What's new with hyperthyroidism in cats (Proceedings)
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 sex predilection.
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 cachexia.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.