GI and Hepatology News

Researchers have developed and internally validated a simple score using clinical factors that can help estimate the likelihood of advanced colorectal neoplasia in adults younger than age 45 years.

While colorectal cancer (CRC) incidence has declined overall due to screening, early-onset CRC is on the rise, particularly in individuals younger than 45 years — an age group not currently recommended for CRC screening.

Studies have shown that the risk for early-onset advanced neoplasia varies based on several factors, including sex, race, family history of CRC, smoking, alcohol consumption, diabetes, hyperlipidemia, obesity, and diet.

A score that incorporates some of these factors to identify which younger adults are at higher risk for advanced neoplasia, a precursor to CRC, could support earlier, more targeted screening interventions.

The simple clinical score can be easily calculated by primary care providers in the office, Carole Macaron, MD, lead author of the study and a gastroenterologist at Cleveland Clinic, told GI & Hepatology News. “Patients with a high-risk score would be referred for colorectal cancer screening.”

The study was published in Digestive Diseases and Sciences.

To develop and validate their risk score, Macaron and colleagues did a retrospective cross-sectional analysis of 9446 individuals aged 18-44 years (mean age, 36.8 years; 61% women) who underwent colonoscopy at their center.

Advanced neoplasia was defined as a tubular adenoma ≥ 10 mm or any adenoma with villous features or high-grade dysplasia, sessile serrated polyp ≥ 10 mm, sessile serrated polyp with dysplasia, traditional serrated adenoma, or invasive adenocarcinoma.

The 346 (3.7%) individuals found to have advanced neoplasia served as the case group, and the remainder with normal colonoscopy or non-advanced neoplasia served as controls.

A multivariate logistic regression model identified three independent risk factors significantly associated with advanced neoplasia: Higher body mass index (BMI; P = .0157), former and current tobacco use (P = .0009 and P = .0015, respectively), and having a first-degree relative with CRC < 60 years (P < .0001) or other family history of CRC (P = .0117).

The researchers used these risk factors to develop a risk prediction score to estimate the likelihood of detecting advanced neoplasia, which ranged from a risk of 1.8% for patients with a score of 1 to 22.2% for those with a score of 12. Individuals with a score of ≥ 9 had a 14% or higher risk for advanced neoplasia.

Based on the risk model, the likelihood of detecting advanced neoplasia in an asymptomatic 32-year-old overweight individual, with a history of previous tobacco use and a first-degree relative younger than age 60 with CRC would be 20.3%, Macaron and colleagues noted.

The model demonstrated “moderate” discriminatory power in the validation set (C-statistic: 0.645), indicating that it can effectively differentiate between individuals at a higher and lower risk for advanced neoplasia.

Additionally, the authors are exploring ways to improve the discriminatory power of the score, possibly by including additional risk factors.

Given the score is calculated using easily obtainable risk factors for individuals younger than 45 who are at risk for early-onset colorectal neoplasia, it could help guide individualized screening decisions for those in whom screening is not currently offered, Macaron said. It could also serve as a tool for risk communication and shared decision-making.

Integration into electronic health records or online calculators may enhance its accessibility and clinical utility.

The authors noted that this retrospective study was conducted at a single center caring mainly for White non-Hispanic adults, limiting generalizability to the general population and to other races and ethnicities.

 

Validation in Real-World Setting Needed

“There are no currently accepted advanced colorectal neoplasia risk scores that are used in general practice,” said Steven H. Itzkowitz, MD, AGAF, professor of medicine, oncological sciences, and medical education, Icahn School of Medicine at Mount Sinai in New York City. “If these lesions can be predicted, it would enable these young individuals to undergo screening colonoscopy, which could detect and remove these lesions, thereby preventing CRC.”

Many of the known risk factors (family history, high BMI, or smoking) for CRC development at any age are incorporated within this tool, so it should be feasible to collect these data,” said Itzkowitz, who was not involved with the study.

But he cautioned that accurate and adequate family histories are not always performed. Clinicians also may not have considered combining these factors into an actionable risk score.

“If this score can be externally validated in a real-world setting, it could be a useful addition in our efforts to lower CRC rates among young individuals,” Itzkowitz said.

The study did not receive any funding. Macaron and Itzkowitz reported no competing interests.

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

Researchers have developed and internally validated a simple score using clinical factors that can help estimate the likelihood of advanced colorectal neoplasia in adults younger than age 45 years.

While colorectal cancer (CRC) incidence has declined overall due to screening, early-onset CRC is on the rise, particularly in individuals younger than 45 years — an age group not currently recommended for CRC screening.

Studies have shown that the risk for early-onset advanced neoplasia varies based on several factors, including sex, race, family history of CRC, smoking, alcohol consumption, diabetes, hyperlipidemia, obesity, and diet.

A score that incorporates some of these factors to identify which younger adults are at higher risk for advanced neoplasia, a precursor to CRC, could support earlier, more targeted screening interventions.

The simple clinical score can be easily calculated by primary care providers in the office, Carole Macaron, MD, lead author of the study and a gastroenterologist at Cleveland Clinic, told GI & Hepatology News. “Patients with a high-risk score would be referred for colorectal cancer screening.”

The study was published in Digestive Diseases and Sciences.

To develop and validate their risk score, Macaron and colleagues did a retrospective cross-sectional analysis of 9446 individuals aged 18-44 years (mean age, 36.8 years; 61% women) who underwent colonoscopy at their center.

Advanced neoplasia was defined as a tubular adenoma ≥ 10 mm or any adenoma with villous features or high-grade dysplasia, sessile serrated polyp ≥ 10 mm, sessile serrated polyp with dysplasia, traditional serrated adenoma, or invasive adenocarcinoma.

The 346 (3.7%) individuals found to have advanced neoplasia served as the case group, and the remainder with normal colonoscopy or non-advanced neoplasia served as controls.

A multivariate logistic regression model identified three independent risk factors significantly associated with advanced neoplasia: Higher body mass index (BMI; P = .0157), former and current tobacco use (P = .0009 and P = .0015, respectively), and having a first-degree relative with CRC < 60 years (P < .0001) or other family history of CRC (P = .0117).

The researchers used these risk factors to develop a risk prediction score to estimate the likelihood of detecting advanced neoplasia, which ranged from a risk of 1.8% for patients with a score of 1 to 22.2% for those with a score of 12. Individuals with a score of ≥ 9 had a 14% or higher risk for advanced neoplasia.

Based on the risk model, the likelihood of detecting advanced neoplasia in an asymptomatic 32-year-old overweight individual, with a history of previous tobacco use and a first-degree relative younger than age 60 with CRC would be 20.3%, Macaron and colleagues noted.

The model demonstrated “moderate” discriminatory power in the validation set (C-statistic: 0.645), indicating that it can effectively differentiate between individuals at a higher and lower risk for advanced neoplasia.

Additionally, the authors are exploring ways to improve the discriminatory power of the score, possibly by including additional risk factors.

Given the score is calculated using easily obtainable risk factors for individuals younger than 45 who are at risk for early-onset colorectal neoplasia, it could help guide individualized screening decisions for those in whom screening is not currently offered, Macaron said. It could also serve as a tool for risk communication and shared decision-making.

Integration into electronic health records or online calculators may enhance its accessibility and clinical utility.

The authors noted that this retrospective study was conducted at a single center caring mainly for White non-Hispanic adults, limiting generalizability to the general population and to other races and ethnicities.

 

Validation in Real-World Setting Needed

“There are no currently accepted advanced colorectal neoplasia risk scores that are used in general practice,” said Steven H. Itzkowitz, MD, AGAF, professor of medicine, oncological sciences, and medical education, Icahn School of Medicine at Mount Sinai in New York City. “If these lesions can be predicted, it would enable these young individuals to undergo screening colonoscopy, which could detect and remove these lesions, thereby preventing CRC.”

Many of the known risk factors (family history, high BMI, or smoking) for CRC development at any age are incorporated within this tool, so it should be feasible to collect these data,” said Itzkowitz, who was not involved with the study.

But he cautioned that accurate and adequate family histories are not always performed. Clinicians also may not have considered combining these factors into an actionable risk score.

“If this score can be externally validated in a real-world setting, it could be a useful addition in our efforts to lower CRC rates among young individuals,” Itzkowitz said.

The study did not receive any funding. Macaron and Itzkowitz reported no competing interests.

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

Researchers have developed and internally validated a simple score using clinical factors that can help estimate the likelihood of advanced colorectal neoplasia in adults younger than age 45 years.

While colorectal cancer (CRC) incidence has declined overall due to screening, early-onset CRC is on the rise, particularly in individuals younger than 45 years — an age group not currently recommended for CRC screening.

Studies have shown that the risk for early-onset advanced neoplasia varies based on several factors, including sex, race, family history of CRC, smoking, alcohol consumption, diabetes, hyperlipidemia, obesity, and diet.

A score that incorporates some of these factors to identify which younger adults are at higher risk for advanced neoplasia, a precursor to CRC, could support earlier, more targeted screening interventions.

The simple clinical score can be easily calculated by primary care providers in the office, Carole Macaron, MD, lead author of the study and a gastroenterologist at Cleveland Clinic, told GI & Hepatology News. “Patients with a high-risk score would be referred for colorectal cancer screening.”

The study was published in Digestive Diseases and Sciences.

To develop and validate their risk score, Macaron and colleagues did a retrospective cross-sectional analysis of 9446 individuals aged 18-44 years (mean age, 36.8 years; 61% women) who underwent colonoscopy at their center.

Advanced neoplasia was defined as a tubular adenoma ≥ 10 mm or any adenoma with villous features or high-grade dysplasia, sessile serrated polyp ≥ 10 mm, sessile serrated polyp with dysplasia, traditional serrated adenoma, or invasive adenocarcinoma.

The 346 (3.7%) individuals found to have advanced neoplasia served as the case group, and the remainder with normal colonoscopy or non-advanced neoplasia served as controls.

A multivariate logistic regression model identified three independent risk factors significantly associated with advanced neoplasia: Higher body mass index (BMI; P = .0157), former and current tobacco use (P = .0009 and P = .0015, respectively), and having a first-degree relative with CRC < 60 years (P < .0001) or other family history of CRC (P = .0117).

The researchers used these risk factors to develop a risk prediction score to estimate the likelihood of detecting advanced neoplasia, which ranged from a risk of 1.8% for patients with a score of 1 to 22.2% for those with a score of 12. Individuals with a score of ≥ 9 had a 14% or higher risk for advanced neoplasia.

Based on the risk model, the likelihood of detecting advanced neoplasia in an asymptomatic 32-year-old overweight individual, with a history of previous tobacco use and a first-degree relative younger than age 60 with CRC would be 20.3%, Macaron and colleagues noted.

The model demonstrated “moderate” discriminatory power in the validation set (C-statistic: 0.645), indicating that it can effectively differentiate between individuals at a higher and lower risk for advanced neoplasia.

Additionally, the authors are exploring ways to improve the discriminatory power of the score, possibly by including additional risk factors.

Given the score is calculated using easily obtainable risk factors for individuals younger than 45 who are at risk for early-onset colorectal neoplasia, it could help guide individualized screening decisions for those in whom screening is not currently offered, Macaron said. It could also serve as a tool for risk communication and shared decision-making.

Integration into electronic health records or online calculators may enhance its accessibility and clinical utility.

The authors noted that this retrospective study was conducted at a single center caring mainly for White non-Hispanic adults, limiting generalizability to the general population and to other races and ethnicities.

 

Validation in Real-World Setting Needed

“There are no currently accepted advanced colorectal neoplasia risk scores that are used in general practice,” said Steven H. Itzkowitz, MD, AGAF, professor of medicine, oncological sciences, and medical education, Icahn School of Medicine at Mount Sinai in New York City. “If these lesions can be predicted, it would enable these young individuals to undergo screening colonoscopy, which could detect and remove these lesions, thereby preventing CRC.”

Many of the known risk factors (family history, high BMI, or smoking) for CRC development at any age are incorporated within this tool, so it should be feasible to collect these data,” said Itzkowitz, who was not involved with the study.

But he cautioned that accurate and adequate family histories are not always performed. Clinicians also may not have considered combining these factors into an actionable risk score.

“If this score can be externally validated in a real-world setting, it could be a useful addition in our efforts to lower CRC rates among young individuals,” Itzkowitz said.

The study did not receive any funding. Macaron and Itzkowitz reported no competing interests.

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

The United States Food and Drug Administration (FDA) approved guselkumab (Tremfya, Johnson & Johnson) for the treatment of adults with moderately to severely active Crohn’s disease (CD).

The approval marks the fourth indication for guselkumab, which was approved for moderate to severe plaque psoriasis in 2017, active psoriatic arthritis in 2020, and moderately to severely active ulcerative colitis in 2024. 

Guselkumab is the first and only interleukin-23 (IL-23) inhibitor that offers both subcutaneous (SC) and intravenous (IV) induction options for CD, the company said in a news release. 

“Despite the progress in the management of Crohn’s disease, many patients experience debilitating symptoms and are in need of new treatment options,” Remo Panaccione, MD, director of the Inflammatory Bowel Disease Unit at the University of Calgary, Calgary, Alberta, Canada, said in the release. 

“The approval of Tremfya offers an IL-23 inhibitor that has shown robust rates of endoscopic remission with both subcutaneous and intravenous induction regimens. Importantly, the fully subcutaneous regimen offers choice and flexibility for patients and providers not available before,” said Panaccione.

The FDA nod in CD was based on positive results from three phase 3 trials evaluating guselkumab in more than 1300 patients with moderately to severely active CD who failed or were intolerant to corticosteroids, immunomodulators, or biologics. 

The GRAVITI trial showed that guselkumab as SC induction and maintenance therapy was superior to placebo in clinical remission as well as endoscopic response and remission and deep remission. 

Results from GALAXI 2 and GALAXI 3 showed that guselkumab was superior to ustekinumab (Stelara) on all pooled endoscopic endpoints. 

Guselkumab is the only IL-23 inhibitor to demonstrate “clinical remission and endoscopic response, both at 1 year, with a fully subcutaneous induction regimen,” the company said. 

The recommended SC induction dose of guselkumab is 400 mg (given as two consecutive injections of 200 mg each, dispensed in one induction pack) at weeks 0, 4 and 8. The drug is also available in a 200 mg prefilled syringe. For the IV induction option, 200 mg IV infusions are administered at weeks 0, 4, and 8.

The recommended maintenance dosage is 100 mg administered by SC injection at week 16, and every 8 weeks thereafter, or 200 mg administered by SC injection at week 12, and every 4 weeks thereafter. 

Use of the lowest effective recommended dosage to maintain therapeutic response is recommended. 

Full prescribing information and medication guide are available online.

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

The United States Food and Drug Administration (FDA) approved guselkumab (Tremfya, Johnson & Johnson) for the treatment of adults with moderately to severely active Crohn’s disease (CD).

The approval marks the fourth indication for guselkumab, which was approved for moderate to severe plaque psoriasis in 2017, active psoriatic arthritis in 2020, and moderately to severely active ulcerative colitis in 2024. 

Guselkumab is the first and only interleukin-23 (IL-23) inhibitor that offers both subcutaneous (SC) and intravenous (IV) induction options for CD, the company said in a news release. 

“Despite the progress in the management of Crohn’s disease, many patients experience debilitating symptoms and are in need of new treatment options,” Remo Panaccione, MD, director of the Inflammatory Bowel Disease Unit at the University of Calgary, Calgary, Alberta, Canada, said in the release. 

“The approval of Tremfya offers an IL-23 inhibitor that has shown robust rates of endoscopic remission with both subcutaneous and intravenous induction regimens. Importantly, the fully subcutaneous regimen offers choice and flexibility for patients and providers not available before,” said Panaccione.

The FDA nod in CD was based on positive results from three phase 3 trials evaluating guselkumab in more than 1300 patients with moderately to severely active CD who failed or were intolerant to corticosteroids, immunomodulators, or biologics. 

