan is supported by the National Institutes of Health, the Leona M. and Harry B. Helmsley Charitable Trust, and the Chleck Family Foundation. He has served on the scientific advisory board for Geneoscopy.

Children who ate a high-quality diet at 1 year of age were at a 25% reduced risk of developing inflammatory bowel disease (IBD) in later life, prospective pooled data from two Scandinavian birth cohorts suggested.

It appears important to feed children a quality diet at a very young age, in particular one rich in vegetables and fish, since by age three, only dietary fish intake had any impact on IBD risk.

Ms. Guo

Although high intakes of these two food categories in very early life correlated with lower IBD risk, exposure to sugar-sweetened beverages (SSBs) was associated with an increased risk. “While non-causal explanations for our results cannot be ruled out, these novel findings are consistent with the hypothesis that early-life diet, possibly mediated through changes in the gut microbiome, may affect the risk of developing IBD,” wrote lead author Annie Guo, a PhD candidate in the Department of Pediatrics, University of Gothenburg, Sweden, and colleagues. The report was published in Gut.

“This is a population-based study investigating the risk for IBD, rather than the specific effect of diet,” Ms. Guo said in an interview. “Therefore, the results are not enough on their own to be translated into individual advice that can be applicable in the clinic. However, the study supports current dietary guidelines for small children, that is, the intake of sugar should be limited and a higher intake of fish and vegetables is beneficial for overall health.”
 

Two-Cohort Study

The investigators prospectively recorded food-group information on children (just under half were female) from the All Babies in Southeast Sweden and The Norwegian Mother, Father and Child Cohort Study to assess the diet quality using a Healthy Eating Index and intake frequency. Parents answered questions about their offspring’s diet at ages 12-18 months and 30-36 months. Quality of diet was measured by intake of meat, fish, fruit, vegetables, dairy, sweets, snacks, and drinks.

The Swedish cohort included 21,700 children born between October 1997 and October 1999, while the Norwegian analysis included 114,500 children, 95,200 mothers, and 75,200 fathers recruited from across Norway from 1999 to 2008. In 1,304,433 person-years of follow-up, the researchers tracked 81,280 participants from birth to childhood and adolescence, with median follow-ups in the two cohorts ranging from 1 year of age to 21.3 years (Sweden) and to 15.2 years of age (Norway). Of these children, 307 were diagnosed with IBD: Crohn’s disease (CD; n = 131); ulcerative colitis (UC; n = 97); and IBD unclassified (n = 79).

Adjusting for parental IBD history, sex, origin, education, and maternal comorbidities, the study found:

• Compared with low-quality diet, both medium- and high-quality diets at 1 year were associated with a roughly 25% reduced risk for IBD (pooled adjusted hazard ratio [aHR], 0.75 [95% CI, 0.58-0.98] and 0.75 [0.56-1.0], respectively).
• The pooled aHR per increase of category was 0.86 (95% CI, 0.74-0.99). The pooled aHR for IBD in 1-year-olds with high vs low fish intake was 0.70 (95% CI, 0.49-1.0), and this diet showed an association with a reduced risk for UC (pooled aHR, 0.46; 95% CI, 0.21-0.99). Higher vegetable intake at 1 year was also associated with a risk reduction in IBD (HR, 0.72; 95% CI, 0.55-0.95). It has been hypothesized that intake of vegetables and vegetable fibers may have programming effects on the immune system.
• AutoWith 72% of children reportedly consuming SSBs at age 1, pooled aHRs showed that some vs no intake of SSBs was associated with an increased risk for later IBD (pooled aHR, 1.42; 95% CI, 1.05-1.90).
• There were no obvious associations between overall IBD or CD/UC risk and meat, dairy, fruit, grains, potatoes, and foods high in sugar and/or fat. Diet at age 3 years was not associated with incident IBD (pooled aHR, 1.02; 95% CI, 0.76-1.37), suggesting that the risk impact of diet is greatest on very young and vulnerable microbiomes.

