April 9-11, 2015 IVIS conf,  Dr. Jorg Steiner, TAMU Gastrointestinal Lab presented the following on EPI   http://www.ivis.org/proceedings/voorjaarsdagen/2015/30.pdf

The Disease & The Pancreas (updated April 23, 2010)

EPI, Exocrine Pancreatic Insufficiency, is the inability of the pancreas to manufacture and secrete the necessary enzymes required by the body to digest food and absorb nutrients......causing the body to starve no matter how much food the dog eats.


One must always be careful when reading medical information on the internet. For this very reason, I have on this website, to include various published medical research reports on EPI from different and well-respected researchers in hopes of giving you, the reader, the most current information and findings on EPI. I have also included earlier research reports so that readers will be able to discern for themselves changes, updates and progress that is being made regarding EPI and to be able to recognize non-current or no longer valid information they may happen upon.

Although this website is dedicated to EPI in Dogs.... now included  is a section dedicated to EPI in Cats too!
Cats with EPI should be fed a highly digestible, good quality and energy dense diet, with an appropriate pancreatic enzyme supplement mixed into it


Proceedings of the 33rd World Small - Animal Veterinary Congress - Dublin, Ireland - 2008


How I Treat - Exocrine Pancreatic Insufficiency
Jörg M. Steiner Dr.med.vet., PhD, DACVIM, DECVIM-CA
Gastrointestinal Laboratory, Dept.VSCS, College of Veterinary Medicine and Biomedical Sciences, Texas A&M
University, 4474 TAMU College Station, TX 77843-4474, USA

Enzyme supplementation
Most dogs and cats with EPI can be successfully treated by dietary supplementation with pancreatic enzymes. Dried extracts of bovine or porcine pancreas are available e.g. Viokase or Pancrezyme). The clinical impression in dogs and cats that powder is more effective
than tablets, capsules, and especially enteric-coated products has also been substantiated in human patients with EPI. Initially, two teaspoons per 20kg body weight and meal should be given in dogs and one teaspoon per cat and meal in cats. Oral bleeding has recently been reported in 3 of 25 dogs with EPI treated with pancreatic enzyme supplements.1 The oral bleeding stopped in all 3 dogs after the dose of pancreatic enzymes was decreased. Moistening the food pancreatic/powder mix also appears to decrease the frequency of this side effect. If the owner has access to fresh pancreas this may be a viable alternative to use of pancreatic powder. However, there is a slight risk of transmission of Aujeszky’s disease from raw pork pancreas, BSE from raw bovine pancreas, and Echinococcus from raw game pancreas. One to three ounces (30-90 g) of raw chopped pancreas can replace one teaspoon of pancreatic extract. Raw bovine pancreas can be kept frozen for several months without loss of enzymatic activity. Preincubation of the food with pancreatic enzymes, supplementation with bile salts, or concurrent antacid therapy are unnecessary in most canine and feline patients with EPI. When clinical signs have resolved the amount of pancreatic enzymes given can be gradually decreased to the lowest effective dose, which may vary from patient to patient, and from batch to batch of the pancreatic supplement. Even though pancreatic enzyme supplementation causes the clinical signs to subside in almost all patients, it has been shown in human beings and dogs with EPI that nutrient absorption, and particularly fat absorption are not normalized by enzyme supplementation. This is thought to be due to the low pH in the stomach leading to irreversible damage of the pancreatic lipase contained in the supplement. Even though gastric pH can be raised by administration of antacids, the negative effect of the increased intraluminal gastric pH on fat digestion by gastric lipase appears to cancel much of the positive effect, so that overall there is only a minimal increase in fat absorption, which is clinically not important in most patients. However, the use of omeprazole has recently been shown to be efficacious in human patients with EPI and may be tried if the patient does not respond to routine therapy.

Dietary considerations
Some authors have suggested feeding low fat diets in order to accommodate impaired fat digestion. However, this may even further decrease fat assimilation and may
potentially lead to serious complications associated with hypovitaminoses of fat-soluble vitamins and conditions associated with a lack of essential fatty acids. Some types of dietary fiber interfere with pancreatic enzyme activity. Therefore, a diet low in insoluble or non-fermentable fiber should be fed.

Vitamin supplementation
Response to enzyme supplementation alone may not be satisfactory in some canine or feline patients with EPI. This is not surprising if one considers that many dogs
and especially cats with EPI also have a serious depletion of total body cobalamin stores. Serum cobalamin and folate concentrations should be routinely evaluated in
small animals with suspected EPI, and dogs and cats with severely decreased serum cobalamin concentrations should be treated with cobalamin parenterally. Even
though hypovitaminoses of other vitamins, especially vitamin K, are not very common, they have been reported in some cats with EPI and should be anticipated as
potential complications. Patients that do not respond to therapy Some dogs and cats do not respond to enzyme supplementation and cobalamin application. These
patients likely have concurrent small intestinal disease. In dogs with EPI small intestinal bacterial overgrowth is common and may need to be treated with antibiotic
therapy. In cats with EPI inflammatory bowel disease can occur concurrently.

EPI is associated with an irreversible loss of pancreatic acinar tissue in most cases, and complete recovery is therefore extremely rare. However, with appropriate
management and monitoring these patients usually gain weight quickly, pass normal stools, and can go on to live a normal life for a normal life span. Reference
1. Rutz GM, Steiner JM, Williams DA (2002) Available on request from author.
Reprinted in IVIS with the permission of the Congress Organizers
Proceedings of the 33rd World Small Animal Veterinary Congress 2008


 In: Encyclopedia of Canine Clinical Nutrition,  Pibot P., Biourge V. and Elliott D.A. (Eds.). International Veterinary Information Service, Ithaca NY http://www.ivis.org/, Last updated: 11-Feb-2008; A4205.0208

The Role of Nutrition in the Pathogenesis and the Management of Exocrine Pancreatic Disorders
By: K. W. Simpson

College of Veterinary Medicine, Cornell University, Ithaca, NY, USA.

The exocrine pancreas has an essential role in the digestion and absorption of nutrients. Pancreatic acini synthesize and secrete enzymes such as lipase, trypsin and amylase that digest fats, proteins and carbohydrates. Pancreatic duct cells secrete bicarbonate that maintains an optimal pH for digestive and absorptive processes, and intrinsic factor that enables the absorption of cobalamin (Vitamin B12). The exocrine pancreas also produces bacteriostatic peptides and defensins that regulate the upper GI flora, and has a role in maintenance of the intestinal mucosa and glucose homeostasis.