The GRAVITI trial showed that guselkumab as SC induction and maintenance therapy was superior to placebo in clinical remission as well as endoscopic response and remission and deep remission. 

Results from GALAXI 2 and GALAXI 3 showed that guselkumab was superior to ustekinumab (Stelara) on all pooled endoscopic endpoints. 

Guselkumab is the only IL-23 inhibitor to demonstrate “clinical remission and endoscopic response, both at 1 year, with a fully subcutaneous induction regimen,” the company said. 

The recommended SC induction dose of guselkumab is 400 mg (given as two consecutive injections of 200 mg each, dispensed in one induction pack) at weeks 0, 4 and 8. The drug is also available in a 200 mg prefilled syringe. For the IV induction option, 200 mg IV infusions are administered at weeks 0, 4, and 8.

The recommended maintenance dosage is 100 mg administered by SC injection at week 16, and every 8 weeks thereafter, or 200 mg administered by SC injection at week 12, and every 4 weeks thereafter. 

Use of the lowest effective recommended dosage to maintain therapeutic response is recommended. 

Full prescribing information and medication guide are available online.

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

The United States Food and Drug Administration (FDA) approved guselkumab (Tremfya, Johnson & Johnson) for the treatment of adults with moderately to severely active Crohn’s disease (CD).

The approval marks the fourth indication for guselkumab, which was approved for moderate to severe plaque psoriasis in 2017, active psoriatic arthritis in 2020, and moderately to severely active ulcerative colitis in 2024. 

Guselkumab is the first and only interleukin-23 (IL-23) inhibitor that offers both subcutaneous (SC) and intravenous (IV) induction options for CD, the company said in a news release. 

“Despite the progress in the management of Crohn’s disease, many patients experience debilitating symptoms and are in need of new treatment options,” Remo Panaccione, MD, director of the Inflammatory Bowel Disease Unit at the University of Calgary, Calgary, Alberta, Canada, said in the release. 

“The approval of Tremfya offers an IL-23 inhibitor that has shown robust rates of endoscopic remission with both subcutaneous and intravenous induction regimens. Importantly, the fully subcutaneous regimen offers choice and flexibility for patients and providers not available before,” said Panaccione.

The FDA nod in CD was based on positive results from three phase 3 trials evaluating guselkumab in more than 1300 patients with moderately to severely active CD who failed or were intolerant to corticosteroids, immunomodulators, or biologics. 

The GRAVITI trial showed that guselkumab as SC induction and maintenance therapy was superior to placebo in clinical remission as well as endoscopic response and remission and deep remission. 

Results from GALAXI 2 and GALAXI 3 showed that guselkumab was superior to ustekinumab (Stelara) on all pooled endoscopic endpoints. 

Guselkumab is the only IL-23 inhibitor to demonstrate “clinical remission and endoscopic response, both at 1 year, with a fully subcutaneous induction regimen,” the company said. 

The recommended SC induction dose of guselkumab is 400 mg (given as two consecutive injections of 200 mg each, dispensed in one induction pack) at weeks 0, 4 and 8. The drug is also available in a 200 mg prefilled syringe. For the IV induction option, 200 mg IV infusions are administered at weeks 0, 4, and 8.

The recommended maintenance dosage is 100 mg administered by SC injection at week 16, and every 8 weeks thereafter, or 200 mg administered by SC injection at week 12, and every 4 weeks thereafter. 

Use of the lowest effective recommended dosage to maintain therapeutic response is recommended. 

Full prescribing information and medication guide are available online.

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

In patients with gastroesophageal reflux (GERD) symptoms undergoing screening upper endoscopy, adjunctive use of wide-area transepithelial sampling with 3D computer-assisted analysis (WATS-3D) increases detection of Barrett’s esophagus (BE) and dysplasia, new research showed. 

Compared with forceps biopsies (FB) alone, the addition of WATS-3D led to confirmation of BE in an additional one fifth of patients, roughly doubled dysplasia diagnoses, and influenced clinical management in the majority of patients. 

“The big take-home point here is that the use of WATS-3D brushing along with conventional biopsies increases the likelihood that intestinal metaplasia will be identified,” first author Nicholas Shaheen, MD, MPH, AGAF, with the Center for Esophageal Diseases and Swallowing, University of North Carolina School of Medicine at Chapel Hill, North Carolina, told GI & Hepatology News. 

“Almost 20% of patients who harbor BE were only identified by WATS-3D and might have otherwise gone undiagnosed had only forceps biopsies been performed,” Shaheen said. 

The study was published in The American Journal of Gastroenterology.

 

Beyond Traditional Biopsies

BE develops as a complication of chronic GERD and is the chief precursor to esophageal adenocarcinoma. Early detection of BE and dysplasia is crucial to enable timely intervention. 

The current gold standard for BE screening involves upper endoscopy with FB following the Seattle protocol, which consists of four-quadrant biopsies from every 1-2 cm of areas of columnar-lined epithelium (CLE) to confirm the presence of intestinal metaplasia. However, this protocol is prone to sampling errors and high false-negative rates, leading to repeat endoscopy, the study team pointed out. 

WATS-3D (CDx Diagnostics) is a complementary technique designed to improve diagnostic yield by using brush biopsy to sample more tissue than routine biopsies.

WATS-3D has been shown to increase detection of dysplasia in patients with BE undergoing surveillance for BE, but less is known about the value of WATS-3D for BE screening in a community-based cohort of patients with GERD. 

To investigate, Shaheen and colleagues studied 23,933 consecutive patients enrolled in a prospective observational registry assessing the utility of WATS-3D in the screening of symptomatic GERD patients for BE. 

Patients had both WATS-3D and FB in the same endoscopic session. No patient had a history of BE, intestinal metaplasia or dysplasia in esophageal mucosa, or esophageal surgery, endoscopic ablation or endoscopic mucosal resection prior to enrollment. 

Overall, 6829 patients (29%) met endoscopic criteria for BE (≥ 1 cm esophageal CLE with accompanying biopsies showing intestinal metaplasia). 

Of these, 2878 (42%) had intestinal metaplasia identified by either FB or WATS-3D, but 19.3% had their BE diagnosis confirmed solely on the basis of WATS-3D findings. 

Among patients who fulfilled the endoscopic criteria for BE, the adjunctive yield of WATS-3D was 76.5% and the absolute yield was 18.1%.

Of the 240 (1.0%) patients with dysplasia, 107 (45%) were found solely by WATS-3D.

 

‘Clinically Valuable Adjunct’

Among patients with positive WATS-3D but negative FB results, clinical management changed in 90.7% of cases, mostly involving initiation or modification of surveillance and proton pump inhibitor therapy. 

These results suggest that WATS-3D is a “clinically valuable adjunct” to FB for the diagnosis of BE when used as a screening tool in symptomatic GERD patients and particularly in patients with endoscopic evidence of > 1 cm esophageal columnar-lined epithelium, the study team wrote. 

Adjunctive use of WATS-3D when BE is suspected “may save endoscopies and lead to quicker, more accurate diagnoses,” they added. 

The investigators said a limitation of the study is the lack of central pathology review, potentially leading to diagnostic variability. They also noted that over half of the detected dysplasia cases were crypt dysplasia or indefinite for dysplasia, raising concerns about clinical significance. 

Reached for comment, Philip O. Katz, MD, AGAF, professor of medicine and director of the GI Function Laboratories, Weill Cornell Medicine in New York, said he’s been using WATS for more than a decade as an adjunct to standard biopsy in patients undergoing screening and surveillance for BE and finds it clinically helpful in managing his patients.

This new study provides “further information that WATS added to biopsy that has been traditionally done with the Seattle protocol increases the yield of intestinal metaplasia and likely dysplasia in patients being screened for Barrett’s,” Katz, who wasn’t involved in the study, told GI & Hepatology News.

Funding for the study was provided by CDx Diagnostics. Shaheen and several coauthors disclosed relationships with the company. Katz disclosed relationships (consultant/advisor) for Phathom Pharmaceuticals and Sebella.

A version of this article appeared on Medscape.com.

In patients with gastroesophageal reflux (GERD) symptoms undergoing screening upper endoscopy, adjunctive use of wide-area transepithelial sampling with 3D computer-assisted analysis (WATS-3D) increases detection of Barrett’s esophagus (BE) and dysplasia, new research showed. 

Compared with forceps biopsies (FB) alone, the addition of WATS-3D led to confirmation of BE in an additional one fifth of patients, roughly doubled dysplasia diagnoses, and influenced clinical management in the majority of patients. 

“The big take-home point here is that the use of WATS-3D brushing along with conventional biopsies increases the likelihood that intestinal metaplasia will be identified,” first author Nicholas Shaheen, MD, MPH, AGAF, with the Center for Esophageal Diseases and Swallowing, University of North Carolina School of Medicine at Chapel Hill, North Carolina, told GI & Hepatology News. 

“Almost 20% of patients who harbor BE were only identified by WATS-3D and might have otherwise gone undiagnosed had only forceps biopsies been performed,” Shaheen said. 

The study was published in The American Journal of Gastroenterology.

 

Beyond Traditional Biopsies

BE develops as a complication of chronic GERD and is the chief precursor to esophageal adenocarcinoma. Early detection of BE and dysplasia is crucial to enable timely intervention. 

The current gold standard for BE screening involves upper endoscopy with FB following the Seattle protocol, which consists of four-quadrant biopsies from every 1-2 cm of areas of columnar-lined epithelium (CLE) to confirm the presence of intestinal metaplasia. However, this protocol is prone to sampling errors and high false-negative rates, leading to repeat endoscopy, the study team pointed out. 

WATS-3D (CDx Diagnostics) is a complementary technique designed to improve diagnostic yield by using brush biopsy to sample more tissue than routine biopsies.

WATS-3D has been shown to increase detection of dysplasia in patients with BE undergoing surveillance for BE, but less is known about the value of WATS-3D for BE screening in a community-based cohort of patients with GERD. 

To investigate, Shaheen and colleagues studied 23,933 consecutive patients enrolled in a prospective observational registry assessing the utility of WATS-3D in the screening of symptomatic GERD patients for BE. 

Patients had both WATS-3D and FB in the same endoscopic session. No patient had a history of BE, intestinal metaplasia or dysplasia in esophageal mucosa, or esophageal surgery, endoscopic ablation or endoscopic mucosal resection prior to enrollment. 

Overall, 6829 patients (29%) met endoscopic criteria for BE (≥ 1 cm esophageal CLE with accompanying biopsies showing intestinal metaplasia). 

Of these, 2878 (42%) had intestinal metaplasia identified by either FB or WATS-3D, but 19.3% had their BE diagnosis confirmed solely on the basis of WATS-3D findings. 

Among patients who fulfilled the endoscopic criteria for BE, the adjunctive yield of WATS-3D was 76.5% and the absolute yield was 18.1%.

Of the 240 (1.0%) patients with dysplasia, 107 (45%) were found solely by WATS-3D.

 

‘Clinically Valuable Adjunct’

Among patients with positive WATS-3D but negative FB results, clinical management changed in 90.7% of cases, mostly involving initiation or modification of surveillance and proton pump inhibitor therapy. 

These results suggest that WATS-3D is a “clinically valuable adjunct” to FB for the diagnosis of BE when used as a screening tool in symptomatic GERD patients and particularly in patients with endoscopic evidence of > 1 cm esophageal columnar-lined epithelium, the study team wrote. 

Adjunctive use of WATS-3D when BE is suspected “may save endoscopies and lead to quicker, more accurate diagnoses,” they added. 

The investigators said a limitation of the study is the lack of central pathology review, potentially leading to diagnostic variability. They also noted that over half of the detected dysplasia cases were crypt dysplasia or indefinite for dysplasia, raising concerns about clinical significance. 

Reached for comment, Philip O. Katz, MD, AGAF, professor of medicine and director of the GI Function Laboratories, Weill Cornell Medicine in New York, said he’s been using WATS for more than a decade as an adjunct to standard biopsy in patients undergoing screening and surveillance for BE and finds it clinically helpful in managing his patients.

This new study provides “further information that WATS added to biopsy that has been traditionally done with the Seattle protocol increases the yield of intestinal metaplasia and likely dysplasia in patients being screened for Barrett’s,” Katz, who wasn’t involved in the study, told GI & Hepatology News.

Funding for the study was provided by CDx Diagnostics. Shaheen and several coauthors disclosed relationships with the company. Katz disclosed relationships (consultant/advisor) for Phathom Pharmaceuticals and Sebella.

A version of this article appeared on Medscape.com.

In patients with gastroesophageal reflux (GERD) symptoms undergoing screening upper endoscopy, adjunctive use of wide-area transepithelial sampling with 3D computer-assisted analysis (WATS-3D) increases detection of Barrett’s esophagus (BE) and dysplasia, new research showed. 

Compared with forceps biopsies (FB) alone, the addition of WATS-3D led to confirmation of BE in an additional one fifth of patients, roughly doubled dysplasia diagnoses, and influenced clinical management in the majority of patients. 

“The big take-home point here is that the use of WATS-3D brushing along with conventional biopsies increases the likelihood that intestinal metaplasia will be identified,” first author Nicholas Shaheen, MD, MPH, AGAF, with the Center for Esophageal Diseases and Swallowing, University of North Carolina School of Medicine at Chapel Hill, North Carolina, told GI & Hepatology News. 

“Almost 20% of patients who harbor BE were only identified by WATS-3D and might have otherwise gone undiagnosed had only forceps biopsies been performed,” Shaheen said. 

The study was published in The American Journal of Gastroenterology.

 

Beyond Traditional Biopsies

BE develops as a complication of chronic GERD and is the chief precursor to esophageal adenocarcinoma. Early detection of BE and dysplasia is crucial to enable timely intervention. 

The current gold standard for BE screening involves upper endoscopy with FB following the Seattle protocol, which consists of four-quadrant biopsies from every 1-2 cm of areas of columnar-lined epithelium (CLE) to confirm the presence of intestinal metaplasia. However, this protocol is prone to sampling errors and high false-negative rates, leading to repeat endoscopy, the study team pointed out. 

WATS-3D (CDx Diagnostics) is a complementary technique designed to improve diagnostic yield by using brush biopsy to sample more tissue than routine biopsies.

WATS-3D has been shown to increase detection of dysplasia in patients with BE undergoing surveillance for BE, but less is known about the value of WATS-3D for BE screening in a community-based cohort of patients with GERD. 

To investigate, Shaheen and colleagues studied 23,933 consecutive patients enrolled in a prospective observational registry assessing the utility of WATS-3D in the screening of symptomatic GERD patients for BE. 

Patients had both WATS-3D and FB in the same endoscopic session. No patient had a history of BE, intestinal metaplasia or dysplasia in esophageal mucosa, or esophageal surgery, endoscopic ablation or endoscopic mucosal resection prior to enrollment. 

Overall, 6829 patients (29%) met endoscopic criteria for BE (≥ 1 cm esophageal CLE with accompanying biopsies showing intestinal metaplasia). 

Of these, 2878 (42%) had intestinal metaplasia identified by either FB or WATS-3D, but 19.3% had their BE diagnosis confirmed solely on the basis of WATS-3D findings. 

Among patients who fulfilled the endoscopic criteria for BE, the adjunctive yield of WATS-3D was 76.5% and the absolute yield was 18.1%.

Of the 240 (1.0%) patients with dysplasia, 107 (45%) were found solely by WATS-3D.

 

‘Clinically Valuable Adjunct’

Among patients with positive WATS-3D but negative FB results, clinical management changed in 90.7% of cases, mostly involving initiation or modification of surveillance and proton pump inhibitor therapy. 

These results suggest that WATS-3D is a “clinically valuable adjunct” to FB for the diagnosis of BE when used as a screening tool in symptomatic GERD patients and particularly in patients with endoscopic evidence of > 1 cm esophageal columnar-lined epithelium, the study team wrote. 

