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Longevity Library · Lab reference

Written by Daniel Tagge, MD
Updated October 23, 2026
Reviewed October 24, 2026
43 sources · Measured in µg/g of stool

System: Gut-Immune Health

Pancreatic elastaseFecal elastase-1 · FE-1 · Stool pancreatic elastase

Fecal elastase-1 is a stool test for whether the pancreas is still making enough digestive enzyme. Pooled across 14 studies it found exocrine pancreatic insufficiency with a sensitivity of 0.77 and a specificity of 0.88 against duodenal testing; it is reliable for severe insufficiency and poor for mild, a watery stool dilutes it into a false low, and in people without weight loss, greasy stools, diabetes or a pancreatic history a mildly low value has never been followed to an outcome, so on a wellness panel it is a question to repeat on a formed sample, not a diagnosis.

Elastase-1 is a protease made only by the pancreas that passes through the gut undegraded, so its concentration in stool tracks how much enzyme the gland secretes. Below 200 µg/g most laboratories call it reduced and below 100 severely reduced; both cutoffs come from studies of people with pancreatic disease. The test is good at severe insufficiency and weak at mild, it reads falsely low in diarrhea, and low values are common in diabetes, celiac disease and older age without proof that digestion has failed. Nobody has followed well people with a mildly low value, and the guidelines say a low number alone does not make the diagnosis.

01 · The scale

Where the laboratory range and the evidence sit.

Pooled sensitivity 0.77 and specificity 0.88 against duodenal testing, strong for severe insufficiency and weak for mild; watery stool reads falsely low; low values are common in diabetes, older age, celiac disease and after gut surgery without proof that digestion has failed; no study has followed a well person with a mildly low value.

0100200300400500600

  1. Severely reduced on most laboratory reports

    0 to 100 µg/g of stool · Hardt 2003; AGA 2023

  2. Mildly to moderately reduced, or indeterminate

    100 to 200 µg/g of stool · AGA 2023; Löser 1996

  3. Reported as normal

    200 and above µg/g of stool · Löser 1996

  4. Central 95 percent of healthy controls, 175 to 1,500

    175 and above µg/g of stool · Stein 1996

  5. Best cutoff in cystic fibrosis 184; a 160 to 200 range suggested

    160 to 200 µg/g of stool · Walkowiak 2002

  6. Below 200 in a watery stool: repeat on a formed sample before reading it

    0 to 200 µg/g of stool · Fischer 2001; UEG 2025

  • Laboratory range
  • Evidence supports
  • Guideline goal or unstudied
  • Higher risk in studies
Scale in µg/g of stool. Reported as micrograms of elastase per gram of stool. Most laboratories print two cutoffs, 200 and 100 µg/g, which come from the diagnostic studies rather than from any outcome trial. Two kinds of assay exist, one built on monoclonal antibodies and one on polyclonal antisera, and their results are not interchangeable. Bands show where studies found something, not a recommendation for any one person.

02 · What it is

What Pancreatic elastase measures.

Elastase-1 is a protein-digesting enzyme made by the acinar cells of the pancreas and secreted into the small intestine with the other pancreatic enzymes. Unlike most of them it is not broken down on the way through: in a 1989 study of pancreatic juice and stool, neither elastase 1 nor chymotrypsin B was degraded during intestinal passage, which is what makes a stool concentration a usable read-out of secretion. The assay is an immunoassay specific for the human enzyme, so it cannot detect the pig-derived enzymes in replacement capsules, and the test can be run while a person is taking them; the 2023 American gastroenterology practice update says so in as many words.1,2,3,4Grade C

The test was validated in 1996 against the secretin-caerulein test, in which pancreatic juice is collected from the duodenum after hormonal stimulation. In 44 patients with mild (8), moderate (14) or severe (22) exocrine insufficiency, 35 patients with non-pancreatic digestive disease and 50 healthy volunteers, a cutoff of 200 µg/g gave a sensitivity of 63 percent for mild, 100 percent for moderate and 100 percent for severe insufficiency, 93 percent overall, with a specificity of 93 percent; day-to-day variation within a person was low (mean coefficient of variation 15 percent) and a sample kept at room temperature for a week. In the companion study, spot stools from controls ranged from 136 to 4,440 µg/g, with 95 percent of values between 175 and 1,500, and the result was unaffected by enzyme replacement.5,6Grade C

What the number is and is not: it is a concentration of one enzyme per gram of stool, a proxy for how much the pancreas secretes, not a measure of whether food is digested. The 2025 European guideline defines exocrine pancreatic insufficiency as secretion reduced below the level that allows normal digestion, states that reduced secretion is not synonymous with insufficiency, calls the test's accuracy low mainly because of low specificity and positive predictive value, and says a cutoff for insufficiency cannot be established although 200 µg/g is frequently used. The gland has a large reserve: fat malabsorption appears only when lipase delivery falls below about 5 to 10 percent of normal output. In many countries this is nonetheless the main, and often the only, test of pancreatic function in routine use.7,8,9Grade A

03 · Origins

Where it came from, and where it sits in the network.

The elastases are chymotrypsin-like serine proteases that digest dietary protein, and the human pancreas carries an odd history: it does not express the archetypal elastase 1 (CELA1) at all but secretes two duplicated elastase 3 isoforms, CELA3A and CELA3B. When their substrate preferences were tested, the duplicated isoforms had not evolved distinct specificities, so a higher gene dose rather than a new enzyme seems to compensate for the lost CELA1 activity, and the stool assay named for elastase 1 in fact measures CELA3. The organ itself is a vertebrate invention: in amphioxus, a small chordate without a pancreas, trypsin, chymotrypsin and elastase are made throughout the digestive tract and concentrated in the hepatic caecum and mid-gut, which suggests that an extensive region of that gut is homologous to the vertebrate exocrine pancreatic cells.10,3,11Grade C

The pancreas functions as the main factory for digestive enzymes, and its two halves grew up together: on current phylogenetic insight the beta cell pioneered the formation of the pancreatic organ, and a constant blood glucose, secured early in vertebrate evolution, is argued to have given the brain an extra degree of freedom to evolve. Elastase-1 is measurable in stool for a simple reason, its stability: it passes through the gastrointestinal tract undergoing only limited degradation, and it survives in a stool sample for about a week at room temperature.12,13,3,5Grade C

