Jones D W
Proc R Soc Med. 1928 May;21(7):1217-30. doi: 10.1177/003591572802100729.
Simple goitre is highly prevalent in New Zealand, and there is considerable incidence of toxic goitre. The aetiology of simple goitre seems fairly well established, and an attempt is being made to apply the data from simple goitre to the problems of toxic goitre.Endemic goitre is of great antiquity among the Maoris, and has been described among Europeans for about fifty years. It occurs in both men and animals. At five years its incidence is similar in boys and girls, later it decreases in boys but increases greatly in girls. It is often hereditary, and many children are born goitrous. In children it is generally small, but may enlarge and cause pressure, myxoedema and toxicity. Its incidence varies greatly in different districts.The only cause found consistent with this variation in distribution is lack of iodine in the soil. An inverse ratio has been demonstrated between the iodine content of the soil and the incidence of goitre in school children in thirty-three districts. The iodine content of the soil is reflected in the food raised upon it.The daily iodine intake was estimated at 35 microgrammes in a non-goitrous, and at 20 microgrammes in a goitrous district.The amount of iodine involved is infinitesimal, and its intake can be ensured by the use of salt for ordinary consumption, which contains four parts per million of potassium iodide.TOXIC GOITRE IS ALSO FREQUENT: in this connexion, the influence of iodine on the thyroid has been investigated. If starved of iodine the thyroid adapts itself either by increasing its colloid or by a diffuse hyperplasia, both may occur in different parts of the same gland. Simple goitre is the response of the healthy thyroid to iodine deficiency, the responding areas may be diffuse or adenomatous, and degenerations may occur. Such goitres may be treated with iodine, in children re-adjustment to the increased intake is readily made, but in adults long accustomed to a low intake, excess often causes too great hormone production, with toxic symptoms, hence the minimal dose alone is permissible in iodized salt.Goitre stored with iodine at low pressures may become toxic under stress, and this may be precipitated by iodine. The prevalence of toxic goitre may be partly due to the prescription of iodides in therapeutic doses for common ailments.Diffuse colloid goitre may subside under physiological iodine, the adenomatous is more prone to toxic symptoms and may go on to secondary Graves' disease or to myxoedema. Diffuse hyperplasia is a possible manifestation of iodine deficiency as primary Graves' disease. Lugol's solution probably allows of a temporary storage in this condition. Iodine has certainly some bearing on the problems of toxic goitre.
单纯性甲状腺肿在新西兰极为常见，毒性甲状腺肿的发病率也相当高。单纯性甲状腺肿的病因似乎已相当明确，人们正尝试将单纯性甲状腺肿的数据应用于毒性甲状腺肿的问题研究中。地方性甲状腺肿在毛利人中由来已久，在欧洲人中也有大约五十年的记载。它在人和动物中都有发生。五岁时，男孩和女孩的发病率相似，之后男孩的发病率下降，而女孩的发病率大幅上升。它常常具有遗传性，许多孩子出生时就患有甲状腺肿。儿童的甲状腺肿通常较小，但可能会增大并导致压迫、黏液性水肿和毒性反应。其发病率在不同地区差异很大。唯一与这种分布差异相符的原因是土壤中缺碘。在33个地区，已证明土壤中的碘含量与学童甲状腺肿的发病率呈反比。土壤中的碘含量反映在其上种植的食物中。在非甲状腺肿流行地区，估计每日碘摄入量为35微克，而在甲状腺肿流行地区为20微克。所需的碘量极少，通过食用含百万分之四碘化钾的普通食盐即可确保碘的摄入。毒性甲状腺肿也很常见：在这方面，已对碘对甲状腺的影响进行了研究。如果缺乏碘，甲状腺会通过增加其胶体或弥漫性增生来进行自我调节，这两种情况可能会在同一腺体的不同部位同时出现。单纯性甲状腺肿是健康甲状腺对碘缺乏的反应，反应区域可能是弥漫性的或腺瘤性的，并且可能会发生退化。这种甲状腺肿可用碘治疗，儿童很容易适应增加的碘摄入量，但成年人长期习惯于低碘摄入，过量碘往往会导致激素分泌过多，出现毒性症状，因此加碘盐中只允许使用最小剂量的碘。在低压下储存碘的甲状腺肿在压力下可能会变得有毒，这可能由碘引发。毒性甲状腺肿的流行可能部分归因于为常见疾病开出治疗剂量的碘化物。弥漫性胶体甲状腺肿在生理碘水平下可能会消退，腺瘤性甲状腺肿更容易出现毒性症状，可能会发展为继发性格雷夫斯病或黏液性水肿。弥漫性增生可能是原发性格雷夫斯病碘缺乏的一种表现形式。卢戈氏溶液可能会在这种情况下允许暂时储存。碘肯定与毒性甲状腺肿的问题有关。
