Canine Idiopathic Chronic Hepatitis

Bexfield, Nick

doi:10.1016/j.cvsm.2016.11.012

Cited by 22 publications

(25 citation statements)

References 63 publications

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“…Chronic hepatitis seemingly has a long subclinical phase consistent with the observation that up to 20% of dogs with CH have increased serum liver enzyme activities in the absence of clinical illness …”

Section: Signalment and Clinical Signssupporting

confidence: 77%

“…The most common toxic injury causing CH in dogs is a consequence of hepatic copper (Cu) excess . Copper‐associated CH (CuCH) may develop in any breed, including mixed breeds, but the Bedlington Terrier (BT), Dalmatian, Labrador Retriever (LR), Doberman Pinscher, and West Highland White Terrier are predisposed.…”

Section: Etiologymentioning

confidence: 99%

“…Reported sex ratios in individual breeds are shown in Supporting Information Table S1. Female predisposition occurs in LR, Dobermans, Dalmatians, and English Springer Spaniels . Male predisposition occurs in American and English Cocker Spaniels …”

Section: Signalment and Clinical Signsmentioning

confidence: 99%

“…Treatment of CH in dog should target the causative agent (Table ). Unfortunately, CH in the dog often is often idiopathic . If thorough diagnostic investigation fails to disclose a plausible etiology, then treatment with nonspecific hepatoprotective agents (see below) with or without a trial of immunosuppressive treatment may be indicated.…”

Section: Treatmentmentioning

confidence: 99%

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ACVIM consensus statement on the diagnosis and treatment of chronic hepatitis in dogs

Webster

Cullen

Penninck

et al. 2019

Veterinary Internal Medicne

198

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This consensus statement on chronic hepatitis (CH) in dogs is based on the expert opinion of 7 specialists with extensive experience in diagnosing, treating, and conducting clinical research in hepatology in dogs. It was generated from expert opinion and information gathered from searching of PubMed for manuscripts on CH, the Veterinary Information Network for abstracts and conference proceeding from annual meetings of the American College of Veterinary Medicine and the European College of Veterinary Medicine, and selected manuscripts from the human literature on CH. The panel recognizes that the diagnosis and treatment of CH in the dog is a complex process that requires integration of clinical presentation with clinical pathology, diagnostic imaging, and hepatic biopsy. Essential to this process is an index of suspicion for CH, knowledge of how to best collect tissue samples, access to a pathologist with experience in assessing hepatic histopathology, knowledge of reasonable medical interventions, and a strategy for monitoring treatment response and complications.

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Section: Signalment and Clinical Signssupporting

confidence: 77%

Section: Etiologymentioning

confidence: 99%

Section: Signalment and Clinical Signsmentioning

confidence: 99%

Section: Treatmentmentioning

confidence: 99%

See 2 more Smart Citations

ACVIM consensus statement on the diagnosis and treatment of chronic hepatitis in dogs

Webster

Cullen

Penninck

et al. 2019

Veterinary Internal Medicne

198

View full text Add to dashboard Cite

show abstract

“…In >60% of dogs with CH, no underlying cause can be found, and these patients are referred to as having idiopathic CH. Copper‐associated and idiopathic CH are reviewed elsewhere. Granulomatous hepatitis is an uncommon form of CH in dogs and may be the result of infectious diseases such as schistosomiasis, histoplasmosis, Angiostrongylus vasorum infection, leishmaniasis, or with lymphoma and histiocytosis .…”

Section: Causes Of Hepatic Fibrosis In Dogsmentioning

confidence: 99%

Hepatic Fibrosis in Dogs

Eulenberg

Lidbury

2017

Veterinary Internal Medicne

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Hepatic fibrosis is commonly diagnosed in dogs, often as a sequela to chronic hepatitis (CH). The development of fibrosis is a crucial event in the progression of hepatic disease that is of prognostic value. The pathophysiology of hepatic fibrosis in human patients and rodent models has been studied extensively. Although less is known about this process in dogs, evidence suggests that fibrogenic mechanisms are similar between species and that activation of hepatic stellate cells is a key step. Diagnosis and staging of hepatic fibrosis in dogs requires histopathological examination of a liver biopsy specimen. However, performing a liver biopsy is invasive and assessment of fibrotic stage is complicated by the absence of a universally accepted staging scheme in veterinary medicine. Serum biomarkers that can discriminate among different fibrosis stages are used in human patients, but such markers must be more completely evaluated in dogs before clinical use. When successful treatment of its underlying cause is feasible, reversal of hepatic fibrosis has been shown to be possible in rodent models and human patients. Reversal of fibrosis has not been well documented in dogs, but successful treatment of CH is possible. In human medicine, better understanding of the pathomechanisms of hepatic fibrosis is leading to the development of novel treatment strategies. In time, these may be applied to dogs. This article comparatively reviews the pathogenesis of hepatic fibrosis, its diagnosis, and its treatment in dogs.

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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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Canine Idiopathic Chronic Hepatitis

Cited by 22 publications

References 63 publications

ACVIM consensus statement on the diagnosis and treatment of chronic hepatitis in dogs

ACVIM consensus statement on the diagnosis and treatment of chronic hepatitis in dogs

Hepatic Fibrosis in Dogs

The effect of ammonia on canine polymorphonuclear cells

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