Adjunctive use of WATS-3D when BE is suspected “may save endoscopies and lead to quicker, more accurate diagnoses,” they added. 

The investigators said a limitation of the study is the lack of central pathology review, potentially leading to diagnostic variability. They also noted that over half of the detected dysplasia cases were crypt dysplasia or indefinite for dysplasia, raising concerns about clinical significance. 

Reached for comment, Philip O. Katz, MD, AGAF, professor of medicine and director of the GI Function Laboratories, Weill Cornell Medicine in New York, said he’s been using WATS for more than a decade as an adjunct to standard biopsy in patients undergoing screening and surveillance for BE and finds it clinically helpful in managing his patients.

This new study provides “further information that WATS added to biopsy that has been traditionally done with the Seattle protocol increases the yield of intestinal metaplasia and likely dysplasia in patients being screened for Barrett’s,” Katz, who wasn’t involved in the study, told GI & Hepatology News.

Funding for the study was provided by CDx Diagnostics. Shaheen and several coauthors disclosed relationships with the company. Katz disclosed relationships (consultant/advisor) for Phathom Pharmaceuticals and Sebella.

A version of this article appeared on Medscape.com.

A recent study supports the importance of intensive nutrition therapy in managing patients with alcohol-related acute-on-chronic liver failure (ACLF).

In a randomized controlled trial, compared with standard care, dietitian-supported, intensive nutritional therapy improved survival, reduced frailty, and lowered hospitalization rates in men with alcohol-related ACLF.

The study, performed by a team from the Postgraduate Institute of Medical Education and Research, Chandigarh, India, was published in Clinical Gastroenterology and Hepatology.

ACLF related to alcohol use is associated with poor outcomes due to poor nutritional intake and frailty. Frail patients with ACLF face higher morbidity, mortality, and hospitalization rates than their nonfrail counterparts. However, research on the role of structured nutritional interventions in improving these outcomes is limited.

Patal Giri, MBBS, MD, and colleagues enrolled 70 men with alcohol-related ACLF and frailty (liver frailty index [LFI] > 4.5) in a single-center, open-label study. Half were randomly allocated to an intervention group receiving outpatient intensive nutrition therapy (OINT) plus standard medical treatment (SMT) and half to a control group receiving SMT alone for 3 months.

The intervention group received a monitored high-calorie, high-protein, and salt-restricted diet as prescribed by a dedicated senior liver dietitian. The control group received regular nutritional recommendations and were managed for the ACLF-associated complications, without intervention or guidance by the study team.

After 3 months follow-up, overall survival (the primary outcome) was significantly improved in the OINT group compared with the control group (91.4% vs 57.1%), “suggesting that the improvement in nutrition status is associated with better survival,” the study team noted. Three patients died in the OINT group vs 15 in the SMT group.

OINT also led to a significant improvement in frailty, with LFI scores decreasing by an average of 0.93 in the intervention group vs 0.33 in the control group; 97% of patients improved from frail to prefrail status in the OINT group, whereas only 20% of patients improved in the SMT group.

The mean change in LFI of 0.93 with OINT is “well above the substantially clinically important difference” (change of 0.8) established in a previous study, the authors noted.

Significant improvements in weight and body mass index were also observed in the OINT group relative to the control group.

Liver disease severity, including model for end-stage liver disease (MELD) scores, showed greater improvement in the OINT group than in the control group (−8.7 vs −6.3 points from baseline to 3 months).

During the follow-up period, fewer patients in the intervention group than in the control group required a hospital stay (17% vs 45.7%).

Limitations of the study include the single-center design and the short follow-up period of 3 months, which limits long-term outcome assessment. Further, the study only included patients meeting Asia Pacific Association for Study of Liver criteria for ACLF, which does not include the patients with organ failure as defined by European Association for the Study of the Liver-Chronic Liver Failure Consortium criteria. Patients with ACLF who had more severe disease (MELD score > 30 or AARC > 10) were also not included.

Despite these limitations, the authors said their study showed that “dietician-monitored goal-directed nutrition therapy is very important in the management of patients with alcohol-related ACLF along with SMT.”

 

Confirmatory Data 

Reached for comment, Katherine Patton, MEd, RD, a registered dietitian with the Center for Human Nutrition at Cleveland Clinic, Cleveland, Ohio, said it’s well known that the ACLF patient population has a “very high rate of morbidity and mortality and their quality of life tends to be poor due to their frailty. It is also fairly well-known that proper nutrition therapy can improve outcomes, however barriers to adequate nutrition include decreased appetite, nausea, pain, altered taste, and early satiety from ascites.”

“Hepatologists are likely stressing the importance of adequate protein energy intake and doctors may refer patients to an outpatient dietitian, but it is up to the patient to make that appointment and act on the recommendations,” Patton told GI & Hepatology News.

“If a dietitian works in the same clinic as the hepatologist and patients can be referred and seen the same day, this is ideal. During a hospital admission, protein/calorie intake can be more closely monitored and encouraged by a multi-disciplinary team,” Patton explained.

She cautioned that “the average patient is not familiar with how to apply general calorie and protein goals to their everyday eating habits. This study amplifies the role of a dietitian and what consistent education and resources can do to improve a patient’s quality of life and survival.”

This study had no specific funding. The authors have declared no relevant conflicts of interest. Patton had no relevant disclosures.

A version of this article appeared on Medscape.com.

A recent study supports the importance of intensive nutrition therapy in managing patients with alcohol-related acute-on-chronic liver failure (ACLF).

In a randomized controlled trial, compared with standard care, dietitian-supported, intensive nutritional therapy improved survival, reduced frailty, and lowered hospitalization rates in men with alcohol-related ACLF.

The study, performed by a team from the Postgraduate Institute of Medical Education and Research, Chandigarh, India, was published in Clinical Gastroenterology and Hepatology.

ACLF related to alcohol use is associated with poor outcomes due to poor nutritional intake and frailty. Frail patients with ACLF face higher morbidity, mortality, and hospitalization rates than their nonfrail counterparts. However, research on the role of structured nutritional interventions in improving these outcomes is limited.

Patal Giri, MBBS, MD, and colleagues enrolled 70 men with alcohol-related ACLF and frailty (liver frailty index [LFI] > 4.5) in a single-center, open-label study. Half were randomly allocated to an intervention group receiving outpatient intensive nutrition therapy (OINT) plus standard medical treatment (SMT) and half to a control group receiving SMT alone for 3 months.

The intervention group received a monitored high-calorie, high-protein, and salt-restricted diet as prescribed by a dedicated senior liver dietitian. The control group received regular nutritional recommendations and were managed for the ACLF-associated complications, without intervention or guidance by the study team.

After 3 months follow-up, overall survival (the primary outcome) was significantly improved in the OINT group compared with the control group (91.4% vs 57.1%), “suggesting that the improvement in nutrition status is associated with better survival,” the study team noted. Three patients died in the OINT group vs 15 in the SMT group.

OINT also led to a significant improvement in frailty, with LFI scores decreasing by an average of 0.93 in the intervention group vs 0.33 in the control group; 97% of patients improved from frail to prefrail status in the OINT group, whereas only 20% of patients improved in the SMT group.

The mean change in LFI of 0.93 with OINT is “well above the substantially clinically important difference” (change of 0.8) established in a previous study, the authors noted.

Significant improvements in weight and body mass index were also observed in the OINT group relative to the control group.

Liver disease severity, including model for end-stage liver disease (MELD) scores, showed greater improvement in the OINT group than in the control group (−8.7 vs −6.3 points from baseline to 3 months).

During the follow-up period, fewer patients in the intervention group than in the control group required a hospital stay (17% vs 45.7%).

Limitations of the study include the single-center design and the short follow-up period of 3 months, which limits long-term outcome assessment. Further, the study only included patients meeting Asia Pacific Association for Study of Liver criteria for ACLF, which does not include the patients with organ failure as defined by European Association for the Study of the Liver-Chronic Liver Failure Consortium criteria. Patients with ACLF who had more severe disease (MELD score > 30 or AARC > 10) were also not included.

Despite these limitations, the authors said their study showed that “dietician-monitored goal-directed nutrition therapy is very important in the management of patients with alcohol-related ACLF along with SMT.”

 

Confirmatory Data 

Reached for comment, Katherine Patton, MEd, RD, a registered dietitian with the Center for Human Nutrition at Cleveland Clinic, Cleveland, Ohio, said it’s well known that the ACLF patient population has a “very high rate of morbidity and mortality and their quality of life tends to be poor due to their frailty. It is also fairly well-known that proper nutrition therapy can improve outcomes, however barriers to adequate nutrition include decreased appetite, nausea, pain, altered taste, and early satiety from ascites.”

“Hepatologists are likely stressing the importance of adequate protein energy intake and doctors may refer patients to an outpatient dietitian, but it is up to the patient to make that appointment and act on the recommendations,” Patton told GI & Hepatology News.

“If a dietitian works in the same clinic as the hepatologist and patients can be referred and seen the same day, this is ideal. During a hospital admission, protein/calorie intake can be more closely monitored and encouraged by a multi-disciplinary team,” Patton explained.

She cautioned that “the average patient is not familiar with how to apply general calorie and protein goals to their everyday eating habits. This study amplifies the role of a dietitian and what consistent education and resources can do to improve a patient’s quality of life and survival.”

This study had no specific funding. The authors have declared no relevant conflicts of interest. Patton had no relevant disclosures.

A version of this article appeared on Medscape.com.

A recent study supports the importance of intensive nutrition therapy in managing patients with alcohol-related acute-on-chronic liver failure (ACLF).

In a randomized controlled trial, compared with standard care, dietitian-supported, intensive nutritional therapy improved survival, reduced frailty, and lowered hospitalization rates in men with alcohol-related ACLF.

The study, performed by a team from the Postgraduate Institute of Medical Education and Research, Chandigarh, India, was published in Clinical Gastroenterology and Hepatology.

ACLF related to alcohol use is associated with poor outcomes due to poor nutritional intake and frailty. Frail patients with ACLF face higher morbidity, mortality, and hospitalization rates than their nonfrail counterparts. However, research on the role of structured nutritional interventions in improving these outcomes is limited.

Patal Giri, MBBS, MD, and colleagues enrolled 70 men with alcohol-related ACLF and frailty (liver frailty index [LFI] > 4.5) in a single-center, open-label study. Half were randomly allocated to an intervention group receiving outpatient intensive nutrition therapy (OINT) plus standard medical treatment (SMT) and half to a control group receiving SMT alone for 3 months.

The intervention group received a monitored high-calorie, high-protein, and salt-restricted diet as prescribed by a dedicated senior liver dietitian. The control group received regular nutritional recommendations and were managed for the ACLF-associated complications, without intervention or guidance by the study team.

After 3 months follow-up, overall survival (the primary outcome) was significantly improved in the OINT group compared with the control group (91.4% vs 57.1%), “suggesting that the improvement in nutrition status is associated with better survival,” the study team noted. Three patients died in the OINT group vs 15 in the SMT group.

OINT also led to a significant improvement in frailty, with LFI scores decreasing by an average of 0.93 in the intervention group vs 0.33 in the control group; 97% of patients improved from frail to prefrail status in the OINT group, whereas only 20% of patients improved in the SMT group.

The mean change in LFI of 0.93 with OINT is “well above the substantially clinically important difference” (change of 0.8) established in a previous study, the authors noted.

Significant improvements in weight and body mass index were also observed in the OINT group relative to the control group.

Liver disease severity, including model for end-stage liver disease (MELD) scores, showed greater improvement in the OINT group than in the control group (−8.7 vs −6.3 points from baseline to 3 months).

During the follow-up period, fewer patients in the intervention group than in the control group required a hospital stay (17% vs 45.7%).

Limitations of the study include the single-center design and the short follow-up period of 3 months, which limits long-term outcome assessment. Further, the study only included patients meeting Asia Pacific Association for Study of Liver criteria for ACLF, which does not include the patients with organ failure as defined by European Association for the Study of the Liver-Chronic Liver Failure Consortium criteria. Patients with ACLF who had more severe disease (MELD score > 30 or AARC > 10) were also not included.

Despite these limitations, the authors said their study showed that “dietician-monitored goal-directed nutrition therapy is very important in the management of patients with alcohol-related ACLF along with SMT.”

 

Confirmatory Data 

Reached for comment, Katherine Patton, MEd, RD, a registered dietitian with the Center for Human Nutrition at Cleveland Clinic, Cleveland, Ohio, said it’s well known that the ACLF patient population has a “very high rate of morbidity and mortality and their quality of life tends to be poor due to their frailty. It is also fairly well-known that proper nutrition therapy can improve outcomes, however barriers to adequate nutrition include decreased appetite, nausea, pain, altered taste, and early satiety from ascites.”

“Hepatologists are likely stressing the importance of adequate protein energy intake and doctors may refer patients to an outpatient dietitian, but it is up to the patient to make that appointment and act on the recommendations,” Patton told GI & Hepatology News.

“If a dietitian works in the same clinic as the hepatologist and patients can be referred and seen the same day, this is ideal. During a hospital admission, protein/calorie intake can be more closely monitored and encouraged by a multi-disciplinary team,” Patton explained.

She cautioned that “the average patient is not familiar with how to apply general calorie and protein goals to their everyday eating habits. This study amplifies the role of a dietitian and what consistent education and resources can do to improve a patient’s quality of life and survival.”

This study had no specific funding. The authors have declared no relevant conflicts of interest. Patton had no relevant disclosures.

A version of this article appeared on Medscape.com.

The American College of Gastroenterology (ACG) has issued its first clinical practice guideline on the diagnosis and management of gastric premalignant conditions (GPMCs) including atrophic gastritis, gastric intestinal metaplasia, dysplasia, and certain gastric epithelial polyps, all of which have an increased risk of progressing to gastric cancer.

The guideline was published online in The American Journal of Gastroenterology.

GPMCs are “common in gastroenterology practices, but in the US, at least, we’ve not had concrete guidance,” first author Douglas Morgan, MD, MPH, AGAF, Division of Gastroenterology, The University of Alabama at Birmingham, noted in an interview.

With these guidelines, we hope there “will be a paradigm shift to finally establish surveillance in the stomach, much like we’ve been doing for decades in the colon and the esophagus,” Morgan said.

Gastric cancer is a common cancer in the United States with disproportionately higher incidence rates in immigrants from countries with a high incidence of gastric cancer and certain non-White populations.

In addition, the 5-year survival rate in the United States for gastric cancer is 36%, which falls short of global standards and is driven by the fact that only a small percentage of these cancers are diagnosed in the early, curable stage.

These guidelines will help address this marked disparity and the burden on minority and marginalized populations, the guideline authors wrote. “The overarching goals are to reduce [gastric cancer] incidence in the United States, increase the detection of early-stage disease (early gastric cancer), and to significantly increase the 5-year survival rates in the near term.”

 

Key Recommendations

The guideline includes recommendations on endoscopic surveillance for high-risk patients, the performance of high-quality endoscopy and image-enhanced endoscopy (IEE) for diagnosis and surveillance, GPMC histology criteria and reporting, endoscopic treatment of dysplasia, the role of Helicobacter pylori eradication, general risk reduction measures, and the management of autoimmune gastritis and gastric epithelial polyps.

In terms of screening, the guidelines recommend against routine upper endoscopy screening for gastric cancer and GPMC in the general US population (low quality of evidence; conditional recommendation).

They also noted that there is “insufficient” direct US evidence to make a recommendation on opportunistic endoscopy screening for gastric cancer and GPMC in patients deemed at high risk based on race/ethnicity and family history. In addition, they recommend against the use of noninvasive biomarkers for screening or surveillance of GPMC or gastric cancer.

