Abstract
This chapter discusses the physiology of iodine deficiency in pregnancy, in addition to outlining the magnitude of the problem and its assessment in clinical practice. Iodine deficiency is still a major public health concern in the world, although substantial progress in the household use of iodized salt has been achieved in the past decade. Even mild iodine deficiency results in suboptimal psychomotor performance in childhood. Iodine deficiency is of critical importance in the pregnant woman, because it results in lowering of maternal thyroxine levels leading to less thyroxine availability for the developing fetus. Adequate maternal thyroxine concentration is essential for fetal nervous system maturation. Assessment of iodine deficiency in pregnancy is obtained by the evaluation of urinary iodine excretion, although there is a debate about iodine loss in early pregnancy. Acute iodine supplementation is by oral potassium iodide or iodized oil. Long-term iodization is optimally achieved by iodized salt. The WHO estimates that 740 million people are presently affected by goiter. However, it is estimated that 68% of the populations of affected countries currently have access to iodized salt, compared to 10% a decade ago. In addition to iodization programs, iodine supplementation to appropriate groups of pregnant women should be considered in iodine-deficient areas until the iodization programs have ensured adequate ambient iodine concentrations.
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