Dysfunction of the exocrine pancreas is broadly characterized by the loss of functional pancreatic mass (exocrine pancreatic insufficiency), or inflammation (pancreatitis), with consequent diarrhea and weight loss, or abdominal pain and vomiting respectively. This chapter will outline the role of nutrition in the pathogenesis and management of exocrine pancreatic disease in the dog.

Kenneth W. SIMPSON

Kenneth W. SIMPSON
Dr. Simpson graduated from the University of Edinburgh (BVM&S) in 1984. His PhD (University of Leicester, 1988) focused on pancreatic and intestinal function in dogs, and was followed by clinical training at the University of Pennsylvania, and the Ohio State University. He is presently an Associate Professor of Medicine at Cornell University with clinical and research interests in internal medicine and gastroenterology.

1. Exocrine Pancreatic Insufficiency



A diagnosis of exocrine pancreatic insufficiency (EPI) is made on the basis of compatible historical and clinical findings nd by ruling out infectious, parasitic, metabolic, and anatomic causes of small bowel diarrhea and weight loss. The diagnosis is confirmed by demonstrating a subnormal serum concentration of trypsin-like immunoreactivity (TLI), recently reviewed by Westermarck & Wiberg (2003).

Table 1. Most Common Signs Observed in 109 German Sherpherd Dogs with Epi* Vs 186 Normal German Sherpherd Dogs
Grey or Yellowish feces99%German Sherpherd
Large amounts of feces95%
Defecation > 3x /day90%
Lean body or cachexia90%
Frequent flatulence88%
Diarrhea several times per week77%
Skin problems14% (not different from control group)
* Exocrine pancreatic insufficiency / from Raiha & Westermack 1989  

Dogs with EPI usually present for investigation of chronic diarrhea (feces of large volume and cow-pat consistency, often yellow to grey in color)  and weight loss (mild to extreme), which is often associated with a ravenous appetite. Pica and coprophagia are also common. A poor hair-coat (hair loss, eczema, dryness, scurf) polydipsia and marked muscle loss are observed in some dogs.

 The feces of canine pancreatic insufficiency patients are often of large volume and cowpat consistency, and are discolored and highly pungent.

The feces of canine pancreatic insufficiency patients are often of large volume and cowpat consistency, and are discolored and highly pungent. (© M. Weber).

Polyuria and polydipsia may be present when exocrine pancreatic insufficiency caused by chronic pancreatitis is complicated by diabetes mellitus. Acute abdomen due to mesenteric torsion has also been associated with EPI.

Supplementary Tests
Clinicopathological Tests

Routine hematology and biochemistry are fairly unremarkable in dogs with EPI. Modest increases in alanine amino-transferase (ALT) and a decrease in cholesterol are observed in some dogs. Pan-hypoproteinemia is not a feature of EPI, and its presence suggests that primary small intestinal disease is causing the diarrhea and weight loss, rather than EPI.

The presence of hyperglycemia and glucosuria in dogs with signs of EPI should prompt consideration of diabetes mellitus secondary to chronic pancreatitis, or pancreatic hypoplasia.

Serum concentrations of cobalamin (Vitamin B12) and Vitamins A and E can also be markedly reduced in dogs with EPI. In contrast, serum folate concentration is often increased. Serum concentrations of zinc and copper are decreased in dogs with experimental pancreatic insufficiency, whereas serum iron and transferrin saturation are increased.

Specific Diagnosis

The specific diagnosis of EPI is made by demonstrating a subnormal concentration of trypsin-like immunoreactivity (TLI) in a fasted serum sample (Williams & Batt 1988). Serum TLI is considered to originate solely from the pancreas and is an indicator of pancreatic mass and inflammtion (Simpson et al 1991)

In dogs with EPI caused by atrophy or chronic inflammation the amount of TLI leaking from the pancreas into the circulation is reduced, and a subnormal TLI concentration can be demonstrated  Interpretation of tyrosin-like immunoreactivity (TLI) values in fasting dogs.

Interpretation of tyrosin-like immunoreactivity (TLI) values in fasting dogs. Patients with persistently intermediate TLI concentrations are likely to have partial EPI that may progress to complete EPI  (Wiberg et al., 1999a; Wiberg & Westermarck 2002)

The TLI test is a simple and reliable way of confirming a diagnosis of EPI. However, if the TLI test result does not fit the patient's clinical signs it is prudent to rerun the test after ensuring an overnight fast to rule out sampling/handling/technician error. The TLI test will not detect conditions that may cause the intra-luminal destruction of pancreatic enzymes e.g., hyperacidic states such as gastrinoma and mast cell tumor, but these conditions have other diagnostic features such as hematemesis and esophagitis to distinguish then from primary EPI.

Diagnostic Pitfalls

EPI must be distinguished from primary intestinal disease.
The combination of diarrhea, weight loss, ravenous appetite, and relatively normal laboratory findings, often in a breed that is predisposed (e.g., German Shepherd) The following two figures strongly suggests EPI is a likely cause.

Frequency distribution of age at diagnosis of canine exocrine pancreatic insufficiency in 199 german shepherd dogs and 102 dogs of other breeds.

 Frequency distribution of age at diagnosis of canine exocrine pancreatic insufficiency in 199 german shepherd dogs and 102 dogs of other breeds. Frequency distribution of breeds for 301 cases of canine pancreatic insufficiency.

Frequency distribution of breeds for 301 cases of canine pancreatic insufficiency. The presence of large bowel diarrhea, frequent vomiting, pallor, jaundice, edema or ascites should prompt consideration of other more likely diagnoses. Hypoproteinemia is not a feature of uncomplicated EPI and usually indicates a protein losing enteropathy.

Do not rely solely on the TLI test result without other supportive evidence of exocrine pancreatic disease.

