Page 177 - WSAVA2018
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P. Watson1
1Department of Veterinary Medicine, University of Cambridge, UK
Pancreatitis in dogs shows a spectrum of disease
from mild, subclinical to acute, necrotising and fatal. Pancreatitis is classified based on histopathological appearance. There is no ‘gold standard’ for histological description of pancreatitis in animals (unlike the liver). The author favours the definitions in human medicine which define pancreatitis as ‘acute’ or ‘chronic’
based on its histological appearance and NOT how it appears clinically. These definitions are summarized
in table 1 below. Chronic pancreatitis (CP) is defined
as: ‘a continuing inflammatory disease characterized
by the destruction of pancreatic parenchyma leading
to progressive or permanent impairment of exocrine
or endocrine function or both. The gold standard for diagnosis is histology but this is rarely indicated or performed in dogs (or humans). Noninvasive diagnosis is difficult with the currently available diagnostic imaging, and blood tests have a lower sensitivity than for acute disease, which may explain why its prevalence is often under-estimated.
Table 1: Proposed histopathological and functional definitions of acute and chronic pancreatitis in dogs based on human definitions
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Causes of chronic pancreatitis
The cause of CP in dogs is usually unknown. Any age
or breed of dog can be affected, but the most typical signalment is a middle-aged to old dog particularly a Cavalier King Charles Spaniel (CKCS), Cocker Spaniel, Collie, or Boxers in the UK. An independent large study of EPI in the UK found an increased prevalence in older CKCS, supporting this breed association. Some cases may represent chronic relapsing cases of acute disease, but many cases are truly ‘chronic’ from the outset, with an initial mononuclear infiltrate.
Autoimmune chronic pancreatitis in the English Cocker Spaniel
The particular form of chronic pancreatitis recognized in English Cocker Spaniels in the UK is thought to be an autoimmune. As in human autoimmune pancreatitis, it typically affects middle-aged to older dogs, with
a higher prevalence in males, and at least 50% of affected dogs subsequently develop DM, EPI, or both. Dogs also often have other concurrent autoimmune disease, particularly keratoconjunctivitis sicca and glomerulonephritis. There is often a mass-like lesion
on ultrasound, and biopsies show a typical perilobular diffuse fibrotic and lymphocytic disease centered on perilobular ducts and vessels, with loss of large ducts and hyperplasia of smaller ducts. Immunohistochemistry shows a preponderance of duct and vein-centered CD3+ lymphocytes (i.e.; T-cells). Recent work in humans has identified a strong association with plasma cells that secrete one subgroup of imuunoglobulin G, IgG4. The disease in humans has been redefined as multisystemic because of the frequent involvement of other organs.
It is now defined as IgG4 positive sclerosing disease
and concurrent keratoconjunctivitis sicca, sialoadenitis, biliary tract disease, and glomerulonephritis are common. Early work in English Cocker Spaniels also shows IgG4- positive plasma cells in the pancreas and kidney (Watson et al, 2012) and also demonstrated an association
with a particular DLA (dog leukocyte antigen) in ECS, supporting the theory of autoimmunity (Bazelle et al 2013). The disease in humans responds well to steroid therapy, including a reduction in insulin requirements
in some diabetics. There are not yet any controlled
trials evaluating the use of immunosuppressive drugs in English Cocker Spaniels with chronic pancreatitis, but there is now enough circumstantial evidence to justify their use in this particular breed. However, the clinician should note that this is very breed- specific; terriers in Britain, for example, have a different histopathologic and clinical picture of disease that does not appear to be autoimmune. The use of steroids in terriers with chronic pancreatitis is not recommended.
   Histopathological appearance
 Neutrophilic inflammation; acinar necrosis, peripancreatic fat necrosis and oedema in varying amounts. Potentially completely reversible with no permanent pancreatic architectural or functional loss
 Mononuclear (lymphocytic +/- plasmacytic) inflammation and fibrosis. Permanent, irreversible disruption of pancreatic architecture. Cases with concurrent neutrophilic inflammation and necrosis but underlying fibrosis fall in to this category.
   Functional changes
  High risk of systemic inflammatory disease and multi-organ failure during acute disease. No permanent pancreatic functional changes on recovery
  Characterised by progressive loss of exocrine and endocrine function. Exocrine pancreatic insufficiency (EPI) and/or diabetes mellitus (DM) develop in end stage disease after 80-90% of pancreatic tissue has been lost
   Clinical appearance
   Spectrum from severe and fatal (usually necrotizing) to mild and subclinical (less common)
   Spectrum from mild, low-grade intermittent gastrointestinal signs (most common) to an acute-on-chronic episode indistinguishable from classical acute pancreatitis
 Histopathological descriptions are useful to understand the pathology and progression of the disease but are not very useful clinically as most cases do not have a pancreatic biopsy performed and either chronic or acute pancreatitis episodes may be mild or severe and either may be recurrent. However, recognizing the potential for underlying chronic disease in an animal which presents acutely is very important for long term management because it allows the clinical to realize that the dog may develop EPI or DM in the future, and to recognize and treat these appropriately.

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