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| + | ==Introduction== |
− | | + | '''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== |
− | Familial predisposition including Doberman pinscher, Bedlington Terrier, Cocker Spaniel, Dalmation, Skye Terrier, Poodle, Labrador Retriever, German Shepherd Dog, Scottish Terrier, Beagle.
| + | *Common in dogs, especially young to middle-aged dogs. |
| + | *Mixed and purebred dogs are affected but there is a familial predisposition in the following breeds: |
| + | <gallery> |
| + | Image:Dobermann.jpg|'''Dobermann'''<p>John Adams (2007) WikiMedia Commons |
| + | Image:Bedlington.jpg|'''Bedlington Terrier'''<p> Pleple2000 (2006) WikiMedia Commons |
| + | Image:Cocker_spaniel.jpg|'''Cocker Spaniel'''<p> Ellen Levy Finch (2004) WikiMedia Commons |
| + | Image:Dalmatian.jpg|'''Dalmatian'''<p> Miroslav Cacik (2006) WikiMedia Commons |
| + | Image:Skye_terrier.jpg|'''Skye Terrier'''<p> Pleple2000 (2007) WikiMedia Commons |
| + | Image:Standard_poodle.jpg|'''Standard Poodle''' <p> John Leslie (2007) WikiMedia Commons |
| + | Image:labrador.jpg|'''Labrador Retriever'''<p> Ellen Levy Finch (2004) WikiMedia Commons |
| + | Image:GermanShep.jpg|'''German Shepherd (Alsatian)'''<p> Ellen Levy Finch (2004) WikiMedia Commons |
| + | Image:Scottish_terrier.jpg|'''Scottish Terrier'''<p> Svencb (2003) WikiMedia Commons |
| + | Image:Beagle.jpg|'''Beagle'''<p> sannse (2003) WikiMedia Commons |
| + | </gallery> |
| + | ==Aetiology== |
| + | A number of aetiologies include: |
| + | *Familial predisposition |
| + | *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. |
| + | *Chronic drug therapy |
| + | *Infectious, for example [[Infectious Canine Hepatitis|infectious canine hepatitis]] |
| + | *Autoimmune or steroid responsive disorder |
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− | ==Description== | + | ===Clinical Signs=== |
− | Chronic, at least 6 months, of hepatocellular necrosis, mostly lymphocytic-plasmacytic infiltration. A number of causes include:
| + | These include: |
− | *Copper accumulation | + | *anorexia, lethargy and depression |
− | *Drugs | + | *weight loss |
− | *Infections | + | *[[Vomiting|vomiting]] and [[Diarrhoea|diarrhoea]] |
− |
| + | *polyuria and polydipsia |
| + | *ascites - most consistent in dogs with [[Cirrhosis|cirrhosis]] |
| + | *and rarely [[Icterus|icterus]], seizures, fever and bleeding diathesis |
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− | ==Diagnosis== | + | ===Laboratory tests=== |
− | ===Clinical Signs===
| + | Haematology: |
− | These include
| + | *Mild non-regenerative anaemia and microcytosis |
− | *Lethargy, weakness, anorexia and weight loss
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− | *Vomiting and diarrhoea
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− | *Polyuria and polydipsia
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− | *Ascites
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− | *Rarely with icterus, seizures, fever and bleeding tendency | |
| | | |
− | ===Haematology & Biochemistry===
| + | Biochemistry: |
− | *Increased ALT and ALP. However these may not be incrased if end-stage cirrhosis is reached. | + | *Increased alanine aminotransferase (ALT) and alkaline phosphatase (ALP). However these may not be increased if end-stage [[Cirrhosis|cirrhosis]] is reached. |
| + | *Hyperbilirubinaemia |
| *Hypoalbuminaemia | | *Hypoalbuminaemia |
− | *Decreased urea | + | *Hyperglobulinaemia |
| + | *Decreased blood urea nitrogen (BUN) |
| + | *Hypoglycaemia |
| + | |
| + | ====Further tests==== |
| *Increased bile acids | | *Increased bile acids |
| + | *Abnormal ammonia tolerance test |
| + | *Increased prolonged activated partial thromboplastin time (APTT) and prothrombin time (PT) indicates severe liver dysfunction or [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation (DIC)]] |
| | | |
− | ===Imaging===
| + | ==Imaging== |
| + | Abdominal radiographs will only reveal microhepatica or ascites when advanced stages of disease are reached. |
| | | |
− | ===Biopsy===
| + | 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. |
− | 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== |
| + | 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. |
| | | |
| ==Treatment== | | ==Treatment== |
− | *Glucocorticoids at 1-2 mg/kg/day PO. Taper down with improved clinical signs and normal liver enzymes values | + | *[[Steroids|Glucocorticoids]] |
| + | **Taper down with improved clinical signs and normal liver enzymes values. |
| + | **This is not indicated for chronic hepatitis caused by drug therapy, primary copper accumulation or infectious agents. |
| + | **Response to treatment should be followed up by liver biopsy 3-6 months later as glucocorticoid causes steroid induced ALP |
| *Ursodeoxycholic acid at 15mg/kg PO SID | | *Ursodeoxycholic acid at 15mg/kg PO SID |
− | *Antioxidants | + | **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. |
− | *Copper chelation with Penicillamine or Zinc if copper exceeds 2000ppm | + | *Vitamin E |
| + | **An antioxidant to scavenge free radicals which may contribute to oxidative hepatocellular injury. |
| + | *Copper chelation if copper exceeds 2000ppm |
| + | **Penicillamine |
| + | **Zinc |
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| ==Prognosis== | | ==Prognosis== |
| + | Response to treatment is variable. Dogs with [[Liver Fibrosis|fibrosis]] and [[Cirrhosis |cirrhosis]] carry a poorer prognosis. |
| + | |
| + | {{Learning |
| + | |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] |
| + | }} |
| + | |
| + | |
| + | ==References== |
| + | *(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. |
| + | *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''. |
| + | *Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''. |
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| + | [[Category:Liver_-_Inflammatory_Pathology]] |
| + | [[Category:Liver Diseases - Dog]][[Category:To Do - Clinical]] |