What we know
Feline hyperthyroidism was first described in 1979 by Peterson and 1980 by Holzworth. It is now estimated that the incidence
is as high as 2% of the feline population seen in tertiary veterinary care facilities. Hyperthyroidism is the most common
endocrine disorder affecting older cats and is caused by adenomatous hyperplasia of the thyroid gland. There is no breed or
Hyperthyroidism is characterized by hypermetabolism including polyuria, polydipsia, and polyphagia with concurrent weight
loss. The sympathetic nervous system is activated as well causing hyperactivity, hypertension, tachycardia, tachyarrhythmia,
and behavioral changes. Long-standing hyperthyroidism results in hypertrophic cardiomyopathy, high-output heart failure and
Common laboratory findings include erythrocytosis, elevated mean corpuscular volume, alanine aminotransferase, and alkaline
phosphatase. Azotemia is not uncommon, which is important considering the glomerular filtration rate decreases substantially
after treatment of hyperthyroidism and can worsen azotemia and result in renal failure. It is important to closely monitor
treated animals for (worsening) renal function.
Hyperthyroidism is diagnosed by measurement of total tetraiodothyronine (TT4) and is diagnostic in about 90% of cases. A
normal TT4 is present in about 10% of the cases due to concurrent non-thyroidal illness, a fluctuating TT4 level, mild hyperthyroid
cases or concurrent medications that lower serum TT4 levels. Free T4 (FT4) by equilibrium dialysis measurements have been
shown to be more diagnostic of early or "occult" hyperthyroidism. Elevated FT4 concentrations should be interpreted concurrently
with the TT4 because non-thyroidal illness (chronic renal failure) can result in spurious elevations of FT4 as well. Elevated
T3 levels only occur in approximately 70% of the cases.
Feline benign functional thyroid adenoma resembles toxic nodular goiter (TNG) of humans. The pathogenesis of TNG is an abnormality
in the signal transduction of the thyroid cell. The TSH receptors of the thyroid cells activate receptor-coupled guanosine
triphosphate binding proteins (G proteins). Recent research showed some hyperthyroid cats express this TSH receptor activation
mutation and have significant decreases in G inhibitory protein.
Does nutrition impact hyperthyroidism? Canned cat food has been implicated as a cause of feline hyperthyroidism in many epidemiological
studies. The suspected goitrogen is bisphenol-A-diglycidyl ester (BADGE). BADGE is used in making the liner of the easy open
'pop-top' cans and suspected to leach into the foods consumed by cats. While this appears safe for human consumption, cats
are proposed to be more susceptible to the toxic effects of this compound due to a greatly reduced ability to detoxify it
via hepatic glucuronidation. Although feline studies are not readily available Bisphenol A reduces triiodothyronine binding
and causes increased TSH secretion resulting in hyperthyroidism and goiter in rats and some humans. Although epidemiological
studies showed association, over 90% of cats in the US consume commercial pet foods and relatively few develop hyperthyroidism.
Does environment impact development of hyperthyroidism? In 2007, Janice Dye, a researcher with the US EPA, implicated polybrominated
diphenyl ethers (PBDEs) as goitrogens associated with feline hyperthyroidism. PBDE wide spread usage started in the 1980's
as a flame retardant. It is used in upholstery, drapes, plastic covering of televisions and computers. This abstract reported
serum PBDE levels 10- to 400-fold higher than humans. It is proposed that these levels are dramatically increased due to increased
exposure to furniture and carpets and meticulous grooming behavior. Another study cited cat litter usage was associated with
increased risk of hyperthyroidism. No recognizable difference between litter types was found suggesting that use of cat litter
is simply a marker of indoor living. Indoor cats are likely to live longer and possibly develop more diseases.