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Exocrine pancreatic insufficiency in dogs

What are the causes of canine exocrine pancreatic insufficiency and how is it best managed?

19 December 2019, at 9:00am

The pancreas of the dog is a V-shaped gland located in the cranial abdomen comprising the exocrine (acinar cells) and endocrine (islets of Langerhans) portions. The exocrine pancreas secretes digestive enzymes, fluid and bicarbonate in response to food ingestion (Singh et al., 2018). Canine exocrine pancreatic insufficiency (EPI) is a digestive disorder resulting from the insufficient secretion of enzymes from the pancreas. This condition is frequently attributed to pancreatic acinar atrophy (PAA) in the dog, in which the enzyme-producing acinar cells are believed to be destroyed by a hereditary autoimmune process (Evans et al., 2015). While EPI has been found to affect many breeds of dog (Batchelor et al., 2007b), EPI attributed to PAA has a documented higher prevalence in the German Shepherd Dog (GSD) population (Tsai et al., 2013); as a result GSDs comprise two thirds of cases of EPI due to pancreatic acinar atrophy in dogs (Hall et al., 2003).

EPI was historically thought to be a simple autosomal recessive disorder; however, a study recently demonstrated that EPI has a more complex mode of inheritance, in which multiple genes combined with environmental factors may contribute towards the variability in clinical presentation and disease progression (Clark and Cox, 2012). Current studies are focused on alleles of the canine major histocompatibility complex and dog leukocyte antigen (DLA) (Tsai et al., 2013). EPI can occur in dogs of any age, but signs are usually first seen between six months and six years of age (Hall et al., 2003).

The exocrine pancreas has a large functional reserve resulting in clinical signs being frequently observed quite late into the disease process where circa 90 percent of the functional mass of the acinar cells have been destroyed (Watson, 2012). Dogs with EPI often present with mild to moderate weight loss, despite showing a good appetite or in some cases, dependent on the condition of the dog, extreme hunger (polyphagia). Other signs include large volumes of diarrhoea with varied consistency, which may be foul-smelling or have a greasy appearance (steatorrhoea), flatulence and intestinal borborygmi. Some cases may display vomiting and increased drinking (polydipsia) and coat condition may become poor and greasy (German, 2012) when presenting to their vet. This variability of clinical signs suggests that EPI is a heterogeneous disorder and that affected dogs can display a spectrum of clinical signs (Batchelor et al., 2007a).

In time, EPI can lead to severe malnutrition because affected dogs, while eating normally, may not be able to digest and absorb sufficient nutrients – namely vitamins B12 (cobalamin), folate (another B vitamin), E and K (Williams, 1996) – due to the role of the pancreatic duct cells in secretion of bicarbonate and intrinsic factor (IF). Bicarbonate regulates the pH of the intestinal lumen environment and IF, which is necessary for the absorption of cobalamin in the small intestine, functions at pH 7; therefore, in EPI the decreased or absent secretion of bicarbonate in this location results in decreased vitamin and cobalamin absorption (Simpson, 2005). It is therefore important to measure serum folate and cobalamin levels when investigating the dog with possible EPI.

In dogs, pancreatic exocrine function is reliably assessed by measuring blood trypsinogen levels using the serum trypsin-like immunoreactivity (TLI) test. A value below 2.5μg/L is highly suggestive of EPI (Suchodolski and Steiner, 2003); however, diagnosis is more difficult when EPI is subclinical (Mansfield, 2015). Any dog presenting with gastrointestinal signs should be considered worthwhile of investigation for EPI because of the varied presentation of these cases, which do not always follow the prescribed list of clinical signs (Batchelor et al., 2007a).

Management of EPI cases revolves largely around supplementation with pancreatic enzymes, which can be provided in numerous forms including tablets, capsules, granules, uncoated enzyme powder and raw pancreas. There has been considerable debate about efficacy of such products, with earlier work suggesting that dogs given uncoated enzymes had a better response to therapy as reported by Hall et al. (1991), but more recent work has not shown such a difference (Simpson, 2005). Due to the associated deficiencies in cobalamin with this condition, supplementation with vitamin B12 is required as part of ongoing management (Simpson et al., 1989) to ensure the dogs are receiving a complete balance of nutrients.

Studies have found significant and independent risk factors for decreased survival in EPI, particularly that hypocobalaminaemia at diagnosis (P=0.04) and not receiving enzyme replacement therapy (P=0.003) were associated with a poorer prognosis. Conversely, hyperfolataemia was associated with improved prognosis (P=0.02) (Allenspach et al., 2007). These results confirm the importance of measuring serum cobalamin and folate concentrations at the time when EPI is diagnosed, as hypocobalaminaemia is negatively associated with prognosis, particularly in the absence of a high serum folate concentration (Soetart et al., 2019).

Historically, dogs with EPI were fed a diet that was digestible with relatively low fibre and low-to-moderate fat levels (Hand et al., 2011), because fat is considered the most difficult nutrient for the intestine to assimilate and lipase activity is the limiting step in digestion of fat (Simpson, 2006). The rationale for lowering the fat content is that intestinal bacteria metabolise unabsorbed fat to hydrolysed fatty acids, which stimulate secretion of fluids in the distal small intestine and colon, potentially worsening the diarrhoea (Westermarck et al., 1995; Simpson, 2006). However, a canine EPI study found that feeding a moderate fat, low fibre, highly digestible food decreased flatulence, borborygmi, faecal volume and defecation frequency compared to feeding the original diets (Westermarck et al., 1995). In another study, a diet with up to 43 percent calories from fat, with a focus on the digestibility of the protein, fat and carbohydrates, yielded positive results in reduction of clinical signs (Suziki et al., 1999) compared to diets containing 18 and 27 percent of calories from fat. In a study of dogs with experimental EPI, a high-fat, high-protein diet in combination with enzyme replacement therapy optimised fat absorption (Suziki et al., 1999).

When considering the available literature, it seems that faecal fat output is more dependent on the digestibility of the fat rather than the total amount fed (Simpson, 2006). In addition, a diet with a high energy density fulfils increased energy requirements while reducing the amount of food given per meal and decreasing the digestive workload and stool volume. A high energy density diet may also support weight regain during convalescence if the dog has presented with marked weight loss as a result of EPI. Dogs suffering from digestive disorders often show a decreased appetite (Batchelor et al., 2007a) and weight loss; therefore, a diet with high palatability should be considered to encourage spontaneous consumption.

In conclusion, canine exocrine pancreatic insufficiency is a complex gastrointestinal condition that results in varied clinical signs and is associated with nutritional deficiencies. In addition to supplementation with replacement pancreatic enzymes and vitamin B12, feeding a highly digestible, high energy density, complete and balanced diet is recommended. High-fibre diets should be avoided, as fibre may interfere with the fat absorption including essential fatty acids and vitamins.

Author Year Title
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Laura Hayes, BVetMed, MRCVS, qualified from the Royal Veterinary College and worked in small animal practice for several years before moving into industry. She joined Royal Canin in 2019 as scientific affairs manager, building collaborative working relationships with key opinion leaders and universities.

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