In terms of endoscopic and histologic diagnosis of GPMC, high-quality endoscopic evaluation is crucial to detect premalignant conditions or gastric cancer, the authors said. This includes adequate mucosal cleansing and insufflation, and photodocumentation of anatomic landmarks, as well as use of high-definition white light endoscopy (HDWLE) and IEE.

Systematic gastric biopsies should follow the updated Sydney protocol, with at least two separate containers for antrum/incisura and corpus biopsies. Histology should document the subtype of gastric intestinal metaplasia — incomplete, complete, or mixed — and severity and extent of atrophic gastritis and metaplasia.

Morgan emphasized the importance of coordination between the gastroenterologist and pathologist. “Several of these measures are not routinely reported, so we need to be in conversations with our collaborating pathologists,” he told this news organization.

In terms of GPMC surveillance, the authors suggest surveillance endoscopy every 3 years in high-risk patients with gastric intestinal metaplasia who meet one of the following criteria: High-risk histology (incomplete vs complete subtype, extending into the corpus); family history of gastric cancer in a first-degree relative; foreign-born individuals from high-gastric cancer incidence nations; or high-risk race/ethnicity (East Asian, Latino/a, Black, American Indian, or Alaska Native).

Individuals with multiple risk factors for gastric cancer may be considered for shorter than 3-year intervals.

Low-risk gastric intestinal metaplasia (limited to antrum, mild atrophy, and complete gastric intestinal metaplasia subtype) does not require routine endoscopic surveillance.

In terms of endoscopic management of dysplastic GPMC, endoscopic resection is suggested for dysplasia with visible margins. If dysplasia is not visible, repeat endoscopy with HDWLE and IEE by an experienced endoscopist is advised.

In patients appropriate for endoscopic resection of dysplasia, particularly endoscopic submucosal dissection, referral to a high-volume center with appropriate expertise in the diagnosis and therapeutic resection of gastric neoplasia is strongly recommended.

In patients with confirmed complete resection of dysplasia, endoscopic surveillance is also strongly recommended. Surveillance examinations should be performed by an experienced endoscopist using HDWLE and IEE, with biopsies according to the systematic biopsy protocol in addition to targeted biopsies.

In terms of nonendoscopic GPMC management, testing for H pylori (and eradication treatment if possible) is strongly recommended for patients with GPMC and those with a history of resected early gastric cancer.

Aspirin, nonsteroidal anti-inflammatory drugs, cyclooxygenase 2 inhibitors, or antioxidants are not recommended for patients with GPMC for the purpose of preventing gastric cancer.

In patients with autoimmune gastritis, testing for H pylori with a nonserological test, eradication treatment if positive, and posttreatment testing to confirm eradication is advised.

There is not enough evidence to make a formal recommendation on endoscopic surveillance in those with autoimmune gastritis; surveillance should be individualized, considering the risk for neuroendocrine tumors and possibly gastric cancer.

In terms of gastric epithelial polyps, endoscopic resection of all gastric adenomas is recommended, regardless of size, to exclude or prevent dysplasia and early gastric cancer. Adenomas that are not amenable to endoscopic resection should be referred for surgical resection, if clinically appropriate.

Morgan noted that the ACG GPMC guideline aligns with the updated ACG/American Society for Gastrointestinal Endoscopy upper endoscopy quality indicators released earlier this year.

Implementation of the ACG GPMC guideline and “change in clinical practice will require concrete targets and include training and quality initiatives,” the authors said.

This research received no commercial support. Morgan disclosed research support from Panbela Therapeutics, Thorne, and American Molecular Laboratories.

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

The American College of Gastroenterology (ACG) has issued its first clinical practice guideline on the diagnosis and management of gastric premalignant conditions (GPMCs) including atrophic gastritis, gastric intestinal metaplasia, dysplasia, and certain gastric epithelial polyps, all of which have an increased risk of progressing to gastric cancer.

The guideline was published online in The American Journal of Gastroenterology.

GPMCs are “common in gastroenterology practices, but in the US, at least, we’ve not had concrete guidance,” first author Douglas Morgan, MD, MPH, AGAF, Division of Gastroenterology, The University of Alabama at Birmingham, noted in an interview.

With these guidelines, we hope there “will be a paradigm shift to finally establish surveillance in the stomach, much like we’ve been doing for decades in the colon and the esophagus,” Morgan said.

Gastric cancer is a common cancer in the United States with disproportionately higher incidence rates in immigrants from countries with a high incidence of gastric cancer and certain non-White populations.

In addition, the 5-year survival rate in the United States for gastric cancer is 36%, which falls short of global standards and is driven by the fact that only a small percentage of these cancers are diagnosed in the early, curable stage.

These guidelines will help address this marked disparity and the burden on minority and marginalized populations, the guideline authors wrote. “The overarching goals are to reduce [gastric cancer] incidence in the United States, increase the detection of early-stage disease (early gastric cancer), and to significantly increase the 5-year survival rates in the near term.”

 

Key Recommendations

The guideline includes recommendations on endoscopic surveillance for high-risk patients, the performance of high-quality endoscopy and image-enhanced endoscopy (IEE) for diagnosis and surveillance, GPMC histology criteria and reporting, endoscopic treatment of dysplasia, the role of Helicobacter pylori eradication, general risk reduction measures, and the management of autoimmune gastritis and gastric epithelial polyps.

In terms of screening, the guidelines recommend against routine upper endoscopy screening for gastric cancer and GPMC in the general US population (low quality of evidence; conditional recommendation).

They also noted that there is “insufficient” direct US evidence to make a recommendation on opportunistic endoscopy screening for gastric cancer and GPMC in patients deemed at high risk based on race/ethnicity and family history. In addition, they recommend against the use of noninvasive biomarkers for screening or surveillance of GPMC or gastric cancer.

In terms of endoscopic and histologic diagnosis of GPMC, high-quality endoscopic evaluation is crucial to detect premalignant conditions or gastric cancer, the authors said. This includes adequate mucosal cleansing and insufflation, and photodocumentation of anatomic landmarks, as well as use of high-definition white light endoscopy (HDWLE) and IEE.

Systematic gastric biopsies should follow the updated Sydney protocol, with at least two separate containers for antrum/incisura and corpus biopsies. Histology should document the subtype of gastric intestinal metaplasia — incomplete, complete, or mixed — and severity and extent of atrophic gastritis and metaplasia.

Morgan emphasized the importance of coordination between the gastroenterologist and pathologist. “Several of these measures are not routinely reported, so we need to be in conversations with our collaborating pathologists,” he told this news organization.

In terms of GPMC surveillance, the authors suggest surveillance endoscopy every 3 years in high-risk patients with gastric intestinal metaplasia who meet one of the following criteria: High-risk histology (incomplete vs complete subtype, extending into the corpus); family history of gastric cancer in a first-degree relative; foreign-born individuals from high-gastric cancer incidence nations; or high-risk race/ethnicity (East Asian, Latino/a, Black, American Indian, or Alaska Native).

Individuals with multiple risk factors for gastric cancer may be considered for shorter than 3-year intervals.

Low-risk gastric intestinal metaplasia (limited to antrum, mild atrophy, and complete gastric intestinal metaplasia subtype) does not require routine endoscopic surveillance.

In terms of endoscopic management of dysplastic GPMC, endoscopic resection is suggested for dysplasia with visible margins. If dysplasia is not visible, repeat endoscopy with HDWLE and IEE by an experienced endoscopist is advised.

In patients appropriate for endoscopic resection of dysplasia, particularly endoscopic submucosal dissection, referral to a high-volume center with appropriate expertise in the diagnosis and therapeutic resection of gastric neoplasia is strongly recommended.

In patients with confirmed complete resection of dysplasia, endoscopic surveillance is also strongly recommended. Surveillance examinations should be performed by an experienced endoscopist using HDWLE and IEE, with biopsies according to the systematic biopsy protocol in addition to targeted biopsies.

In terms of nonendoscopic GPMC management, testing for H pylori (and eradication treatment if possible) is strongly recommended for patients with GPMC and those with a history of resected early gastric cancer.

Aspirin, nonsteroidal anti-inflammatory drugs, cyclooxygenase 2 inhibitors, or antioxidants are not recommended for patients with GPMC for the purpose of preventing gastric cancer.

In patients with autoimmune gastritis, testing for H pylori with a nonserological test, eradication treatment if positive, and posttreatment testing to confirm eradication is advised.

There is not enough evidence to make a formal recommendation on endoscopic surveillance in those with autoimmune gastritis; surveillance should be individualized, considering the risk for neuroendocrine tumors and possibly gastric cancer.

In terms of gastric epithelial polyps, endoscopic resection of all gastric adenomas is recommended, regardless of size, to exclude or prevent dysplasia and early gastric cancer. Adenomas that are not amenable to endoscopic resection should be referred for surgical resection, if clinically appropriate.

Morgan noted that the ACG GPMC guideline aligns with the updated ACG/American Society for Gastrointestinal Endoscopy upper endoscopy quality indicators released earlier this year.

Implementation of the ACG GPMC guideline and “change in clinical practice will require concrete targets and include training and quality initiatives,” the authors said.

This research received no commercial support. Morgan disclosed research support from Panbela Therapeutics, Thorne, and American Molecular Laboratories.

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

The American College of Gastroenterology (ACG) has issued its first clinical practice guideline on the diagnosis and management of gastric premalignant conditions (GPMCs) including atrophic gastritis, gastric intestinal metaplasia, dysplasia, and certain gastric epithelial polyps, all of which have an increased risk of progressing to gastric cancer.

The guideline was published online in The American Journal of Gastroenterology.

GPMCs are “common in gastroenterology practices, but in the US, at least, we’ve not had concrete guidance,” first author Douglas Morgan, MD, MPH, AGAF, Division of Gastroenterology, The University of Alabama at Birmingham, noted in an interview.

With these guidelines, we hope there “will be a paradigm shift to finally establish surveillance in the stomach, much like we’ve been doing for decades in the colon and the esophagus,” Morgan said.

Gastric cancer is a common cancer in the United States with disproportionately higher incidence rates in immigrants from countries with a high incidence of gastric cancer and certain non-White populations.

In addition, the 5-year survival rate in the United States for gastric cancer is 36%, which falls short of global standards and is driven by the fact that only a small percentage of these cancers are diagnosed in the early, curable stage.

These guidelines will help address this marked disparity and the burden on minority and marginalized populations, the guideline authors wrote. “The overarching goals are to reduce [gastric cancer] incidence in the United States, increase the detection of early-stage disease (early gastric cancer), and to significantly increase the 5-year survival rates in the near term.”

 

Key Recommendations

The guideline includes recommendations on endoscopic surveillance for high-risk patients, the performance of high-quality endoscopy and image-enhanced endoscopy (IEE) for diagnosis and surveillance, GPMC histology criteria and reporting, endoscopic treatment of dysplasia, the role of Helicobacter pylori eradication, general risk reduction measures, and the management of autoimmune gastritis and gastric epithelial polyps.

In terms of screening, the guidelines recommend against routine upper endoscopy screening for gastric cancer and GPMC in the general US population (low quality of evidence; conditional recommendation).

They also noted that there is “insufficient” direct US evidence to make a recommendation on opportunistic endoscopy screening for gastric cancer and GPMC in patients deemed at high risk based on race/ethnicity and family history. In addition, they recommend against the use of noninvasive biomarkers for screening or surveillance of GPMC or gastric cancer.

In terms of endoscopic and histologic diagnosis of GPMC, high-quality endoscopic evaluation is crucial to detect premalignant conditions or gastric cancer, the authors said. This includes adequate mucosal cleansing and insufflation, and photodocumentation of anatomic landmarks, as well as use of high-definition white light endoscopy (HDWLE) and IEE.

Systematic gastric biopsies should follow the updated Sydney protocol, with at least two separate containers for antrum/incisura and corpus biopsies. Histology should document the subtype of gastric intestinal metaplasia — incomplete, complete, or mixed — and severity and extent of atrophic gastritis and metaplasia.

Morgan emphasized the importance of coordination between the gastroenterologist and pathologist. “Several of these measures are not routinely reported, so we need to be in conversations with our collaborating pathologists,” he told this news organization.

In terms of GPMC surveillance, the authors suggest surveillance endoscopy every 3 years in high-risk patients with gastric intestinal metaplasia who meet one of the following criteria: High-risk histology (incomplete vs complete subtype, extending into the corpus); family history of gastric cancer in a first-degree relative; foreign-born individuals from high-gastric cancer incidence nations; or high-risk race/ethnicity (East Asian, Latino/a, Black, American Indian, or Alaska Native).

Individuals with multiple risk factors for gastric cancer may be considered for shorter than 3-year intervals.

Low-risk gastric intestinal metaplasia (limited to antrum, mild atrophy, and complete gastric intestinal metaplasia subtype) does not require routine endoscopic surveillance.

In terms of endoscopic management of dysplastic GPMC, endoscopic resection is suggested for dysplasia with visible margins. If dysplasia is not visible, repeat endoscopy with HDWLE and IEE by an experienced endoscopist is advised.

In patients appropriate for endoscopic resection of dysplasia, particularly endoscopic submucosal dissection, referral to a high-volume center with appropriate expertise in the diagnosis and therapeutic resection of gastric neoplasia is strongly recommended.

In patients with confirmed complete resection of dysplasia, endoscopic surveillance is also strongly recommended. Surveillance examinations should be performed by an experienced endoscopist using HDWLE and IEE, with biopsies according to the systematic biopsy protocol in addition to targeted biopsies.

In terms of nonendoscopic GPMC management, testing for H pylori (and eradication treatment if possible) is strongly recommended for patients with GPMC and those with a history of resected early gastric cancer.

Aspirin, nonsteroidal anti-inflammatory drugs, cyclooxygenase 2 inhibitors, or antioxidants are not recommended for patients with GPMC for the purpose of preventing gastric cancer.

In patients with autoimmune gastritis, testing for H pylori with a nonserological test, eradication treatment if positive, and posttreatment testing to confirm eradication is advised.

There is not enough evidence to make a formal recommendation on endoscopic surveillance in those with autoimmune gastritis; surveillance should be individualized, considering the risk for neuroendocrine tumors and possibly gastric cancer.

In terms of gastric epithelial polyps, endoscopic resection of all gastric adenomas is recommended, regardless of size, to exclude or prevent dysplasia and early gastric cancer. Adenomas that are not amenable to endoscopic resection should be referred for surgical resection, if clinically appropriate.

Morgan noted that the ACG GPMC guideline aligns with the updated ACG/American Society for Gastrointestinal Endoscopy upper endoscopy quality indicators released earlier this year.

Implementation of the ACG GPMC guideline and “change in clinical practice will require concrete targets and include training and quality initiatives,” the authors said.

This research received no commercial support. Morgan disclosed research support from Panbela Therapeutics, Thorne, and American Molecular Laboratories.

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

New research highlights the promise of artificial intelligence (AI) for opportunistic screening of chronic liver disease (CLD) through routine echocardiography. 

An AI algorithm called EchoNet-Liver demonstrated strong performance for detecting cirrhosis and steatotic liver disease (SLD) from routinely acquired transthoracic echocardiography studies containing subcostal images of the liver, the developers reported in NEJM AI.

“We hope that this algorithm enables physicians to opportunistically screen for chronic liver disease to identify asymptomatic and undiagnosed patients, thus enabling us to treat comorbidities relevant to the patient’s cardiovascular and noncardiovascular health,” Alan C. Kwan, MD, assistant professor, Department of Cardiology, Smidt Heart Institute at Cedars-Sinai, Los Angeles, California, told this news organization.

 

Harnessing Echo to Reveal Liver Trouble 

CLD affects over 1.5 billion people globally, with many cases remaining undiagnosed due to the asymptomatic nature of early disease and a lack of routine screening. Traditional diagnostic methods such as liver function tests, ultrasonography, and MRI are often limited by cost, availability, and patient access.