Decision Tree

The differential diagnosis of EPI includes other causes of small bowel diarrhea and weight loss

Table 2. Differential Diagnosis of Chronic Small Bowell Diarrhea
InfectiousGiardia, Histoplasmosis, pathogenic bacteria (Salmonella, Campylobacter), Phycomycoses, Mycobacteria
MetabolicHypoadrenocorticism, liver disease, kidney disease
DietaryIntolerance / Allergy
Exocrine pancreatic insufficiencyPrimary or secondary
Small intestinal diseaseStructuralPartial obstruction : intussusception, foreign object, neoplasia, lymphangiectasia, congenital anomalies
InflammatoryEosinophilic, lymphoplasmacytic, granulomatous
NeoplasticLymphosarcoma, adenocarcinoma, leiomyoma, fibrosarcoma
Bacterial overgrowthSecondary, idiopathic
FunctionalMotility disorders, idiopathic


Risk Factors

Pancreatic acinar atrophy (PAA) is probably the most common cause of exocrine pancreatic insufficiency (EPI) in the dog. Dogs under five years of age diagnosed with EPI are usually suspected of having pancreatic acinar atrophy, whereas older dogs likely have a higher incidence of pancreatitis induced degeneration (Hall et al.,1991).  Dogs with chronic relapsing pancreatitis are considered at increased risk of developing EPI.

Breed Predispositions

Many different breeds have been diagnosed with EPI .

A familial predisposition to pancreatic acinar atrophy has been reported in German Shepherd Dogs, Collies and English Setters (Westermarck 1980; Boari et al 1994; Moeller et al 2002; Wiberg 2004). As it is impossible to determine the cause of atrophy in an end stage pancreas, prospective studies of the development of canine PAA have been conducted. These longitudinal studies have identified German Shepherd dogs and Rough Coated Collies with sub-clinical exocrine pancreatic insufficiency, detected by assay of circulating TLI, in whom pancreatic atrophy is preceded by a marked lymphocytic infiltration Westermarck et al 1993a; Wiberg wet al 1999b, 2000). This strongly suggests an autoimmune basis for PAA. There is no evidence that a lack of trophic factors e.g., CCK, or anti-pancreatic antibodies play a role in the genesis of PAA.

Breeds such as Miniature Schnauzers appear to be overrepresented with relapsing pancreatitis and may be predisposed to EPI.

Pathophysiological Mechanisms of EPI

Exocrine pancreatic insufficiency (EPI) in the dog is most often a consequence of a severe reduction of pancreatic mass caused by pancreatic acinar atrophy, or chronic pancreatitis

 Chronic pancreatitis. Fibrosis and atrophy are evident in this section from the pancreas of a dog with EPI secondary to pancreatitis (x10; H&E coloration).

Photographs of EPI due to pancratic acinar and chronic atrophy and chronic pancreatitis. Chronic pancreatitis. Fibrosis and atrophy are evident in this section from the pancreas of a dog with EPI secondary to pancreatitis (x10; H&E coloration).

Lymphocytic inflammation precedes the development of EPI in dogs with familial acinar atrophy (x40; H&E coloration).

Photographs of EPI due to pancratic acinar and chronic atrophy and chronic pancreatitis. Lymphocytic inflammation precedes the development of EPI in dogs with familial acinar atrophy (x40; H&E coloration).

Islet cells, stained for insulin (brown), and surrounded by a sea of atrophied exocrine tissue are relatively normal in dogs with EPI. (Glucose tolerance is abnormal but responds to enzyme supplementation - see text for details) (x20; immunocoloration for insulin).

Photographs of EPI due to pancratic acinar and chronic atrophy and chronic pancreatitis. Islet cells, stained for insulin (brown), and surrounded by a sea of atrophied exocrine tissue are relatively normal in dogs with EPI. (Glucose tolerance is abnormal but responds to enzyme supplementation - see text for details) (x20; immunocoloration for insulin).

Pancreatic hypoplasia with concomitant EPI and diabetes mellitus has been rarely documented. In theory, EPI can also occur secondary to:

  • The increased destruction, or decreased activity, of pancreatic enzymes in patients with acid hypersecretion
  • Decreased synthesis and secretion of enzymes in the presence of severe malnutrition.

Extensive loss of exocrine pancreatic mass (approx. 90%), whether by atrophy or chronic inflammation is required before signs of EPI are evident Simpson et al 1992 The predominant clinical signs of EPI, diarrhea, weight loss and a ravenous appetite can be directly attributed to decreased intra-duodenal concentrations of pancreatic enzymes, bicarbonate, and various other factors with resultant malassimilation of fats, carbohydrates and proteins

 Pathophysiology of exocrine pancreatic insufficiency.

 Pathophysiology of exocrine pancreatic insufficiency. Malabsorption of fat soluble vitamins and cobalamin, and changes in the number and composition of the small intestinal bacterial flora have also been documented in dogs with EPI and may contribute to their clinical condition  (Williams et al 1987; Westermarck et al 1993b; Adamama-Moraitou et al 2002) . Subnormal serum concentrations of cobalamin are frequently documented (approximately 75% of cases) in dogs with EPI and are likely a consequence of intrinsic factor deficiency, disrupted binding of cobalamin to IF (by intestinal pH, lack of proteases) and bacterial consumption of cobalamin (Batt et al 1989; Simpson et al 1989a; Simpson et al 1993) .

Following ingestion, cobalamin is released from food in the stomach. It is then bound to a non-specific cobalamin-binding protein of salivary and gastric origin called haptocorrin. Intrinsic factor (IF), a cobalamin binding protein that promotes cobalamin absorption in the ileum, is produced by the stomach and pancreas in dogs. The affinity of cobalamin for haptocorrin is higher at acid pH than for IF, so most is bound to haptocorrin in the stomach.

Upon entering the duodenum haptocorrin is degraded by pancreatic proteases, and cobalaminis transferred from haptocorrin to IF, a process facilitated by the high affinity of IF for cobalamin at neutral pH. Cobalamin-IF complexes traverse the intestine until they bind to specific receptors (previously called IFCR, but recently dubbed cubilin) located in the microvillus pits of the apical brush-border membrane of ileal enterocytes.

Cobalamin is then transcytosed to the portal bloodstream and binds to a protein called transcobalamin 2 (TC II), which mediates cobalamin absorption by target cells. A portion of cobalamin taken up by hepatocytes is rapidly (within an hour in the dog) re-excreted in bilebound to haptocorrin.

Cobalamin of hepatobiliary origin, in common with dietary derived cobalamin, under goes transfer to IF and receptor mediated absorption, thus establishing enterohepatic recirculation of the vitamin.

