Clinical hyperthyroidism in cats and dogs is produced from excessive secretion of the thyroid hormones, T4 and T3, resulting in signs that reflect an increased metabolic rate. It is most common in middle-aged to old cats but also develops rarely in dogs.
Functional thyroid adenoma (adenomatous hyperplasia) is the most common cause of feline hyperthyroidism; in ~70% of cases, both thyroid lobes are enlarged. Thyroid carcinoma, the primary cause of hyperthyroidism in dogs, is rare in cats (1%–2% of hyperthyroidism cases).
The most common signs include weight loss, increased appetite, hyperexcitability, polydipsia, polyuria, and palpable enlargement of the thyroid gland. GI signs are also common and may include vomiting, diarrhea, and increased fecal volume. Cardiovascular signs include tachycardia, systolic murmurs, dyspnea, cardiomegaly, and congestive heart failure. Rarely, hyperthyroid cats exhibit apathetic signs (eg, anorexia, lethargy, and depression); weight loss remains a common sign in these cats.
High basal serum total thyroid hormone concentration is the hallmark of hyperthyroidism and confirms the diagnosis. Although serum total T4 concentrations are high in most cats with hyperthyroidism, ~5%–10% of cats have normal T4 values. Most cats with normal serum T4 values have either mild or early hyperthyroidism or hyperthyroidism with concurrent nonthyroidal illness, which has caused suppression of a high total T4 concentration to within reference range limits. In these cats, a high free T4 concentration along with consistent history and physical examination findings is diagnostic of hyperthyroidism.
Cats with hyperthyroidism can be treated by radioiodine therapy, thyroidectomy, chronic administration of an antithyroid drug, or lifelong nutritional therapy (iodine-deficient diet). Radioactive iodine provides a simple, effective, and safe treatment and is considered the treatment of choice. The radioiodine is concentrated within the thyroid tumor, where it selectively irradiates and destroys hyperfunctioning thyroid tissue.
Surgical thyroidectomy is also an effective treatment for hyperthyroidism in cats. With unilateral thyroid tumors, hemithyroidectomy corrects the hyperthyroid state, and thyroxine supplementation usually is not necessary. For bilateral thyroid tumors, complete thyroidectomy is indicated, but parathyroid function must be preserved to avoid postoperative hypocalcemia. Thyroxine supplementation should be started 1–2 days after complete thyroidectomy. If iatrogenic hypoparathyroidism develops, treatment with vitamin D and calcium is also indicated.
Treatment with methimazole, an antithyroid drug, controls hyperthyroidism by blocking thyroid hormone synthesis. Carbimazole is a similar antithyroid drug available in many European countries, Australia, and Japan; it exerts its effects through immediate conversion to methimazole after administration. Propylthiouracil, another antithyroid drug, is not recommended for use in cats because of the high incidence of serious adverse effects (especially hemolytic anemia and thrombocytopenia). The recommended initial daily dose of methimazole is 2.5–5 mg in two divided doses. The dosage is adjusted to maintain circulating thyroid hormone concentrations within the mid-normal range and is given daily. Adverse effects, the more serious of which are agranulocytosis and thrombocytopenia, develop in <5% of treated cats. If this occurs, methimazole should be discontinued and supportive therapy instituted; these adverse reactions should resolve within 2 wk. To maintain normal levels of thyroid hormone and to monitor for adverse reactions during the first 3 mo of treatment (when the most serious adverse effects associated with methimazole therapy develop), CBCs and serum thyroid hormone determinations should be repeated at 2- to 4-wk intervals, with the drug dosage adjusted as necessary. Subsequently, serum T4 concentrations should be measured at 3- to 6-mo intervals to monitor dosage requirements and response to treatment.
The use of medical therapy other than methimazole may be required if adverse effects develop. For the most part, these alternative medical therapies are for short-term use and are only recommended before use of a more permanent treatment option.
Propranolol and atenolol are the most frequently used β-adrenoceptor blocking agents in hyperthyroid cats. These drugs do not lower the circulating T4 concentration but are used to symptomatically control the tachycardia, tachypnea, hypertension, and hyperexcitability associated with hyperthyroidism.
Oral cholecystographic agents (eg, ipodate, iopanoic acid, or diatrizoate meglumine) acutely inhibit conversion of peripheral T4 to T3. In one study of hyperthyroid cats, administration of calcium ipodate normalized serum total T3 concentrations and produced clinical improvement in >60% of cats treated. Ipodate (308 mg iodine/500 mg calcium ipodate) is no longer marketed in the USA, but iopanoic acid (333 mg iodine/500 mg iopanoic acid) and diatrizoate meglumine (370 mg iodine/mL) have been used anecdotally in hyperthyroid cats at comparable dosages. None of these drugs provides complete resolution of clinical signs or biochemical features associated with hyperthyroidism. In addition, waning of the thyroid-lowering effect is common after 3 mo of therapy with any of these drugs.
A fouth treatment option for cats with hyperthyroidism is the use of a prescription diet with severely restricted iodine levels (Hill’s® y/d Feline Thyroid HealthTM). The basis for using this diet is that iodine is an essential component of both T4 and T3; without sufficient iodine, the thyroid cannot produce excess thyroid hormones. This is an iodine-deficient diet, containing iodine levels below the minimum daily requirement for adult cats. A major indication for use of this diet for management of feline hyperthyroidism is in cats that are not candidates for definitive treatment of the underlying thyroid tumor(s) with surgery or radioiodine, which remain the treatments of choice. In addition, nutritional management could be considered in cats whose owners are not able to give oral medication or in cats that develop adverse effects from methimazole or carbimazole.
Most hyperthyroid cats exclusively fed this iodine-restricted diet become euthyroid in 8–12 wk. This therapy appears to be more effective in cats with only moderate increases of T4 than in cats with severe hyperthyroidism. Despite some advantages, nutritional management has disadvantages: 1) feeding this diet can only control (by withholding "fuel" for the thyroid tumor) but not cure hyperthyroidism; 2) cats fed this diet must not eat any other cat diet, table food, or treats, because even tiny amounts of iodine can render the diet ineffective in controlling hyperthyroidism; and 3) relapse will occur if the diet is stopped, so the cat must eat only this diet for the rest of its life.
In dogs, a thyroid tumor causing hyperthyroidism should always be presumed to be a carcinoma until proved otherwise. This is in contrast to the case in hyperthyroid cats, in which thyroid carcinoma is present in <5%.
Treatment of thyroid neoplasia and hyperthyroidism in dogs is dictated by the size of the primary tumor, extent of local tissue invasion, presence of detectable metastasis, and available treatment options. Surgery, chemotherapy, cobalt irradiation, and use of radioactive iodine therapy, alone or in combination, may be indicated depending on the individual. The hyperthyroid state can be medically controlled by daily administration of an antithyroid drug such as methimazole or carbimazole (5–15 mg/dog, bid), but such treatment will not prevent tumor growth or metastasis. Because canine hyperthyroidism is almost always associated with thyroid carcinoma, the longterm prognosis in these dogs is poor to grave.