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Based on discussions during PancreasFest 2021, , according to a recent report in Gastro Hep Advances
Due to its complex and individualized nature, EPI requires multidisciplinary approaches to therapy, as well as better pancreas function tests and biomarkers for diagnosis and treatment, wrote researchers who were led by David C. Whitcomb, MD, PhD, AGAF, emeritus professor of medicine in the division of gastroenterology, hepatology and nutrition at the University of Pittsburgh.
“This condition remains challenging even to define, and serious limitations in diagnostic testing and therapeutic options lead to clinical confusion and frequently less than optimal patient management,” the authors wrote.
EPI is clinically defined as inadequate delivery of pancreatic digestive enzymes to meet nutritional needs, which is typically based on a physician’s assessment of a patient’s maldigestion. However, there’s not a universally accepted definition or a precise threshold of reduced pancreatic digestive enzymes that indicates “pancreatic insufficiency” in an individual patient.
Current guidelines also don’t clearly outline the role of pancreatic function tests, the effects of different metabolic needs and nutrition intake, the timing of pancreatic enzyme replacement therapy (PERT), or the best practices for monitoring or titrating multiple therapies.
In response, Dr. Whitcomb and colleagues proposed a new mechanistic definition of EPI, including the disorder’s physiologic effects and impact on health. First, they said, EPI is a disorder caused by failure of the pancreas to deliver a minimum or threshold level of specific pancreatic digestive enzymes to the intestine in concert with ingested nutrients, followed by enzymatic digestion of individual meals over time to meet certain nutritional and metabolic needs. In addition, the disorder is characterized by variable deficiencies in micronutrients and macronutrients, especially essential fats and fat-soluble vitamins, as well as gastrointestinal symptoms of nutrient maldigestion.
The threshold for EPI should consider the nutritional needs of the patient, dietary intake, residual exocrine pancreas function, and the absorptive capacity of the intestine based on anatomy, mucosal function, motility, inflammation, the microbiome, and physiological adaptation, the authors wrote.
Due to challenges in diagnosing EPI and its common chronic symptoms such as abdominal pain, bloating, and diarrhea, several conditions may mimic EPI, be present concomitantly with EPI, or hinder PERT response. These include celiac disease, small intestinal bacterial overgrowth, disaccharidase deficiencies, inflammatory bowel disease (IBD), bile acid diarrhea, giardiasis, diabetes mellitus, and functional conditions such as irritable bowel syndrome. These conditions should be considered to address underlying pathology and PERT diagnostic challenges.
Although there is consensus that exocrine pancreatic function testing (PFT) is important to diagnosis EPI, no optimal test exists, and pancreatic function is only one aspect of digestion and absorption that should be considered. PFT may be needed to make an objective EPI diagnosis related to acute pancreatitis, pancreatic cancer, pancreatic resection, gastric resection, cystic fibrosis, or IBD. Direct or indirect PFTs may be used, which typically differs by center.
“The medical community still awaits a clinically useful pancreas function test that is easy to perform, well tolerated by patients, and allows personalized dosing of PERT,” the authors wrote.
After diagnosis, a general assessment should include information about symptoms, nutritional status, medications, diet, and lifestyle. This information can be used for a multifaceted treatment approach, with a focus on lifestyle changes, concomitant disease treatment, optimized diet, dietary supplements, and PERT administration.
PERT remains a mainstay of EPI treatment and has shown improvements in steatorrhea, postprandial bloating and pain, nutrition, and unexplained weight loss. The Food and Drug Administration has approved several formulations in different strengths. The typical starting dose is based on age and weight, which is derived from guidelines for EPI treatment in patients with cystic fibrosis. However, the recommendations don’t consider many of the variables discussed above and simply provide an estimate for the average subject with severe EPI, so the dose should be titrated as needed based on age, weight, symptoms, and the holistic management plan.
For optimal results, regular follow-up is necessary to monitor compliance and treatment response. A reduction in symptoms can serve as a reliable indicator of effective EPI management, particularly weight stabilization, improved steatorrhea and diarrhea, and reduced postprandial bloating, pain, and flatulence. Physicians may provide patients with tracking tools to record their PERT compliance, symptom frequency, and lifestyle changes.
For patients with persistent concerns, PERT can be increased as needed. Although many PERT formulations are enteric coated, a proton pump inhibitor or H2 receptor agonist may improve their effectiveness. If EPI symptoms persist despite increased doses, other causes of malabsorption should be considered, such as the concomitant conditions mentioned above.
