Glinoer D
Université Libre de Bruxelles, University Hospital Saint-Pierre, Department of Internal Medicine/Endocrinology, Thyroid Investigation Clinic 322, Rue Haute, B-1000 Brussels/Belgium.
Ann Endocrinol (Paris). 2003 Feb;64(1):37-44.
The main changes in thyroid function associated with the pregnant state are increased thyroid hormone requirements. These increased requirements can only be met by a proportional increase in hormone production, that directly depends upon the availability of dietary iodine. When the iodine intake is adequate, normal "physiological" adaptation takes place. When the intake is restricted, physiological adaptation is progressively replaced by pathological alterations, in parallel with the degree of iodine deprivation, leading to excessive glandular stimulation, hypothyroxinemia, and goiter formation. Thus, pregnancy acts typically as a revelator of underlying iodine restriction and gestation results in an iodine deficient status, even in conditions with only a moderately restricted iodine intake, characteristic of many European regions. Iodine deficiency during pregnancy has important repercussions for both mother and fetus, namely thyroid underfunction and goitrogenesis. Furthermore, iodine deficiency may be associated with alterations of the psychoneuro-intellectual outcome in the progeny. The risk of an abnormal progeny's development is further enhanced because mother and offspring are exposed to iodine deficiency, both during gestation and the postnatal period. Because iodine deficiency is still prevalent in many European regions and remains a subject of great concern, investigators have proposed, since several years, that iodine prophylaxis be introduced systematically during pregnancy, in order to provide mothers with an adequate iodine supply. In areas with a severe iodine deficiency, correcting the iodine lack has proved highly beneficial to prevent mental deficiency disorders. The many actions undertaken to eradicate severe iodine deficiency have allowed to prevent the occurrence of mental retardation in millions young infants throughout the world. In most public health programmes dealing with the correction of iodine deficiency disorders, iodized salt has been used as the preferred strategy in order to convey the iodine supplements to the household. Iodized salt, however, is not the ideal vector in the specific instance of pregnancy (or breastfeeding) or in young infants, because of the necessity to limit salt intake. Hence, particular attention is required in our countries to ensure that pregnant women have an adequate iodine intake, by administering multi-vitamin tablets containing iodide supplements (+125 micro g/d). Finally, it is with some concern that the results of a recent nutritional survey in the USA have disclosed that iodine deficiency, long thought to have been eradicated since many years, may actually show a resurgence, particularly in women in the child-bearing period. This issue needs to be considered seriously by the medical community and public health authorities.
与妊娠状态相关的甲状腺功能的主要变化是甲状腺激素需求增加。这些增加的需求只能通过激素产生的相应增加来满足,而激素产生的增加直接取决于膳食碘的供应。当碘摄入量充足时,会发生正常的“生理”适应。当摄入量受限,生理适应会逐渐被病理改变所取代,这与碘缺乏的程度平行,导致腺体过度刺激、甲状腺素血症和甲状腺肿形成。因此,妊娠通常是潜在碘缺乏的揭示因素,即使在许多欧洲地区仅存在适度碘摄入受限的情况下,妊娠也会导致碘缺乏状态。孕期碘缺乏对母亲和胎儿都有重要影响,即甲状腺功能减退和甲状腺肿形成。此外,碘缺乏可能与后代心理神经智力发育的改变有关。由于母亲和后代在妊娠期和产后都暴露于碘缺乏环境中,异常后代发育的风险进一步增加。由于碘缺乏在许多欧洲地区仍然普遍存在且仍然是一个备受关注的问题,多年来研究人员一直提议在孕期系统地引入碘预防措施,以便为母亲提供充足的碘供应。在碘严重缺乏的地区,纠正碘缺乏已被证明对预防智力缺陷障碍非常有益。为消除严重碘缺乏所采取的诸多行动已在全世界范围内预防了数百万幼儿智力发育迟缓的发生。在大多数应对碘缺乏障碍纠正的公共卫生项目中,加碘盐一直被用作首选策略,以便将碘补充剂输送到家庭。然而,在妊娠(或哺乳)的特定情况下或对于幼儿来说,加碘盐并不是理想的载体,因为有必要限制盐的摄入量。因此,在我们国家需要特别关注,通过给予含有碘补充剂(+125微克/天)的多种维生素片来确保孕妇有充足的碘摄入。最后,令人有些担忧的是,美国最近一项营养调查的结果显示,长期以来被认为已消除多年的碘缺乏实际上可能正在卷土重来,尤其是在育龄妇女中。这个问题需要医学界和公共卫生当局认真考虑。