甲状腺功能亢进症与妊娠

甲状腺功能亢进症（下简称甲亢）好发于生育年龄妇女，可导致育龄妇女月经紊甜，受孕率下降，甚至出现不孕现象，但仍有少数患者在甲亢期间受孕或在妊娠期间发生甲亢。研究显示甲亢可导致妊娠并发症，如流产、早产、妊娠高血压发生的危险性增加，使胎儿和新生儿生长、发育受限，出现胎儿宫内发育停滞、早产低出生体重儿发生率增加，胎儿、新生儿甲状腺功能异常率增加，直至导致围生期死亡率增加。妊娠期间甲亢的正确诊断、及时合理的治疗对减少甲亢对孕产妇及其胎儿和新生儿造成不良影响有着十分重要的临床意义。     

精神病患者甲状腺激素检测的应用分析

正甲状腺激素对人体的生长与发育、物质与能量代谢、中枢神经系统的发育和功能具有重要作用。甲状腺激素在胎儿及婴幼儿时期对神经系统发育的重要性已得到公认,但对成年人大脑的作用机制仍存在争议。甲状腺激素异常伴发的神经精神障碍的病理、生理机制仍不明确~([1])。目前临床常见的是甲状腺激素异常所致的甲状腺功能亢进、甲状腺功能减低等疾病。为了解精神病患者甲状腺激素水平,探讨其对精神疾病的影     

妊娠合并甲状腺功能亢进诊治体会

甲状腺功能亢进（甲亢）是甲状腺激素分泌过多引起神经、循环、消化等系统兴奋性增高和代谢亢进为主要表现的临床综合征。妊娠后脑垂体前叶促甲状腺激素和胎盘分泌的促甲状腺激素释放激素和绒毛膜促性腺激素共同引起甲状腺组织增生、肥大、血运增加,新生腺泡腺腔胶样物质增多使甲状腺激素合成和分泌增多,若不正确处理可导致母儿严重并发症。 1甲亢对妊娠结局的影响 （1）不正确、及时治疗甲状腺功能亢进,则易合并妊娠期高血压疾病、妊娠期糖尿病、神经肌肉疾病、营养不良、在应激情况下如：分娩、手术、感染、精神紧张、疲劳、饥饿等情况下大量甲状腺素入血可发生甲状腺危象,致心、肝功能衰竭,水电解质紊乱可造成生命危险,还可致胎死宫内、流产、早产[1]。（2）可使胎儿、新生儿甲状腺增大,出现甲亢或甲减,甲减妇女可致胎儿畸形。新生儿还可出现广泛性自身免疫性疾病,如：淋巴组织肥大、血小板减少症。2诊断多数甲亢合并妊娠的孕妇,孕前有甲状腺疾病的现病史或既往史,诊断已经明确;但也有一些孕妇处在甲亢的早期阶段,同时合并妊娠,因此应首先区分是妊娠本身引起的代谢变化,还是确实存在甲亢,妊娠期孕妇有情绪不安、易怒、怕热、多虑、易激动、脉搏快等症状,     

1例流产后甲状腺炎合并妊娠的护理

流产后甲状腺炎是产后由于甲状腺滤泡细胞被自身免疫性炎症破坏引起的甲状腺功能异常,属于自身免疫性甲状腺炎的一种类型[1,2].临床型自身免疫性甲状腺炎表现为临床型甲状腺功能减退症,亚临床型则表现为亚临床甲状腺功能减退症,或者甲状腺功能正常,仅表现为甲状腺自身抗体阳性.甲状腺激素是胎儿神经发育的必需激素,胎儿甲状腺激素缺乏可以导致神经系统发育障碍,严重者可发生呆小症.孕妇甲状腺功能减退,生殖能力降低,但也有怀孕可能,一旦怀孕,母体及胎儿可出现多种并发症,如:妊娠期高血压疾病发生率增加,引起流产、先天畸形、发育缓慢,小儿智力不同程度受损,但是总的胎儿先天异常发生率与普通人群比较没有明显增加[3].笔者对1例产后甲状腺炎合并妊娠的病例实施了精心的治疗护理,病人及其子健康出院.现将护理体会介绍如下.     