Echocardiography is a commonly performed imaging study that incidentally captures images of the liver but is not utilized for liver disease assessment.

EchoNet-Liver is an AI algorithm that can identify high-quality subcostal images from full echocardiography studies and detect the presence of cirrhosis and SLD. 

Kwan and colleagues trained it using nearly 1.6 million echocardiogram videos from 66,922 studies and 24,276 adult patients at Cedars-Sinai Medical Center (CSMC). The model predictions were compared with diagnoses from clinical evaluations of paired abdominal ultrasound or MRI studies. External validation studies were conducted using similar data from Stanford Health Care. 

In the “held-out” CSMC ultrasound dataset, EchoNet-Liver detected cirrhosis with an area under the receiver operating characteristic curve (AUROC) of 0.837 (95% CI, 0.828-0.848) and SLD with an AUROC of 0.799 (95% CI, 0.788-0.811).

The algorithm showed a sensitivity of 69.6% and a specificity of 84.6% for detecting cirrhosis, and a sensitivity of 74.1% and a specificity of 72.0% for detecting SLD. 

In the Stanford Health Care external-validation test ultrasound cohort, the model detected cirrhosis with an AUROC of 0.830 (95% CI, 0.799-0.859) and SLD with an AUROC of 0.769 (95% CI, 0.733-0.813), with sensitivity and specificity of 80.0% and 70.9%, respectively, for cirrhosis and 66.7% and 78.0%, respectively, for SLD. 

In the CSMC MRI-paired cohort, EchoNet-Liver detected cirrhosis with an AUROC of 0.704 (95% CI, 0.699-0.708) and SLD with an AUROC of 0.725 (95% CI, 0.707-0.762).

 

Identifying Subclinical Liver Disease to Improve Outcomes

“Across diverse populations and disease definitions, deep-learning-enhanced echocardiography enabled high-throughput, automated detection of CLD, which could enable opportunistic screening for asymptomatic liver disease,” the authors wrote. 

“By improving the diagnosis of subclinical CLD, we may be able to limit or reverse disease progression and improve care by triaging patients toward appropriate clinical and diagnostic management,” they said. 

By way of limitations, the researchers noted that the tool was developed using a cohort of patients who had both abdominal ultrasound and echocardiography within 30 days, and thus probably had a higher prevalence of liver disease compared with the general population receiving echocardiography. The true clinical utility of EchoNet-Liver will depend on whether its application to a general echocardiography population can efficiently detect undiagnosed CLD, they cautioned. 

“While we developed this algorithm based on clinical data, the application within the clinic would typically require FDA approval, which we have not yet applied for,” Kwan told this news organization.

“We plan to prospectively validate this algorithm at multiple sites to ensure that application of this algorithm improves patient care without causing excess diagnostic testing, thus providing value to patients and the healthcare system as a whole,” Kwan said.

Funding was provided in part by KAKENHI (Japan Society for the Promotion of Science). Kwan reported receiving consulting fees from InVision.

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

New research highlights the promise of artificial intelligence (AI) for opportunistic screening of chronic liver disease (CLD) through routine echocardiography. 

An AI algorithm called EchoNet-Liver demonstrated strong performance for detecting cirrhosis and steatotic liver disease (SLD) from routinely acquired transthoracic echocardiography studies containing subcostal images of the liver, the developers reported in NEJM AI.

“We hope that this algorithm enables physicians to opportunistically screen for chronic liver disease to identify asymptomatic and undiagnosed patients, thus enabling us to treat comorbidities relevant to the patient’s cardiovascular and noncardiovascular health,” Alan C. Kwan, MD, assistant professor, Department of Cardiology, Smidt Heart Institute at Cedars-Sinai, Los Angeles, California, told this news organization.

 

Harnessing Echo to Reveal Liver Trouble 

CLD affects over 1.5 billion people globally, with many cases remaining undiagnosed due to the asymptomatic nature of early disease and a lack of routine screening. Traditional diagnostic methods such as liver function tests, ultrasonography, and MRI are often limited by cost, availability, and patient access.

Echocardiography is a commonly performed imaging study that incidentally captures images of the liver but is not utilized for liver disease assessment.

EchoNet-Liver is an AI algorithm that can identify high-quality subcostal images from full echocardiography studies and detect the presence of cirrhosis and SLD. 

Kwan and colleagues trained it using nearly 1.6 million echocardiogram videos from 66,922 studies and 24,276 adult patients at Cedars-Sinai Medical Center (CSMC). The model predictions were compared with diagnoses from clinical evaluations of paired abdominal ultrasound or MRI studies. External validation studies were conducted using similar data from Stanford Health Care. 

In the “held-out” CSMC ultrasound dataset, EchoNet-Liver detected cirrhosis with an area under the receiver operating characteristic curve (AUROC) of 0.837 (95% CI, 0.828-0.848) and SLD with an AUROC of 0.799 (95% CI, 0.788-0.811).

The algorithm showed a sensitivity of 69.6% and a specificity of 84.6% for detecting cirrhosis, and a sensitivity of 74.1% and a specificity of 72.0% for detecting SLD. 

In the Stanford Health Care external-validation test ultrasound cohort, the model detected cirrhosis with an AUROC of 0.830 (95% CI, 0.799-0.859) and SLD with an AUROC of 0.769 (95% CI, 0.733-0.813), with sensitivity and specificity of 80.0% and 70.9%, respectively, for cirrhosis and 66.7% and 78.0%, respectively, for SLD. 

In the CSMC MRI-paired cohort, EchoNet-Liver detected cirrhosis with an AUROC of 0.704 (95% CI, 0.699-0.708) and SLD with an AUROC of 0.725 (95% CI, 0.707-0.762).

 

Identifying Subclinical Liver Disease to Improve Outcomes

“Across diverse populations and disease definitions, deep-learning-enhanced echocardiography enabled high-throughput, automated detection of CLD, which could enable opportunistic screening for asymptomatic liver disease,” the authors wrote. 

“By improving the diagnosis of subclinical CLD, we may be able to limit or reverse disease progression and improve care by triaging patients toward appropriate clinical and diagnostic management,” they said. 

By way of limitations, the researchers noted that the tool was developed using a cohort of patients who had both abdominal ultrasound and echocardiography within 30 days, and thus probably had a higher prevalence of liver disease compared with the general population receiving echocardiography. The true clinical utility of EchoNet-Liver will depend on whether its application to a general echocardiography population can efficiently detect undiagnosed CLD, they cautioned. 

“While we developed this algorithm based on clinical data, the application within the clinic would typically require FDA approval, which we have not yet applied for,” Kwan told this news organization.

“We plan to prospectively validate this algorithm at multiple sites to ensure that application of this algorithm improves patient care without causing excess diagnostic testing, thus providing value to patients and the healthcare system as a whole,” Kwan said.

Funding was provided in part by KAKENHI (Japan Society for the Promotion of Science). Kwan reported receiving consulting fees from InVision.

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

New research highlights the promise of artificial intelligence (AI) for opportunistic screening of chronic liver disease (CLD) through routine echocardiography. 

An AI algorithm called EchoNet-Liver demonstrated strong performance for detecting cirrhosis and steatotic liver disease (SLD) from routinely acquired transthoracic echocardiography studies containing subcostal images of the liver, the developers reported in NEJM AI.

“We hope that this algorithm enables physicians to opportunistically screen for chronic liver disease to identify asymptomatic and undiagnosed patients, thus enabling us to treat comorbidities relevant to the patient’s cardiovascular and noncardiovascular health,” Alan C. Kwan, MD, assistant professor, Department of Cardiology, Smidt Heart Institute at Cedars-Sinai, Los Angeles, California, told this news organization.

 

Harnessing Echo to Reveal Liver Trouble 

CLD affects over 1.5 billion people globally, with many cases remaining undiagnosed due to the asymptomatic nature of early disease and a lack of routine screening. Traditional diagnostic methods such as liver function tests, ultrasonography, and MRI are often limited by cost, availability, and patient access.

Echocardiography is a commonly performed imaging study that incidentally captures images of the liver but is not utilized for liver disease assessment.

EchoNet-Liver is an AI algorithm that can identify high-quality subcostal images from full echocardiography studies and detect the presence of cirrhosis and SLD. 

Kwan and colleagues trained it using nearly 1.6 million echocardiogram videos from 66,922 studies and 24,276 adult patients at Cedars-Sinai Medical Center (CSMC). The model predictions were compared with diagnoses from clinical evaluations of paired abdominal ultrasound or MRI studies. External validation studies were conducted using similar data from Stanford Health Care. 

In the “held-out” CSMC ultrasound dataset, EchoNet-Liver detected cirrhosis with an area under the receiver operating characteristic curve (AUROC) of 0.837 (95% CI, 0.828-0.848) and SLD with an AUROC of 0.799 (95% CI, 0.788-0.811).

The algorithm showed a sensitivity of 69.6% and a specificity of 84.6% for detecting cirrhosis, and a sensitivity of 74.1% and a specificity of 72.0% for detecting SLD. 

In the Stanford Health Care external-validation test ultrasound cohort, the model detected cirrhosis with an AUROC of 0.830 (95% CI, 0.799-0.859) and SLD with an AUROC of 0.769 (95% CI, 0.733-0.813), with sensitivity and specificity of 80.0% and 70.9%, respectively, for cirrhosis and 66.7% and 78.0%, respectively, for SLD. 

In the CSMC MRI-paired cohort, EchoNet-Liver detected cirrhosis with an AUROC of 0.704 (95% CI, 0.699-0.708) and SLD with an AUROC of 0.725 (95% CI, 0.707-0.762).

 

Identifying Subclinical Liver Disease to Improve Outcomes

“Across diverse populations and disease definitions, deep-learning-enhanced echocardiography enabled high-throughput, automated detection of CLD, which could enable opportunistic screening for asymptomatic liver disease,” the authors wrote. 

“By improving the diagnosis of subclinical CLD, we may be able to limit or reverse disease progression and improve care by triaging patients toward appropriate clinical and diagnostic management,” they said. 

By way of limitations, the researchers noted that the tool was developed using a cohort of patients who had both abdominal ultrasound and echocardiography within 30 days, and thus probably had a higher prevalence of liver disease compared with the general population receiving echocardiography. The true clinical utility of EchoNet-Liver will depend on whether its application to a general echocardiography population can efficiently detect undiagnosed CLD, they cautioned. 

“While we developed this algorithm based on clinical data, the application within the clinic would typically require FDA approval, which we have not yet applied for,” Kwan told this news organization.

“We plan to prospectively validate this algorithm at multiple sites to ensure that application of this algorithm improves patient care without causing excess diagnostic testing, thus providing value to patients and the healthcare system as a whole,” Kwan said.

Funding was provided in part by KAKENHI (Japan Society for the Promotion of Science). Kwan reported receiving consulting fees from InVision.

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

Diets in wealthier countries often include processed foods that contain additives, particularly emulsifiers. These additives are increasingly associated with the development of various diseases, including inflammatory bowel disease (IBD).

A research team led by Benoit Chassaing, PhD, research director at the French National Institute of Health and Medical Research (Inserm), focused on one such emulsifier — carboxymethylcellulose (CMC) — which is commonly found in processed baked goods, such as brioche and sandwich bread, and ice cream.

The study, published in the journal Gut, describes how the team developed a new method that uses a simple stool sample to predict an individual’s sensitivity to CMC.

 

Sensitivity Detection

In a previous clinical trial conducted on healthy volunteers, Chassaing and colleagues found that CMC consumption altered the gut microbiota and fecal metabolome in some healthy individuals. In mice, transplanting fecal microbiota from CMC-sensitive animals made other animals susceptible. This has led researchers to investigate the characteristics of sensitive microbiota.

To explore this, the researchers developed an in vitro microbiota model capable of replicating multiple healthy human microbiota. CMC sensitivity was tested using this model, and the findings were validated in vivo by transplanting microbiota classified as sensitive or resistant to mice. Only mice that received microbiota predicted to be CMC-sensitive developed severe colitis after consuming CMC.

 

Predictive Signature

Next, the team analyzed the stool metagenomes of individuals with microbiotas classified as sensitive or resistant to CMC. They identified a specific microbial signature that could predict whether a given microbiota would react negatively to emulsifiers. Using molecular analyses, this signature allows researchers to predict whether an individual’s microbiota is susceptible or resistant to CMC exposure.

For the research team, these findings open the possibility of determining whether an individual is sensitive to a particular emulsifier, allowing for personalized dietary recommendations. This is particularly relevant for patients with chronic IBD and may also help prevent these conditions in those not previously affected.

These findings could pave the way for personalized dietary recommendations, particularly for patients with chronic IBD. By identifying individuals sensitive to specific emulsifiers, clinicians can tailor diets to reduce inflammation and potentially prevent disease onset in those at risk.

To further validate these insights, the team is launching a cohort study in patients with Crohn’s to explore why some individuals are more susceptible to food additives than others.

This story was translated from Univadis France using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

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

Diets in wealthier countries often include processed foods that contain additives, particularly emulsifiers. These additives are increasingly associated with the development of various diseases, including inflammatory bowel disease (IBD).

A research team led by Benoit Chassaing, PhD, research director at the French National Institute of Health and Medical Research (Inserm), focused on one such emulsifier — carboxymethylcellulose (CMC) — which is commonly found in processed baked goods, such as brioche and sandwich bread, and ice cream.

The study, published in the journal Gut, describes how the team developed a new method that uses a simple stool sample to predict an individual’s sensitivity to CMC.

 

Sensitivity Detection

In a previous clinical trial conducted on healthy volunteers, Chassaing and colleagues found that CMC consumption altered the gut microbiota and fecal metabolome in some healthy individuals. In mice, transplanting fecal microbiota from CMC-sensitive animals made other animals susceptible. This has led researchers to investigate the characteristics of sensitive microbiota.

To explore this, the researchers developed an in vitro microbiota model capable of replicating multiple healthy human microbiota. CMC sensitivity was tested using this model, and the findings were validated in vivo by transplanting microbiota classified as sensitive or resistant to mice. Only mice that received microbiota predicted to be CMC-sensitive developed severe colitis after consuming CMC.

 

Predictive Signature

Next, the team analyzed the stool metagenomes of individuals with microbiotas classified as sensitive or resistant to CMC. They identified a specific microbial signature that could predict whether a given microbiota would react negatively to emulsifiers. Using molecular analyses, this signature allows researchers to predict whether an individual’s microbiota is susceptible or resistant to CMC exposure.

For the research team, these findings open the possibility of determining whether an individual is sensitive to a particular emulsifier, allowing for personalized dietary recommendations. This is particularly relevant for patients with chronic IBD and may also help prevent these conditions in those not previously affected.

These findings could pave the way for personalized dietary recommendations, particularly for patients with chronic IBD. By identifying individuals sensitive to specific emulsifiers, clinicians can tailor diets to reduce inflammation and potentially prevent disease onset in those at risk.

To further validate these insights, the team is launching a cohort study in patients with Crohn’s to explore why some individuals are more susceptible to food additives than others.

This story was translated from Univadis France using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

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

Diets in wealthier countries often include processed foods that contain additives, particularly emulsifiers. These additives are increasingly associated with the development of various diseases, including inflammatory bowel disease (IBD).

A research team led by Benoit Chassaing, PhD, research director at the French National Institute of Health and Medical Research (Inserm), focused on one such emulsifier — carboxymethylcellulose (CMC) — which is commonly found in processed baked goods, such as brioche and sandwich bread, and ice cream.

The study, published in the journal Gut, describes how the team developed a new method that uses a simple stool sample to predict an individual’s sensitivity to CMC.

 

Sensitivity Detection

In a previous clinical trial conducted on healthy volunteers, Chassaing and colleagues found that CMC consumption altered the gut microbiota and fecal metabolome in some healthy individuals. In mice, transplanting fecal microbiota from CMC-sensitive animals made other animals susceptible. This has led researchers to investigate the characteristics of sensitive microbiota.

