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Thyroid and hepatic function after high‐dose 131 I‐metaiodobenzylguanidine ( 131 I‐MIBG) therapy for neuroblastoma
Author(s) -
Quach Alekist,
Ji Lingyun,
Mishra Vikash,
Sznewajs Aimee,
Veatch Janet,
Huberty John,
Franc Benjamin,
Sposto Richard,
Groshen Susan,
Wei Denice,
Fitzgerald Paul,
Maris John M.,
Yanik Gregory,
Hawkins Randall A.,
Villablanca Judith G.,
Matthay Katherine K.
Publication year - 2011
Publication title -
pediatric blood and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.116
H-Index - 105
eISSN - 1545-5017
pISSN - 1545-5009
DOI - 10.1002/pbc.22767
Subject(s) - medicine , neuroblastoma , thyroid , toxicity , thyroid function , gastroenterology , liver function , asymptomatic , radiation therapy , thyroid function tests , genetics , biology , cell culture
Background 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. Procedure 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. Results 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. Conclusion 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. Pediatr Blood Cancer 2011;56:191–201. © 2010 Wiley‐Liss, Inc.