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1.
H. David Mosier 《The Western journal of medicine》1959,90(1):32-36
Five to 10 per cent of cretinism in the United States is due to some congenital enzymatic defect in thyroid hormone synthesis. The clinical signs of hypothyroidism appear in early infancy. Differentiation from athyreotic cretinism is important because the metabolic defect tends to be familial and its presence in the patient''s infant relatives should be diagnosed as early as possible. The differentiation is easily made if a goiter is discernible, but if it is not, radioiodine uptake should be measured, for in this condition the uptake is normal or greater. Thyroid replacement is the treatment in either the athyreotic state or the metabolic deficiency.The three known defects in thyroid hormone synthesis are (1) failure to oxidize iodine to elemental iodine resulting in failure of all subsequent processes; (2) failure to deiodinate free iodotyrosine, and (3) failure to form iodothyronine although the previous steps are accomplished. 相似文献
2.
Paul Starr 《The Western journal of medicine》1962,97(5):263-267
Often patients in whom there is little to suggest myxedema or cretinism have subclinical hypothyroidism. Once the condition is suspected, it can be diagnosed by determination of protein-bound iodine and, if the PBI is low, by response to therapy with thyroid hormone.Patients in the following categories should have protein-bound iodine determination: Those having (1) a history of previous treatment for hypothyroidism; (2) suboptimal development in children; (3) ovarian dysfunction, infertility, habitual abortion or unusual menopausal disorders; (4) symptoms of malaise and debility, such as undue fatigue, somnolence, mental asthenia and anxiety; (5) unexplained anemia; (6) colloid goiter, adenomatous goiter and cancer of the thyroid gland.If hypothyroidism is diagnosed, administration of thyroid hormone in increasing amounts, as determined by serial serum PBI tests, should be carried out indefinitely. Instruction of the patient is essential. 相似文献
3.
The role of iodine in human growth and development 总被引:1,自引:0,他引:1
Zimmermann MB 《Seminars in cell & developmental biology》2011,22(6):645-652
Iodine is an essential component of the hormones produced by the thyroid gland. Thyroid hormones, and therefore iodine, are essential for mammalian life. Iodine deficiency is a major public health problem; globally, it is estimated that two billion individuals have an insufficient iodine intake. Although goiter is the most visible sequelae of iodine deficiency, the major impact of hypothyroidism due to iodine deficiency is impaired neurodevelopment, particularly early in life. In the fetal brain, inadequate thyroid hormone impairs myelination, cell migration, differentiation and maturation. Moderate-to-severe iodine deficiency during pregnancy increases rates of spontaneous abortion, reduces birth weight, and increases infant mortality. Offspring of deficient mothers are at high risk for cognitive disability, with cretinism being the most severe manifestation. It remains unclear if development of the offspring is affected by mild maternal iodine deficiency. Moderate-to-severe iodine deficiency during childhood reduces somatic growth. Correction of mild-to-moderate iodine deficiency in primary school aged children improves cognitive and motor function. Iodine prophylaxis of deficient populations with periodic monitoring is an extremely cost effective approach to reduce the substantial adverse effects of iodine deficiency throughout the life cycle. 相似文献
4.
Serum angiotensin converting enzyme activities were significantly increased in 26 untreated hyperthyroid patients (20.3 +/- 5.4 U/ml; P less than 0.001) compared with healthy control subjects (13.1 +/- 2.3 U/ml). In 12 patients a significant fall in enzyme activities was observed after treatment compared with pretreatment serum ACE levels (P less than 0.001). Eight patients with hypothyroidism (15.7 +/- 5.1 U/ml) and 11 athyreotic patients, totally thyroidectomized for well-differentiated thyroid cancer, showed no significant differences in serum ACE activities (14.3 +/- 2.2 U/ml) compared with control subjects. After thyroid hormone supplementation a significant increase in serum ACE activity (P less than 0.05) was found in the athyreotic patients. Addition of increasing amounts of L-thyroxine to a serum sample of an athyreotic patient showed no significant effect on ACE activity in vitro. We suggest that the elevated serum ACE activity in hyperthyroidism is not from the thyroid gland, but represents a direct effect of thyroid hormone on ACE synthesis and/or release from endothelial cells. 相似文献
5.
