Brief Reports1 October 1988Calcitonin Deficiency after Radioactive Iodine TreatmentJ. J. Body, MD, N. Demeester-Mirkine, MD, J. Corvilain, MDJ. J. Body, MDSearch for more papers by this author, N. Demeester-Mirkine, MDSearch for more papers by this author, J. Corvilain, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-109-7-590 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptBecause the long-feared carcinogenic and genetic hazards of radioactive iodine (131I) have been refuted (1), many authors now consider this therapy the treatment of choice for patients with toxic multinodular goiter and for most patients with Graves disease. Moreover, the use of ablative doses was recently recommended to correct hyperthyroidism rapidly and to cause hypothyroidism predictably, contrasting with the delayed and unpredictable occurrence of hypothyroidism after conventional131I treatment (2). Intrathyroidal C cells do not trap radioactive iodine but could be damaged indirectly due to their contiguity to follicular cells, as suggested by some reports (3) of an antitumoral effect...