Exocrine Pancreatic Insufficiency in Dogs

Chapter 136

Exocrine Pancreatic Insufficiency in Dogs

Chronic diseases of the exocrine pancreas may affect pancreatic function and lead to inadequate production of digestive enzymes with associated maldigestion signs of exocrine pancreatic insufficiency (EPI). The exocrine pancreas has a large reserve in terms of secretory capacity, and clinical signs do not occur until about 90% of secretory capacity is lost. EPI in dogs can be the result of pancreatic acinar atrophy, chronic pancreatitis, pancreatic hypoplasia, and pancreatic neoplasia. EPI has been found in many different breeds, and breed-specific pathogenetic differences have been reported.


Pancreatic acinar atrophy is by far the most common reason for the clinical signs of EPI. The breeds most commonly affected with the acinar atrophy are German shepherds, rough-coated collies, and Eurasians. In these breeds, an autosomal-recessive inheritance model has been suggested. Thus far genetic studies have not been able to identify the genes involved (Clark et al, 2005; Proschowsky and Fredholm, 2007). Females and males usually are affected equally.

Studies with German shepherds and collies suggest that pancreatic atrophy is a result of an autoimmune-mediated atrophic lymphocytic pancreatitis, which gradually may lead to almost total destruction of pancreatic acinar tissue (Wiberg, Saari, and Westermarck, 2000). Typically the endocrine part of the pancreas is unaffected. A long-term follow-up study of a German shepherd litter revealed that the disease was not congenital, and a polygenic inheritance pattern has been suggested (Westermarck, Saari, and Wiberg, 2010). Genetic predisposition to the disease and the typical histologic findings during the progression of acinar atrophy have been taken as primary evidence of the autoimmune nature of the disease.

Wiberg, Saari, and Westermarck (1999b) divided the progression of acinar atrophy into subclinical and clinical phases. The subclinical phase is characterized by marked lymphocytic inflammation into a partially atrophied acinar parenchyma. Cytotoxic T cells are predominant when the tissue destruction is in progress. When the disease progresses to end-stage atrophy, the clinical phase of EPI develops. An atrophied pancreas is thin and transparent with no increase of fibrotic tissue.

The natural progression of the atrophic pancreatitis can vary markedly. Clinical signs of EPI usually appear at 1 to 5 years of age but also can be seen in older dogs. Dogs may remain in the subclinical phase for years and sometimes for life (Wiberg and Westermarck, 2002). Markers that predict which dogs are likely to develop clinical disease or environmental factors that trigger disease have not been identified thus far.

Chronic pancreatitis is the most common cause of EPI in cats and humans. In dogs, chronic pancreatitis has been recognized increasingly as a cause of EPI. Chronic pancreatitis usually affects older dogs, and breed-specific clinical and histopathologic features have been reported (Batchelor et al, 2007b; Watson et al, 2011). Unlike the situation of atrophic pancreatitis, in chronic pancreatitis usually a progressive destruction of the exocrine and endocrine pancreas is accompanied by fibrosis. Clinical signs are nonspecific gastrointestinal signs and sometimes are related to the development of diabetes mellitus. The congenital form of exocrine or exocrine and endocrine pancreatic hypoplasia sometimes is found in young puppies. EPI is reported rarely in association with pancreatic neoplasia.


Diagnosis of exocrine pancreatic dysfunction is based on typical clinical findings and confirmed with abnormal pancreatic function testing. Routine serum biochemistry profile and complete blood count often show unremarkable changes. Serum amylase and lipase activities are not useful in the diagnosis of EPI. Various pancreatic function tests that measure pancreatic enzymes in the blood and feces have been used to diagnose canine EPI. The diagnostic value of the tests has relied mostly on their ability to distinguish whether the clinical maldigestion signs are caused by EPI or a disease of the small intestine.

Serum Trypsin-like Immunoreactivity

The measurement of serum canine trypsin-like immunoreactivity (TLI) has become one of the most commonly used pancreatic function tests to diagnose canine EPI (see Chapter 136). Serum TLI measurement is species and pancreas specific, with high sensitivity and specificity for diagnosing EPI. The reference range for canine TLI (cTLI) in healthy dogs is greater than 5.7 to 45.2 µg/L (RIA). In dogs showing clinical maldigestion signs of EPI, cTLI concentrations are usually very low (<2.5 µg/L), indicating severe loss of digestive enzyme–producing acinar tissue. However, the interpretation of cTLI values is not always straightforward. Pathologic processes affecting exocrine pancreatic function are gradually progressive, and cTLI levels can vary from normal to abnormal, depending of the degree of pancreatic tissue lost. Overlapping results between normal and affected dogs can be expected, and a normal cTLI greater than 5 µg/L does not necessarily exclude the possibility of mild-to-moderate pancreatic dysfunction. In general, the lower the cTLI value, the more valuable a single measurement is in assessing the pancreatic dysfunction. Dogs with serum cTLI concentrations in the range of 2.5 to 5 µg/L and gastrointestinal signs can be a diagnostic challenge. Whether the signs are caused by a decreased exocrine pancreatic function or disease of the small intestine may be difficult to assess, and further diagnostic procedures repeating the cTLI measurement or treatment trials are needed. In breeds predisposed to autoimmune atrophic pancreatitis, repeatedly subnormal cTLI values (2.5 to 5 µg/L) in dogs showing no typical signs of EPI indicate subclinical EPI and suggest partial atrophy (Wiberg, Nurmi, and Westermarck, 1999a).

< div class='tao-gold-member'>

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Exocrine Pancreatic Insufficiency in Dogs

Full access? Get Clinical Tree

Get Clinical Tree app for offline access