News

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.

Despite universal hepatitis C virus (HCV) screening recommendations issued in 2020, HCV screening rates remain suboptimal among US women, a new analysis showed. 

“We found that screening rates were higher and rose more steeply in pregnant individuals compared to nonpregnant reproductive age females after this guidance.” However overall, HCV screening in women still remained low by the end of 2022, authors Roshni Singh, MD, and Rachel Epstein, MD, MSc, with the section of infectious diseases, Boston Medical Center, noted in an email to this news organization.

The study was published online in JAMA.

The researchers leveraged TriNetX LIVE electronic health record data to compare HCV screening rates from 68 US healthcare organizations covering more than 115 million patients.

Using a multiple-group interrupted time series analysis, they compared HCV screening rates for pregnant and nonpregnant women for each 6-month period before (January 2014 to December 2019) and after (July 2020 to December 2022) the 2020 guidelines. January to June 2020 was considered a washout period to account for the COVID-19 pandemic peak and guideline dissemination.

For the entire 9-year study period (2014-2022), a total of 79,231 incident HCV tests occurred among pregnant women and 678,951 occurred among nonpregnant women. 

In the 6 months before the guidance, HCV screening per 1000 person-years increased from 52 to 117 tests among pregnant women and 16 to 24 tests among nonpregnant women.

In the 6 months after the guidance, screening per 1000 person-years increased from 141 to 253 among pregnant women and from 29 to 37 among nonpregnant women.

Yet by the end of 2022, only 38.7% of women with a pregnancy and 8.7% of nonpregnant women were ever tested for the HCV.

 

How to Boost HCV Screening

These results suggest that “innovative strategies are needed to improve HCV diagnosis and treatment,” the authors wrote. 

“Several interventions have been demonstrated to be effective in increasing screening in general, including electronic medical record alerts for opt-out testing, routine test offer by nonclinician office staff, offering testing in nontraditional spaces, including substance use treatment programs, harm reduction centers, STI clinics, and mobile health units,” Singh and Epstein told this news organization.

“A key step is educating primary care providers in addition to addiction medicine and emergency medicine clinicians about the updated guidelines as they interface with a large number of at-risk individuals,” they said. And the most important measure is creating clear work flows that respond to positive results to link people to treatment and cure. 

“Clinicians need to feel empowered that their work screening a patient can make a meaningful difference in both the patient’s life and in helping end this epidemic,” the two researchers explained. 

Aaron Glatt, MD, a spokesperson for the Infectious Diseases Society of America, who wasn’t involved in the study, told this news organization that the low HCV screening rates are not surprising. 

“We tend not to do well with screening. It’s not necessarily anybody’s fault, but patients don’t necessarily want to be screened. Sometimes physicians are very busy. Sometimes screening is not the most important thing for them to do. Sometimes there are processes in place that fall through,” said Glatt, chief of infectious diseases and hospital epidemiologist at Mount Sinai South Nassau, Oceanside, New York. 

“We tend to do a better job of screening in pregnant than nonpregnant women because pregnancy is a focus and there is 9 months that you can be following-up, so there is more opportunity. A healthy nonpregnant woman may not see her doctor for another year,” Glatt noted. 

“I think that many physicians are very good at screening for hepatitis C in patients that are clearly at risk,” he added. “We’re not so good at screening for people” that don’t have a clear risk but do “have risk factors.”

The study had no commercial funding. Singh, Epstein, and Glatt had no relevant disclosures.

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

Despite universal hepatitis C virus (HCV) screening recommendations issued in 2020, HCV screening rates remain suboptimal among US women, a new analysis showed. 

“We found that screening rates were higher and rose more steeply in pregnant individuals compared to nonpregnant reproductive age females after this guidance.” However overall, HCV screening in women still remained low by the end of 2022, authors Roshni Singh, MD, and Rachel Epstein, MD, MSc, with the section of infectious diseases, Boston Medical Center, noted in an email to this news organization.

The study was published online in JAMA.

The researchers leveraged TriNetX LIVE electronic health record data to compare HCV screening rates from 68 US healthcare organizations covering more than 115 million patients.

Using a multiple-group interrupted time series analysis, they compared HCV screening rates for pregnant and nonpregnant women for each 6-month period before (January 2014 to December 2019) and after (July 2020 to December 2022) the 2020 guidelines. January to June 2020 was considered a washout period to account for the COVID-19 pandemic peak and guideline dissemination.

For the entire 9-year study period (2014-2022), a total of 79,231 incident HCV tests occurred among pregnant women and 678,951 occurred among nonpregnant women. 

In the 6 months before the guidance, HCV screening per 1000 person-years increased from 52 to 117 tests among pregnant women and 16 to 24 tests among nonpregnant women.

In the 6 months after the guidance, screening per 1000 person-years increased from 141 to 253 among pregnant women and from 29 to 37 among nonpregnant women.