In the network the exocrine pancreas sits upstream of several markers on this shelf. Without its lipase, fat and the fat-soluble vitamins go unabsorbed: in 40 patients with chronic pancreatitis, 70 percent of them exocrine insufficient, vitamin D deficiency was present in 53 percent and vitamin K deficiency in 63 percent, with osteopenia in 45 percent and osteoporosis in 10 percent, and bone loss was more frequent than expected even in the exocrine-sufficient patients; pooled across 10 studies of 513 patients with chronic pancreatitis, 23.4 percent had osteoporosis and 65 percent had either osteoporosis or osteopenia. In 115 outpatients with chronic pancreatitis, vitamin D deficiency (22 percent), zinc deficiency (20 percent) and magnesium deficiency (17 percent) were the commonest deficits, while vitamin A and E deficiency were seen only in those with exocrine insufficiency. Vitamin B12 depends on the pancreas too: in the stomach B12 binds almost exclusively to salivary R protein, and only partial digestion of that protein by pancreatic proteases lets it transfer to intrinsic factor, which is why pancreatic insufficiency causes B12 malabsorption. Zinc is the exception that keeps the reading honest: in 150 patients with chronic pancreatitis, 26 percent were zinc deficient, and the deficiency tracked age and smoking rather than exocrine insufficiency.14,15,16,17,18Grade C

The pancreas-diabetes link runs in both directions. Insulin from the islets has a trophic effect on the surrounding acinar tissue, so diabetes is proposed to thin exocrine secretion through loss of that effect, atrophy, autonomic dysfunction, fibrosis, fatty infiltration and disordered glucagon and somatostatin; and exocrine disease destroys islets, so diabetes caused by pancreatic disease (type 3c) is estimated at 5 to 10 percent of diabetes in Western populations, or 8 percent or more, and regulation of beta-cell mass and incretin secretion is argued to depend directly on normal exocrine function. The two systems are so closely linked, anatomically and physiologically, that a systematic review of the field calls exocrine impairment in diabetes frequent and largely overlooked.7,19,20,21Grade C

04 · The laboratory range

What a laboratory calls normal.

Above 200 µg/g reported as normal, 100 to 200 as mildly to moderately reduced or indeterminate, below 100 as severely reduced; most US laboratory reports print these two cutoffs.

The 200 µg/g line is the cutoff from the 1996 validation against duodenal testing. The 100 µg/g line marks severe insufficiency in the same tradition: the largest diabetes screening study called above 200 normal and below 100 severely reduced, and the 2023 American gastroenterology practice update states that a level below 100 µg/g provides good evidence of exocrine pancreatic insufficiency, that 100 to 200 is indeterminate, and that the test must be performed on a semi-solid or solid stool specimen.5,22,4Grade A

These are diagnostic thresholds for a disease, not a range for health. The 2025 European guideline says a cutoff for insufficiency cannot be established although 200 is frequently used, and that the test is at risk of false-positive results in people with a low pre-test probability and false-negative results in those with a high one. The meta-analysis makes that concrete: at a 5 percent pre-test probability a positive result would be wrong about 11 percent of the time while a negative would be wrong 1.1 percent of the time, so a normal value rules insufficiency out in low-probability people but an abnormal one does not rule it in.7,23Grade A

The assays differ. A monoclonal-antibody test and a polyclonal-antisera test are both in use; the polyclonal assay has been reported to be less specific for elastase-1 and to overestimate the overall concentration, and unlike the monoclonal assay it is affected by enzyme replacement. Cutoffs also move with the population: across 725 people with cystic fibrosis and 243 healthy subjects from four countries the best single cutoff was 184 µg/g, country subgroups differed, and the authors suggested a range of 160 to 200 rather than one line. A number from one laboratory's assay cannot be read against another's without knowing which assay it was.24,25,26Grade C

05 · The evidence

What the studies support.

The 2018 meta-analysis pooled 14 studies, 428 people with exocrine pancreatic insufficiency and 673 without. Against the secretin stimulation test the stool assay had a pooled sensitivity of 0.77 (0.58 to 0.89) and specificity of 0.88 (0.78 to 0.93); against quantitative fecal fat, in 6 studies of 345 cases and 312 controls, sensitivity was 0.96 and specificity 0.88. In people with a low pre-test probability (5 percent) the false-negative rate would be 1.1 percent and the false-positive rate 11 percent, a high yield for ruling insufficiency out and a poor one for finding it; at a 40 percent pre-test probability about 10 percent of true cases would be missed. The authors' conclusion: a normal level above 200 can rule out insufficiency in low-probability people such as those with diarrhea-predominant irritable bowel, and in those same people a level below 200 has a high false-positive rate.23Grade A

Mild disease is where it fails. In 64 patients with suspected insufficiency graded by the secretin-pancreozymin test and fecal fat, 94 percent of the 34 with normal function had a normal elastase, but only 53 percent of the 30 with insufficiency had an abnormal one; among the severe cases 73 to 91 percent of fecal enzyme results were abnormal, while in mild to moderate insufficiency fewer than half were, and the authors concluded the test is helpful only in detecting severe insufficiency, not the mild to moderate form that poses the more frequent and difficult clinical problem. Sensitivity in mild to moderate insufficiency has been reported as low as 30 percent.27,8Grade C

Water is the commonest artifact. In 519 stool samples from 310 patients, the 151 classed as diarrhea (mean water content 88.8 percent) averaged 279 µg/g when measured as received and 606 after freeze-drying to a standard water content; in 16 of the 151 (11 percent) a result below 200 proved normal once corrected. Because the result is a concentration, a watery stool will almost invariably read low, and the European guideline asks for a formed stool sample whenever possible to reduce false positives.28,8,7Grade C

Diabetes lowers the number more often than it lowers digestion. Among 1,021 people with diabetes (323 type 1, 697 type 2, mean age 50, mean duration 11 years) the value was above 200 in 59.3 percent and below 100 in 22.9 percent, lower with early onset, long duration and low body mass; and in 544 people with type 2 diabetes matched to 544 controls, medians were 308 against 418 µg/g, with values below 100 in 11.9 percent against 3.7 percent (adjusted odds ratio 4.5). Of 101 diabetic patients selected for a low value, 39.6 percent excreted more than 10 g of fat a day. But when 33 people with type 1 diabetes had the secretin-cerulein test itself, the 11 with abnormal results had only mild to moderate insufficiency, stimulated lipase secretion was never less than 10 percent of the level at which pancreatic steatorrhea first occurs, the stool test correlated poorly with the direct test, and the non-pancreatic steatorrhea in two-thirds was probably bacterial overgrowth; those authors concluded a low elastase should not be used as the indicator for enzyme treatment in type 1 diabetes. The 2025 European guideline puts reduced secretion by this test at 10 to 50 percent of people with diabetes, a pooled 22 percent in type 2, and 5.4 percent in studies that strictly excluded pancreatic-origin diabetes; it recommends screening for symptoms and nutritional deficits, not routine elastase testing.22,29,30,25,7Grade B

