Exocrine Pancreatic Insufficiency

What characteristics or symptoms do you look for to identify patients who are at risk for exocrine pancreatic insufficiency (EPI)?

Dr. Barkin: The first thing we have to understand is which patient populations we should consider. EPI traditionally has been a disease associated with chronic pancreatitis, and that still makes up the majority of patients. But in addition to those with chronic pancreatitis, we have to think about patients who have had severe acute pancreatitis and who may have had loss of functional pancreatic parenchyma or pancreatic surgery, as well as patients with pancreatic cancer that may cause both ductal obstruction and parenchyma loss.

This might also include patients with foregut surgery who may develop postcibal dyskinesia, meaning they do not get appropriate mixing of the gastric chyme and food contents with the pancreatic enzymes and pancreatic juice in the duodenum. For example, this might be evident in patients who have had a Roux-en-Y gastric bypass, or in patients with untreated celiac disease, who do not get stimulation for pancreatic secretion based on the amount of small bowel mucosal damage.

A series of other conditions may present with EPI, such as inflammatory bowel disease, although these make up the minority of cases. When we think about symptoms, the end symptom of EPI from fat malabsorption is gross steatorrhea. Unfortunately, by the time the patient gets to that point, the cat is out of the bag—especially in patients with chronic pancreatitis. So, we want to try to identify these patients earlier.

Realistically, a series of symptoms can be seen far earlier than gross steatorrhea. In fact, most patients will present with symptoms like increased stool frequency or decreased stool consistency in their daily life. Some abdominal discomfort or bloating may be seen that is associated with maldigestion of  food, among other factors.

In some patients, night vision changes from fat-soluble vitamin deficiencies may be the first or an early presenting symptom if they have other conditions masking their diarrheal symptoms. Patients who do not feel well when they are eating or feel uncomfortable after they eat may avoid certain types of foods. You may see weight loss in these populations because they are avoiding foods, feeling sitophobia, or not appropriately digesting their food.

Unfortunately, even before we see clinically relevant symptoms, we may see micronutrient deficiencies and fat-soluble vitamin deficiencies. That is why it is so important, for example, in the chronic pancreatitis population, to screen these patients on a regular basis for the presence of EPI, whether with symptom questionnaires or by testing.

Can you expand on some of the risk factors and the importance of screening, particularly for malnutrition?

Dr. Barkin: The risk factors usually involve patients who have had some kind of damage to the gland. For example, many patients with cystic fibrosis are actually exocrine pancreatic insufficient from early in life to diagnosis. They have loss of the gland and loss of function at the gland.

Our patients with chronic pancreatitis, who may have had either recurrent acute pancreatitis or chronic pancreatitis for a variety of reasons, are screened for EPI on a regular basis. That may mean that you ask them a symptom questionnaire at each clinic visit and check a fecal elastase level on a regular basis. It is not just the symptoms that we have to worry about; we have to think about the effects of maldigestion on a patient’s weight and nutritional status and the impact of micronutrient deficiencies.

A series of new studies has looked at the impact of exocrine insufficiency. For example, a study from Spain found an increased risk of all-cause mortality with exocrine insufficiency. When we think about metabolic bone disease in this population with exocrine insufficiency, we see that there is decreased bone density and increased risk of pathologic low-trauma fractures. For example, the patient who has fallen from a standing position at home and suddenly has a hip fracture has substantial morbidity and mortality associated with that fracture. The decreases in bone density and increased risk of fracture are reversed when we identify EPI and treat it appropriately.

What is your approach to diagnosing EPI?

Dr. Barkin: For a patient who walks in the door with an obvious diagnosis or prior diagnosis of chronic pancreatitis, it is relatively easy to ask them a series of questions about whether they have symptoms that may be associated with EPI. So, first, I ask them about their bowel habits and stool frequency and consistency.

A couple of years ago, we showed that if you treat a patient with EPI using pancreatic enzyme replacement therapy, their stool consistency and frequency are the two reliable markers that get better. They not only get better, but these improvements directly correlate with objective stool markers of improvement in fat maldigestion.

Obviously, we want improvement in other symptoms—abdominal discomfort, bloating, etc.—but I have to set very realistic expectations for patients. Along with stool frequency and consistency, there should be subsequent improvement of steatorrhea. I talk to them about the importance of taking a multivitamin to prevent those micronutrient deficiencies. We check for micronutrient deficiencies and fat-soluble vitamin deficiencies routinely.

Patients who do not have obvious chronic pancreatitis who get diagnosed with EPI are a little bit harder to parse out. I want to make sure that they do not have celiac disease, or that they do not have a concomitant mimicking symptom that may result in, for example, a low fecal elastase level. I also check for small intestinal bacterial overgrowth (SIBO) as a mimicking condition.

Regarding fecal elastase testing, the gold standard for diagnosis of EPI was historically a 72-hour fecal fat collection on a standardized-fat-intake diet. That required patient confinement in the hospital. It is cumbersome, not widely available, and not realistic in practice.

In some centers, endoscopic pancreatic function testing, secretin-enhanced magnetic resonance cholangiopancreatography (MRCP), or breath testing, as is done in Europe, may be options to help diagnose EPI, but these tests are not widely available. Unfortunately, we do not have a great diagnostic test for exocrine insufficiency. As a result, we use fecal elastase level. If you have a patient who has a high pretest probability of having EPI, it is a relatively good test. If they have a low pretest probability, then a series of false-positive test results may occur in this patient population. That means they may not actually have exocrine insufficiency.

If a diarrheal stool is submitted for testing, a false-positive fecal elastase test may result. That is really key, because I see a number of patients with potentially functional diarrheal symptoms who also have low fecal elastase levels. As a result, they have been labeled as exocrine insufficient when, in fact, they may not actually have the disease, which is why it is so important to understand and think about that.

How do you choose the appropriate approach to managing EPI, and how do you consider the impact it has on the quality of life overall?

Dr. Barkin: There are two key points. The treatment for EPI is not to tell your patient to not eat fat and hope that it gets better. Rather, it is appropriate supplementation of pancreatic enzymes. This is done with pancreatic enzyme replacement therapy. A few FDA-approved medications are on the market. I recommend against the ones that have been labeled as pancreatic enzyme digestive aids that are available online. Those are not pancreatic enzymes; a regulatory push about 15 to 20 years ago got these digestive aids appropriately regulated.

The FDA-approved medications are dosed at approximately 40,000 to 50,000 lipase units per meal to start, according to the guidelines. Some of us may prescribe higher doses than that to start. These are taken with meals and about a half-dose with snacks.

If you have a patient who is taking, for example, two pills per meal or two capsules per meal, it is important that they take one at the very beginning of the meal and one about halfway through the meal. The pills should not be taken a half hour before or a half hour after the meal. The goal is to simulate normal pancreatic function as much as possible to get the food contents mixing.

The pancreatic enzymes come in a coated version that does not require coadministration with proton pump inhibitors or an uncoated version that does require coadministration of proton pump inhibitors to prevent degradation by gastric acid. Patients need to understand that, although they may take a large number of pills per day, adhering to this regimen is important, not only for treating their symptoms, but also for combating long-term morbidity and mortality.

I use the symptomatic response to assess response to therapy because, as discussed, there is a direct correlation between improvements in stool frequency and consistency and objective markers of response to therapy.

If a patient is not responding, we first check to make sure that there are no adherence issues and that they are able to access therapy, because sometimes there are issues with cost or insurance approvals. Second, I make sure that patients are taking it correctly, and that they understand the difference between a meal and a snack. For example, if somebody says, “Oh, I just had a small cheeseburger and that's my snack,” that is actually a meal and may require more enzymes. Once we ensure that those are not issues, I make sure again, as part of my approach, that there are no comorbid conditions that may be driving some of the symptoms, such as celiac disease or SIBO, with SIBO being very common in this population.

