Circulatory disorders of the liver in dogs and cats

Ingh, T.S.G.A.M. van den; Rothuizen, J.; Meyer, H.

doi:10.1080/01652176.1995.9694536

Cited by 66 publications

(73 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MVD in cats has been seldom reported up to the present [17]. In the present study, however, the disease accounted for 12.7% (9 of 71) of liver diseases.…”

Section: Discussioncontrasting

confidence: 49%

A Retrospective Histopathological Survey on Canine and Feline Liver Diseases at the University of Tokyo between 2006 and 2012

et al. 2014

View full text Add to dashboard Cite

To determine the incidence of hepatic diseases in dogs and cats in Japan, a retrospective study was performed using data of 463 canine and 71 feline liver biopsies at the Veterinary Medical Center of the University of Tokyo. The most common canine hepatic disease was microvascular dysplasia (MVD) and occupied 29.4% of all diagnoses. This terminology might contain “real” MVD and primary portal vein hypoplasia, because these two conditions were difficult to be clearly distinguished histopathologically. Parenchymal and interstitial hepatitis and primary hepatic tumors accounted for 23.5% and 21.0% of the diagnoses, respectively. Parenchymal and interstitial hepatitis occupied 34.1% of non-proliferative canine hepatic diseases, while hepatocellular adenoma and carcinoma were 26.6% and 24.5% of proliferative hepatic diseases, respectively. Breed-specificity was seen in MVD for Yorkshire terrier, Papillon and Toy poodle, in hepatitis for Doberman pinscher and Labrador retriever, in cholangiohepatitis for American cocker spaniel, Miniature schnauzer and Pomeranian, in hepatocellular adenoma for Golden retriever and Shiba and in hepatocellular carcinoma for Shih Tzu. The most common feline liver disease was parenchymal and interstitial hepatitis (45.1% of all diagnoses). Among feline hepatitis, neutrophilic cholangiohepatitis (23.9%), lymphocytic cholangiohepatitis (14.1%) and chronic hepatitis (5.6%) were recorded. Adult polycystic liver disease was 5.6%. Among proliferative diseases in the feline liver (11.3% of the all), lymphoma (4.2%) and primary epithelial tumors (4.2%) including hepatocellular carcinoma, cholangiocellular adenoma and cholangiocellular carcinoma were observed. Hepatic degeneration was 14.1%, and MVD was 12.7%, respectively.

show abstract

“…MVD in cats has been seldom reported up to the present [17]. In the present study, however, the disease accounted for 12.7% (9 of 71) of liver diseases.…”

Section: Discussioncontrasting

confidence: 49%

A Retrospective Histopathological Survey on Canine and Feline Liver Diseases at the University of Tokyo between 2006 and 2012

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Maintenance of liver mass and function is provided mostly by hepatic perfusion, especially by the quantity and quality of portal blood (van den Ingh et al 1995). Normally, the abdominal organs connected to the splanchnic vascular bed (gastrointestinal tract, pancreas, and spleen) supply their efflux blood to the portal vein.…”

Section: Congenital Portosystemic Shunts and Associated Liver Dysfuncmentioning

confidence: 99%

Inherited liver shunts in dogs elucidate pathways regulating embryonic development and clinical disorders of the portal vein

et al. 2011

View full text Add to dashboard Cite

Congenital disorders of the hepatic portal vasculature are rare in man but occur frequently in certain dog breeds. In dogs, there are two main subtypes: intrahepatic portosystemic shunts, which are considered to stem from defective closure of the embryonic ductus venosus, and extrahepatic shunts, which connect the splanchnic vascular system with the vena cava or vena azygos. Both subtypes result in nearly complete bypass of the liver by the portal blood flow. In both subtypes the development of the smaller branches of the portal vein tree in the liver is impaired and terminal branches delivering portal blood to the liver lobules are often lacking. The clinical signs are due to poor liver growth, development, and function. Patency of the ductus venosus seems to be a digenic trait in Irish wolfhounds, whereas Cairn terriers with extrahepatic portosystemic shunts display a more complex inheritance. The genes involved in these disorders cannot be identified with the sporadic human cases, but in dogs, the genome-wide study of the extrahepatic form is at an advanced stage. The canine disease may lead to the identification of novel genes and pathways cooperating in growth and development of the hepatic portal vein tree. The same pathways likely regulate the development of the vascular system of regenerating livers during liver diseases such as hepatitis and cirrhosis. Therefore, the identification of these molecular pathways may provide a basis for future proregenerative intervention.

show abstract

“…It is therefore clinically relevant to investigate the function of the ammonia metabolizing pathways in such canine liver diseases. CPSS are inherited single large vascular anomalies that directly connect the portal venous system with the systemic venous circulation bypassing the liver parenchyma [28]. This occurs via an intrahepatic (IHPSS) or an extrahepatic portosystemic shunt (EHPSS).…”

Section: Introductionmentioning

confidence: 99%

Aberrant Expression and Distribution of Enzymes of the Urea Cycle and Other Ammonia Metabolizing Pathways in Dogs with Congenital Portosystemic Shunts

et al. 2014

View full text Add to dashboard Cite

The detoxification of ammonia occurs mainly through conversion of ammonia to urea in the liver via the urea cycle and glutamine synthesis. Congenital portosystemic shunts (CPSS) in dogs cause hyperammonemia eventually leading to hepatic encephalopathy. In this study, the gene expression of urea cycle enzymes (carbamoylphosphate synthetase (CPS1), ornithine carbamoyltransferase (OTC), argininosuccinate synthetase (ASS1), argininosuccinate lyase (ASL), and arginase (ARG1)), N-acetylglutamate synthase (NAGS), Glutamate dehydrogenase (GLUD1), and glutamate-ammonia ligase (GLUL) was evaluated in dogs with CPSS before and after surgical closure of the shunt. Additionally, immunohistochemistry was performed on urea cycle enzymes and GLUL on liver samples of healthy dogs and dogs with CPSS to investigate a possible zonal distribution of these enzymes within the liver lobule and to investigate possible differences in distribution in dogs with CPSS compared to healthy dogs. Furthermore, the effect of increasing ammonia concentrations on the expression of the urea cycle enzymes was investigated in primary hepatocytes in vitro. Gene-expression of CPS1, OTC, ASL, GLUD1 and NAGS was down regulated in dogs with CPSS and did not normalize after surgical closure of the shunt. In all dogs GLUL distribution was localized pericentrally. CPS1, OTC and ASS1 were localized periportally in healthy dogs, whereas in CPSS dogs, these enzymes lacked a clear zonal distribution. In primary hepatocytes higher ammonia concentrations induced mRNA levels of CPS1. We hypothesize that the reduction in expression of urea cycle enzymes, NAGS and GLUD1 as well as the alterations in zonal distribution in dogs with CPSS may be caused by a developmental arrest of these enzymes during the embryonic or early postnatal phase.

show abstract

Circulatory disorders of the liver in dogs and cats

Cited by 66 publications

References 20 publications

A Retrospective Histopathological Survey on Canine and Feline Liver Diseases at the University of Tokyo between 2006 and 2012

A Retrospective Histopathological Survey on Canine and Feline Liver Diseases at the University of Tokyo between 2006 and 2012

Inherited liver shunts in dogs elucidate pathways regulating embryonic development and clinical disorders of the portal vein

Aberrant Expression and Distribution of Enzymes of the Urea Cycle and Other Ammonia Metabolizing Pathways in Dogs with Congenital Portosystemic Shunts

Contact Info

Product

Resources

About