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Exocrine Pancreatic Insufficiency |  |
| Exocrine pancreatic insufficiency (EPI) is a syndrome caused by insufficient synthesis and secretion of digestive enzymes by the exocrine portion of the pancreas. It is much more common in dogs than cats. |
| Etiology and Pathogenesis: |
| Pancreatic acinar atrophy is the most common cause of EPI in dogs, while chronic pancreatitis is the most common cause in cats. Less common causes of EPI in dogs and cats are pancreatic or extrapancreatic masses that lead to obstruction of the pancreatic duct. The exocrine pancreas has a remarkable functional reserve, 90% of which must be lost before clinical signs of EPI develop. Pancreatic acinar enzymes play an integral role in the assimilation of all major dietary
components, and a lack of pancreatic digestive enzymes leads to maldigestion and malabsorption (see also
malabsorption syndromes,
Malabsorption Syndromes). The nutrients remaining in the intestinal lumen lead to loose, voluminous stools and steatorrhea. The lack of nutrients also causes weight loss and may lead to vitamin deficiencies. In animals with EPI caused by chronic pancreatitis, destruction of pancreatic tissue may not be limited to the acinar cells, and concurrent diabetes mellitus may develop. |
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| Clinical Findings: |
| EPI due to pancreatic acinar atrophy is most frequent in young adult German Shepherds. Dogs and cats with EPI due to other causes are usually middle-aged to older and can be of any breed. Clinical signs most commonly reported are polyphagia, weight loss, and diarrhea. Vomiting and anorexia are observed in some animals with EPI and may be a sign of concurrent conditions. The feces are most commonly pale, loose, and voluminous and may be malodorous. In rare cases watery diarrhea
may be seen. The high fat content of the feces can lead to a greasy appearance of the hair coat, especially in the perianal and tail region of cats. |
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| Diagnosis: |
| A serum trypsin-like immunoreactivity (TLI) concentration of ≤2.5 µg/L (dogs) or ≤8.0 µg/L (cats) is diagnostic for EPI. A few German Shepherds with subclinical EPI had severely decreased serum TLI concentrations, a lack of exocrine pancreatic tissue at abdominal exploratory, but no or only intermittent clinical signs of EPI. Recently, a new assay for measurement of fecal elastase in dogs has been developed and validated. Unfortunately, some healthy dogs or dogs with chronic
small-intestinal disease may have a decreased fecal elastase concentration, making this test less reliable than serum TLI concentration. |
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| Treatment: |
| Most dogs and cats with EPI can be successfully treated by dietary supplementation with pancreatic enzymes. Powder is more effective than tablets, capsules, and especially enteric-coated products. Initially, 2 tsp/20 kg body wt should be given with each meal for dogs and 1 tsp/cat with each meal for cats. Oral bleeding has been reported in 3 of 25 dogs with EPI treated with pancreatic enzyme supplements; the bleeding stopped in all 3 dogs after a dose reduction. Moistening the
food and pancreatic powder mix may also decrease the frequency of this side effect. When clinical signs have resolved, the amount of pancreatic enzymes given can be gradually decreased to the lowest effective dose, which may vary from animal to animal, and from batch to batch of the pancreatic supplement. Fresh pancreas may be a viable alternative to the use of powder; 1-3 oz (30-90 g) of raw chopped pancreas can replace 1 tsp of pancreatic extract. Because of a slight risk of
transmission of Aujeszky’s disease from raw porcine pancreas, only raw bovine pancreas should be used. Raw pancreas can be kept frozen for several months without loss of enzymatic activity. Preincubation of the food with pancreatic enzymes or supplementation with bile salts is not necessary. Concurrent antacid therapy has little effect on overall digestive ability and is unnecessary in almost all EPI patients. |
| Even though pancreatic enzyme supplementation decreases the clinical signs in almost all animals, nutrient absorption, especially of fats, is not normalized. Feeding low-fat diets to accommodate impaired fat digestion has been suggested, but this may further decrease fat assimilation and lead to deficiencies of fat-soluble vitamins and/or essential fatty acids. Some types of dietary fiber interfere with pancreatic enzyme activity, and a diet low in insoluble or nonfermentable
fiber should be fed. |
| Enzyme supplementation alone may not lead to complete resolution of clinical signs; cobalamin deficiency should be considered as a possible cause. Cobalamin absorption depends on adequate synthesis and secretion of intrinsic factor. In cats, ~99% of intrinsic factor is secreted by the exocrine pancreas, and most cats with EPI are cobalamin deficient. In contrast, in dogs, ~90% of intrinsic factor is secreted by the exocrine pancreas, and cobalamin deficiency is seen in
slightly <50% of dogs with EPI. Thus, serum cobalamin and folate concentrations should be routinely evaluated in small animals with suspected EPI. Dogs and cats with cobalamin deficiency, suggested by a severely decreased serum cobalamin concentration, should be treated with cobalamin parenterally. Other hypovitaminoses have been reported. For example, vitamin K deficiency leading to a coagulopathy has been reported in some cats with EPI. Some animals may not respond to enzyme
supplementation and cobalamin therapy and likely have concurrent small-intestinal disease. Dogs with EPI commonly have concurrent small-intestinal bacterial overgrowth and may need antibiotic therapy, while cats with EPI often have concurrent inflammatory bowel disease. |
| Prognosis: |
| EPI results from an irreversible loss of pancreatic acinar tissue in most cases, and recovery is rare. However, with appropriate management and monitoring, these animals usually gain weight quickly, pass normal stools, and can live a normal life for a normal life span. |
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