Low serum cobalamin concentrations in dogs have been associated with exocrine pancreatic insufficiency (EPI), severe intestinal disease, IF-Cbl receptor abnormalities, and conditions associated with the proliferation of enteric abacteria e.g stagnant loops.

Cobalamin absorption in the dog.

 Cobalamin absorption in the dog.

Other abnormalities encountered in dogs with EPI include alterations in:

  • Glucose homeostasis (subclinical glucose intolerance) (Rogers et al 1983)
  • Pancreatic and gastrointestinal regulatory peptides (e.g., vasoactive intestinal polypeptide, gastric inhibitory polypeptide, somatostatin, pancreatic polypeptide) (Hellmann et al 1991)  
  • The regulation of small intestinal mucosal growth, enzyme synthesis and enzyme degradation  (Batt et al 1979; Sorensen et al 1988; Simpson et al 1989b) .

Trace element status in EPI has received relatively little study. One report of German Shepherd dogs with EPI indicates normal serum concentrations of copper and zinc. However, it has been recently demonstrated that serum copper and zinc decline, and serum iron and transferrin saturation increase, after pancreatic duct ligation (Adamama-Moraitou et al 2001)  

The clinical significance of these abnormalities is unclear. The severe malassimilation of nutrients in EPI can lead to protein calorie malnutrition  that may further compromise residual pancreatic function, intestinal absorption and metabolic homeostasis.

Dermatological abnormalities are variably present in German Shepherd dogs with EPI and their presence may be related to protein calorie malnutrition, deficiencies in trace elements and minerals and potentially adverse reactions to food.

EPI Case Study - Neutered Female Boxer Age 7 Years

History and Clinical Examination
  • Weight loss (6 months), chronic diarrhea (>6 times per day for 3 months), ravenous appetite
  • Emaciated (1/5 body score), 3mm cutaneous nodules x 2 on left neck and right flank
  • Referral veterinarian treated with fluoroquinolone  (enrofloxacin), prednisone   (10 days) and metronidazole:  no signs of improvement
Stat Blood Tests
Packed cell volume39%
Total Protein7.5 g/dL
Blood urea nitrogen30 - 40 mg/dL
Glucose86 mg/dL
Complete Blood Count Profile
PCV (%)44(42 - 57) Albumin (g/dL)3.9(3.1 - 4.1)
MCV (fl)74(63 - 74)Globulin (g/dL)3.0(1.9 - 3.6)
WBC (thou/µL)8.1(6.2 - 14.4)ALP (IU/L)1130(12 - 122)
Neutrophilis (thou/µL)6.6(3.4 - 9.7)ALT (IU/L)357(25 - 106)
Lymphocytes (thou/µL)1.4(1.3 - 4.7)GGT (IU/L)33(0 - 10)
Platelets (thou/µL)475(179 - 483)Cholesterol (mg/dL)106(124 - 335)
Figure 8
Figure 8.
Pancreas: Atrophy with lymphoplasmacytic inflammation, still residual acinar tissue fibrosis
Liver: Vacuolar hepatopathy - multifocal, clusters
Stomach: Moderate lymphoplasmocytic infiltrate lymphoid nodules in deep lamina propria; +++helicobacter organisms
Duodenum/jejunum/ileum: Peyers patches sampled
Mesenteric lymph node: Hyperplasia
Urinalysis Fecal
USG1.041 Giardia ELISA negative, zinc sulphate negative. Many Clostridium perfringens- like organisms on a smear
pH6.5TLI5.58 µg/L (5 - 25)
protein++ (meaningless because of the urine specific gravity) Cobalamin184 pg/mL (175 - 550)
Folate27 ng/mL (4 - 13)
Ultrasound: Questionable diffuse hyperechoic liver
Thoracic radiographs: Normal
Cutaneous aspirates: Blood
Coagulation tests: Normal (OSPT, APTT)
Working Diagnosis After Surgery
Exocrine pancreatic insufficiency, possible Helicobacter related gastritis, reactive lymphadenopathy presumed secondary to gastrointestinal disease.
Over the next two months the dog gained 10lbs (42# to 52#), fecal consistency normalized and the energy level of the dog increased.
Chronic diarrhea, weight loss and polyphagia suggestive of maldigestion or malabsorption. Elevated liver enzymes suggest a primary or secondary hepatopathy in response to exogenous corticoteroids or GI disease. Low cholesterol suggests small intestinal disease, EPI or liver disease. Lack of other evidence of hepatic synthetic failure (normal protein, BUN) suggests low cholesterol may be due to GI disease or EPI.

Normal TLI test lowers the likelihood of EPI suggesting that high folate and low normal cobalamin are due to intestinal disease. Due to the degree of weight loss and lack of a definitive diagnosis an exploratory laparotomy was performed to biopsy the gastrointestinal tract, liver and mesenteric lymph nodes.

At surgery a 10 cm tangled cloth in the stomach and a 6cm cloth in the jejunum were found. These were considered incidental as they were not causing obstruction and likely secondary to the polyphagia. A thickened gastric wall and severe atrophy of the pancreas were observed.
The history of marked weight loss, diarrhea and polyphagia coupled with normal serum protein but low cholesterol are typical for EPI. The increases in liver enzymes, particularly ALP are higher than might be anticipated in EPI, but the prior steroid treatment and intestinal foreign bodies may have contributed to these changes. The changes in cobalamin and folate are suggestive of EPI or a blind loop syndrome.

No obstruction was visualized by ultrasound or at surgery, so the changes in cobalamin and folate are likely a consequence of EPI. However the TLI test result at 5.28 argued strongly against EPI. Usually dogs with signs of EPI have TLI < 2.5. In this case histology confirmed atrophy secondary to lymphocytic infiltration. Perhaps the small amount of inflammation in the residual pancreatic tissue was enough to keep the TLI in the normal range while exocrine secretion was severely impaired. Unfortunately the owner declined further TLI tests to further investigate the normal TLI.


Enzyme Supplement (additional information/ updates from website owner, not author of this article, is printed in red)

An enzyme preparation must be given at mealtimes in situations of insufficient enzyme secretion by the exocrine pancreas. There are many variations of powdered porcine enzymes, and/or appropriate enteric preparations that are now available. Please view http://www.epi4dogs.com/enzymesdigestion.htm for the list. Also feeding fresh pancreas is another alternative.

