Radioiodine Treatment is Associated with Worsening of Graves' Ophthalmopathy
ABSTRACT & COMMENTARY
Synopsis: Radioiodine therapy for Graves' hyperthyroidism is followed by worsening of ophthalmopathy, but worsening can be prevented with prednisone.
Source: Bartalena L. N Engl J Med 1998;338:73-78.
The effect of the treatment used for graves' hyperthyroidism and the course of the associated ophthalmopathy has been controversial. A total of 443 patients with Graves' hyperthyroidism and slight or no ophthalmopathy were randomly assigned to receive radioiodine, radioiodine followed by a three- month course of prednisone, or methimazole for 18 months. The patients were evaluated for changes in the function and appearance of the thyroid and progression of ophthalmopathy at intervals of 1-2 months for 12 months. Hypothyroidism and persistent hyperthyroidism were promptly corrected.
Among the 150 patients treated with radioiodine, ophthalmopathy developed or worsened in 23 (15%) 2-6 months after treatment. The change was transient in 15 patients, but it persisted in eight (5%), who subsequently required treatment for their eye disease. Among the 145 patients treated with radioiodine and prednisone, 50 (67%) of the 75 with ophthalmopathy at baseline had improvement, and no patient had progression. Among the 148 patients treated with methimazole, three (2%) who had ophthalmopathy at baseline improved, four (3%) had worsening of eye disease, and the remaining 141 had no change.
The authors conclude that radioiodine therapy for Graves' hyperthyroidism is followed by the appearance or worsening of ophthalmopathy more often than is therapy with methimazole. Worsening of ophthalmopathy after radioiodine therapy is often transient and can be prevented by the administration of prednisone.
COMMENT BY RALPH R. HALL, MD, FACP
As the author indicates, the ophthalmopathy of Graves' disease, its cause, acceleration, and progression in relation to the type of therapy have been debated for years. The majority of the publications suggest that radioactive iodine (RAI) was more likely to be associated with worsening and progression of the ophthalmologic problems than antithyroid drug administration.1 The results of this study are in accord with my long-term impression that RAI is an aggravating factor in some patients. The accompanying editorial asks the important question, "What is the appropriate treatment?" and suggests the appropriate approach until we know the cause or causes of ophthalmopathy.1
Environmental factors that are associated with more severe and worsening of the eye problems are smoking, high serum tricodothyromine concentrations before treatment, high concentration of thyrotropin receptor antibodies, and high serum thyrotropin concentrations after treatment. Patients with these conditions are more appropriately treated with antithyroid medication and/or RAI plus prednisone for those in whom prednisone is not counter-indicated.
In my experience, rapid deterioration of eye pathology has occurred only after RAI or surgery. Further, patients who have not responded to one type of therapy (i.e., RAI, antithyroid drugs, or surgery) may fail or be difficult to control with the other treatment regimens.
The biological explanation for the association between smoking and the ophthalmopathy of Graves' disease is unknown, but the association is strong. Patients should be made aware of this association. It is usually an effective way to encourage the patient to stop smoking permanently. The use of antithyroid medication prior to treatment with RAI in this study
may have actually decreased the incidence of eye disease. Antithyroid medication has been reported to decrease abnormal thyrotropins associated with eye disease.2 Treatment with antithyroid drugs alone works well with young patients who have small glands and disease of recent onset. The failure rate is high, with patients who have larger glands and disease that has been present for more than 3-4 months, be they young or old.3
References
1. Kang AWC. J Clin Endocrinol Metab 1994;79:542-546.
2. Meek JC, et al. Proc Natl Med Sci 1964;52(2):343-349.
3. Karlsson FA. J Clin Endocrinol Metab 1998;83: 1398-1399.
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