Yet by the end of 2022, only 38.7% of women with a pregnancy and 8.7% of nonpregnant women were ever tested for the HCV.

 

How to Boost HCV Screening

These results suggest that “innovative strategies are needed to improve HCV diagnosis and treatment,” the authors wrote. 

“Several interventions have been demonstrated to be effective in increasing screening in general, including electronic medical record alerts for opt-out testing, routine test offer by nonclinician office staff, offering testing in nontraditional spaces, including substance use treatment programs, harm reduction centers, STI clinics, and mobile health units,” Singh and Epstein told this news organization.

“A key step is educating primary care providers in addition to addiction medicine and emergency medicine clinicians about the updated guidelines as they interface with a large number of at-risk individuals,” they said. And the most important measure is creating clear work flows that respond to positive results to link people to treatment and cure. 

“Clinicians need to feel empowered that their work screening a patient can make a meaningful difference in both the patient’s life and in helping end this epidemic,” the two researchers explained. 

Aaron Glatt, MD, a spokesperson for the Infectious Diseases Society of America, who wasn’t involved in the study, told this news organization that the low HCV screening rates are not surprising. 

“We tend not to do well with screening. It’s not necessarily anybody’s fault, but patients don’t necessarily want to be screened. Sometimes physicians are very busy. Sometimes screening is not the most important thing for them to do. Sometimes there are processes in place that fall through,” said Glatt, chief of infectious diseases and hospital epidemiologist at Mount Sinai South Nassau, Oceanside, New York. 

“We tend to do a better job of screening in pregnant than nonpregnant women because pregnancy is a focus and there is 9 months that you can be following-up, so there is more opportunity. A healthy nonpregnant woman may not see her doctor for another year,” Glatt noted. 

“I think that many physicians are very good at screening for hepatitis C in patients that are clearly at risk,” he added. “We’re not so good at screening for people” that don’t have a clear risk but do “have risk factors.”

The study had no commercial funding. Singh, Epstein, and Glatt had no relevant disclosures.

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

Despite universal hepatitis C virus (HCV) screening recommendations issued in 2020, HCV screening rates remain suboptimal among US women, a new analysis showed. 

“We found that screening rates were higher and rose more steeply in pregnant individuals compared to nonpregnant reproductive age females after this guidance.” However overall, HCV screening in women still remained low by the end of 2022, authors Roshni Singh, MD, and Rachel Epstein, MD, MSc, with the section of infectious diseases, Boston Medical Center, noted in an email to this news organization.

The study was published online in JAMA.

The researchers leveraged TriNetX LIVE electronic health record data to compare HCV screening rates from 68 US healthcare organizations covering more than 115 million patients.

Using a multiple-group interrupted time series analysis, they compared HCV screening rates for pregnant and nonpregnant women for each 6-month period before (January 2014 to December 2019) and after (July 2020 to December 2022) the 2020 guidelines. January to June 2020 was considered a washout period to account for the COVID-19 pandemic peak and guideline dissemination.

For the entire 9-year study period (2014-2022), a total of 79,231 incident HCV tests occurred among pregnant women and 678,951 occurred among nonpregnant women. 

In the 6 months before the guidance, HCV screening per 1000 person-years increased from 52 to 117 tests among pregnant women and 16 to 24 tests among nonpregnant women.

In the 6 months after the guidance, screening per 1000 person-years increased from 141 to 253 among pregnant women and from 29 to 37 among nonpregnant women.

Yet by the end of 2022, only 38.7% of women with a pregnancy and 8.7% of nonpregnant women were ever tested for the HCV.

 

How to Boost HCV Screening

These results suggest that “innovative strategies are needed to improve HCV diagnosis and treatment,” the authors wrote. 

“Several interventions have been demonstrated to be effective in increasing screening in general, including electronic medical record alerts for opt-out testing, routine test offer by nonclinician office staff, offering testing in nontraditional spaces, including substance use treatment programs, harm reduction centers, STI clinics, and mobile health units,” Singh and Epstein told this news organization.

“A key step is educating primary care providers in addition to addiction medicine and emergency medicine clinicians about the updated guidelines as they interface with a large number of at-risk individuals,” they said. And the most important measure is creating clear work flows that respond to positive results to link people to treatment and cure. 

“Clinicians need to feel empowered that their work screening a patient can make a meaningful difference in both the patient’s life and in helping end this epidemic,” the two researchers explained. 

Aaron Glatt, MD, a spokesperson for the Infectious Diseases Society of America, who wasn’t involved in the study, told this news organization that the low HCV screening rates are not surprising. 

“We tend not to do well with screening. It’s not necessarily anybody’s fault, but patients don’t necessarily want to be screened. Sometimes physicians are very busy. Sometimes screening is not the most important thing for them to do. Sometimes there are processes in place that fall through,” said Glatt, chief of infectious diseases and hospital epidemiologist at Mount Sinai South Nassau, Oceanside, New York. 