S Miura Y Hara M Iitaka N Fukasawa K Hase M Urabe Y Sakatsume M Yanagisawa J Ishii S Kawazu 《Endocrinologia japonica》1991,38(6):647-653
To investigate the thyroid function in Bio-Breeding Worcester (BB/W) rats, we have examined the iodine metabolism, serum TSH and thyroid hormone levels in 8- and 16-week-old BB/W and normal Wistar (W) rats. At 8 weeks of age, serum TSH levels were significantly higher in BB/W rats than in W rats, although there was no difference in the serum levels of free T3 and free T4. Furthermore, the thyroidal radioactive iodine incorporation at 48 h was significantly lower in BB/W rats, suggesting that they might have some defects in iodine organification. At 16 weeks of age, serum TSH levels were also significantly higher in BB/W rats than in W rats. Furthermore, serum TSH levels in 16-week-old BB/W rats were significantly higher than in 8-week-old BB/W rats. The thyroid weight was significantly greater in BB/W rats, probably due to the increased serum TSH. The thyroidal radioactive iodine uptake at 48 h and the iodine content in the thyroid homogenates were significantly lower in BB/W rats. These results suggest that BB/W rats have some defect in iodine metabolism resulting in impaired thyroid hormone synthesis. 相似文献
6.
In the course of lactoperoxidase-catalysed I- oxidation, which is a model for the initial step of thyroid hormone biosynthesis, irreversible enzyme inactivation can occur if free molecular iodine (I2) or other oxidized iodine species accumulate. Evidence is presented that the breakdown of the catalytic activity is the result of the iodination of the peroxidase-apoprotein. This kind of enzyme inactivation, which can be prevented by iodine acceptors' such as thyroglobulin or high concentrations of I-, may well play a role in the regulation of the synthesis of thyroid hormones in vivo. 相似文献
7.
The effect of diazepam on thyroid function tests was examined in 12 euthyroid patients requiring the drug for psychiatric reasons and in six patients with thyrotoxicosis. Assessment was made before and after four weeks'' therapy.There was no significant difference in results from tests of thyroid iodide trapping and binding (thyroid radioiodine uptake, thyroid clearance, and absolute iodine uptake) except in the one-hour thyroid uptake in the euthyroid group, which was increased after diazepam. This increase occurred without alteration in serum thyroid stimulating hormone levels. No change occurred in either group in tests of thyroid hormone release (protein-bound iodine, T-3 resin uptake, or Thyopac-3 and free thyroxine index).Patients with suspected thyroid disease who are taking diazepam do not need to stop therapy while their thyroid status is being determined. 相似文献
8.
Fetal and maternal thyroid hormones 总被引:2,自引:0,他引:2
It is well known that insufficient production of thyroid hormones during the fetal and neonatal period of development may result in permanent brain damage unless treatment with thyroid hormone is instituted very soon after birth. But congenital hypothyroidism is not the only situation in which brain damage may be related to insufficient thyroid function. Cretinism is the most severe manifestation of iodine deficiency disorders found in areas where iodine intake is greatly reduced. Some of the manifestations of cretinism suggest that the insult to the developing brain starts earlier than in the case of congenital hypothyroidism. Hypothyroxinemia of mothers with adequate iodine intake may also leave permanent, though less severe, mental retardation. For these reasons the possible role of maternal transfer of thyroid hormones during early fetal development have been reinvestigated, using the rat to obtain various experimental models. It has been shown that thyroid hormones are found in embryonic tissues before onset of fetal thyroid function and that thyroidectomy of the mother results in delayed development of the concepta. The concentrations of T4 and T3 in embryonic tissues from thyroidectomized dams were undetectable before the onset of fetal thyroid function, and still reduced in some tissues near term, despite the onset of fetal thyroid function. Treatment of control and thyroidectomized dams with methyl-mercaptoimidazole to block fetal thyroid function reduced thyroid hormone concentrations in fetal tissues near term, but this decrease could be partially avoided by infusion of physiological doses of thyroxine to the mothers. Iodine deficiency of the mothers resulted in thyroid hormone deficiency of the developing embryo, which was very marked until term in all tissues including the brain. The results strongly support a role of maternal thyroid hormones in fetal thyroid hormone economy both before and after the onset of the fetal thyroid function, at least in the rat. They also support a role of the hypothyroxinemia of iodine-deficient mothers in initiating the brain damage of the endemic cretin, a damage which would not be corrected once the fetal thyroid becomes active, as iodine-deficiency of the fetus would impair adequate production of hormones by its own thyroid, and maternal transfer would continue to be low. 相似文献
9.