“As EPI escalates, a lower fat diet may become necessary to alleviate distressing gastrointestinal symptoms,” the authors wrote. “A close working relationship between the treating provider and the [registered dietician] is crucial so that barriers to optimum nutrient assimilation can be identified, communicated, and overcome. Frequent monitoring of the nutritional state with therapy is also imperative.”
PancreasFest 2021 received no specific funding for this event. The authors declared grant support, adviser roles, and speaking honoraria from several pharmaceutical and medical device companies and health care foundations, including the National Pancreas Foundation.
Recognition of recent advances and unaddressed gaps can clarify key issues around exocrine pancreatic insufficiency (EPI).
The loss of pancreatic digestive enzymes and bicarbonate is caused by exocrine pancreatic and proximal small intestine disease. EPI’s clinical impact has been expanded by reports that 30% of subjects can develop EPI after a bout of acute pancreatitis. Diagnosing and treating EPI challenges clinicians and investigators.
The contribution on EPI by Whitcomb and colleagues provides state-of-the-art content relating to diagnosing EPI, assessing its metabolic impact, enzyme replacement, nutritional considerations, and how to assess the effectiveness of therapy.
Though the diagnosis and treatment of EPI have been examined for over 50 years, a consensus for either is still needed. Assessment of EPI with luminal tube tests and endoscopic collections of pancreatic secretion are the most accurate, but they are invasive, limited in availability, and time-consuming. Indirect assays of intestinal activities of pancreatic enzymes by the hydrolysis of substrates or stool excretion are frequently used to diagnose EPI. However, they need to be more insensitive and specific to meet clinical and investigative needs.
Indeed, all tests of exocrine secretion are surrogates of unclear value for the critical endpoint of EPI, its nutritional impact. An unmet need is the development of nutritional standards for assessing EPI and measures for the adequacy of pancreatic enzyme replacement therapy. In this context, a patient’s diet, and other factors, such as the intestinal microbiome, can affect pancreatic digestive enzyme activity and must be considered in designing the best EPI treatments. The summary concludes with a thoughtful and valuable road map for moving forward.
Fred Sanford Gorelick, MD, is the Henry J. and Joan W. Binder Professor of Medicine (Digestive Diseases) and of Cell Biology for Yale School of Medicine, New Haven, Conn. He also serves as director of the Yale School of Medicine NIH T32-funded research track in gastroenterology; and as deputy director of Yale School of Medicine MD-PhD program.
Potential conflicts: Dr. Gorelick serves as chair of NIH NIDDK DSMB for Stent vs. Indomethacin for Preventing Post-ERCP Pancreatitis (SVI) study. He also holds grants for research on mechanisms of acute pancreatitis from the U.S. Department of Veterans Affairs and the Department of Defense.
Recognition of recent advances and unaddressed gaps can clarify key issues around exocrine pancreatic insufficiency (EPI).
The loss of pancreatic digestive enzymes and bicarbonate is caused by exocrine pancreatic and proximal small intestine disease. EPI’s clinical impact has been expanded by reports that 30% of subjects can develop EPI after a bout of acute pancreatitis. Diagnosing and treating EPI challenges clinicians and investigators.
The contribution on EPI by Whitcomb and colleagues provides state-of-the-art content relating to diagnosing EPI, assessing its metabolic impact, enzyme replacement, nutritional considerations, and how to assess the effectiveness of therapy.
Though the diagnosis and treatment of EPI have been examined for over 50 years, a consensus for either is still needed. Assessment of EPI with luminal tube tests and endoscopic collections of pancreatic secretion are the most accurate, but they are invasive, limited in availability, and time-consuming. Indirect assays of intestinal activities of pancreatic enzymes by the hydrolysis of substrates or stool excretion are frequently used to diagnose EPI. However, they need to be more insensitive and specific to meet clinical and investigative needs.
Indeed, all tests of exocrine secretion are surrogates of unclear value for the critical endpoint of EPI, its nutritional impact. An unmet need is the development of nutritional standards for assessing EPI and measures for the adequacy of pancreatic enzyme replacement therapy. In this context, a patient’s diet, and other factors, such as the intestinal microbiome, can affect pancreatic digestive enzyme activity and must be considered in designing the best EPI treatments. The summary concludes with a thoughtful and valuable road map for moving forward.
