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Exocrine Pancreatic Insufficiency: Not Just Pancreatitis— 20+ Additional Factors to Consider

Exocrine pancreatic insufficiency (EPI) involves reduced pancreatic enzymes, leading to impaired digestion. The prevalence of EPI in the general population is estimated to be around 10-20%.1 Because EPI presents with non-specific GI symptoms, diagnosis may be missed or delayed, resulting in an underestimation of its true prevalence, particularly in patients with diabetes and diarrhea-predominant irritable bowel syndrome (IBS-D).2 Awareness of symptoms, causes, risk factors, testing, and treatment for EPI can help clinicians identify affected patients earlier, initiate appropriate therapy, and improve nutritional status and overall quality of life.

A Review of Normal Exocrine Pancreatic Physiology

Both neural (entero-pancreatic, cholinergic, vagal reflexes) and hormonal (cholecystokinin [CCK], secretin) pathways mediate the release of pancreatic enzymes in response to intestinal stimuli. CCK is the major mediator in response to amino acids and fatty acids. Cells that release CCK are located within the duodenum and jejunum, and mucosal integrity is necessary for normal secretion.3

Sufficient hydrochloric acid (HCl) is also important for downstream digestive events. When acidic chyme enters the duodenum, it triggers the release of secretin and CCK, which in turn stimulate pancreatic fluid secretion.4,5 Pancreatic enzymes are released from pancreatic acinar cells. Pancreatic fluid contains pancreatic enzymes such as amylase, lipase, and protease, along with water and ions like bicarbonate and phosphate.6 CCK also stimulates gallbladder contraction and bile release.7

These components play an essential role in digestion within the small intestine, and diseases or conditions affecting them can cause EPI.

How Do Pancreatic and Non-Pancreatic Diseases Contribute to EPI?

EPI has multiple pathophysiological mechanisms. Conditions that impair acinar cell function decrease digestive enzyme production. Loss of pancreatic parenchyma impairs enzyme production. Tumors and ductal stenoses decrease enzyme outflow.6 Surgeries such as a Whipple procedure can create a mis-timing of pancreatic enzyme output mixing with chyme.7

EPI can also be caused by non-pancreatic disease. Small intestine enteropathy, such as celiac disease, alters the stimulation of CCK, decreasing the stimulation of enzyme release.3,6,8,9 Studies show exocrine pancreatic function is decreased in villous atrophy regardless of underlying disease. After mucosal regeneration, fecal elastase levels stabilize.9

EPI Symptoms and Complications

Most patients with EPI have symptoms, although some with mild EPI may be asymptomatic. EPI symptoms include:7,10,11

  • Abdominal pain, cramping
  • Bloating
  • Gas
  • Diarrhea
  • Constipation
  • Steatorrhea (clay-colored, loose, greasy, foul-smelling, sticky, large stools)
  • Unexplained weight loss
  • Dyspepsia
  • Nausea and vomiting

Prolonged malabsorption due to EPI can lead to nutritional deficiencies resulting in sarcopenia, osteopenia, neurologic effects, coagulation abnormalities, skin rashes, anemia, fatigue, weakness, and impaired quality of life.12 Pancreatic enzymes have anti-bacterial properties, and deficiencies can lead to small intestinal bacterial overgrowth (SIBO).13 A systematic review and meta-analysis showed that 38% of chronic pancreatitis patients are predisposed to having SIBO.14 Addressing EPI and managing its downstream consequences can improve symptoms and quality of life.

Causes and Risk Factors for Exocrine Pancreatic Insufficiency

While chronic pancreatitis may not be frequently diagnosed in general practice, clinicians routinely manage patients with diabetes, obesity, unhealthy lifestyle habits, and other prevalent risk factors associated with EPI. Many of these underlying conditions or risk factors can be addressed, and in some cases, EPI can be reversed.