The trace element selenium and the thyroid gland. 总被引:6,自引:0,他引:6
J K?hrle 《Biochimie》1999,81(5):527-533
Apart from the essential trace element iodine, which is the central constituent of thyroid hormones, a second essential trace element, selenium, is required for appropriate thyroid hormone synthesis, activation and metabolism. The human thyroid gland has the highest selenium content per gram of tissue among all organs. Several selenocysteine-containing proteins respectively enzymes are functionally expressed in the thyroid, mainly in thyrocytes themselves: three forms of glutathione peroxidases (cGPx, pGPx, and PH-GPx), the type I 5-deiodinase, thioredoxin reductase and selenoprotein P. The thyroidal expression of type II 5-deiodinase still is controversial. As thyrocytes produce H2O2 continuously throughout life an effective cell defense system against H2O2 and reactive oxygen intermediates derived thereof is essential for maintenance of normal thyroid function and protection of the gland. In experimental animal models long-term and strong selenium deficiency leads to necrosis and fibrosis after high iodide loads. Combined iodide and selenium deficiency such as in central Zaire is thought to cause the myxedematous form of endemic cretinism. Inadequate selenium supply and prediagnostically low serum selenium levels are significantly correlated with the development of thyroid carcinoma and other tumors. Though selenium supply controls expression and translation of selenocysteine-containing proteins no direct correlation is found between selenium tissue content and expression of various thyroidal selenoproteins, indicating that other regulatory factors contribute to or override selenium-dependent expression control, e.g., in thyroid adenoma, carcinoma or autoimmune disease. As both trace elements, iodine and selenium, were washed out from the upper layers of the soil during and after the ice ages in many regions of the world adequate supply with these essential compounds needs to be provided either by a balanced diet or supplementation. 相似文献
10.
Pearce EN 《Journal of trace elements in medicine and biology》2012,26(2-3):131-133
Dietary iodine requirements are increased in pregnancy due to increased thyroid hormone production, increased renal iodine losses, and fetal iodine requirements. Adverse effects of iodine deficiency in pregnancy include maternal and fetal goiter, cretinism, intellectual impairments, neonatal hypothyroidism, and increased pregnancy loss and infant. Dietary iodine requirements remain increased in lactation due to the concentration of iodine in breast milk. Iodine deficiency remains a significant global public health problem. Excess iodine ingestion in pregnancy, while a relatively uncommon problem, may also have adverse fetal effects. However, the safe upper limit for chronic iodine ingestion in pregnancy and lactation is not currently well defined. 相似文献
11.
