How I Diagnose/How I Treat--Chronic Pancreatitis in Dogs
World Small Animal Veterinary Association World Congress Proceedings, 2010
Jörg M. Steiner,, PhD, DACVIM, DECVIM-CA
College Station, TX, USA


Historically, canine pancreatitis was believed to be acute in the majority of cases. However, in a large necropsy study conducted at the Animal Medical Center in New York, histopathologic evidence of chronic pancreatic inflammation was observed almost twice as frequently as was evidence of acute pancreatic inflammation.1 As a result, it is now recognized that dogs not only may have acute pancreatitis with classical clinical signs, such as vomiting and abdominal discomfort, but may also have chronic pancreatitis, which may be associated with atypical clinical signs or may even be subclinical.


Chronic pancreatitis should be considered as a potential differential diagnosis in any dog with chronic gastrointestinal signs, where an underlying cause cannot be readily identified. A careful history should be taken and a thorough physical examination should be completed. Then the patient should be evaluated for endoparasites by a routine fecal smear, fecal flotation, and a therapeutic trial with a broad-spectrum anthelminthic agent. Next, the patient should be evaluated for secondary causes of gastrointestinal disease by performing a complete blood count, a serum chemistry profile, and a urinalysis. If no abnormalities are found that identify a definitive secondary cause for the chronic gastrointestinal signs the patient should be evaluated for exocrine pancreatic insufficiency by measurement of a serum canine trypsin-like immunoreactivity concentration (cTLI) and for chronic pancreatitis by measurement of a serum canine pancreatic lipase immunoreactivity concentration (measured by Spec cPL®).

Many different cell types in the body synthesize and secrete lipases. In contrast to catalytic assays for the measurement of lipase activity, use of immunoassays does allow for the specific measurement of lipase originated from the exocrine pancreas. Serum cPLI was measured in a group of dogs with exocrine pancreatic insufficiency and the median serum cPLI concentration was significantly decreased compared to clinically healthy dogs. In addition, serum cPLI concentration was non-detectable in most of the dogs and minimal serum cPLI concentrations were observed in the rest of the dogs, indicating that serum cPLI concentration originates from the exocrine pancreas and is specific for exocrine pancreatic function. In another study serum cPLI was evaluated in dogs with experimentally induced chronic renal failure. While serum cPLI was significantly higher in dogs with experimentally induced chronic renal failure than in clinically healthy dogs, most dogs had serum cPLI concentrations within the reference range and none of the dogs had serum cPLI concentrations that were above the currently recommended cut-off value for pancreatitis. These data would suggest that serum cPLI concentration can be used as a diagnostic test for pancreatitis even in dogs with renal failure. Also, long-term oral administration of prednisone did not have any effect on serum cPLI concentration. Finally, the sensitivity of different minimally-invasive diagnostic tests was compared in dogs with biopsy-proven pancreatitis. The sensitivity of serum TLI concentration was below 35% and that of serum lipase activity was less than 55%.2 In contrast, the sensitivity for serum cPLI concentration for pancreatitis was above 80%.2 Thus, measurement of serum cPLI concentration is currently the most sensitive and specific diagnostic test for pancreatitis in dogs.


Often canine patients with chronic pancreatitis have concurrent conditions, most notably IBD. Very little is known about appropriate therapy for these patients and management is often limited to evaluation and treatment of the concurrent condition, and careful monitoring of the pancreatitis. Serum calcium and triglyceride concentrations should always be evaluated in these patients in order to identify any risk factors that can potentially be addressed therapeutically. Also, the use of an ultra low-fat diet is recommended in these patients. Patients should be monitored for a decrease in serum cPLI concentration, initially every 2-3 weeks and less frequently as the condition improves.

Over the last two decades a new form of pancreatitis, autoimmune pancreatitis, has been described in humans. Like many cases of chronic pancreatitis in dogs, autoimmune pancreatitis is characterized by a lymphocytic-plasmacytic infiltration of the pancreas.3,4 Human patients with autoimmune pancreatitis respond favourably to the administration of corticosteroids.4 Recently, several clinicians have started to cautiously treat canine patients with chronic pancreatitis with corticosteroids and have found this treatment strategy to be beneficial in a portion of cases, but further research is needed before this treatment strategy can be recommended for routine use.


1.  Steiner JM, Newman S, Xenoulis P, et al. Sensitivity of serum markers for pancreatitis in dogs with macroscopic evidence of pancreatitis. Vet Ther 2008; 9:263-273;

2.  Steiner JM, Broussard J, Mansfield CS, Gumminger SR, Williams DA. Serum canine pancreatic lipase immunoreactivity (cPLI) concentrations in dogs with spontaneous pancreatitis. J. Vet. Int. Med. 2001;15:274 (abstract);

3.  Newman SJ, Steiner JM, Woosley K, et al. Localization of pancreatic inflammation and necrosis in dogs. J Vet Int Med 2004; 18:488-493;

4.  Church NI, Pereira SP, Deheragoda MG, et al. Autoimmune pancreatitis: Clinical and radiological features and objective response to steroid therapy in a UK Series. Am J Gastroenterol 2007; 102:2417-2425.


Speaker Information
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Jörg M. Steiner, Dr. med. vet., PhD, DACVIM, DECVIM-CA
College Station, TX, USA