The enzyme supplement should be mixed into the food. Pre-incubation does not "significantly" impact outcome (Pidgeon & Strombeck 1982) However, many folks claim that their dog only did better when the enzymes are incubated in room temperature food  for approximately 20 minutes.  A new batch, change of preparation or increased amounts may produce a response. If cessation of diarrhea and weight gain are observed over a two week period the animal is maintained on this regimen and an attempt is made to decrease the enzyme supplement to the lowest effective dose.

If the therapy fails, the lot or the mode of presentation may be changed, or the enzyme quantities increased. If a response is not being achieved with a dose of 0.4 g/kg of non-enteric coated powdered extract or 3 g/kg body weight/meal whole pancreas, inadequate enzyme replacement is an unlikely reason for treatment failure.


Fat soluble vitamins are likely candidates for malabsorption, and low levels of Vitamins A and E have been reported in German Shepherd dogs with EPI. Vitamin E  can be given orally (400 500 IU SID q 1 month). It seems prudent to examine the vitamin K status of dogs with EPI who have laboratory evidence of a coagulopathy (bleeding).

Cobalamin deficiency can have a myriad of effects on the body and the provision of supplementary parenteral cobalamin  (cyanocobalamin, vitamin B12)  is recommended because pancreatic enzyme supplementation does not reverse the deficiency. Studies in dogs indicate that the parenteral administration of a single dose of cyanocobalamin  (250 - 500 µg SQ once per month) is enough to prevent recurrence of metabolic abnormalities for up to one month. Please read the B12 section:
  there is a recommended protocol now for B12 treatment one injection weekly for 6 weeks, one injection bi weekly for 6 weeks and then injection monthly and test to verify that monthly holds the dog's B12 levels. Recently there have even been cases of EPI dogs being managed with a combination of certain B12 pills and Injections. again, please  review the B12 section on this website.  The cobalamin malabsorption does not resolve after enzyme supplementation and lifelong therapy is recommended.

Role of vitamin b12 in the organism.

 Role of vitamin B12 in the organism. Vitamin B12 plays a fundamental role in protein synthesis and red blood cell production and has an enzyme function in many essential biochemical reactions.

Feeding Dogs with EPI

The pivotal role of the exocrine pancreas in the digestion and assimilation of nutrients would suggest that EPI is a disease that would be particularly amenable to nutritional intervention. In "theory" a highly digestible, fat restricted diet (fat is considered the most difficult nutrient to assimilate and lipase activity is the limiting step in its digestion) that is low in fiber (fiber is indigestible, lowers energy density and hinders pancreatic enzyme activity) would seem justified in dogs with EPI. However, analysis of the outcome (survival) of 116 dogs with EPI indicates that dogs that received a modified diet (n=73, 30% dead) did not outlive those receiving a standard diet (n=43, 35% dead) (Hall et al 1991)  ...Please read below on "Potential Advantages of a High Fat Content"  because more recent additional research has proven fat restriction may not be the best treatment.

A 50% reduction of the initial dose is possible in the majority of the dogs (after stabilization is achieved (Simpson et al 1994) (This adaptation of the dose is important, because the cost of pancreatic enzymes is an obstacle to treatment for many owners, who prefer to euthanize their dogs.

Potential Advantages of a High Fat Content

In complete contrast to the paradigm of fat restriction in EPI, diets with 43% calories from fat have been shown to promote better protein, fat and carbohydrate digestibility compared to diets containing 18 and 27% calories from fat in dogs with experimental EPI (Suzuki et al 1999). Improved preservation of exogenous pancreatic enzymes, especially lipase, could explain this observation. It is of note that studies in dogs with experimental exocrine pancreatic insufficiency demonstrated that fecal fat output is more dependant on the digestibility of the fat, rather than the amount fed (Pidgeon 1982; Pidgeon & Strombeck 1982)  

A case report of 3 German Shepherd dogs with EPI and poor haircoat demonstrated that a 19% fat DM (40.8 % of calories from fat), soy protein isolate hydrolysate and rice diet was well tolerated and improved fecal quality, haircoat and weight gain (2 - 10 kg) compared with the dogs previous diets. The dogs recovered optimal body condition within a 2-month period  (Biourge & Fontaine 2004) 

These observations suggest that high fat, highly digestible diets are not contra-indicated in the management of EPI. Traditionally, dietary supplementation with medium chain triglyceride oil  (24 mL/meal) has been considered a beneficial way of providing calories to severely malnourished patients fed a highly digestible fat restricted diet but supportive data are lacking. However feeding a higher fat and thus more energy dense diet could promote a rapid restoration of optimal body weight without recourse to medium chain triglyceride oil.

As the importance of nutritional modification in the management of EPI is far from clear, and the costs associated with special diets are a common reason for euthanasia this author recommends initially feeding a good quality maintenance dog food (i.e., high digestibility) with an appropriate exogenous enzyme supplement mixed into it. If the response to treatment is poor then dietary modification is an option (see treatment failure - below).

Treatment Failures
Inadequate Enzyme Supplementation

This is probably the number one cause of treatment failure. Some dogs develop an aversion to the enzyme supplement and raw pancreas may have to be used (or enteric coated capsules of enzymes such as CREON, recently approved by the FDA), if attempts to disguise the powder are unsuccessful. Stomatitis has been reported as a side effect of exogenous enzyme supplementation and may be remedied by decreasing the supplement by 50%  (Rutz et al 2002).  Decreasing the enzyme supplement may also be considered in the majority of dogs with EPI.

Bacterial Overgrowth/intolerance

EPI may impact the quantity and composition of the small intestinal flora and compromise the host response to a normal or abnormal flora. These alterations are usually addressed by treatment with an enzyme supplement. However, in some patients, diarrhea cannot be eliminated until antibiotics are administered. In these patients treatment failure may reflect decreased synthesis of intestinal mucosal enzymes associated with EPI. The presence of an abnormal flora cannot be predicted accurately by measuring serum concentrations of cobalamin and folate, so a trial with an antibiotic such as oxytetracycline  (20 mg/kg PO TID 28d), ortylosin (10 mg/kg PO TID) can be undertaken.

