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1. Simpson KW. Inflammation. In: Washabau RJ, Day MJ, eds. Canine and feline gastroenterology. St Louis: Saunders, 2013;616–619.
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2. Day MJ, Bilzer T, Mansell J, et al. Histopathological standards for the diagnosis of gastrointestinal inflammation in endoscopic biopsy samples from the dog and cat: a report from the World Small Animal Veterinary Association Gastrointestinal Standardization Group. J Comp Pathol 2008;138(suppl 1):S1–S43.
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Comparison of clinical, endoscopic, and histologic features between dogs with chronic gastritis with and without lymphofollicular hyperplasia
Abstract
OBJECTIVE
To compare clinical, endoscopic, and histopathologic features between dogs with chronic gastritis (CG) with and without lymphofollicular hyperplasia (LFH).
ANIMALS
64 and 56 dogs with CG with (cases) and without (controls) LFH, respectively.
PROCEDURES
The medical record database of a referral clinic was searched to identify dogs that underwent endoscopic examination of the upper portion of the gastrointestinal tract and were subsequently determined to have CG with or without LFH between October 2006 and February 2011. Signalment and clinical, endoscopic, and histologic findings were compared between cases and controls. Logistic regression was used to identify factors associated with CG with LFH.
RESULTS
Compared with controls, cases were significantly younger and more likely to be of a brachycephalic phenotype. The proportions of dogs with a poor body condition or diarrhea were significantly lower and the proportions of dogs with inspiratory dyspnea, exercise intolerance, or hyperemia and discoloration of the gastric mucosa were significantly higher for the case group, compared with the control group. Inspiratory dyspnea, gastric mucosal hyperemia, and gastritis severity were positively associated, whereas poor body condition was negatively associated, with CG with LFH on multivariable logistic regression.
CONCLUSIONS AND CLINICAL RELEVANCE
The strong positive association between inspiratory dyspnea and CG with LFH suggested that the condition may be a consequence of an increase in negative intrathoracic pressure rather than a distinct clinical entity. Prospective studies are warranted to elucidate the mechanism by which inspiratory dyspnea contributes to the development of CG with LFH.
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