“We tend to do a better job of screening in pregnant than nonpregnant women because pregnancy is a focus and there is 9 months that you can be following-up, so there is more opportunity. A healthy nonpregnant woman may not see her doctor for another year,” Glatt noted. 

“I think that many physicians are very good at screening for hepatitis C in patients that are clearly at risk,” he added. “We’re not so good at screening for people” that don’t have a clear risk but do “have risk factors.”

The study had no commercial funding. Singh, Epstein, and Glatt had no relevant disclosures.

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

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are associated with retained gastric contents and aborted procedures among patients undergoing upper endoscopy, according to a meta-analysis of more than 80,000 patients.

Safety profiles, however, were comparable across groups, suggesting that prolonged fasting may be a sufficient management strategy, instead of withholding GLP-1RAs, lead author Antonio Facciorusso, MD, PhD, of the University of Foggia, Italy, and colleagues reported.

“The impact of GLP-1RAs on slowing gastric motility has raised concerns in patients undergoing endoscopic procedures, particularly upper endoscopies,” the investigators wrote in Clinical Gastroenterology and Hepatology. “This is due to the perceived risk of aspiration of retained gastric contents in sedated patients and the decreased visibility of the gastric mucosa, which can reduce the diagnostic yield of the examination.”

The American Society of Anesthesiologists (ASA) recommends withholding GLP-1RAs before procedures or surgery, whereas AGA suggests an individualized approach, citing limited supporting data. 

A previous meta-analysis reported that GLP-1RAs mildly delayed gastric emptying, but clinical relevance remained unclear. 

The present meta-analysis aimed to clarify this uncertainty by analyzing 13 retrospective studies that involved 84,065 patients undergoing upper endoscopy. Outcomes were compared among GLP-1RA users vs non-users, including rates of retained gastric contents, aborted procedures, and adverse events. 

Patients on GLP-1RAs had significantly higher rates of retained gastric contents than non-users (odds ratio [OR], 5.56), a finding that held steady (OR, 4.20) after adjusting for age, sex, diabetes, body mass index, and other therapies. 

GLP-1RAs were also associated with an increased likelihood of aborted procedures (OR, 5.13; 1% vs. 0.3%) and a higher need for repeat endoscopies (OR, 2.19; 1% vs 2%); however, Facciorusso and colleagues noted that these events, in absolute terms, were relatively uncommon.

“The rate of aborted and repeat procedures in the included studies was low,” the investigators wrote. “This meant that only for every 110 patients undergoing upper endoscopy while in GLP-1RA therapy would we observe an aborted procedure and only for every 120 patients would we need to repeat the procedure.”

The overall safety profile of GLP-1RAs in the context of upper endoscopy remained largely reassuring, they added. Specifically, rates of bronchial aspiration were not significantly different between users and non-users. What’s more, no single study reported a statistically significant increase in major complications, including pulmonary adverse events, among GLP-1RA users. 

According to Facciorusso and colleagues, these findings suggest that retained gastric contents do not appear to substantially heighten the risk of serious harm, though further prospective studies are needed.

“Our comprehensive analysis indicates that, while the use of GLP-1RA results in higher rates of [retained gastric contents], the actual clinical impact appears to be limited,” they wrote. “Therefore, there is no strong evidence to support the routine discontinuation of the drug before upper endoscopy procedures.”

Instead, they supported the AGA task force’s recommendation for an individualized approach, and not withholding GLP-1RAs unnecessarily, calling this “the best compromise.”

“Prolonging the duration of fasting for solids could represent the optimal approach in these patients, although this strategy requires further evaluation,” the investigators concluded.

The investigators disclosed no conflicts of interest.







 

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are associated with retained gastric contents and aborted procedures among patients undergoing upper endoscopy, according to a meta-analysis of more than 80,000 patients.

Safety profiles, however, were comparable across groups, suggesting that prolonged fasting may be a sufficient management strategy, instead of withholding GLP-1RAs, lead author Antonio Facciorusso, MD, PhD, of the University of Foggia, Italy, and colleagues reported.

“The impact of GLP-1RAs on slowing gastric motility has raised concerns in patients undergoing endoscopic procedures, particularly upper endoscopies,” the investigators wrote in Clinical Gastroenterology and Hepatology. “This is due to the perceived risk of aspiration of retained gastric contents in sedated patients and the decreased visibility of the gastric mucosa, which can reduce the diagnostic yield of the examination.”

The American Society of Anesthesiologists (ASA) recommends withholding GLP-1RAs before procedures or surgery, whereas AGA suggests an individualized approach, citing limited supporting data. 

A previous meta-analysis reported that GLP-1RAs mildly delayed gastric emptying, but clinical relevance remained unclear. 

The present meta-analysis aimed to clarify this uncertainty by analyzing 13 retrospective studies that involved 84,065 patients undergoing upper endoscopy. Outcomes were compared among GLP-1RA users vs non-users, including rates of retained gastric contents, aborted procedures, and adverse events. 

