Smyth P P
Endocrine Laboratory, Department of Medicine and Therapeutics, University College Dublin, Ireland.
Thyroid. 1999 Jul;9(7):637-42. doi: 10.1089/thy.1999.9.637.
Reports in the literature are divided on changes in thyroid volume and urinary iodine excretion (UI) during normal pregnancy. Reports from Ireland, an area of modest dietary iodine intake (median UI 70 microg/L) showed an increase in UI that rose to a median value of 135 microg/L in the first trimester (T1) and continued at 124 microg/L in the second (T2) and 122 microg/L in the third trimester (T3). In parallel with the increase in UI, mean ultrasound measured thyroid volume increased by a maximum of 47% over nonpregnant values in the third trimester (T3). Although these findings were consistent with studies in Cardiff, UK (median UI 73 microg/L), which also showed a pregnancy-associated rise in UI excretion (maximum 176 microg/L) accompanied by a 30% increase in median thyroid volume, they differed from findings in Sri Lanka (median UI 146 microg/L), a country in which a successful program of salt iodination has recently been implemented, which showed no significant changes in UI excretion (T3 maximum 154 microg/L) but did show a modest (20%) maximum increase in median thyroid volume at T3. Prospective studies on Irish subjects showed that median UI fell precipitously to nonpregnant control values (76 microg/L) at delivery. In addition, UI in neonates sampled at 3-days postdelivery showed that excretion was greater in breast-fed than in bottle fed infants. Differences in reported UI excretion patterns during pregnancy may may reflect the existence of a threshold above which increased renal clearance results in increased iodine loss but that is masked at higher iodine intakes. Assuming constant dietary iodine intake during pregnancy, any increased urine loss will inevitably lead to negative iodine balance and thyroid depletion. In these circumstances, increased thyroid volume may in part be a compensatory mechanism to allow for greater iodine storage.
文献报道对于正常孕期甲状腺体积和尿碘排泄(UI)的变化存在分歧。爱尔兰是一个膳食碘摄入量适中的地区(尿碘中位数为70微克/升),其报告显示尿碘排泄增加,在孕早期(T1)升至中位数135微克/升,并在孕中期(T2)持续为124微克/升,在孕晚期(T3)为122微克/升。与尿碘排泄增加同时,超声测量的甲状腺平均体积在孕晚期(T3)比非孕期值最大增加了47%。尽管这些发现与英国加的夫的研究结果一致(尿碘中位数为73微克/升),该研究也显示孕期尿碘排泄增加(最大值为176微克/升),同时甲状腺中位数体积增加了30%,但它们与斯里兰卡的研究结果不同(尿碘中位数为146微克/升),该国最近实施了一项成功的食盐碘化计划,该研究显示尿碘排泄无显著变化(T3最大值为154微克/升),但在T3时甲状腺中位数体积确实有适度的(20%)最大增加。对爱尔兰受试者的前瞻性研究表明,分娩时尿碘中位数急剧降至非孕期对照值(76微克/升)。此外,分娩后3天采集的新生儿尿碘显示,母乳喂养婴儿的排泄量高于人工喂养婴儿。孕期报告的尿碘排泄模式差异可能反映了存在一个阈值,高于该阈值时肾清除率增加会导致碘流失增加,但在碘摄入量较高时会被掩盖。假设孕期膳食碘摄入量恒定,任何尿碘流失增加都将不可避免地导致碘负平衡和甲状腺耗竭。在这种情况下,甲状腺体积增加可能部分是一种补偿机制,以允许更多的碘储存。