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− | ==Introduction==
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− | '''Chronic hepatitis''' is an inflammatory-necrotising disease of at least 6 months duration. It is characterised by hepatocellular [[Adaptive Immunity to Viruses|apoptosis]] or [[Necrosis - Pathology|necrosis]], a variable mononuclear or mixed inflammatory cell infiltrate, [[Liver Regeneration|regeneration]] and [[Liver Fibrosis|fibrosis]] (1). It predominantly consists of lymphocytic-plasmacytic inflammatory infiltration, and the disease process typically involves a slowly progressive inflammation which leads to fibrosis and possibly cirrhosis.
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| ==Signalment== | | ==Signalment== |
− | *Common in dogs, especially young to middle-aged dogs.
| + | Familial predisposition including Doberman pinscher, Bedlington Terrier, Cocker Spaniel, Dalmation, Skye Terrier, Poodle, Labrador Retriever, German Shepherd Dog, Scottish Terrier, Beagle. |
− | *Mixed and purebred dogs are affected but there is a familial predisposition in the following breeds:
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− | <gallery>
| + | ==Description== |
− | Image:Dobermann.jpg|'''Dobermann'''<p>John Adams (2007) WikiMedia Commons
| + | Chronic hepatitis is an inflammatory-nectorising disease of at least 6 months duration. It predominantly consists of lymphocytic-plasmacytic inflammatory infiltration. A number of causes include: |
− | Image:Bedlington.jpg|'''Bedlington Terrier'''<p> Pleple2000 (2006) WikiMedia Commons
| + | *Copper accumulation |
− | Image:Cocker_spaniel.jpg|'''Cocker Spaniel'''<p> Ellen Levy Finch (2004) WikiMedia Commons
| + | *Drugs |
− | Image:Dalmatian.jpg|'''Dalmatian'''<p> Miroslav Cacik (2006) WikiMedia Commons
| + | *Infections |
− | Image:Skye_terrier.jpg|'''Skye Terrier'''<p> Pleple2000 (2007) WikiMedia Commons
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− | Image:Standard_poodle.jpg|'''Standard Poodle''' <p> John Leslie (2007) WikiMedia Commons
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− | Image:labrador.jpg|'''Labrador Retriever'''<p> Ellen Levy Finch (2004) WikiMedia Commons
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− | Image:GermanShep.jpg|'''German Shepherd (Alsatian)'''<p> Ellen Levy Finch (2004) WikiMedia Commons
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− | Image:Scottish_terrier.jpg|'''Scottish Terrier'''<p> Svencb (2003) WikiMedia Commons
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− | Image:Beagle.jpg|'''Beagle'''<p> sannse (2003) WikiMedia Commons
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− | </gallery>
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− | ==Aetiology== | |
− | A number of aetiologies include: | |
− | *Familial predisposition
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− | *Copper accumulation (copper storage disease) | |
− | **This may be a cause or consequence of chronic hepatitis. Copper is normally excreted in bile, therefore it can occur with any cholestatic hepatobiliary disorder.
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− | *Chronic drug therapy | |
− | *Infectious, for example [[Infectious Canine Hepatitis|infectious canine hepatitis]] | |
− | *Autoimmune or steroid responsive disorder
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| + | ==Diagnosis== |
| ===Clinical Signs=== | | ===Clinical Signs=== |
− | These include: | + | These include |
− | *anorexia, lethargy and depression | + | *Lethargy, weakness, anorexia and weight loss |
− | *weight loss
| + | *Vomiting and diarrhoea |
− | *[[Vomiting|vomiting]] and [[Diarrhoea|diarrhoea]] | + | *Polyuria and polydipsia |
− | *polyuria and polydipsia | + | *Ascites |
− | *ascites - most consistent in dogs with [[Cirrhosis|cirrhosis]] | + | *Rarely with icterus, seizures, fever and bleeding tendency |
− | *and rarely [[Icterus|icterus]], seizures, fever and bleeding diathesis | |
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− | ===Laboratory tests===
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− | Haematology:
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− | *Mild non-regenerative anaemia and microcytosis
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− | Biochemistry: | + | ===Haematology & Biochemistry=== |
− | *Increased alanine aminotransferase (ALT) and alkaline phosphatase (ALP). However these may not be increased if end-stage [[Cirrhosis|cirrhosis]] is reached. | + | *Increased ALT and ALP. However these may not be incrased if end-stage cirrhosis is reached. |
− | *Hyperbilirubinaemia
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| *Hypoalbuminaemia | | *Hypoalbuminaemia |
− | *Hyperglobulinaemia
| + | *Decreased urea |
− | *Decreased blood urea nitrogen (BUN) | |
− | *Hypoglycaemia
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− | | |
− | ====Further tests====
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| *Increased bile acids | | *Increased bile acids |
− | *Abnormal ammonia tolerance test
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− | *Increased prolonged activated partial thromboplastin time (APTT) and prothrombin time (PT) indicates severe liver dysfunction or [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation (DIC)]]
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− | ==Imaging== | + | ===Imaging=== |
− | Abdominal radiographs will only reveal microhepatica or ascites when advanced stages of disease are reached.
