RESUMEN
The fetus is totally dependent in early pregnancy on maternal thyroxine for normal brain development. Adequate maternal dietary intake of iodine during pregnancy is essential for maternal thyroxine production and later for thyroid function in the fetus. If iodine insufficiency leads to inadequate production of thyroid hormones and hypothyroidism during pregnancy, then irreversible fetal brain damage can result. In the United States, the median urinary iodine (UI) was 168 microg/L in 2001-2002, well within the range of normal established by the World Health Organization (WHO), but whereas the UI of pregnant women (173 microg/L; 95% CI 75-229 microg/L) was within the range recommended by WHO (150-249 microg/L), the lower 95% CI was less than 150 microg/L. Therefore, until additional physiologic data are available to make a better judgment, the American Thyroid Association recommends that women receive 150 microg iodine supplements daily during pregnancy and lactation and that all prenatal vitamin/mineral preparations contain 150 microg of iodine.
Asunto(s)
Suplementos Dietéticos , Yodo , Lactancia/fisiología , Embarazo/fisiología , Glándula Tiroides/fisiología , Adolescente , Adulto , Canadá , Femenino , Humanos , Hipotiroidismo/fisiopatología , Hipotiroidismo/prevención & control , Necesidades Nutricionales , Complicaciones del Embarazo/fisiopatología , Sociedades Científicas , Tiroxina/biosíntesis , Estados UnidosRESUMEN
UNLABELLED: (131)I-Iodide is the treatment of choice in most cases of hyperthyroidism, with a standard 7,000-cGy (rad) thyroid absorbed dose generally resulting in an incidental blood absorbed dose of less than 10 cGy (rad). However, in approximately 15% of patients there is a small, rapidly secreted thyroid iodine pool (small-pool patients) and, based on theoretic calculations, an incidental blood absorbed dose of up to 150 cGy (rad) could result. In such small-pool patients, continuing antithyroid drugs (ATDs) at a reduced dosage during (131)I therapy should inhibit the formation of (131)I-labeled levothyroxine and triiodothyronine and thereby reduce the protein-bound (131)I-iodine concentration in blood and the blood absorbed dose. METHODS: To test this hypothesis, thyroid and blood time-activity data were measured and absorbed doses were calculated for an (131)I tracer administered to small-pool hyperthyroid patients (n = 9) not receiving ATDs (off ATDs) and then receiving ATDs (on ATDs). RESULTS: The blood absorbed dose (cGy/37 MBq [rad/mCi] administered) was reduced from 2.54 +/- 0.91 (mean +/- SD) without ATDs to 1.27 +/- 0.54 with ATDs (P < 0.0001), whereas the thyroid absorbed dose was unchanged (1,870 +/- 700 vs. 2,080 +/- 1,080). The blood absorbed dose for an administered (131)I activity required to deliver a standard prescribed absorbed dose of 7,000 cGy (rad) to the thyroid therefore was reduced by over 50% with ATDs, from 11.3 +/- 6.5 to 4.9 +/- 2.8 cGy (rad) (P < 0.001). CONCLUSION: Continued administration of ATDs during (131)I therapy thus can effectively reduce extrathyroid radiation in small-pool patients without significantly reducing the target tissue (i.e., thyroid) dose.