Benefits of dietary modification in dogs (n=14) fed a "moderate fat, highly digestible low fiber diet" for four weeks versus a maintenance diet were restricted to a tendency (8/14 dogs) to reduced borborygmi, flatulence and fecal volume (Westermarck et al, 1990). A study in 21 EPI dogs, evaluating the benefit of feeding a low fat (13% of calories), low fiber diet compared to the usual commercial or home cooked diet failed to show any significant benefit of severe fat restriction (Westermarck et al 1995)  

Finally, feeding a low fat (13% of calories) diet in combination with exogenous enzymes (2.5 g/300 g food) to dogs (n=20) has been shown to promote a 24% average weight gain over a four month period, and a good response in 17/20 dogs (Simpson et al 1994.)   However, the role of the diet in this study is unclear as 11/20 dogs were subsequently successfully maintained on a variety of diets after the trial period.

Small Intestinal Disease

Routine hematology and biochemistry are almost always normal in uncomplicated EPI, so abnormalities such as hypoproteinemia (which may indicate a protein losing enteropathy) should be pursued.

Dietary Modifications

Once these common reasons for treatment failure (inadequate enzyme supplementation, the presence of bacterial overgrowth or intolerance, and concomitant small intestinal disease) have been addressed, nutritional modification must be considered.

Dietary management of small intestinal disease is typically based on feeding a highly digestible, usually a rice based diet that is restricted in fat.However, rice is a grain and tends to disagree with most (but not all) EPI dogs.There are now many grain-free foods available that are much more suited to an EPI dog. If dietary sensitivity is suspected an antigen restricted or protein hydrolysate diet (prescription diet) may be employed. Hydrolysates are produced by enzymatic proteolysis of native proteins which results in an array of peptides that are small enough so that they may not be recognized by, nor trigger a reaction by the immune system  (Guilford 1996). These peptides are also highly digestible, therefore reducing their retention time in the lumen of the intestine. Soy hydrolysates have been used extensively in the prevention of food sensitivity in babies and in calves  (Lalles et al 1995; Terracciano et al 2002).  If gastrointestinal signs resolve after the dietary trial (usually one to two weeks) it is necessary to rechallenge the individual with the original diet to confirm a diagnosis of dietary intolerance. The addition of specific antigens such as beef, soy, chicken to the diet that induced remission is required to document hypersensitivity.

It is of interest that the use of a soy hydrolysate diet with relatively high fat content was effective in facilitating weight gain, decreasing diarrhea and improving haircoat in three dogs with EPI that had failed to respond to diet and pancreatic extracts( Biourge & Fontaine 2004)  German sherpherd suffering from exocrine pancreatic insufficiency.

 German Shepherd suffering from exocrine pancreatic insufficiency.

If response to treatment is still poor then acid suppression to protect pancreatic enzymes and empirical dietary modifications can be made, while carefully reviewing the diagnosis of EPI and considering other underlying disorders.Please review this website's diet section http://www.epi4dogs.com/diet.htm

Dogs with confirmed EPI that respond poorly to appropriate enzyme supplementation and antimicrobial therapy usually require investigation of the small intestine.


In a majority of dogs suffering from EPI a high quality maintenance diet supplemented with powdered pancreatic enzymes resolves most of the abnormalities associated with the disease. The relatively high cost of enzyme supplementation and special diets can significantly impact the outcome, precipitating euthanasia. If pancreatitis or diabetes is associated, prognosis is more reserved.

  • 1. Adamama-Moraitou K, Rallis T, Papasteriadis A et al. Iron, zinc, and copper concentration in serum, various organs, and hair of dogs with experimentally induced exocrine pancreatic insufficiency. Dig Dis Sci 2001;46(7):1444-57. - PubMed- - 
  • 2. Adamama-Moraitou KK, Rallis TS, Prassinos NN et al. Serum vitamin A concentration in dogs with experimentally induced exocrine pancreatic insufficiency. Int J Vitam Nutr Res 2002; 72(3):177-82. - PubMed  
  • 3. Batt RM, Bush BM, Peters TJ. Biochemical changes in the jejunal mucosa of dogs with naturally occurring exocrine pancreatic insufficiency. Gut 1979; 20(8):709-15.
  • 4. Batt RM, Horadagoda NU, McLean L et al. Identification and characterization of a pancreatic intrinsic factor in the dog. Am J Physiol 1989; 256(3 Pt 1):G517-23. - PubMed
  • 5. Biourge V, Fontaine J. Exocrine Pancreatic Insufficiency and Adverse Reaction to Food in Dogs: a Positive Response to a High-Fat, Soy Isolate Hydrolysate-Based diet. J of Nutrition 2004; 134:2166S-2168S.
  • 6. Boari A, Williams DA, Famigli-Bergamini P. Observations on exocrine pancreatic insufficiency in a family of English setter dogs. J Small Anim Pract 1994; 35:247-251.
  • 7. Guilford WG. Adverse reactions to food and Nutritional management of gastrointestinal diseases. In: Guilford WG, Center SA, Strombeck DR, Williams DA & Meyer DJ eds. Strombeck's small animal gastroenterology. Philadelphia: WB Saunders Company, 1996; 436-450 & 889-910. - Available at Amazon.com  
  • 8. Hall EJ, Bond PM, Butt RM et al. A survey of the diagnosis and treatment of canine exocrine pancreatic insufficiency. J Small Anim Pract 1991; 32:613-619.
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  • 11. Moeller EM, Steiner JM, Clark LA et al. Inheritance of pancreatic acinar atrophy in German Shepherd Dogs. Am J Vet Res 2002; 63(10):1429-34. - PubMed 
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  • 14. Raiha M, Westermack E. The signs of pancreatic degenerative atrophy in dogs and the role of external factors in the etiology of the disease. Acta Vet Scand. 1989; 30(4):447-52.
  • 15. Rogers WA, O'Dorisio TM, Johnson SE et al. Postprandial release of gastric inhibitory polypeptide (GIP) and pancreatic polypeptide in dogs with pancreatic acinar atrophy. Correction of blunted GIP response by addition of pancreatic enzymes to a meal. Dig Dis Sci 1983; 28(4):345-9. - PubMed  
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  • 18. Simpson KW, Johnstone JMS, Bell PRF et al. Pancreatic function following partial pancreatectomy and anastomosis of the pancreatic duct to the stomach or duodenum in dogs. Res Vet Sci 1992; 52:97-104.
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  • 20. Simpson KW, Morton DB, Batt RM. Effect of exocrine pancreatic insufficiency on cobalamin absorption in dogs. Am J Vet Res 1989a; 50(8):1233-6. - PubMed  
  • 21. Simpson KW, Morton DB, Sorensen SH et al. Biochemical changes in the jejunal mucosa of dogs with exocrine pancreatic insufficiency following pancreatic duct ligation. Res Vet Sci 1989b; 47(3):338-45. - PubMed  
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  • 23. Sorensen SH, Riley JE, Lobley RW et al. Investigation of the physical properties of dog intestinal microvillar membrane proteins by polyacrylamide gel electrophoresis: a comparison between normal dogs and dogs with exocrine pancreatic insufficiency. Biochim Biophys Acta 1988; 955(3):275-82. - PubMed  
  • 24. Suzuki A, Mizumoto A, Rerknimitr R et al. Effect of bacterial or porcine lipase with low- or high fat diets on nutrient absorption in pancreatic-insufficient dogs. Gastroenterology 1999; 116:431-437. - PubMed 
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  • 34. Wiberg ME, Lautala HM, Westermarck E. Response to long-term enzyme replacement treatment in dogs with exocrine pancreatic insufficiency. J Am Vet Med Assoc 1998; 1;213(1):86-90. - PubMed  
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  ...as adapted from http://www.veterinarypartner.com/Content.plx?P=A&A=1627&S=1&SourceID=42


