Objective—To measure serum calprotectin concentration in dogs with inflammatory bowel disease (IBD) before and after initiation of treatment and evaluate its correlation with a clinical scoring system (canine IBD activity index), serum canine C-reactive protein concentration, and severity of histopathologic changes.
Animals—34 dogs with idiopathic IBD and 139 healthy control dogs.
Procedures—From dogs with IBD, blood samples were collected immediately before (baseline) and 3 weeks after initiation of 1 of 2 treatments: prednisone (1 mg/kg, PO, q 12 h; n = 21) or a combination of prednisone and metronidazole (10 mg/kg, PO, q 12 h; 13). Blood samples were collected once from each of the control dogs. For all samples, serum calprotectin concentration was determined via radioimmunoassay.
Results—Mean serum calprotectin concentrations for dogs with IBD at baseline (431.1 μg/L) and 3 weeks after initiation of treatment (676.9 μg/L) were significantly higher, compared with that (219.4 μg/L) for control dogs, and were not significantly correlated with the canine IBD activity index, serum C-reactive protein concentration, or severity of histopathologic changes. The use of a serum calprotectin concentration of ≥ 296.0 μg/L as a cutoff had a sensitivity of 82.4% (95% confidence interval, 65.5% to 93.2%) and specificity of 68.4% (95% confidence interval, 59.9% to 76.0%) for distinguishing dogs with idiopathic IBD from healthy dogs.
Conclusions and Clinical Relevance—Serum calprotectin concentration may be a useful biomarker for the detection of inflammation in dogs, but the use of certain drugs (eg, glucocorticoids) appears to limit its clinical usefulness.
We would like to comment on the JAVMA News article in the November 15, 2021, issue “Taking the chronic out of enteropathies.”1 The article discusses the use of a panel of new serologic tests for inflammatory bowel disease, relying heavily on a research paper published in 2021 in the Journal of Veterinary Internal Medicine (JVIM) by Estruch et al.2 However, the News article fails to mention that the results of this study have been questioned due to lack of reporting and analytical assay
Objective—To determine whether substantial interobserver
variation exists among diagnostic pathologists
for descriptions of intestinal mucosal cell populations
and whether histopathologic descriptions
accurately predict when a patient does not have clinically
evident intestinal disease.
Sample Population—14 histologic slides of duodenal,
ileal, or colonic tissue from 10 dogs and 3
Procedure—Each histologic slide was evaluated
independently by 5 pathologists at 4 institutions.
Pathologists, who had no knowledge of the tissues'
origin, indicated whether slides were adequate for
histologic evaluation and whether the tissue was normal
or abnormal. They also identified the main infiltrating
cell type in specimens that were considered
abnormal, and whether infiltrates were mild, moderate,
severe, or neoplastic.
Results—Quality of all slides was considered adequate
or superior by at least 4 of the 5 pathologists.
For intensity of mucosal cellular infiltrates, there was
uniformity of opinion for 1 slide, near-uniformity for 6
slides, and nonuniformity for 7 slides. Five dogs did
not have clinical evidence of intestinal disease, yet
the pathologists' descriptions indicated that their
intestinal tissue specimens were abnormal.
Conclusions and Clinical Relevance—Substantial
interobserver variation was detected. Standardization
of pathologic descriptions of intestinal tissue is necessary
for meaningful comparisons with published
articles. Clinicians must be cautious about correlating
clinical signs and histopathologic descriptions of
intestinal biopsy specimens. (J Am Vet Med Assoc
Objective—To characterize mucosal gene expression in dogs with chronic enteropathy (CE).
Animals—18 dogs with CE and 6 healthy control dogs.
Procedures—Small intestinal mucosal biopsy specimens were endoscopically obtained from dogs. Disease severity in dogs with CE was determined via inflammatory bowel index scores and histologic grading of biopsy specimens. Total RNA was extracted from biopsy specimens and microchip array analysis (approx 43,000 probe sets) and quantitative reverse transcriptase PCR assays were performed.
Results—1,875 genes were differentially expressed between dogs with CE and healthy control dogs; 1,582 (85%) genes were downregulated in dogs with CE, including neurotensin, fatty acid–binding protein 6, fatty acid synthase, aldehyde dehydrogenase 1 family member B1, metallothionein, and claudin 8, whereas few genes were upregulated in dogs with CE, including genes encoding products involved in extracellular matrix degradation (matrix metallopeptidases 1, 3, and 13), inflammation (tumor necrosis factor, interleukin-8, peroxisome proliferator–activated receptor γ, and S100 calcium-binding protein G), iron transport (solute carrier family 40 member 1), and immunity (CD96 and carcinoembryonic antigen–related cell adhesion molecule [CEACAM] 18). Dogs with CE and protein-losing enteropathy had the greatest number of differentially expressed genes. Results of quantitative reverse transcriptase PCR assay for select genes were similar to those for microchip array analysis.
Conclusions and Clinical Relevance—Expression of genes encoding products regulating mucosal inflammation was altered in dogs with CE and varied with disease severity.
Impact for Human Medicine—Molecular pathogenesis of CE in dogs may be similar to that in humans with inflammatory bowel disease.