List of causes and associated risk factors for EPI:

EPI Causes/ Risk Factors
EPI Prevalence
EPI Pathophysiology
Chronic pancreatitis [2,6,15,16] 30%-90% within 10-12 years of diagnosis Loss of pancreatic parenchyma, necrosis, tissue calcifications
Acute pancreatitis [2,16] 62% during hospitalization and 35% after discharge Loss of pancreatic parenchyma, necrosis
Type 1 and 2 diabetes [2,7,16-20] 14% to 77.5% for DM1 and 16.8%-49.2% for DM2 Microvascular damage may induce pancreatic fibrosis; pancreatic volume is reduced; pancreatic steatosis impairs function; lack of trophic action of insulin on acinar cells
Obesity [19,21-23] Data not available Mechanism unknown; possibly similar to metabolic-associated fatty liver disease (MAFLD), pancreatic steatosis results in acinar cell death
Celiac disease [2,6,16,24-26] 17%-61% with some studies showing persistence of EPI despite adherence to a gluten-free diet Reduced CCK secretion from the atrophied intestinal lining; negative relationship with fecal elastase levels and degree of bowel damage
Cystic fibrosis [2,27] 85%-90% Inherited genetic disease that damages the lungs, pancreas, and other organs, affecting the cells that make mucus, sweat, and digestive enzymes
Aging [16,19,28] 15%-30% Age >80 years; pancreatic steatosis increases with age, impairing pancreatic function
Excessive alcohol intake [29] Alcohol is involved in about 45% of EPI cases; severe chronic pancreatitis develops with alcohol intake of 60-80 g/day for an average of 12 years Risk factor for chronic pancreatitis; damages pancreatic parenchyma, acinar and ductal cells; causes pancreatic fibrosis
Smoking [16] 10%-20% Risk factor for chronic pancreatitis; damages pancreatic parenchyma; causes pancreatic fibrosis
Inflammatory Bowel Disease (IBD) [2] 18% to 80% EPI linked to extent of Crohn’s disease, especially when the ileum is affected, and active disease is present; reduction of pancreatic stimulationby the inflamed intestine
Small intestinal bacterial overgrowth [9,14,25,26,30-32] Data not available for SIBO patients in general>1/3 of chronic pancreatitis patients have SIBO Severe SIBO can cause villous blunting, lamina propria inflammation, and intraepithelial lymphocytosis, similar to celiac pathophysiology; this may lead to reduced CCK secretion from the atrophied intestinal lining, although there is no literature to support this theory for SIBO in particular
Zollinger-Ellison syndrome [33,34] EPI common, but condition rare Increased gastric acid hypersecretion due to ectopic gastrin secretion by neuroendocrine tumor leads to destruction of pancreatic enzymes by acid
Infectious enteritis [3,35] Data not available; one study showed 28% of children with acute enteritis had EPI Bacterial and viral infections transiently damage the small intestine, reducing enteric CCK secretion
GI surgery (gastric bypass, pancreatic resection, etc.) [2] >1/3 of gastric carcinoma patients who underwent gastrectomy developed asymptomatic EPI based on fecal elastase evaluationUp to 41.6% of patients who underwent bariatric surgery developed EPI Pancreatectomy for various malignant pancreatic diseases; structural or functional changes could lead to inadequate production, insufficient secretion, and/or inactivation of pancreatic enzymes
Pancreatic cancer [2,16] 20%-60% Loss of functional pancreatic tissue and obstruction of the main pancreatic duct
Autoimmune pancreatitis [16] 30%-60% Loss of pancreatic parenchyma
Certain cancer therapies and antiretroviral medications [16,36-38] 10%-50% Side effects of medications may cause pancreatic atrophy or damage, and chronic pancreatitis
IBS-D [2] 1.8%-6.1% IBS diagnosis may mask EPI
Schwachman–Diamond syndrome [16] 80% Inherited disease characterized by fatty replacement of acinar cells
Cow’s milk-related enteropathy [9] Data not available Damage to the small intestine reduces enteric CCK secretion
Disordered eating and malnutrition (studies mixed) [39] Data not available Atrophy of pancreatic acinar cells
PPI usage [40] hypochlorhydria PPI use doubled the odds of having EPI in one study Literature describes an association of EPI and PPI usage, not necessarily causation, and the mechanism is unknown; however, normal physiology relies on acidic chyme for the stimulation of CCK and pancreatic enzymes

