Keynote Message

• There has been modest progress in the treatment of pancreatitis in dogs and cats. Such progress is based on the identification and treatment of the underlying cause, improved understanding of the nutritional needs of the patient, prevention of SIRS, and, in patients with chronic pancreatitis, treatment of a suspected immune-mediated etiology.
• Currently, the majority of both acute and chronic pancreatitis cases in both dogs and cats are considered idiopathic. However, careful study of various groups of patients with pancreatitis has led to identification of certain risk factors that can be managed therapeutically:
• Hypertriglyceridemia: a series of studies has provided evidence that, as in humans, severe hypertriglyceridemia is a significant risk factor for acute pancreatitis in dogs.
• Management includes the use of a low-fat diet (i.e., a commercial diet with less than 20 g of fat/1000 kcal or a homemade diet with an even lower fat content) and using low-fat treats (i.e., vegetables, fruits, and commercial or homemade low-fat treats).
• Fibrates and statins can also be used in patients that do not respond to dietary management alone.
• Hypercalcemia: some dogs and cats have acute pancreatitis secondary to hypercalcemia; such patients should be carefully evaluated for any possible underlying disease process (e.g., lymphoma, granulomatous infections, hypoadrenocorticism) and be managed accordingly.
• Many pharmaceutical agents can rarely cause acute or sometimes chronic pancreatitis as an idiosyncratic reaction; thus, a careful drug history is important in any canine or feline patient presenting with pancreatitis; non-essential drugs should be discontinued and essential drugs should be replaced with an alternative drug.
• Until recently, nothing per os was considered the standard nutritional recommendation for a patient with acute pancreatitis. However, more recent data have shown that acute pancreatitis, especially when severe, is a highly catabolic disease and early caloric support is essential for treatment success. Enteral nutritional support is preferable over parenteral support and pre-pancreatic delivery is as effective as post-pancreatic delivery.
• Many patients with severe acute pancreatitis ultimately succumb to a systemic inflammatory response syndrome and it has long been recognized in humans that addressing this systemic inflammation has the biggest hope for treating these patients successfully. One such approach is the treatment with fuzapladib:
• Fuzapladib sodium monohydrate (fuzapladib) is a leucocyte function-associated activation (LFA-1) inhibitor that has been shown to effectively block neutrophil extravasation in experimental animals.
• In a proof-of-concept study in Japan, the mortality in dogs with experimentally induced pancreatitis was decreased from 50% to 0% after treatment with fuzapladib.
• In two controlled clinical trials (one performed in Japan and another one performed in the USA), treatment with fuzapladib was associated with faster clinical recovery and a more rapid decrease in serum C-reactive protein or Spec cPL concentrations.
• However, fuzapladib is not yet licensed for use in dogs in the USA or in Europe, but is only licensed for use in Japan under the brand name Brenda Z.
• In cats with chronic pancreatitis (CP), the most common histopathological findings are lymphocytic or lymphocytic-plasmacytic cell infiltration and fibrosis of various degree. Based on a suspected immune-mediated etiology, treatment with corticosteroids has been suggested, but clinical trials are lacking. Cyclosporine, a calcineurin inhibitor that blocks cytokine production and inhibit T cell proliferation and activation, is a potential treatment option in cats with CP.
• In a study in mice with experimentally induced autoimmune pancreatitis, the histopathological severity index was significantly reduced after 28 days of cyclosporine treatment when compared to placebo. Cyclosporine treatment was associated with less prominent inflammatory infiltration, less fibrosis, and preserved tissue architecture, compared to the placebo group.
• In a very recent retrospective study in cats with suspected CP, a significant reduction in serum feline pancreatic lipase immunoreactivity (Spec fPL) concentration was demonstrated after daily oral cyclosporine treatment for a minimum of 23 days. Serum Spec fPL concentrations decreased in 16/19 cats.
• Dose tapering or cessation of therapy in 11 of the cats responding to cyclosporine resulted in a significant increase in Spec fPL concentration. In a small number of those cats, the cyclosporine dose was again increased to the starting dose. This was associated with a subsequent decrease in serum Spec fPL concentration in all cats, although statistical calculations were not possible due to the small sample size.

Key References

1.  De Cock HE, Forman MA, Farver TB, Marks SL. Prevalence and histopathologic characteristics of pancreatitis in cats. Vet Pathol. 2007;44(1):39–49.

2.  Fragkou FC, Adamama-Moraitou KK, Poutahidis T, Prassinos NN, Kritsepi-Konstantinou M, Xenoulis PG, Steiner JM, Lidbury JA, Suchodolski JS, Rallis TS. Prevalence and clinicopathological features of triaditis in a prospective case series of symptomatic and asymptomatic cats. J Vet Intern Med. 2016;30(4):1031–45. (doi: 10.1111/jvim.14356).

3.  Jergens AE, Allenspach K. Feline inflammatory gastrointestinal disease. In: Little SE, ed. August's Consultations in Feline Internal Medicine. Vol 7, 1st edition. St. Louis, MO: Elsevier; 2016: 129–137.

4.  Mansfield CS, James FE, Steiner JM, Suchodolski JS, Robertson ID, Hosgood G. A pilot study to assess tolerability of early enteral nutrition via esophagostomy tube feeding in dogs with severe acute pancreatitis. J Vet Intern Med. 2011;25:419–425.

5.  Schwaiger T, van den Brandt C, Fitzner B, Zaatreh S, Kraatz F, Dummer A, Nizze H, Evert M, Bröker BM, Brunner-Weinzierl MC, Wartmann T, Salem T, Lerch MM, Jaster R, Mayerle J. Autoimmune pancreatitis in MRL/Mp mice is a T cell-mediated disease responsive to cyclosporine A and rapamycin treatment. Gut. 2014;63(3):494–505.

6.  Steiner JM. Canine pancreatitis: diagnosis and treatment. In: Ettinger SJ, Feldman EC, Côté E, eds. Textbook of Veterinary Internal Medicine. 8th edition. St. Louis, MO: Elsevier; 2017:1683–1688.

7.  Xenoulis PG, Cammarata PJ, Walzem RL, Suchodolski JS, Steiner JM. Serum triglyceride and cholesterol concentrations and lipoprotein profiles in dogs with naturally occurring pancreatitis and healthy control dogs. J Vet Intern Med. 2020;34(2):644–652 (doi.org/10.1111/jvim.15715).

8.  Xenoulis PG, Levinski MD, Suchodolski JS, Steiner JM. Serum triglyceride concentrations in Miniature Schnauzers with and without a history of probable pancreatitis. J Vet Intern Med. 2011;25:20–25.

9.  Yotsuya S, Shikama H, Nakano I, Sakai K, Kato M, Sugi H, Takada H, Kog Y. A novel synthetic anti-acute pancreatitis agent, IS-741. Digestion. 1999;60 (supplement 1):34–39.