Hyperthyroidism in cats


Feline hyperthyroidism (FHT) was first recognized in early 1980s [1] and has since grown in prevalence to become the most common endocrine disease of cats, with 10% of cats over 10 years being affected [2]. Now, the disease is more commonly screened for in at-risk cats, with total serum thyroxine (T4) being included in geriatric blood panels; however, this increased awareness is unlikely to be the sole reason for the apparent increase in prevalence.

Etiology & Epidemiology

Approximately 97% – 99% of cases result from bilateral benign nodular hyperplasia, adenomatous hyperplasia or adenoma of the thyroid gland [3]. Clinically and histopathologically it resembles toxic goitre seen in humans rather than the autoimmune disease, Graves’.

The underlying cause of these thyroid changes has not been definitively identified; however, it is thought both genetic and environmental factors contribute [4]. The incidence appears to vary geographically. Other consistent associations  found include increased risk with age, decreased risk in Siamese and Himalayan cats, and increased risk in cats that consume canned cat food [5]. Exposure to pesticides and herbicides and cat litter also increased risk [5]. It should be noted that this could simply be a marker for indoor, regularly deflea-ed and wormed, high welfare cats that are more likely to be diagnosed with FHT.

Clinical signs

Thyroid hormones affect a variety of different body systems, so the clinical presentation can vary from cat to cat.  In the 1980s, cases commonly presented in what we now recognise as the typical skinny, unkempt, hypermetabolic state, with cardiorespiratory disease being the most common comorbidity [6]. However latterly, with increased recognition and screening this advanced presentation is much less commonly seen. With earlier presentation, clinical signs are more subtle and may also be complicated by comorbidities.

The classic signs of FHT are weight loss, polyphagia, polyuria, polydipsia, increased vocalisation, agitation, increased activity, tachypnoea, tachycardia, vomiting, diarrhoea and an unkempt hair coat. Differential diagnoses for cats with such clinical signs include diabetes mellitus, gastrointestinal (GI) malabsorption or maldigestion, neoplasia (especially GI lymphoma), chronic kidney disease (CKD) and parasitism. A palpably enlarged thyroid is present in 80-90% cats [7] [8]. Owners can often report the cat is ‘kitten-like’ in his behaviour, ‘losing weight as he is so active’, ‘senile’ or ‘always hungry’.

A definitive diagnosis of FHT requires demonstration of persistently elevated thyroid hormone concentrations occurring concurrently with one or more of the typical clinical signs. Total serum T4 is usually used owing to its better diagnostic sensitivity over T3. A normal T4 result in a cat showing clinical signs may be because of T4 suppression by concurrent illness, or owing to fluctuations in circulating T4 levels. Free T4 or dynamic thyroid function tests can also be employed [9].


There are now 6 established groups when considering FHT diagnosis, ranging from overt clinical disease supported by laboratory confirmation, to clinically normal but with elevated T4.

GROUP 1: Classic clinical disease. Cats with uncomplicated clinical hyperthyroidism and elevated T4.

GROUP 2: Possible FHT with probable non-thyroidal disease. Cats with clinical hyperthyroidism and normal T4.

GROUP 3: Enlarged thyroid without clinical FHT. Cats without clinical hyperthyroidism, T4 within the reference interval, but with enlarged thyroid gland(s).

GROUP 4: Subclinical FHT. Cats without overt clinical hyperthyroidism, but with an elevated T4 and with some physical exam findings suggestive of hyperthyroidism.

GROUP 5: Clinical FHT with confirmed non-thyroidal disease. Cats with clinical hyperthyroidism confirmed by elevated T4, and one or more concurrent diseases.

GROUP 6: Clinically normal. Cats with no clinical signs of hyperthyroidism and no palpable thyroid nodule, but with an elevated T4 on screening lab test.

Each of these groups has an established management strategy, details of which can be found in 2016 AAFP Guidelines for the Management of FHT (Guidelines) [10].


The identification of hypertension in cats with FHT is vital for their health. At every veterinary visit the blood pressure should be monitored, although of course results can be variable in cats out of their home environment. In addition, performing a complete fundic exam may determine whether hypertensive retinopathy is present. This monitoring should continue throughout treatment, if hypertension fails to resolve with FHT treatment it may be owing to concurrent disease.