Age lowers it in people with nothing wrong. In 914 adults aged 50 to 75 recruited during a general health examination, 11.5 percent had a value of 200 or below and 5.1 percent below 100, rising with age, with smoking an independent risk factor; among 106 adults aged 60 to 92 with no special diet, digestive disease, surgery or diabetes, 21.7 percent were below 200 and 9 were below 100, and the value fell with age (r = -0.35). The European guideline quotes both figures and states that the clinical relevance of exocrine insufficiency in aging is unknown.31,32,7Grade C

Gut diseases that are not pancreatic also lower it. Among 314 people meeting criteria for diarrhea-predominant irritable bowel syndrome, 19 (6.1 percent) had a value below 100 against none of 105 people with other chronic diarrhea and none of 95 controls; in those 19, enzyme treatment improved stool frequency, consistency and pain at 12 weeks, without a placebo arm. In celiac disease a low elastase was found in 11 percent at diagnosis, 6 percent on a gluten-free diet without symptoms, 30 percent on the diet with persistent diarrhea and 4 percent of non-celiac controls, and in a separate series of 90 celiac patients in 4.4 percent. The 2025 European guideline reports values below 200 in 7.1 to 13.3 percent and below 100 in 4.4 to 6 percent of diarrhea-predominant irritable bowel, a pooled 26.2 percent in newly diagnosed celiac disease falling to 8 percent on a gluten-free diet, attributes the celiac finding to reduced hormonal stimulation of a normal pancreas, and states that in the absence of pancreatic disease false-positive results cannot be excluded and that no randomized or blinded trial of enzymes has been done in this setting.33,34,35,7Grade C

When insufficiency is real, it matters and it is treatable. In 430 people with chronic pancreatitis followed for a mean of 8.6 years, insufficiency diagnosed by a breath test (prevalence 29.3 percent) carried 2.59 times the mortality (1.42 to 4.71) after adjustment, with cancer, infection and cardiovascular events the leading causes of death. Across 17 randomized trials of 511 patients with chronic pancreatitis, enzyme replacement raised the coefficient of fat absorption from 63.1 to 83.7 percent against baseline and to 83.2 against 67.4 on placebo, improved nitrogen absorption, stool weight and abdominal pain, and in follow-up studies raised nutritional markers and quality of life without significant adverse events. The practice update's rule follows: once insufficiency is diagnosed, enzyme replacement is required, taken with meals, with fat-soluble vitamins monitored and a baseline bone density scan.36,37,4Grade A

After gut surgery and after acute pancreatitis the test is both more often low and less reliable. The 2025 European guideline puts insufficiency after upper gastrointestinal surgery at 9 to 67 percent and after bariatric surgery at 9 to 48 percent depending on the operation and the test, and states that elastase is not a reliable test in these patients because it measures secretion but not the mistiming between stomach emptying and pancreatic juice that the surgery creates; in a bariatric clinic, only 11.9 percent of 310 stool tests were suggestive of insufficiency and they did not correlate with symptoms. After a first attack of acute pancreatitis, pooled insufficiency was 62 percent during the admission and 35 percent at follow-up, higher after severe or alcohol-related attacks, and the stool test detected significantly fewer cases than other methods.7,38,39,40Grade C

06 · What moves it

The levers with evidence behind them.

What is listed here has been tested. The size of each effect, and the size of the study, are in the sentence, so a small effect reads as a small effect.

  • Alcohol

    drives the disease behind most low values

    Chronic pancreatitis, the leading cause of exocrine insufficiency, is most commonly caused by toxins such as alcohol or tobacco, genetic variants and recurrent acute pancreatitis; after acute pancreatitis, insufficiency was more frequent when the cause was alcohol. Reducing alcohol and stopping smoking are part of the treatment of insufficiency in every guide, and a heavy drinking history is one of the clearest reasons to order the test at all.41,40,8Grade A

  • Smoking

    lowers it, with or without pancreatitis

    In the population study of 914 adults aged 50 to 75, smoking was an independent risk factor for a value of 200 or below and for one below 100; a cross-sectional study of people without pancreatic disease found moderate (18 percent) and severe (10 percent) reductions more often in smokers than in controls, and smoking is associated with reduced exocrine function as well as with acute and chronic pancreatitis and pancreatic cancer. In chronic pancreatitis, smokers were also about three times as likely to be zinc deficient.31,24,8,18Grade C

  • Glucose control

    poor control tracks with lower values

    Among people with type 2 diabetes, an HbA1c of 7 percent or more carried 5.6 times the odds of an elastase below 100 (confidence interval 1.5 to 37), with no association found for diabetes duration, neuropathy or alcohol; in 101 people with type 2 diabetes, those with an HbA1c of 7 or more averaged 385.9 µg/g against 454.6 in those below 7, a difference not explained by pancreas size or fat. Whether enzyme replacement improves glucose control in return is unsettled; the European guideline calls the evidence conflicting.29,42,7Grade C

  • Enzyme replacement, when insufficiency is real

    does not change the number; changes digestion

    Replacement enzymes are pig-derived and the assay does not see them, so the stool value stays where it was and the test can be repeated on treatment; what moves is fat absorption, from 63 to 84 percent across the pooled trials in chronic pancreatitis, with better nitrogen absorption, less pain and better nutritional markers. The benefit is established in people with pancreatic disease; no trial has treated a mildly low number in well adults.6,2,4,37,7Grade A

  • Stool water

    dilutes it into a false low

    A loose or watery sample lowers the concentration without any change in the pancreas: 11 percent of diarrheal samples that read below 200 were normal after correction for water content, and the mean rose from 279 to 606 µg/g. A formed sample, or a repeat once a diarrheal illness has settled, is the fix; the American practice update requires a semi-solid or solid specimen and the European guideline asks for a formed one.28,4,7Grade C

  • Surgery on the stomach or pancreas

    lowers it and lowers its reliability

    Gastrectomy, bariatric bypass and pancreatic resection reduce the hormonal and nerve signals that stimulate the pancreas and uncouple stomach emptying from enzyme delivery, so insufficiency is common after them and the stool test, which measures secretion only, is declared unreliable by the European guideline for diagnosing it; the bariatric review's advice is to consider insufficiency in anyone with prolonged digestive complaints after the operation and to confirm it before treating.7,38,39Grade C

07 · Reading it well

Caveats, and what belongs with a physician.

