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Sodium iodide I 131 treatment of dogs with nonresectable thyroid tumors: 39 cases (1990–2003)

Jane M. TurrelVeterinary Oncology Specialties, 1072 Valencia Way, Pacifica, CA 94044.

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 DVM, MS, DACVR, DACVIM
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Margaret C. McEnteeDepartment of Clinical Sciences and Sprecher Institute for Comparative Cancer Research, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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Blaise P. BurkeDepartment of Clinical Sciences and Sprecher Institute for Comparative Cancer Research, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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Rodney L. PageDepartment of Clinical Sciences and Sprecher Institute for Comparative Cancer Research, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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Abstract

Objective—To determine outcome for dogs with nonresectable thyroid carcinomas treated with sodium iodide I 131 and identify factors associated with outcome.

Design—Retrospective case series.

Animals—39 dogs.

Procedures—A definitive or presumptive diagnosis of thyroid tumor was made on the basis of cytologic or histologic examination, abnormal accumulation of sodium pertechnetate Tc 99m during scintigraphy, or both, and dogs were treated with sodium iodide I 131. Dogs with cervical thyroid tumors were evaluated 3 to 6 weeks after 131I therapy, and residual tumor was resected when feasible.

Results—Prior to 131I therapy, 32 dogs had a solitary mass and 7 had metastases; 21 were hyperthyroid, 16 were euthyroid, and 2 were hypothyroid. Median survival time for dogs with local or regional tumors (ie, stage II or III) was significantly longer (839 days) than median survival time for dogs with metastasis (366 days). Tumor site (cervical vs ectopic), dose of sodium iodide I 131, age, body weight, treatment (131I therapy alone vs 131I therapy followed by surgery), and serum T4 concentration prior to 131I therapy were not significantly associated with survival time. Three dogs died of radioiodine-associated myelosuppression within 3 months after treatment, but no specific factor associated with development of toxicosis was identified.

Conclusions and Clinical Relevance—Results suggested that 131I therapy may result in prolonged survival times in dogs with nonresectable thyroid tumors, regardless of serum thyroxine concentration prior to treatment. Dogs undergoing 131I therapy should be monitored for signs of bone marrow suppression.

Abstract

Objective—To determine outcome for dogs with nonresectable thyroid carcinomas treated with sodium iodide I 131 and identify factors associated with outcome.

Design—Retrospective case series.

Animals—39 dogs.

Procedures—A definitive or presumptive diagnosis of thyroid tumor was made on the basis of cytologic or histologic examination, abnormal accumulation of sodium pertechnetate Tc 99m during scintigraphy, or both, and dogs were treated with sodium iodide I 131. Dogs with cervical thyroid tumors were evaluated 3 to 6 weeks after 131I therapy, and residual tumor was resected when feasible.

Results—Prior to 131I therapy, 32 dogs had a solitary mass and 7 had metastases; 21 were hyperthyroid, 16 were euthyroid, and 2 were hypothyroid. Median survival time for dogs with local or regional tumors (ie, stage II or III) was significantly longer (839 days) than median survival time for dogs with metastasis (366 days). Tumor site (cervical vs ectopic), dose of sodium iodide I 131, age, body weight, treatment (131I therapy alone vs 131I therapy followed by surgery), and serum T4 concentration prior to 131I therapy were not significantly associated with survival time. Three dogs died of radioiodine-associated myelosuppression within 3 months after treatment, but no specific factor associated with development of toxicosis was identified.

Conclusions and Clinical Relevance—Results suggested that 131I therapy may result in prolonged survival times in dogs with nonresectable thyroid tumors, regardless of serum thyroxine concentration prior to treatment. Dogs undergoing 131I therapy should be monitored for signs of bone marrow suppression.

Contributor Notes

Supported by the John and Eloise Turrel Endowment and the Sprecher Institute for Comparative Cancer Research, Cornell University.

The authors thank Drs. Clifford Berry and Sharon Ullman for technical assistance and Dr. John Periou for assistance with histologic analyses.

Address correspondence to Dr. McEntee.