To explore this, the researchers developed an in vitro microbiota model capable of replicating multiple healthy human microbiota. CMC sensitivity was tested using this model, and the findings were validated in vivo by transplanting microbiota classified as sensitive or resistant to mice. Only mice that received microbiota predicted to be CMC-sensitive developed severe colitis after consuming CMC.

 

Predictive Signature

Next, the team analyzed the stool metagenomes of individuals with microbiotas classified as sensitive or resistant to CMC. They identified a specific microbial signature that could predict whether a given microbiota would react negatively to emulsifiers. Using molecular analyses, this signature allows researchers to predict whether an individual’s microbiota is susceptible or resistant to CMC exposure.

For the research team, these findings open the possibility of determining whether an individual is sensitive to a particular emulsifier, allowing for personalized dietary recommendations. This is particularly relevant for patients with chronic IBD and may also help prevent these conditions in those not previously affected.

These findings could pave the way for personalized dietary recommendations, particularly for patients with chronic IBD. By identifying individuals sensitive to specific emulsifiers, clinicians can tailor diets to reduce inflammation and potentially prevent disease onset in those at risk.

To further validate these insights, the team is launching a cohort study in patients with Crohn’s to explore why some individuals are more susceptible to food additives than others.

This story was translated from Univadis France using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

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

The United States multi-society task force on colorectal cancer (CRC) has updated its 2014 guidance for optimizing the adequacy of bowel preparation for colonoscopy.

The latest consensus recommendations emphasize the importance of verbal and written patient education, refine diet restrictions, update optimal purgative regimens, and advise tracking bowel prep adequacy rates at both the individual endoscopist and unit levels.

“Colorectal cancer remains the second most common cause of cancer death in the United States, and colonoscopy is considered the gold standard for evaluating the colon, including assessing causes of colon-related signs or symptoms and the detection of precancerous lesions. It is well recognized that the adequacy of bowel preparation is essential for optimal colonoscopy performance,” the task force wrote.

 

Choice of Prep, Dosing and Timing, and Dietary Restrictions 

When choosing bowel preparation regimens, the task force recommends considering the individual’s medical history, medications, and, when available, the adequacy of bowel preparation reported from prior colonoscopies. Other considerations include patient preference, associated additional costs to the patient, and ease in obtaining and consuming any purgatives or adjuncts.

In terms of timing and dose, the task force now “suggests that lower-volume bowel preparation regimens, such as those that rely on only 2 liters of fluid compared to the traditional 4L, are acceptable options for individuals considered unlikely to have an inadequate bowel preparation. This assumes that the purgative is taken in a split-dose fashion (half the evening prior to colonoscopy and half the morning of the colonoscopy),” co–lead author Brian C. Jacobson, MD, MPH, AGAF, with Massachusetts General Hospital and Harvard Medical School, both in Boston, said in an interview.

The task force also states that a same-day bowel preparation regimen for afternoon, but not morning, colonoscopy is a “reasonable alternative to the now-common split-dose regimen,” Jacobson said.

The group did not find one bowel preparation purgative to be better than others, although table 7 in the document details characteristics of commonly used prep regimens including their side effects and contraindications.

Recommendations regarding dietary modifications depend upon the patient’s risk for inadequate bowel prep. For patients at low risk for inadequate bowel prep, the task force recommends limiting dietary restrictions to the day before a colonoscopy, relying on either clear liquids or low-fiber/low-residue diets for the early and midday meals. Table 5 in the document provides a list of low-residue foods and sample meals.

The task force also suggests the adjunctive use of oral simethicone (≥ 320 mg) to bowel prep as a way to potentially improve visualization, although they acknowledge that further research is needed.

How might these updated consensus recommendations change current clinical practice? 

Jacobson said: “Some physicians may try to identify individuals who will do just as well with a more patient-friendly, easily tolerated bowel preparation regimen, including less stringent dietary restrictions leading up to colonoscopy.” 

He noted that the task force prefers the term “guidance” to “guidelines.”

 

New Quality Benchmark 

The task force recommends documenting bowel prep quality in the endoscopy report after all washing and suctioning have been completed using reliably understood descriptors that communicate the adequacy of the preparation.

They recommend the term “adequate bowel preparation” be used to indicate that standard screening or surveillance intervals can be assigned based on the findings of the colonoscopy.

Additionally, the task force recommends that endoscopy units and individual endoscopists track and aim for ≥ 90% adequacy rates in bowel preparation — up from the 85% benchmark contained in the prior recommendations.

Jacobson told this news organization it’s “currently unknown” how many individual endoscopists and endoscopy units track and meet the 90% benchmark at present.

David Johnson, MD, professor of medicine and chief of gastroenterology at Eastern Virginia Medical School, Norfolk, who wasn’t on the task force, said endoscopy units and providers “need to be accountable and should be tracking this quality metric.”

Johnson noted that bowel prep inadequacy has “intrinsic costs,” impacting lesion detection, CRC incidence, and patient outcomes. Inadequate prep leads to “increased risk for morbidity, mortality, longer appointment and wait times for rescheduling, and negative connotations that may deter patients from returning.”

 

Brian Sullivan, MD, MHS, assistant professor of medicine, division of gastroenterology, Duke University School of Medicine, Durham, North Carolina, who wasn’t on the task force, said the recommendation to target a 90% or higher bowel preparation adequacy rate is “appreciated.”

“This benchmark encourages practices to standardize measurement, tracking, and reporting of preparation quality at both the individual and unit levels. Specifically, it should motivate providers to critically evaluate their interpretation of preparation quality and ensure adequate cleansing before making determinations,” Sullivan said in an interview.

“At the unit level, this metric can identify whether there are opportunities for quality improvement, such as by implementing evidence-based initiatives (provided in the guidance) to enhance outpatient preparation processes,” Sullivan noted.

The task force emphasized that the majority of consensus recommendations focus on individuals at average risk for inadequate bowel prep. Patients at high risk for inadequate bowel prep (eg, diabetes, constipation, opioid use) should receive tailored instructions, including a more extended dietary prep and high-volume purgatives.

 

‘Timely and Important’ Updates

Sullivan said the updated consensus recommendations on optimizing bowel preparation quality for colonoscopy are both “timely and important.” 

“Clear guidance facilitates dissemination and adoption, promoting flexible yet evidence-based approaches that enhance patient and provider satisfaction while potentially improving CRC prevention outcomes. For instance, surveys reveal that some practices still do not utilize split-dose bowel preparation, which is proven to improve preparation quality, particularly for the right-side of the colon. This gap underscores the need for standardized guidance to ensure high-quality colonoscopy and effective CRC screening,” Sullivan said.

He also noted that the inclusion of lower-volume bowel prep regimens and less intensive dietary modifications for selected patients is a “welcome update.”

“These options can improve patient adherence and satisfaction, which are critical not only for the quality of the index exam but also for ensuring patients return for future screenings, thereby supporting long-term CRC prevention efforts,” Sullivan said.

The task force includes representatives from the American Gastroenterological Association, the American College of Gastroenterology, and the American Society for Gastrointestinal Endoscopy.

The consensus document was published online in the three societies’ respective scientific journals — Gastroenterology, the American Journal of Gastroenterology, and Gastrointestinal Endsocopy.

This research had no financial support. Jacobson is a consultant for Curis and Guardant Health. Sullivan had no disclosures. Johnson is an adviser to ISOThrive and a past president of the American College of Gastroenterology.

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

The United States multi-society task force on colorectal cancer (CRC) has updated its 2014 guidance for optimizing the adequacy of bowel preparation for colonoscopy.

The latest consensus recommendations emphasize the importance of verbal and written patient education, refine diet restrictions, update optimal purgative regimens, and advise tracking bowel prep adequacy rates at both the individual endoscopist and unit levels.

“Colorectal cancer remains the second most common cause of cancer death in the United States, and colonoscopy is considered the gold standard for evaluating the colon, including assessing causes of colon-related signs or symptoms and the detection of precancerous lesions. It is well recognized that the adequacy of bowel preparation is essential for optimal colonoscopy performance,” the task force wrote.

 

Choice of Prep, Dosing and Timing, and Dietary Restrictions 

When choosing bowel preparation regimens, the task force recommends considering the individual’s medical history, medications, and, when available, the adequacy of bowel preparation reported from prior colonoscopies. Other considerations include patient preference, associated additional costs to the patient, and ease in obtaining and consuming any purgatives or adjuncts.

In terms of timing and dose, the task force now “suggests that lower-volume bowel preparation regimens, such as those that rely on only 2 liters of fluid compared to the traditional 4L, are acceptable options for individuals considered unlikely to have an inadequate bowel preparation. This assumes that the purgative is taken in a split-dose fashion (half the evening prior to colonoscopy and half the morning of the colonoscopy),” co–lead author Brian C. Jacobson, MD, MPH, AGAF, with Massachusetts General Hospital and Harvard Medical School, both in Boston, said in an interview.

The task force also states that a same-day bowel preparation regimen for afternoon, but not morning, colonoscopy is a “reasonable alternative to the now-common split-dose regimen,” Jacobson said.

The group did not find one bowel preparation purgative to be better than others, although table 7 in the document details characteristics of commonly used prep regimens including their side effects and contraindications.

Recommendations regarding dietary modifications depend upon the patient’s risk for inadequate bowel prep. For patients at low risk for inadequate bowel prep, the task force recommends limiting dietary restrictions to the day before a colonoscopy, relying on either clear liquids or low-fiber/low-residue diets for the early and midday meals. Table 5 in the document provides a list of low-residue foods and sample meals.

The task force also suggests the adjunctive use of oral simethicone (≥ 320 mg) to bowel prep as a way to potentially improve visualization, although they acknowledge that further research is needed.

How might these updated consensus recommendations change current clinical practice? 

Jacobson said: “Some physicians may try to identify individuals who will do just as well with a more patient-friendly, easily tolerated bowel preparation regimen, including less stringent dietary restrictions leading up to colonoscopy.” 

He noted that the task force prefers the term “guidance” to “guidelines.”

 

New Quality Benchmark 

The task force recommends documenting bowel prep quality in the endoscopy report after all washing and suctioning have been completed using reliably understood descriptors that communicate the adequacy of the preparation.

They recommend the term “adequate bowel preparation” be used to indicate that standard screening or surveillance intervals can be assigned based on the findings of the colonoscopy.

Additionally, the task force recommends that endoscopy units and individual endoscopists track and aim for ≥ 90% adequacy rates in bowel preparation — up from the 85% benchmark contained in the prior recommendations.

Jacobson told this news organization it’s “currently unknown” how many individual endoscopists and endoscopy units track and meet the 90% benchmark at present.

David Johnson, MD, professor of medicine and chief of gastroenterology at Eastern Virginia Medical School, Norfolk, who wasn’t on the task force, said endoscopy units and providers “need to be accountable and should be tracking this quality metric.”

Johnson noted that bowel prep inadequacy has “intrinsic costs,” impacting lesion detection, CRC incidence, and patient outcomes. Inadequate prep leads to “increased risk for morbidity, mortality, longer appointment and wait times for rescheduling, and negative connotations that may deter patients from returning.”

 

Brian Sullivan, MD, MHS, assistant professor of medicine, division of gastroenterology, Duke University School of Medicine, Durham, North Carolina, who wasn’t on the task force, said the recommendation to target a 90% or higher bowel preparation adequacy rate is “appreciated.”

“This benchmark encourages practices to standardize measurement, tracking, and reporting of preparation quality at both the individual and unit levels. Specifically, it should motivate providers to critically evaluate their interpretation of preparation quality and ensure adequate cleansing before making determinations,” Sullivan said in an interview.

“At the unit level, this metric can identify whether there are opportunities for quality improvement, such as by implementing evidence-based initiatives (provided in the guidance) to enhance outpatient preparation processes,” Sullivan noted.

The task force emphasized that the majority of consensus recommendations focus on individuals at average risk for inadequate bowel prep. Patients at high risk for inadequate bowel prep (eg, diabetes, constipation, opioid use) should receive tailored instructions, including a more extended dietary prep and high-volume purgatives.

 

‘Timely and Important’ Updates

Sullivan said the updated consensus recommendations on optimizing bowel preparation quality for colonoscopy are both “timely and important.” 

“Clear guidance facilitates dissemination and adoption, promoting flexible yet evidence-based approaches that enhance patient and provider satisfaction while potentially improving CRC prevention outcomes. For instance, surveys reveal that some practices still do not utilize split-dose bowel preparation, which is proven to improve preparation quality, particularly for the right-side of the colon. This gap underscores the need for standardized guidance to ensure high-quality colonoscopy and effective CRC screening,” Sullivan said.

He also noted that the inclusion of lower-volume bowel prep regimens and less intensive dietary modifications for selected patients is a “welcome update.”

“These options can improve patient adherence and satisfaction, which are critical not only for the quality of the index exam but also for ensuring patients return for future screenings, thereby supporting long-term CRC prevention efforts,” Sullivan said.

The task force includes representatives from the American Gastroenterological Association, the American College of Gastroenterology, and the American Society for Gastrointestinal Endoscopy.

The consensus document was published online in the three societies’ respective scientific journals — Gastroenterology, the American Journal of Gastroenterology, and Gastrointestinal Endsocopy.

This research had no financial support. Jacobson is a consultant for Curis and Guardant Health. Sullivan had no disclosures. Johnson is an adviser to ISOThrive and a past president of the American College of Gastroenterology.

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

The United States multi-society task force on colorectal cancer (CRC) has updated its 2014 guidance for optimizing the adequacy of bowel preparation for colonoscopy.

The latest consensus recommendations emphasize the importance of verbal and written patient education, refine diet restrictions, update optimal purgative regimens, and advise tracking bowel prep adequacy rates at both the individual endoscopist and unit levels.

“Colorectal cancer remains the second most common cause of cancer death in the United States, and colonoscopy is considered the gold standard for evaluating the colon, including assessing causes of colon-related signs or symptoms and the detection of precancerous lesions. It is well recognized that the adequacy of bowel preparation is essential for optimal colonoscopy performance,” the task force wrote.

 

Choice of Prep, Dosing and Timing, and Dietary Restrictions 

When choosing bowel preparation regimens, the task force recommends considering the individual’s medical history, medications, and, when available, the adequacy of bowel preparation reported from prior colonoscopies. Other considerations include patient preference, associated additional costs to the patient, and ease in obtaining and consuming any purgatives or adjuncts.

In terms of timing and dose, the task force now “suggests that lower-volume bowel preparation regimens, such as those that rely on only 2 liters of fluid compared to the traditional 4L, are acceptable options for individuals considered unlikely to have an inadequate bowel preparation. This assumes that the purgative is taken in a split-dose fashion (half the evening prior to colonoscopy and half the morning of the colonoscopy),” co–lead author Brian C. Jacobson, MD, MPH, AGAF, with Massachusetts General Hospital and Harvard Medical School, both in Boston, said in an interview.

The task force also states that a same-day bowel preparation regimen for afternoon, but not morning, colonoscopy is a “reasonable alternative to the now-common split-dose regimen,” Jacobson said.

The group did not find one bowel preparation purgative to be better than others, although table 7 in the document details characteristics of commonly used prep regimens including their side effects and contraindications.

Recommendations regarding dietary modifications depend upon the patient’s risk for inadequate bowel prep. For patients at low risk for inadequate bowel prep, the task force recommends limiting dietary restrictions to the day before a colonoscopy, relying on either clear liquids or low-fiber/low-residue diets for the early and midday meals. Table 5 in the document provides a list of low-residue foods and sample meals.

The task force also suggests the adjunctive use of oral simethicone (≥ 320 mg) to bowel prep as a way to potentially improve visualization, although they acknowledge that further research is needed.

How might these updated consensus recommendations change current clinical practice? 

