ArticlePloS one2015
Attenuation of congenital portosystemic shunt reduces inflammation in dogs.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Clinical presentation, treatment, and outcomes for 15 dogs with two or three congenital extrahepatic portosystemic shunts.Veterinary surgery : VS · 2026Article
- Diagnosis and classification of portosystemic shunts: a machine learning retrospective case-control study.Frontiers in veterinary science · 2024Article
- Comparison of diet, lactulose, and metronidazole combinations in the control of pre-surgical clinical signs in dogs with congenital extrahepatic portosystemic shunts.Journal of veterinary internal medicine · 2022Article
- Measurement and clinical applications of C-reactive protein in gastrointestinal diseases of dogs.Veterinary clinical pathology · 2022Review
- Astrocyte lesions in cerebral cortex and cerebellum of dogs with congenital ortosystemic shunting.Journal of veterinary science · 2020Article
- ACVIM consensus statement on the diagnosis and treatment of chronic hepatitis in dogs.Journal of veterinary internal medicine · 2019Article
- The effect of ammonia on canine polymorphonuclear cells.Veterinary research communications · 2018Article
- Haematology and coagulation profiles in cats with congenital portosystemic shunts.Journal of feline medicine and surgery · 2017Article
- Vasoactive intestinal peptide in canine portosystemic shunt in the absence of portal hypertension.Open veterinary journalArticle
- Comparison of hematologic variables between dogs with congenital intrahepatic and extrahepatic portosystemic shunts.Journal of veterinary internal medicineArticle
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
Abstract
Liver disease is a major cause of morbidity and mortality. One of the most significant complications in patients with liver disease is the development of neurological disturbances, termed hepatic encephalopathy. The pathogenesis of hepatic encephalopathy is incompletely understood, which has resulted in the development of a wide range of experimental models. Congenital portosystemic shunt is one of the most common congenital disorders diagnosed in client owned dogs. Our recent studies have demonstrated that the pathophysiology of canine hepatic encephalopathy is very similar to human hepatic encephalopathy, which provides strong support for the use of dogs with a congenital portosystemic shunt as a naturally occurring model of human hepatic encephalopathy. Specifically, we have demonstrated an important role for ammonia and inflammation in the development of hepatic encephalopathy in dogs with a congenital portosystemic shunt. Despite the apparent importance of inflammation in driving hepatic encephalopathy in dogs, it is unclear whether inflammation resolves following the successful treatment of liver disease. We hypothesized that haematological and biochemical evidence of inflammation, as gauged by neutrophil, lymphocyte and monocyte concentrations together with C-reactive protein concentrations, would decrease following successful treatment of congenital portosystemic shunts in dogs. One hundred and forty dogs with a congenital portosystemic shunt were enrolled into the study. We found that the proportion of dogs with a monocyte concentration above the reference range was significantly greater in dogs with hepatic encephalopathy at time of initial diagnosis. Importantly, neutrophil and monocyte concentrations significantly decreased following surgical congenital portosystemic shunt attenuation. We also found a significant decrease in C-reactive protein concentrations following surgical attenuation of congenital portosystemic shunts. Our study demonstrates that haematological and biochemical indices of inflammation reduce following successful treatment of the underlying liver disorder.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.