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Feline Hyperthyroidism

David S. Bruyette, DVM, DACVIM (SAIM)

Anivive Lifesciences, Long Beach, CA, USA

Etiology/Pathophysiology
and Epidemiology the univariate analysis were selected for further, a persis­
tent protective effect of breed (Siamese or Himalayan)
Two recent large studies have looked at possible environ­ was found. In addition, results suggested a 2–3‐fold
mental or dietary factors involved in the pathogenesis of increase in risk of developing hyperthyroidism among
hyperthyroidism. One of the studies with a case–control cats eating a diet composed mostly of canned cat food
design looked at 100 cats with hyperthyroidism and 163 and a threefold increase in risk among those using cat
control cats. The cats’ medical records were reviewed litter. In contrast, the use of commercial flea products
and the owners were asked to complete a mailed ques­ did not retain a strong association. The results of this
tionnaire. Data included demographic variables, envi­ study indicate that further research into dietary and
ronmental exposures, and diet to include the preferred other potentially important environmental factors (cat
flavors of canned cat food. In this study, housing, expo­ litter) is warranted.
sure to fertilizers, herbicides, regular use of flea prod­ Altered G protein expression was found in thyroid
ucts, and the presence of a smoker in the house were not gland tissue from hyperthyroid cats compared to normal
associated with an increased risk but cats that preferred control cats. Adenomatous thyroid glands obtained from
fish or liver and giblets flavors of canned cat food had an eight hyperthyroid cats and thyroid glands obtained from
increased risk. The results suggested that cats that prefer four age‐matched euthyroid cats were examined for
to eat certain flavors of canned cat food may have a sig­ expression of G inhibitory protein (Gi) and G stimulatory
nificantly increased risk of hyperthyroidism. protein (Gs). Expression of Gi was significantly reduced
In the second case–control study, owners of 379 hyper­ in thyroid gland adenomas from hyperthyroid cats, com­
thyroid and 351 control cats were questioned about their pared with normal thyroid gland tissue from euthyroid
cats’ exposure to potential risk factors, including breed, cats. Expression of Gs was similar between the two
demographic factors, medical history, indoor environ­ groups. A decrease in expression of Gi in adenomatous
ment, chemicals applied to the cat and environment, and thyroid glands of cats may reduce the negative inhibition
diet. The association between these hypothesized risk of the cAMP cascade in thyroid cells, leading to autono­
factors and outcome of disease was evaluated. Two mous growth and hypersecretion of thyroxine. What we
genetically related cat breeds (Siamese and Himalayan) don’t know is what causes the reduction in Gi in hyper­
were found to have diminished risk of developing hyper­ thyroid cats. The factors mentioned above in the studies
thyroidism. Cats that used litter had higher risk of devel­ of environmental and dietary risk factors may play a role
oping hyperthyroidism than those that did not. Use of in altering the G protein expression found in this study.
topical ectoparasite preparations was associated with Oncogenes and the tumor suppressor gene p53 were
increased risk of developing hyperthyroidism. Compared examined in cats with hyperthyroidism. Formalin‐fixed,
with cats that did not eat canned food, those that ate paraffin‐embedded thyroid glands from 18 cats diag­
commercially prepared canned food had an approximate nosed with hyperthyroidism were evaluated immunohis­
twofold increase in risk of disease. When these four vari­ tochemically for overexpression of the products of
ables (breed, use of cat litter, consumption of canned cat oncogenes c‐ras (a mitogenic oncogene) and bcl2 (an
food, and use of topical ectoparasite preparations) from apoptosis inhibitor) and the tumor suppressor gene p53.

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical