Radioiodine and Graves Orbitopathy

Radioiodine and Graves orbitopathy

H.X. Li’s 2016 Journal of Endocrinolog Investigation meta-analysis of nine trials with 1773 patients suggested that radioiodine therapy is a significant risk factor for development or worsening of GO in GD. But GO progression can be prevented by prophylactic glucocorticoids in patients with preexisting GO. (Steroids however have health risks.)

Compared with Thyroidectomy alone, Total thyroid ablation induces an earlier and steadier GO improvement in patients with mild to moderate-severe and active GO. Whether this is sufficient to offer Total Thyroid Ablation to patients needs further investigation. (TTA:  achieved by near total thyroidectomy followed by radioiodine)

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Older articles:

N Engl J Med. 1998 Jan 8;338(2):73-8.  Relation between therapy for hyperthyroidism and the course of Graves’ ophthalmopathy.

Source

Istituto di Endocrinologia, University of Pisa,  Italy.

METHODS: We studied 443 patients with Graves’ hyperthyroidism and slight or no ophthalmopathy who were randomly assigned to receive radioiodine, radioiodine followed by a 3-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 to 2 months for 12 months. Hypothyroidism and persistent nyperthyroiaism were promptly corrected.


RESULTS: Among the 150 patients treated with radioiodine, ophthalmopathy developed or worsened in 23 (15 percent) two to six months after treatment. The change was transient in 15 patients, but it persisted in 8 (5 percent), who subsequently required treatment for their eye disease. None of the 55 other patients in this group who had ophthalmopathy at base line had improvement in their eye disease. Among the 145 patients treated with radioiodine and prednisone, 50 (67 percent) of the 75 with ophthalmopathy at base line had improvement, and no patient had progression. The effects of radioiodine on thyroid function were similar in these two groups. Among the 148 patients treated with methimazole, 3 (2 percent) who had ophthalmopathy at base line improved, 4 (3 percent) had worsening of eye disease, and the remaining 141 had no change.

CONCLUSIONS: 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.

 

British Medical Journal. 1999 July 10; 319(7202): 68–69.
Radioiodine and thyroid eye disease.  Use with caution
 
John P Walsh, Locum lecturer

Colin M Dayan, Consultant senior lecturer

University Department of Medicine, Bristol Royal Infirmary, Bristol BS2 8HW (
Michael J Potts, Consultant ophthalmic surgeon
British Medical Journal. 1999 October 23; 319(7217): 1133.
James Ahlquistconsultant endocrinologist  editor—The relation between treatment with radioiodine and thyroid eye disease, discussed in Walsh et al’s editorial, troubles many endocrinologists and patients.1 There have been concerns that the use of radioiodine for thyrotoxicosis due to Graves’ disease may be associated with a deterioration in ophthalmopathy, raising the question of whether radioiodine is safe for patients with mild ophthalmic Graves’ disease. This question has been addressed recently by Bartalena et al, who showed that there is a small but significant risk of deterioration in mild ophthalmopathy after the use of radioiodine and that this risk may be reduced by simultaneous administration of systemic glucocorticoids.2 
Walsh et al go further and advocate that high dose prednisone, as used in Bartalena et al’s trial, should be used routinely in all patients with mild ophthalmopathy who are to receive radioiodine, to reduce the risk of deterioration in eye disease. Surely this is not yet justified. No account has been taken of the appreciable adverse effects of giving prednisone for three months (typically 30-40 mg/day for the first month and then reducing over the next two months). In Bartalena et al’s study under a tenth of patients (7/72) with mild pre-existing ophthalmopathy who received radioiodine had a deterioration that was more than transient and required treatment. 

Routine use of glucocorticoids exposes all patients who receive them to important adverse effects, while the benefit is limited to a few. Certain clinical features (for example, mild but active or progressive ophthalmopathy) are likely to mark out those who are at risk. Further studies are needed to examine this and to determine the minimum dose and duration of glucocorticoid treatment that protects against deterioration of eye disease.

At present there is a case for limiting treatment with glucocorticoids to those who have an appreciable symptomatic worsening of ophthalmopathy rather than treating all routinely. Bartalena et al did not go so far as to advocate routine glucocorticoid treatment for all patients with mild ophthalmopathy who receive radioiodine, and with good reason. Clinical trials showing that a treatment is effective are immensely useful but need to be supported by further, balanced evaluation of the risks and benefits of treatment before the original demonstration of efficacy is translated directly into routine clinical practice—a message for all clinicians, not just endocrinologists. First do no harm.