Triaditis in Cats - Does It Exist?
World Small Animal Veterinary Association World Congress Proceedings, 2014
Caroline Mansfield, BSc, BVMS, MVM, PhD, MANZCVSc, DECVIM-CA
Faculty of Veterinary Science, The University of Melbourne, Werribee, VIC, Australia

Over recent years, there has been an increasing awareness of pancreatic disease in cats. Similarly, the ability to diagnose intestinal and hepatic conditions less invasively than previously has also increased. The cat has a unique anatomy of the hepatic-pancreatic-intestinal region. Most cats only have one pancreatic duct that enters the small intestine through the major duodenal papilla, with this opening being contiguous with the bile duct. Cats also have a higher number of duodenal bacteria than dogs and do not seem to develop pancreatitis from dietary factors.

This unique and interrelated anatomy of the pancreas, small intestine, and the biliary system is thought to predispose to the development of inflammation in all three systems. Triaditis is the term used to refer to concurrent inflammatory bowel disease (IBD), chronic pancreatitis, and cholangiohepatitis. One postmortem study identified a greater prevalence of pancreatitis (9/18) and intestinal inflammation (15/18) in cats with cholangiohepatitis.1 As a result of this report, there has been an increasing trend in making a 'diagnosis' of triaditis, or at least assuming it could be present if inflammation in one of the three organ systems is identified. Generally however, as the pancreatitis seen in cats is generally of low clinical importance, usually treatment of either the IBD or cholangiohepatitis results in clinical improvement. This means that often the assumption there is concurrent pancreatic disease is not tested fully, especially if the diagnosis of IBD or cholangiohepatitis is made with minimally invasive techniques - as pancreatic biopsies may not be obtained.

Chronic non-suppurative pancreatitis is the histological form of pancreatitis that occurs most commonly in cats. With this form, a mononuclear (often lymphocytic) inflammation occurs, along with disruption of the pancreatic architecture due to concurrent fibrosis. The amount of inflammation may be minimal and recurrent at the time of biopsy, yet still fulfil this definition. Histologically, acute pancreatitis is defined as a neutrophilic inflammation, without fibrosis or exocrine atrophy, and is present within the body of the pancreas and/or peripancreatic fat. Clinically, the term chronic pancreatitis is given to cases where there are only mild clinical signs and acute pancreatitis when there are severe clinical signs. In cats, there appears to be a reasonable correlation between the clinical and histologic classifications. There is no specific treatment for chronic pancreatitis in cats. If clinical signs are suspicious of recurrent bouts of inflammation, then anti-inflammatory medication such as prednisolone could be tried.2 A survey of 115 feline postmortems at a tertiary referral institution found that there was an overall prevalence for pancreatitis of 67%, with 45% of clinically healthy cats also having pancreatic lesions.3 This study demonstrates that chronic pancreatitis may be grossly underrecognised in cats. However, it also raises the possibility that mild histological changes in the pancreas may not be clinically important and actually represent a spectrum of normal.

Inflammatory bowel disease is defined as a chronic inflammation of the intestinal lamina propria resulting in clinical signs (generally diarrhoea, vomiting, or weight loss) for which there is no predisposing cause. The inflammatory infiltrate is generally composed of lymphocytes and plasma cells, and there may be a poor correlation between the degree of infiltration histologically and the severity of clinical signs. In cats, there is a large degree of overlap between IBD (the lymphocytic-plasmacytic form) and low-grade intestinal lymphoma. Differentiation between the two is sometimes difficult, especially when endoscopic biopsies have been obtained. Increased diagnostic certainty can be obtained by performing clonality testing on biopsy samples, obtaining samples from the distal ileum and obtaining full-thickness samples.4 Currently, treatment of IBD is centred on removing antigenic stimulation (modifying the diet and/or treating with antibiotics) or suppressing the immune response (prednisolone and/or chlorambucil).

Cholangiohepatitis refers to inflammation (not necessarily infectious) centred on the bile ducts as well as the hepatic parenchyma. Cholangiohepatitis can have acute and chronic forms. With the acute form, neutrophils are present in the bile ducts and adjacent portal areas with associated necrosis; whilst with chronic, the infiltrate is more mixed and there is associated fibrosis. In areas where parasitic disease is a concern, there is a high number of eosinophils present in the cell infiltrate. Causes of cholangiohepatitis are thought to include inspissation of bile, ascending infection or bile duct anomalies. Clinical signs are variable and can wax and wane, but frequently include anorexia and weight loss. This makes clinical differentiation between cholangiohepatitis and IBD difficult. When severely affected, cats are often jaundiced and have a corresponding increase in serum bilirubin, as well as hepatocellular blood markers (ALT and AST) and cholestatic enzymes (ALKP). Treatment is variable depending on the severity of illness. If cats are dehydrated and severely ill, then IV fluid replacement along with parenteral antibiotics and nutritional support is often administered. If cats are not seriously ill, then oral antibiotic therapy along with supportive treatment is tried first. If there is a poor response, then anti-inflammatory medication can be administered.