Reduced secretion is not insufficiency. The European definition of exocrine pancreatic insufficiency is secretion below the level that allows normal digestion, the gland's reserve means malabsorption appears only when enzyme delivery falls to roughly 5 to 10 percent of normal, and the diagnosis rests on symptoms, nutritional status and a function test read together in a clinical context, never on the stool number alone.7,8Grade A

In a person with no reason to suspect pancreatic disease, a low result is more likely to be wrong than right: at a 5 percent pre-test probability the pooled false-positive rate is 11 percent against a false-negative rate of 1.1 percent, which is why the meta-analysis recommends the test for ruling insufficiency out rather than for finding it in low-probability people, and why the European guideline warns of false positives in that setting.23,7Grade A

Conditions outside the pancreas can mimic or cause a low value: celiac disease, inflammatory bowel disease, gastric resection and hypersecretory states can either mimic or cause insufficiency, diabetes lowers the number without proof of maldigestion, small intestinal bacterial overgrowth explains non-pancreatic steatorrhea in diabetes and should be considered when enzymes do not help, and the test is unreliable after upper gastrointestinal surgery. Imaging cannot diagnose insufficiency, but it is how the causes of a low value are found.12,25,7,4Grade B

Blood markers help interpret a low value in people with pancreatic disease and were never validated as a substitute in well people. Among 114 patients with chronic pancreatitis, a serum magnesium below 2.05 mg/dL detected insufficiency with a sensitivity of 0.88 and a negative predictive value of 0.91, and low hemoglobin, albumin, prealbumin and retinol-binding protein and a raised HbA1c were also associated; the European guideline finds that evidence limited and makes no strong recommendation on it.43,7Grade C

No study has followed symptom-free adults with a mildly low value, 100 to 200 µg/g or just under 200 on a formed sample, to see whether anything happens to them, and no trial has treated such a value in well adults; the one double-blind trial of enzymes in diarrhea-predominant irritable bowel found no benefit and did not measure pancreatic function. The within-person stability of the test (coefficient of variation about 15 percent) means a repeat on a formed sample is informative; it does not supply the missing outcome data.7,5Grade D

See a physician

  • Unexplained weight loss, pale, greasy, floating or foul-smelling stools, or oily leakage, with any elastase result, because these are the symptoms of insufficiency and the number is secondary to them.
  • A value below 100 µg/g on a formed stool sample, which the American practice update calls good evidence of exocrine pancreatic insufficiency and which belongs with a gastroenterologist and imaging of the pancreas before any treatment.
  • A low value together with diabetes, particularly diabetes that began in adulthood with weight loss or without the usual features of type 2, since diabetes caused by pancreatic disease is underdiagnosed, often taken for type 2, and in chronic pancreatitis carries a raised risk of pancreatic cancer.
  • Low vitamin D, A, E or K, bone loss, or a low B12 or magnesium that does not respond to replacement, alongside digestive symptoms or a low elastase.
  • A heavy drinking history or long smoking history with recurrent upper abdominal pain, with or without a low value, since the stool test misses mild disease.
  • Persistent diarrhea, bloating or weight loss after pancreatic, gastric or bariatric surgery, where the stool test is unreliable and a different test of digestion is needed.

This page is education, not individual medical advice, and reading it creates no physician-patient relationship.

08 · Open questions

What the literature does not settle.

  • No study has followed well adults with a mildly low elastase (100 to 200 µg/g, or just under 200 on a formed sample) to any outcome; what such a value means on a wellness panel in someone without weight loss, steatorrhea, diabetes or a pancreatic history is unknown.
  • Whether a low value in diabetes represents insufficiency that benefits from enzymes is contested: the large screening studies say it is common, the one study that used the direct duodenal test in type 1 diabetes found only mild changes and poor correlation, and the European guideline recommends against routine testing in diabetes.
  • Between 11 and 22 percent of older adults without digestive disease have a low value; whether this is disease, normal aging of the gland or a mixture, and whether anyone benefits from acting on it, has not been studied.
  • In diarrhea-predominant irritable bowel syndrome, whether insufficiency coexists with the syndrome or causes it remains unclear, and no randomized or blinded trial of enzymes guided by the stool test has been done.
  • The monoclonal and polyclonal assays do not give interchangeable results, the European guideline says a cutoff cannot be established, and there is no agreed harmonization; a value is only as readable as the assay named on the report.
  • Whether treating real insufficiency improves survival rather than digestion and nutrition is supported by observational data only, and whether enzyme replacement improves glucose control in diabetes is conflicting.

09 · In practice

How Dr. Tagge reads it in his own practice.

I order elastase for a reason, not as a screen. The reasons are unexplained weight loss, stools that are pale, greasy or hard to flush, diabetes with gut symptoms, a vitamin D or other fat-soluble vitamin that will not come up on replacement, a heavy drinking history, and anyone who has had surgery on the pancreas or stomach. When it comes back low I do not read it alone; one marker is a clue, three are a story. I put it beside vitamin D, B12, zinc, ferritin and magnesium, beside HbA1c and fasting glucose, beside albumin, and beside the stool itself, because a watery sample reads low whatever the pancreas is doing, and a low value in a loose stool gets repeated on a formed sample before I believe it. The two cutoffs on the report, 200 and 100 µg/g, are the diagnostic studies' lines for insufficiency, not mine, and they were drawn in people with pancreatic disease. A mildly low value on a wellness panel in a well person is a question, not a diagnosis; the literature has never followed such a person, and I say so plainly. I will also say where I am ahead of the evidence: ordering the test for a vitamin D that will not rise, with no gut symptoms, is reasoning from the physiology, not from a study, and I treat what it finds with that in mind. Where it is real, a low result earns a gastroenterologist and imaging of the pancreas, because the number points to a disease and it is the disease we treat. It does not earn an enzyme capsule bought online: a response to enzymes proves nothing, the trials that showed benefit were in people with known pancreatic disease, and the first job is to find out why the gland is quiet.