SG Obican GD Jahnke OP Soldin AR Scialli 《Birth defects research. Part A, Clinical and molecular teratology》2012,94(9):677-682
Iodine deficiency is an important nutritional deficiency, with more than 2 billion people worldwide estimated to be at risk. The developing fetus and young children are particularly at risk. During pregnancy and lactation, iodine requirements increase, whether in iodine-poor or iodine-sufficient countries, making the mother and the developing fetus vulnerable. The American Thyroid Association (ATA) recommends 250 micrograms per day of iodine intake for pregnant and lactating women. The thyroid gland is able to adapt to the changes associated with pregnancy as long as sufficient iodine is present. Dietary intake is the sole source of iodine, which is essential to the synthesis of thyroid hormones. Iodine is found in multiple dietary sources including iodized salt, dairy products, seaweed, and fish. Prenatal vitamins containing iodine are a good source of iodine, but iodine content in multivitamin supplements is highly variable. Congenital hypothyroidism is associated with cretinism. Clinical hypothyroidism has been associated with increased risk of poor perinatal outcome including prematurity, low birth weight, miscarriage, preeclampsia, fetal death, and impaired fetal neurocognitive development. Subclinical hypothyroidism is also associated with poor pregnancy outcomes and potential fetal neurocognitive deficits, but the data are more variable than those for clinical hypothyroidism. We concur with the ATA recommendation that all pregnant and lactating women should ingest (through diet and supplements) 250 micrograms of iodine daily. To achieve this goal, we recommend that all pregnant and lactating women take daily iodine supplementation of 150 micrograms. Birth Defects Research (Part A) 94:677-682, 2012. ? 2012 Wiley Periodicals, Inc. 相似文献
12.
碘是人体必需的微量元素,是合成甲状腺激素(thyroid hormone,TH)的主要原料。人体内的碘主要从饮水及食物中获取。碘的摄入缺乏或过量,不仅对TH的合成及分泌有至关重要的影响,而且与甲状腺形态及多种甲状腺疾病的发生、发展及转归密切相关。加碘盐的推广有效预防了碘缺乏可能引起的相关疾病;而碘过量导致的甲状腺疾病谱和发病率的急剧变化,也引起各界高度重视。流行病学调查表明,碘的摄入量与甲状腺功能亢进、自身免疫性甲状腺炎、甲状腺功能减退、甲状腺肿大和甲状腺癌等疾病的发病率密切相关。针对碘的相关生物学问题,对近年来的基础研究和人群研究进行综述,希望借此抛砖引玉,引起相关部门的重视,提高人民群众对碘营养的科学认识水平。 相似文献
13.
硒缺乏与甲状腺激素代谢及功能 总被引:4,自引:0,他引:4
I型脱碘酶为含硒酶,缺硒时,该酶活性下降,使循环T4增高,外周组织T3水平下降。缺硒可加速甲状腺组织碘的耗竭,并加重某些缺碘的生物学效应,缺硒还可能与碘缺乏病的发生发展有关。以缺硒为主要病因的克山病存在甲状腺激素代谢异常,其心肌呼吸酶活性变化与缺碘引起的甲状腺功能低下相似,缺碘可缺硒引起的甲状腺激素代谢改变与克山病的发生可能有关。 相似文献
14.
Slices of dog thyroid gland were incubated with liposomes consisting of (125)I-labelled phosphatidylcholine (the iodine was covalently linked to unsaturated fatty acyl chains). The (125)I label of (125)I-labelled liposomes was incorporated into thyroid protein and/or thyroglobulin at a higher rate than was the (131)I label of either Na(131)I or (131)I(2). The iodine was shown to be protein-bound by the co-migration of the labelled iodine with protein under conditions where free iodine, iodide and lipid-bound iodine were removed from protein. The uptake of iodine from the iodinated phospholipid was probably due to phospholipid exchange between the iodinated liposomes and the thyroid cell membrane, since (a) (14)C-labelled phospholipid was metabolized to (14)CO(2) and (b) many lipids in the tissue slice became (14)C-labelled. A very strong inhibition of iodide ;uptake' from Na(131)I, caused by thiosulphate, produced only a minor inhibition of the incorporation of (125)I from (125)I-labelled liposomes into thyroid protein and/or thyroglobulin. This implies that free iodide may not necessarily be formed from the iodinated phospholipids before their entrance or utilization in the cell. Synthetic polytyrosine polypeptide suspensions showed some iodination by (131)I-labelled liposomes. In tissues with low tyrosine contents, such as liver and kidney, only a trace uptake was observed. Salivary gland showed some uptake. Endoplasmic reticulum of thyroid gland showed a higher iodine uptake than that of the corresponding plasma membranes. These experiments, together with the demonstration of the diet-dependent presence of iodinated phospholipids in dog thyroid, leads us to suggest that iodination of the membrane phospholipids of thyroid cells may be directly or indirectly involved at some stage in the synthesis of thyroglobulin, or exists as a scavenger mechanism, to re-utilize and/or recover released iodine from unstable compounds inside the thyroid cell. 相似文献
15.
