Excessive secretion of the thyroid hormones, T4 and T3, results in signs that reflect an increased metabolic rate and produces clinical hyperthyroidism. 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).
Clinical Findings and Diagnosis
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 will 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, or chronic administration of an antithyroid drug. 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. 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, ideally in two divided doses. The dose is adjusted to maintain circulating thyroid hormone concentrations within the 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 side effects associated with methimazole therapy develop), complete blood counts and serum thyroid hormone determinations should be repeated at 2- to 4-wk intervals, and the drug dose 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 reaction develop. For the most part, these alternative medical therapies are for short-term use and are only recommended prior to 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 peripheral T4 to T3 conversion. 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, at least 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 doses. 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.
In dogs, a thyroid tumor causing hyperthyroidism should always be presumed to be a carcinoma until proven 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. Medical control of the hyperthyroid state can be achieved by daily administration of an antithyroid drug such as methimazole or carbimazole (5–15 mg/dog, bid), but such medical 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.
Last full review/revision March 2012 by Mark E. Peterson, DVM, DACVIM; Janice E. Kritchevsky, 'VMD, MS, DACVIM