Primary hypothyroidism commonly occurs after
radiotherapy (RT), and coincides with increased circulating
thyroid-stimulating hormone (TSH) levels.We tested therefore the protective effect of suppressing TSH with
L-thyroxine during RT for
medulloblastoma/
PNET and
Hodgkin lymphoma (HL) in a prospective cohort study. From1998 to 2001, a total of 37 euthyroid children with
medulloblastoma/
PNET plus 14 with HL, scheduled for
craniospinal irradiation and mediastinum/neck
radiotherapy, respectively, underwent thyroid ultrasound and free
triiodothyronine (FT3), free
thyroxine (FT4), and TSH evaluation at the beginning and end of craniospinal iiradiation. From 14 days before and up to the end of
radiotherapy, patients were administered
L-thyroxine checking every 3 days TSH to ensure a value < 0.3 μIU/mL. During follow-up, blood tests and ultrasound were repeated;
primary hypothyroidism was considered an increased TSH level greater than normal range. Twenty-two/37 patients with
medulloblastoma/
PNET and all the 14 patients with HL were alive after a median 231 months from
radiotherapy with 7/22 and 8/14 having correctly reached TSH levels < 0.3 μIU/mL and well matched for other variables. Twenty years on,
hypothyroidism-free survival rates differed significantly, being 60% ± 15% and 15.6% ± 8.2% in TSH-suppressed vs. not-TSH suppressed patients, respectively (P = 0.001). These findings suggest that
hypothyroidism could be durably prevented in two populations at risk of late RT sequelae, but it should be confirmed in a larger cohort.