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  • Author or Editor: Keith P. Richter x
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Summary

The medical records of 7 hypercalcemic cats with primary hyperparathyroidism were evaluated. Mean age was 12.9 years, with ages ranging from 8 to 15 years; 5 were female; 5 were Siamese, and 2 were of mixed breed. The most common clinical signs detected by owners were anorexia and lethargy. A cervical mass was palpable in 4 cats. Serum calcium concentrations were 11.1 to 22.8 mg/dl, with a mean of 15.8 mg/dl calculated from each cat's highest preoperative value. The serum phosphorus concentration was low in 2 cats, within reference limits in 4, and slightly high in 1 cat. The bun concentration was > 60 mg/dl in 2 cats, 31 to 35 mg/dl in 2 cats, and < 30 mg/dl in 3 cats. Abnormalities were detected in serum alanine transaminase, aspartate transaminase, and alkaline phosphatase activities from 2 or 3 cats. Parathormone (pth) concentrations were measured in 2 cats before and after surgery. The preoperative pth concentration was within reference limits in 1 cat and was high in 1 cat. The pth concentrations were lower after surgery in both cats tested. A solitary parathyroid adenoma was surgically removed from 5 cats, bilateral parathyroid cystadenomas were surgically resected in 1 cat, and a parathyroid carcinoma was diagnosed at necropsy in 1 cat. None of the cats had clinical problems with hypocalcemia after surgery, although 2 cats developed hypocalcemia without tetany, one of which was controlled with oral administration of dihydrotachysterol and the other with oral administration of 1,25 dihydroxyvitamin D. All 5 of the cats that underwent removal of an adenoma were alive at least 240 days after surgery. Four of these 5 cats were normocalcemic at the last examination. The cat that had bilateral cystadenomas was lost to follow-up evaluation 110 days after surgery. One of the cats with a parathyroid adenoma was reevaluated 569 days after the first surgery. It was found to be hypercalcemic (21.5 mg/dl), subsequently died, and was identified as having a parathyroid adenoma and a parathyroid carcinoma on histologic evaluation of tissue removed from the neck at necropsy.

Free access
in Journal of the American Veterinary Medical Association

Abstract

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.

Animals—14 dogs.

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.

Full access
in Journal of the American Veterinary Medical Association