Prevalence and underlying causes of histologic abnormalities in cats suspected to have chronic small bowel disease: 300 cases (2008-2013).

OBJECTIVE: To determine prevalence of histologic abnormalities in cats suspected, on the basis of compatible clinical signs and ultrasonographic findings, to have chronic small bowel disease; identify the most common underlying causes in affected cats; and compare methods for differentiating among the various causes of chronic small bowel disease. DESIGN: Retrospective case series. ANIMALS: 300 client-owned domestic cats suspected to have chronic small bowel disease. PROCEDURES: Medical records were reviewed to identify cats evaluated because of chronic vomiting, chronic small bowel diarrhea, or weight loss that also had ultrasonographic evidence of thickening of the small intestine. Cats were included in the study if full-thickness biopsy specimens had been obtained from ≥ 3 locations of the small intestine by means of laparotomy and biopsy specimens had been examined by means of histologic evaluation and, when necessary to obtain a diagnosis, immunohistochemical analysis and a PCR assay for antigen receptor rearrangement. RESULTS: Chronic small bowel disease was diagnosed in 288 of the 300 (96%) cats. The most common diagnoses were chronic enteritis (n = 150) and intestinal lymphoma (124). CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that a high percentage of cats with clinical signs of chronic small bowel disease and ultrasonographic evidence of thickening of the small intestine had histologic abnormalities. Furthermore, full-thickness biopsy specimens were useful in differentiating between intestinal lymphoma and chronic enteritis, but such differentiation was not possible with ultrasonography or clinicopathologic testing alone.

Dickkopf-1 regulates bone formation in young growing rodents and upon traumatic injury.

The physiological role of Dickkopf-1 (Dkk1) during postnatal bone growth in rodents and in adult rodents was examined utilizing an antibody to Dkk1 (Dkk1-Ab) that blocked Dkk1 binding to both low density lipoprotein receptor-related protein 6 (LRP6) and Kremen2, thereby preventing the Wnt inhibitory activity of Dkk1. Treatment of growing mice and rats with Dkk1-Ab resulted in a significant increase in bone mineral density because of increased bone formation. In contrast, treatment of adult ovariectomized rats did not appreciably impact bone, an effect that was associated with decreased Dkk1 expression in the serum and bone of older rats. Finally, we showed that Dkk1 plays a prominent role in adult bone by mediating fracture healing in adult rodents. These data suggest that, whereas Dkk1 significantly regulates bone formation in younger animals, its role in older animals is limited to pathologies that lead to the induction of Dkk1 expression in bone and/or serum, such as traumatic injury.