目的:了解食盐加碘后健康人及甲亢患者甲状腺摄131I 率的变化及其与24 小时尿碘含量的相关性,探讨甲状腺摄131I 率与
碘营养状况的关系。方法:对比食盐加碘前后健康体检者及甲亢患者甲状腺摄131I 率的变化,分析健康体检者甲状腺摄131I 率、晨
尿碘浓度及经肌酐校正的尿碘含量与24小时尿碘含量的相关关系。结果:健康人及甲亢患者食盐加碘后3、6 及24 小时甲状腺
摄131I 率均显著降低;健康体检者甲状腺摄131I 率与24 小时尿碘含量呈负相关(r=-0.7651, P<0.001),晨尿碘浓度与24 小时尿碘
含量呈正相关(r=0.8231, P<0.001),经肌酐校正的尿碘含量与24 小时尿碘含量呈正相关(r=0.9054, P<0.001)。结论:食盐加碘对甲
状腺摄131I 率有显著影响,应重新确立甲状腺摄131I 率的正常范围及甲亢的诊断标准;经肌酐校正的尿碘含量较晨尿碘浓度能更
准确地反映碘营养状况;甲状腺摄131I率可作为评估个体碘营养状况的指标,可以稳定地反映近期的碘营养状况。 相似文献
16.
Authors present the long-term development of two monozygotic twin sisters. One of them was detected by newborn screening as athyreotic (gemelus A) and healthy gemelus B sister. Therapy in athyreotic girl started at 4 weeks after birth and was monitored in order to maintain serum thyroxine and TSH in normal range. Both sisters spent their chilhood and adolescence together in the same family, school and work together as tailors in the same factory. Their development was very similar. In order to detect subclinical difference of their development, the school achievements were tested using their school certificates. Studies were divided to testing mechanical memory, logical thinking and skills. The evaluation of all classes of school attendance (13 years) reveals subtle differences - deficit of patient at approximately 6-15% level, mainly in studies demanding skills. However, dynamic evaluation after years reveals that the worse results of the patient (gemelus A) occurred during the first years of basic school whereas during adolescence having attended the special school tailor, she attained better results than her healthy sister. It seems that mental deficit in early treated hypothyroid patient is not severe and varies even during the life. Problem of the fetal hypothyroidism is probably more related to the iodine deficiency, which assures necessity of thyroid hormones for athyreotic child from mother's or twin's normally supplemented thyroid glands. 相似文献
17.
《Médecine Nucléaire》2020,44(4):277-283
The treatment of large, complicated goiters with iodine 131 constitutes an interesting alternative to surgery. It is minimally invasive, safe, and effective in most cases, and is particularly valuable in elderly, fragile patients with multiple co-morbidities. Also, it does not preclude the possibility of surgery, should it become a necessary alternative, for whatever reason in the future. The precise pre-treatment evaluation includes thyroid scintigraphy, calculation of thyroid volume and tracheal surface measurement. Patients who are most at risk of acute complications (very small cross sectional tracheal area, underlying respiratory pathology, and hyperthyroidism) should be managed during hospitalization for possible respiratory distress, or rhythm disturbances induced by hormone release. The choice of the iodine 131 activity depends on individual routine practice, either standardized or modulated by thyroid mass. Administration may be repeated depending on the effect obtained and the cumulative dose. Efficacy in terms of volume reduction is practically constant at an early stage. Its effectiveness is difficult to predict, often less in the case of large size goiters. It can be improved by increasing iodine fixation, for example, using synthetic antithyroid drugs. Permanent hypothyroidism is the most frequent and minor complication of the treatment. It involves biological monitoring in order to introduce hormone replacement therapy to avoid thyroid growth stimulation and negate the benefits of radioiodine treatment. 相似文献
18.