Ms. Guo noted that a Swedish national survey among 4-year-olds found a mean SSB consumption of 187 g/d with a mean frequency of once daily. The most desired changes in food habits are a lower intake of soft drinks, sweets, crisps, cakes, and biscuits and an increase in the intake of fruits and vegetables. A similar Norwegian survey among 2-year-olds showed that SSBs were consumed by 36% of all children with a mean intake of 40 g/d.

The exact mechanism by which sugar affects the intestinal microbiota is not established. “However, what we do know is that an excessive intake of sugar can disrupt the balance of the gut microbiome,” Ms. Guo said. “And if the child has a high intake of foods with high in sugar, that also increases the chances that the child’s overall diet has a lower intake of other foods that contribute to a diverse microbiome such as fruits and vegetables.”

An ‘Elegant’ Study

In an accompanying editorial, gastroenterologist Ashwin N. Ananthakrishnan, MBBS, MPH, AGAF, of Mass General Brigham and the Mass General Research Institute, Boston, cautioned that accurately measuring food intake in very young children is difficult, and dietary questionnaires in this study did not address food additives and emulsifiers common in commercial baby food, which may play a role in the pathogenesis of IBD.

Mass General Brigham

Another study limitation is that the dietary questionnaire used has not been qualitatively or quantitatively validated against other more conventional methods, said Dr. Ananthakrishnan, who was not involved in the research.

Nevertheless, he called the study “elegant” and expanding of the data on the importance of this period in IBD development. “Although in the present study there was no association between diet at 3 years and development of IBD (in contrast to the association observed for dietary intake at 1 year), other prospective cohorts of adult-onset IBD have demonstrated an inverse association between vegetable or fish intake and reduced risk for CD while sugar-sweetened beverages have been linked to a higher risk for IBD.”

As to the question of recommending early preventive diet for IBD, “thus far, data on the impact of diet very early in childhood, outside of breastfeeding, on the risk for IBD has been lacking,” Dr. Ananthakrishnan said in an interview. “This important study highlights that diet as early as 1 year can modify subsequent risk for IBD. This raises the intriguing possibility of whether early changes in diet could be used, particularly in those at higher risk, to reduce or even prevent future development of IBD. Of course, more works needs to be done to define modifiability of diet as a risk factor, but this is an important supportive data.”

In his editorial, Dr. Ananthakrishnan stated that despite the absence of gold-standard interventional data demonstrating a benefit of dietary interventions, “in my opinion, it may still be reasonable to suggest such interventions to motivate individuals who incorporate several of the dietary patterns associated with lower risk for IBD from this and other studies. This includes ensuring adequate dietary fiber, particularly from fruits and vegetables, intake of fish, minimizing sugar-sweetened beverages and preferring fresh over processed and ultra-processed foods and snacks.” According to the study authors, their novel findings support further research on the role of childhood diet in the prevention of IBD.

The All Babies in Southeast Sweden Study is supported by Barndiabetesfonden (Swedish Child Diabetes Foundation), the Swedish Council for Working Life and Social Research, the Swedish Research Council, the Medical Research Council of Southeast Sweden, the JDRF Wallenberg Foundation, ALF and LFoU grants from Region Östergötland and Linköping University, and the Joanna Cocozza Foundation.

The Norwegian Mother, Father and Child Cohort Study is supported by the Norwegian Ministry of Health and Care Services and the Ministry of Education and Research.

Ms. Guo received grants from the Swedish Society for Medical Research and the Henning and Johan Throne-Holst Foundation to conduct this study. Co-author Karl Mårild has received funding from the Swedish Society for Medical Research, the Swedish Research Council, and ALF, Sweden’s medical research and education co-ordinating body. The authors declared no competing interests. Dr. Ananthakrishnan is supported by the National Institutes of Health, the Leona M. and Harry B. Helmsley Charitable Trust, and the Chleck Family Foundation. He has served on the scientific advisory board for Geneoscopy.

Gastroenterology

January 2024

Hirano I, et al; ASCENT WORKING GROUP. Ascending to New Heights for Novel Therapeutics for Eosinophilic Esophagitis. Gastroenterology. 2024 Jan;166(1):1-10. doi: 10.1053/j.gastro.2023.09.004. Epub 2023 Sep 9. PMID: 37690772; PMCID: PMC10872872.