Fred Sanford Gorelick, MD, is the Henry J. and Joan W. Binder Professor of Medicine (Digestive Diseases) and of Cell Biology for Yale School of Medicine, New Haven, Conn. He also serves as director of the Yale School of Medicine NIH T32-funded research track in gastroenterology; and as deputy director of Yale School of Medicine MD-PhD program.
Potential conflicts: Dr. Gorelick serves as chair of NIH NIDDK DSMB for Stent vs. Indomethacin for Preventing Post-ERCP Pancreatitis (SVI) study. He also holds grants for research on mechanisms of acute pancreatitis from the U.S. Department of Veterans Affairs and the Department of Defense.
Recognition of recent advances and unaddressed gaps can clarify key issues around exocrine pancreatic insufficiency (EPI).
The loss of pancreatic digestive enzymes and bicarbonate is caused by exocrine pancreatic and proximal small intestine disease. EPI’s clinical impact has been expanded by reports that 30% of subjects can develop EPI after a bout of acute pancreatitis. Diagnosing and treating EPI challenges clinicians and investigators.
The contribution on EPI by Whitcomb and colleagues provides state-of-the-art content relating to diagnosing EPI, assessing its metabolic impact, enzyme replacement, nutritional considerations, and how to assess the effectiveness of therapy.
Though the diagnosis and treatment of EPI have been examined for over 50 years, a consensus for either is still needed. Assessment of EPI with luminal tube tests and endoscopic collections of pancreatic secretion are the most accurate, but they are invasive, limited in availability, and time-consuming. Indirect assays of intestinal activities of pancreatic enzymes by the hydrolysis of substrates or stool excretion are frequently used to diagnose EPI. However, they need to be more insensitive and specific to meet clinical and investigative needs.
Indeed, all tests of exocrine secretion are surrogates of unclear value for the critical endpoint of EPI, its nutritional impact. An unmet need is the development of nutritional standards for assessing EPI and measures for the adequacy of pancreatic enzyme replacement therapy. In this context, a patient’s diet, and other factors, such as the intestinal microbiome, can affect pancreatic digestive enzyme activity and must be considered in designing the best EPI treatments. The summary concludes with a thoughtful and valuable road map for moving forward.
Fred Sanford Gorelick, MD, is the Henry J. and Joan W. Binder Professor of Medicine (Digestive Diseases) and of Cell Biology for Yale School of Medicine, New Haven, Conn. He also serves as director of the Yale School of Medicine NIH T32-funded research track in gastroenterology; and as deputy director of Yale School of Medicine MD-PhD program.
Potential conflicts: Dr. Gorelick serves as chair of NIH NIDDK DSMB for Stent vs. Indomethacin for Preventing Post-ERCP Pancreatitis (SVI) study. He also holds grants for research on mechanisms of acute pancreatitis from the U.S. Department of Veterans Affairs and the Department of Defense.
Based on discussions during PancreasFest 2021, , according to a recent report in Gastro Hep Advances
Due to its complex and individualized nature, EPI requires multidisciplinary approaches to therapy, as well as better pancreas function tests and biomarkers for diagnosis and treatment, wrote researchers who were led by David C. Whitcomb, MD, PhD, AGAF, emeritus professor of medicine in the division of gastroenterology, hepatology and nutrition at the University of Pittsburgh.
“This condition remains challenging even to define, and serious limitations in diagnostic testing and therapeutic options lead to clinical confusion and frequently less than optimal patient management,” the authors wrote.
EPI is clinically defined as inadequate delivery of pancreatic digestive enzymes to meet nutritional needs, which is typically based on a physician’s assessment of a patient’s maldigestion. However, there’s not a universally accepted definition or a precise threshold of reduced pancreatic digestive enzymes that indicates “pancreatic insufficiency” in an individual patient.
Current guidelines also don’t clearly outline the role of pancreatic function tests, the effects of different metabolic needs and nutrition intake, the timing of pancreatic enzyme replacement therapy (PERT), or the best practices for monitoring or titrating multiple therapies.