Patients on GLP-1RAs had significantly higher rates of retained gastric contents than non-users (odds ratio [OR], 5.56), a finding that held steady (OR, 4.20) after adjusting for age, sex, diabetes, body mass index, and other therapies. 

GLP-1RAs were also associated with an increased likelihood of aborted procedures (OR, 5.13; 1% vs. 0.3%) and a higher need for repeat endoscopies (OR, 2.19; 1% vs 2%); however, Facciorusso and colleagues noted that these events, in absolute terms, were relatively uncommon.

“The rate of aborted and repeat procedures in the included studies was low,” the investigators wrote. “This meant that only for every 110 patients undergoing upper endoscopy while in GLP-1RA therapy would we observe an aborted procedure and only for every 120 patients would we need to repeat the procedure.”

The overall safety profile of GLP-1RAs in the context of upper endoscopy remained largely reassuring, they added. Specifically, rates of bronchial aspiration were not significantly different between users and non-users. What’s more, no single study reported a statistically significant increase in major complications, including pulmonary adverse events, among GLP-1RA users. 

According to Facciorusso and colleagues, these findings suggest that retained gastric contents do not appear to substantially heighten the risk of serious harm, though further prospective studies are needed.

“Our comprehensive analysis indicates that, while the use of GLP-1RA results in higher rates of [retained gastric contents], the actual clinical impact appears to be limited,” they wrote. “Therefore, there is no strong evidence to support the routine discontinuation of the drug before upper endoscopy procedures.”

Instead, they supported the AGA task force’s recommendation for an individualized approach, and not withholding GLP-1RAs unnecessarily, calling this “the best compromise.”

“Prolonging the duration of fasting for solids could represent the optimal approach in these patients, although this strategy requires further evaluation,” the investigators concluded.

The investigators disclosed no conflicts of interest.







 

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are associated with retained gastric contents and aborted procedures among patients undergoing upper endoscopy, according to a meta-analysis of more than 80,000 patients.

Safety profiles, however, were comparable across groups, suggesting that prolonged fasting may be a sufficient management strategy, instead of withholding GLP-1RAs, lead author Antonio Facciorusso, MD, PhD, of the University of Foggia, Italy, and colleagues reported.

“The impact of GLP-1RAs on slowing gastric motility has raised concerns in patients undergoing endoscopic procedures, particularly upper endoscopies,” the investigators wrote in Clinical Gastroenterology and Hepatology. “This is due to the perceived risk of aspiration of retained gastric contents in sedated patients and the decreased visibility of the gastric mucosa, which can reduce the diagnostic yield of the examination.”

The American Society of Anesthesiologists (ASA) recommends withholding GLP-1RAs before procedures or surgery, whereas AGA suggests an individualized approach, citing limited supporting data. 

A previous meta-analysis reported that GLP-1RAs mildly delayed gastric emptying, but clinical relevance remained unclear. 

The present meta-analysis aimed to clarify this uncertainty by analyzing 13 retrospective studies that involved 84,065 patients undergoing upper endoscopy. Outcomes were compared among GLP-1RA users vs non-users, including rates of retained gastric contents, aborted procedures, and adverse events. 

Patients on GLP-1RAs had significantly higher rates of retained gastric contents than non-users (odds ratio [OR], 5.56), a finding that held steady (OR, 4.20) after adjusting for age, sex, diabetes, body mass index, and other therapies. 

GLP-1RAs were also associated with an increased likelihood of aborted procedures (OR, 5.13; 1% vs. 0.3%) and a higher need for repeat endoscopies (OR, 2.19; 1% vs 2%); however, Facciorusso and colleagues noted that these events, in absolute terms, were relatively uncommon.

“The rate of aborted and repeat procedures in the included studies was low,” the investigators wrote. “This meant that only for every 110 patients undergoing upper endoscopy while in GLP-1RA therapy would we observe an aborted procedure and only for every 120 patients would we need to repeat the procedure.”

The overall safety profile of GLP-1RAs in the context of upper endoscopy remained largely reassuring, they added. Specifically, rates of bronchial aspiration were not significantly different between users and non-users. What’s more, no single study reported a statistically significant increase in major complications, including pulmonary adverse events, among GLP-1RA users. 

According to Facciorusso and colleagues, these findings suggest that retained gastric contents do not appear to substantially heighten the risk of serious harm, though further prospective studies are needed.

“Our comprehensive analysis indicates that, while the use of GLP-1RA results in higher rates of [retained gastric contents], the actual clinical impact appears to be limited,” they wrote. “Therefore, there is no strong evidence to support the routine discontinuation of the drug before upper endoscopy procedures.”

Instead, they supported the AGA task force’s recommendation for an individualized approach, and not withholding GLP-1RAs unnecessarily, calling this “the best compromise.”

“Prolonging the duration of fasting for solids could represent the optimal approach in these patients, although this strategy requires further evaluation,” the investigators concluded.

