PDF(Pubmed)
Abstract：
Endemic cretinism is the most severe manifestation among the iodine deficiency-related disorders. The clinical status of the cretins may be modified subsequently by the duration and severity of the disease. We aimed to reassess the clinical status and thyroid function of 31 surviving \"neurological cretins\" after 42 years of iodine supplementation in a historically severely iodine deficiency area of China.
It was a cross-sectional study in design and we investigated all 31 surviving neurological cretins and 85 controls. A detailed neurological examination was conducted on each patients. All the participants were given a questionnaire and underwent B-mode ultrasonography of the thyroid. The serum levels of thyroid hormones, thyroid antibodies, serum iodine concentration (SIC) and urine iodine concentration (UIC) were measured.
The neurological cretins had shorter stature than that of the control. Neurological damage is still present in patients with cretinism. The prevalence of subclinical hypothyroidism and thyroid nodule in the cretins was significantly higher (χ2 =4.766, P=0.029 and χ2 =17.077, P<0.0001, respectively) compared with the control. After adjusting for confounding factors, endemic neurocretinism was found to be an independent risk factor for subclinical hypothyroidism (OR=4.412; 95% CI: 1.358-14.334; P=0.014) and thyroid nodule (OR=6.433; 95% CI: 2.323-17.816; P<0.0001).
Iodine supplementation after birth does not reverse the neurological damage that results from maternal/foetal hypothyroidism in utero and is subsequently manifested as neurological cretinism. There is a cross-sectional association between endemic neurocretinism and subclinical hypothyroidism and thyroid nodule.
It was a cross-sectional study in design and we investigated all 31 surviving neurological cretins and 85 controls. A detailed neurological examination was conducted on each patients. All the participants were given a questionnaire and underwent B-mode ultrasonography of the thyroid. The serum levels of thyroid hormones, thyroid antibodies, serum iodine concentration (SIC) and urine iodine concentration (UIC) were measured.
The neurological cretins had shorter stature than that of the control. Neurological damage is still present in patients with cretinism. The prevalence of subclinical hypothyroidism and thyroid nodule in the cretins was significantly higher (χ2 =4.766, P=0.029 and χ2 =17.077, P<0.0001, respectively) compared with the control. After adjusting for confounding factors, endemic neurocretinism was found to be an independent risk factor for subclinical hypothyroidism (OR=4.412; 95% CI: 1.358-14.334; P=0.014) and thyroid nodule (OR=6.433; 95% CI: 2.323-17.816; P<0.0001).
Iodine supplementation after birth does not reverse the neurological damage that results from maternal/foetal hypothyroidism in utero and is subsequently manifested as neurological cretinism. There is a cross-sectional association between endemic neurocretinism and subclinical hypothyroidism and thyroid nodule.
摘要：
地方性克汀病是碘缺乏相关疾病中最严重的表现。可随后通过疾病的持续时间和严重程度来改变cretin的临床状态。我们的目的是在中国历史上严重的碘缺乏地区补充碘42年后，重新评估31名幸存的“神经性cretins”的临床状况和甲状腺功能。
这是一项设计中的横断面研究，我们调查了所有31例存活的神经学克理菌素和85例对照。对每位患者进行了详细的神经系统检查。对所有参与者进行了问卷调查，并进行了甲状腺B超检查。血清甲状腺激素水平,甲状腺抗体，测定血清碘浓度(SIC)和尿碘浓度(UIC)。
与对照相比,神经学上的cretin具有较短的身材。克汀病患者仍然存在神经系统损害。与对照组相比，cretins中的亚临床甲状腺功能减退症和甲状腺结节的患病率显着升高（分别为χ2=4.766，P=0.029和χ2=17.077，P<0.0001）。在调整混杂因素后，发现地方性神经克汀病是亚临床甲状腺功能减退症（OR=4.412；95％CI：1.358-14.334；P=0.014）和甲状腺结节（OR=6.433；95％CI：2.323-17.816；P<0.0001）的独立危险因素。
出生后补充碘不能逆转子宫内母体/胎儿甲状腺功能减退症导致的神经损伤，随后表现为神经克汀病。地方性神经克汀病与亚临床甲状腺功能减退症和甲状腺结节之间存在横断面关联。
这是一项设计中的横断面研究，我们调查了所有31例存活的神经学克理菌素和85例对照。对每位患者进行了详细的神经系统检查。对所有参与者进行了问卷调查，并进行了甲状腺B超检查。血清甲状腺激素水平,甲状腺抗体，测定血清碘浓度(SIC)和尿碘浓度(UIC)。
与对照相比,神经学上的cretin具有较短的身材。克汀病患者仍然存在神经系统损害。与对照组相比，cretins中的亚临床甲状腺功能减退症和甲状腺结节的患病率显着升高（分别为χ2=4.766，P=0.029和χ2=17.077，P<0.0001）。在调整混杂因素后，发现地方性神经克汀病是亚临床甲状腺功能减退症（OR=4.412；95％CI：1.358-14.334；P=0.014）和甲状腺结节（OR=6.433；95％CI：2.323-17.816；P<0.0001）的独立危险因素。
出生后补充碘不能逆转子宫内母体/胎儿甲状腺功能减退症导致的神经损伤，随后表现为神经克汀病。地方性神经克汀病与亚临床甲状腺功能减退症和甲状腺结节之间存在横断面关联。