Then we have to decide whether we need to change the dose. Do we need to increase the dose? Some of us start a little bit higher than the 40,000 to 50,000 units of lipase per meal, as suggested in some of our national and international guidelines, and go from there.

What characteristics or symptoms do you look for to identify patients who are at risk for exocrine pancreatic insufficiency (EPI)?

Dr. Barkin: The first thing we have to understand is which patient populations we should consider. EPI traditionally has been a disease associated with chronic pancreatitis, and that still makes up the majority of patients. But in addition to those with chronic pancreatitis, we have to think about patients who have had severe acute pancreatitis and who may have had loss of functional pancreatic parenchyma or pancreatic surgery, as well as patients with pancreatic cancer that may cause both ductal obstruction and parenchyma loss.

This might also include patients with foregut surgery who may develop postcibal dyskinesia, meaning they do not get appropriate mixing of the gastric chyme and food contents with the pancreatic enzymes and pancreatic juice in the duodenum. For example, this might be evident in patients who have had a Roux-en-Y gastric bypass, or in patients with untreated celiac disease, who do not get stimulation for pancreatic secretion based on the amount of small bowel mucosal damage.

A series of other conditions may present with EPI, such as inflammatory bowel disease, although these make up the minority of cases. When we think about symptoms, the end symptom of EPI from fat malabsorption is gross steatorrhea. Unfortunately, by the time the patient gets to that point, the cat is out of the bag—especially in patients with chronic pancreatitis. So, we want to try to identify these patients earlier.

Realistically, a series of symptoms can be seen far earlier than gross steatorrhea. In fact, most patients will present with symptoms like increased stool frequency or decreased stool consistency in their daily life. Some abdominal discomfort or bloating may be seen that is associated with maldigestion of  food, among other factors.

In some patients, night vision changes from fat-soluble vitamin deficiencies may be the first or an early presenting symptom if they have other conditions masking their diarrheal symptoms. Patients who do not feel well when they are eating or feel uncomfortable after they eat may avoid certain types of foods. You may see weight loss in these populations because they are avoiding foods, feeling sitophobia, or not appropriately digesting their food.

Unfortunately, even before we see clinically relevant symptoms, we may see micronutrient deficiencies and fat-soluble vitamin deficiencies. That is why it is so important, for example, in the chronic pancreatitis population, to screen these patients on a regular basis for the presence of EPI, whether with symptom questionnaires or by testing.

Can you expand on some of the risk factors and the importance of screening, particularly for malnutrition?

Dr. Barkin: The risk factors usually involve patients who have had some kind of damage to the gland. For example, many patients with cystic fibrosis are actually exocrine pancreatic insufficient from early in life to diagnosis. They have loss of the gland and loss of function at the gland.

Our patients with chronic pancreatitis, who may have had either recurrent acute pancreatitis or chronic pancreatitis for a variety of reasons, are screened for EPI on a regular basis. That may mean that you ask them a symptom questionnaire at each clinic visit and check a fecal elastase level on a regular basis. It is not just the symptoms that we have to worry about; we have to think about the effects of maldigestion on a patient’s weight and nutritional status and the impact of micronutrient deficiencies.

A series of new studies has looked at the impact of exocrine insufficiency. For example, a study from Spain found an increased risk of all-cause mortality with exocrine insufficiency. When we think about metabolic bone disease in this population with exocrine insufficiency, we see that there is decreased bone density and increased risk of pathologic low-trauma fractures. For example, the patient who has fallen from a standing position at home and suddenly has a hip fracture has substantial morbidity and mortality associated with that fracture. The decreases in bone density and increased risk of fracture are reversed when we identify EPI and treat it appropriately.

What is your approach to diagnosing EPI?

Dr. Barkin: For a patient who walks in the door with an obvious diagnosis or prior diagnosis of chronic pancreatitis, it is relatively easy to ask them a series of questions about whether they have symptoms that may be associated with EPI. So, first, I ask them about their bowel habits and stool frequency and consistency.

A couple of years ago, we showed that if you treat a patient with EPI using pancreatic enzyme replacement therapy, their stool consistency and frequency are the two reliable markers that get better. They not only get better, but these improvements directly correlate with objective stool markers of improvement in fat maldigestion.

Obviously, we want improvement in other symptoms—abdominal discomfort, bloating, etc.—but I have to set very realistic expectations for patients. Along with stool frequency and consistency, there should be subsequent improvement of steatorrhea. I talk to them about the importance of taking a multivitamin to prevent those micronutrient deficiencies. We check for micronutrient deficiencies and fat-soluble vitamin deficiencies routinely.

Patients who do not have obvious chronic pancreatitis who get diagnosed with EPI are a little bit harder to parse out. I want to make sure that they do not have celiac disease, or that they do not have a concomitant mimicking symptom that may result in, for example, a low fecal elastase level. I also check for small intestinal bacterial overgrowth (SIBO) as a mimicking condition.

Regarding fecal elastase testing, the gold standard for diagnosis of EPI was historically a 72-hour fecal fat collection on a standardized-fat-intake diet. That required patient confinement in the hospital. It is cumbersome, not widely available, and not realistic in practice.

In some centers, endoscopic pancreatic function testing, secretin-enhanced magnetic resonance cholangiopancreatography (MRCP), or breath testing, as is done in Europe, may be options to help diagnose EPI, but these tests are not widely available. Unfortunately, we do not have a great diagnostic test for exocrine insufficiency. As a result, we use fecal elastase level. If you have a patient who has a high pretest probability of having EPI, it is a relatively good test. If they have a low pretest probability, then a series of false-positive test results may occur in this patient population. That means they may not actually have exocrine insufficiency.

If a diarrheal stool is submitted for testing, a false-positive fecal elastase test may result. That is really key, because I see a number of patients with potentially functional diarrheal symptoms who also have low fecal elastase levels. As a result, they have been labeled as exocrine insufficient when, in fact, they may not actually have the disease, which is why it is so important to understand and think about that.

How do you choose the appropriate approach to managing EPI, and how do you consider the impact it has on the quality of life overall?

Dr. Barkin: There are two key points. The treatment for EPI is not to tell your patient to not eat fat and hope that it gets better. Rather, it is appropriate supplementation of pancreatic enzymes. This is done with pancreatic enzyme replacement therapy. A few FDA-approved medications are on the market. I recommend against the ones that have been labeled as pancreatic enzyme digestive aids that are available online. Those are not pancreatic enzymes; a regulatory push about 15 to 20 years ago got these digestive aids appropriately regulated.

The FDA-approved medications are dosed at approximately 40,000 to 50,000 lipase units per meal to start, according to the guidelines. Some of us may prescribe higher doses than that to start. These are taken with meals and about a half-dose with snacks.

If you have a patient who is taking, for example, two pills per meal or two capsules per meal, it is important that they take one at the very beginning of the meal and one about halfway through the meal. The pills should not be taken a half hour before or a half hour after the meal. The goal is to simulate normal pancreatic function as much as possible to get the food contents mixing.

The pancreatic enzymes come in a coated version that does not require coadministration with proton pump inhibitors or an uncoated version that does require coadministration of proton pump inhibitors to prevent degradation by gastric acid. Patients need to understand that, although they may take a large number of pills per day, adhering to this regimen is important, not only for treating their symptoms, but also for combating long-term morbidity and mortality.

I use the symptomatic response to assess response to therapy because, as discussed, there is a direct correlation between improvements in stool frequency and consistency and objective markers of response to therapy.

