# Transmural Ileal Fibroplasia Causing Mechanical Obstruction in a Dog: Surgical Management, Histopathology, and Molecular Findings

## TL;DR

A dog developed a rare intestinal blockage due to fibroplasia, and the study highlights the role of specific genes in this condition.

## Contribution

The study identifies PDGFRB and FGFR upregulation in non-cancerous intestinal fibroplasia in dogs.

## Key findings

- Transmural ileal fibroplasia caused mechanical obstruction in a dog with no malignancy.
- PDGFRB and FGFR gene expression was significantly increased, suggesting a role in fibroplasia.
- Hyperadrenocorticism may contribute to chronic fibrotic changes in the intestine.

## Abstract

This case report describes a mechanical small bowel obstruction caused by transmural ileal fibroplasia at the ileocolic junction in a dog. Diagnostic imaging and histopathological examination confirmed a severe fibrotic stricture at the ileocolic junction, accompanied by marked dilation of the distal ileum, with no evidence of malignancy. Cancer Gene Expression analysis revealed a 2.38-fold increase in both PDGFRB and FGFR expression, suggesting a potential role for aberrant receptor tyrosine kinase signaling in the development of pathological fibroplasia. In addition, concurrent hyperadrenocorticism may have acted as a permissive systemic factor, contributing to the chronic fibrotic remodeling observed in this case.

Small bowel obstruction (SBO) in dogs is most commonly caused by foreign bodies or neoplasia; however, SBO secondary to transmural fibroplasia remains a rare clinical complication of canine chronic enteropathy. This report describes the complex case of mechanical SBO caused by transmural ileal fibroplasia and inflammation at the ileocolic junction in a 9-year-old mixed-breed dog with concomitant hyperadrenocorticism (HAC). The primary presentation involved chronic severe weight loss and intermittent anorexia, contrasting with the acute presentation typical of most SBO cases. Imaging studies revealed severe, circumferential thickening up to 10 mm of the small intestine wall at the ileocolic junction (ICJ), resulting in complete luminal stricture and marked proximal dilation. Surgical intestinal resection and anastomosis were performed for alleviation of the obstruction, and histopathology confirmed severe mural and serosal enteritis with extensive fibroplasia extending into the adjacent mesentery, thereby excluding neoplastic processes. Quantitative PCR analysis demonstrated a significant upregulation of mRNA expression for PDGFRB and FGFR compared to normal tissue. Postoperative recovery was rapid; although soft feces persisted for one month, normal stool consistency was subsequently restored, and the patient achieved significant weight gain. This case underscores the diagnostic and therapeutic challenges associated with non-neoplastic, inflammation-driven SBO and suggests that activation of the PDGFR-β/FGFR pathways may play a key role in fibroplasia-related intestinal strictures, offering a novel molecular perspective beyond conventional SBO etiologies.