Proceeding of the NAVC - North American Veterinary Conference- Jan. 8-12, 2005, Orlando, Florida


Denise A. Elliott, BVSc, PhD, Dipl ACVIM, Dipl ACVN
Royal Canin USA, Inc
St Charles, MO

Exocrine pancreatic insufficiency (EPI) is a clinical syndrome that arises secondary to a deficiency of pancreatic enzymes. The predominate cause of EPI is an immune
mediated, lympocytic pancreatic acinar atropy. Less common causes include pancreatitis and neoplasia. In these situations, concurrent diabetes mellitus may also be
observed. EPI typically affects young dogs, 1-5 years of age, with reported breed dispositions including the German Shepard, Rough Collie, English and Irish Setters. Clinical signs are the result of nutrient malabsorption secondary to failure of intraluminal digestion. Although the digestion of protein and carbohydrate will be affected, the digestion of fat is most severely impaired since lipases are absent from the normal array of intestinal brush border enzymes. Studies have suggested that 70% of dogs with EPI have concurrent small intestinal bacterial overgrowth (SIBO) and secondary damage to the small intestine. Bacteria in the intestinal tract can metabolize undigested fat to hydroxy-fatty acids which can lead to secretory diarrhea in the largeintestine. Bacteria also deconjugate bile acids further impairing fat digestion and absorption. Some dogs will also exhibit reduced duodenal enzyme activity. This can arise because of SIBO, or as a result of generalized cachexia. The clinical signs of EPI include severe weight loss (cachexia), large, voluminous pale feces, ravenous appetite, copraphagia, borborygmus, abdominal discomfort, poor skin and haircoat. Diagnosis is confirmed by a serum TLI concentration less than 2.5 μg/L in the dog, and < 9 μg/L in the cat. Recently, it has been shown that measurement of serum TLI can be utilized to diagnose subclinical EPI, beforethe onset of clinical signs of severe pancreatic loss. Subclinical EPI is suspected in dogs with repeatedly low
serum c TLI concentrations (< 5.0 μg/L) but no clinical signs of EPI. Measurement of vitamin B12 (cobalamin) and folate is also useful in patients with EPI. A diagnosis of concurrent smallintestinal bacterial overgrowth is supported by an elevated folate and low vitamin B12 concentrations.

Client understanding and compliance are key to successful therapeutic management. The client should be informed that several weeks to months maybe required for the therapeutic response to occur, and therapy is life-long. Dietary management in conjunction with pancreatic enzyme supplementation is the cornerstone of management. The amount of food to feed the EPI patient should be calculated on the current body weight. Once the maldigestion and malabsorption are controlled with concurrent enzyme therapy, the amount fed can be gradually increased to facilitate weight gain. The food should be offered in at least two meals per day.
Since fat is the most difficult nutrient to digest, requiring the interplay between the intestine, liver and pancreas, fat digestion is most severely affected by pancreatic enzymedeficiency. Therefore, it is intuitive that a highly digestible, low fat diet is appropriate for the management of exocrine pancreatic insufficiency. However, what constitutes a restricted fat diet varies considerably among manufacturers. Nutritionists consider a restricted fat diet to be one that contains less than 18% of the energy from fat. Using this recommendation, it is clear that many diets formulated for the management of gastrointestinal disease are not actually low fat diets.
Simpson et al evaluated the effect of a low fat diet in conjunction with enzyme supplementation in the management of 20 dogs with exocrine pancreatic insufficiency. Clinical signs resolved in all 20 dogs within 4 months of instituting therapy. The body weight of the dogs increased on average by 24%. Long term contact was available for 17 of 20 dogs. Eleven of these dogs were progressing well, 3 were euthanized for poor progress, and 3 were euthanized for unrelated reasons. Once the dogs were stabilized, they required 6-58% less enzyme supplementation compared tothe initial dose needed for stabilization. A study by Westermarck et al failed to demonstrate a benefit of severe dietary fat restriction in 21 dogs with naturally occurring EPI. However, there was considerable variation between dogs in this study. Suzuki et al reported that dogs with experimental EPI tolerated a diet consisting of 43% fat (ME basis). The dogs in this study absorbed protein, fat and carbohydrate more effectively compared to when they were fed diets with 18 and 27% of the calories from fat. The improved digestibility was attributed to preservation of theexogenous pancreatic enzymes, particularly lipase, in the higher fat diets. Medium chain triglyerides, which contain 8-12 carbons,
have been recommended by some authors. It has been suggested that MCT’s are less dependent on micelle formation and the lymphatic vasculature for digestion and absorption. It has been suggested that MCT’s reduce the palatability of the diet. In addition, MCT’s have been associated with the development of hepatic lipidosis in cats. Dietary fiber can interfere with the effect of pancreatic enzymes. Dutta et al evaluated the effect of high dietary fiber in twelve human patients with EPI. The high fiber diet (28.75 g TDF/1000 kcal) was associated with an increase in fecal weight, fecal fat excretion and flatulence. In vitro studies using different concentrations of cellulose, pectin, and wheat bran incubated with amylase, lipase, and trypsin demonstrated that increasing the dietary fiber concentration
reduced pancreatic enzyme activity.Maldigestion of fat may result in malabsorption of the fat soluble vitamins. Indeed, very low concentrations of tocopherols and vitamin K coagulopathies have been reported in patients with EPI. Therefore the diet should contain adequate fat soluble vitamins. Additional subcutaneous
supplementation with vitamin K may be necessary in some patients. Malabsorption of cobalamin can occur from a combination of decreased availability of pancreatic intrinsic factor and pancreatic proteases necessary to release cobalamin from R proteins, coupled with overgrowth of cobalamin binding intestinal bacteria. Therefore, cobalamin concentrations should be measured every 3 to 6 months and subcutaneous therapy instituted where necessary. Some studies have suggested that patients with EPI may be zinc and/or copper deficient from depressed absorption. Therefore, the diet that is chosen should have adequate zinc and copper concentrations.