If a patient is not responding, we first check to make sure that there are no adherence issues and that they are able to access therapy, because sometimes there are issues with cost or insurance approvals. Second, I make sure that patients are taking it correctly, and that they understand the difference between a meal and a snack. For example, if somebody says, “Oh, I just had a small cheeseburger and that's my snack,” that is actually a meal and may require more enzymes. Once we ensure that those are not issues, I make sure again, as part of my approach, that there are no comorbid conditions that may be driving some of the symptoms, such as celiac disease or SIBO, with SIBO being very common in this population.

Then we have to decide whether we need to change the dose. Do we need to increase the dose? Some of us start a little bit higher than the 40,000 to 50,000 units of lipase per meal, as suggested in some of our national and international guidelines, and go from there.

What characteristics or symptoms do you look for to identify patients who are at risk for exocrine pancreatic insufficiency (EPI)?

Dr. Barkin: The first thing we have to understand is which patient populations we should consider. EPI traditionally has been a disease associated with chronic pancreatitis, and that still makes up the majority of patients. But in addition to those with chronic pancreatitis, we have to think about patients who have had severe acute pancreatitis and who may have had loss of functional pancreatic parenchyma or pancreatic surgery, as well as patients with pancreatic cancer that may cause both ductal obstruction and parenchyma loss.

This might also include patients with foregut surgery who may develop postcibal dyskinesia, meaning they do not get appropriate mixing of the gastric chyme and food contents with the pancreatic enzymes and pancreatic juice in the duodenum. For example, this might be evident in patients who have had a Roux-en-Y gastric bypass, or in patients with untreated celiac disease, who do not get stimulation for pancreatic secretion based on the amount of small bowel mucosal damage.

A series of other conditions may present with EPI, such as inflammatory bowel disease, although these make up the minority of cases. When we think about symptoms, the end symptom of EPI from fat malabsorption is gross steatorrhea. Unfortunately, by the time the patient gets to that point, the cat is out of the bag—especially in patients with chronic pancreatitis. So, we want to try to identify these patients earlier.

Realistically, a series of symptoms can be seen far earlier than gross steatorrhea. In fact, most patients will present with symptoms like increased stool frequency or decreased stool consistency in their daily life. Some abdominal discomfort or bloating may be seen that is associated with maldigestion of  food, among other factors.

In some patients, night vision changes from fat-soluble vitamin deficiencies may be the first or an early presenting symptom if they have other conditions masking their diarrheal symptoms. Patients who do not feel well when they are eating or feel uncomfortable after they eat may avoid certain types of foods. You may see weight loss in these populations because they are avoiding foods, feeling sitophobia, or not appropriately digesting their food.

Unfortunately, even before we see clinically relevant symptoms, we may see micronutrient deficiencies and fat-soluble vitamin deficiencies. That is why it is so important, for example, in the chronic pancreatitis population, to screen these patients on a regular basis for the presence of EPI, whether with symptom questionnaires or by testing.

Can you expand on some of the risk factors and the importance of screening, particularly for malnutrition?

Dr. Barkin: The risk factors usually involve patients who have had some kind of damage to the gland. For example, many patients with cystic fibrosis are actually exocrine pancreatic insufficient from early in life to diagnosis. They have loss of the gland and loss of function at the gland.

Our patients with chronic pancreatitis, who may have had either recurrent acute pancreatitis or chronic pancreatitis for a variety of reasons, are screened for EPI on a regular basis. That may mean that you ask them a symptom questionnaire at each clinic visit and check a fecal elastase level on a regular basis. It is not just the symptoms that we have to worry about; we have to think about the effects of maldigestion on a patient’s weight and nutritional status and the impact of micronutrient deficiencies.

A series of new studies has looked at the impact of exocrine insufficiency. For example, a study from Spain found an increased risk of all-cause mortality with exocrine insufficiency. When we think about metabolic bone disease in this population with exocrine insufficiency, we see that there is decreased bone density and increased risk of pathologic low-trauma fractures. For example, the patient who has fallen from a standing position at home and suddenly has a hip fracture has substantial morbidity and mortality associated with that fracture. The decreases in bone density and increased risk of fracture are reversed when we identify EPI and treat it appropriately.

What is your approach to diagnosing EPI?

Dr. Barkin: For a patient who walks in the door with an obvious diagnosis or prior diagnosis of chronic pancreatitis, it is relatively easy to ask them a series of questions about whether they have symptoms that may be associated with EPI. So, first, I ask them about their bowel habits and stool frequency and consistency.

A couple of years ago, we showed that if you treat a patient with EPI using pancreatic enzyme replacement therapy, their stool consistency and frequency are the two reliable markers that get better. They not only get better, but these improvements directly correlate with objective stool markers of improvement in fat maldigestion.

Obviously, we want improvement in other symptoms—abdominal discomfort, bloating, etc.—but I have to set very realistic expectations for patients. Along with stool frequency and consistency, there should be subsequent improvement of steatorrhea. I talk to them about the importance of taking a multivitamin to prevent those micronutrient deficiencies. We check for micronutrient deficiencies and fat-soluble vitamin deficiencies routinely.

Patients who do not have obvious chronic pancreatitis who get diagnosed with EPI are a little bit harder to parse out. I want to make sure that they do not have celiac disease, or that they do not have a concomitant mimicking symptom that may result in, for example, a low fecal elastase level. I also check for small intestinal bacterial overgrowth (SIBO) as a mimicking condition.

Regarding fecal elastase testing, the gold standard for diagnosis of EPI was historically a 72-hour fecal fat collection on a standardized-fat-intake diet. That required patient confinement in the hospital. It is cumbersome, not widely available, and not realistic in practice.

In some centers, endoscopic pancreatic function testing, secretin-enhanced magnetic resonance cholangiopancreatography (MRCP), or breath testing, as is done in Europe, may be options to help diagnose EPI, but these tests are not widely available. Unfortunately, we do not have a great diagnostic test for exocrine insufficiency. As a result, we use fecal elastase level. If you have a patient who has a high pretest probability of having EPI, it is a relatively good test. If they have a low pretest probability, then a series of false-positive test results may occur in this patient population. That means they may not actually have exocrine insufficiency.

If a diarrheal stool is submitted for testing, a false-positive fecal elastase test may result. That is really key, because I see a number of patients with potentially functional diarrheal symptoms who also have low fecal elastase levels. As a result, they have been labeled as exocrine insufficient when, in fact, they may not actually have the disease, which is why it is so important to understand and think about that.

How do you choose the appropriate approach to managing EPI, and how do you consider the impact it has on the quality of life overall?

Dr. Barkin: There are two key points. The treatment for EPI is not to tell your patient to not eat fat and hope that it gets better. Rather, it is appropriate supplementation of pancreatic enzymes. This is done with pancreatic enzyme replacement therapy. A few FDA-approved medications are on the market. I recommend against the ones that have been labeled as pancreatic enzyme digestive aids that are available online. Those are not pancreatic enzymes; a regulatory push about 15 to 20 years ago got these digestive aids appropriately regulated.

The FDA-approved medications are dosed at approximately 40,000 to 50,000 lipase units per meal to start, according to the guidelines. Some of us may prescribe higher doses than that to start. These are taken with meals and about a half-dose with snacks.

If you have a patient who is taking, for example, two pills per meal or two capsules per meal, it is important that they take one at the very beginning of the meal and one about halfway through the meal. The pills should not be taken a half hour before or a half hour after the meal. The goal is to simulate normal pancreatic function as much as possible to get the food contents mixing.

The pancreatic enzymes come in a coated version that does not require coadministration with proton pump inhibitors or an uncoated version that does require coadministration of proton pump inhibitors to prevent degradation by gastric acid. Patients need to understand that, although they may take a large number of pills per day, adhering to this regimen is important, not only for treating their symptoms, but also for combating long-term morbidity and mortality.

I use the symptomatic response to assess response to therapy because, as discussed, there is a direct correlation between improvements in stool frequency and consistency and objective markers of response to therapy.

