Parenchymal changes of the liver during systemicdisease
7.5.2.1 Steroid hepatopathy plasma to 65°C for 2 min. However, later on in the disease process, both the steroid-induced as well as hepatic AP may be increased.
Management
The glucocorticoid-induced changes of the liver disappear spontaneously within 4-12 weeks after the discontinuation of steroid administration or successful therapy of hyperadreno- corticism.
7.5.2.2 Hepatic steatosis in diabetes mellitus
Pathogenesis
In patients with diabetes mellitus, lipolysis in the adipose tissue is increased leading to an increased delivery of fatty acids to the liver. In addition, the production of triglycerides is also increased. As a result, fat accumulates in the hepatocytes and causes microvesicular, and in advanced cases, macrovesicular steatosis (lipidosis).5
Symptoms
Hepatic steatosis is mostly subclinical, and patients usually present with clinical signs due to the underlying diabetes mel- litus, such as PU/ PD and weight gain.
Pathogenesis
Diagnosis
Cushing’s disease and the administration of exogenous corticosteroids cause glycogen accumulation in hepatocytes and vacuolization, also known as ballooning. The liver cells are enlarged leading to hepatomegaly. Steroids cause induction of alkaline phosphatase (AP) activity. However, steroid hepatopa- thy does not dramatically affect hepatic function, so that the symptoms are usually due to the primary disease process rather than the hepatic changes.5,70,71
Symptoms
The symptoms seen with steroid hepatopathy are those of hy- peradrenocorticism.
Serum hepatic enzyme activities and bile acids concentrations can be slightly to moderately increased in patients with hepatic steatosis. The histological or cytological demonstration of steatosis in combination with persistent hyperglycemia is diagnostic. Indeed, the cytological evaluation of smears from fine needle aspirates is diagnostic in most cases.
Management
Specific treatment of the fatty change of the liver is not necessary, as it gradually disappears with regulation of the diabetes mellitus. There are idiopathic forms of hepatic steatosis, which may be chronic, but do not cause considerable hepatic dysfunction. There is no known treatment for these cases.
Diagnosis
The diagnosis of steroid hepatopathy is made by liver histology or cytology. The steroid-induced AP can be differentiated from other sources of AP as it remains active after heating the
7.4.1.1 Hypoxic liver damage
Symptoms
Pathogenesis
Hepatic degeneration or necrosis can occur due to hypoxia of the liver. The usual causes of hepatic hypoxia are severe hemolysis and shock. Hepatic hypoxia leads to centrolobular necrosis, followed by a secondary inflammatory reaction of polymorphonuclear cells and intrahepatic cholestasis.5,41
Symptoms
Hypoxic liver damage normally does not lead to recognizable clinical signs as the patient usually displays pronounced clinical signs of the underlying hemolysis or shock.
Diagnosis
Hepatic changes due to hypoxia are specific, but they can only be confirmed by histopathology. However, in most patients with severe hemolysis or shock, the secondary hepatic changes are not of primary interest and instead the diagnostic effort is directed at identifying the underlying cause of the hemolysis or shock. It is important to note that patients with primary liver diseases also often show icterus in combination with anemia, but in patients with hypoxic liver damage, the anemia is much less pronounced than in patients with primary hemolytic anemia.
Management
Management involves treatment of the underlying cause. The liver usually recovers spontaneously.
7.4.1.2 Amyloidosis
Pathogenesis
Amyloidosis of the liver is very rare in dogs and is most commonly seen in Shar Peis. It occurs more commonly in Siamese cats. Deposits of amyloid in the liver are visible as amorphous hyaline and eosinophilic material in the space of Disse. Depending on the amount of amyloid deposit, the liver may be enlarged on abdominal palpation. Hepatic enzyme activities and bile acids concentrations in serum or plasma are usually increased. Amyloidosis usually causes concurrent glomerular damage and proteinuria. The liver becomes severely enlarged and fragile. Many patients die suddenly due to spontaneous hepatic rupture.
Sudden death due to hepatic rupture and abdominal blood loss may occur. Renal lesions are usually present and may cause proteinuria and nephrotic syndrome.
Diagnosis
Amyloidosis is diagnosed by cytological examination of a hepatic aspirate.
Management
There is no know treatment for this disease and it is usually lethal. 7
7.4.2