A practice judgment, labeled as one (Grade D): it is how one physician reads the number for the people he cares for, not a recommendation for you.

10

Questions

11 · Sources

43 sources, read in full.

Numbered in the order they appear. Each line says what this page relies on from the paper; the link opens the record at PubMed or the publisher.

  1. 1.

    Sziegoleit A, Krause E, Klör HU, Kanacher L, Linder D. Elastase 1 and chymotrypsin B in pancreatic juice and feces. Clinical Biochemistry. 1989. PMID 2720968. DOI 10.1016/s0009-9120(89)80003-7.

    Laboratory method study · Neither elastase 1 nor chymotrypsin B was degraded during intestinal passage, and both reflected pancreatic function in a clinical study.

  2. 2.

    Dominici R, Franzini C. Fecal elastase-1 as a test for pancreatic function: a review. Clinical Chemistry and Laboratory Medicine. 2002. PMID 12059069. DOI 10.1515/CCLM.2002.051.

    Review · Elastase-1 is a human-specific protease of the acinar cells, undetectable in porcine or bovine enzyme preparations, very stable, unaffected by enzyme treatment, and correlates with direct function tests.

  3. 3.

    Weiss FU, Budde C, Lerch MM. Specificity of a Polyclonal Fecal Elastase ELISA for CELA3. PLoS One. 2016. PMID 27459204. DOI 10.1371/journal.pone.0159363.

    Laboratory method study · Elastase passes through the gut with only limited degradation; the polyclonal assay is specific for the CELA3 isoform and does not cross-react with pig pancreatin; CELA1 is not expressed in the adult human pancreas.

  4. 4.

    Whitcomb DC, Buchner AM, Forsmark CE. AGA Clinical Practice Update on the Epidemiology, Evaluation, and Management of Exocrine Pancreatic Insufficiency: Expert Review. Gastroenterology. 2023. PMID 37737818. DOI 10.1053/j.gastro.2023.07.007.

    Consensus statement · Fecal elastase is the most appropriate initial test and must be run on a semi-solid or solid stool; below 100 µg/g is good evidence of insufficiency and 100 to 200 is indeterminate; testing can be done on enzyme therapy; a therapeutic trial is unreliable for diagnosis; imaging cannot identify insufficiency; once diagnosed, enzyme replacement is required with fat-soluble vitamin monitoring and a baseline bone density scan.

  5. 5.

    Löser C, Möllgaard A, Fölsch UR. Faecal elastase 1: a novel, highly sensitive, and specific tubeless pancreatic function test. Gut. 1996. PMID 8944569. DOI 10.1136/gut.39.4.580.

    Laboratory method study · Against the secretin-caerulein test in 44 patients, 35 disease controls and 50 healthy volunteers, a 200 µg/g cutoff gave sensitivity 63 percent (mild), 100 percent (moderate and severe), 93 percent overall, specificity 93 percent; day-to-day CV 15 percent; stable a week at room temperature.

  6. 6.

    Stein J, Jung M, Sziegoleit A, Zeuzem S, Caspary WF, Lembcke B. Immunoreactive elastase I: clinical evaluation of a new noninvasive test of pancreatic function. Clinical Chemistry. 1996. PMID 8595714.

    Laboratory method study · Control spot stools ranged from 136 to 4,440 µg/g with 95 percent between 175 and 1,500; output correlated with amylase, lipase and trypsin; results unaffected by enzyme replacement.

  7. 7.

    Dominguez-Muñoz JE, Vujasinovic M, de la Iglesia D, et al.; European PEI Multidisciplinary Group. European guidelines for the diagnosis and treatment of pancreatic exocrine insufficiency: UEG, EPC, EDS, ESPEN, ESPGHAN, ESDO, and ESPCG evidence-based recommendations. United European Gastroenterology Journal. 2025. PMID 39639485. DOI 10.1002/ueg2.12674.

    Guideline · Insufficiency is secretion below what allows normal digestion and is not synonymous with reduced secretion; FE-1 accuracy is low from poor specificity, a cutoff cannot be established though 200 µg/g is frequently used, and a formed stool is needed; low values in 10 to 50 percent of diabetes (pooled 22 percent in type 2, 5.4 percent when pancreatic-origin diabetes excluded) with no routine screening; 11.5 to 21.7 percent of older adults, relevance unknown; 26.2 percent of new celiac disease; 4 to 13 percent of diarrhea-predominant IBS with false positives not excludable; not reliable after upper gastrointestinal surgery.

  8. 8.

    Struyvenberg MR, Martin CR, Freedman SD. Practical guide to exocrine pancreatic insufficiency - Breaking the myths. BMC Medicine. 2017. PMID 28183317. DOI 10.1186/s12916-017-0783-y.

    Review · Fat malabsorption occurs when duodenal lipase falls below 5 to 10 percent of normal; sensitivity in mild to moderate insufficiency as low as 30 percent; watery stools almost invariably read low so a formed stool is required; enzymes need not be stopped for testing; smoking is associated with reduced exocrine function and alcohol and smoking cessation are part of treatment.

  9. 9.

    Leeds JS, Oppong K, Sanders DS. The role of fecal elastase-1 in detecting exocrine pancreatic disease. Nature Reviews Gastroenterology and Hepatology. 2011. PMID 21629239. DOI 10.1038/nrgastro.2011.91.

    Review · In many countries fecal elastase-1 is the main and often the only available test of exocrine pancreatic function; exocrine insufficiency occurs in a range of conditions beyond alcohol-related disease.

  10. 10.

    Boros E, Szabó A, Zboray K, Héja D, Pál G, Sahin-Tóth M. Overlapping Specificity of Duplicated Human Pancreatic Elastase 3 Isoforms and Archetypal Porcine Elastase 1 Provides Clues to Evolution of Digestive Enzymes. Journal of Biological Chemistry. 2017. PMID 28062577. DOI 10.1074/jbc.M116.770560.

    Laboratory method study · The human pancreas does not express CELA1 but secretes two CELA3 isoforms, which did not evolve distinct substrate preferences; increased gene dosage rather than new specificity appears to compensate for the lost CELA1 activity.

  11. 11.