If a patient is not responding, we first check to make sure that there are no adherence issues and that they are able to access therapy, because sometimes there are issues with cost or insurance approvals. Second, I make sure that patients are taking it correctly, and that they understand the difference between a meal and a snack. For example, if somebody says, “Oh, I just had a small cheeseburger and that's my snack,” that is actually a meal and may require more enzymes. Once we ensure that those are not issues, I make sure again, as part of my approach, that there are no comorbid conditions that may be driving some of the symptoms, such as celiac disease or SIBO, with SIBO being very common in this population.

Then we have to decide whether we need to change the dose. Do we need to increase the dose? Some of us start a little bit higher than the 40,000 to 50,000 units of lipase per meal, as suggested in some of our national and international guidelines, and go from there.

This month’s round up of clinical studies is a fitting end to 2021 – they provide a close look at the intersection between pancreatic pathology and SARS CoV-2 infection.  The first study, out of the UK, speculated that SARS CoV-2 virus may be associated with development of idiopathic pancreatitis.¹  They followed 1,476 patients with acute pancreatitis for 12 months (118 of whom were positive for SARS CoV-2, and 1,358 of whom were negative for the virus).  The patients underwent magnetic resonance cholangiopancreatography, endoscopic ultrasound, or biochemical investigations to exclude other causes of pancreatitis.  Remarkably, as the paper states, “Patients who were SARS-CoV-2 positive were more likely to have idiopathic acute pancreatitis (AP, 34.7% vs 13.9%, P < .001) with over five times increased risk after adjusting for age, smoking status, body mass index and ethnicity (odds ration [OR] 5.34, P < .001).”  

Secondarily, the authors aimed to determine if SARS CoV-2 infection would increase risk for diabetes mellitus (DM) and pancreatic exocrine insufficiency (PEI).  Notably, SARS-CoV-2 did not increase the risk of DM (2.3% vs 2.5%, OR 0.61, P = .541) or PEI (OR 1.11, P = .828) (P > .05).  The relationship between pancreatitis and SARS CoV-2 infection is indeed an important one – the authors point out that autopsy studies have demonstrated the presence of virus in pancreatic tissue.  There is clear mechanistic reason for trophism as ACE 2 receptors are found on exocrine and endocrine cells of the pancreas.  

Another study, out of Hubei Province, China, looked at the association of elevated serum amylase (ESA) with mortality and other adverse outcomes  in hospitalized patients with COVID-19.²  Their retrospective study included 1,515 inpatients with COVID-19.  Overall, 196 patients had ESA, of which 9.7% had an ESA of >3 times the upper limit of normal (ULN).  Somewhat not unexpectedly, hyperamylasemia was independently associated with mortality (1-3-times ULN [1-3 ULN]: hazard ratio [HR] 1.63; P = .034; >3-fold ULN [>3 ULN]: HR 8.90; P < .001) and adverse outcomes, such as sepsis (1-3 ULN: odds ratio [OR] 1.15; >3 ULN: OR 1.87), disseminated intravascular coagulation (1-3 ULN: OR 1.13; >3 ULN: OR 1.65), cardiac injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.71), acute respiratory distress syndrome (1-3 ULN: OR 1.21; >3 ULN: OR 1.62), and acute kidney injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.79).  The authors conclude that, “​​Since early intervention might change the outcome, serum amylase should be monitored dynamically during hospitalization.”  It appears to be unclear what would be practice changing, assuming patients would already be receiving appropriate resuscitation.  

More interesting, perhaps, is the question of whether or not the pancreas is merely a bystander casualty or an active protagonist in the role of sepsis and disease severity in highly morbid diseases, such as COVID-19.  

References

1.           Nayar M et al. SARS-CoV-2 infection is associated with an increased risk of idiopathic acute pancreatitis but not pancreatic exocrine insufficiency or diabetes: long-term results of the COVIDPAN study. Gut 2021(Nov 11).

2.           Li G et al. Serum amylase elevation is associated with adverse clinical outcomes in patients with coronavirus disease 2019. Aging (Albany NY) 2021;13(20):23442–58 (Oct 2021).

This month’s round up of clinical studies is a fitting end to 2021 – they provide a close look at the intersection between pancreatic pathology and SARS CoV-2 infection.  The first study, out of the UK, speculated that SARS CoV-2 virus may be associated with development of idiopathic pancreatitis.¹  They followed 1,476 patients with acute pancreatitis for 12 months (118 of whom were positive for SARS CoV-2, and 1,358 of whom were negative for the virus).  The patients underwent magnetic resonance cholangiopancreatography, endoscopic ultrasound, or biochemical investigations to exclude other causes of pancreatitis.  Remarkably, as the paper states, “Patients who were SARS-CoV-2 positive were more likely to have idiopathic acute pancreatitis (AP, 34.7% vs 13.9%, P < .001) with over five times increased risk after adjusting for age, smoking status, body mass index and ethnicity (odds ration [OR] 5.34, P < .001).”  

Secondarily, the authors aimed to determine if SARS CoV-2 infection would increase risk for diabetes mellitus (DM) and pancreatic exocrine insufficiency (PEI).  Notably, SARS-CoV-2 did not increase the risk of DM (2.3% vs 2.5%, OR 0.61, P = .541) or PEI (OR 1.11, P = .828) (P > .05).  The relationship between pancreatitis and SARS CoV-2 infection is indeed an important one – the authors point out that autopsy studies have demonstrated the presence of virus in pancreatic tissue.  There is clear mechanistic reason for trophism as ACE 2 receptors are found on exocrine and endocrine cells of the pancreas.  

Another study, out of Hubei Province, China, looked at the association of elevated serum amylase (ESA) with mortality and other adverse outcomes  in hospitalized patients with COVID-19.²  Their retrospective study included 1,515 inpatients with COVID-19.  Overall, 196 patients had ESA, of which 9.7% had an ESA of >3 times the upper limit of normal (ULN).  Somewhat not unexpectedly, hyperamylasemia was independently associated with mortality (1-3-times ULN [1-3 ULN]: hazard ratio [HR] 1.63; P = .034; >3-fold ULN [>3 ULN]: HR 8.90; P < .001) and adverse outcomes, such as sepsis (1-3 ULN: odds ratio [OR] 1.15; >3 ULN: OR 1.87), disseminated intravascular coagulation (1-3 ULN: OR 1.13; >3 ULN: OR 1.65), cardiac injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.71), acute respiratory distress syndrome (1-3 ULN: OR 1.21; >3 ULN: OR 1.62), and acute kidney injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.79).  The authors conclude that, “​​Since early intervention might change the outcome, serum amylase should be monitored dynamically during hospitalization.”  It appears to be unclear what would be practice changing, assuming patients would already be receiving appropriate resuscitation.  

More interesting, perhaps, is the question of whether or not the pancreas is merely a bystander casualty or an active protagonist in the role of sepsis and disease severity in highly morbid diseases, such as COVID-19.  

References

1.           Nayar M et al. SARS-CoV-2 infection is associated with an increased risk of idiopathic acute pancreatitis but not pancreatic exocrine insufficiency or diabetes: long-term results of the COVIDPAN study. Gut 2021(Nov 11).

2.           Li G et al. Serum amylase elevation is associated with adverse clinical outcomes in patients with coronavirus disease 2019. Aging (Albany NY) 2021;13(20):23442–58 (Oct 2021).

