Improved radiation protection of the thyroid gland with thyroxine, methimazole, and potassium iodide during diagnostic and therapeutic use of radiolabeled metaiodobenzylguanidine in children with neuroblastoma.

BACKGROUND: During radiolabeled metaiodobenzylguanidine (MIBG) administration in children with neuroblastoma, the thyroid is protected from (123/131)I uptake by potassium iodide. Despite this protection, up to 64% of patients develop thyroid dysfunction. The authors introduce a new method of radiation protection for the thyroid gland. METHODS: In a prospective cohort study, 34 children with neuroblastoma who received MIBG were given thyroxine, methimazole, and potassium iodide for protection of the thyroid gland. Protection started 1 day before the start of diagnostic 123I-MIBG and was continued until 4 weeks after the last therapeutic 131I-MIBG dose. Follow-up measurements were performed every 3 months after the protection was stopped. Visualization of the thyroid on MIBG images was reviewed by three nuclear medicine physicians. Results were compared with a historic control group of children who had received potassium iodide for thyroid protection during MIBG administration. RESULTS: After a mean follow-up of 19 months, there were 23 evaluable patients. Thyroid function was normal in 86% of survivors compared with 44% of children in the historic control group (P=0.011; Pearson chi-square test). Scintigraphic visualization of the thyroid diminished substantially after the new protection (21.5% vs. 5.3%, respectively; P=0.000). CONCLUSIONS: The results of the current study indicate that compared with potassium iodide alone, combined thyroxine, methimazole, and potassium iodide protect the thyroid more effectively against radiation damage from (123/131)I during diagnostic and therapeutic MIBG administration in children with neuroblastoma.

High incidence of thyroid dysfunction despite prophylaxis with potassium iodide during (131)I-meta-iodobenzylguanidine treatment in children with neuroblastoma.

BACKGROUND: Treatment modalities like targeted radiotherapy with (131)I-meta-iodobenzylguanidine ((131)I-MIBG) improve survival rates after neuroblastoma (NB). Radiation to the thyroid gland can lead to hypothyroidism and even malignancy. Because hypothyroidism after (131)I-MIBG treatment was reported, the current KI prophylaxis against thyroidal radiation damage was evaluated. METHODS: The incidence, pathogenesis, and consequences of thyroid dysfunction among 42 NB patients treated with (131)I-MIBG were evaluated retrospectively. Efficacy of KI prophylaxis was established by measuring thyroidal radioiodide uptake. Thyroid damage was expressed as thyrotropin elevation (TE, plasma concentration of thyroid stimulating hormone > or = 4.5 mU/L). RESULTS: The mean followup was 2.3 years (range, 0.1-8.5). The mean number of treatments with (131)I-MIBG was 3.3. Of 428 scintigrams, uptake of (131)I in the thyroid was visible in 92 (21.0%). Twenty two patients (52.4 %) presented TE after a mean period of 1.4 years (range, 0.1-5.8). Clinical signs of hypothyroidism were not observed. Eight patients received suppletion therapy with thyroxine. Thyrotropin elevation was transient in four patients. Of 25 survivors, with a mean followup of 3.5 years, 16 (64%) developed TE. No correlation was found between TE and thyroid visualization after (131)I-MIBG administration or the number of treatments. No abnormalities were seen by ultrasound imaging of the thyroid. CONCLUSIONS: Occurrence of thyroid dysfunction after treatment with (131)I-MIBG for NB is high, in spite of KI prophylaxis. Close followup of thyroid function and structure is required in patients treated with (131)I-MIBG. New ways of protecting the thyroid during exposure to radioiodine should be developed.