    Li H, Gao Z, Zhang S. Localization of trypsin, chymotrypsin and elastase in the digestive tract of amphioxus Branchiostoma japonicum with implications to the origin of vertebrate pancreas. Tissue and Cell. 2022. PMID 36174270. DOI 10.1016/j.tice.2022.101943.

    Laboratory method study · Trypsin, chymotrypsin and elastase are widely distributed in the amphioxus digestive tract, especially the hepatic caecum and mid-gut, suggesting that region is homologous to vertebrate exocrine pancreatic cells.

  12. 12.

    Keller J, Aghdassi AA, Lerch MM, Mayerle JV, Layer P. Tests of pancreatic exocrine function - clinical significance in pancreatic and non-pancreatic disorders. Best Practice and Research Clinical Gastroenterology. 2009. PMID 19505669. DOI 10.1016/j.bpg.2009.02.013.

    Review · The pancreas is the main factory for digestive enzymes; celiac disease, inflammatory bowel disease, Zollinger-Ellison syndrome and gastric resection can mimic or cause exocrine insufficiency; available function tests lose accuracy in mild impairment.

  13. 13.

    Madsen OD. Pancreas phylogeny and ontogeny in relation to a 'pancreatic stem cell'. Comptes Rendus Biologies. 2007. PMID 17631449. DOI 10.1016/j.crvi.2007.03.006.

    Review · Blood glucose regulation likely evolved during early vertebrate evolution to secure the evolution of complex brains, and on current phylogenetic insight the beta cell pioneered the formation of the pancreatic organ.

  14. 14.

    Sikkens EC, Cahen DL, Koch AD, et al.. The prevalence of fat-soluble vitamin deficiencies and a decreased bone mass in patients with chronic pancreatitis. Pancreatology. 2013. PMID 23719594. DOI 10.1016/j.pan.2013.02.008.

    Cross-sectional study · In 40 patients with chronic pancreatitis (70 percent exocrine insufficient), deficiency of vitamins A, D, E and K in 3, 53, 10 and 63 percent; osteopenia 45 percent and osteoporosis 10 percent, more than expected even in exocrine-sufficient patients.

  15. 15.

    Duggan SN, Smyth ND, Murphy A, Macnaughton D, O'Keefe SJ, Conlon KC. High prevalence of osteoporosis in patients with chronic pancreatitis: a systematic review and meta-analysis. Clinical Gastroenterology and Hepatology. 2014. PMID 23856359. DOI 10.1016/j.cgh.2013.06.016.

    Systematic review and meta-analysis · Across 10 studies of 513 patients with chronic pancreatitis, pooled prevalence of osteoporosis 23.4 percent, osteopenia 39.8 percent, either 65 percent.

  16. 16.

    Jøker-Jensen H, Mathiasen AS, Køhler M, Rasmussen HH, Drewes AM, Olesen SS. Micronutrient deficits in patients with chronic pancreatitis: prevalence, risk factors and pitfalls. European Journal of Gastroenterology and Hepatology. 2020. PMID 32732813. DOI 10.1097/MEG.0000000000001866.

    Cross-sectional study · In 115 outpatients with chronic pancreatitis, vitamin D deficiency 22 percent, zinc 20 percent, magnesium 17 percent; vitamin A (10 percent) and E (7 percent) deficiency only in those with exocrine insufficiency; trace-element deficits tracked albumin.

  17. 17.

    Allen RH, Seetharam B, Podell E, Alpers DH. Effect of proteolytic enzymes on the binding of cobalamin to R protein and intrinsic factor. In vitro evidence that a failure to partially degrade R protein is responsible for cobalamin malabsorption in pancreatic insufficiency. Journal of Clinical Investigation. 1978. PMID 22556. DOI 10.1172/JCI108924.

    Laboratory method study · In the stomach B12 binds almost exclusively to R protein; pancreatic proteases partially degrade R protein and transfer B12 to intrinsic factor within minutes (trypsin more than chymotrypsin more than elastase), so lack of pancreatic proteases is the primary defect in B12 malabsorption of pancreatic insufficiency.

  18. 18.

    Vujasinovic M, Hedström A, Maisonneuve P, et al.. Zinc deficiency in patients with chronic pancreatitis. World Journal of Gastroenterology. 2019. PMID 30774274. DOI 10.3748/wjg.v25.i5.600.

    Cross-sectional study · In 150 patients with chronic pancreatitis, zinc deficiency in 26 percent, associated with age 60 and over and with smoking (about three times the risk in current and heavy smokers) but not with exocrine insufficiency, diabetes or HbA1c.

  19. 19.

    Hardt PD, Brendel MD, Kloer HU, Bretzel RG. Is pancreatic diabetes (type 3c diabetes) underdiagnosed and misdiagnosed?. Diabetes Care. 2008. PMID 18227480. DOI 10.2337/dc08-s244.

    Review · Exocrine insufficiency is frequent in diabetes; diabetes caused by exocrine pancreatic disease may comprise 8 percent or more of all diabetes; beta-cell mass and incretin secretion depend on normal exocrine function.

  20. 20.

    Ewald N, Bretzel RG. Diabetes mellitus secondary to pancreatic diseases (Type 3c)--are we neglecting an important disease?. European Journal of Internal Medicine. 2013. PMID 23375619. DOI 10.1016/j.ejim.2012.12.017.

    Review · Type 3c diabetes is 5 to 10 percent of diabetes in Western populations, underdiagnosed; physicians should screen for exocrine insufficiency and fat-soluble vitamin lack, especially vitamin D; most cases arise from chronic pancreatitis with its raised pancreatic cancer risk.

  21. 21.

    Zsóri G, Illés D, Terzin V, Ivány E, Czakó L. Exocrine pancreatic insufficiency in type 1 and type 2 diabetes mellitus: do we need to treat it? A systematic review. Pancreatology. 2018. PMID 29779830. DOI 10.1016/j.pan.2018.05.006.

    Review · The exocrine and endocrine pancreas are closely linked anatomically and physiologically; exocrine impairment appears to be a frequent, largely overlooked complication of diabetes.

  22. 22.

    Hardt PD, Hauenschild A, Nalop J, et al.; S2453112/S2453113 Study Group. High prevalence of exocrine pancreatic insufficiency in diabetes mellitus. A multicenter study screening fecal elastase 1 concentrations in 1,021 diabetic patients. Pancreatology. 2003. PMID 14526149. DOI 10.1159/000073655.

