Treatment of thyrotoxicosis — the current position Part III: Radioiodine therapy. Special considerations

Summary

Radioiodine (¹³¹I) therapy for thyrotoxicosis has the advantages of simplicity, effectiveness and safety in patients over 40 years of age and especially in the frail and elderly when there is often associated cardiac disease. ¹³¹I should not be used in children except in unusual circumstances such as drug sensitivity and refusal to have an operation. There is, however, only a relative contra-indication to its use in adults less than 40 years of age and it is the best treatment for a post-operative recurrence irrespective of the age of the patient. The physician must be sure the patient is not in early pregnancy and she should avoid this state for several months.

¹³¹I therapy does not cause leukaemia, thyroid cancer nor other damage, but all patients made euthyroid are at risk to the development of hypothyroidism, although its onset may be delayed for up to 15 years; once a patient is made firmly euthyroid with ¹³¹I therapy a true recurrence of thyrotoxicosis is exceptionally rare.

Since ¹³¹I therapy seems to destroy the whole thyroid (or damage all the cells) leading to hypothyroidism and because ¹²⁵I, an alternative nuclide, may not do this it is being tried in special trials. The results are very promising although it is too early to advise the routine use of ¹²⁵I.

This final section ends with an account of the management of severe thyrotoxicosis (including crisis), thyrocardiac disease including the use of β-adrenergic blocking drugs. A short note on the management of thyrotoxicosis in pregnancy and in children and of eye-signs is added.

In this three-part review, those aspects of causation relevant to the course and treatment of thyrotoxicosis are presented. The large majority in the United Kingdom have Graves' disease. LATS is linked in some way to Graves' disease, but its unique stimulating effect on thyroid function is puzzling as autoantibodies are usually destructive. LATS may be an antichalone which reacts with thyroid chalone, probably a 4S compound in thyroid cell sap, and so neutralises the chalone's normal inhibitory control of mitosis. This speculative hypothesis is worth further study. LATS activity correlates in a general way with control of the thyrotoxic process but as yet it has not been shown to be of value in selecting therapy or predicting its results.

Antibody studies also suggest that in Graves' disease there is an inherited abnormality of immune homeostasis, which probably explains the familial nature of the condition. Patients with high titres of thyroid autoantibodies are more prone to hypothyroidism after surgery, but not after antithyroid drugs or ¹³¹I therapy and this is puzzling too.

The indications for, efficacy, advantages and disadvantages, and complications of antithyroid drug therapy, thyroidectomy and ¹³¹I therapy are discussed in detail.

There is a renewed interest in antithyroid drugs, the best of which seems to be carbimazole. The majority of young patients with Graves' disease are best treated in the first instance with carbimazole and the T3 thyroid suppression test is of some value in following the disease process and predicting remissions after antithyroid drug therapy.

The results and complications of surgery are scrutinised. There is more awareness of postoperative hypothyroidism, which is more common than at one time appreciated; its frequency varies and evidence that it is cumulative is conflicting. Its incidence reflects the extent of the resection and the care taken with follow-up. Autoimmunity is a contributory factor. The frequency of permanent damage to the recurrent laryngeal nerve and of persistent severe parathyroid insufficiency is fortunately low. Changes in the voice without impairment of cord movement and biochemical parathyroid insufficiency are, however, more frequent. There is a correlation between hypoparathyroidism and recurrent laryngeal nerve damage which is related to the extent of gland mobilisation at operation. Second thyroidectomies are contra-indicated because of the risk of damage to adjacent structures and of the poor functional results achieved.

The present position of ¹³¹I therapy is presented. In particular, its single but significant shortcoming, namely a cumulative incidence of hypothyroidism is noted. The reasons for this are mentioned. Modifications to current practice are discussed, including a regime of reduced ¹³¹I dosage supplemented by an antithyroid drug, and the use of a different isotope of iodine, namely ¹²⁵I. ¹²⁵I has different energy characteristics from ¹³¹I and these are likely to restrict its irradiation effects on the thyroid cell chiefly to the area where hormone is synthesised. As a result, cell function should be impaired and the thyrotoxic process controlled while the cell nucleus should be spared and the likelihood of future hypothyroidism diminished.

Brief consideration is given to current standard practice in the management of severe thyrotoxicosis, including thyroid crisis and thyrocardiacs, thyrotoxicosis in pregnancy and in children, and the ophthalmopathy of Graves' disease.

Key Words: :

• Hyperthyrodism
• drug therapy
• radiotherapy
• thyroidectomy