Testing for Exocrine Pancreatic Insufficiency

Fecal Elastase 1 (FE-1)

According to the American Gastroenterological Association (AGA) guidelines, fecal elastase 1 (FE-1), also called pancreatic elastase 1 (PE-1), is the most appropriate initial test recommended for EPI. Although it’s not a direct pancreatic function test, it’s simple, noninvasive, and relatively inexpensive compared to direct testing. Direct measurement of pancreatic secretions into the duodenum via endoscopy is the most accurate method.12

FE-1 is an enzyme produced by the pancreas that remains intact during intestinal transit. Since it does not degrade like other enzymes in the process of digestion, it’s a suitable marker of exocrine pancreatic output and serves as a proxy marker for other pancreatic enzymes, including lipase, amylase, and protease. A watery stool sample can dilute FE-1, causing falsely low results; testing should only be performed on formed or semi-formed samples.7,36

Many studies show that fecal elastase levels are well over 500 µg/g in healthy adults or control subjects. Yet, the reference cutpoint for EPI is <200 µg/g.17,28,41,42 Many clinicians ignore findings above 200 µg/g  that are in the “green zone” on test reports because it’s generally considered optimal. In my experience as a medical education specialist with a functional medicine laboratory, I often advise clinicians that >500 µg/g would be the optimal finding consistent with studies. The British Society of Gastroenterology suggests that a cutoff of <500 µg/g may indicate EPI.26 The FE-1 test lacks sensitivity for mild EPI.12

It’s important to understand the FE-1 methodology used by laboratories. Enzyme-Linked Immunosorbent Assay (ELISA) tests either polyclonal or monoclonal antibodies. A test using monoclonal antibodies specific to human FE-1 is best, because it is unaffected by exogenous enzymes. A test using polyclonal antibodies that are not specific to humans may measure exogenous supplementation and may not accurately reflect endogenous production and output.16,43

Chymotrypsin

Another fecal enzyme test that has largely been replaced by FE-1 testing is chymotrypsin. The chymotrypsin test cross-reacts with enzyme replacement therapy, which could therefore result in a false negative finding. Whereas exogenous enzymes do not alter FE-1 levels; FE-1 is a true measure of endogenous exocrine pancreatic output.12 It has been suggested that chymotrypsin could be used as a marker for assessing treatment response.

Comprehensive Stool Testing

A study on comprehensive stool testing panels in people with diagnoses suggestive of IBS showed that 7.1% of samples had low PE-1 levels. Comprehensive testing included markers of digestion and absorption, inflammation and immune status, and measured parasites, commensal and pathogenic bacteria, and yeast. Abnormal fecal biomarkers were found in 82.8% of tests.44 This means that many patients who receive a diagnosis of IBS or are merely prescribed medications to manage symptoms without testing are improperly diagnosed and mismanaged. Comprehensive stool testing can reveal underlying IBS causes, including EPI and others.

Pancreatic Enzyme Replacement Therapy (PERT) and Digestive Enzymes

When FE-1 levels fall below 200 μg/g, pancreatic enzyme replacement therapy (PERT) is indicated. A retrospective study was conducted on 82 patients with FE-1 levels between 200 and 500 μg/g. Symptoms that prompted testing included diarrhea, steatorrhea, bloating, flatulence, and abdominal pain. Creon was given with food (2 capsules with meals, 1 capsule with snacks), and symptoms improved in 71% of patients. Patients not offered PERT continued to remain symptomatic despite other interventions.36 This study suggests that a trial of PERT may be beneficial despite “normal” FE-1 findings.