    Cross-sectional study · Among 1,021 people with diabetes (323 type 1, 697 type 2), elastase was above 200 µg/g in 59.3 percent and below 100 in 22.9 percent, lower with early onset, long duration and low body mass index.

  23. 23.

    Vanga RR, Tansel A, Sidiq S, El-Serag HB, Othman MO. Diagnostic Performance of Measurement of Fecal Elastase-1 in Detection of Exocrine Pancreatic Insufficiency: Systematic Review and Meta-analysis. Clinical Gastroenterology and Hepatology. 2018. PMID 29374614. DOI 10.1016/j.cgh.2018.01.027.

    Systematic review and meta-analysis · 14 studies, 428 cases and 673 controls: pooled sensitivity 0.77 and specificity 0.88 against secretin testing, 0.96 and 0.88 against fecal fat; at 5 percent pre-test probability false-negative 1.1 percent and false-positive 11 percent; at 40 percent about 10 percent of cases missed.

  24. 24.

    Capurso G, Traini M, Piciucchi M, Signoretti M, Arcidiacono PG. Exocrine pancreatic insufficiency: prevalence, diagnosis, and management. Clinical and Experimental Gastroenterology. 2019. PMID 30962702. DOI 10.2147/CEG.S168266.

    Review · Two assays exist, monoclonal and polyclonal; the polyclonal is less specific for elastase-1, overestimates concentration and is affected by enzyme replacement while the monoclonal is not; measurement must be on solid stool; smokers without pancreatic disease showed moderate (18 percent) and severe (10 percent) reductions more often than controls.

  25. 25.

    Hahn JU, Kerner W, Maisonneuve P, Lowenfels AB, Lankisch PG. Low fecal elastase 1 levels do not indicate exocrine pancreatic insufficiency in type-1 diabetes mellitus. Pancreas. 2008. PMID 18362841. DOI 10.1097/MPA.0b013e3181656f8.

    Cross-sectional study · In 33 people with type 1 diabetes tested by secretin-cerulein and by both monoclonal and polyclonal elastase assays, 11 had only mild to moderate insufficiency, elastase correlated poorly with the direct test, non-pancreatic steatorrhea in two thirds was probably bacterial overgrowth, and a low value should not indicate enzyme substitution.

  26. 26.

    Walkowiak J, Nousia-Arvanitakis S, Cade A, et al.. Fecal elastase-1 cut-off levels in the assessment of exocrine pancreatic function in cystic fibrosis. Journal of Cystic Fibrosis. 2002. PMID 15463824. DOI 10.1016/s1569-1993(02)00096-6.

    Cross-sectional study · In 725 people with cystic fibrosis and 243 healthy subjects from four countries, the best cutoff was 184 µg/g with inter-country differences; the authors suggest a 160 to 200 range rather than a single line.

  27. 27.

    Lankisch PG, Schmidt I, König H, et al.. Faecal elastase 1: not helpful in diagnosing chronic pancreatitis associated with mild to moderate exocrine pancreatic insufficiency. Gut. 1998. PMID 9616319. DOI 10.1136/gut.42.4.551.

    Cross-sectional study · In 64 patients graded by the secretin-pancreozymin test and fecal fat, 94 percent of those with normal function had a normal elastase but only 53 percent of those with insufficiency had an abnormal one; abnormal in 73 to 91 percent of severe and under half of mild to moderate cases.

  28. 28.

    Fischer B, Hoh S, Wehler M, Hahn EG, Schneider HT. Faecal elastase-1: lyophilization of stool samples prevents false low results in diarrhoea. Scandinavian Journal of Gastroenterology. 2001. PMID 11444478. DOI 10.1080/003655201300192058.

    Laboratory method study · Of 519 samples from 310 patients, the 151 diarrheal samples averaged 279 µg/g unprocessed and 606 after freeze-drying to standard water content; 16 of 151 (11 percent) below 200 proved normal after correction.

  29. 29.

    Rathmann W, Haastert B, Icks A, et al.. Low faecal elastase 1 concentrations in type 2 diabetes mellitus. Scandinavian Journal of Gastroenterology. 2001. PMID 11589378. DOI 10.1080/003655201750422657.

    Cross-sectional study · 544 people with type 2 diabetes against 544 matched controls: median 308 versus 418 µg/g; below 100 in 11.9 versus 3.7 percent (adjusted odds ratio 4.5); HbA1c of 7 percent or more carried 5.6 times the odds of a low value.

  30. 30.

    Hardt PD, Hauenschild A, Jaeger C, Teichmann J, Bretzel RG, Kloer HU; S2453112/S2453113 Study Group. High prevalence of steatorrhea in 101 diabetic patients likely to suffer from exocrine pancreatic insufficiency according to low fecal elastase 1 concentrations: a prospective multicenter study. Digestive Diseases and Sciences. 2003. PMID 14560984. DOI 10.1023/a:1025422423435.

    Cross-sectional study · In 101 diabetic patients with low elastase, mean fat excretion was 9.19 g a day; 40.6 percent were normal (under 7 g) and 39.6 percent exceeded 10 g a day, uncorrelated with diabetes type, duration or symptoms.

  31. 31.

    Rothenbacher D, Löw M, Hardt PD, Klör HU, Ziegler H, Brenner H. Prevalence and determinants of exocrine pancreatic insufficiency among older adults: results of a population-based study. Scandinavian Journal of Gastroenterology. 2005. PMID 16036530. DOI 10.1080/00365520510023116.

    Cross-sectional study · Among 914 adults aged 50 to 75, 11.5 percent had elastase of 200 µg/g or below and 5.1 percent below 100, increasing with age; smoking was an independent risk factor.

  32. 32.

    Herzig KH, Purhonen AK, Räsänen KM, et al.. Fecal pancreatic elastase-1 levels in older individuals without known gastrointestinal diseases or diabetes mellitus. BMC Geriatrics. 2011. PMID 21266058. DOI 10.1186/1471-2318-11-4.

    Cross-sectional study · Among 106 adults aged 60 to 92 without digestive disease, surgery or diabetes, 23 (21.7 percent) were below 200 µg/g and 9 below 100; elastase correlated negatively with age (r = -0.35).

  33. 33.