Concurrent CKD

Many clinicians falsely believe that elevated T4 supports renal function. However, the Guidelines clearly states that any FHT patient with concurrent CKD should still be treated for FHT [10]. The recommendations for treatment do differ depending on whether the cat is azotemic or not at the time of FHT diagnosis. Treatment for CKD should be in accordance with the IRIS guidelines.  Both guidelines should be referred to for further details, as it is beyond the scope of this article.

Concurrent heart disease

Concurrent heart disease is common in FHT patients and may or may not be a direct result of FHT. It is recommended to first correct the hyperthyroidism and then evaluate the heart disease once the cat is euthyroid.

Treatment modalities

The goal of therapy is to restore euthyroidism, avoid hypothyroidism and minimize side effects of treatment. There are several commonly employed treatment modalities that should be considered according to suitability for each case.

Therapies can be implemented individually or in combination: radioactive iodine (131I), pharmaceutical therapy (methimazole or carbimazole), surgical thyroidectomy and dietary therapy. The choice is often influenced by the cat’s age, comorbidities, cost- ongoing or upfront payment, availability and clinician’s expertise.

Most clinicians now recommend definitive curative therapy with 131I or thyroidectomy, especially if the cat is relatively young and otherwise healthy. 131I is considered the gold standard treatment currently. Pre-treatment with anti-thyroid drugs prior to 131I or surgery is common practice as will decrease surgical risk and may improve long-term outcome post 131I [11].

In the case of geriatric cats, cats with concurrent disease (especially CKD), the long-term administration of the antithyroid drugs and/ or a commercial iodine-restricted diet are options. These options are very successful in managing FHT, however all cats will relapse when therapy is discontinued [12] [9]. The lifetime total cost of surgery, medication or radioactive iodine are all approximately comparable. However, dietary therapy for ONE year with a specific low iodine prescription diet equals the lifetime total cost of the other treatment modalities.


Regardless of the treatment modality used, regular monitoring to assess therapeutic efficacy and to detect iatrogenic hypothyroidism is very important. In addition, some comorbidities may become evident with resolution of the hyperthyroid state. The cat’s physical condition, T4, CBC, chemistry and renal parameters should all be considered. Initial follow up should be 2-4 weeks after implementation of therapy and 2-4 weeks after any change in medication dose. Stable uncomplicated FHT cats should be assessed every 4-6 months.


The median survival time for FHT cats without concurrent CKD is 5.3 years after diagnosis [11]. Morbidity and mortality in the well-managed hyperthyroid cat are more strongly influenced by the presence and severity of the comorbid disease than by FHT itself.


Many cats with FHT have lost weight and lean body mass. In addition, most are geriatric cats with increased protein requirements compared with younger cats. Due to their hypermetabolic state, vitamin and other trace nutrient stores may be depleted. Insulin resistance and glucose intolerance are common problems in FHT cats and seem to remain even after treatment. Highly digestible, high protein (>40% dry matter), low-carbohydrate (<25% dry matter) diets are recommended to help restore weight and lean body mass [13]. Such diets include Royal Canin Mature Consult or Early Renal.

Myths about FHT

  1. Methimazole and other treatment modalities causes kidney damage.

They do not [14, 15]. This myth may have come about as FHT may mask the concurrent signs of CKD, which become apparent as the FHT is controlled.

  • Maintaining T4 slightly above the reference interval will help patients with comorbidities like CKD, through improved renal blood flow and appetite.

This myth is now confirmed to be untrue. In actual fact, even mild FHT can cause or exacerbate CKD and early treatment can help reduce damage to the kidneys from hyperthyroidism [16]. Furthermore, unregulated FHT creates a false sense of security in the patient’s health and masks clinical signs of comorbid disease due to increased appetite and activity level.

  • The cost of 131I is prohibitive and the stress of isolation post treatment makes it a poor choice for treatment.

Although any time a cat is away from home it may experience stress, this stress is much less than that of the illness or other treatments. It is important to fully explain to the owner that any illness and treatment can be stressful, and this must be weighed against the benefits. In fact, the stress is likely no different to time spent in boarding facilities when owners go away on holidays.

The cost of 131I treatment is the same as surgery or long-term medication. The cost is a one-off, upfront payment, so may seem more than that of regular small payments for medication.

