Difference between revisions of "Hepatitis, Chronic"

From WikiVet English
Jump to navigation Jump to search
(61 intermediate revisions by 7 users not shown)
Line 1: Line 1:
==Introduction==
+
{{unfinished}}
'''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.
+
 
  
 
==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:
+
 
<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
+
 
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
 
  
 +
==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
 
 
 
===Laboratory tests===
 
Haematology:
 
*Mild non-regenerative anaemia and microcytosis
 
  
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
 
 
*Hypoalbuminaemia
 
*Hypoalbuminaemia
*Hyperglobulinaemia
+
*Decreased urea
*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.
 
  
Ultrasonographically, liver may be normal or non specific changes in echogenecity may be seen in early stages of the diseaseIn 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 diagnosisHistology reveals lymphoplasmacellular inflammation and necrosis of the hepatocytes adjacent to the portal tracts.
  
==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==
*[[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.
 
**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
**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.
 
*Copper chelation if copper exceeds 2000ppm
 
**Penicillamine
 
**Zinc
 
  
 
==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''.
 
 
[[Category:Liver_-_Inflammatory_Pathology]]
 
[[Category:Liver Diseases - Dog]][[Category:To Do - Clinical]]
 

Revision as of 16:00, 6 August 2009




Signalment

Familial predisposition including Doberman pinscher, Bedlington Terrier, Cocker Spaniel, Dalmation, Skye Terrier, Poodle, Labrador Retriever, German Shepherd Dog, Scottish Terrier, Beagle.

Description

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:

  • Copper accumulation
  • Drugs
  • Infections


Diagnosis

Clinical Signs

These include

  • Lethargy, weakness, anorexia and weight loss
  • Vomiting and diarrhoea
  • Polyuria and polydipsia
  • Ascites
  • Rarely with icterus, seizures, fever and bleeding tendency

Haematology & Biochemistry

  • Increased ALT and ALP. However these may not be incrased if end-stage cirrhosis is reached.
  • Hypoalbuminaemia
  • Decreased urea
  • Increased bile acids

Imaging

Biopsy

This is required for definitive diagnosis. Histology reveals lymphoplasmacellular inflammation and necrosis of the hepatocytes adjacent to the portal tracts.


Treatment

  • Glucocorticoids at 1-2 mg/kg/day PO. Taper down with improved clinical signs and normal liver enzymes values
  • Ursodeoxycholic acid at 15mg/kg PO SID
  • Antioxidants
  • Copper chelation with Penicillamine or Zinc if copper exceeds 2000ppm

Prognosis