title: Thyroglobulin in smoking mothers and their newborns at delivery suggests autoregulation of placental iodide transport overcoming thiocyanate inhibition.
abstract: 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
  One hundred and forty 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 nonsmokers (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 were analyzed.
  
  
  RESULTS
  In a context of mild-to-moderate iodine deficiency, smoking mothers had significantly higher serum Tg than nonsmoking mothers (mean Tg smokers 40.2 vs nonsmokers 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 nonsmokers (smoking 2.06 vs nonsmoking 2.22, P=0.69).
  
  
  CONCLUSIONS
  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.
authors: Department of Endocrinology, Aalborg University Hospital, Aalborg, Denmark. stine.a@rn.dk
authors: Stine L
authors: SL
authors: Andersen
authors: Susanne B
authors: SB
authors: Nøhr
authors: Chun S
authors: CS
authors: Wu
authors: Jørn
authors: J
authors: Olsen
authors: Klaus M
authors: KM
authors: Pedersen
authors: Peter
authors: P
authors: Laurberg
mesh_terms: D000328:Adult; D003430:Cross-Sectional Studies; D036861:Delivery, Obstetric; D003718:Denmark; D005260:Female; D005312:Fetal Blood / Q000378:metabolism*; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D007231:Infant, Newborn; D007455:Iodine / Q000172:deficiency*; D008297:Male; D008431:Maternal-Fetal Exchange; D011247:Pregnancy; D012907:Smoking; D013954:Thyroglobulin / Q000097:blood*
chemical_list: D013954:Thyroglobulin; D007455:Iodine