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Letter to the editor |
University of Insubria (L.B.), Varese, Italy; and University of Pisa (F.B., A.P., E.M.), Pisa, Italy
Address correspondence to: Prof. Luigi Bartalena, Department of Clinical Medicine, University of Insubria, Division of Endocrinology, Ospedale di Circolo, Viale Borri, 57, 21100 Varese, Italy. E-mail: l.bartalena{at}libero.it or luigi.bartalena{at}uninsubria.it.
To the editor:
We read with great interest the paper by Bonnema et al. published in a recent issue of the Journal of Clinical Endocrinology and Metabolism (1). This randomized clinical trial showed that the efficacy of radioiodine (RAI) therapy for hyperthyroidism was reduced when RAI was administered after pretreatment with propylthiouracil (PTU) (1). Although the results of Bonnema et al. are convincing, this effect might be specific for PTU. In fact, two well-designed, prospective, randomized trials (2, 3) failed to show any consequence of methimazole (MMI) pretreatment on the efficacy of RAI therapy. This difference might be related to the longer radioprotective effect of PTU. Because data of the literature and our own experience indicated that MMI pretreatment does not affect successful management of hyperthyroidism by RAI therapy, we treat all hyperthyroid patients with MMI for 2–3 months before RAI administration to restore euthyroidism and to deplete intrathyroidal iodine stores (4). In our opinion, this approach is particularly important in patients who are old or have underlying nonthyroidal illness. In addition, prompt correction of hyperthyroidism is required in Graves’ patients with associated orbitopathy, because restoration of euthyroidism is associated with a more favorable course of eye disease (5).
In the paper by Bonnema et al. (1), as well as in a previous report by Burch et al. (6), RAI therapy was not followed by an increase in serum thyroid hormone concentrations. However, because thyroid function was evaluated 3 wk after RAI therapy (1), early and transient changes in serum thyroid hormone levels might have been missed. In addition, the results of Bonnema et al. clearly showed that, when RAI therapy was given, serum thyroid hormone concentrations were markedly higher in nonpretreated patients than in pretreated patients (1). Thus, although the interval between randomization and RAI therapy was not specified, nonpretreated patients were presumably exposed to a longer period of uncontrolled hyperthyroidism than patients receiving thionamide pretreatment. As we mentioned earlier, we believe that this is not acceptable in patients whose hyperthyroidism represents a threatening condition and must be promptly and effectively controlled. Many thyroidologists are concerned about the consequences of subclinical hyperthyroidism; in our opinion, we should worry even more about the potential untoward effects of overt hyperthyroidism. In this regard, we recently demonstrated that lithium administration for a few days before RAI therapy and for 2 wk thereafter can effectively prevent the increase in serum thyroid hormone concentrations that follows RAI administration and/or MMI withdrawal before RAI therapy (7). Lithium adjuvant therapy was also associated with a prompter goiter shrinkage after RAI therapy (7).
In conclusion: 1) the study by Bonnema et al. (1) demonstrated that PTU pretreatment is associated with a lower efficacy of RAI therapy, but MMI does not seem to share this effect; accordingly, we support the view that MMI pretreatment should be given for a better control of hyperthyroidism before RAI therapy; 2) uncontrolled hyperthyroidism is an unacceptable and potentially dangerous situation that requires a more aggressive approach, particularly in at-risk patients; and 3) a short course of lithium adjuvant therapy, shortly before and after RAI therapy, is helpful to prevent the increase in serum thyroid hormone concentrations related to RAI therapy and/or thionamide withdrawal, to obtain a prompter control of hyperthyroidism, and to achieve a more rapid shrinkage of goiter.
Received October 11, 2004.
References
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