Abstract
During pregnancy the thyroid is subjected to increased demands which results in: 1. increase of the serum total T4 and T3 and of the TGB; 2. decrease of the serum free T4 and T3; 3. increased nuclear capacity of binding for T4; 4. signs of increased TRH-TSH response; 5. increased thyroid uptake of radioiodine; 6. lowering of inorganic plasma iodine; 7. increase of the renal clearance of iodine [Aboul-Khair et al. 1965; Beckers 1991, Burrow 1980; Crooks et al. 1967, Gent et al. 1982; Glinoer et al. 1990; Kvetny et al. 1984; Weeke et al. 1982]. In this phase of increased endocrine demand the iodine metabolism is characterized by the tendency to develop an endogenous iodine deficiency (ID). The causes are supposedly: 1. increased demand of iodine of the mother and the fetus; 2. enlarged extracellular space; 3. increased renal iodine clearance from the second trimester to the week 6th post partum and renal excretion of iodine. So far the increased renal excretion of iodine was considered as an essential factor causing ID during pregnancy [Cassano et al. 1960; Aboul-Khair et al. 1965; Hoff et al. 1982;]. Since under the conditions of alimentary ID the effect of endogenous and exogenous ID are combined all investigations of the thyroidal status during pregnancy must be carried out and interpreted in relation to the actual supply of iodine.
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Bauch, K. et al. (1993). Goitre in Pregnancy in Germany. In: Delange, F., Dunn, J.T., Glinoer, D. (eds) Iodine Deficiency in Europe. NATO ASI Series, vol 241. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1245-9_22
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