Thyroid and Hepatic Function After High-Dose I-131-Metaiodobenzylguanidine (I-131-MIBG) Therapy for Neuroblastoma PEDIATRIC BLOOD & CANCER Quach, A., Ji, L., Mishra, V., Sznewajs, A., Veatch, J., Huberty, J., Franc, B., Sposto, R., Groshen, S., Wei, D., Fitzgerald, P., Maris, J. M., Yanik, G., Hawkins, R. A., Villablanca, J. G., Matthay, K. K. 2011; 56 (2): 191–201


(131) I-Metaiodobenzylguanidine ((131) I-MIBG) provides targeted radiotherapy for children with neuroblastoma, a malignancy of the sympathetic nervous system. Dissociated radioactive iodide may concentrate in the thyroid, and (131) I-MIBG is concentrated in the liver after (131) I-MIBG therapy. The aim of our study was to analyze the effects of (131) I-MIBG therapy on thyroid and liver function.Pre- and post-therapy thyroid and liver functions were reviewed in a total of 194 neuroblastoma patients treated with (131) I-MIBG therapy. The cumulative incidence over time was estimated for both thyroid and liver toxicities. The relationship to cumulative dose/kg, number of treatments, time from treatment to follow-up, sex, and patient age was examined.In patients who presented with Grade 0 or 1 thyroid toxicity at baseline, 12? ± ?4% experienced onset of or worsening to Grade 2 hypothyroidism and one patient developed Grade 2 hyperthyroidism by 2 years after (131) I-MIBG therapy. At 2 years post-(131) I-MIBG therapy, 76? ± ?4% patients experienced onset or worsening of hepatic toxicity to any grade, and 23? ± ?5% experienced onset of or worsening to Grade 3 or 4 liver toxicity. Liver toxicity was usually transient asymptomatic transaminase elevation, frequently confounded by disease progression and other therapies.The prophylactic regimen of potassium iodide and potassium perchlorate with (131) I-MIBG therapy resulted in a low rate of significant hypothyroidism. Liver abnormalities following (131) I-MIBG therapy were primarily reversible and did not result in late toxicity. (131) I-MIBG therapy is a promising treatment for children with relapsed neuroblastoma with a relatively low rate of symptomatic thyroid or hepatic dysfunction.

View details for DOI 10.1002/pbc.22767

View details for Web of Science ID 000286017500005

View details for PubMedID 20830775

View details for PubMedCentralID PMC3006009