Gastroduodenal Ulceration in Dogs

Abstract

Forty three dogs with non-neoplastic canine gastric and/or duodenal ulcers were diagnosed at the University of Tennessee Veterinary Teaching Hospital (UTVTH) and reviewed in conjunction with dogs reported in the literature. No age, sex, or breed predilection was found. Most of the 43 UTVTH dogs presented with clinical signs referable to gastrointestinal disease, but evidence of hemorrhage was not always present. Nonregenerative anemia was a common (33/43 dogs) finding. Diagnosis of ulcer disease was made by contrast radiography, with clinical evidence of gastrointestinal hemorrhage, or surgery, endoscopy, or necropsy. Treatment with nonsteroidal, anti-inflammatory drugs (NSAIDs) and hepatic disease were the two most common predisposing factors for ulcer disease. Dogs with liver disease tended to have duodenal ulcers, dogs receiving NSAID treatment tended to have pyloroantral ulcers, and dogs with mastocytosis had ulcers in multiple locations. Three dogs with duodenal ulcers receiving NSAID treatment had an additional predisposing factor. Surgical treatment (with or without medical treatment) had a good outcome when the predisposing factors could be controlled or eliminated. Only 3 of 27 dogs in both the surgical and medically treated groups died from ulcer disease, whereas 6 of 16 dogs in the untreated group died from ulcer disease.

Lyophilized Aspirin with Trehalose May Decrease the Incidence of Gastric Injuries in Healthy Dogs

“…However, gastric ulcer formation resulting from NSAID administration in dogs is still controversial [23,24,28]. Aspirin was produced in 1897 as the first NSAID and is still widely used as an antiinflammatory and anticoagulant drug.…”

Gastritis and Peptic Ulcer Diseases in Dogs: A Review

“…Gastrin directly stimulates to hydrochloric acid secretion from the parietal cells, as well as indirectly stimulating acid production by releasing histamine from fundic enterochromaffin-like cells in response to compromising the protective mechanisms and reducing the epithelial cell turnover of the gastric mucosa (Hughes, 2006). Gross and histological appearances of gastric erosions and ulcers are well documented, erosions involve only surface epithelium with a minimal inflammatory response but ulcers can extend into the muscularis mucosae (Sullivan and Yool, 1998).The chronic liver disease leads to ischemia in GI mucosa that causes portal hypertension and thrombus formation into the gastric vessels (Stanton and Bright, 1989). The renal system has been involved in the elimination of at least 40 % circulating Gastrin-17, with up to 40 percent of circulating Gastrin-17.…”

“…The peptic ulcer is the imperfection in the mucosal barrier that continues to the muscularis mucosa of the stomach (Stanton and Bright, 1989). The most common clinical symptoms are sudden onset of acute vomiting with or without blood, dehydration, anorexia, weight loss and depression.…”

“…Chronic gastric ulcers and local ulcerative neoplastic lesions are macroscopically relatively similar; they can be differentiated through histopathological examination (Stanton and Bright, 1989). Based on histological examination (relative control of the reparative processes and the severity of ulceration), the gastric ulcers are classified as acute or chronic.…”

“…Animals with mastocytosis may have numerous all over gastric ulcers (Stanton and Bright, 1989;Ozaki et al, 2002). The mast cell tumor produces and releases histamine, which binds to H2 receptors on gastric parietal cells, gives a powerful stimulant to acid secretion.…”