Congenital portosystemic shunts (CPSS) are abnormal vascular communications between the portal and the systemic circulation, bypassing the hepatic parenchyma and resulting in liver hypoplasia and hepatic insufficiency. Such connections develop in utero and persist postnatally. CPSS are among the two most common congenital vascular anomalies of the liver in small animals, along with primary hypoplasia of the portal vein without portal hypertension (PHPV without PH). CPSS can be extrahepatic (ECPSS), most commonly diagnosed in small and toy breed dogs and cats, or intrahepatic (ICPSS), most commonly seen in large breed dogs. Single ECPSS is the most common type encountered in both dogs and cats. Clinical signs of CPSS are non-specific and may wax and wane, while laboratory findings can raise clinical suspicion for CPSS, but they are also not specific. Definitive diagnosis will be established by evaluation of liver function tests, such as determination of fasting plasma ammonia (FA) levels, and pre- and postprandial serum bile acids concentrations, and diagnostic imaging. The purpose of this article is to review the definition, classification, pathogenesis, clinical presentation, and diagnosis of CPSS in dogs and cats, highlighted by the authors’ clinical experience.

Congenital portosystemic shunts (CPSS) are a common vascular anomaly of the liver in dogs and cats. Clinical signs of CPSS are non-specific and may wax and wane, while laboratory findings can raise the clinical suspicion for CPSS, but they are also not specific. Definitive diagnosis will be established by evaluation of liver function tests and diagnostic imaging. The aim of this article is to review the management, both medical and surgical, complications, and prognosis of CPSS in dogs and cats. Attenuation of the CPSS is the treatment of choice and may be performed by open surgical intervention using ameroid ring constrictors, thin film banding, and partial or complete suture ligation or by percutaneous transvenous coil embolization. There is no strong evidence to recommend one surgical technique over another. Medical treatment strategies include administration of non-absorbable disaccharides (i.e., lactulose), antibiotics, and dietary changes, and are indicated for pre-surgical stabilization or when surgical intervention is not feasible. After CPSS attenuation, short- and long-term post-surgical complications may be seen, such as post-operative seizures and recurrence of clinical signs, respectively. Prognosis after surgical attenuation of CPSS is generally favorable for dogs and fair for cats.

Canine inflammatory bowel disease (IBD) is a group of chronic gastrointestinal disorders, the pathogenesis of which remains elusive, but it possibly involves the interaction of the intestinal immune system with luminal microbiota and food-derived antigens. Mucosal cytokines profiles in canine IBD have been investigated mainly in small intestinal disease, while data on cytokine profiles in large intestinal IBD are limited. The objective of this study was to measure colonic mucosal and cytobrush sample messenger (m)RNA expression of interleukin (IL)-1β, IL-2, IL-12p40, IL-23p19, tumor necrosis factor-alpha (TNF-α) and chemokine C‐C motif ligand (CCL28) in dogs with IBD and healthy controls using quantitative real-time polymerase chain reaction (PCR), and assess their correlation with clinical disease activity, endoscopic and histopathologic score. Dogs with IBD had a significantly increased mRNA expression of IL-1β, IL-23p19 and CCL28 in the colonic mucosa, compared to healthy controls. None of the selected cytokines had significantly different mRNA expression in the colonic cytobrush samples between the two groups or between the colonic mucosa and cytobrush samples of dogs with IBD. Finally, there was a statistically significant correlation of clinical disease activity with endoscopic activity score and fibrosis and atrophy of the colonic mucosa in dogs with large intestinal IBD. IL-1β, IL-23p19 and CCL28 could play a role in the pathogenesis of canine large intestinal IBD. Colonic cytokine expression does not correlate with clinical disease activity and/or endoscopic score. However, clinical signs reflect the severity of endoscopic lesions.

This retrospective study assessed the potential of blood leukocyte ratios as diagnostic biomarkers in cats with chronic enteropathies (CE). Absolute neutrophil-to-lymphocyte (NLR), neutrophil-to-monocyte (NMR), and lymphocyte-to-monocyte (LMR) ratios were calculated from the hematological profiles of 221 cats, including healthy controls (n = 73), and those diagnosed with food-responsive enteropathy (FRE, n = 59), steroid-responsive enteropathy (SRE, n = 56), or small cell lymphoma (SCL, n = 33). SCL cats had higher NLRs than SRE (p = 0.002) and FRE (p = 0.028), and lower LMRs than SRE (p = 0.012) and FRE (p = 0.001). Healthy cats had lower NLRs compared to the FRE (p < 0.001), SRE (p < 0.001), and SCL (p < 0.001) cats and higher LMRs compared to the FRE (p < 0.001), SRE (p < 0.001), and SCL (p < 0.001) cats. Receiver operating characteristic (ROC) curve analysis demonstrated that NLR ≥ 11.6 differentiated SCL from SRE with 87.5% specificity but low sensitivity (39.4%). NMR ≥ 34.5 distinguished FRE from SRE with 52.5% sensitivity and 69.6% specificity. LMR ≥ 3.72 differentiated SRE from SCL with 67.9% sensitivity and 60.6% specificity. Although significant differences in leukocyte ratios were observed among groups, their diagnostic accuracy in differentiating CE phenotypes was suboptimal. These findings suggest that the utility of NLR, NMR, and LMR as standalone diagnostic tools is limited.