Åkerström JH, et al. Antireflux Surgery Versus Antireflux Medication and Risk of Esophageal Adenocarcinoma in Patients With Barrett’s Esophagus. Gastroenterology. 2024 Jan;166(1):132-138.e3. doi: 10.1053/j.gastro.2023.08.050. Epub 2023 Sep 9. PMID: 37690771.



Barnes EL, et al; AGA Clinical Guidelines Committee. AGA Clinical Practice Guideline on the Management of Pouchitis and Inflammatory Pouch Disorders. Gastroenterology. 2024 Jan;166(1):59-85. doi: 10.1053/j.gastro.2023.10.015. PMID: 38128971.

February 2024

Yoo HW, et al. Helicobacter pylori Treatment and Gastric Cancer Risk After Endoscopic Resection of Dysplasia: A Nationwide Cohort Study. Gastroenterology. 2024 Feb;166(2):313-322.e3. doi: 10.1053/j.gastro.2023.10.013. Epub 2023 Oct 18. PMID: 37863270.



Yang J, et al. High Soluble Fiber Promotes Colorectal Tumorigenesis Through Modulating Gut Microbiota and Metabolites in Mice. Gastroenterology. 2024 Feb;166(2):323-337.e7. doi: 10.1053/j.gastro.2023.10.012. Epub 2023 Oct 18. PMID: 37858797.



Young E, et al. Texture and Color Enhancement Imaging Improves Colonic Adenoma Detection: A Multicenter Randomized Controlled Trial. Gastroenterology. 2024 Feb;166(2):338-340.e3. doi: 10.1053/j.gastro.2023.10.008. Epub 2023 Oct 14. PMID: 37839498.
 

Clinical Gastroenterology and Hepatology

January 2024

Overbeek KA, et al; Dutch Familial Pancreatic Cancer Surveillance Study work group. Intraductal Papillary Mucinous Neoplasms in High-Risk Individuals: Incidence, Growth Rate, and Malignancy Risk. Clin Gastroenterol Hepatol. 2024 Jan;22(1):62-71.e7. doi: 10.1016/j.cgh.2023.03.035. Epub 2023 Apr 7. PMID: 37031711.

Reddy CA, et al. Achalasia is Strongly Associated With Eosinophilic Esophagitis and Other Allergic Disorders. Clin Gastroenterol Hepatol. 2024 Jan;22(1):34-41.e2. doi: 10.1016/j.cgh.2023.06.013. Epub 2023 Jun 28. PMID: 37391057; PMCID: PMC10753026.

Thiruvengadam NR, et al. The Clinical Impact and Cost-Effectiveness of Surveillance of Incidentally Detected Gastric Intestinal Metaplasia: A Microsimulation Analysis. Clin Gastroenterol Hepatol. 2024 Jan;22(1):51-61. doi: 10.1016/j.cgh.2023.05.028. Epub 2023 Jun 9. Erratum in: Clin Gastroenterol Hepatol. 2024 Jan 19;: PMID: 37302442.

February 2024

Goodoory VC, et al. Systematic Review and Meta-analysis: Efficacy of Mesalamine in Irritable Bowel Syndrome. Clin Gastroenterol Hepatol. 2024 Feb;22(2):243-251.e5. doi: 10.1016/j.cgh.2023.02.014. Epub 2023 Feb 27. PMID: 36858143.

Brenner DM, et al. Development and Current State of Digital Therapeutics for Irritable Bowel Syndrome. Clin Gastroenterol Hepatol. 2024 Feb;22(2):222-234. doi: 10.1016/j.cgh.2023.09.013. Epub 2023 Sep 22. PMID: 37743035.
 

Techniques and Innovations in Gastrointestinal Endoscopy

January 2024

Ramirez PR, et al. Gaps and Improvement Opportunities in Post-Colonoscopy Communication. Tech Innov Gastrointest Endosc. 2024 Jan;26(1):90-92. doi: 10.1016/j.tige.2023.10.001. Epub 2023 Oct 22.

Gonzaga ER, et al. Gastric Peroral Endoscopic Myotomy (G-POEM) for the Management of Gastroparesis. Tech Innov Gastrointest Endosc. 2024 Jan; 26(1): 46-55. doi: 10.1016/j.tige.2023.09.002. Epub 2023 Oct 13.