The tissue-specific pathways regulating cell proliferation are inherited independently in somatic hybrid between thyroid and liver cells 总被引:1,自引:1,他引:0
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《The Journal of cell biology》1990,111(6):2703-2711
Thyroid stimulating hormone (TSH) and insulin-like growth factors type 1 (IGF-I) regulate the proliferation and differentiation of cultured thyroid cells but not of cultured liver cells. We have examined the influence of TSH and IGF-I on the metabolic functions and proliferation of somatic hybrids obtained by fusing rat thyroid cells (FRTL5) with rat liver cells (BRL). While IGF-I is able to stimulate the proliferation of the hybrid cells (TxL) TSH fails to induce their growth. However, the hybrid TxL cells have surface TSH receptors with normal ligand characteristics. The addition of TSH to TxL cells led to typical enhancement of cAMP production and depolymerization of actin filaments. Yet, TSH failed to stimulate iodine uptake in the hybrid cells. Interestingly, iodine inhibited TxL proliferation induced by IGF- I but not by serum. It is concluded that the hybrid TxL cells inherited from the parental thyroid cells several important differentiated traits including mitogenic pathways induced and used by IGF-I, functional TSH receptors, and sensitivity to the inhibitory action of iodine. 相似文献
19.
《Endocrinología y nutrición》2008,55(9):436-438
Thyrotoxicosis factitia is defined as thyrotoxicosis resulting from exogenous ingestion of thyroid hormone, usually in patients with a psychiatric disorder. Diagnosis can be difficult and this entity should be suspected in patients with high free tiroxine (T4) concentrations, low or suppressed thyroglobulin concentrations, normal urinary iodide excretion and low or suppressed 131I uptake. To establish the differential diagnosis, thyrotoxicosis factitia must be distinguished from several diseases with low 131I uptake, such as Graves’ disease, subacute thyroiditis, hyperthyroidism due to excessive iodine intake, struma ovarii and metastasis from thyroid cancer. Treatment is based on b-blockers to reduce symptoms and avoid iatrogeny. We present a case of thyrotoxicosis factitia treated in our outpatient clinic. 相似文献
20.
目的:了解食盐加碘后健康人及甲亢患者甲状腺摄131I率的变化及其与24小时尿碘含量的相关性,探讨甲状腺摄131I率与碘营养状况的关系。方法:对比食盐加碘前后健康体检者及甲亢患者甲状腺摄131I率的变化,分析健康体检者甲状腺摄131I率、晨尿碘浓度及经肌酐校正的尿碘含量与24小时尿碘含量的相关关系。结果:健康人及甲亢患者食盐加碘后3、6及24小时甲状腺摄131I率均显著降低;健康体检者甲状腺摄131I率与24小时尿碘含量呈负相关(r=-0.7651,P〈0.001),晨尿碘浓度与24小时尿碘含量呈正相关(r=0.8231,P〈0.001),经肌酐校正的尿碘含量与24小时尿碘含量呈正相关(r=0.9054,P〈0.001)。结论:食盐加碘对甲状腺摄131I率有显著影响,应重新确立甲状腺摄131I率的正常范围及甲亢的诊断标准;经肌酐校正的尿碘含量较晨尿碘浓度能更准确地反映碘营养状况;甲状腺摄131I率可作为评估个体碘营养状况的指标,可以稳定地反映近期的碘营养状况。 相似文献