Peterson M.E., Becker D.V. and Hurley J.R.
Conference Proceedings, (1980). American College of Veterinary Internal Medicine:
Spontaneous hyperthyroidism resulting from toxic nodular goiter was studied in 28 cats aged 9-18 years. Clinical signs included weight loss, polyphagia, nervousness, hyperdefecation, polyuria, diarrhea, tremor, tachycardia, and congestive heart failure. Hemograms, biochemistries (SMA 19-60) and urinalyses were noncontributory. In 4 cats with voluminous stools, 48-hour fecal fat analysis revealed marked steatorrhea (5.5-35.3 gm fat; normal <3.5 gm). ECGS showed evidence of left-ventricular enlargement (RII >0.9 mV) in 20, tachycardia (rate >240) in 15, atrial premature contractions in 4, right bundle branch in 2, ventricular premature contractions in 1, and right-ventricular bigeminy in 1. T4 (RIA) ranged from 6.5-45 mg/100 mL (normal = 2.1 ± 0.5 mg/100 mL). T3 (RIA) ranged from 127-768 ng/100 ml (normal = 26.3 ± 12.6 ng/100 mL). Scintiscans performed 24 hours post IV injection 0f 25 mCi 131I revealed increased uptake in 1 thyroid lobe in 20 cats with suppression of uptake in the contralateral lobe. 8 cats had diffuse or nodular uptake in both lobes. Radioiodine uptake (RAIU) at 24 hours ranged from 19-58% (normal 10.0 ± 2.0%). Measurements of thyroidal kinetics showed rapid turnover of 131I in 5 of 16 cats. Disposition kinetics of 131I were studied in 4 cats. Urinary excretion predominated over fecal loss, but approximately 25% of administered 131I remained unaccounted for suggesting either vapor loss or a slow releasing compartment. To block the effects of excessive thyroid hormone, propranolol (2.5 mg TID for 7 days) was administered preoperatively. Following hemi- or total thyroidectomy, T4 and T3 fell to normal within 24-48 hours. Histopathology revealed adenomatous changes in 26 and carcinoma in 1. Clinical signs of hyperthyroidism resolved postoperatively. 1 cat was successfully treated with 131I. It was concluded that (1) spontaneous hyperthyroidism due to toxic nodular goiter is a common disorder in the cat; (2) the clinical signs, ECG, laboratory findings, and 131I studies (RAIU, scintiscans, and kinetics) mimic those in man; (3) the frequency and close analogy to the human disorder make feline hyperthyroidism a suitable model for the study of toxic nodular goiter in man.