This month’s round up of clinical studies is a fitting end to 2021 – they provide a close look at the intersection between pancreatic pathology and SARS CoV-2 infection.  The first study, out of the UK, speculated that SARS CoV-2 virus may be associated with development of idiopathic pancreatitis.¹  They followed 1,476 patients with acute pancreatitis for 12 months (118 of whom were positive for SARS CoV-2, and 1,358 of whom were negative for the virus).  The patients underwent magnetic resonance cholangiopancreatography, endoscopic ultrasound, or biochemical investigations to exclude other causes of pancreatitis.  Remarkably, as the paper states, “Patients who were SARS-CoV-2 positive were more likely to have idiopathic acute pancreatitis (AP, 34.7% vs 13.9%, P < .001) with over five times increased risk after adjusting for age, smoking status, body mass index and ethnicity (odds ration [OR] 5.34, P < .001).”  

Secondarily, the authors aimed to determine if SARS CoV-2 infection would increase risk for diabetes mellitus (DM) and pancreatic exocrine insufficiency (PEI).  Notably, SARS-CoV-2 did not increase the risk of DM (2.3% vs 2.5%, OR 0.61, P = .541) or PEI (OR 1.11, P = .828) (P > .05).  The relationship between pancreatitis and SARS CoV-2 infection is indeed an important one – the authors point out that autopsy studies have demonstrated the presence of virus in pancreatic tissue.  There is clear mechanistic reason for trophism as ACE 2 receptors are found on exocrine and endocrine cells of the pancreas.  

Another study, out of Hubei Province, China, looked at the association of elevated serum amylase (ESA) with mortality and other adverse outcomes  in hospitalized patients with COVID-19.²  Their retrospective study included 1,515 inpatients with COVID-19.  Overall, 196 patients had ESA, of which 9.7% had an ESA of >3 times the upper limit of normal (ULN).  Somewhat not unexpectedly, hyperamylasemia was independently associated with mortality (1-3-times ULN [1-3 ULN]: hazard ratio [HR] 1.63; P = .034; >3-fold ULN [>3 ULN]: HR 8.90; P < .001) and adverse outcomes, such as sepsis (1-3 ULN: odds ratio [OR] 1.15; >3 ULN: OR 1.87), disseminated intravascular coagulation (1-3 ULN: OR 1.13; >3 ULN: OR 1.65), cardiac injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.71), acute respiratory distress syndrome (1-3 ULN: OR 1.21; >3 ULN: OR 1.62), and acute kidney injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.79).  The authors conclude that, “​​Since early intervention might change the outcome, serum amylase should be monitored dynamically during hospitalization.”  It appears to be unclear what would be practice changing, assuming patients would already be receiving appropriate resuscitation.  

More interesting, perhaps, is the question of whether or not the pancreas is merely a bystander casualty or an active protagonist in the role of sepsis and disease severity in highly morbid diseases, such as COVID-19.  

References

1.           Nayar M et al. SARS-CoV-2 infection is associated with an increased risk of idiopathic acute pancreatitis but not pancreatic exocrine insufficiency or diabetes: long-term results of the COVIDPAN study. Gut 2021(Nov 11).

2.           Li G et al. Serum amylase elevation is associated with adverse clinical outcomes in patients with coronavirus disease 2019. Aging (Albany NY) 2021;13(20):23442–58 (Oct 2021).

Key clinical point: Exocrine pancreatic insufficiency (EPI) is the major cause of nutrient malabsorption in cystic fibrosis (CF), with the likelihood of restoration of pancreatic function significantly higher if CF transmembrane conductance regulator (CFTR) modulator therapies are initiated as early in life as possible.

Main finding: In the ARRIVAL study, ivacaftor led to a mean decrease of 56% in immunoreactive trypsinogen in 12-24 month old patients with CFTR gating mutation. Similar improvements were observed in older children aged 2-5 years treated with ivacaftor in the KIWI and the open-label extension KLIMB study. However, the results are not as promising in older patients aged 5-61 years.

Study details: These are highlights from a review that summarizes the effects of highly effective CFTR modulators on growth and nutrition in patients with CF.

Disclosures: The manuscript did not receive any additional funding. The authors declared receiving grant support and serving as consultants for various sources.

Source: Bass R et al. Nutrients. 2021(Aug 24);13(9):2907. Doi: 10.3390/nu13092907.

Key clinical point: Exocrine pancreatic insufficiency (EPI) is the major cause of nutrient malabsorption in cystic fibrosis (CF), with the likelihood of restoration of pancreatic function significantly higher if CF transmembrane conductance regulator (CFTR) modulator therapies are initiated as early in life as possible.

Main finding: In the ARRIVAL study, ivacaftor led to a mean decrease of 56% in immunoreactive trypsinogen in 12-24 month old patients with CFTR gating mutation. Similar improvements were observed in older children aged 2-5 years treated with ivacaftor in the KIWI and the open-label extension KLIMB study. However, the results are not as promising in older patients aged 5-61 years.

Study details: These are highlights from a review that summarizes the effects of highly effective CFTR modulators on growth and nutrition in patients with CF.

Disclosures: The manuscript did not receive any additional funding. The authors declared receiving grant support and serving as consultants for various sources.

Source: Bass R et al. Nutrients. 2021(Aug 24);13(9):2907. Doi: 10.3390/nu13092907.

Key clinical point: Exocrine pancreatic insufficiency (EPI) is the major cause of nutrient malabsorption in cystic fibrosis (CF), with the likelihood of restoration of pancreatic function significantly higher if CF transmembrane conductance regulator (CFTR) modulator therapies are initiated as early in life as possible.

Main finding: In the ARRIVAL study, ivacaftor led to a mean decrease of 56% in immunoreactive trypsinogen in 12-24 month old patients with CFTR gating mutation. Similar improvements were observed in older children aged 2-5 years treated with ivacaftor in the KIWI and the open-label extension KLIMB study. However, the results are not as promising in older patients aged 5-61 years.

Study details: These are highlights from a review that summarizes the effects of highly effective CFTR modulators on growth and nutrition in patients with CF.

Disclosures: The manuscript did not receive any additional funding. The authors declared receiving grant support and serving as consultants for various sources.

Source: Bass R et al. Nutrients. 2021(Aug 24);13(9):2907. Doi: 10.3390/nu13092907.

Key clinical point: Pancreatic enzyme replacement therapy (PERT) administration in patients with advanced pancreatic ductal adenocarcinoma (PDAC) undergoing standard first-line chemotherapy with gemcitabine plus nab-paclitaxel improved survival, along with weight gain and reduction in maldigestion-related symptoms.

Major finding: PERT administration was associated with longer overall survival (hazard ratio 2.85; P < .001), weight gain at 3 months (P = .02), and a significant reduction in feeling of indigestion (P = .001), bloating (P < .0001), frequent stools (P < .0001), and floating or greasy/fatty stool (P = .003).

Study details: This retrospective study included 110 patients with advanced PDAC treated with first-line chemotherapy with gemcitabine plus nab-paclitaxel with (n = 55) or without (n = 55) PERT administration.

Disclosures: No specific source of funding was identified for this study. Some investigators, including the lead author, reported receiving speaker’s fees, honoraria, travel expenses, consultant’s fees, and institutional research grants and participation in advisory boards and steering committee activities from various sources.

Source: Trestini I et al. Front Oncol. 2021(Sep 9).Doi: 10.3389/fonc.2021.688889.

Key clinical point: Pancreatic enzyme replacement therapy (PERT) administration in patients with advanced pancreatic ductal adenocarcinoma (PDAC) undergoing standard first-line chemotherapy with gemcitabine plus nab-paclitaxel improved survival, along with weight gain and reduction in maldigestion-related symptoms.

Major finding: PERT administration was associated with longer overall survival (hazard ratio 2.85; P < .001), weight gain at 3 months (P = .02), and a significant reduction in feeling of indigestion (P = .001), bloating (P < .0001), frequent stools (P < .0001), and floating or greasy/fatty stool (P = .003).