Wang D, et al. Sphincterotomy vs Sham Procedure for Pain Relief in Sphincter of Oddi Dysfunction: Systematic Review and Meta-analysis. Tech Innov Gastrointest Endosc. 2024 Jan;26(1): 30-37. doi: 10.1016/j.tige.2023.10.003. Epub 2023 Nov 8.
 

Gastro Hep Advances

January 2024

Adeniran E, et al. Intense and Sustained Alcohol Consumption Associated With Acute Pancreatitis Warrants Early Intervention. Gastro Hep Advances. 2024 Jan;3(1):61-63. doi: 10.1016/j.gastha.2023.08.017. Epub 2023 Sep 2.

Alkhouri N, et al. A Novel Prescription Digital Therapeutic Option for the Treatment of Metabolic Dysfunction-Associated Steatotic Liver Disease. Gastro Hep Advances. 2024 Jan;3(1): 9-16. doi: 10.1016/j.gastha.2023.08.019. Epub 2023 Oct 1.

Gastroenterology

January 2024

Hirano I, et al; ASCENT WORKING GROUP. Ascending to New Heights for Novel Therapeutics for Eosinophilic Esophagitis. Gastroenterology. 2024 Jan;166(1):1-10. doi: 10.1053/j.gastro.2023.09.004. Epub 2023 Sep 9. PMID: 37690772; PMCID: PMC10872872.



Åkerström JH, et al. Antireflux Surgery Versus Antireflux Medication and Risk of Esophageal Adenocarcinoma in Patients With Barrett’s Esophagus. Gastroenterology. 2024 Jan;166(1):132-138.e3. doi: 10.1053/j.gastro.2023.08.050. Epub 2023 Sep 9. PMID: 37690771.



Barnes EL, et al; AGA Clinical Guidelines Committee. AGA Clinical Practice Guideline on the Management of Pouchitis and Inflammatory Pouch Disorders. Gastroenterology. 2024 Jan;166(1):59-85. doi: 10.1053/j.gastro.2023.10.015. PMID: 38128971.

February 2024

Yoo HW, et al. Helicobacter pylori Treatment and Gastric Cancer Risk After Endoscopic Resection of Dysplasia: A Nationwide Cohort Study. Gastroenterology. 2024 Feb;166(2):313-322.e3. doi: 10.1053/j.gastro.2023.10.013. Epub 2023 Oct 18. PMID: 37863270.



Yang J, et al. High Soluble Fiber Promotes Colorectal Tumorigenesis Through Modulating Gut Microbiota and Metabolites in Mice. Gastroenterology. 2024 Feb;166(2):323-337.e7. doi: 10.1053/j.gastro.2023.10.012. Epub 2023 Oct 18. PMID: 37858797.



Young E, et al. Texture and Color Enhancement Imaging Improves Colonic Adenoma Detection: A Multicenter Randomized Controlled Trial. Gastroenterology. 2024 Feb;166(2):338-340.e3. doi: 10.1053/j.gastro.2023.10.008. Epub 2023 Oct 14. PMID: 37839498.
 

Clinical Gastroenterology and Hepatology

January 2024

Overbeek KA, et al; Dutch Familial Pancreatic Cancer Surveillance Study work group. Intraductal Papillary Mucinous Neoplasms in High-Risk Individuals: Incidence, Growth Rate, and Malignancy Risk. Clin Gastroenterol Hepatol. 2024 Jan;22(1):62-71.e7. doi: 10.1016/j.cgh.2023.03.035. Epub 2023 Apr 7. PMID: 37031711.

Reddy CA, et al. Achalasia is Strongly Associated With Eosinophilic Esophagitis and Other Allergic Disorders. Clin Gastroenterol Hepatol. 2024 Jan;22(1):34-41.e2. doi: 10.1016/j.cgh.2023.06.013. Epub 2023 Jun 28. PMID: 37391057; PMCID: PMC10753026.

