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Hypothyroidism after treatment of metastatic neuroblastoma

To the Editor: With great interest we read the report by Bhandari et al. [1] on hypothyroidism after 131I-monoclonal antibody treatment of neuroblastoma. Thirty-two of 51 treated subjects (63%) developed primary hypothyroidism despite pretreatment with oral iodide plus liothyronine sodium, and the authors conclude that there was evidence for an association between thyroidal uptake of 131I and development of hypothyroidism. Since hypothyroidism after multimodal treatment of neuroblastoma might be caused also by different other mechanisms including radiotherapy with 131I-MIBG [2] and/or busulfan based high-dose chemotherapy [3] we would like to report on our 25 years of experience with thyroid function in children surviving neuroblastoma stage IV. Between 1984 and 2009, 34 patients were diagnosed with metastatic neuroblastoma at our institution. Treatment was given according to the current protocols including preoperative chemotherapy, surgery, high-dose chemotherapy followed by autologous stem cell transplantation and occasionally 131I-MIBG therapy. Before and during 131I-MIBG therapy and diagnostic MIBG scans, all patients received 15 drops (750 mg) orally/day of saturated solution of potassium iodide for protection of the thyroid gland. None of the patients received external beam radiation to the neck region. There were 16 long-term survivors (5 females, 11 males) with a median follow-up of 5.7 years (range 1.1–25.2 years). Thyroid function was assessed by measuring TSH values every 6 months during the first 3 years of followup and then annually. Ten of the 16 patients (62.5%) developed primary hypothyroidism with a median TSH value of 6.84 U/L (range 4.24–16.2 U/L). Patient characteristics and treatment of 16 long-term survivors of neuroblastoma IV with hypothyroidism (n = 10) and normal thyroid function (n = 6) are shown in Table I. In the group with hypothyroidism, 5/10 patients were conditioned with a busulfan-based regimen and 3/10 patients additionally received 131I-MIBG therapy. In contrast, in the group with normal thyroid function only 1 patient received busulfan and none 131IMIBG therapy. Interestingly, 5/10 patients with hypothyroidism neither received busulfan nor 131I-MIBG therapy. We agree with Bhandari et al. that hypothyroidism is a major problem for children surviving metastatic neuroblastoma and that investigators should be aware of this late effect during long-term care of these patients. However, hypothyroidism can be caused not only by treatment with 131I-monoclonal antibody but also by different other mechanisms including busulfan, 131I-MIBG therapy, external beam radiation to the neck or even currently unknown mechanisms.