Prevention of thyroid eye disease and final conclusions.

Abstract

pathogenesis of graves' ophthalmopathy or thyroid eye disease (TED) is almost certainly multifactorial including activated T cells directed against a thyroid follicular cell antigen(s) that then recognize and bind to a similar antigen(s) in orbital tissue (1). These activated orbital T cells then release a variety of cytokines that stimulate excess production of glycosaminoglycans and collagen by orbital fibroblasts resulting in the inflammatory and edematous changes of TED. There are conflicting data as to the culprit common antigen in the orbit and thyroid, the thyrotropin (TSH) receptor or a variant, as well as the role of circulating antibodies against extraocular muscle and fibroblasta components. The speakers at this symposium have addressed many of the problems in defining the pathogenesis of TED and, I believe, a unipotential etiology of TED remains elusive. There has been a great deal of controversy as to whether radioiodine (131I) therapy of Graves' disease incites the onset of TED or aggravates existing TED. There are few prospective studies comparing 131I and antithyroid drug therapy (ATD) on TED, but those that have been published do suggest that 131I therapy does aggravate TED, almost certainly due to the release of thyroid antigens and the subsequent rise in antibodies that would be conducive to the worsening of TED. I have been reluctant to use 131I in patients with pre-existing TED, especially in patients who smoke, because I have not infrequently observed worsening of the TED, a finding rarely observed in patients treated with ATD. Furthermore, thyroidectomy for patients with very large goiters is an alternative treatment and I have not observed the onset or worsening of TED after a near-total thyroidectomy. Very recently, Bartalena and colleagues (2) have reported in a careful prospective study that ATD rarely results in the appearance or worsening of TED, whereas 131I therapy does so more frequently. The administration of corticosteroids after 131I administration prevents this worsening of TED. In an accompanying editorial, Wiersinga emphasizes the following points: because only 15% of patients developed TED after 131I therapy and it was usually mild and transient, the administration of corticosteroids for months after 131I therapy with its attendant risks is probably not indicated; in patients with more severe TED, ATD is the treament of choice and if 131I is to be given, corticosteroids should probably be used as well; conclusive evidence has been presented that 131I does carry a small but definite risk for the onset or worsening of TED (3). We have used large ablative doses of 131I followed by steroids and prompt administration of levothyroxine when hypothyroidism ensues in patients with preexisting TED who have problems with ATD or in younger patients with large goiters who refuse surgery after ATD failure.