Thiruvengadam NR, et al. The Clinical Impact and Cost-Effectiveness of Surveillance of Incidentally Detected Gastric Intestinal Metaplasia: A Microsimulation Analysis. Clin Gastroenterol Hepatol. 2024 Jan;22(1):51-61. doi: 10.1016/j.cgh.2023.05.028. Epub 2023 Jun 9. Erratum in: Clin Gastroenterol Hepatol. 2024 Jan 19;: PMID: 37302442.

February 2024

Goodoory VC, et al. Systematic Review and Meta-analysis: Efficacy of Mesalamine in Irritable Bowel Syndrome. Clin Gastroenterol Hepatol. 2024 Feb;22(2):243-251.e5. doi: 10.1016/j.cgh.2023.02.014. Epub 2023 Feb 27. PMID: 36858143.

Brenner DM, et al. Development and Current State of Digital Therapeutics for Irritable Bowel Syndrome. Clin Gastroenterol Hepatol. 2024 Feb;22(2):222-234. doi: 10.1016/j.cgh.2023.09.013. Epub 2023 Sep 22. PMID: 37743035.
 

Techniques and Innovations in Gastrointestinal Endoscopy

January 2024

Ramirez PR, et al. Gaps and Improvement Opportunities in Post-Colonoscopy Communication. Tech Innov Gastrointest Endosc. 2024 Jan;26(1):90-92. doi: 10.1016/j.tige.2023.10.001. Epub 2023 Oct 22.

Gonzaga ER, et al. Gastric Peroral Endoscopic Myotomy (G-POEM) for the Management of Gastroparesis. Tech Innov Gastrointest Endosc. 2024 Jan; 26(1): 46-55. doi: 10.1016/j.tige.2023.09.002. Epub 2023 Oct 13.



Wang D, et al. Sphincterotomy vs Sham Procedure for Pain Relief in Sphincter of Oddi Dysfunction: Systematic Review and Meta-analysis. Tech Innov Gastrointest Endosc. 2024 Jan;26(1): 30-37. doi: 10.1016/j.tige.2023.10.003. Epub 2023 Nov 8.
 

Gastro Hep Advances

January 2024

Adeniran E, et al. Intense and Sustained Alcohol Consumption Associated With Acute Pancreatitis Warrants Early Intervention. Gastro Hep Advances. 2024 Jan;3(1):61-63. doi: 10.1016/j.gastha.2023.08.017. Epub 2023 Sep 2.

Alkhouri N, et al. A Novel Prescription Digital Therapeutic Option for the Treatment of Metabolic Dysfunction-Associated Steatotic Liver Disease. Gastro Hep Advances. 2024 Jan;3(1): 9-16. doi: 10.1016/j.gastha.2023.08.019. Epub 2023 Oct 1.

Gastroenterology

January 2024

Hirano I, et al; ASCENT WORKING GROUP. Ascending to New Heights for Novel Therapeutics for Eosinophilic Esophagitis. Gastroenterology. 2024 Jan;166(1):1-10. doi: 10.1053/j.gastro.2023.09.004. Epub 2023 Sep 9. PMID: 37690772; PMCID: PMC10872872.



Åkerström JH, et al. Antireflux Surgery Versus Antireflux Medication and Risk of Esophageal Adenocarcinoma in Patients With Barrett’s Esophagus. Gastroenterology. 2024 Jan;166(1):132-138.e3. doi: 10.1053/j.gastro.2023.08.050. Epub 2023 Sep 9. PMID: 37690771.



Barnes EL, et al; AGA Clinical Guidelines Committee. AGA Clinical Practice Guideline on the Management of Pouchitis and Inflammatory Pouch Disorders. Gastroenterology. 2024 Jan;166(1):59-85. doi: 10.1053/j.gastro.2023.10.015. PMID: 38128971.

February 2024

Yoo HW, et al. Helicobacter pylori Treatment and Gastric Cancer Risk After Endoscopic Resection of Dysplasia: A Nationwide Cohort Study. Gastroenterology. 2024 Feb;166(2):313-322.e3. doi: 10.1053/j.gastro.2023.10.013. Epub 2023 Oct 18. PMID: 37863270.



