Hypothyroidism after 131 I‐monoclonal antibody treatment of neuroblastoma

• Published in: Pediatric blood & cancer Vol. 55; no. 1; pp. 76 - 80
• Main Authors: Bhandari, Sonal, Cheung, Nai‐Kong V., Kushner, Brian H., Kramer, Kim, Modak, Shakeel, Larson, Steven M., Yeh, Samuel, Heller, Glenn, Sklar, Charles A.
• Format: Journal Article
• Language: English
• Published: 15.07.2010
• ISSN: 1545-5009; 1545-5017
• DOI: 10.1002/pbc.22452

Abstract Background To determine the prevalence of and risk factors for primary hypothyroidism following treatment with a radiolabeled monoclonal antibody ( 131 I‐3F8) in children with neuroblastoma. Procedure In the current study, we assessed thyroid function in 51 neuroblastoma patients who survived for ≥3 months after treatment with 131 I‐3F8 (a murine IgG3 monoclonal antibody that reacts with the ganglioside GD2) at 4 mCi/kg/day × 5 days (total 20 mCi/kg). Prior therapy in all subjects included dose‐intensive chemotherapy; 13 subjects also received external beam radiation to the neck. Oral iodide and liothyronine sodium (T3) were administered for protection of the thyroid gland. Results Thirty‐two of 51 subjects (63%) developed hormonal evidence of primary hypothyroidism. The median time to hypothyroidism after treatment with 131 I‐3F8 was 6.4 months. The probability of developing hypothyroidism was 56% at 2 years following treatment with 131 I‐3F8. There was evidence for an association between thyroidal uptake of 131 I and development of hypothyroidism (hazard ratio 1.83, 95% confidence interval 0.91–3.30; P  = 0.09). Conclusions We conclude that hormonal evidence of primary hypothyroidism developed in a majority of subjects treated with 131 I‐3F8, despite pretreatment with oral iodide plus liothyronine sodium. Alternative strategies for thyroid gland protection are needed. Pediatr Blood Cancer 2010;55:76–80. © 2010 Wiley‐Liss, Inc.