Study details: This retrospective study included 110 patients with advanced PDAC treated with first-line chemotherapy with gemcitabine plus nab-paclitaxel with (n = 55) or without (n = 55) PERT administration.

Disclosures: No specific source of funding was identified for this study. Some investigators, including the lead author, reported receiving speaker’s fees, honoraria, travel expenses, consultant’s fees, and institutional research grants and participation in advisory boards and steering committee activities from various sources.

Source: Trestini I et al. Front Oncol. 2021(Sep 9).Doi: 10.3389/fonc.2021.688889.

Key clinical point: Pancreatic enzyme replacement therapy (PERT) administration in patients with advanced pancreatic ductal adenocarcinoma (PDAC) undergoing standard first-line chemotherapy with gemcitabine plus nab-paclitaxel improved survival, along with weight gain and reduction in maldigestion-related symptoms.

Major finding: PERT administration was associated with longer overall survival (hazard ratio 2.85; P < .001), weight gain at 3 months (P = .02), and a significant reduction in feeling of indigestion (P = .001), bloating (P < .0001), frequent stools (P < .0001), and floating or greasy/fatty stool (P = .003).

Study details: This retrospective study included 110 patients with advanced PDAC treated with first-line chemotherapy with gemcitabine plus nab-paclitaxel with (n = 55) or without (n = 55) PERT administration.

Disclosures: No specific source of funding was identified for this study. Some investigators, including the lead author, reported receiving speaker’s fees, honoraria, travel expenses, consultant’s fees, and institutional research grants and participation in advisory boards and steering committee activities from various sources.

Source: Trestini I et al. Front Oncol. 2021(Sep 9).Doi: 10.3389/fonc.2021.688889.

Key clinical point: Elevated serum amylase (ESA) was associated with adverse clinical outcomes and mortality in hospitalized patients with COVID-19.

Major finding: Hyperamylasemia (amylase > upper limit of normal [ULN] of 115 U/L) was independently associated with mortality (1-3-times ULN [1-3 ULN]: hazard ratio [HR] 1.63; P = .034; >3-fold ULN [>3 ULN]: HR 8.90; P < .001) and adverse outcomes (all P < .001), such as sepsis (1-3 ULN: odds ratio [OR] 1.15; >3 ULN: OR 1.87), disseminated intravascular coagulation (1-3 ULN: OR 1.13; >3 ULN: OR 1.65), cardiac injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.71), acute respiratory distress syndrome (1-3 ULN: OR 1.21; >3 ULN: OR 1.62), and acute kidney injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.79).

Study details: This retrospective study included 1,515 inpatients with COVID-19. Overall, 196 patients had ESA, of which 9.7% had an ESA of >3 ULN.

Disclosures: This study was supported by the National Nature Science Foundation of China and Chen Xiao-ping Foundation for the Development of Science and Technology of Hubei Province. The authors declared no conflict of interests.

Source: Li G et al. Aging (Albany NY). 2021(Oct 29);13(20):23442-23458. Doi: 10.18632/aging.203653.

Key clinical point: Elevated serum amylase (ESA) was associated with adverse clinical outcomes and mortality in hospitalized patients with COVID-19.

Major finding: Hyperamylasemia (amylase > upper limit of normal [ULN] of 115 U/L) was independently associated with mortality (1-3-times ULN [1-3 ULN]: hazard ratio [HR] 1.63; P = .034; >3-fold ULN [>3 ULN]: HR 8.90; P < .001) and adverse outcomes (all P < .001), such as sepsis (1-3 ULN: odds ratio [OR] 1.15; >3 ULN: OR 1.87), disseminated intravascular coagulation (1-3 ULN: OR 1.13; >3 ULN: OR 1.65), cardiac injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.71), acute respiratory distress syndrome (1-3 ULN: OR 1.21; >3 ULN: OR 1.62), and acute kidney injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.79).

Study details: This retrospective study included 1,515 inpatients with COVID-19. Overall, 196 patients had ESA, of which 9.7% had an ESA of >3 ULN.

Disclosures: This study was supported by the National Nature Science Foundation of China and Chen Xiao-ping Foundation for the Development of Science and Technology of Hubei Province. The authors declared no conflict of interests.

Source: Li G et al. Aging (Albany NY). 2021(Oct 29);13(20):23442-23458. Doi: 10.18632/aging.203653.

Key clinical point: Elevated serum amylase (ESA) was associated with adverse clinical outcomes and mortality in hospitalized patients with COVID-19.

Major finding: Hyperamylasemia (amylase > upper limit of normal [ULN] of 115 U/L) was independently associated with mortality (1-3-times ULN [1-3 ULN]: hazard ratio [HR] 1.63; P = .034; >3-fold ULN [>3 ULN]: HR 8.90; P < .001) and adverse outcomes (all P < .001), such as sepsis (1-3 ULN: odds ratio [OR] 1.15; >3 ULN: OR 1.87), disseminated intravascular coagulation (1-3 ULN: OR 1.13; >3 ULN: OR 1.65), cardiac injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.71), acute respiratory distress syndrome (1-3 ULN: OR 1.21; >3 ULN: OR 1.62), and acute kidney injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.79).

Study details: This retrospective study included 1,515 inpatients with COVID-19. Overall, 196 patients had ESA, of which 9.7% had an ESA of >3 ULN.

Disclosures: This study was supported by the National Nature Science Foundation of China and Chen Xiao-ping Foundation for the Development of Science and Technology of Hubei Province. The authors declared no conflict of interests.

Source: Li G et al. Aging (Albany NY). 2021(Oct 29);13(20):23442-23458. Doi: 10.18632/aging.203653.

Key clinical point: An increased intrapancreatic fat deposition (IPFD) following acute pancreatitis (AP) was associated with a decrease in pancreatic tail diameter (PTD), and in turn, decreased circulating levels of pancreatic amylase.

Major finding: An increased IPFD was significantly associated with reduced PTD in patients with AP (P = .036). Pancreatic amylase was associated with PTD in AP (P = .042).

Study details: This cross-sectional study included 108 individuals with previous AP (median, 20 months post-AP) and 60 healthy controls.

Disclosures: This study was supported by the Rutherford Discovery Fellowship by the Royal Society of New Zealand to MS Petrov. The authors declared no conflict of interests.

Source: Ko J et al. Obes Facts. 2021(Nov 9). Doi: 10.1159/000519621.

Key clinical point: An increased intrapancreatic fat deposition (IPFD) following acute pancreatitis (AP) was associated with a decrease in pancreatic tail diameter (PTD), and in turn, decreased circulating levels of pancreatic amylase.

Major finding: An increased IPFD was significantly associated with reduced PTD in patients with AP (P = .036). Pancreatic amylase was associated with PTD in AP (P = .042).

Study details: This cross-sectional study included 108 individuals with previous AP (median, 20 months post-AP) and 60 healthy controls.

Disclosures: This study was supported by the Rutherford Discovery Fellowship by the Royal Society of New Zealand to MS Petrov. The authors declared no conflict of interests.

Source: Ko J et al. Obes Facts. 2021(Nov 9). Doi: 10.1159/000519621.

Key clinical point: An increased intrapancreatic fat deposition (IPFD) following acute pancreatitis (AP) was associated with a decrease in pancreatic tail diameter (PTD), and in turn, decreased circulating levels of pancreatic amylase.

Major finding: An increased IPFD was significantly associated with reduced PTD in patients with AP (P = .036). Pancreatic amylase was associated with PTD in AP (P = .042).

Study details: This cross-sectional study included 108 individuals with previous AP (median, 20 months post-AP) and 60 healthy controls.

Disclosures: This study was supported by the Rutherford Discovery Fellowship by the Royal Society of New Zealand to MS Petrov. The authors declared no conflict of interests.

Source: Ko J et al. Obes Facts. 2021(Nov 9). Doi: 10.1159/000519621.

