Endocrine 18321 Thyroid Function

Primary hypothyroidism is a common late effect observed in cancer survivors who received head and neck radiation (Kaplan et al. 1983; Halperin et al. 1999). The occurrence of thyroid dysfunction is related, primarily, to the dose of radiotherapy administered but is also influenced by the age and gender of the patient and the time elapsed since the end of treatment (Sklar et al. 2000).

A higher incidence of clinically significant hy-pothyroidism is observed above radiation doses of 2000 cGy (Kaplan et al. 1983; Constine et al. 1984).

Current radiotherapy doses used for local control in high-risk neuroblastoma patients with thoracic or cervical tumors are often in this range (Halperin et al. 1999; Kushner et al. 2001). Patients who received total-body irradiation (TBI) are also at risk for hypothyroidism (Ogilvy-Stuart et al. 1992). The radiation-related risk persists more than 25 years after treatment (Hancock et al. 1991; Sklar et al. 2000). The addition of chemotherapy to radiation therapy does not seem to increase the risk of hypothyroidism (Van Santen et al. 2003).

Many cases of subclinical primary hypothy-roidism have been described in neuroblastoma patients following the administration of 131I-metaiodo-benzylguanidine (131 I-MIBG; Garaventa et al. 1991; Picco et al. 1993; Picco et al. 1995; Van Santen et al. 2002). The reported incidence is 50-80% despite thyroid protection with high doses of potassium iodide before, during, and after the 131I-MIBG (Picco et al. 1995; Van Santen et al. 2002). Optimal prophylaxis against the thyroidal damage induced by radio-iodi-nated substances is still unknown (Van Santen et al. 2002).

In our cohort, 23 % of the patients developed primary hypothyroidism. Of these patients, 66% received 131I-3F8 antibody (despite protection with potassium iodide and thyroid hormone suppression) and 33% received chest/mantle external-beam radiation therapy.

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