Jacobson said: “Some physicians may try to identify individuals who will do just as well with a more patient-friendly, easily tolerated bowel preparation regimen, including less stringent dietary restrictions leading up to colonoscopy.” 

He noted that the task force prefers the term “guidance” to “guidelines.”

 

New Quality Benchmark 

The task force recommends documenting bowel prep quality in the endoscopy report after all washing and suctioning have been completed using reliably understood descriptors that communicate the adequacy of the preparation.

They recommend the term “adequate bowel preparation” be used to indicate that standard screening or surveillance intervals can be assigned based on the findings of the colonoscopy.

Additionally, the task force recommends that endoscopy units and individual endoscopists track and aim for ≥ 90% adequacy rates in bowel preparation — up from the 85% benchmark contained in the prior recommendations.

Jacobson told this news organization it’s “currently unknown” how many individual endoscopists and endoscopy units track and meet the 90% benchmark at present.

David Johnson, MD, professor of medicine and chief of gastroenterology at Eastern Virginia Medical School, Norfolk, who wasn’t on the task force, said endoscopy units and providers “need to be accountable and should be tracking this quality metric.”

Johnson noted that bowel prep inadequacy has “intrinsic costs,” impacting lesion detection, CRC incidence, and patient outcomes. Inadequate prep leads to “increased risk for morbidity, mortality, longer appointment and wait times for rescheduling, and negative connotations that may deter patients from returning.”

 

Brian Sullivan, MD, MHS, assistant professor of medicine, division of gastroenterology, Duke University School of Medicine, Durham, North Carolina, who wasn’t on the task force, said the recommendation to target a 90% or higher bowel preparation adequacy rate is “appreciated.”

“This benchmark encourages practices to standardize measurement, tracking, and reporting of preparation quality at both the individual and unit levels. Specifically, it should motivate providers to critically evaluate their interpretation of preparation quality and ensure adequate cleansing before making determinations,” Sullivan said in an interview.

“At the unit level, this metric can identify whether there are opportunities for quality improvement, such as by implementing evidence-based initiatives (provided in the guidance) to enhance outpatient preparation processes,” Sullivan noted.

The task force emphasized that the majority of consensus recommendations focus on individuals at average risk for inadequate bowel prep. Patients at high risk for inadequate bowel prep (eg, diabetes, constipation, opioid use) should receive tailored instructions, including a more extended dietary prep and high-volume purgatives.

 

‘Timely and Important’ Updates

Sullivan said the updated consensus recommendations on optimizing bowel preparation quality for colonoscopy are both “timely and important.” 

“Clear guidance facilitates dissemination and adoption, promoting flexible yet evidence-based approaches that enhance patient and provider satisfaction while potentially improving CRC prevention outcomes. For instance, surveys reveal that some practices still do not utilize split-dose bowel preparation, which is proven to improve preparation quality, particularly for the right-side of the colon. This gap underscores the need for standardized guidance to ensure high-quality colonoscopy and effective CRC screening,” Sullivan said.

He also noted that the inclusion of lower-volume bowel prep regimens and less intensive dietary modifications for selected patients is a “welcome update.”

“These options can improve patient adherence and satisfaction, which are critical not only for the quality of the index exam but also for ensuring patients return for future screenings, thereby supporting long-term CRC prevention efforts,” Sullivan said.

The task force includes representatives from the American Gastroenterological Association, the American College of Gastroenterology, and the American Society for Gastrointestinal Endoscopy.

The consensus document was published online in the three societies’ respective scientific journals — Gastroenterology, the American Journal of Gastroenterology, and Gastrointestinal Endsocopy.

This research had no financial support. Jacobson is a consultant for Curis and Guardant Health. Sullivan had no disclosures. Johnson is an adviser to ISOThrive and a past president of the American College of Gastroenterology.

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

The most common pathology affecting the pancreas is excess intra-pancreatic fat deposition (IPFD), often called fatty pancreas disease (FPD) — a disorder experienced by roughly one fifth of the world’s population. Although it is more common than type 2 diabetes, pancreatitis, and pancreatic cancer combined, it has remained relatively obscure.

By contrast, fatty liver — once called nonalcoholic fatty liver disease and recently renamed metabolic dysfunction–associated steatotic liver disease (MASLD) — is well-known.

“When it comes to diseases of the liver and pancreas, the liver is the big brother that has gotten all the attention, while the pancreas is the neglected little stepbrother that’s not sufficiently profiled in most medical textbooks and gets very little attention,” Max Petrov, MD, MPH, PhD, professor of pancreatology, University of Auckland, New Zealand, said in an interview. “The phenomenon of fatty pancreas has been observed for decades, but it is underappreciated and underrecognized.”

 

As early as 1926, fat depositions were identified during autopsies, but the condition remained relatively unknown, Mohammad Bilal, MD, associate professor of medicine-gastroenterology, University of Colorado Anschutz Medical Campus, Aurora, said in an interview. “Fortunately, FPD has recently been receiving more focus.”

Generally, healthy individuals have small amounts of fat in their pancreas. IPFD is defined as “the diffuse presence of fat in the pancreas, measured on a continuous scale,” and FPD refers to IPFD above the upper limit of normal. While there is no clear consensus as to what the normal range is, studies suggest it’s a pancreatic fat content ranging from 1.8% to 10.4%.

FPD’s “most important implication is that it can be a precursor for more challenging and burdensome diseases of the pancreas,” Petrov said.

Fatty changes in the pancreas affect both its endocrine and exocrine systems. FPD is associated with type 2 diabetes, the most common disease of the endocrine pancreas, as well as pancreatitis and pancreatic cancer, the most common diseases of the exocrine pancreas. It’s also implicated in the development of carotid atherosclerosis, pancreatic fistula following surgery, and exocrine pancreatic insufficiency (EPI).

 

A ‘Pandora’s Box’

Up to half of people with fatty pancreas are lean. The condition isn’t merely caused by an overflow of fat from the liver into the pancreas in people who consume more calories than they burn, Petrov said. Neither robust postmortem nor biopsy studies have found a statistically significant association between fatty deposition in the pancreas and liver fat.

Compared with the way people accumulate liver fat, the development of FPD is more complex, Petrov said.

“Hepatic fat is a relatively simple process: Lipid droplets accumulate in the hepatocytes; but, in the pancreas, there are several ways by which fat may accumulate,” he said.

One relates to the location of the pancreas within visceral, retroperitoneal fat, Petrov said. That fat can migrate and build up between pancreatic lobules.

Fat also can accumulate inside the lobes. This process can involve a buildup of fat droplets in acinar and stellate cells on the exocrine side and in the islets of Langerhans on the endocrine side. Additionally, when functional pancreatic cells die, particularly acinar cells, adult stem cells may replace them with adipocytes. Transformation of acinar cells into fat cells — a process called acinar-to-adipocyte transdifferentiation — also may be a way fat accumulates inside the lobes, Petrov said.

The accumulation of fat is a response to a wide array of insults to the pancreas over time. For example, obesity and metabolic syndrome lead to the accumulation of adipocytes and fat infiltration, whereas alcohol abuse and viral infections may lead to the death of acinar cells, which produce digestive enzymes.

Ultimately, the negative changes produced by excess fat in the pancreas are the origin of all common noninherited pancreatic diseases, bringing them under one umbrella, Petrov maintained. He dubbed this hypothesis PANcreatic Diseases Originating from intRapancreatic fAt (PANDORA).

The type of cells involved has implications for which disease may arise. For example, fat infiltration in stellate cells may promote pancreatic cancer, whereas its accumulation in the islets of Langerhans, which produce insulin and glucagon, is associated with type 2 diabetes.

The PANDORA hypothesis has eight foundational principles:

• Fatty pancreas is a key driver of pancreatic diseases in most people.
• Inflammation within the pancreatic microenvironment results from overwhelming lipotoxicity fueled by fatty pancreas.
• Aberrant communication between acinar cells involving lipid droplets drives acute pancreatitis.
• The pancreas responds to lipotoxicity with fibrosis and calcification — the hallmarks of chronic pancreatitis.
• Fat deposition affects signaling between stellate cells and other components of the microenvironment in ways that raise the risk for pancreatic cancer.
• The development of diabetes of the exocrine pancreas and EPI is affected by the presence of fatty pancreas.
• The higher risk for pancreatic disease in older adults is influenced by fatty pancreas.
• The multipronged nature of intrapancreatic fat deposition accounts for the common development of one pancreatic disease after another.

The idea that all common pancreatic diseases are the result of pathways emanating from FPD could “explain the bidirectional relationship between diabetes and pancreatitis or pancreatic cancer,” Petrov said.

 

Risk Factors, Symptoms, and Diagnosis

A variety of risk factors are involved in the accumulation of fat that may lead to pancreatic diseases, including aging, cholelithiasis, dyslipidemia, drugs/toxins (eg, steroids), genetic predisposition, iron overload, diet (eg, fatty foods, ultraprocessed foods), heavy alcohol use, overweight/obesity, pancreatic duct obstruction, tobacco use, viral infection (eg, hepatitis B, COVID-19), severe malnutrition, prediabetes, and dysglycemia.

Petrov described FPD as a “silent disease” that’s often asymptomatic, with its presence emerging as an incidental finding during abdominal ultrasonography for other reasons. However, patients may sometimes experience stomach pain or nausea if they have concurrent diseases of the pancreas, he said.

There are no currently available lab tests that can definitively detect the presence of FPD. Rather, the gold standard for a noninvasive diagnosis of FPD is MRI, with CT as the second-best choice, Petrov said.

In countries where advanced imaging is not available, a low-cost alternative might be a simple abdominal ultrasound, but it is not definitive, he said. “It’s operator-dependent and can be subjective.”

Some risk factors, such as derangements of glucose and lipid metabolism, especially in the presence of heavy alcohol use and a high-fat diet, can “be detected on lab tests,” Petrov said. “This, in combination with the abdominal ultrasound, might suggest the patients will benefit from deeper investigation, including MRI.”

Because the exocrine pancreas helps with digestion of fatty food, intralobular fatty deposits or replacement of pancreatic exocrine cells with adipose cells can lead to steatorrhea, Bilal said.

“Fat within the stool or oily diarrhea is a clue to the presence of FPD,” Bilal said.

Although this symptom isn’t unique to FPD and is found in other types of pancreatic conditions, its presence suggests that further investigation for FPD is warranted, he added.

 

Common-Sense Treatment Approaches

At present, there are no US Food and Drug Administration–approved treatments for FPD, Petrov said.

“What might be recommended is something along the lines of treatment of MASLD — appropriate diet and physical activity,” he said. Petrov hopes that as the disease entity garners more research attention, more clinical drug trials will be initiated, and new medications are found and approved.

Petrov suggested that there could be a “theoretical rationale” for the use of glucagon-like peptide 1 receptor agonists (GLP-1 RAs) as a treatment, given their effectiveness in multiple conditions, including MASLD, but no human trials have robustly shown specific benefits of these drugs for FPD.

Petrov added that, to date, 12 classes of drugs have been investigated for reducing IPFD: biguanides, sulfonylureas, GLP-1 RAs, thiazolidinediones, dipeptidyl peptidase–4 (DPP-4) inhibitors, sodium-glucose cotransporter 2 inhibitors, statins, fibrates, pancreatic lipase inhibitors, angiotensin II receptor blockers, somatostatin receptor agonists, and antioxidants.

Of these, most have shown promise in preclinical animal models. But only thiazolidinediones, GLP-1 RAs, DPP-4 inhibitors, and somatostatin receptor agonists have been investigated in randomized controlled trials in humans. The findings have been inconsistent, with the active treatment often not achieving statistically significant improvements.

“At this stage of our knowledge, we can’t recommend a specific pharmacotherapy,” Petrov said. But we can suggest dietary changes, such as saturated fat reduction, alcohol reduction, smoking cessation, reduction in consumption of ultraprocessed food, physical exercise, and addressing obesity and other drivers of metabolic disease.

Bilal, who is also a spokesperson for AGA, suggested that pancreatic enzyme replacement therapy, often used to treat pancreatic EPI, may treat some symptoms of FPD such as diarrhea.

Bariatric surgery has shown promise for FPD, in that it can decrease the patient’s body mass and potentially reduce the fat in the pancreas as well as it can improve metabolic diseases and hyperlipidemia. One study showed that it significantly decreased IPFD, fatty acid uptake, and blood flow, and these improvements were associated with more favorable glucose homeostasis and beta-cell function.

However, bariatric surgery is only appropriate for certain patients; is associated with potentially adverse sequelae including malnutrition, anemia, and digestive tract stenosis; and is currently not indicated for FPD.

Bilal advises clinicians to “keep an eye on FPD” if it’s detected incidentally and to screen patients more carefully for MASLD, metabolic disease, and diabetes.

“Although there are no consensus guidelines and recommendations for managing FPD at present, these common-sense approaches will benefit the patient’s overall health and hopefully will have a beneficial impact on pancreatic health as well,” he said.

Petrov reported no relevant financial relationships. Bilal reported being a consultant for Boston Scientific, Steris Endoscopy, and Cook Medical.

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

The most common pathology affecting the pancreas is excess intra-pancreatic fat deposition (IPFD), often called fatty pancreas disease (FPD) — a disorder experienced by roughly one fifth of the world’s population. Although it is more common than type 2 diabetes, pancreatitis, and pancreatic cancer combined, it has remained relatively obscure.

By contrast, fatty liver — once called nonalcoholic fatty liver disease and recently renamed metabolic dysfunction–associated steatotic liver disease (MASLD) — is well-known.

“When it comes to diseases of the liver and pancreas, the liver is the big brother that has gotten all the attention, while the pancreas is the neglected little stepbrother that’s not sufficiently profiled in most medical textbooks and gets very little attention,” Max Petrov, MD, MPH, PhD, professor of pancreatology, University of Auckland, New Zealand, said in an interview. “The phenomenon of fatty pancreas has been observed for decades, but it is underappreciated and underrecognized.”

 

As early as 1926, fat depositions were identified during autopsies, but the condition remained relatively unknown, Mohammad Bilal, MD, associate professor of medicine-gastroenterology, University of Colorado Anschutz Medical Campus, Aurora, said in an interview. “Fortunately, FPD has recently been receiving more focus.”

Generally, healthy individuals have small amounts of fat in their pancreas. IPFD is defined as “the diffuse presence of fat in the pancreas, measured on a continuous scale,” and FPD refers to IPFD above the upper limit of normal. While there is no clear consensus as to what the normal range is, studies suggest it’s a pancreatic fat content ranging from 1.8% to 10.4%.

FPD’s “most important implication is that it can be a precursor for more challenging and burdensome diseases of the pancreas,” Petrov said.

Fatty changes in the pancreas affect both its endocrine and exocrine systems. FPD is associated with type 2 diabetes, the most common disease of the endocrine pancreas, as well as pancreatitis and pancreatic cancer, the most common diseases of the exocrine pancreas. It’s also implicated in the development of carotid atherosclerosis, pancreatic fistula following surgery, and exocrine pancreatic insufficiency (EPI).

 

A ‘Pandora’s Box’

Up to half of people with fatty pancreas are lean. The condition isn’t merely caused by an overflow of fat from the liver into the pancreas in people who consume more calories than they burn, Petrov said. Neither robust postmortem nor biopsy studies have found a statistically significant association between fatty deposition in the pancreas and liver fat.

Compared with the way people accumulate liver fat, the development of FPD is more complex, Petrov said.

“Hepatic fat is a relatively simple process: Lipid droplets accumulate in the hepatocytes; but, in the pancreas, there are several ways by which fat may accumulate,” he said.

One relates to the location of the pancreas within visceral, retroperitoneal fat, Petrov said. That fat can migrate and build up between pancreatic lobules.