Key clinical point: Cystic fibrosis (CF) transmembrane conductance regulator (CFTR) modulator use was associated with reduced incidence of acute pancreatitis (AP) hospitalizations in pancreas-sufficient (PS) and pancreas-insufficient (PI) patients with CF.

Major finding: Estimated rates of AP hospitalizations per 1000 patient-years in patients with PS-CF and PI-CF treated with CFTR modulator were 3.26 (95% CI 0.94-11.33) and 0.66 (95% CI 0.26-1.68), respectively, and those not treated with CFTR modulator were 10.20 (95% CI 6.19-16.81) and 1.76 (95% CI 0.98-3.17), respectively.

Study details: Findings are from a retrospective analysis of 10,417 patients with CF (PS n = 3,759; PI n = 6,658) with (17.2%) or without previous CFTR modulator use.

Disclosures: This study was supported by the US National Center for Advancing Translational Sciences. The authors declared no conflict of interests.

Source: Ramsey ML et al. Am J Gastroenterol. 2021(Oct 19). Doi: 10.14309/ajg.0000000000001527.

Key clinical point: Cystic fibrosis (CF) transmembrane conductance regulator (CFTR) modulator use was associated with reduced incidence of acute pancreatitis (AP) hospitalizations in pancreas-sufficient (PS) and pancreas-insufficient (PI) patients with CF.

Major finding: Estimated rates of AP hospitalizations per 1000 patient-years in patients with PS-CF and PI-CF treated with CFTR modulator were 3.26 (95% CI 0.94-11.33) and 0.66 (95% CI 0.26-1.68), respectively, and those not treated with CFTR modulator were 10.20 (95% CI 6.19-16.81) and 1.76 (95% CI 0.98-3.17), respectively.

Study details: Findings are from a retrospective analysis of 10,417 patients with CF (PS n = 3,759; PI n = 6,658) with (17.2%) or without previous CFTR modulator use.

Disclosures: This study was supported by the US National Center for Advancing Translational Sciences. The authors declared no conflict of interests.

Source: Ramsey ML et al. Am J Gastroenterol. 2021(Oct 19). Doi: 10.14309/ajg.0000000000001527.

Key clinical point: Cystic fibrosis (CF) transmembrane conductance regulator (CFTR) modulator use was associated with reduced incidence of acute pancreatitis (AP) hospitalizations in pancreas-sufficient (PS) and pancreas-insufficient (PI) patients with CF.

Major finding: Estimated rates of AP hospitalizations per 1000 patient-years in patients with PS-CF and PI-CF treated with CFTR modulator were 3.26 (95% CI 0.94-11.33) and 0.66 (95% CI 0.26-1.68), respectively, and those not treated with CFTR modulator were 10.20 (95% CI 6.19-16.81) and 1.76 (95% CI 0.98-3.17), respectively.

Study details: Findings are from a retrospective analysis of 10,417 patients with CF (PS n = 3,759; PI n = 6,658) with (17.2%) or without previous CFTR modulator use.

Disclosures: This study was supported by the US National Center for Advancing Translational Sciences. The authors declared no conflict of interests.

Source: Ramsey ML et al. Am J Gastroenterol. 2021(Oct 19). Doi: 10.14309/ajg.0000000000001527.

Key clinical point: After 12 months, SARS-CoV-2 infection increased the risk for idiopathic acute pancreatitis (AP) but not of diabetes or exocrine pancreatic insufficiency (EPI).

Major finding: Patients who were SARS-CoV-2 positive vs. negative were at a higher risk of idiopathic AP (34.7% vs. 13.9%; odds ratio [OR] 5.34; P < .001) but not of diabetes (2.3% vs. 2.5%; OR 0.61; P = .541) or EPI (OR 1.11; P = .828).

Study details: Findings are from a 12-month follow-up analysis of 1,476 patients with (n = 118) or without (n = 1,358) SARS-CoV-2 infection.

Disclosures: No source of funding was identified. The authors declared no conflict of interests.

Source: Nayar M et al. Gut. 2021(Nov 11). Doi: 10.1136/gutjnl-2021-326218.

Key clinical point: After 12 months, SARS-CoV-2 infection increased the risk for idiopathic acute pancreatitis (AP) but not of diabetes or exocrine pancreatic insufficiency (EPI).

Major finding: Patients who were SARS-CoV-2 positive vs. negative were at a higher risk of idiopathic AP (34.7% vs. 13.9%; odds ratio [OR] 5.34; P < .001) but not of diabetes (2.3% vs. 2.5%; OR 0.61; P = .541) or EPI (OR 1.11; P = .828).

Study details: Findings are from a 12-month follow-up analysis of 1,476 patients with (n = 118) or without (n = 1,358) SARS-CoV-2 infection.

Disclosures: No source of funding was identified. The authors declared no conflict of interests.

Source: Nayar M et al. Gut. 2021(Nov 11). Doi: 10.1136/gutjnl-2021-326218.

Key clinical point: After 12 months, SARS-CoV-2 infection increased the risk for idiopathic acute pancreatitis (AP) but not of diabetes or exocrine pancreatic insufficiency (EPI).

Major finding: Patients who were SARS-CoV-2 positive vs. negative were at a higher risk of idiopathic AP (34.7% vs. 13.9%; odds ratio [OR] 5.34; P < .001) but not of diabetes (2.3% vs. 2.5%; OR 0.61; P = .541) or EPI (OR 1.11; P = .828).

Study details: Findings are from a 12-month follow-up analysis of 1,476 patients with (n = 118) or without (n = 1,358) SARS-CoV-2 infection.

Disclosures: No source of funding was identified. The authors declared no conflict of interests.

Source: Nayar M et al. Gut. 2021(Nov 11). Doi: 10.1136/gutjnl-2021-326218.

While this month’s journal scan for clinical research reviews in exocrine pancreatic insufficiency (EPI) may not reveal a landmark paper, there certainly are novel findings worthy of note.  In particular researchers Halabitska and Babinets¹ from Ternopil National Medical University in Ukraine¹ looked at the impact of NSAID use on fecal elastase and nutritional parameters in patients with baseline EPI.

The researchers’ primary aim is based on the idea that osteoarthritis (OA) accounts for a significant global disease burden, particularly in advanced age with other concomitant comorbidities, yet most attention is paid to the study of peptic ulcer disease (PUD) and nonsteroidal anti-inflammatory drug (NSAID)-related enteropathies of the gastrointestinal tract after NSAID use. Researchers state, “however, no studies have been found to study the effect of NSAIDs on the progression of EPI and the development of trophological disorders, especially under conditions of primary OA comorbidity with diseases accompanied by EPI.”

This study included 87 adult patients with primary OA along with EPI and 30 healthy controls. The patients in the interventional group received a 14-day course of NSAIDs which are officially recommended for the treatment of pain in primary OA (15 mg/day meloxicam, 200 mg/day nimesulide, 150 mg/day diclofenac sodium).  Fecal α-elastase levels were analyzed before and after NSAID treatment in patients with primary OA and concomitant EPI. After NSAID treatment, there was a statistically significant decrease in EPI levels, which was most pronounced in the subgroup of patients with EPI from chronic pancreatitis. Further, the levels of trophologic parameters (magnesium, calcium, iron, zinc, selenium, albumin, and vitamins A, E, and K) decreased significantly after NSAID treatment (all P < .05).

The authors concluded that NSAID use likely worsens EPI and nutritional parameters in patients with primary osteoarthritis with concomitant EPI at baseline. This is potentially practice changing, which might suggest that a closer monitoring of EPI parameters during a course of NSAID treatment is needed. Patients with EPI are of course already at risk of fat soluble vitamin deficiencies, and it may provide only more reason to check and replenish micronutrients and vitamin levels after a course of NSAID therapy. 

