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Calcitonin Deficiency after Radioactive Iodine Treatment

J. J. Body, MD; N. Demeester-Mirkine, MD; and J. Corvilain, MD
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Grant Support. Partial support by a grant from the Fondation Lefèvre of Belgium.

Requests for Reprints: J. J. Body, MD, Service de Médecine, Unité d'Endocrinologie, Institut Jules Bordet, 1 rue Héger-Bordet, 1000 Bruxelles, Belgium.

Current Author Addresses: Dr. Body: Unité d'Endocrinologie, Institut Jules Bordet, 1000 Bruxelles, Belgium.

Drs. Demeester-Mirkine and Corvilain: Service de Médecine, Hôpital Universitaire Brugmann, Bruxelles, Belgium.

Ann Intern Med. 1988;109(7):590-591. doi:10.7326/0003-4819-109-7-590
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This excerpt has been provided in the absence of an abstract.

Because 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 conventional 131I 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


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