Surgical attenuation of spontaneous congenital portosystemic shunts in dogs resolves hepatic encephalopathy but not hypermanganesemia

Gow, Adam; Frowde, Polly; Elwood, Clive; Burton, C.; Powell, Roger M.; Tappin, Simon; Foale, Rob; Duncan, Andrew; Mellanby, Richard J.

doi:10.1007/s11011-015-9676-y

Cited by 4 publications

(2 citation statements)

References 30 publications

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“…The increase of Mn concentrations in the liver of CH‐Cu greater than 100 dogs in our study could also be explained by a cholestatic phenomenon, although Gow et al () demonstrated that resolution of congenital portosystemic shunts in dogs resolves the encephalopathy but not the hypermanganesaemia. The liver plays a pivotal role in Mn metabolism because the majority of the gastrointestinally‐absorbed element is removed by the liver and excreted into bile, allowing for only approximately 2% of absorbed Mn to reach the systemic circulation (Aschner & Aschner ).…”

Section: Discussionmentioning

confidence: 44%

“…The liver plays a pivotal role in Mn metabolism because the majority of the gastrointestinally‐absorbed element is removed by the liver and excreted into bile, allowing for only approximately 2% of absorbed Mn to reach the systemic circulation (Aschner & Aschner ). Very limited information is available on the role of Mn in canine liver disease, even though recent studies have demonstrated that whole‐blood Mn concentrations were higher in dogs with primary hepatitis (Kilpatrick et al ) and hepatic encephalopathy (Gow et al ). Studies in humans have shown increased blood Mn concentrations and deposition in the central nervous system (CNS) in cases of hepatic insufficiency (Zheng et al , Tuschl et al ).…”

Section: Discussionmentioning

confidence: 99%

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Hepatic concentrations of copper and other metals in dogs with and without chronic hepatitis

Cedeño

López‐Alonso

Miranda

2016

J of Small Animal Practice

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Section: Discussionmentioning

confidence: 44%

Section: Discussionmentioning

confidence: 99%

Hepatic concentrations of copper and other metals in dogs with and without chronic hepatitis

Cedeño

López‐Alonso

Miranda

2016

J of Small Animal Practice

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The effect of ammonia on canine polymorphonuclear cells

et al. 2018

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Hyperammonaemia is a common complication of liver disease in dogs. High concentrations of ammonia can be detrimental to dogs with liver disease for several reasons, notably by causing hepatic encephalopathy (HE) which describes the wide range of neurological abnormalities ranging from altered behaviour to seizures that are well recognised complications in dogs with hepatic disorders. In human patients with liver disease, hyperammonaemia has also been linked to the development of other systemic complications such as dysregulation of the innate immune system. In contrast, the effects of hyperammonaemia on the canine innate immune system is currently unknown. The aim of this study was to investigate the effects of ammonia on the oxidative burst activity of canine polymorphonuclear cells in vitro. Blood obtained from healthy dogs (n = 8) was incubated with escalating concentrations of ammonia ranging from 0 to 250 μM, and the percentage of cells experiencing an oxidative burst was evaluated using a commercial kit (Phagoburst™) and flow cytometry. The spontaneous oxidative burst was evaluated without stimulation and also following stimulation with E coli. The pH of the blood was also measured at the differing ammonia concentrations. There was an increase in the percentage of cells experiencing a spontaneous oxidative burst from ammonia concentrations of 125 μM (p = <0.05) and above (p = <0.01), with a 4.9 fold increase at 200 μM (p = < 0.001). In those cells stimulated with E coli, incubation with increasing ammonia concentrations did not result in a significant difference in oxidative burst from baseline (p = 0.953). There was no statistically significant difference between the pH of the blood at the various ammonia concentrations (p = 0.2) suggesting that the difference in spontaneous oxidative burst was due to the ammonia rather than simply a change in pH conditions. In summary, the spontaneous oxidative burst of neutrophils was significantly increased from baseline. This supports a potential role of ammonia in contributing to innate immune system dysfunction in dogs with liver disease, and may present a future therapeutic target.

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Dietary management of liver disorders

Chandler¹

2019

Companion Animal

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The liver is responsible for many important functions, including metabolism of ingested nutrients and toxins, and production of plasma proteins, clotting factors and bile salts. When the liver is diseased or damaged, dietary therapy is beneficial in preventing further damage; supporting hepatic repair and liver function; and decreasing signs of hepatic encephalopathy. The nutritional status of patients with liver disease is often compromised by anorexia; nutrient malassimilation due to portal hypertension and cirrhosis; and decreased hepatic nutrient synthesis or storage capacity. Appetite and the amounts of protein, carbohydrates, fats, vitamins and minerals should all be considered. Previously, reduced dietary protein was often recommended; however, reducing dietary protein concentrations in all animals with liver disease is not appropriate. Nutraceuticals may have a beneficial effect in some cases. Nutritional support specifically for feline hepatic lipidosis, copper associated liver disease and hepatic encephalopathy are discussed.

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Surgical attenuation of spontaneous congenital portosystemic shunts in dogs resolves hepatic encephalopathy but not hypermanganesemia

Cited by 4 publications

References 30 publications

Hepatic concentrations of copper and other metals in dogs with and without chronic hepatitis

Hepatic concentrations of copper and other metals in dogs with and without chronic hepatitis

The effect of ammonia on canine polymorphonuclear cells

Dietary management of liver disorders

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