Graves' ophthalmopathy and I-131 therapy

Graves' ophthalmopathy is an autoimmune process initiated and maintained by antigen(s) shared by the thyroid and the orbit. A matter of argument conce rns the choice of the method of treatment for Graves' hyperthyroidism when clinically evident ophthalmopathy is present. Restoration of euthyroidism a ppears to be beneficial for ophthalmopathy, On the other hand the continuin g disease activity associated with the recurrence of hyperthyroidism appear s to adversely affect the course of ophthalmopathy, For these reasons it is our opinion that in patients with Graves' hyperthyroidism and ophthalmopat hy the permanent control of thyroid hyperfunction by ablation of thyroid ti ssue should be obtained by radioiodine therapy or thyroidectomy, The ration ale for an ablative strategy is the following: i) permanent control of hype rthyroidism avoids exacerbations of eye disease associated with recurrence of hyperthyroidism; ii) hypothyroidism, which follows thyroid tissue ablati on, should be regarded as a therapeutic end point rather than as an undesir able result; iii) ablation of thyroid tissue may result in the removal of b oth the thyroid-orbit cross-reacting antigen(s) and the major source of thy roid-autoreactive lymphocytes, The relationship between radioiodine therapy and the course of GO is a matter of controversy, and some authors have sug gested that radioiodine administration may be associated with a worsening o f preexisting ophthalmopathy, This was not observed when radioiodine treatm ent was associated with a S-month oral course of prednisone, The developmen t or progression of GO after radioiodine therapy might be due to the releas e of thyroid antigens following radiation injury and to subsequent exacerba tions of autoimmune reactions directed towards antigens shared by the thyro id and the orbit. The view that radioiodine therapy may be associated with a progression of ophthalmopathy is not shared by some authors who claim tha t the apparent link between progression of ophthalmopathy and radioiodine t herapy might simply be coincidental, reflecting the natural history of the disease. The radioiodine-associated exacerbation of eye disease might be us ed as an argument against the use of radioiodine therapy in patients with o phthalmopathy, We do not share this view, since the outword effects of radi oiodine on eye disease can easily be prevented by concomitant administratio n of glucocorticoids. Glucocorticoid treatment should be limited, in our op inion, to patients with clinically evident eye disease and to those without ophthalmopathy but with other known risk factors, such as smoking.