妊娠合并甲状腺功能减退症的研究进展

妊娠期甲状腺激素的合成、分泌、代谢及调节均发生改变,妊娠合并甲状腺功能减退症(甲减)既可增加流产、早产、妊娠期高血压疾病、胎盘早剥等产科并发症的发生率,又可导致胎儿神经系统、视力等发育异常.目前促甲状腺激素(TSH)仍作为诊断妊娠期甲状腺疾病的首选指标,2.5 mU/L是其普遍接受的上限标准.妊娠合并甲减首选替代治疗药物是左甲状腺素(L-T4),其治疗安全有效.妊娠合并甲减与多种不良妊娠结局有关,是否应对所有孕妇常规进行甲状腺功能筛查以及如何筛查尚存在争议,需进一步研究.     

妊娠合并甲状腺功能异常的处理

妊娠合并甲状腺功能异常指妊娠过程中发现的甲状腺功能亢进症(甲亢)和甲状腺功能减退症(甲减).由于甲减可能危害胎儿神经系统发育,增加流产和早产率,因此避免孕妇及胎儿甲状腺功能降低具有重大意义.在处理妊娠合并甲亢的时候需要考虑到胎儿甲状腺功能的相应变化,抗甲状腺药物治疗被推荐为一线治疗方式,在某些情况下可以考虑手术治疗,但在怀孕期间不选择同位素治疗.     

漳州地区1160例妊娠与非妊娠妇女甲状腺激素水平的比较

目的通过对妊娠期及非妊娠期妇女体内甲状腺水平的检测及对比,研究妊娠期甲状腺激素水平减低在临床中的应用。方法用化学发光免疫学方法测定漳州地区775例妊娠期妇女和385例健康体检非妊娠妇女的体内甲状腺激素(FT3、FT4、TSH)含量。结果妊娠组单独FT3水平低于参考值的例数高于对照组,两者之间有显著差异(P0.01);单独FT4水平低于参考值的例数高于对照组,两者之间有显著差异(P0.01);FT3、FT4水平同时低于参考值的例数高于对照组,两者之间有显著差异(P0.01);TSH水平参考值例数高于对照组,二者无显著差异(P0.05)。结论妇女在妊娠后体内甲状腺激素水平明显降低,建议妊娠妇女在妊娠期间应筛查甲状腺激素水平,建立妊娠期特异性甲状腺功能参考值范围,如发现甲状腺水平降低及时跟踪处理,以避免对胎儿的发育造成影响。     

孕早期女性甲状腺功能失调临床观察

目的探讨孕早期女性甲状腺功能失调的发生情况,分析甲状腺功能失调与不良妊娠结局的关系。方法行常规产前检查并分娩孕妇527例,均于孕1~12周检测甲状腺功能,统计孕早期临床甲状腺功能亢进(甲亢)、亚临床甲亢、临床甲状腺功能减退(甲减)、亚临床甲减、低甲状腺素(T4)血症等甲状腺功能失调发生情况;对临床甲减和甲亢患者进行常规治疗,对亚临床甲亢、亚临床甲减及低T4血症患者进行知情选择治疗;比较发生与未发生甲状腺功能失调者不良妊娠结局发生情况。结果527例中41例(7.78%)发生甲状腺功能失调为甲状腺功能失调组,其中临床甲亢3例(0.57%),亚临床甲亢3例(0.57%),临床甲减4例(0.76%),亚临床甲减23例(4.36%),低T4血症8例(1.51%);41例中发生早产1例(2.44%),子痫前期1例(2.44%),妊娠期糖尿病3例(7.32%),新生儿低体质量2例(4.88%);余486例为无甲状腺功能失调组;甲状腺功能失调组新生儿低体质量发生率(4.88%)高于无甲状腺功能失调组(0.21%)(P0.01),2组早产、妊娠高血压疾病、子癫前期和妊娠期糖尿病的发生率比较差异无统计学意义(P0.05)。结论孕早期女性甲状腺功能失调发生率较高,经积极干预可有效控制妊娠结局,但应注意胎儿甲状腺发育,预防胎儿低出生体质量发生。     

