Dietary management of labrador retrievers with subclinical hepatic copper accumulation.

Abstract

BackgroundGenetic and environmental factors, including dietary copper intake, contribute to the pathogenesis of copper‐associated hepatitis in Labrador retrievers. Clinical disease is preceded by a subclinical phase in which copper accumulates in the liver.ObjectiveTo investigate the effect of a low‐copper, high‐zinc diet on hepatic copper concentration in Labrador retrievers with increased hepatic copper concentrations.AnimalsTwenty‐eight clinically healthy, client‐owned Labrador retrievers with a mean hepatic copper concentration of 919 ± 477 mg/kg dry weight liver (dwl) that were related to dogs previously diagnosed with clinical copper‐associated hepatitis.MethodsClinical trial in which dogs were fed a diet containing 1.3 ± 0.3 mg copper/Mcal and 64.3 ± 5.9 mg zinc/Mcal. Hepatic copper concentrations were determined in liver biopsy samples approximately every 6 months. Logistic regression was performed to investigate effects of sex, age, initial hepatic copper concentration and pedigree on the ability to normalize hepatic copper concentrations.ResultsIn responders (15/28 dogs), hepatic copper concentrations decreased from a mean of 710 ± 216 mg/kg dwl copper to 343 ± 70 mg/kg dwl hepatic copper after a median of 7.1 months (range, 5.5–21.4 months). Dogs from a severely affected pedigree were at increased risk for inability to have their hepatic copper concentrations normalized with dietary treatment.Conclusions and Clinical ImportanceFeeding a low‐copper, high‐zinc diet resulted in a decrease in hepatic copper concentrations in a subset of clinically normal Labrador retrievers with previous hepatic copper accumulation. A positive response to diet may be influenced by genetic background. Determination of clinical benefit requires further study.