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Aspects of canine hypothyroidism and feline hyperthyroidism

01 October 2010, at 1:00am

LIBBY SHERIDAN reviews the contrasting presentations in dogs and cats

WE are always reminded that “cats are not small dogs” and, amongst other examples, this is dramatically illustrated by the very different way in which they present with thyroid disease. 

Hyperthyroid disease in cats, since its emergence in the late 1970s is now the most common endocrine disease seen in cats with a prevalence estimated at 2%. By way of contrast, hyperthyroid disease in dogs is extremely rare and hypothyroidism is more common. The feline equivalent of this latter disease is usually iatrogenic and rarely seen spontaneously. 

Feline hyperthyroidism aetiology

The exact aetiology and pathogenesis of feline hyperthyroidism remains unclear. Cats are often presented late in the course of the disease; many owners happily live with their cat displaying an increased appetite and lively demeanour, thinking it a good thing in an older animal. This can make investigation of the progression of normal thyroid tissue to adenomatous hyperplasia difficult.

Suspicions of a goitrogenic component in the pathogenesis of the disease is put down to several observed factors: the changes in thyroid tissue seen at presentation tend to be that of benign hyperplasia rather than neoplasia; histological changes are often seen in both thyroid lobes at presentation and cases often progress from unilateral to bilateral disease; finally there is diversity in the severity of tissue involvement between the lobes. This, combined with the apparent sudden emergence of the disease at a time when the husbandry of cats was changing (an increasing number of indoor-housed cats along with changes in the way in which cats were fed), has led to theories of potential involvement of environmental and/or nutritional as well as endogenous factors. Some epidemiological and case-controlled studies have observed associations with certain chemicals including flea sprays, cat litter and pesticides. It was also observed that cats fed canned food were at a two- to three-fold increased risk of developing the disease.

One subsequent study showed a possible link with cats fed from “pop- top” cans and it was suggested that components from plasticisers, notably bisphenol A, may have disrupted endocrine function and increased TSH.

Other suggestions for a goitrogenic component in the food itself came from observations that cats fed fish, liver or giblet-based canned foods also showed an increased risk of developing the disease.

Iodine itself is a goitrogen and variability in intake has been associated with iodine- induced hyperthyroidism in people. Some authors suggest though that dietary iodine is less likely to cause adenomatous change in the gland. 

Soybean, a common vegetable ingredient in cat food, may have a goitrogenic effect through the isoflavones genistein and daidzein causing inhibition of an enzyme involved in synthesis of thyroid hormone. One study showed a modest increase in Total T4 and Free T4 concentrations relative to Total T3 concentrations in healthy cats fed dietary soy. 

Endogenous factors such as auto- immunity and over expression or mutation of oncogenes and G protein genes are also undergoing investigation. It may be that a combination of environmental, nutritional, infectious and genetic factors in susceptible animals is involved. Future studies will hopefully clarify any interaction leading to the development of the disease.


Treatment of hyperthyroidism involves three options: administration of long- term anti-thyroid medication, surgical thyroidectomy, and radioactive iodine therapy.

Choice of treatment is often influenced by the personal experience of the clinician, the client’s attitude and ability towards medication, and the temperament of the cat itself. There are advantages and disadvantages with each option.

Medical management is a life-long treatment and requires ongoing monitoring and compliance on the part of the owner. The disease itself will progress and the patient is likely to need increasing doses of medication.

Surgical thyroidectomy is also commonly performed, though involvement of ectopic thyroid tissue may mean that euthyroidism is not achieved in all cases. One study reported up to a third of surgical cases not leading to a permanent resolution of the disease in a retrospective review of cases from two first- opinion practices.

Access to radioactive iodine facilities is increasing, though it still requires a long period of hospitalisation, which may be a cause of significant stress in this species.

Canine hypothyroidism

At the other end of the spectrum, the pathogenesis of canine hypothyroidism involves destruction of the thyroid gland.

Histopathology shows two different presentations, that of lymphocytic thyroiditis in about 50% of cases, with a known genetic and breed-related component and the other half showing idiopathic atrophy.

The cause of the atrophy is postulated to be either a primary degenerative disorder, or the end-stage of lymphocytic thyroiditis.


The challenge for clinicians tends to be in achieving a clear diagnosis of the disease and avoiding unnecessary treatment, rather than in the management itself.

Clinical signs of thyroid disease in the dog are non-specific and sometimes subtle. Non-thyroidal illness (NTI) or euthyroid sick syndrome can also be a complicating factor. This is characterised by a decrease in circulating thyroid hormone levels but without an increase in TSH levels.

This physiological phenomenon is seen with many other diseases and is thought to be a protective mechanism. Treatment with exogenous thyroxine in these cases is not advised.

Other non-thyroidal factors may also lead to suppressed thyroid hormone levels, often seen as a low level of TT4 (Total T4). Treatment with glucocorticoids, anaesthetics, some NSAIDs and potentiated sulphonamides, and anti-convulsants such as phenobarbitone should also be taken into account when interpreting results and, where possible, expert advice sought on either withdrawing the treatment prior to hormone testing, or on interpretation of the results where they have been given concurrently. Sight hounds and some older dogs also have lower levels of thyroid hormones.

Because of the cross-over in presentation and potential effect of non-thyroidal factors, endocrine experts recommend careful evaluation of the clinical signs and presentation of the case before embarking on laboratory testing. Ruling out concurrent disease helps to allow clearer evaluation of any test results subsequently.

There are a number of laboratory tests available to help in the diagnosis of hypothyroidism, though no one test should be used in isolation. Amongst those commonly used and widely available are measurements of total thyroxine (TT4) and circulating thyrotropin (cTSH).

Used in combination in a case with suggestive clinical signs and free of other illnesses, these allow a fairly reliable diagnosis. Confusion can arise from potential interference by any thyroglobulin auto-antibodies which may be circulating at the same time. These are directed against the protein thyroglobulin (an intrinsic part of T4 and T3) during the inflammatory process of lymphocytic thyroiditis, and can interfere with thyroid hormone measurement.

Some specialist labs are able to measure these auto-antibodies directly (which may help indicate lymphocytic thyroiditis, if caught early in the disease) and advise on interpretation.

Most of the time, following careful pre-assessment, a combined finding of high cTSH and low TT4 is reliable diagnostically, and further tests are not needed.

The finding of a low TT4 with a “normal” cTSH is more challenging, and measuring free thyroxine (not protein-bound) FT or auto-antibody levels may be helpful. The FT4 result will help to rule out NTIs and the auto-antibody tests can help to confirm thyroid disease.


Treatment of the disease in dogs is usually straight-forward and associated with few side-effects. Administration of synthetic thyroid hormone, levothyroxine (L- thyroxine), in titrated once or twice daily doses (depending on the preparation used) usually leads to clinical improvement within 4-6 weeks.

Measurement of both “peak” (4-6 hours post treatment) and “trough” (immediately before the next dose is due) T4 levels is recommended every six months after stabilisation.

  • Further reading available on request from the author.