孕晚期亚临床甲状腺功能异常对孕妇糖代谢及妊娠并发症的影响

目的探讨孕晚期亚临床甲状腺功能异常对孕妇糖代谢及妊娠并发症的影响。方法选取62例孕晚期亚临床甲状腺功能减退孕妇(亚甲减组)、38例亚临床甲亢孕妇(亚甲亢组)和50例甲状腺功能正常孕妇(对照组)为研究对象。观察3组甲状腺功能及糖代谢指标情况,对比各组孕妇妊娠并发症和胎儿不良结局情况。结果亚甲减组孕妇血清促甲状腺激素(TSH)水平明显高于对照组,而亚甲亢组TSH水平则明显低于对照组(P<0.05)。亚甲减组孕妇空腹血糖(FBG)、餐后1 h血糖(1hPBG)、2hPBG及糖化血红蛋白(HbA1c)等糖代谢指标均明显高于对照组(P<0.05);而亚甲亢组和对照组孕妇各糖代谢指标比较,差异无统计学意义(P>0.05)。血TSH水平与孕妇FBG、1hPBG、2hPBG及HbA1c呈显著正相关(P<0.05)。亚甲减组和亚甲亢组产妇胎盘早剥发生率均显著高于对照组(P<0.05);亚甲减组产妇妊娠糖尿病以及胎儿窘迫、低出生体重儿、新生儿窒息发生率也高于对照组(P<0.05)。结论孕晚期甲状腺功能与孕妇糖代谢紊乱密切相关,甲状腺功能异常会增加妊娠期并发症和胎儿不良结局的发生率,其中亚甲减对母婴的影响更为严重。     

三维超声检测胎儿甲状腺体积

胎儿甲状腺功能减低(简称甲减)或甲状腺功能亢进(简称甲亢)与甲状腺体积相关,并严重影响胎儿正常发育[1-3]。目前,三维超声体积自动测量系统(3DUS-VOCAL)可较准确地测量胎儿肺、肾脏、胸腺等器官体积[4]。本研究采用3DUS-VOCAL技术检测胎儿甲状腺体积,并与二维超声测量值和实际体积对比,探讨3DUS-VOCAL技术在检测胎儿甲状腺体积     

Thyroid disorders during pregnancy

Thyroid disorders are common in women during pregnancy. If left untreated, both hypothyroidism and hyperthyroidism are associated with adverse effects on pregnancy and fetal outcomes. It is important to correctly identify these disorders and treat them appropriately to prevent pregnancy-related complications. Levothyroxine is the indicated treatment for hypothyroidism, and thionamides are the treatment of choice for hyperthyroidism; thyroidectomy may be indicated in select cases. When thyroid cancer is diagnosed during pregnancy, a decision must be made regarding performing thyroidectomy during the pregnancy or postponing surgical resection until the postpartum period. Radioactive iodine is absolutely contraindicated during pregnancy and lactation.     

Thyroid disease and pregnancy

Thyroid disease is common in younger women and may be a factor in reproductive dysfunction. This probably only applies to severe cases of hyper- or hypothyroidism. Once adequately treated, neither of these disorders significantly impacts on fertility. The key is to recognize and to treat thyroid disorders in the reproductive-age woman before conception. Thyroxine therapy and even antithyroid drug therapy should be continued during pregnancy as necessary. Pregnancy is a euthyroid state that is normally maintained by complex changes in thyroid physiology. The fetal and neonatal hypothalamic-pituitary-thyroid system develops independently, but it may be influenced by thyroid disease in the mother. Early pregnancy is characterized by an increase in maternal T4 secretion stimulated by hCG and an increase in TBG, resulting in the elevated total serum T4 in pregnancy. The debate continues as to whether maternal T4 is important in early or late fetal brain development. If so, the physiologic changes in thyroid hormone secretion and transport in early pregnancy would help to ensure that a sufficient amount of thyroid hormone was available. There is new evidence in human subjects that substantial maternal T4 can cross the placenta during pregnancy, and this may be particularly important when fetal thyroid function is compromised as a result of congenital hypothyroidism. Maternal and fetal/neonatal outcomes in pregnancy are adversely affected if severe hypothyroidism is undiagnosed or inadequately treated. Thyroid function tests should be obtained during gestation in women taking T4 and appropriate dose adjustments should be made for TSH levels outside a normal range. The TSH-receptor blocking antibodies from the mother are a recognized cause of congenital hypothyroidism in the fetus and neonate that can be permanent or transient. If neonatal hypothyroidism is detected through neonatal screening programs, and prompt and adequate T4 replacement therapy is instituted as soon as possible following delivery, subsequent growth and development are usually normal. Paradoxically, pregnancy often has a favorable effect on the course of maternal Hashimoto's disease, although there is the risk of relapse postpartum. Pathophysiologic conditions of hCG secretion such as gestational trophoblastic disease and hyperemesis gravidarum may present as thyrotoxicosis in pregnancy, but the main cause of this syndrome is Graves' disease. The mainstay of treatment is antithyroid drugs and either propylthiouracil or methimazole may be used safely. Subtotal thyroidectomy, after medical control, is the alternative treatment, but radioiodine ablation is contraindicated.(ABSTRACT TRUNCATED AT 400 WORDS)     

