Over the past 15 to 20 years, we have seen what we believe to be an increased incidence of copper-associated hepatopathy in dogs. The onset of this increase appears to have coincided with a change in the type of copper used in premixes added to commercial dog foods. And, more recently, the increased incidence may have been exacerbated by consumer-driven desire for pet foods formulated with a high content of animal-based ingredients (eg, evolutionary diets), including certain organ meats, that might introduce additional copper and by trends favoring foods containing vegetables with a high copper content (eg, sweet potatoes).
Objective—To describe findings in dogs with exogenous thyrotoxicosis attributable to consumption of commercially available dog foods or treats containing high concentrations of thyroid hormone.
Design—Retrospective and prospective case series.
Procedures—Medical records were retrospectively searched to identify dogs with exogenous thyrotoxicosis attributable to dietary intake. One case was found, and subsequent cases were identified prospectively. Serum thyroid hormone concentrations were evaluated before and after feeding meat-based products suspected to contain excessive thyroid hormone was discontinued. Scintigraphy was performed to evaluate thyroid tissue in 13 of 14 dogs before and 1 of 13 dogs after discontinuation of suspect foods or treats. Seven samples of 5 commercially available products fed to 6 affected dogs were analyzed for thyroxine concentration; results were subjectively compared with findings for 10 other commercial foods and 6 beef muscle or liver samples.
Results—Total serum thyroxine concentrations were high (median, 8.8 μg/dL; range, 4.65 to 17.4 μg/dL) in all dogs at initial evaluation; scintigraphy revealed subjectively decreased thyroid gland radionuclide in 13 of 13 dogs examined. At ≥ 4 weeks after feeding of suspect food or treats was discontinued, total thyroxine concentrations were within the reference range for all dogs and signs associated with thyrotoxicosis, if present, had resolved. Analysis of tested food or treat samples revealed a median thyroxine concentration for suspect products of 1.52 μg of thyroxine/g, whereas that of unrelated commercial foods was 0.38 μg of thyroxine/g.
Conclusions and Clinical Relevance—Results indicated that thyrotoxicosis can occur secondary to consumption of meat-based products presumably contaminated by thyroid tissue, and can be reversed by identification and elimination of suspect products from the diet.
We would like to comment on the JAVMA News article in the November 15, 2021, issue “Taking the chronic out of enteropathies.”1 The article discusses the use of a panel of new serologic tests for inflammatory bowel disease, relying heavily on a research paper published in 2021 in the Journal of Veterinary Internal Medicine (JVIM) by Estruch et al.2 However, the News article fails to mention that the results of this study have been questioned due to lack of reporting and analytical assay