As is apparent, the clinical presentation, diagnostic findings and treatment of cholangiohepatitis, IBD, and chronic pancreatitis have large overlap. It is therefore perhaps not clinically relevant that the presence or absence of each of these diseases is determined in an individual cat. This is particularly true for pancreatitis, as often the inflammation is subclinical and treatment of the primary condition will result in clinical improvement. The major consequences of chronic pancreatitis that will affect prognosis are the potential development of endocrine (diabetes mellitus) or exocrine dysfunction secondary to fibrosis and loss of functional pancreatic tissue.

Recently, the concept of 'triaditis' has been challenged. The association between cholangiohepatitis and pancreatitis appears to be low, whilst the association between IBD and pancreatitis is high.2 There are two major hypotheses as to why there could be a relationship between IBD and pancreatitis. Firstly, inflammation in the gut may cause distant inflammation in the pancreas. This could occur via upregulation of inflammatory mediators or their receptors. Secondly, there may be inflammation in response to enteric bacteria that have travelled from the intestine to the pancreas. Enteric bacteria have been identified in the pancreas of some cats via fluorescence in situ hybridization (FISH).5 Other possible relationships between pancreatitis and IBD could be due to treatment, changes in cholesterol or anatomic abnormalities of the duodenum.

Bacterial involvement in pancreatitis appears to be more common in cats with acute pancreatitis and with concurrent hepatic disease than in those with chronic pancreatitis. However, the hepatic disease most commonly associated with pancreatitis is not cholangiohepatitis but is either cholangitis (infection of the biliary system) or cholecystitis (infection of the gall bladder). In one retrospective study, 60% of cats with cholangitis had concurrent pancreatitis, whilst in a case series 50% cats with cholecystitis had pancreatic inflammation.6,7

As such, if a cat presents with acute pancreatitis it would be prudent to assess the biliary system for infection (by obtaining a gall bladder aspirate under ultrasound guidance). If this is not possible, then treatment with a broad-spectrum antibiotic that is excreted in the bile is recommended. As opposed to pancreatitis in dogs, there could be a reasonable assumption that pancreatitis in cats may have a bacterial component and again antibiotic therapy could be considered.

If a cat is diagnosed with IBD, then the possibility of concurrent pancreatitis could be considered. As chronic pancreatitis of low clinical significance is most likely, rigorous pursuit of a diagnosis may not be necessary. Treatment of IBD may result in clinical resolution of any signs attributable to pancreatitis. There is no evidence to date that concurrent pancreatitis worsens the prognosis of IBD in cats, although this is suggested in people.

References

1.  Weiss DJ, Gagne JM, Armstrong PJ. Relationship between inflammatory hepatic disease and inflammatory bowel disease, pancreatitis, and nephritis in cats. Journal of the American Veterinary Medical Association. 1996;209(6):1114–1116.

2.  Armstrong PJ, Williams DA. Pancreatitis in cats. Topics in Companion Animal Medicine. 2012;27(3):140–147.

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

4.  Scott KD, Zoran D, Mansell J, Norby B, Willard M. Utility of endoscopic biopsies of the duodenum and ileum for diagnosis of inflammatory bowel disease and small cell lymphoma in cats. Journal of Veterinary Internal Medicine. 2011;25(6):1253–1257.

5.  Simpson KW, Twedt D, McDonough SP, Craven MD, Steffey M, Dudak JL. Culture-independent detection of bacteria in feline pancreatitis (abstract). Journal of Veterinary Internal Medicine. 2011;25.

6.  Brain PH, Barrs VR, Martin P, Baral R, White JD, Beatty JA. Feline cholecystitis and acute neutrophilic cholangitis: clinical findings, bacterial isolates and response to treatment in six cases. Journal of Feline Medicine and Surgery. 2006;8(2):91–103.

7.  Callahan Clark JE, Haddad JL, Brown DC, Morgan MJ, Van Winkle TJ, Rondeau MP. Feline cholangitis: a necropsy study of 44 cats (1986–2008). Journal of Feline Medicine and Surgery. 2011;13(8):570–576.

  

Speaker Information
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Caroline Mansfield, BSc, BVMS, MVM, PhD, MANZCVSc, DECVIM-CA
Faculty of Veterinary Science
The University of Melbourne
Werribee, VIC, Australia


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