  • Post-treatment T4 should be below the reference interval because producing a hypothyroid state does not harm cats.

Cats can develop clinically significant hypothyroidism even if the T4 is within the reference interval. While treatment of FHT does not cause or exacerbate renal disease, overtreatment (iatrogenic hypothyroidism) can cause progression of renal disease and increase patient morbidity and mortality [17].

FHT is a disease of aging cats that is now classed in 6 different groups according to presence of clinical signs, T4 levels and presence of comorbidities. Each group has a specific diagnostic and treatment strategy, described in the AAFP Guidelines for FHT. 131I is currently felt to be the gold standard treatment for FHT. The role of diet is mainly supportive, high protein, low carbohydrate to help lean muscle mass gain. Royal Canin Mature Consult or Early Renal are good available options.


1.         Holzworth, J., et al., Hyperthyroidism in the cat: ten cases. J Am Vet Med Assoc, 1980. 176(4): p. 345-53.

2.         Peterson, M., Hyperthyroidism in cats: what’s causing this epidemic of thyroid disease and can we prevent it? J Feline Med Surg, 2012. 14(11): p. 804-18.

3.         Gunn-Moore, D., Feline endocrinopathies. Vet Clin North Am Small Anim Pract, 2005. 35(1): p. 171-210, vii.

4.         McLean, J.L., R.G. Lobetti, and J.P. Schoeman, Worldwide prevalence and risk factors for feline hyperthyroidism: A review. J S Afr Vet Assoc, 2014. 85(1): p. 1097.

5.         Kass, P.H., et al., Evaluation of environmental, nutritional, and host factors in cats with hyperthyroidism. J Vet Intern Med, 1999. 13(4): p. 323-9.

6.         Fox, P.R., M.E. Peterson, and J.D. Broussard, Electrocardiographic and radiographic changes in cats with hyperthyroidism: comparison of populations evaluated during 1992-1993 vs. 1979-1982. J Am Anim Hosp Assoc, 1999. 35(1): p. 27-31.

7.         Peterson, M.E., Diagnostic tests for hyperthyroidism in cats. Clin Tech Small Anim Pract, 2006. 21(1): p. 2-9.

8.         Norsworthy, G.D., et al., Relationship between semi-quantitative thyroid palpation and total thyroxine concentration in cats with and without hyperthyroidism. J Feline Med Surg, 2002. 4(3): p. 139-43.

9.         Mooney, C.T., Feline hyperthyroidism. Diagnostics and therapeutics. Vet Clin North Am Small Anim Pract, 2001. 31(5): p. 963-83, viii.

10.       Carney, H.C., et al., 2016 AAFP Guidelines for the Management of Feline Hyperthyroidism. J Feline Med Surg, 2016. 18(5): p. 400-16.

11.       Milner, R.J., et al., Survival times for cats with hyperthyroidism treated with iodine 131, methimazole, or both: 167 cases (1996-2003). J Am Vet Med Assoc, 2006. 228(4): p. 559-63.

12.       Daminet, S., et al., Best practice for the pharmacological management of hyperthyroid cats with antithyroid drugs. J Small Anim Pract, 2014. 55(1): p. 4-13.

13.       Laflamme, D. and D. Gunn-Moore, Nutrition of aging cats. Vet Clin North Am Small Anim Pract, 2014. 44(4): p. 761-74, vi.

14.       Norrgran, J., et al., Decabromobiphenyl, polybrominated diphenyl ethers, and brominated phenolic compounds in serum of cats diagnosed with the endocrine disease feline hyperthyroidism. Arch Environ Contam Toxicol, 2012. 63(1): p. 161-8.

15.       Vaske, H.H., T. Schermerhorn, and G.F. Grauer, Effects of feline hyperthyroidism on kidney function: a review. J Feline Med Surg, 2016. 18(2): p. 55-9.

16.       Williams, T.L., et al., Survival and the development of azotemia after treatment of hyperthyroid cats. J Vet Intern Med, 2010. 24(4): p. 863-9.

17.       Williams, T.L., J. Elliott, and H.M. Syme, Association of iatrogenic hypothyroidism with azotemia and reduced survival time in cats treated for hyperthyroidism. J Vet Intern Med, 2010. 24(5): p. 1086-92.


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