Hyperthyroidism

What it is

Feline hyperthyroidism is a state of thyrotoxicosis caused by autonomous, excessive production of thyroxine (T4) and triiodothyronine (T3). In the great majority of cats the lesion is benign adenomatous hyperplasia or adenoma, affecting both thyroid lobes in many cases; thyroid carcinoma is rare. The hyperfunctioning tissue escapes regulation by pituitary TSH, which is suppressed, and the normal thyroid tissue atrophies. The excess hormone speeds up the metabolism of almost every organ. The cause is poorly understood; dietary and environmental factors (such as goitrogenic compounds and flame retardants) have been studied, but none has been shown to be the single cause.

Who it affects

Middle-aged and older cats, usually over 10 years of age; it is very rare in young cats. There is no clear sex predisposition. Siamese and Himalayan cats appear to be at lower risk.

Anatomy involved

• Thyroid gland: two lobes on either side of the trachea, caudal to the larynx, not joined by an obvious isthmus in the cat. As they enlarge they may descend along the neck and be felt as a mobile nodule ("goitre"); sometimes the hyperfunctioning tissue is ectopic, in the neck or the cranial mediastinum. The external parathyroid glands lie at the cranial pole of each lobe and must be preserved during surgery.
• Heart: thyrotoxicosis causes tachycardia, increased cardiac output and left ventricular hypertrophy (thyrotoxic cardiomyopathy), which usually improves once the hyperthyroidism is controlled.
• Kidneys: increased renal blood flow and glomerular filtration can mask chronic kidney disease, which becomes evident when the hyperthyroidism is treated.
• Vessels and eyes: systemic hypertension with retinal lesions may be present.

Clinical signs

Weight loss with a normal or increased appetite (polyphagia), polyuria and polydipsia, hyperactivity or restlessness, vocalisation, vomiting, diarrhoea or bulky faeces, an unkempt coat and muscle wasting. On examination: a palpable thyroid nodule, tachycardia, a murmur, gallop sound or arrhythmias. A minority show the "apathetic" form, with lethargy and inappetence. Severe cases may develop heart failure or blindness from hypertensive retinal detachment.

Diagnosis

• Serum total T4: increased in most hyperthyroid cats and, with compatible signs, enough for the diagnosis.
• If total T4 is in the upper reference range with compatible signs (mild hyperthyroidism or concurrent illness lowering it): free T4 by equilibrium dialysis together with total T4, repeat total T4 after a few weeks, T3 suppression test or thyroid scintigraphy.
• Pertechnetate scintigraphy confirms the diagnosis and locates the hyperfunctioning tissue, including ectopic tissue and metastases.
• General blood work: increased ALT and alkaline phosphatase, mild erythrocytosis; creatinine, SDMA and urine specific gravity must be interpreted with caution because renal function is overestimated.
• Blood pressure and, when there are cardiac abnormalities, echocardiography.

Treatment

There are four options:

• Radioactive iodine (I-131): the treatment of choice; a single injection destroys the hyperfunctioning tissue, including ectopic tissue, while sparing the atrophied normal tissue, and cures the great majority of cats. It requires hospitalisation in licensed facilities.
• Antithyroid drugs (methimazole or its prodrug carbimazole): control hormone production but do not cure, and must be given for life. Adverse effects include vomiting, facial pruritus with excoriations, liver disease and haematological abnormalities.
• Thyroidectomy: curative if all affected tissue is removed; the main risk of bilateral thyroidectomy is hypocalcaemia from injury or removal of the parathyroid glands.
• Iodine-restricted diet: controls T4 if the cat eats no other food.

A trial with antithyroid drugs is advised before definitive treatment to see how renal function responds. Iatrogenic hypothyroidism after treatment is associated with azotaemia and should be corrected. The prognosis of treated cats is good, limited mainly by concurrent kidney and heart disease.

Key studies

• AAFP guidelines (Carney et al., 2016): the reference guideline. It proposes testing sequences to avoid misdiagnosis, divides the diagnosis into six clinical categories with their management, recommends treating every hyperthyroid cat regardless of comorbidities and explains how to monitor treated cats so as not to worsen concurrent disease.
• Peterson and Broome (2015), thyroid scintigraphy of 2096 consecutive hyperthyroid cats. Disease was unilateral in 31.7%, bilateral in 62.9% (asymmetric in 50.6%, symmetric in 12.3%) and multifocal in 3.9%. Ectopic thyroid tissue was found in 3.9% of cats, tissue in the thoracic cavity in 5.5%, and carcinoma was suspected in 1.7%.
• Peterson et al. (2001), 917 untreated hyperthyroid cats, 221 cats with non-thyroidal illness and 172 healthy cats. Free T4 by equilibrium dialysis was more sensitive than total T4 or T3, but was high in 14 of the 221 cats with non-thyroidal illness, so it should not be used on its own to diagnose hyperthyroidism.
• Peterson and Becker (1995), prospective series of 524 cats treated with subcutaneous radioiodine, with the dose adjusted to severity. By 6 months only 8 cats (1.5%) remained hyperthyroid; 2.1% developed clinical hypothyroidism needing thyroxine and 2.5% relapsed 1.1 to 6.5 years later. There was no comparison group.
• Peterson et al. (2018), prospective study of 262 hyperthyroid cats treated with radioiodine and 206 healthy cats of similar age. None was azotaemic before treatment, but 16% became azotaemic afterwards. A high SDMA before treatment predicted this with 97.7% specificity but only 33.3% sensitivity: a high value is a warning, a normal one does not rule out masked kidney disease.
• Williams et al. (2010), retrospective study of 75 treated cats. Azotaemia was more frequent in cats with iatrogenic hypothyroidism (16 of 28) than in euthyroid cats (14 of 47), and hypothyroid cats that became azotaemic lived less (median 456 versus 905 days).