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− | Ultrasonographically, liver may be normal or non specific changes in echogenecity may be seen in early stages of the disease. In cases of [[Cirrhosis|cirrhosis]], microhepatica, irregularity in hepatic margin, focal lesions corresponding to regenerative nodules, hyperechogenicity of liver parenchyma associated with increased fibrous tissue and ascites may be seen.
| + | ===Biopsy=== |
| + | This is required for definitive diagnosis. Histology reveals lymphoplasmacellular inflammation and necrosis of the hepatocytes adjacent to the portal tracts. |
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− | ==Histopathology==
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− | This is required for definitive diagnosis and to differentiate chronic hepatitis from other hepatopathies. Chronic hepatitis is characterised by moderate to severe lymphoplasmacellular [[Inflammation - Pathology|inflammation]] and [[Liver Necrosis|necrosis]] of the hepatocytes adjacent to the portal tracts.
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| ==Treatment== | | ==Treatment== |
− | *[[Steroids|Glucocorticoids]] | + | *Glucocorticoids at 1-2 mg/kg/day PO. Taper down with improved clinical signs and normal liver enzymes values |
− | **Taper down with improved clinical signs and normal liver enzymes values.
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− | **This is not indicated for chronic hepatitis caused by drug therapy, primary copper accumulation or infectious agents.
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− | **Response to treatment should be followed up by liver biopsy 3-6 months later as glucocorticoid causes steroid induced ALP
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| *Ursodeoxycholic acid at 15mg/kg PO SID | | *Ursodeoxycholic acid at 15mg/kg PO SID |
− | **It is a synthetic hydrophilic bile acid that has hepatoprotective (anti-inflammatory, immunomodulatory and antifibrotic effects) properties and choleretic effect. It expands the bile acid pool and displaces potentially hepatotoxic hydrophobic bile acids that accumulate in cholestasis. | + | *Antioxidants |
− | *Vitamin E
| + | *Copper chelation with Penicillamine or Zinc if copper exceeds 2000ppm |
− | **An antioxidant to scavenge free radicals which may contribute to oxidative hepatocellular injury.
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− | *Copper chelation if copper exceeds 2000ppm | |
− | **Penicillamine
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− | **Zinc
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| ==Prognosis== | | ==Prognosis== |
− | Response to treatment is variable. Dogs with [[Liver Fibrosis|fibrosis]] and [[Cirrhosis |cirrhosis]] carry a poorer prognosis.
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− | {{Learning
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− | |Vetstream = [https://www.vetstream.com/felis/Content/Disease/dis01088.asp Liver: chronic disease in feline]<br>[https://www.vetstream.com/canis/Content/Disease/dis01089.asp Chronic heptatitis in canines]
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− | }}
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− | ==References==
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− | *(1) Van den Ingh, TSGAM et. al. (2006). Morphological classification of parenchymal disorders of the canine and feline liver. In Rothuizen J et. al., editors: WSAVA standards for clinical and histological diagnosis of canine and feline liver disease, Oxford, England, Saunders.
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− | *Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition) ''W.B. Saunders Company''.
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− | *Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.
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− | [[Category:Liver_-_Inflammatory_Pathology]]
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− | [[Category:Liver Diseases - Dog]][[Category:To Do - Clinical]]
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