Abstract

We are in agreement that the most probable culprit in the etiology of DTC was the exposure to 131I-MIBG. For this reason, thyroid protection during exposure to MIBG must be optimized.
Although we could not demonstrate a lasting negative influence of chemotherapy to the thyroid gland in the past, we agree that in the future, the exact role of chemotherapy must be further elucidated. Considering the literature on NBL survivors and thyroid damage, the genetic susceptibility of these patients must be studied. Indeed, genome-wide array CGH chips might contribute to this knowledge in the future.