The investigators disclosed no conflicts of interest.







 

Placing two cystic duct stents instead of one during endoscopic transpapillary gallbladder drainage (ETGBD) is associated with a lower rate of unplanned reintervention, according to a retrospective multicenter study.

These findings suggest that endoscopists should prioritize dual stent placement when feasible, and consider adding a second stent in patients who previously received a single stent, James D. Haddad, MD, of the University of Texas Southwestern, Dallas, and colleagues reported.

 

The American Gastroenterological Association (AGA) has recognized the role of endoscopic drainage in managing acute cholecystitis in high-risk patients, but specific guidance on optimal technique and follow-up remains unclear, the investigators wrote in Techniques and Innovations in Gastrointestinal Endoscopy.

“Despite accumulating data and increased interest in this technique, clear guidance on the ideal strategy for ETGBD is lacking,” Dr. Haddad and colleagues wrote. “For example, the optimal size, number, and follow-up of cystic duct stents for patients undergoing ETGBD has not been well established.”

To address this knowledge gap, the investigators analyzed data from 75 patients at five academic medical centers who had undergone ETGBD between June 2013 and October 2022. Patients were divided into two groups based on whether they received one or two cystic duct stents. 

The primary outcome was clinical success, defined as symptom resolution without requiring another drainage procedure. Secondary outcomes included technical success (defined as successful stent placement), along with rates of adverse events and unplanned reinterventions. 

Out of the 75 patients, 59 received a single stent, while 16 received dual stents. The median follow-up time was 407 days overall, with a longer follow-up in the single-stent group (433 days), compared with the double-stent group (118 days).

Clinical success was reported in 81.3% of cases, which technical success was achieved in 88.2% of cases. 

Patients who received two stents had significantly lower rates of unplanned reintervention, compared with those who received a single stent (0% vs 25.4%; P = .02). The median time to unplanned reintervention in the single-stent group was 210 days.

Use of a 7 French stent was strongly associated with placement of two stents (odd ratio [OR], 15.5; P = .01). Similarly, patients with a prior percutaneous cholecystostomy tube were significantly more likely to have two stents placed (OR, 10.8; P = .001).

Adverse event rates were uncommon and not statistically different between groups, with an overall rate of 6.7%. Post-endoscopic retrograde cholangiopancreatography pancreatitis was the most common adverse event, occurring in two patients in the single-stent group and one patient in the double-stent group. There were no reported cases of cystic duct or gallbladder perforation.

“In conclusion,” the investigators wrote, “ETGBD with dual transpapillary gallbladder stenting is associated with a lower rate of unplanned reinterventions, compared with that with single stenting, and has a low rate of adverse events. Endoscopists performing ETGBD should consider planned exchange of solitary transpapillary gallbladder stents or interval ERCP for reattempted placement of a second stent if placement of two stents is not possible at the index ERCP.”

The investigators disclosed relationships with Boston Scientific, Motus GI, and ConMed.







 

Placing two cystic duct stents instead of one during endoscopic transpapillary gallbladder drainage (ETGBD) is associated with a lower rate of unplanned reintervention, according to a retrospective multicenter study.

These findings suggest that endoscopists should prioritize dual stent placement when feasible, and consider adding a second stent in patients who previously received a single stent, James D. Haddad, MD, of the University of Texas Southwestern, Dallas, and colleagues reported.

 

The American Gastroenterological Association (AGA) has recognized the role of endoscopic drainage in managing acute cholecystitis in high-risk patients, but specific guidance on optimal technique and follow-up remains unclear, the investigators wrote in Techniques and Innovations in Gastrointestinal Endoscopy.

“Despite accumulating data and increased interest in this technique, clear guidance on the ideal strategy for ETGBD is lacking,” Dr. Haddad and colleagues wrote. “For example, the optimal size, number, and follow-up of cystic duct stents for patients undergoing ETGBD has not been well established.”

To address this knowledge gap, the investigators analyzed data from 75 patients at five academic medical centers who had undergone ETGBD between June 2013 and October 2022. Patients were divided into two groups based on whether they received one or two cystic duct stents. 

The primary outcome was clinical success, defined as symptom resolution without requiring another drainage procedure. Secondary outcomes included technical success (defined as successful stent placement), along with rates of adverse events and unplanned reinterventions. 

Out of the 75 patients, 59 received a single stent, while 16 received dual stents. The median follow-up time was 407 days overall, with a longer follow-up in the single-stent group (433 days), compared with the double-stent group (118 days).

Clinical success was reported in 81.3% of cases, which technical success was achieved in 88.2% of cases. 

Patients who received two stents had significantly lower rates of unplanned reintervention, compared with those who received a single stent (0% vs 25.4%; P = .02). The median time to unplanned reintervention in the single-stent group was 210 days.

