Feline Hyperthyroidism

Feline hyperthyroidism (FH) is becoming one of the most common and important endocrinopathies that we see in every day practice. It is important to identify these patients before they become clinically apparent due to, sometimes, irreversible effects on multiple organs.

Feline hyperthyroidism can cause a myriad of clinical signs including unexplained weight loss, vomiting, and/or diarrhea, increased vocalization, inappropriate elimination (urinating or defecating outside the litter box), increased thirst, agitation, aggressiveness, and in some severe, well-established, cases, anorexia (not eating), lethargy, severe dehydration, cachexia (wasting disease) and death.

FH is generally diagnosed by blood tests. The group of tests that are the most specific and accurate for determining FH is through the measurements of thyroxine and Thyroid stimulating hormone (TSH) in the blood stream. Thyroxine is measured via T4 and Free T4.

Elevations of T4 and Free T4 are generally sufficient to make a diagnosis of FH in the cat. Most internists or endocrinologists believe that levels greater than 2.5 ug/dl are suggestive of hyperthyroidism. Levels above 4.0 ug/dl are diagnostic. In many patients, with clinical disease, their T4 may reach 16-20 ug/dl!

Feline hyperthyroidism looks very similar to "toxic nodular goiter" in humans.¹ FH in the cat is caused by nodular hyperplasia or nodular adenoma of the thyroid gland. Since the incidence of the disease, or the number of patients with the disease, is increasing, a great deal of research has been directed at finding the cause(s). Hyperthyroidism is a multifactorial disease in the cat. There have been numerous risk factors identified over the years. Unfortunately, some of these risk factors are common place in the home of the patient, including use of litter boxes, canned foods containing fish, liver, and giblets, use of topical preparations for ectoparasites (fleas, ticks).² It has been noted, in research, that feeding canned foods containing fish, liver, or giblets increases the risk 2-fold of developing FH. Cats using a litter box have a 2-3-fold increase. Clearly, there are goitrogenic chemicals or dietary items that remain unknown. It is apparent that, finally, females are at a greater risk to this disease.³

Treatment of this important disease has changed over the years. Surgical removal of the thyroid glands was initially advocated, but other sites, in the cat's body, was found to secrete the hormone. The surgical option has all but been discarded. The gold standard for medical treatment involves the use of Methimazole. Methimazole destroys the gland's ability to produce and secrete thyroid hormone. It is taken daily or even twice daily either by mouth (tablets and flavored liquids) or topically through the newer "transdermal gels."

Radioactive Iodine has been used and advocated for nearly twenty years for its ability to ablate the thyroid gland and the secretion of thyroid hormone. Iodine therapy involves the injection of I-131 under the skin of the patient. The patient remains in the center for eight days, allowing deterioration of the isotope. In our area, only one veterinary clinic is licensed and approved for use of I-131.⁴

Methimazole must be given for the life of the pet.