مقایسه دفع ادراری ید در خانم های حامله همراه با گواتر و خانم های حامله بدون گواتر و نوزادانشان

Iodine availability for the maternal thyroid is reduced during pregnancy as a result of the loss of the nutrient by increased renal clearance, and competition by the fetoplacental unit. So with a marginal iodine intake, pregnancy constitutes a stimulus for both the maternal and fetal thyroids. On the other hand, iodine deficiency in the first trimester of pregnancy results in impaired development of the central nervous system, lack of T4 then results in smaller brain size associated with fewer neurons which are also shorter in length. This cross-sectional study was undertaken to evaluate pregnant women and their newborns, these two susceptible groups to IDD in an endemic area such as Shiraz. Urinary excretion of iodine as iodine (µg/dl)/creatinine (gr) ratios in two groups of pregnant women, one group without goiter (52.88%) and the other with goiter (grade Ib and II 47.2%) and their newborns were compared. There was no significant difference in urinary excretion of iodine in mothers and newborns of the 2 groups. In all newborns even in those of mothers excreting <50 mg iodine/gr creatinine, there was a significantly greater excretion of iodine probably due to increased renal clearance of iodine by the immature kidney, and their excretion of iodine was not parallel to those of mothers. There was no significant difference between weight, height and head circumference of the two groups of newborns. It is concluded that iodine excretion in neonates can not be used as an indicator of iodine deficiency disorder. In iodine deficient areas pregnancy justifies monitoring thyroid function and volume and therapeutic intervention to avoid hypothyroxinemia and goiterogenesis in both mother and newborn. Likewise neonatal thyroid screening constitutes a valuable and sensitive index for detecting the presence of iodine deficiency.