Radiotherapy

From Cat

Radiotherapy for hyperthyroidism in cats is reliable and highly effective when a dose of between 160 and 250 MBq is given (depending on the size and number of thyroid nodules, and the extent of the T4 elevation; most cats need 150 to 200 MBq)[1]. Young healthy female cats appear to have a greater likelihood of survival from radioiodine therapy, and pre-existing chronic renal disease and neoplasia significantly reduce survival rates[2].

From the point of view of the cat, I-131 is safe and not stressful to administer as either a capsule or a subcutaneous injection. Cats are required, by regulatory authorities, to be hospitalised for about 5-7 days. There is no requirement for anaesthesia or surgery, and no risk of post-operative hypocalcaemia, laryngeal paralysis etc. It fixes the problem, generally permanently, at the first attempt and without side effects. In most facilities, in Australia at least, I-131 therapy will “cost out” cheaper than bilateral staged thyroid surgery. A variety of therapy centres exist in different areas. The development of commercially available purpose-built cages makes radio-iodine therapy possible in any practice with a startup cost of less than $10,000 AUD, including training and licensing. There is insufficient evidence in the peer reviewed literature to recommend the additional cost of routine thyroid scans prior to I-131 therapy. Simple tables that take into consideration the size of the thyroid lesion(s) and the extent of the T4 elevation seem adequate to determine the radioiodine dose.

From a pathophysiological point-of-view, radio-iodine fixes the underlying problem, i.e. the abnormal thyroid tissue is ablated. Other non-specific effects of the thyroid lesion e.g. paraneoplastic substances, mass effects are avoided. There is no requirement for twice daily medication and regular trips to the veterinary clinic to maintain a euthyroid state. In contrast, cats treated with carbimazole or methimazole typically require frequent and careful monitoring. The dose of medication may change as the primary lesion gets larger[3]. The presence of concurrent parathyroid lesions becomes apparent, as abnormal thyroid tissue is ablated by the I-131. Thus, the detection of concurrent parathyroid lesions – either functional or non-functional – is facilitated. Under dosing with radio-iodine requires that the cat be given a 2nd dose at some point in time, typically after waiting 6 months for delayed effects of treatment.

Over dosage with radio-iodine can result in permanent hypothyroidism, although this is rare. Transient hypothyroidism occurs in many patients, and is the stimulus for increased TSH levels to “kick start” normal thyroid tissue that was previously quiescent. Another complication is that up to 39% of treated cats have chronic renal disease diagnosed after treatment of hyperthyroidism[4].

Signs of permanent hypothyroidism include lethargy, a poor coat and myxoedema of the head, resulting in thickened facial features and mild stridor referable to the upper airways. Hypothyroidism is easily treated with replacement therapy, typically 100 μg of thyroxine once daily. This requirement is constant. It is noteworthy that many human patients with Graves’ disease are treated with ablative radio-iodine, and subsequently given life-long replacement therapy. Because thyroxine is a natural substance, it is well tolerated.


Much is made of the risk of “unmasking” renal insufficiency following treatment of hyperthyroidism. However, if cats have urea and creatinine concentrations within the reference range, and a urine sg > 1.025 (>1.035 is even better!), it is rare for them to develop clinically significant azotaemia following therapy with I-131. It should be emphasised that urea and creatinine concentrations in cats with hyperthyroidism generally do rise to some extent following re-establishment of euthyroidism. unfortunately some cats develop the uraemic syndrome following therapy (particularly very old cats).The only definitive way to determine whether this will occur is with a carbimazole trial, which adds greatly to the cost and complexity of therapy. Renal insufficiency following I-131 therapy can still be managed using prescription diets, phosphate binders, and attention to hydration; it is prudent to also treat them with supra-physiological doses of thyroxine to re-establish a slightly hyperthyroid state and thereby increase renal blood flow. It may be prudent not to treat cats with clinical or biochemical evidence of renal insufficiency – even though some of these cats will actually benefit from correction of their thyrotoxicosis. A good way forward in this situation is a trial with carbimazole – although sometimes adverse effects from this drug trial can be problematic. Another strategy is to manage the cardiac signs of thyrotoxicosis with atenolol, treat hypertension with amlodopine and forgo any attempt to treat the underlying problem specifically. The current cost of therapy ($900-1200 AUD) is acceptable and less expensive in the long term than on-going medical management for 6-12 months.

References

  1. Malik, R 2009) Hyperthyroidism, hyperparathyroidism and ventral cervical nodules. WSAVA conference
  2. Slater MR, Geller S, Rogers K (2001) Long-term health and predictors of survival for hyperthyroid cats treated with iodine 131 Journal of Veterinary Internal Medicine 15(1):47-51
  3. van Hoek IM et al (2009) Effect of reconbinant human thyroid stimulating hormone on serum thyroxin and thyroid scintigraphy in euthyroid cats. JFMS 11:309-314
  4. van Hoek, IM et al (2010) Thyroid stimulation with recombinant human thyrotropin in healthy cats, cats with non-thyroidal illness and in cats with low serum thyroxin and azotemia after treatment of hyperthyroidism. JFMS 12:117-121