Diagnosis of canine inflammatory bowel disease (IBD) requires confirmation of histopathologic inflammation in intestinal biopsies. Different studies have found it difficult to correlate histopathologic findings with clinical disease severity due to a lack of consistency between pathologists when describing histopathologic changes and the questionable quality of specimens submitted for diagnostic evaluation. The WSAVA* GI standardization grading scheme (Day 2008) was an attempt to rectify some of these problems but even it is associated with poor agreement among pathologists. The aim of the present study was to utilize a new grading scheme for improved consistency of evaluation of GI histopathologic findings and to correlate these features to clinical disease activity in dogs with IBD.

Paraffin-embedded tissues from the stomach, duodenum, ileum, and colon of 70 healthy dogs and 163 IBD dogs were evaluated for histopathologic lesions using a simplified model for defining GI inflammation (Jergens 2013). Morphologic/inflammatory features were independently scored by 8 pathologists for total lesion scores for each GI organ and sub-scores within each organ. Clinical disease activity was calculated using CCECAI/CIBDAI scores. Pearson's correlation coefficients were used to evaluate the association between clinical and histopathologic scores.

The estimated correlation between CCECAI/CIBDAI and total histology score was found to be significant (p<0.05) for duodenum (r=0.42, 95% CI=[0.08–0.65]) and colon (r=0.33, 95% CI=[0.04–0.57]). The correlation was borderline significant for ileum (p: 0.06, r=0.29, 95% CI=[-0.02–0.55]) but non-significant for stomach (p: 0.7, r=0.05, 95% CI=[-0.24–0.34]). In evaluating the relationship between histopathologic sub-scores and disease activity, the correlation was significant for: i) crypt dilation (p<0.001, r=0.52), ii) LP macrophages (p<0.01, r=0.34), iii) LP neutrophils (p: 0.03, r=0.28), iv) mucosal fibrosis (p<0.001, r=0.53), v) surface epithelium (p: 0.01, r=0.34), and vi) villus stunting (p: 0.002, r=0.43). The correlation to CCECAI/CIBDAI for colonic goblet cells, intraepithelial lymphocytes, LP eosinophils, LP lymphocytes, and lacteal dilation was non-significant. There was agreement between pathologists for total histology scores, while sub-scores for mucosal fibrosis and villus stunting differed significantly (p<0.05).

In conclusion, a simplified model for GI inflammation shows utility in correlating histologic features to clinical disease activity. Gastric biopsies would appear to be less clinically useful versus duodenal and colonic biopsies for defining intestinal inflammation in canine IBD.

Disclosures

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