Goslings B M, Djokomoeljanto R, Docter R, van Hardeveld C, Hennemann G, Smeenk D, Querido A
J Clin Endocrinol Metab. 1977 Mar;44(3):481-90. doi: 10.1210/jcem-44-3-481.
In an area of severe endemic goiter in Central Java, Indonesia, clinical overt or mild hypothyroidism appeared to be present in 7 out of 20 cretins and also in 12 out of 94 non-cretinous subjects, all 5-20 years of age, living in the village of Sengi. Hypothyroidism was not found in a control group of 70 subjects of the same age living in Londjong just outside the edemia. In hypothyroid subjects the plasma PBI-concentration was 0.98+/-0.32 mug/100 ml (mean+/-SD) vs. 2.72+/-1.24 mug/100 ml in euthyroid subjects from Sengi and 4.86+/-0.80 mug/100 ml in controls from Londjong. Values for T3 were 56.3+/-3.17 ng/100 ml in hypothyroids, 140.5+/-38.5 ng/100 ml in euthyroids from Sengi and 121.6+/-27.4 ng/100 ml in controls. The TSH levels (geometric mean and range) in these 3 groups were, respectively, 210.1 (108.0-342), 15.6 (3.0-372) and 4.1 (0.8-7.0) muU/ml. The differences between the mean concentration of PBI, T3 and TSH in the hypothyroid and euthyroid groups were highly significant (P less than 0.001). These data strengthen the clinical diagnosis of hypothyroidism in cretins as well as in non-cretinous subjects. All hypothyroid subjects had a PBI less than 1.8 mug/100 ml and T3 less than 120 ng/100 ml and TSH greater than 100 muU/ml. In 8 hypothyroid subjects, restudied 18 months after iodized oil injection, hypothyroidism was either corrected or markedly improved. It therefore appears that iodine deficiency per se in postnatal life may lead to (juvenile) hypothyroidism, which can be corrected by iodine therapy. Our findings have implications for the definition and diagnosis of endemic cretinism. Not all hypothyroid subjects in an area of endemic iodine deficiency should be classified as cretins.
在印度尼西亚爪哇中部严重地方性甲状腺肿流行区,在森吉村生活的20名克汀病患者中有7名以及94名非克汀病患者(年龄均在5至20岁)中有12名存在临床显性或轻度甲状腺功能减退。在水肿区外的隆宗村生活的70名同龄对照者中未发现甲状腺功能减退。甲状腺功能减退患者的血浆蛋白结合碘(PBI)浓度为0.98±0.32微克/100毫升(均值±标准差),而森吉村甲状腺功能正常者为2.72±1.24微克/100毫升,隆宗村对照者为4.86±0.80微克/100毫升。甲状腺功能减退患者的三碘甲状腺原氨酸(T3)值为56.3±3.17纳克/100毫升,森吉村甲状腺功能正常者为140.5±38.5纳克/100毫升,对照者为121.6±27.4纳克/100毫升。这3组的促甲状腺激素(TSH)水平(几何均值及范围)分别为210.1(108.0 - 342)、15.6(3.0 - 372)和4.1(0.8 - 7.0)微国际单位/毫升。甲状腺功能减退组与甲状腺功能正常组的PBI、T3和TSH平均浓度差异具有高度显著性(P小于0.001)。这些数据强化了克汀病患者以及非克汀病患者甲状腺功能减退的临床诊断。所有甲状腺功能减退患者的PBI均低于1.8微克/100毫升,T3低于120纳克/100毫升,TSH高于100微国际单位/毫升。8名甲状腺功能减退患者在注射碘化油18个月后复查,甲状腺功能减退要么得到纠正,要么明显改善。因此,似乎出生后生活中的碘缺乏本身可能导致(青少年)甲状腺功能减退,而这种情况可通过碘治疗得到纠正。我们的研究结果对地方性克汀病的定义和诊断具有启示意义。在地方性碘缺乏地区,并非所有甲状腺功能减退患者都应被归类为克汀病患者。