    Leeds JS, Hopper AD, Sidhu R, et al.. Some patients with irritable bowel syndrome may have exocrine pancreatic insufficiency. Clinical Gastroenterology and Hepatology. 2010. PMID 19835990. DOI 10.1016/j.cgh.2009.09.032.

    Cross-sectional study · Elastase below 100 µg/g in 19 of 314 (6.1 percent) with diarrhea-predominant IBS, none of 105 with chronic diarrhea and none of 95 controls; enzyme therapy improved stool frequency, consistency and pain in the low group.

  34. 34.

    Leeds JS, Hopper AD, Hurlstone DP, et al.. Is exocrine pancreatic insufficiency in adult coeliac disease a cause of persisting symptoms?. Alimentary Pharmacology and Therapeutics. 2007. PMID 17269988. DOI 10.1111/j.1365-2036.2006.03206.x.

    Cross-sectional study · Low elastase in 11 percent of new celiac disease, 6 percent on a gluten-free diet without symptoms, 30 percent on the diet with chronic diarrhea and 4 percent of non-celiac controls; enzymes cut stool frequency from four a day to one in 18 of 20.

  35. 35.

    Vujasinovic M, Tepes B, Volfand J, Rudolf S. Exocrine pancreatic insufficiency, MRI of the pancreas and serum nutritional markers in patients with coeliac disease. Postgraduate Medical Journal. 2015. PMID 26253920. DOI 10.1136/postgradmedj-2015-133262.

    Cross-sectional study · Among 90 celiac patients, exocrine insufficiency by elastase in 4 (4.4 percent), with normal pancreatic MRI in all four and at least one low nutritional marker in each.

  36. 36.

    de la Iglesia-Garcia D, Vallejo-Senra N, Iglesias-Garcia J, López-López A, Nieto L, Domínguez-Muñoz JE. Increased Risk of Mortality Associated With Pancreatic Exocrine Insufficiency in Patients With Chronic Pancreatitis. Journal of Clinical Gastroenterology. 2018. PMID 28858943. DOI 10.1097/MCG.0000000000000917.

    Prospective cohort · In 430 patients with chronic pancreatitis followed a mean 8.6 years, insufficiency by breath test (29.3 percent) carried a mortality hazard ratio of 2.59 (1.42 to 4.71); cancer, infection and cardiovascular events led the causes of death.

  37. 37.

    de la Iglesia-García D, Huang W, Szatmary P, et al.; NIHR Pancreas Biomedical Research Unit Patient Advisory Group. Efficacy of pancreatic enzyme replacement therapy in chronic pancreatitis: systematic review and meta-analysis. Gut. 2017. PMID 27941156. DOI 10.1136/gutjnl-2016-312529.

    Systematic review and meta-analysis · 17 randomized studies, 511 patients: enzyme replacement raised the coefficient of fat absorption from 63.1 to 83.7 percent versus baseline and to 83.2 versus 67.4 on placebo, improved nitrogen absorption, stool weight and pain, and in follow-up raised nutritional markers and quality of life without significant adverse events.

  38. 38.

    Vujasinovic M, Valente R, Thorell A, et al.. Pancreatic Exocrine Insufficiency after Bariatric Surgery. Nutrients. 2017. PMID 29137169. DOI 10.3390/nu9111241.

    Review · Insufficiency is a multifactorial complication of upper gastrointestinal surgery whose symptoms overlap with those of gastric bypass; it should be considered in anyone with prolonged complaints suggesting maldigestion after bariatric surgery and treated once confirmed.

  39. 39.

    Guman MSS, van Olst N, Yaman ZG, et al.. Pancreatic exocrine insufficiency after bariatric surgery. Surgery for Obesity and Related Diseases. 2022. PMID 35074297. DOI 10.1016/j.soard.2021.12.017.

    Cross-sectional study · In a bariatric clinic, 63.4 percent of postoperative patients scored abnormally on a symptom questionnaire, yet only 11.9 percent of 310 fecal elastase tests suggested insufficiency and the two did not correlate (c-index 0.55); specificity of the test seems reduced after surgery.

  40. 40.

    Huang W, de la Iglesia-García D, Baston-Rey I, et al.. Exocrine Pancreatic Insufficiency Following Acute Pancreatitis: Systematic Review and Meta-Analysis. Digestive Diseases and Sciences. 2019. PMID 31161524. DOI 10.1007/s10620-019-05568-9.

    Systematic review and meta-analysis · Pooled insufficiency 62 percent during admission for acute pancreatitis and 35 percent at follow-up (1,795 patients, 39 studies), twice as common after severe attacks and higher with necrosis or alcohol; fecal elastase detected significantly fewer cases than other tests.

  41. 41.

    Gardner TB, Adler DG, Forsmark CE, Sauer BG, Taylor JR, Whitcomb DC. ACG Clinical Guideline: Chronic Pancreatitis. American Journal of Gastroenterology. 2020. PMID 32022720. DOI 10.14309/ajg.0000000000000535.

    Guideline · Chronic pancreatitis is most commonly caused by toxins such as alcohol or tobacco, genetic variants and recurrent acute pancreatitis; exocrine insufficiency and diabetes develop at variable rates; diagnosis rests on cross-sectional imaging with function tests in a secondary role.

  42. 42.

    Terzin V, Várkonyi T, Szabolcs A, et al.. Prevalence of exocrine pancreatic insufficiency in type 2 diabetes mellitus with poor glycemic control. Pancreatology. 2014. PMID 25278304. DOI 10.1016/j.pan.2014.07.004.

    Cross-sectional study · In 101 people with type 2 diabetes, elastase averaged 385.9 µg/g with HbA1c of 7 percent or more against 454.6 below 7, not explained by pancreas size or steatosis.

  43. 43.

    Lindkvist B, Domínguez-Muñoz JE, Luaces-Regueira M, Castiñeiras-Alvariño M, Nieto-Garcia L, Iglesias-Garcia J. Serum nutritional markers for prediction of pancreatic exocrine insufficiency in chronic pancreatitis. Pancreatology. 2012. PMID 22898630. DOI 10.1016/j.pan.2012.04.006.

    Cross-sectional study · In 114 patients with chronic pancreatitis (33 percent insufficient by breath test), magnesium below 2.05 mg/dL detected insufficiency with sensitivity 0.88, specificity 0.66 and negative predictive value 0.91; low hemoglobin, albumin, prealbumin and retinol-binding protein and a raised HbA1c were also associated.

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