Use of a 7 French stent was strongly associated with placement of two stents (odd ratio [OR], 15.5; P = .01). Similarly, patients with a prior percutaneous cholecystostomy tube were significantly more likely to have two stents placed (OR, 10.8; P = .001).

Adverse event rates were uncommon and not statistically different between groups, with an overall rate of 6.7%. Post-endoscopic retrograde cholangiopancreatography pancreatitis was the most common adverse event, occurring in two patients in the single-stent group and one patient in the double-stent group. There were no reported cases of cystic duct or gallbladder perforation.

“In conclusion,” the investigators wrote, “ETGBD with dual transpapillary gallbladder stenting is associated with a lower rate of unplanned reinterventions, compared with that with single stenting, and has a low rate of adverse events. Endoscopists performing ETGBD should consider planned exchange of solitary transpapillary gallbladder stents or interval ERCP for reattempted placement of a second stent if placement of two stents is not possible at the index ERCP.”

The investigators disclosed relationships with Boston Scientific, Motus GI, and ConMed.







 

Placing two cystic duct stents instead of one during endoscopic transpapillary gallbladder drainage (ETGBD) is associated with a lower rate of unplanned reintervention, according to a retrospective multicenter study.

These findings suggest that endoscopists should prioritize dual stent placement when feasible, and consider adding a second stent in patients who previously received a single stent, James D. Haddad, MD, of the University of Texas Southwestern, Dallas, and colleagues reported.

 

The American Gastroenterological Association (AGA) has recognized the role of endoscopic drainage in managing acute cholecystitis in high-risk patients, but specific guidance on optimal technique and follow-up remains unclear, the investigators wrote in Techniques and Innovations in Gastrointestinal Endoscopy.

“Despite accumulating data and increased interest in this technique, clear guidance on the ideal strategy for ETGBD is lacking,” Dr. Haddad and colleagues wrote. “For example, the optimal size, number, and follow-up of cystic duct stents for patients undergoing ETGBD has not been well established.”

To address this knowledge gap, the investigators analyzed data from 75 patients at five academic medical centers who had undergone ETGBD between June 2013 and October 2022. Patients were divided into two groups based on whether they received one or two cystic duct stents. 

The primary outcome was clinical success, defined as symptom resolution without requiring another drainage procedure. Secondary outcomes included technical success (defined as successful stent placement), along with rates of adverse events and unplanned reinterventions. 

Out of the 75 patients, 59 received a single stent, while 16 received dual stents. The median follow-up time was 407 days overall, with a longer follow-up in the single-stent group (433 days), compared with the double-stent group (118 days).

Clinical success was reported in 81.3% of cases, which technical success was achieved in 88.2% of cases. 

Patients who received two stents had significantly lower rates of unplanned reintervention, compared with those who received a single stent (0% vs 25.4%; P = .02). The median time to unplanned reintervention in the single-stent group was 210 days.

Use of a 7 French stent was strongly associated with placement of two stents (odd ratio [OR], 15.5; P = .01). Similarly, patients with a prior percutaneous cholecystostomy tube were significantly more likely to have two stents placed (OR, 10.8; P = .001).

Adverse event rates were uncommon and not statistically different between groups, with an overall rate of 6.7%. Post-endoscopic retrograde cholangiopancreatography pancreatitis was the most common adverse event, occurring in two patients in the single-stent group and one patient in the double-stent group. There were no reported cases of cystic duct or gallbladder perforation.

“In conclusion,” the investigators wrote, “ETGBD with dual transpapillary gallbladder stenting is associated with a lower rate of unplanned reinterventions, compared with that with single stenting, and has a low rate of adverse events. Endoscopists performing ETGBD should consider planned exchange of solitary transpapillary gallbladder stents or interval ERCP for reattempted placement of a second stent if placement of two stents is not possible at the index ERCP.”

The investigators disclosed relationships with Boston Scientific, Motus GI, and ConMed.







 

Circulating blood proteins could enable early identification of Crohn’s disease (CD) years before clinical signs, according to investigators.

The 29-protein biosignature, which was validated across multiple independent cohorts, could potentially open doors to new preclinical interventions, lead author Olle Grännö, MD, of Örebro University in Sweden, and colleagues reported. 

“Predictive biomarkers of future clinical onset of active inflammatory bowel disease could detect the disease during ‘a window of opportunity’ when the immune dysregulation is potentially reversible,” the investigators wrote in Gastroenterology.

Preclinical biomarker screening has proven effective in other immune-mediated diseases, such as type 1 diabetes, where risk stratification using autoantibodies enabled early intervention that delayed disease onset, they noted. 

Previous studies suggested similar potential for inflammatory bowel disease (IBD) via predictive autoantibodies and serum proteins, although the accuracy of these markers was not validated in external cohorts. The present study aimed to fill this validation gap.

First, the investigators measured 178 plasma proteins in blood samples taken from 312 individuals before they were diagnosed with IBD. Using machine learning, Dr. Grännö and colleagues compared these findings with blood-matched controls who remained free of IBD through follow-up. This process revealed the 29-protein signature. 