Recently, protein hydrolysate diets have become available for the management of adverse food reactions. These diets are highly digestible with “pre-digested” protein, and are of interest in the management of dogs with EPI. Biourge et al recently reported the use of a commercially available hydrolyzed soy isolate protein diet (consisting of 40% of calories from fat) in four male German Shepard Dogs with EPI and severe skin disease. The age of the dogs ranged from 2.5 years to 9.0 years. All four dogs had a previous diagnosis of EPI on the basis of history, clinical signs, indirect pancreatic function test (one dog) and serum canine TLI (three dogs). All dogs were lean (BSC 2/5), and, at the time of presentation, managed with high digestible diets, pancreatic enzyme supplementation and occasional antibiotic
therapy. Within 7 days of feeding the hydrolyzed soy protein isolate diet, all dogs had well formed feces, and no episode of diarrhea was observed over the 3 month follow-up. In addition, all 4 dogs gained weight (2-10kg), and were in optimal body condition after two months of dietary therapy. The results of this case series suggested that a high fat, highly digestible, soy-protein isolate hydrolysate diet is effective for the management of EPI in dogs. EPI requires life-time enzyme replacement therapy. Commercial enzyme replacers are available in powder, capsule and tablet format. Generally, enteric coated capsules and tablets appear to be less effective than enzyme powder. The enzyme should be mixed with the food prior to feeding. There have also been reports that suggest utilizing beef or pig pancreas. The only concern with this approach is the health risks associated with handling and feeding raw meats. Up to 83% of the lipase activity and 65% of the trypsin activity are lost in the acid pH of the stomach. Therefore the actual dose needed to control the clinical signs will need to be tailored to each patient. Some authors have suggested that controlling the acidity of the stomach using histamine-blocking agents may increase the effectiveness of the pancreatic enzyme supplementation This theory remains to be proven. With diet and enzyme replacer therapy, the diarrhea typically resolves in 3-7 days. The time to respond will also depend on concurrent small intestine bacterial overgrowth and mucosal dysfunction. Small intestinal overgrowth can be managed with antibiotic therapy such as metronizadole.
Wiberg et al studied the effect of long term enzyme replacement treatment in 76 German Shepherd Dogs or Rough Coated Collies with EPI. The gastrointestinal signs of EPI were controlled in approximately half of the dogs, and their general health was considered to be similar to normal dogs. Twenty percent of the dogs had a poor response to treatment, characterized by persistent high fecal volume, yellow feces and flatulence. Nonenteric-coated enzyme supplement, powdered enzyme, and raw chopped pancreas appeared to be equally effective in controlling clinical signs. Published in IVIS with the permission of the NAVC - ww.ivis.org

1. Biourge VC, Fontaine J. Exocrine pancreatic
insufficiency (EPI) and adverse reaction to food: A
positive response to a high fat, soy isolate hydrolysate
based diet. Waltham International Science Symposium,
Bangkok, Thailand, October 28-31, 2003 p, 58
2. Hall EJ, Bond PM, McLean C, et al. A survey of the
diagnosis and treatment of canine exocrine pancreatic
insufficiency. J Small Anim Pract 1991;32:613-619.
3. Simpson KW, Morton DB, Batt RM. Effect of exocrine
pancreatic insufficiency on cobalamin absorption in dogs.
Am J Vet Res 1989;50:1233-1236.
4. Simpson KW, Batt RM, Jones D, et al. Effects of exocrine
pancreatic insufficiency and replacement therapy on the
bacterial flora of the duodenum in dogs. Am J Vet Res
5. Simpson JW, Maskell IE, Quigg J, et al. The long-term
management of canine exocrine pancreatic insufficiency.
J Small Anim Pract 1994;35:133-138.
6. Suzuki A, Mizumoto A, Rerknimitr R, et al. Effect of
bacterial or porcine lipase with low- or high-fat diets on
nutrient absorption in pancreatic insufficient dogs.
Gastroenterology 1999;116: 431-437.
7. Westermarck E: Treatment of pancreatic degenerative
atrophy with raw pancreas homogenate and various
enzyme preparations. J Vet Med Assoc. 1987;34:728-
8. Westermarck E, Junttila J, Wiberg M. The role of low
dietary fat in the treatment of dogs with exocrine
pancreatic insufficiency. Am J Vet Res 1995;56:600-605.
9. Wiberg ME, Lautala H-M, Westermarck E. Response to
long-term enzyme replacement treatment in dogs with
exocrine pancreatic insufficiency. J Am Vet Med Assoc
10. Wiberg ME, Westermarck E. Subclinical exocrine
pancreatic insufficiency in dogs. J Am Vet Med Assoc
11. Williams DA, Batt RM. Sensitivity and specificity of
radioimmunoassay of serum trypsin-like immunoreactivity
for the diagnosis of canine exocrine pancreatic
insufficiency. J Am Vet Med Assoc. 1988;192:195-200.
12. Williams DA, Batt RM, Mclean L. Bacterial overgrowth in
the duodenum of dogs with exocrine pancreatic

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