Thyroid hormone and the cardiovascular system

Thyroid hormone has many effects on the heart and vascular system. Many of the clinical manifestations of hyperthyroidism are due to the ability of thyroid hormone to alter cardiovascular hemodynamics. The hemodynamic effects of hypothyroidism are opposite to those of hyperthyroidism, although the clinical manifestations are less obvious. This review will integrate what is known about the mechanisms of thyroid hormone action on the heart with recent observations from both experimental and clinical studies of hyperthyroidism and hypothyroidism. Thyroid hormone has both direct and indirect actions on the cardiovascular system. Patients with thyroid disease, especially those with hyperthyroidism, often have symptoms and signs indicating changes in cardiovascular hemodynamics. Indeed, symptoms and signs referable to the cardiovascular system may be the only manifestations of thyroid dysfunction, and thyroid function should therefore be assessed by the measurement of serum thyrotropin concentrations in all patients with cardiovascular disease. Some suggest that the administration of triiodothyronine may benefit some patients with cardiovascular disease.     

Thyroid function during pregnancy

BACKGROUND: This Case Conference reviews the normal changes in thyroid activity that occur during pregnancy and the proper use of laboratory tests for the diagnosis of thyroid dysfunction in the pregnant patient. CASE: A woman in the 18th week of pregnancy presented with tachycardia, increased blood pressure, severe vomiting, increased total and free thyroid hormone concentrations, a thyroid-stimulating hormone (TSH) concentration within the reference interval, and an increased human chorionic gonadotropin (hCG) beta-subunit concentration. ISSUES: During pregnancy, normal thyroid activity undergoes significant changes, including a two- to threefold increase in thyroxine-binding globulin concentrations, a 30-100% increase in total triiodothyronine and thyroxine concentrations, increased serum thyroglobulin, and increased renal iodide clearance. Furthermore, hCG has mild thyroid stimulating activity. Pregnancy produces an overall increase in thyroid activity, which allows the healthy individual to remain in a net euthyroid state. However, both hyper- and hypothyroidism can occur in pregnant patients. In addition, two pregnancy-specific conditions, hyperemesis gravidarum and gestational trophoblastic disease, can lead to clinical hyperthyroidism. The normal changes in thyroid activity and the association of pregnancy with conditions that can cause hyperthyroidism necessitates careful interpretation of thyroid function tests during pregnancy. CONCLUSION: Assessment of thyroid function during pregnancy should be done with a careful clinical evaluation of the patient's symptoms as well as measurement of TSH and free, not total, thyroid hormones. Measurement of thyroid autoantibodies may also be useful in selected cases to detect maternal Graves disease or Hashimoto thyroiditis and to assess risk of fetal or neonatal consequences of maternal thyroid dysfunction.     

Hyperthyroidism and thyroid storm

Thyrotoxicosis and thyroid storm are disease states that result from thyroid hormone-induced hypermetabolism. The excess thyroid hormone is released from the thyroid gland as a result of excess thyroid hormone production, or by processes that disrupt the follicular structure of the gland with subsequent release of stored hormone. True hyperthyroidism results from increased synthesis and release of thyroid hormone and can be distinguished from other causes of thyrotoxicosis by the thyroid 131I uptake. Graves' disease is the most common cause of hyperthyroidism and occurs most often in women aged 30 to 50 years. The classic features of a patient with fully developed Graves' disease are difficult to overlook, but the clinical features of thyrotoxicosis vary with the etiology of the disease and the sensitivity of the patient's peripheral tissues. Thyroid storm presents with an exaggeration of the features of uncomplicated thyrotoxicosis and, in addition, an alteration in mental status. Thyroid storm may lead to irreversible cardiovascular collapse and death if proper treatment is not initiated in the Emergency Department. Specific therapy of hyperthyroidism follows several strategies, including inhibition of hormone synthesis and release, inhibition of peripheral conversion of T4 to T3, and blocking of the systemic effects of excess thyroid hormone. Treatments directed at these ends may be initiated rapidly in the emergency setting.     

