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1190 Small Animal Clinical Nutrition
CASE 68-5
VetBooks.ir Increased Hepatic Enzyme Activities in a
Bedlington Terrier
David C. Twedt, DVM, Dipl. ACVIM (Internal Medicine)
College of Veterinary Medicine and Biomedical Sciences
Colorado State University
Fort Collins, Colorado, USA
Patient Assessment
A one-and-one-half-year-old female Bedlington terrier (Figure
1) was evaluated because a littermate had recently been diag-
nosed with copper-associated hepatotoxicity. A serum biochem-
istry profile obtained by the referring veterinarian identified an
abnormal alanine aminotransferase (ALT) activity of 161 IU/l
(reference range 10 to 120 IU/l). The dog was considered to be Figure 1. A one-and-one-half-year-old female Bedlington terrier
affected with inherited copper hepatotoxicity.
normal by the owner and a physical examination was unremark-
able. The dog weighed 6.6 kg and had normal body condition
(body condition score [BCS] 3/5).
Another serum biochemistry profile confirmed an elevated
ALT of 189 IU/l. Serum protein and bile acid concentrations,
and clotting times were normal suggesting adequate hepatic
function. The liver was grossly normal when biopsy specimens
were collected at laparoscopy.Evaluation of the biopsy specimens
revealed mild focal necrosis with many hepatocytes containing
golden brown granules. These granules stained positive for cop-
per using rhodamine copper stain (Figure 2). Hepatic copper
quantitation was 4,901 µg/g dry weight liver (normal reference
120 to 400 µg/g dry weight liver). A diagnosis of inherited cop-
per hepatotoxicity was made.
Assess the Food and Feeding Method
The diet was currently a mixture of a commercial dry grocery Figure 2. A photomicrograph of a liver specimen from a Bedlington
a
brand dog food (Purina Dog Chow ) and various commercial terrier. Granules located in hepatocytes (arrows) stained positive for
moist grocery brand foods with occasional table foods.The foods copper (rhodamine copper stain).
were mixed together at each meal so that approximately two-
thirds of the volume came from dry food and one-third from
moist food. The exact daily caloric intake was unknown. The patient was eating approximately the same amount of food and there
had been no change in body weight during the last year.
Questions
1. What are the key nutritional factors to consider for this patient?
2. What nutritional supplements might benefit patients with copper hepatotoxicity?
Answers and Discussion
1. Key nutritional factors to consider in patients with copper-associated hepatoxicosis include energy, protein, copper, zinc and
antioxidant vitamins. Providing adequate daily energy intake is important to allow protein synthesis and prevent tissue catabo-
lism that generates ammonia. The exact caloric needs of these patients have not been determined but would be expected to be
similar to those of other dogs of similar age and body condition.
Most dogs with copper toxicosis develop clinical problems or liver disease is detected during adulthood (i.e., two to six years
of age). Protein requirements have not been established for these dogs, but they would be expected to be similar to those of other
adult dogs (15 to 30% dry matter [DM]). Patients with evidence of hepatic encephalopathy will often need more restricted
dietary protein levels.
Foods low in copper are recommended for affected dogs that accumulate hepatic copper. Restriction of dietary copper as the
primary therapy probably does little to lower abnormal hepatic copper concentrations in diseased dogs. Copper-restricted foods
have a minimal depleting effect for hepatic copper.