In the same discovery cohort, the panel of 29 proteins differentiated preclinical CD cases from controls with an area under the curve (AUC) of 0.85. The signature was then validated in an independent preclinical cohort of CD patients, with an AUC of 0.87. 

While accuracy increased in proximity to clinical disease onset, the model was still highly predictive up to 16 years before CD diagnosis, at which time the AUC was 0.82. The panel showed perfect performance among newly diagnosed CD patients, with an AUC of 1.0, supporting clinical relevance.

Predictive power was statistically significant but less compelling among individuals with preclinical ulcerative colitis (UC). In this IBD subgroup, AUC for identification and validation cohorts was 0.77 and 0.67, respectively, while newly diagnosed patients had an AUC of 0.95.

“In preclinical samples, downregulated (but not upregulated) proteins related to gut barrier integrity and macrophage functionality correlated with time to diagnosis of CD,” Dr. Grännö and colleagues wrote. “Contrarily, all proteins associated with preclinical UC were upregulated, and only one protein marker correlated with the time to diagnosis.”

These findings suggest that disruptions in gut barrier integrity and macrophage function precede clinical CD onset, they explained, potentially serving as an early signal of inflammation-driven intestinal damage. In contrast, the preclinical UC signature primarily involved upregulated inflammatory markers.

Dr. Grännö and colleagues also examined the influence of genetic and environmental factors by comparing preclinical IBD signatures in unrelated and related twin pairs. 

The CD biosignature had an AUC of 0.89 when comparing individuals with preclinical CD to matched external (unrelated) healthy twins. Predictive ability dropped significantly (AUC = 0.58) when comparing CD cases to their own healthy twin siblings, suggesting that genetic and shared environmental factors have a “predominant influence” on protein dysregulation. 

In contrast, AUC among unrelated vs related twin controls was more similar for UC, at 0.76 and 0.64, respectively, indicating “a limited impact” of genetic and environmental factors on the protein signature.

Altogether, this study reinforces the concept of a long preclinical phase in CD, and highlights the potential for early detection and intervention, according to the investigators.

“The long preclinical period in CD endorses the adoption of early preventive strategies (e.g., diet alterations and medication) to potentially attenuate disease progression and improve the natural history of CD,” they concluded.

This study was funded by the Swedish Research Council, the Swedish Foundation for Strategic Research, the Örebro University Hospital Research Foundation, and others. The investigators disclosed relationships with Pfizer, Janssen, AbbVie, and others.

Circulating blood proteins could enable early identification of Crohn’s disease (CD) years before clinical signs, according to investigators.

The 29-protein biosignature, which was validated across multiple independent cohorts, could potentially open doors to new preclinical interventions, lead author Olle Grännö, MD, of Örebro University in Sweden, and colleagues reported. 

“Predictive biomarkers of future clinical onset of active inflammatory bowel disease could detect the disease during ‘a window of opportunity’ when the immune dysregulation is potentially reversible,” the investigators wrote in Gastroenterology.

Preclinical biomarker screening has proven effective in other immune-mediated diseases, such as type 1 diabetes, where risk stratification using autoantibodies enabled early intervention that delayed disease onset, they noted. 

Previous studies suggested similar potential for inflammatory bowel disease (IBD) via predictive autoantibodies and serum proteins, although the accuracy of these markers was not validated in external cohorts. The present study aimed to fill this validation gap.

First, the investigators measured 178 plasma proteins in blood samples taken from 312 individuals before they were diagnosed with IBD. Using machine learning, Dr. Grännö and colleagues compared these findings with blood-matched controls who remained free of IBD through follow-up. This process revealed the 29-protein signature. 

In the same discovery cohort, the panel of 29 proteins differentiated preclinical CD cases from controls with an area under the curve (AUC) of 0.85. The signature was then validated in an independent preclinical cohort of CD patients, with an AUC of 0.87. 

While accuracy increased in proximity to clinical disease onset, the model was still highly predictive up to 16 years before CD diagnosis, at which time the AUC was 0.82. The panel showed perfect performance among newly diagnosed CD patients, with an AUC of 1.0, supporting clinical relevance.

Predictive power was statistically significant but less compelling among individuals with preclinical ulcerative colitis (UC). In this IBD subgroup, AUC for identification and validation cohorts was 0.77 and 0.67, respectively, while newly diagnosed patients had an AUC of 0.95.

“In preclinical samples, downregulated (but not upregulated) proteins related to gut barrier integrity and macrophage functionality correlated with time to diagnosis of CD,” Dr. Grännö and colleagues wrote. “Contrarily, all proteins associated with preclinical UC were upregulated, and only one protein marker correlated with the time to diagnosis.”

These findings suggest that disruptions in gut barrier integrity and macrophage function precede clinical CD onset, they explained, potentially serving as an early signal of inflammation-driven intestinal damage. In contrast, the preclinical UC signature primarily involved upregulated inflammatory markers.

