Page 922 - Cote clinical veterinary advisor dogs and cats 4th

Hepatitis (Chronic), Breed-Associated 451

hepatobiliary disease are strongly suggestive of Acute General Treatment phosphatidylcholine] 24-70 mg/kg PO q
the diagnosis; confirmation is obtained with a • Crystalloid fluid support, as appropriate 24h). Combination antioxidants are available
VetBooks.ir Differential Diagnosis (see Chronic Treatment below) (pp. 174, • Ursodeoxycholic acid 10-15 mg/kg PO q 24h Diseases and Disorders
(e.g., Denamarin).
• Treatment of HE, ascites, and GI ulceration
liver biopsy.
is given for antioxidant activity, antiinflam-
380, and 440)
• Hepatic disease from other causes
occur.
• Nonhepatic conditions associated with abnor- • Coagulopathies and sepsis are treated as they matory effects, immunomodulating effects,
and to promote choleresis.
mal liver enzyme activities, often referred to • Antifibrotics (e.g., colchicine 0.03 mg/kg
as nonspecific reactive hepatopathy Chronic Treatment PO q 24h) have failed to prolong survival
• Anti-inflammatory or immunosuppressive in humans, and few studies report their use
Initial Database therapy in dogs. Angiotensin II receptor blockers
• Subclinical disease ○ Glucocorticoid therapy (prednisolone have shown promise in inhibiting fibrosis
○ Elevation in serum alanine aminotransferase 1-2 mg/kg PO q 24-48h; maximum dose in humans and may have an application
(ALT), aspartate aminotransferase (AST), of 60 mg q 24h) may be beneficial in in dogs (e.g., telmisartan 1 mg/kg PO q
gamma-glutamyltransferase (GGT), and/or slowing inflammatory component of the 12-24h), but veterinary studies on safety
alkaline phosphatase (ALP) activity; ALT liver disease. With clinical improvement, and efficacy are lacking. Phosphatidylcholine
elevations are the most consistent labora- dose may be slowly tapered to 0.5 mg/kg q 20-70 mg/kg/d PO may also have antifibrotic
tory change 48h. With ascites, dexamethasone 0.2 mg/ effects.
• Clinical disease kg PO q 24h should be used instead of • Advanced clinical hepatitis
○ Elevations in serum ALT, AST, GGT, ALP prednisolone to avoid mineralocorticoid ○ Treatment for HE (p. 440): high-quality,
activities effect. Anecdotally, cocker spaniels have limited-protein diet; lactulose 0.1-0.5 mL/
○ Elevated serum bile acid concentrations improved survival after prednisolone kg PO q 12h, titrated to achieve loose fecal
in most; not useful in icteric animals therapy. Springer spaniels are reported consistency; and/or intestinal antibiotics
○ Hypoalbuminemia is common. to have improved liver enzymes and (metronidazole 7.5-10 mg/kg PO q 12h;
• Advanced disease prolonged survival with therapy. amoxicillin-clavulanate 15 mg/kg q 12h,
○ Elevation of serum total bilirubin ○ Immunosuppressive therapy using or 15 neomycin 20 mg/kg PO q 12h).
concentration cyclosporine 5 mg/kg q 12h followed by ○ Ascites therapy: spironolactone 1 mg/kg
○ Low serum albumin, blood urea nitrogen, dose taper is reported to result in remission PO q 12h or furosemide 0.5-2 mg/kg PO
and glucose concentrations in many cases based on normalization of q 12h
○ Prolonged clotting times liver enzymes during therapy. With liver ○ Gastric ulceration: omeprazole 1 mg/kg
enzyme improvement, cyclosporine dose PO q 12-24h and/or sucralfate 0.25-1 g
Advanced or Confirmatory Testing and frequency of administration can be PO q 8-12h.
• Abdominal radiographs: normal or micro- tapered. Vomiting often transiently occurs
hepatica ± ascites (loss of serosal detail) as a side effect of the medication, and Drug Interactions
• Ultrasound: early hepatitis may be normal or giving the drug with food or freezing • Avoid drugs that require hepatic metabolism
have altered parenchymal echogenicity; with the capsules before administration often or alter hepatic biotransformation (e.g.,
advanced hepatitis, there is microhepatica ± resolves this. Gingival hyperplasia is cimetidine).
ascites ± vascular changes associated with sometimes observed. There are no reported • Glucocorticoids may cause sodium reten-
portal hypertension. Acquired portosystemic studies evaluating other immunosuppres- tion, promote GI ulceration, precipitate
shunts may be evident. sive drugs, although some authors recom- hepatic failure in advanced disease, and
• Surgery or laparoscopy (p. 1128): varies mend mycophenolate mofetil 10-15 mg/ cause increased liver enzymes (making
from normal to small liver; micronodular kg q 12h as the immunosuppressive drug interpretation difficult).
or macronodular and fibrotic in advanced of choice. • Penicillamine and zinc should not be given
cirrhosis. Test coagulation first. • Copper chelation using penicillamine together because penicillamine chelates zinc.
• Liver histopathology: subclinical disease is 10-15 mg/kg q 12h may be required in some • Diuretics may worsen HE, promote dehydra-
associated with mixed inflammation varying Doberman pinchers (p. 458). Treatment is tion or metabolic alkalosis, and should be
from mild-moderate to marked lymphoplas- generally for 4 months or longer based on used only in otherwise stable patients for
macytic infiltrates and evidence of hepatocyte repeated measurement of hepatic copper the long-term delay of return of ascites or
death (apoptosis or necrosis). Variable fibrosis, concentrations. Concentration of ALT often for concurrent conditions (e.g., congestive
ductular response, and regenerative nodule returns to normal if copper is removed and heart failure).
formation occur as hepatitis progresses. inflammation controlled. • Nonsteroidal antiinflammatory drugs may
• Hepatic metal quantitative analysis: hepatic • Palatability is important in advanced cases exacerbate GI ulceration.
copper is usually normal in cocker and because adequate caloric intake is required.
springer spaniels but often high in Doberman Feed a high-quality, moderate-protein Possible Complications
pinchers. Hepatic iron may be increased in diet in small, multiple feedings. Dietary • Glucocorticoids may precipitate ascites and
all breeds and is thought to be secondary to protein restriction is necessary only when HE and result in early death in advanced
chronic hepatic inflammation. protein intolerance occurs (i.e., HE); milk cases.
and vegetable protein sources are better for • Because von Willebrand disease is common
TREATMENT avoiding HE than meat protein–based diets. in Doberman pinschers, von Willebrand
Fermentable fiber may also be beneficial in factor, buccal mucosal bleeding time, or
Treatment Overview controlling HE. Doberman pinschers with both should be evaluated before biopsy
Goals of treatment are to slow progression of abnormal hepatic copper should be fed a procedures.
the inflammatory component, provide general low-copper diet (homemade formulated diet
supportive care, and treat complications of liver or veterinary therapeutic liver diets). Recommended Monitoring
disease such as HE, ascites, GI ulceration, and • Provide liver support with anti- • Young adult dogs of these breeds should have
nutritional imbalance. If abnormal hepatic oxidants (vitamin E 10 IU/kg PO q 24h; periodic liver enzymes measured as screening
copper is a component of the disease, specific S-adenosylmethionine 20 mg/kg PO q 24h; tests to help identify affected dogs early in
therapy is required. and/or milk thistle [silybin complexed with the disease process.

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