Development of neonatal Graves' disease--prediction, prevention and treatment

It is well known that neonatal hyperthyroidism or neonatal Graves' disease is caused by trans-placental transfer of TSH receptor antibodies. The antibodies stimulate the thyroid gland in the fetal and neonatal stages, which induces hyperfunction of the thyroid gland and increased thyroid hormone production. In this paper, I would like to focus on four clinically interesting issues related neonatal hyperthyroidism. 1. High risk of mothers whose infants develop neonatal Graves' disease. 2. How to predict for development of neonatal Graves' disease. 3. How to prevent for development of neonatal Graves' disease. 4. How to treat the infants with Graves' disease. I also mention on the neonatal thyrotoxicosis and fetal hyperthyroidism.     

Frequency and outcomes of maternal thyroid function abnormalities in early pregnancy

Thyroid function in pregnant women is of clinical importance considering the crucial role of thyroid hormones during fetal brain development, but the current level of evidence is insufficient to recommend for or against the routine testing of thyroid function in pregnant women. As part of this debate, it is important to evaluate the frequency of undiagnosed and untreated thyroid function abnormalities in pregnant women and to address challenges related to the biochemical assessment of maternal thyroid function in early pregnancy. A hypothesis of fetal programming by maternal thyroid disease has been proposed, but more evidence in humans is needed to extend the hypothesis and to evaluate child neurodevelopmental outcomes after in utero exposure to different abnormalities in maternal thyroid function. The nationwide registers in the Nordic countries provide unique opportunities within reproductive epidemiology to study the impact of various in utero exposures, and stored blood samples from pregnant women in nationwide birth cohorts provide a valuable source for the establishment of pregnancy specific reference ranges. This review addresses the frequency and outcomes of thyroid function abnormalities in pregnant women mainly focusing on observational studies that combine data from the Danish nationwide registers and biological specimens from the Danish National Birth Cohort. Dynamic changes in the reference range of maternal TSH and free T4 during the first trimester of pregnancy are described and discussed. A high frequency of unidentified maternal thyroid function abnormalities is illustrated, and outcomes of child neurodevelopment are evaluated according to subtypes and severity of maternal thyroid dysfunction.     

Ultrasonography of the thyroid gland in pregnancies complicated by autoimmune thyroid disease

Thyroid function and ultrasonographically determined thyroid volume were studied in nine pregnant women with diagnosed autoimmune thyroid disease at regular intervals during pregnancy and two months after delivery. The results were compared to the findings in ten healthy pregnant women. In ultrasound examinations seven of the patients showed definite morphological changes such as hypoechogeneity and inhomogeneity of the thyroid gland, which did not change during the course of pregnancy nor during the post-partum period of eight weeks. There were no morphological changes in the thyroid glands of the control group. The mean thyroid volume did not significantly change during pregnancy and after delivery in both the patient group and controls. The mean thyroid volume was smaller in the study group, with 7.55 ml (SD 6.01) compared to the controls with 11.29 ml (SD 5.61), a difference which was not statistically significant. Neither course of pregnancy nor fetal outcome was influenced by inactive autoimmune disease of the thyroid. © 1993 John Wiley & Sons, Inc.     

Transient hyperthyroidism after total parathyroidectomy for tertiary hyperparathyroidism: A report of two cases

Surgical removal of enlarged parathyroid glands is the treatment of choice in most cases of tertiary renal hyperparathyroidism. Complications of this surgical procedure are rare. We report two cases of patients who developed acute hyperthyroidism after total parathyroidectomy with parathyroid autotransplantation for refractory tertiary hyperparathyroidism. The patients had no history or biochemical or radiologic evidence of thyroid disease. They were not taking drugs affecting thyroid function. Thyroid function (thyroid stimulating hormone, free T(3) and free T(4)) was measured preoperatively, immediately after surgery and again three months later. Total parathyroidectomy was successful in both patients. Circulating levels of parathyroid hormone were at the lower limit of normal values. Postoperative thyroid function tests demonstrated acute hyperthyroidism with a rapid increase in free T(3) and T(4) levels above normal and a drop in thyroid stimulating hormone below normal in both patients. The course of hyperthyroidism was short (normalization of fT(3) and fT(4) values within 14-21 days). Neither patient had symptoms of thyrotoxicosis. Transient hyperthyroidism may be an under-recognized complication of total parathyroidectomy for tertiary hyperparathyroidism. These patients should be monitored with thyroid function tests and assessed for clinical signs attributable to thyrotoxicosis.