In response, Dr. Whitcomb and colleagues proposed a new mechanistic definition of EPI, including the disorder’s physiologic effects and impact on health. First, they said, EPI is a disorder caused by failure of the pancreas to deliver a minimum or threshold level of specific pancreatic digestive enzymes to the intestine in concert with ingested nutrients, followed by enzymatic digestion of individual meals over time to meet certain nutritional and metabolic needs. In addition, the disorder is characterized by variable deficiencies in micronutrients and macronutrients, especially essential fats and fat-soluble vitamins, as well as gastrointestinal symptoms of nutrient maldigestion.
The threshold for EPI should consider the nutritional needs of the patient, dietary intake, residual exocrine pancreas function, and the absorptive capacity of the intestine based on anatomy, mucosal function, motility, inflammation, the microbiome, and physiological adaptation, the authors wrote.
Due to challenges in diagnosing EPI and its common chronic symptoms such as abdominal pain, bloating, and diarrhea, several conditions may mimic EPI, be present concomitantly with EPI, or hinder PERT response. These include celiac disease, small intestinal bacterial overgrowth, disaccharidase deficiencies, inflammatory bowel disease (IBD), bile acid diarrhea, giardiasis, diabetes mellitus, and functional conditions such as irritable bowel syndrome. These conditions should be considered to address underlying pathology and PERT diagnostic challenges.
Although there is consensus that exocrine pancreatic function testing (PFT) is important to diagnosis EPI, no optimal test exists, and pancreatic function is only one aspect of digestion and absorption that should be considered. PFT may be needed to make an objective EPI diagnosis related to acute pancreatitis, pancreatic cancer, pancreatic resection, gastric resection, cystic fibrosis, or IBD. Direct or indirect PFTs may be used, which typically differs by center.
“The medical community still awaits a clinically useful pancreas function test that is easy to perform, well tolerated by patients, and allows personalized dosing of PERT,” the authors wrote.
After diagnosis, a general assessment should include information about symptoms, nutritional status, medications, diet, and lifestyle. This information can be used for a multifaceted treatment approach, with a focus on lifestyle changes, concomitant disease treatment, optimized diet, dietary supplements, and PERT administration.
PERT remains a mainstay of EPI treatment and has shown improvements in steatorrhea, postprandial bloating and pain, nutrition, and unexplained weight loss. The Food and Drug Administration has approved several formulations in different strengths. The typical starting dose is based on age and weight, which is derived from guidelines for EPI treatment in patients with cystic fibrosis. However, the recommendations don’t consider many of the variables discussed above and simply provide an estimate for the average subject with severe EPI, so the dose should be titrated as needed based on age, weight, symptoms, and the holistic management plan.
For optimal results, regular follow-up is necessary to monitor compliance and treatment response. A reduction in symptoms can serve as a reliable indicator of effective EPI management, particularly weight stabilization, improved steatorrhea and diarrhea, and reduced postprandial bloating, pain, and flatulence. Physicians may provide patients with tracking tools to record their PERT compliance, symptom frequency, and lifestyle changes.
For patients with persistent concerns, PERT can be increased as needed. Although many PERT formulations are enteric coated, a proton pump inhibitor or H2 receptor agonist may improve their effectiveness. If EPI symptoms persist despite increased doses, other causes of malabsorption should be considered, such as the concomitant conditions mentioned above.
“As EPI escalates, a lower fat diet may become necessary to alleviate distressing gastrointestinal symptoms,” the authors wrote. “A close working relationship between the treating provider and the [registered dietician] is crucial so that barriers to optimum nutrient assimilation can be identified, communicated, and overcome. Frequent monitoring of the nutritional state with therapy is also imperative.”
PancreasFest 2021 received no specific funding for this event. The authors declared grant support, adviser roles, and speaking honoraria from several pharmaceutical and medical device companies and health care foundations, including the National Pancreas Foundation.
Based on discussions during PancreasFest 2021, , according to a recent report in Gastro Hep Advances
Due to its complex and individualized nature, EPI requires multidisciplinary approaches to therapy, as well as better pancreas function tests and biomarkers for diagnosis and treatment, wrote researchers who were led by David C. Whitcomb, MD, PhD, AGAF, emeritus professor of medicine in the division of gastroenterology, hepatology and nutrition at the University of Pittsburgh.
“This condition remains challenging even to define, and serious limitations in diagnostic testing and therapeutic options lead to clinical confusion and frequently less than optimal patient management,” the authors wrote.
