Endocrine ophthalmopathy and radioiodine therapy

Figures & data

Figure 1.  Effects of radioiodine treatment (350 MBq ¹³¹I) of TSH receptor antibody levels (TSH binding inhibition immunoglobulin, TBII) in patients with newly diagnosed Graves disease randomized to three treatment groups, I radioiodine only (n = 23), II methimazole and radioiodine (n = 17), III betamethasone (n = 20). From reference 25 with permission from J Clin Endocrinol Metab.

Table I.  Thirty consecutive patients with severe endocrine ophthalmopathy.

Region of referral: 1 million inhabitants, 5 year period
Chemosis, periorbital swelling	22/30
Diplopia	26/30
Visual acuity and/or field defect	11/30
Proptosis (mean)	right 26.0 mm
	left 26.5 mm

Note the presence of marked proptosis among the subjects, 35% of whom had optic nerve damage.

Table II.  Treatment-induced thyroid activation in 30 patients with severe endocrine ophthalmopathy.

Hypothyroid episodes (median TSH 30, range 7–78 mU/L)	(n = 16)
Radioiodine treated without documented hypothyroid episode	(n = 8)
Antithyroid drugs interrupted early with flare-up	(n = 3)
No remarkable event identified	(n = 3)
Total	(n = 30)

Table III.  Protocols for glucocorticoid-treatment of patients with eye signs subjected to radioiodine therapy.

Prednisolone (Uppsala^1)		Prednisone (Pisa^2)
20 mg	2 weeks	30 mg	1 month
15 mg	3 weeks	15 mg	2 weeks
10 mg	1 month	7.5 mg	2 weeks
7.5 mg	1 month	5 mg	2 weeks
5 mg	1 month	5 mg eod	2 weeks
5 mg eod	1 month	eod = every other day

¹ Prednisolone over a five months period, started on the third day after Rx.

² Prednisone 0.4 to 0.5 mg per kilogram of body weight tapered over three months [6].

Bartalena L, Marcocci C, Bogazzi F, Panicucci M, Lepri A, Pinchera A. Use of corticosteroids to prevent progression of Graves’ ophthalmopathy after radioiodine therapy for hyperthyroidism. N Engl J Med 1989; 321: 1349–52

 PubMed Web of Science ®Google Scholar