TY - JOUR

T1 - Thyroglobulin in smoking mothers and their newborns at delivery suggests autoregulation of placental iodide transport overcoming thiocyanate inhibition

AU - Andersen, Stine Linding

AU - Nøhr, Susanne Backman

AU - Wu, Chunsen

AU - Olsen, Jørn

AU - Pedersen, Klaus Michael

AU - Laurberg, Peter

PY - 2013/4

Y1 - 2013/4

N2 - BACKGROUND: Placental transport of iodide is required for fetal thyroid hormone production. The sodium iodide symporter (NIS) mediates active iodide transport into the thyroid and the lactating mammary gland, and is also present in placenta. NIS is competitively inhibited by thiocyanate from maternal smoking, but compensatory autoregulation of iodide transport differs between organs. The extent of autoregulation of placental iodide transport remains to be clarified. OBJECTIVE: To compare the impact of maternal smoking on thyroglobulin (Tg) levels in maternal serum at delivery and in cord serum as markers of maternal and fetal iodine deficiency. METHODS: 140 healthy, pregnant women admitted for delivery and their newborns were studied before the iodine fortification of salt in Denmark. Cotinine in urine and serum classified mothers as smokers (n=50) or non-smokers (n=90). The pregnant women reported on intake of iodine containing supplements during pregnancy and Tg in maternal serum at delivery and in cord serum was analyzed. RESULTS: In a context of mild to moderate iodine deficiency, smoking mothers had significantly higher serum Tg than non-smoking mothers (mean Tg smokers 40.2 vs. non-smokers 24.4 μg/l, p = 0.004) and so had their respective newborns (cord Tg 80.2 vs. 52.4 μg/l, p = 0.006), but the ratio between Tg in cord serum and maternal serum was not significantly different in smokers compared with non-smokers (smoking 2.06 vs. non-smoking 2.22, p = 0.69). CONCLUSION: Maternal smoking increased the degree of iodine deficiency in parallel in the mother and the fetus, as reflected by increased Tg levels. However, placental iodide transport seemed unaffected despite high thiocyanate levels, suggesting that thiocyanate-insensitive iodide transporters alternative to NIS are active or that NIS in the placenta is autoregulated to keep iodide transport unaltered.

AB - BACKGROUND: Placental transport of iodide is required for fetal thyroid hormone production. The sodium iodide symporter (NIS) mediates active iodide transport into the thyroid and the lactating mammary gland, and is also present in placenta. NIS is competitively inhibited by thiocyanate from maternal smoking, but compensatory autoregulation of iodide transport differs between organs. The extent of autoregulation of placental iodide transport remains to be clarified. OBJECTIVE: To compare the impact of maternal smoking on thyroglobulin (Tg) levels in maternal serum at delivery and in cord serum as markers of maternal and fetal iodine deficiency. METHODS: 140 healthy, pregnant women admitted for delivery and their newborns were studied before the iodine fortification of salt in Denmark. Cotinine in urine and serum classified mothers as smokers (n=50) or non-smokers (n=90). The pregnant women reported on intake of iodine containing supplements during pregnancy and Tg in maternal serum at delivery and in cord serum was analyzed. RESULTS: In a context of mild to moderate iodine deficiency, smoking mothers had significantly higher serum Tg than non-smoking mothers (mean Tg smokers 40.2 vs. non-smokers 24.4 μg/l, p = 0.004) and so had their respective newborns (cord Tg 80.2 vs. 52.4 μg/l, p = 0.006), but the ratio between Tg in cord serum and maternal serum was not significantly different in smokers compared with non-smokers (smoking 2.06 vs. non-smoking 2.22, p = 0.69). CONCLUSION: Maternal smoking increased the degree of iodine deficiency in parallel in the mother and the fetus, as reflected by increased Tg levels. However, placental iodide transport seemed unaffected despite high thiocyanate levels, suggesting that thiocyanate-insensitive iodide transporters alternative to NIS are active or that NIS in the placenta is autoregulated to keep iodide transport unaltered.

U2 - 10.1530/EJE-12-0759

DO - 10.1530/EJE-12-0759

M3 - Journal article

C2 - 23444413

VL - 168

SP - 723

EP - 731

JO - European Journal of Endocrinology

JF - European Journal of Endocrinology

SN - 0804-4643

IS - 5

ER -