While hyperthyroidism is an extremely common disease of domestic cats, spontaneous adult onset hypothyroidism is extremely rarely recognized (though the congenital form is occasionally seen). It may, however, be under recognized due to the generally vague clinical signs and lack of data on the condition. This paper sought to describe the clinical signs, clinicipathologic data, diagnostics, treatment, and outcome for cats with spontaneous adult onset hypothyroidism.
This study was designed as a prospective case series on seven cats presenting to a referral veterinary endrocrinology clinic over a 3.5 year period. Demographic data, medical history, PE findings, CBC/Biochemistry/Urinalysis findings and full body radiographs were collected. Full thyroid testing (total T4, free T4, and TSH) and thyroid scintigraphy were also assessed. Two cats had thyroid aspirates done and one had a thyroid biopsy.
Three cats had hypothyroidism detected on routine thyroid testing at the regular clinic; two had testing done for evaluation of a palpable goiter; and two were investigated for clinical signs of hypothyroidism. Six cats gad a palpable goiter. Clinical signs in affected cats included poor haircoats, polyuria and polydipsia, weight gain, and lethargy. Clinical pathology findings included azotemia, isosthenuria, and anemia. All changes were considered to be mild. All cats had normal radiographic findings (ie closure of the physes).
Six cats had both a low total T4 and free T4. One cat had normal thyroxine levels. All cats had significant elevations to TSH. On scintigraphy, six of seven cats had markedly increased thyroid volumes and Thyroid: Salivary ratios. The remaining cat had no detectable thyroid tissue. Two cats had thyroid aspirates analyzed, both of which were considered consistent with thyroid hyperplasia. A single cat had a biopsy evaluated which was diagnosed as follicular hyperplasia.
All cats were treated with 100-200ug/cat/day of levothyroxine for 3-7 months. All cats had an increase in total and free T4 into the normal range and a decrease in TSH into the reference interval. Azotemia resolved in all animals with an elevated creatinine. Five of seven animals had a significant decrease in goiter size on scintigraphy; one had no change in size and the last had no detectable thyroid tissue to start with. All cats were alive, clinically well, non-azotemic, and receiving levothyroxine therapy at the time of publication (mean 739 days).
The authors suggest that hypothyroidism in cats may be more common than previously reported, and is often associated with mild clinical signs. While the majority of cats had a goiterous form of hypothyroidism (thyroid hyperplasia), they suggest that this may be a selection bias as cats with palpable goiter were more likely to be referred for evaluation. It was theorized that their cases were more likely due to an inborn defect in thyroid function rather than nutritional deficiencies or goitrogen exposure. While males were over represented in this population, the numbers were small enough that this may be sampling error.
The authors recommend that larger numbers of cats be screened for hypothyroidism to determine the true provenance and demographics of the disease. They further suggest that TSH is the most appropriate test to screen for adult onset hypothyroidism, and that cats respond very well to therapy with levothyroxine.
Reference: Spontaneous primary hypothyroidism in 7 adult cats. J Vet Intern Med. 2018 Oct 7