Fat also can accumulate inside the lobes. This process can involve a buildup of fat droplets in acinar and stellate cells on the exocrine side and in the islets of Langerhans on the endocrine side. Additionally, when functional pancreatic cells die, particularly acinar cells, adult stem cells may replace them with adipocytes. Transformation of acinar cells into fat cells — a process called acinar-to-adipocyte transdifferentiation — also may be a way fat accumulates inside the lobes, Petrov said.

The accumulation of fat is a response to a wide array of insults to the pancreas over time. For example, obesity and metabolic syndrome lead to the accumulation of adipocytes and fat infiltration, whereas alcohol abuse and viral infections may lead to the death of acinar cells, which produce digestive enzymes.

Ultimately, the negative changes produced by excess fat in the pancreas are the origin of all common noninherited pancreatic diseases, bringing them under one umbrella, Petrov maintained. He dubbed this hypothesis PANcreatic Diseases Originating from intRapancreatic fAt (PANDORA).

The type of cells involved has implications for which disease may arise. For example, fat infiltration in stellate cells may promote pancreatic cancer, whereas its accumulation in the islets of Langerhans, which produce insulin and glucagon, is associated with type 2 diabetes.

The PANDORA hypothesis has eight foundational principles:

• Fatty pancreas is a key driver of pancreatic diseases in most people.
• Inflammation within the pancreatic microenvironment results from overwhelming lipotoxicity fueled by fatty pancreas.
• Aberrant communication between acinar cells involving lipid droplets drives acute pancreatitis.
• The pancreas responds to lipotoxicity with fibrosis and calcification — the hallmarks of chronic pancreatitis.
• Fat deposition affects signaling between stellate cells and other components of the microenvironment in ways that raise the risk for pancreatic cancer.
• The development of diabetes of the exocrine pancreas and EPI is affected by the presence of fatty pancreas.
• The higher risk for pancreatic disease in older adults is influenced by fatty pancreas.
• The multipronged nature of intrapancreatic fat deposition accounts for the common development of one pancreatic disease after another.

The idea that all common pancreatic diseases are the result of pathways emanating from FPD could “explain the bidirectional relationship between diabetes and pancreatitis or pancreatic cancer,” Petrov said.

 

Risk Factors, Symptoms, and Diagnosis

A variety of risk factors are involved in the accumulation of fat that may lead to pancreatic diseases, including aging, cholelithiasis, dyslipidemia, drugs/toxins (eg, steroids), genetic predisposition, iron overload, diet (eg, fatty foods, ultraprocessed foods), heavy alcohol use, overweight/obesity, pancreatic duct obstruction, tobacco use, viral infection (eg, hepatitis B, COVID-19), severe malnutrition, prediabetes, and dysglycemia.

Petrov described FPD as a “silent disease” that’s often asymptomatic, with its presence emerging as an incidental finding during abdominal ultrasonography for other reasons. However, patients may sometimes experience stomach pain or nausea if they have concurrent diseases of the pancreas, he said.

There are no currently available lab tests that can definitively detect the presence of FPD. Rather, the gold standard for a noninvasive diagnosis of FPD is MRI, with CT as the second-best choice, Petrov said.

In countries where advanced imaging is not available, a low-cost alternative might be a simple abdominal ultrasound, but it is not definitive, he said. “It’s operator-dependent and can be subjective.”

Some risk factors, such as derangements of glucose and lipid metabolism, especially in the presence of heavy alcohol use and a high-fat diet, can “be detected on lab tests,” Petrov said. “This, in combination with the abdominal ultrasound, might suggest the patients will benefit from deeper investigation, including MRI.”

Because the exocrine pancreas helps with digestion of fatty food, intralobular fatty deposits or replacement of pancreatic exocrine cells with adipose cells can lead to steatorrhea, Bilal said.

“Fat within the stool or oily diarrhea is a clue to the presence of FPD,” Bilal said.

Although this symptom isn’t unique to FPD and is found in other types of pancreatic conditions, its presence suggests that further investigation for FPD is warranted, he added.

 

Common-Sense Treatment Approaches

At present, there are no US Food and Drug Administration–approved treatments for FPD, Petrov said.

“What might be recommended is something along the lines of treatment of MASLD — appropriate diet and physical activity,” he said. Petrov hopes that as the disease entity garners more research attention, more clinical drug trials will be initiated, and new medications are found and approved.

Petrov suggested that there could be a “theoretical rationale” for the use of glucagon-like peptide 1 receptor agonists (GLP-1 RAs) as a treatment, given their effectiveness in multiple conditions, including MASLD, but no human trials have robustly shown specific benefits of these drugs for FPD.

Petrov added that, to date, 12 classes of drugs have been investigated for reducing IPFD: biguanides, sulfonylureas, GLP-1 RAs, thiazolidinediones, dipeptidyl peptidase–4 (DPP-4) inhibitors, sodium-glucose cotransporter 2 inhibitors, statins, fibrates, pancreatic lipase inhibitors, angiotensin II receptor blockers, somatostatin receptor agonists, and antioxidants.

Of these, most have shown promise in preclinical animal models. But only thiazolidinediones, GLP-1 RAs, DPP-4 inhibitors, and somatostatin receptor agonists have been investigated in randomized controlled trials in humans. The findings have been inconsistent, with the active treatment often not achieving statistically significant improvements.

“At this stage of our knowledge, we can’t recommend a specific pharmacotherapy,” Petrov said. But we can suggest dietary changes, such as saturated fat reduction, alcohol reduction, smoking cessation, reduction in consumption of ultraprocessed food, physical exercise, and addressing obesity and other drivers of metabolic disease.

Bilal, who is also a spokesperson for AGA, suggested that pancreatic enzyme replacement therapy, often used to treat pancreatic EPI, may treat some symptoms of FPD such as diarrhea.

Bariatric surgery has shown promise for FPD, in that it can decrease the patient’s body mass and potentially reduce the fat in the pancreas as well as it can improve metabolic diseases and hyperlipidemia. One study showed that it significantly decreased IPFD, fatty acid uptake, and blood flow, and these improvements were associated with more favorable glucose homeostasis and beta-cell function.

However, bariatric surgery is only appropriate for certain patients; is associated with potentially adverse sequelae including malnutrition, anemia, and digestive tract stenosis; and is currently not indicated for FPD.

Bilal advises clinicians to “keep an eye on FPD” if it’s detected incidentally and to screen patients more carefully for MASLD, metabolic disease, and diabetes.

“Although there are no consensus guidelines and recommendations for managing FPD at present, these common-sense approaches will benefit the patient’s overall health and hopefully will have a beneficial impact on pancreatic health as well,” he said.

Petrov reported no relevant financial relationships. Bilal reported being a consultant for Boston Scientific, Steris Endoscopy, and Cook Medical.

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

The most common pathology affecting the pancreas is excess intra-pancreatic fat deposition (IPFD), often called fatty pancreas disease (FPD) — a disorder experienced by roughly one fifth of the world’s population. Although it is more common than type 2 diabetes, pancreatitis, and pancreatic cancer combined, it has remained relatively obscure.

By contrast, fatty liver — once called nonalcoholic fatty liver disease and recently renamed metabolic dysfunction–associated steatotic liver disease (MASLD) — is well-known.

“When it comes to diseases of the liver and pancreas, the liver is the big brother that has gotten all the attention, while the pancreas is the neglected little stepbrother that’s not sufficiently profiled in most medical textbooks and gets very little attention,” Max Petrov, MD, MPH, PhD, professor of pancreatology, University of Auckland, New Zealand, said in an interview. “The phenomenon of fatty pancreas has been observed for decades, but it is underappreciated and underrecognized.”

 

As early as 1926, fat depositions were identified during autopsies, but the condition remained relatively unknown, Mohammad Bilal, MD, associate professor of medicine-gastroenterology, University of Colorado Anschutz Medical Campus, Aurora, said in an interview. “Fortunately, FPD has recently been receiving more focus.”

Generally, healthy individuals have small amounts of fat in their pancreas. IPFD is defined as “the diffuse presence of fat in the pancreas, measured on a continuous scale,” and FPD refers to IPFD above the upper limit of normal. While there is no clear consensus as to what the normal range is, studies suggest it’s a pancreatic fat content ranging from 1.8% to 10.4%.

FPD’s “most important implication is that it can be a precursor for more challenging and burdensome diseases of the pancreas,” Petrov said.

Fatty changes in the pancreas affect both its endocrine and exocrine systems. FPD is associated with type 2 diabetes, the most common disease of the endocrine pancreas, as well as pancreatitis and pancreatic cancer, the most common diseases of the exocrine pancreas. It’s also implicated in the development of carotid atherosclerosis, pancreatic fistula following surgery, and exocrine pancreatic insufficiency (EPI).

 

A ‘Pandora’s Box’

Up to half of people with fatty pancreas are lean. The condition isn’t merely caused by an overflow of fat from the liver into the pancreas in people who consume more calories than they burn, Petrov said. Neither robust postmortem nor biopsy studies have found a statistically significant association between fatty deposition in the pancreas and liver fat.

Compared with the way people accumulate liver fat, the development of FPD is more complex, Petrov said.

“Hepatic fat is a relatively simple process: Lipid droplets accumulate in the hepatocytes; but, in the pancreas, there are several ways by which fat may accumulate,” he said.

One relates to the location of the pancreas within visceral, retroperitoneal fat, Petrov said. That fat can migrate and build up between pancreatic lobules.

Fat also can accumulate inside the lobes. This process can involve a buildup of fat droplets in acinar and stellate cells on the exocrine side and in the islets of Langerhans on the endocrine side. Additionally, when functional pancreatic cells die, particularly acinar cells, adult stem cells may replace them with adipocytes. Transformation of acinar cells into fat cells — a process called acinar-to-adipocyte transdifferentiation — also may be a way fat accumulates inside the lobes, Petrov said.

The accumulation of fat is a response to a wide array of insults to the pancreas over time. For example, obesity and metabolic syndrome lead to the accumulation of adipocytes and fat infiltration, whereas alcohol abuse and viral infections may lead to the death of acinar cells, which produce digestive enzymes.

Ultimately, the negative changes produced by excess fat in the pancreas are the origin of all common noninherited pancreatic diseases, bringing them under one umbrella, Petrov maintained. He dubbed this hypothesis PANcreatic Diseases Originating from intRapancreatic fAt (PANDORA).

The type of cells involved has implications for which disease may arise. For example, fat infiltration in stellate cells may promote pancreatic cancer, whereas its accumulation in the islets of Langerhans, which produce insulin and glucagon, is associated with type 2 diabetes.

The PANDORA hypothesis has eight foundational principles:

• Fatty pancreas is a key driver of pancreatic diseases in most people.
• Inflammation within the pancreatic microenvironment results from overwhelming lipotoxicity fueled by fatty pancreas.
• Aberrant communication between acinar cells involving lipid droplets drives acute pancreatitis.
• The pancreas responds to lipotoxicity with fibrosis and calcification — the hallmarks of chronic pancreatitis.
• Fat deposition affects signaling between stellate cells and other components of the microenvironment in ways that raise the risk for pancreatic cancer.
• The development of diabetes of the exocrine pancreas and EPI is affected by the presence of fatty pancreas.
• The higher risk for pancreatic disease in older adults is influenced by fatty pancreas.
• The multipronged nature of intrapancreatic fat deposition accounts for the common development of one pancreatic disease after another.

The idea that all common pancreatic diseases are the result of pathways emanating from FPD could “explain the bidirectional relationship between diabetes and pancreatitis or pancreatic cancer,” Petrov said.

 

Risk Factors, Symptoms, and Diagnosis

A variety of risk factors are involved in the accumulation of fat that may lead to pancreatic diseases, including aging, cholelithiasis, dyslipidemia, drugs/toxins (eg, steroids), genetic predisposition, iron overload, diet (eg, fatty foods, ultraprocessed foods), heavy alcohol use, overweight/obesity, pancreatic duct obstruction, tobacco use, viral infection (eg, hepatitis B, COVID-19), severe malnutrition, prediabetes, and dysglycemia.

Petrov described FPD as a “silent disease” that’s often asymptomatic, with its presence emerging as an incidental finding during abdominal ultrasonography for other reasons. However, patients may sometimes experience stomach pain or nausea if they have concurrent diseases of the pancreas, he said.

There are no currently available lab tests that can definitively detect the presence of FPD. Rather, the gold standard for a noninvasive diagnosis of FPD is MRI, with CT as the second-best choice, Petrov said.

In countries where advanced imaging is not available, a low-cost alternative might be a simple abdominal ultrasound, but it is not definitive, he said. “It’s operator-dependent and can be subjective.”

Some risk factors, such as derangements of glucose and lipid metabolism, especially in the presence of heavy alcohol use and a high-fat diet, can “be detected on lab tests,” Petrov said. “This, in combination with the abdominal ultrasound, might suggest the patients will benefit from deeper investigation, including MRI.”

Because the exocrine pancreas helps with digestion of fatty food, intralobular fatty deposits or replacement of pancreatic exocrine cells with adipose cells can lead to steatorrhea, Bilal said.

“Fat within the stool or oily diarrhea is a clue to the presence of FPD,” Bilal said.

Although this symptom isn’t unique to FPD and is found in other types of pancreatic conditions, its presence suggests that further investigation for FPD is warranted, he added.

 

Common-Sense Treatment Approaches

At present, there are no US Food and Drug Administration–approved treatments for FPD, Petrov said.

“What might be recommended is something along the lines of treatment of MASLD — appropriate diet and physical activity,” he said. Petrov hopes that as the disease entity garners more research attention, more clinical drug trials will be initiated, and new medications are found and approved.

Petrov suggested that there could be a “theoretical rationale” for the use of glucagon-like peptide 1 receptor agonists (GLP-1 RAs) as a treatment, given their effectiveness in multiple conditions, including MASLD, but no human trials have robustly shown specific benefits of these drugs for FPD.

Petrov added that, to date, 12 classes of drugs have been investigated for reducing IPFD: biguanides, sulfonylureas, GLP-1 RAs, thiazolidinediones, dipeptidyl peptidase–4 (DPP-4) inhibitors, sodium-glucose cotransporter 2 inhibitors, statins, fibrates, pancreatic lipase inhibitors, angiotensin II receptor blockers, somatostatin receptor agonists, and antioxidants.

Of these, most have shown promise in preclinical animal models. But only thiazolidinediones, GLP-1 RAs, DPP-4 inhibitors, and somatostatin receptor agonists have been investigated in randomized controlled trials in humans. The findings have been inconsistent, with the active treatment often not achieving statistically significant improvements.

“At this stage of our knowledge, we can’t recommend a specific pharmacotherapy,” Petrov said. But we can suggest dietary changes, such as saturated fat reduction, alcohol reduction, smoking cessation, reduction in consumption of ultraprocessed food, physical exercise, and addressing obesity and other drivers of metabolic disease.

Bilal, who is also a spokesperson for AGA, suggested that pancreatic enzyme replacement therapy, often used to treat pancreatic EPI, may treat some symptoms of FPD such as diarrhea.

Bariatric surgery has shown promise for FPD, in that it can decrease the patient’s body mass and potentially reduce the fat in the pancreas as well as it can improve metabolic diseases and hyperlipidemia. One study showed that it significantly decreased IPFD, fatty acid uptake, and blood flow, and these improvements were associated with more favorable glucose homeostasis and beta-cell function.

However, bariatric surgery is only appropriate for certain patients; is associated with potentially adverse sequelae including malnutrition, anemia, and digestive tract stenosis; and is currently not indicated for FPD.

Bilal advises clinicians to “keep an eye on FPD” if it’s detected incidentally and to screen patients more carefully for MASLD, metabolic disease, and diabetes.

“Although there are no consensus guidelines and recommendations for managing FPD at present, these common-sense approaches will benefit the patient’s overall health and hopefully will have a beneficial impact on pancreatic health as well,” he said.

Petrov reported no relevant financial relationships. Bilal reported being a consultant for Boston Scientific, Steris Endoscopy, and Cook Medical.

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