Page 205 - ONLINE PROCEEDING BOOK WSAVA 2017
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In ammatory Bowel Disease (IBD): The in ammatory process located in the GI mucosa may lead to protein loss both by preventing the absorption of nutrients
and by compromising the integrity of the intestinal mucosal barrier leading to exudation of proteins into the intestinal lumen. PLE of soft-coated wheaten terriers is
a speci c form of IBD affecting this breed worldwide. In approximately 50% of these dogs, PLE and protein- losing nephropathy (PLN) occur concurrently. The pathogenesis of PLE in these dogs includes a dietary hypersensitivity component.
Crypt disease: Crypt dilation and necrosis have been frequently associated with PLE. Dogs with small intestinal crypt abscesses have signi cant hypoalbuminemia and ultrasound changes of their intestinal mucosa, and their clinical presentation is generally severe.
THERAPY
Diet: Dogs with PLE are in a catabolic state, and adequate nutrition is essential. Dietary modi cation centers on feeding a highly digestible diet with low to very low fat content of less than 20% on a Metabolizable Energy (ME) basis (this is equivalent to less than 10%
on a dry matter [DM] basis) to prevent further dilation and rupture of lacteals. Many common intestinal support diets may be too high in fat (have between 20-30% fat ME, which is between 10-15% fat on a DM basis) and may perpetuate the lacteal dilation despite initiation of other medical managements. Feeding higher fat diets should be avoided during the initial course of treatment whenever possible. Additionally, the diet should contain highly bioavailable dietary proteins and be low in crude  ber (less than 2% crude  ber on a DM basis).
The long-term dietary strategy will depend on whether the animal has a primary fat malabsorption (primary idiopathic IL) or fat malabsorption secondary to an intestinal in ammatory condition (PLE associated with underlying IBD). In dogs with primary idiopathic IL, feeding a highly digestible, fat-restricted diet (i.e. less than 20% fat ME) may be required life-long. In dogs
with PLE associated with underlying IBD, good success has been reported with exclusive feeding of low- to moderate-fat diets consisting of either hydrolyzed or novel protein diets. Diet selection should be based on a detailed diet history including all treats and supplements that have been fed in the past. Diet history information may not be readily available during the initial course of treatment and starting with a hydrolyzed protein diet would be prudent until a more detailed diet history can be obtained. In dogs with PLE associated with underlying IBD feeding of fat-restricted diets may not be required for long-term management.
Acceptance of the diet is a critical issue in PLE dogs, particularly in the most severely affected animals, which may be anorexic. Initially, it might be more important to
An Urban Experience
feed a less optimal diet that the dog will be interested in eating, and progressively transition to a more desirable diet. Home-prepared diet formulations may be required for animals requiring both fat restriction and a novel ingredient diet for long-term management.
Management of in ammation: In dogs with primary IL, anti-in ammatory glucocorticoid therapy (e.g. prednisone at 1 mg/kg/day) is useful and often required for proper management of the disease. Its main desired effect is to decrease in ammation associated with lipogranulomas secondary to chyle leakage and therefore help restoring an adequate  ow in intestinal lymphatics. In some dogs, anti-in ammatory treatment can be slowly weaned off over 2-3 months or longer.
Immunosuppressive therapy: Immunosuppression is the basis for treatment of severe IBD with PLE. The  rst approach consists of administering prednisone or prednisolone initially at 2 mg/kg q12 h during 3-5 days, then 2 mg/kg once daily until the dog’s condition has signi cantly improved and appears stable (clinical improvement and serum albumin reliably > 20 g/L). Subsequently the dose can be decreased in 2-week steps with 1 mg/kg/day, then 1 mg/kg every other day and so on.
Other corticosteroids: budesonide is known to be locally ef cient and undergo high  rst pass hepatic metabolism in people, making systemic complications of steroid treatment less likely. In dogs, the drug signi cantly in uences the pituitary-adrenal axis. A recent study reported that budesonide was ef cacious in the treatment of canine IBD. The recommended doses are 0.5-3 mg/dog daily (depending on the dog’s size). Concurrent use with other glucocorticoids is not recommended.
Chlorambucil has recently been shown to be
more effective when used with prednisolone than a combination of azathioprine and prednisolone in dogs with chronic enteropathies and severe PLE. The survival was greatly improved in dogs receiving the chlorambucil combination. The recommended initial canine dose
of chlorambucil is approximately 4 mg/m2 q24-48h,
and it comes in 2 mg tablets (the drug will need to be appropriately reformulated or compounded for small dogs). Side effects of chlorambucil are rare and include bone marrow suppression. A CBC should be performed after 1 and 3 weeks of treatment and repeated every 2-3 months or if the dog’s condition deteriorates to look for neutropenia.
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