Pancrelipase is a pharmaceutical prescription of porcine-derived lipase, protease, and amylase, offered by many brands, including Creon, Zenpep, etc. Dosing is individualized based on body weight, severity of illness, and fat intake, often calculated by lipase units. A typical starting dose for adults is about 50,000 lipase units per meal and 25,000 units per snack.7

Conventional preparations are FDA-regulated and are enteric-coated to be acid-resistant and pH-sensitive to protect lipase from denaturation by gastric acid. Conventional guidelines suggest adding acid-inhibiting medication to improve PERT efficacy if unresponsive, or to non-enteric-coated PERT preparations.7 While blocking HCl may improve PERT efficacy, it decreases normal physiological functioning, where HCl is important for endogenous activation of pancreatic enzyme output.4,5 This presents a conundrum in trying to optimize digestive health. One study showed that PPI use doubled the odds of having EPI.40

In my experience speaking with clinicians, many have successfully used reputable supplement companies with similar USP dosing. Supplements are not FDA-regulated and may or may not be enteric-coated. There is evidence to suggest that unprotected (non-enteric-coated) enzymes may not improve nutrient digestion.7 Furthermore, many supplement companies design comprehensive formulas that include pancreatic enzymes, hydrochloric acid (HCl), and bile salts. The addition of HCl may inactivate pancreatic enzymes.16,45

How Do I Know If PERT Dosage is Successful?

Indications that PERT is successful include reduced symptoms, weight gain, improved muscle mass and function, and normalized fat-soluble vitamin levels.12

In patients with chronic pancreatitis who do not respond to PERT, it is suggested to test for SIBO, which occurs frequently in this population. SIBO treatment is shown to alleviate symptoms.14,30 Other concurrent conditions resulting in a poor response to PERT include lactose intolerance, bacterial infection, parasites (especially giardia), cholestasis, colitis, celiac disease, short bowel syndrome, and Crohn’s disease.7 Once the cause(s) are identified and treated, it’s helpful to monitor FE-1 levels for improvement and to assess the need for continued PERT.3

What About Digestive Enzyme Supplements?

I’m often asked to recommend the best digestive enzyme supplement when FE-1 results are low on stool testing. There are many digestive enzyme formulas out there containing a variety of enzymes. If someone has EPI or suboptimal FE-1 levels, it’s important to make sure the product at least contains pancreatic enzymes lipase, amylase, and protease, because that’s what’s deficient and needs to be replaced. I tell clinicians that if the product has other types of enzymes in addition to PERT, it may help with overall digestion.

When Should Pancreatic Enzymes or Digestive Enzymes Be Taken?

Enzymes should be taken with meals, rather than before or after.36 This mimics the action of our own endogenous enzyme output, where secretion occurs throughout a meal.7

Identify and Treat the Cause (Tolle causam)

Clinicians are eager to treat with PERT, but it’s always important to ask, “Why does this patient have EPI, or why are their FE-1 levels suboptimal (<500 μg/g)?” Some underlying causes can be treated, which means pancreatic function can return to normal, and patients are not reliant on PERT with every meal long-term.20 For instance, in celiac patients with EPI, adopting a gluten-free diet can help restore the intestinal mucosa, often leading to normalization of pancreatic function and FE-1 levels within a few months.24 Some patients may have more than one cause that needs to be explored. Some causes may not be treatable, such as cystic fibrosis, and the patient is reliant on PERT indefinitely.

Key Takeaways on EPI

  • EPI and suboptimal FE-1 levels are underdiagnosed and undertreated.
  • FE-1 testing in symptomatic patients helps assess disease.
  • As functional medicine practitioners, digging for the root cause is foundational to practice.
  • Treating the cause may eliminate EPI and the need for long-term PERT.

References

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