Difference between revisions of "Hepatitis, Chronic"
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| Line 23: | Line 23: | ||
*Familial predisposition | *Familial predisposition | ||
*Copper accumulation (copper storage disease) | *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 | *Chronic drug therapy | ||
*Infectious for examplae infectious canine hepatitis- | *Infectious for examplae infectious canine hepatitis- | ||
| Line 30: | Line 31: | ||
===Clinical Signs=== | ===Clinical Signs=== | ||
These include | These include | ||
| − | *lethargy | + | *anorexia, lethargy and depression |
| + | *weight loss | ||
*vomiting and diarrhoea | *vomiting and diarrhoea | ||
*polyuria and polydipsia | *polyuria and polydipsia | ||
| − | *ascites | + | *ascites - most consistent in dogs with cirrhosis |
*and rarely icterus, seizures, fever and bleeding disthesis | *and rarely icterus, seizures, fever and bleeding disthesis | ||
===Laboratory tests=== | ===Laboratory tests=== | ||
| + | |||
| + | ====Haematology==== | ||
| + | *Mild non-regenerative anaemia and microcytosis | ||
| + | |||
====Biochemistry==== | ====Biochemistry==== | ||
*Increased alanine aminotransferase (ALT) and alkaline phosphatase (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 incrased if end-stage 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 (DIC) | ||
===Imaging=== | ===Imaging=== | ||
| + | *Abdominal radiographs will only reveal microhepatica or ascites when advanced stages of disease is reached. | ||
| + | *Ultrasonographically, a normal liver or non specific changes in echogenecity may be seen in early stages of the disease. In cases of 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. | ||
| + | |||
===Histopathology=== | ===Histopathology=== | ||
Revision as of 12:27, 7 August 2009
 |
This article is still under construction. |
Signalment
- Common in dogs, especially young to middle-aged dogs.
- Mixed and purebred dogs are affected but there is a familial predisposition in
- Doberman pinscher
- Bedlington Terrier
- Cocker Spaniel
- Dalmation
- Skye Terrier
- Poodle
- Labrador Retriever
- German Shepherd Dog
- Scottish Terrier
- Beagle
Description
Chronic hepatitis is an inflammatory-necrotising disease of at least 6 months duration. It is characterised by hepatocellular apoptosis or necrosis, a variable mononuclear or mixed inflammatory cell infiltrate, regeneration and fibrosis (1). It predominantly consists of lymphocytic-plasmacytic inflammatory infiltration.
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 examplae infectious canine hepatitis-
- Autoimmune or steroid responsive disorder
Diagnosis
Clinical Signs
These include
- anorexia, lethargy and depression
- weight loss
- vomiting and diarrhoea
- polyuria and polydipsia
- ascites - most consistent in dogs with cirrhosis
- and rarely icterus, seizures, fever and bleeding disthesis
Laboratory tests
Haematology
- Mild non-regenerative anaemia and microcytosis
Biochemistry
- Increased alanine aminotransferase (ALT) and alkaline phosphatase (ALP). However these may not be incrased if end-stage cirrhosis is reached.
- Hyperbilirubinaemia
- Hypoalbuminaemia
- Hyperglobulinaemia
- Decreased blood urea nitrogen (BUN)
- Hypoglycaemia
Further tests
- 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 (DIC)
Imaging
- Abdominal radiographs will only reveal microhepatica or ascites when advanced stages of disease is reached.
- Ultrasonographically, a normal liver or non specific changes in echogenecity may be seen in early stages of the disease. In cases of 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.
Histopathology
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
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.