Dr. Grännö and colleagues also examined the influence of genetic and environmental factors by comparing preclinical IBD signatures in unrelated and related twin pairs. 

The CD biosignature had an AUC of 0.89 when comparing individuals with preclinical CD to matched external (unrelated) healthy twins. Predictive ability dropped significantly (AUC = 0.58) when comparing CD cases to their own healthy twin siblings, suggesting that genetic and shared environmental factors have a “predominant influence” on protein dysregulation. 

In contrast, AUC among unrelated vs related twin controls was more similar for UC, at 0.76 and 0.64, respectively, indicating “a limited impact” of genetic and environmental factors on the protein signature.

Altogether, this study reinforces the concept of a long preclinical phase in CD, and highlights the potential for early detection and intervention, according to the investigators.

“The long preclinical period in CD endorses the adoption of early preventive strategies (e.g., diet alterations and medication) to potentially attenuate disease progression and improve the natural history of CD,” they concluded.

This study was funded by the Swedish Research Council, the Swedish Foundation for Strategic Research, the Örebro University Hospital Research Foundation, and others. The investigators disclosed relationships with Pfizer, Janssen, AbbVie, and others.

Circulating blood proteins could enable early identification of Crohn’s disease (CD) years before clinical signs, according to investigators.

The 29-protein biosignature, which was validated across multiple independent cohorts, could potentially open doors to new preclinical interventions, lead author Olle Grännö, MD, of Örebro University in Sweden, and colleagues reported. 

“Predictive biomarkers of future clinical onset of active inflammatory bowel disease could detect the disease during ‘a window of opportunity’ when the immune dysregulation is potentially reversible,” the investigators wrote in Gastroenterology.

Preclinical biomarker screening has proven effective in other immune-mediated diseases, such as type 1 diabetes, where risk stratification using autoantibodies enabled early intervention that delayed disease onset, they noted. 

Previous studies suggested similar potential for inflammatory bowel disease (IBD) via predictive autoantibodies and serum proteins, although the accuracy of these markers was not validated in external cohorts. The present study aimed to fill this validation gap.

First, the investigators measured 178 plasma proteins in blood samples taken from 312 individuals before they were diagnosed with IBD. Using machine learning, Dr. Grännö and colleagues compared these findings with blood-matched controls who remained free of IBD through follow-up. This process revealed the 29-protein signature. 

In the same discovery cohort, the panel of 29 proteins differentiated preclinical CD cases from controls with an area under the curve (AUC) of 0.85. The signature was then validated in an independent preclinical cohort of CD patients, with an AUC of 0.87. 

While accuracy increased in proximity to clinical disease onset, the model was still highly predictive up to 16 years before CD diagnosis, at which time the AUC was 0.82. The panel showed perfect performance among newly diagnosed CD patients, with an AUC of 1.0, supporting clinical relevance.

Predictive power was statistically significant but less compelling among individuals with preclinical ulcerative colitis (UC). In this IBD subgroup, AUC for identification and validation cohorts was 0.77 and 0.67, respectively, while newly diagnosed patients had an AUC of 0.95.

“In preclinical samples, downregulated (but not upregulated) proteins related to gut barrier integrity and macrophage functionality correlated with time to diagnosis of CD,” Dr. Grännö and colleagues wrote. “Contrarily, all proteins associated with preclinical UC were upregulated, and only one protein marker correlated with the time to diagnosis.”

These findings suggest that disruptions in gut barrier integrity and macrophage function precede clinical CD onset, they explained, potentially serving as an early signal of inflammation-driven intestinal damage. In contrast, the preclinical UC signature primarily involved upregulated inflammatory markers.

Dr. Grännö and colleagues also examined the influence of genetic and environmental factors by comparing preclinical IBD signatures in unrelated and related twin pairs. 

The CD biosignature had an AUC of 0.89 when comparing individuals with preclinical CD to matched external (unrelated) healthy twins. Predictive ability dropped significantly (AUC = 0.58) when comparing CD cases to their own healthy twin siblings, suggesting that genetic and shared environmental factors have a “predominant influence” on protein dysregulation. 

In contrast, AUC among unrelated vs related twin controls was more similar for UC, at 0.76 and 0.64, respectively, indicating “a limited impact” of genetic and environmental factors on the protein signature.

Altogether, this study reinforces the concept of a long preclinical phase in CD, and highlights the potential for early detection and intervention, according to the investigators.

“The long preclinical period in CD endorses the adoption of early preventive strategies (e.g., diet alterations and medication) to potentially attenuate disease progression and improve the natural history of CD,” they concluded.

This study was funded by the Swedish Research Council, the Swedish Foundation for Strategic Research, the Örebro University Hospital Research Foundation, and others. The investigators disclosed relationships with Pfizer, Janssen, AbbVie, and others.