BackgroundRadioiodine is the treatment of choice for hyperthyroidism in cats. The ideal method of dose determination of radioiodine remains controversial.ObjectiveTo compare a method of radioiodine dose determination that utilized thyroid scintigraphy with a standard fixed dose for treatment of hyperthyroidism.AnimalsFifty‐seven and 23 client‐owned hyperthyroid cats in the variable and fixed dose groups, respectively.MethodsCats with a percent dose uptake using 99mTc‐pertechnetate uptake on thyroid scintigraphy <5%, 5%‐10%, and >10% were to receive 3, 3.5, or 4.5 millicuries (mCi) of radioiodine, respectively, administered SC. Radioiodine dose was adjusted according to thyroid gland size as determined by the thyroid:salivary size ratio and categorized as <5:1, 5‐10:1, and >10:1. If the thyroid size fell into a higher dosing category than the percent dose uptake, the dose was increased accordingly. Cats in the fixed dose group received 4.5 mCi. Six months after treatment, cats were determined to be euthyroid, hypothyroid, or hyperthyroid based on serum thyroxine and thyroid stimulating hormone concentrations.ResultsNo difference in outcome was found between the variable and fixed dose treatment groups. Euthyroidism, hypothyroidism, and persistent hyperthyroidism developed in 61, 30, and 9% of cats in the fixed dose group compared to 58, 26, and 16%, respectively, in the variable dose group.ConclusionsA variable dosing method of radioiodine based on percent dose uptake primarily and thyroid gland size secondarily did not improve outcome compared to a standard fixed dose method.

Objectives The purpose of this study was to evaluate symmetric dimethylarginine (SDMA) in hyperthyroid cats before and after treatment with radioactive iodine and to determine how pretreatment SDMA relates to the development of post-treatment azotemia. Methods Eighty-four non-azotemic hyperthyroid cats had serum SDMA and creatinine evaluated before and 1, 3 and 6 months after treatment with radioiodine therapy. Results Baseline SDMA was increased in 7% (n = 6/84) of cats, whereas SDMA was increased in 19% (n = 15/81), 20% (n = 16/80) and 32% (n = 26/81) at 1 month, 3 months and 6 months after treatment, respectively. Creatinine was not elevated in any of the cats at baseline because of the study design, and was elevated in 6% (n = 5/81), 15% (n = 12/80) and 15% (n = 12/81) of cats at 1, 3 and 6 months after treatment, respectively. SDMA (median 11 μg/dl, range 1–22 μg/dl) was significantly higher at 3 (12 μg/dl, range 6–45 μg/dl; P = 0.005) and 6 months (11 μg/dl, 6–25 μg/dl; P <0.001) compared with baseline (11 μg /dl, range 1–21 μg/dl). The median baseline SDMA was significantly higher in the azotemic group (13 μg/dl, range 11–22 μg/dl) compared with the non-azotemic group (10 μg/dl, range 1–21 μg/dl, P = 0.002). The sensitivity of SDMA for detecting azotemia after treatment was 15.4%, with a specificity of 94.4%. Baseline serum SDMA concentration had a moderately positive association with baseline creatinine concentration ( P <0.001, r = 0.437). At 6 months, there was a strong positive correlation between SDMA and creatinine concentrations ( P <0.001, r = 0.721). There was no significant correlation with SDMA and thyroxine at baseline ( P = 0.772, r = −0.034) or 6 months ( P = 0.492, r = −0.078). Conclusions and relevance SDMA increases in cats treated for hyperthyroidism with radioactive iodine and likely reflects associated changes in glomerular filtration rate. An increased SDMA concentration above the reference interval prior to treatment has a high specificity but poor sensitivity for the prediction of post-treatment azotemia.

CASE DESCRIPTION A 7-year-old castrated male Havanese was evaluated at a veterinary teaching hospital because of a 12-week history of hyperactivity, aggression, and progressive weight loss despite a healthy appetite. CLINICAL FINDINGS Tachycardia was the only remarkable finding during physical examination. Serum 3,5,3'-triiodothyronine (T3) and free T3 concentrations were markedly increased, and thyroxine (T4), free T4, and thyroid-stimulating hormone concentrations were at or decreased from the respective reference ranges. Thyroid scintigraphy revealed suppressed uptake of sodium pertechnetate Tc 99m by the thyroid gland but no ectopic thyroid tissue, which was indicative of thyrotoxicosis induced by an exogenous source of T3. TREATMENT AND OUTCOME The dog was hospitalized for 24 hours, and its diet was changed, after which the clinical signs rapidly resolved and serum T3 and free T3 concentrations returned to within the respective reference ranges. This raised suspicion of an exogenous source of T3 in the dog's home environment. Analysis of the commercial beef-based canned food the dog was being fed revealed a high concentration of T3 (1.39 μg/g) and an iodine (82.44 μg/g) concentration that exceeded industry recommendations. No other source of T3 was identified in the dog's environment. CLINICAL RELEVANCE To our knowledge, this is the first report of clinical thyrotoxicosis in a dog induced by exogenous T3, although the source of exogenous T3 was not identified. This case highlights the importance of measuring serum T3 and thyroid-stimulating hormone concentrations in addition to T4 and free T4 concentrations when there is incongruity between clinical findings and thyroid function test results.