Food-responsive enteropathy (FRE) is the most frequent form of canine chronic inflammatory enteropathy (CIE). It can be diagnosed if, after excluding known causes of diarrhea, clinical signs resolve or significantly improve after an appropriate dietary trial. No universal diet can resolve the clinical signs in every case of FRE, as genetic predisposition and environment (e.g., the possible role of the diet feed before the disease onset) are suggested as possible players. The study aimed to retrospectively evaluate the possible correlations between disease, diet, and breed in a large cohort of dogs (n = 222) suffering from FRE. Throughout the study, dogs differed based on dietary options: commercial diet group, homemade diet group, and mixed diet group. Diet, breed, age, body weight, body condition score (BCS), fecal score (FS), canine chronic enteropathy activity index (CCECAI), and selected clinical signs were variably evaluated at T0 and at final time (FT—based on response to the diet[s], but between 30 and 60 days). Significant differences between T0 and FT were found regarding FS, BCS, and CCECAI, as well as between age, BCS, and CCECAI at FT with the FS at FT. The CCECAI at FT was significantly directly correlated only with the shift from a mixed to a homemade diet. Finally, the multiple linear regression analysis between the covariables of different breeds versus clinical response to the dietary trials did not highlight any difference except for the passage from commercial to mixed diet in a specific subgroup of breeds. The present study reports the clinical progression in 222 dogs suffering from FRE, and it could represent a reference for the variables investigated, considering the large number of patients included.

This study describes the clinicopathological features of seven canine cases showing a diffuse cobblestone-like gastric mucosal pattern on endoscopy. Cases were retrospectively retrieved from endoscopic databases (2017–2025). Clinical data, treatment history, endoscopic findings, and histology were reviewed. Endoscopically, all dogs exhibited thickened, irregular, and poorly distensible gastric folds. Histopathologic examination showed mild-to-moderate foveolar hyperplasia, variable cystic dilation of the fundic glands, mild chronic lymphoplasmacytic inflammation, and interstitial fibrosis. Parietal-cell population was variably increased and predominant (hyperplasia). Because these features can overlap widely among reactive and hyperplastic gastropathies, interpretation required correlation with clinical and endoscopic findings in addition to histopathology. All dogs had a history of prolonged omeprazole administration, and most showed clinical improvement after dose reduction or treatment withdrawal. Follow-up endoscopy in two dogs documented divergent outcomes, with marked improvement in one dog and only minimal changes in the other. These findings suggest that this cobblestone-like pattern represents a benign, reactive, and potentially regressive gastropathy, possibly associated with chronic acid suppression. Recognition of this appearance may assist clinicians in differentiating reactive gastropathy from proliferative or neoplastic conditions and supports prudent use of long-term proton pump inhibitors in dogs with chronic gastrointestinal disease.