Exocrine Pancreatic Insufficiency (EPI) is a syndrome that is characterized by a lack of effective pancreatic exocrine secretion in the small intestine.

EPI is not a rare clinical condition in both dogs and cats. The most common cause of EPI in dogs is pancreatic acinar atrophy (PAA). The etiopathogenesis of PAA has not yet been determined. Although PAA has been reported in many breeds, a familiar predisposition exists in German Shepherd dogs, collies and English setters. Chronic pancreatitis, repeated episodes of acute or subacute pancreatitis and pancreatic neoplasia are also reported as a cause of canine EPI. In cats chronic pancreatitis is the most common cause of EPI. Eurytrema procyonis flukes attached in the pancreatic ducts have been reported as a cause of EPI in some cats.

EPI is characterized by loss of the majority of the functional reserve capacity of the exocrine pancreas. Therefore, a decrease of intraduodenal concentration of pancreatic enzymes, bicarbonate, antibacterial and enteric mucosal "trophic" factors, as well as pancreatic and GI regulatory peptides are observed. Finally, malassimilation of nutrients (fats, carbohydrates, proteins, vitamins, trace elements), small intestinal bacterial overgrowth, morphologic and functional changes of small intestine are produced as a result of EPI.

Dogs and cats with EPI usually have a history and clinical signs of small bowel diarrhoea with voluminous, semiformed, yellowish or gray feces, polyphagia, pica especially in young dogs with inherited EPI, extreme weight loss, intestinal borborygmus, and dermatological problems such as poor coat and seborrhoea sicca. Anorexia has also been observed in some cats.

Although the symptoms of EPI are typical, they are not pathognomonic. In dogs, the differential diagnosis includes the small intestinal disorders that cause malabsorption or maldigestion (intestinal parasites, inflammatory bowel disease, small intestinal villus atrophy, lymphangiectasia, diffuse small intestinal malignancies, short bowel syndrome, changes of the intestinal brush border enzyme activities). Differential diagnosis in cats includes intestinal parasites, inflammatory bowel disease, hyperthyroidism, chronic renal failure and triaditis (chronic pancreatitis-cholangiohepatitis-inflammatory bowel disease) and intestinal lymphoma.

Routine haematology results are usually within normal limits. Liver enzyme activity such as serum alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase are mildly increased and may reflect hepatocyte damage secondary to increased uptake of hepatotoxic substances through an abnormally permeable small intestinal mucosa or hepatic lipidosis. Concurrent hyperglycemia or abnormal glucose tolerance test are not common in dogs with EPI. Some dogs have subnormal cobalamin and high folate concentration. Cats with EPI have decreased serum cobalamin and folate concentration. Serum vitamin E and A concentrations are decreased in dogs, while serum vitamin K is decreased in some cats with EPI. Absorption of trace elements in EPI may be promoted or inhibited secondary to either loss of specific factors affecting absorption or to a change in intraluminal pH. In experimentally induced EPI in dogs, as well as in some clinical cases, serum total iron concentration and % transferring saturation have been increased, while serum copper and zinc concentration have been decreased.

The histopathological lesions of dogs with EPI include pancreatic atrophy and fibrosis, foci of fatty infiltration in the liver, destruction of villi epithelium and infiltration of small intestinal lamina propria with lymphocytes and plasmacytes.

The confirmation of clinical diagnosis of EPI is based on the measurement of serum trypsin-like immunoreactivity (cTLI) by radioimmunoassay. The cTLI is a species and pancreas specific test and determines trypsin and trypsinogen that have entered the blood from pancreas. The values of TLI test are characteristic and help in differentiating EPI of small intestinal diseases. Low-fasting serum cTLI concentrations (< 2.5 μg/L) are typical of EPI. Reference range of TLI in normal dogs is 5.0 to 35 μg/L. cTLI values between 2.5-5 μg/L are indicative of early phase of EPI, before severe destruction of exocrine pancreas.

A new fecal test for diagnosis of EPI is based on the determination of fecal elastase activity using the ELISA method. It is also a species and pancreas--specific test. A single fecal sample is sufficient and values less than 10 μg/g are suggestive of EPI. A disadvantage of this test is that low results can occasionally be found in normal dogs.

The fasting serum feline TLI test (fTLI) was developed and validated for the diagnosis of EPI in cats. Values of less than 8 μg/L are suggestive of EPI. fTLI values between 8-17 μg/L are indicative of early phase of EPI. For the diagnosis of exocrine pancreatic disorders, a radioimmunoassay has been recently developed and validated that measures canine and feline pancreatic lipase immunoreactivity (PLI). The PLI test is more sensitive and specific than TLI test.

The management of EPI is based on the dietary modification and pancreatic enzyme supplementation. A highly digestible, lowfat, low-fiber diet has been shown to ameliorate clinical signs of EPI. On the contrary, some small animal gastroenterologists insist that feeding a low-fat diet does not significantly improve clinical symptoms. Dietary supplementation of medium-chain triglyceride oil (2 ml/meal every other day) may further improve the patient situation.

Exogenous pancreatic enzyme supplementation is the cornerstone of treatment of canine and feline EPI. Powdered pancreatic extracts (2 teaspoons/20 kg BW/meal for dogs, 0-1 teaspoon/cat/meal for cats) are usually adequate. The powdered form of pancreatic extracts is more suitable compared to the enteric-coated tablets, capsules or raw-chopped pancreas. Dogs and cats with EPI require parenteral cobalamin, vitamin K and oral vitamin E supplementation.

Inadequate enzyme supplementation may be a cause of treatment EPI failure. In these cases reevaluation of dose is indicated. Lipase is acid-sensitive enzyme. In some dogs with EPI the enzyme supplementation must followed by an antacid administration (ranitidine, cimetidine).

Other causes of treatment failure in dogs with EPI are small intestinal bacterial overgrowth and/or inflammatory small intestinal disease. In these cases metronidazole and/or prednisone administration is respectively indicated.

References

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