Yang J, et al. High Soluble Fiber Promotes Colorectal Tumorigenesis Through Modulating Gut Microbiota and Metabolites in Mice. Gastroenterology. 2024 Feb;166(2):323-337.e7. doi: 10.1053/j.gastro.2023.10.012. Epub 2023 Oct 18. PMID: 37858797.



Young E, et al. Texture and Color Enhancement Imaging Improves Colonic Adenoma Detection: A Multicenter Randomized Controlled Trial. Gastroenterology. 2024 Feb;166(2):338-340.e3. doi: 10.1053/j.gastro.2023.10.008. Epub 2023 Oct 14. PMID: 37839498.
 

Clinical Gastroenterology and Hepatology

January 2024

Overbeek KA, et al; Dutch Familial Pancreatic Cancer Surveillance Study work group. Intraductal Papillary Mucinous Neoplasms in High-Risk Individuals: Incidence, Growth Rate, and Malignancy Risk. Clin Gastroenterol Hepatol. 2024 Jan;22(1):62-71.e7. doi: 10.1016/j.cgh.2023.03.035. Epub 2023 Apr 7. PMID: 37031711.

Reddy CA, et al. Achalasia is Strongly Associated With Eosinophilic Esophagitis and Other Allergic Disorders. Clin Gastroenterol Hepatol. 2024 Jan;22(1):34-41.e2. doi: 10.1016/j.cgh.2023.06.013. Epub 2023 Jun 28. PMID: 37391057; PMCID: PMC10753026.

Thiruvengadam NR, et al. The Clinical Impact and Cost-Effectiveness of Surveillance of Incidentally Detected Gastric Intestinal Metaplasia: A Microsimulation Analysis. Clin Gastroenterol Hepatol. 2024 Jan;22(1):51-61. doi: 10.1016/j.cgh.2023.05.028. Epub 2023 Jun 9. Erratum in: Clin Gastroenterol Hepatol. 2024 Jan 19;: PMID: 37302442.

February 2024

Goodoory VC, et al. Systematic Review and Meta-analysis: Efficacy of Mesalamine in Irritable Bowel Syndrome. Clin Gastroenterol Hepatol. 2024 Feb;22(2):243-251.e5. doi: 10.1016/j.cgh.2023.02.014. Epub 2023 Feb 27. PMID: 36858143.

Brenner DM, et al. Development and Current State of Digital Therapeutics for Irritable Bowel Syndrome. Clin Gastroenterol Hepatol. 2024 Feb;22(2):222-234. doi: 10.1016/j.cgh.2023.09.013. Epub 2023 Sep 22. PMID: 37743035.
 

Techniques and Innovations in Gastrointestinal Endoscopy

January 2024

Ramirez PR, et al. Gaps and Improvement Opportunities in Post-Colonoscopy Communication. Tech Innov Gastrointest Endosc. 2024 Jan;26(1):90-92. doi: 10.1016/j.tige.2023.10.001. Epub 2023 Oct 22.

Gonzaga ER, et al. Gastric Peroral Endoscopic Myotomy (G-POEM) for the Management of Gastroparesis. Tech Innov Gastrointest Endosc. 2024 Jan; 26(1): 46-55. doi: 10.1016/j.tige.2023.09.002. Epub 2023 Oct 13.



Wang D, et al. Sphincterotomy vs Sham Procedure for Pain Relief in Sphincter of Oddi Dysfunction: Systematic Review and Meta-analysis. Tech Innov Gastrointest Endosc. 2024 Jan;26(1): 30-37. doi: 10.1016/j.tige.2023.10.003. Epub 2023 Nov 8.
 

Gastro Hep Advances

January 2024

Adeniran E, et al. Intense and Sustained Alcohol Consumption Associated With Acute Pancreatitis Warrants Early Intervention. Gastro Hep Advances. 2024 Jan;3(1):61-63. doi: 10.1016/j.gastha.2023.08.017. Epub 2023 Sep 2.

Alkhouri N, et al. A Novel Prescription Digital Therapeutic Option for the Treatment of Metabolic Dysfunction-Associated Steatotic Liver Disease. Gastro Hep Advances. 2024 Jan;3(1): 9-16. doi: 10.1016/j.gastha.2023.08.019. Epub 2023 Oct 1.