Toxic thyroid nodule
Toxic thyroid nodule or Plummer's Disease is a condition where there is a single nodule (a benign adenoma) producing excess thyroid hormone.
The clinical features are similar to any patient with thyrotoxicosis, but without the extra manifestations caused by the autoantibodies found in Graves’ disease. The overactive nodule is not always readily palpable, but may only be found on imaging.
Diagnosis is initially made with thyroid function tests, which show the classical changes of thyrotoxicosis. Imaging is performed with radioactive iodine or technetium scanning, which in contrast to Graves’ disease, shows a solitary ‘hot’ nodule (Fig. 1).
The treatment of choice depends on the patient's wishes. Radioactive Iodine (131I) gives good results with a low dose, and can also be repeated if necessary. The risk of radioiodine-induced hypothyroidism after treatment is small, as the toxic nodule preferentially takes up the RAI, while suppressing uptake in the remaining thyroid, allowing it to be relatively protected.
Surgical excision, in the form of a thyroid lobectomy, may be preferred in some cases as it works more quickly in controlling the thyrotoxicosis, and controls the pressure symptoms that may be a feature of larger nodules. The risk of postoperative hypothyroidism is low, and surgery has the advantage of providing tissue for histology (microscopic pathology examination).
Toxic Multinodular Goitre
Toxic multinodular goitre is usually found in older patients, compared with those with Graves' disease. It is the most common cause of thyrotoxicosis in the elderly. The condition is thought to occur because of recurrent periods of thyroid growth and involution, which over the long term results in the formation of an autonomous nodule (not responding to control from TSH), which becomes overactive.
There does seem to be some autoimmune component however, as thyroid autoantibodies have been found in 25% of patients.
Toxic multinodular goitre is almost always preceded by long-standing multinodular goitre and probably, in most patients, by episodes of subclinical thyrotoxicosis. This thyrotoxicosis is often precipitated by exposure to excessive iodine from outside sources, such as medications and radiology contrast media used in imaging procedures like CT scanning.
The clinical features are again similar to Graves’ patients, but without the extra manifestations due to the autoantibodies, and diagnostic tests are the same.
Thyroid function tests show a suppressed TSH with a normal T3 and T4 in the early stages, an indication of incipient autonomous nodules and potential toxicity.
The scan however will reveal a patchy uptake, rather than a single nodule (Plummer’s) or uniform uptake (Graves’) (Fig. 2).
Antithyroid drugs are of no value as a long term treatment as the thyrotoxicosis is due to autonomous nodules within the goitre, which will continue to produce excess hormone once the antithyroid drug is stopped.
This means that all patients will need definitive treatment. The choice of definitive treatment depends on the wishes of the patient. Radioactive iodine is fine if the goitre is small and non-compressive, or if the patient wishes to avoid surgery.
If the goitre is large, symptomatic or cosmetically unacceptable however, then surgery (total thyroidectomy) is the best option, after the gland has been suppressed with antithyroid drugs in the short term to make the patient safe to undergo operation.