| If the patient is hyperthyroid our primary choice of therapy is radioiodine, with the aims to render the patient euthyroid and to reduce thyroid size by 50 % in 2 years (see Thyroid International 2- 1999 for a discussion 3 ). Antithyroid drugs may be used, but they will not reduce goitre size and medication will have to continue life long. Treatment of multinodular toxic goitre with antithyroid drugs does not lead to remission of the basic disease process as it has been found to occur in 90–95 % of patients with Graves’ disease. Hence hyperthyroidism will return rapidly after cessation of therapy in most patients with multinodu-lar toxic goitre. This is different from Graves’ disease where relapses due to reactivation of the autoimmune aberration occur more gradually over the years after withdraval of therapy, with a frequency depending on goitre size (fig. 2). Life-long therapy with antithyroid drugs may be the option in very old subjects with multinodular toxic goitre. Subclinical hyperthyroidism with suppressed serum TSH and serum T4 and T3 in the normal range is common in multinodular goitre. The lab-oratory reference ranges for serum T4 and T3 are twice as broad as the individual spontaneous variations in serum T4 and T3 . This indicate that 50% of the laboratory reference range is not nor-mal for the individual subject and patients with subclinical hyperthyroidism probably all have a thyroid hormone secretion above their individual set point. Accordingly atrial fibrillation and other complications to hyperthyroidism are more com-mon in subclinical hyperthyroidism. Radioiodine therapy is recommended for patients with multi-nodular goitre and subclinical hyperthyroidism. |