References

1. Halabitska IM et al. Different consequences of the treatment of osteoarthritis in gastrointestinal comorbidity with exocrine pancreatic insufficiency. Fam Med Prim Care Rev. 2021 (Oct 5);23(4):10.5114/fmpcr.2021.108207.

While this month’s journal scan for clinical research reviews in exocrine pancreatic insufficiency (EPI) may not reveal a landmark paper, there certainly are novel findings worthy of note.  In particular researchers Halabitska and Babinets¹ from Ternopil National Medical University in Ukraine¹ looked at the impact of NSAID use on fecal elastase and nutritional parameters in patients with baseline EPI.

The researchers’ primary aim is based on the idea that osteoarthritis (OA) accounts for a significant global disease burden, particularly in advanced age with other concomitant comorbidities, yet most attention is paid to the study of peptic ulcer disease (PUD) and nonsteroidal anti-inflammatory drug (NSAID)-related enteropathies of the gastrointestinal tract after NSAID use. Researchers state, “however, no studies have been found to study the effect of NSAIDs on the progression of EPI and the development of trophological disorders, especially under conditions of primary OA comorbidity with diseases accompanied by EPI.”

This study included 87 adult patients with primary OA along with EPI and 30 healthy controls. The patients in the interventional group received a 14-day course of NSAIDs which are officially recommended for the treatment of pain in primary OA (15 mg/day meloxicam, 200 mg/day nimesulide, 150 mg/day diclofenac sodium).  Fecal α-elastase levels were analyzed before and after NSAID treatment in patients with primary OA and concomitant EPI. After NSAID treatment, there was a statistically significant decrease in EPI levels, which was most pronounced in the subgroup of patients with EPI from chronic pancreatitis. Further, the levels of trophologic parameters (magnesium, calcium, iron, zinc, selenium, albumin, and vitamins A, E, and K) decreased significantly after NSAID treatment (all P < .05).

The authors concluded that NSAID use likely worsens EPI and nutritional parameters in patients with primary osteoarthritis with concomitant EPI at baseline. This is potentially practice changing, which might suggest that a closer monitoring of EPI parameters during a course of NSAID treatment is needed. Patients with EPI are of course already at risk of fat soluble vitamin deficiencies, and it may provide only more reason to check and replenish micronutrients and vitamin levels after a course of NSAID therapy. 

References

1. Halabitska IM et al. Different consequences of the treatment of osteoarthritis in gastrointestinal comorbidity with exocrine pancreatic insufficiency. Fam Med Prim Care Rev. 2021 (Oct 5);23(4):10.5114/fmpcr.2021.108207.

While this month’s journal scan for clinical research reviews in exocrine pancreatic insufficiency (EPI) may not reveal a landmark paper, there certainly are novel findings worthy of note.  In particular researchers Halabitska and Babinets¹ from Ternopil National Medical University in Ukraine¹ looked at the impact of NSAID use on fecal elastase and nutritional parameters in patients with baseline EPI.

The researchers’ primary aim is based on the idea that osteoarthritis (OA) accounts for a significant global disease burden, particularly in advanced age with other concomitant comorbidities, yet most attention is paid to the study of peptic ulcer disease (PUD) and nonsteroidal anti-inflammatory drug (NSAID)-related enteropathies of the gastrointestinal tract after NSAID use. Researchers state, “however, no studies have been found to study the effect of NSAIDs on the progression of EPI and the development of trophological disorders, especially under conditions of primary OA comorbidity with diseases accompanied by EPI.”

This study included 87 adult patients with primary OA along with EPI and 30 healthy controls. The patients in the interventional group received a 14-day course of NSAIDs which are officially recommended for the treatment of pain in primary OA (15 mg/day meloxicam, 200 mg/day nimesulide, 150 mg/day diclofenac sodium).  Fecal α-elastase levels were analyzed before and after NSAID treatment in patients with primary OA and concomitant EPI. After NSAID treatment, there was a statistically significant decrease in EPI levels, which was most pronounced in the subgroup of patients with EPI from chronic pancreatitis. Further, the levels of trophologic parameters (magnesium, calcium, iron, zinc, selenium, albumin, and vitamins A, E, and K) decreased significantly after NSAID treatment (all P < .05).

The authors concluded that NSAID use likely worsens EPI and nutritional parameters in patients with primary osteoarthritis with concomitant EPI at baseline. This is potentially practice changing, which might suggest that a closer monitoring of EPI parameters during a course of NSAID treatment is needed. Patients with EPI are of course already at risk of fat soluble vitamin deficiencies, and it may provide only more reason to check and replenish micronutrients and vitamin levels after a course of NSAID therapy. 

References

1. Halabitska IM et al. Different consequences of the treatment of osteoarthritis in gastrointestinal comorbidity with exocrine pancreatic insufficiency. Fam Med Prim Care Rev. 2021 (Oct 5);23(4):10.5114/fmpcr.2021.108207.

Key clinical point: Among pediatric patients with pancreatic neoplasms who underwent pancreatic surgery, exocrine pancreatic insufficiency (EPI) occurred early after surgery but did not affect growth course with prompt treatment. Endocrine failure was less common and developed later, highlighting the need for long-term monitoring in this patient population.

Major finding: EPI occurred in 25% of patients within 6 months after surgery, and endocrine failure developed in 12.5% of patients 8-10 years after surgery. All patients with EPI required pancrelipase supplementation. No significant difference was observed in the body mass index z-score at diagnosis vs. the last follow-up.

Study details: This retrospective study included 16 pediatric patients with pancreatic neoplasms who underwent pancreatic surgery (pancreaticoduodenectomy, 50%).

Disclosures: No source of funding was identified. The authors declared no conflict of interests.

Source: Bolasco G et al. World J Clin Cases. 2021;9(25):7340-7349. doi: 10.12998/wjcc.v9.i25.7340.

Key clinical point: Among pediatric patients with pancreatic neoplasms who underwent pancreatic surgery, exocrine pancreatic insufficiency (EPI) occurred early after surgery but did not affect growth course with prompt treatment. Endocrine failure was less common and developed later, highlighting the need for long-term monitoring in this patient population.

Major finding: EPI occurred in 25% of patients within 6 months after surgery, and endocrine failure developed in 12.5% of patients 8-10 years after surgery. All patients with EPI required pancrelipase supplementation. No significant difference was observed in the body mass index z-score at diagnosis vs. the last follow-up.

Study details: This retrospective study included 16 pediatric patients with pancreatic neoplasms who underwent pancreatic surgery (pancreaticoduodenectomy, 50%).

Disclosures: No source of funding was identified. The authors declared no conflict of interests.

Source: Bolasco G et al. World J Clin Cases. 2021;9(25):7340-7349. doi: 10.12998/wjcc.v9.i25.7340.

Key clinical point: Among pediatric patients with pancreatic neoplasms who underwent pancreatic surgery, exocrine pancreatic insufficiency (EPI) occurred early after surgery but did not affect growth course with prompt treatment. Endocrine failure was less common and developed later, highlighting the need for long-term monitoring in this patient population.

Major finding: EPI occurred in 25% of patients within 6 months after surgery, and endocrine failure developed in 12.5% of patients 8-10 years after surgery. All patients with EPI required pancrelipase supplementation. No significant difference was observed in the body mass index z-score at diagnosis vs. the last follow-up.

Study details: This retrospective study included 16 pediatric patients with pancreatic neoplasms who underwent pancreatic surgery (pancreaticoduodenectomy, 50%).

Disclosures: No source of funding was identified. The authors declared no conflict of interests.

Source: Bolasco G et al. World J Clin Cases. 2021;9(25):7340-7349. doi: 10.12998/wjcc.v9.i25.7340.