EPI is clinically defined as inadequate delivery of pancreatic digestive enzymes to meet nutritional needs, which is typically based on a physician’s assessment of a patient’s maldigestion. However, there’s not a universally accepted definition or a precise threshold of reduced pancreatic digestive enzymes that indicates “pancreatic insufficiency” in an individual patient.
Current guidelines also don’t clearly outline the role of pancreatic function tests, the effects of different metabolic needs and nutrition intake, the timing of pancreatic enzyme replacement therapy (PERT), or the best practices for monitoring or titrating multiple therapies.
In response, Dr. Whitcomb and colleagues proposed a new mechanistic definition of EPI, including the disorder’s physiologic effects and impact on health. First, they said, EPI is a disorder caused by failure of the pancreas to deliver a minimum or threshold level of specific pancreatic digestive enzymes to the intestine in concert with ingested nutrients, followed by enzymatic digestion of individual meals over time to meet certain nutritional and metabolic needs. In addition, the disorder is characterized by variable deficiencies in micronutrients and macronutrients, especially essential fats and fat-soluble vitamins, as well as gastrointestinal symptoms of nutrient maldigestion.
The threshold for EPI should consider the nutritional needs of the patient, dietary intake, residual exocrine pancreas function, and the absorptive capacity of the intestine based on anatomy, mucosal function, motility, inflammation, the microbiome, and physiological adaptation, the authors wrote.
Due to challenges in diagnosing EPI and its common chronic symptoms such as abdominal pain, bloating, and diarrhea, several conditions may mimic EPI, be present concomitantly with EPI, or hinder PERT response. These include celiac disease, small intestinal bacterial overgrowth, disaccharidase deficiencies, inflammatory bowel disease (IBD), bile acid diarrhea, giardiasis, diabetes mellitus, and functional conditions such as irritable bowel syndrome. These conditions should be considered to address underlying pathology and PERT diagnostic challenges.
Although there is consensus that exocrine pancreatic function testing (PFT) is important to diagnosis EPI, no optimal test exists, and pancreatic function is only one aspect of digestion and absorption that should be considered. PFT may be needed to make an objective EPI diagnosis related to acute pancreatitis, pancreatic cancer, pancreatic resection, gastric resection, cystic fibrosis, or IBD. Direct or indirect PFTs may be used, which typically differs by center.
“The medical community still awaits a clinically useful pancreas function test that is easy to perform, well tolerated by patients, and allows personalized dosing of PERT,” the authors wrote.
After diagnosis, a general assessment should include information about symptoms, nutritional status, medications, diet, and lifestyle. This information can be used for a multifaceted treatment approach, with a focus on lifestyle changes, concomitant disease treatment, optimized diet, dietary supplements, and PERT administration.
PERT remains a mainstay of EPI treatment and has shown improvements in steatorrhea, postprandial bloating and pain, nutrition, and unexplained weight loss. The Food and Drug Administration has approved several formulations in different strengths. The typical starting dose is based on age and weight, which is derived from guidelines for EPI treatment in patients with cystic fibrosis. However, the recommendations don’t consider many of the variables discussed above and simply provide an estimate for the average subject with severe EPI, so the dose should be titrated as needed based on age, weight, symptoms, and the holistic management plan.
For optimal results, regular follow-up is necessary to monitor compliance and treatment response. A reduction in symptoms can serve as a reliable indicator of effective EPI management, particularly weight stabilization, improved steatorrhea and diarrhea, and reduced postprandial bloating, pain, and flatulence. Physicians may provide patients with tracking tools to record their PERT compliance, symptom frequency, and lifestyle changes.
For patients with persistent concerns, PERT can be increased as needed. Although many PERT formulations are enteric coated, a proton pump inhibitor or H2 receptor agonist may improve their effectiveness. If EPI symptoms persist despite increased doses, other causes of malabsorption should be considered, such as the concomitant conditions mentioned above.
“As EPI escalates, a lower fat diet may become necessary to alleviate distressing gastrointestinal symptoms,” the authors wrote. “A close working relationship between the treating provider and the [registered dietician] is crucial so that barriers to optimum nutrient assimilation can be identified, communicated, and overcome. Frequent monitoring of the nutritional state with therapy is also imperative.”
PancreasFest 2021 received no specific funding for this event. The authors declared grant support, adviser roles, and speaking honoraria from several pharmaceutical and medical device companies and health care foundations, including the National Pancreas Foundation.
FROM GASTRO HEP ADVANCES