Hypothyroidism Food List

The Hypothyroidism Revolution

During Phase 1 of the Hypothyroidism Revolution Program, the magic begins to happen as you begin to notice many positive changes occurring. You will begin your progressive transition towards the ideal thyroid healing diet that will give your thyroid the big boost that it needs to help your cells produce more than enough energy for you. By the end of Phase 1, your energy levels will be rapidly on the rise and you will feel amazingly satisfied with zero food cravings. You will feel in control again as your mood drastically improves and any sign of depression and anxiety begin to disappear. Your family and friends are going to notice some major positive changes in you. You will also begin to experience many of the outer changes that come with improved thyroid function. Youre skin will begin to clear up and glow while your hair and nails will begin to look healthy again. As you ease into the thyroid healing diet, you will progressively remove the foods that suppress your thyroid, disrupt your hormone pathways, cause digestive upset and irritation, and cause toxic byproducts that congest your liver. At the same time, you will be progressively adding the foods that will be supplying your cells with the right balance and combination of nutrients that they need to thrive and produce endless amounts of energy. Read more...

The Hypothyroidism Revolution Overview


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Thyroid Disease during Pregnancy

The prevalence of hyperthyroidism is around 5 per 1,000 and hypothyroidism about 3 per 1,000 in women. As the conditions are generally much more common in the female it is to be expected that they will appear during pregnancy. Developments in our understanding of thyroid physiology 1 and immunology 2 in pregnancy as well as improvements in thyroid function testing 3 have highlighted the importance of recognising and providing appropriate therapy to women with gestational thyroid disorders.

Fetal Thyroid Function and Maternal Thyroid Hormones

Consequently, if the mother has T4 deficiency then the fetus will be T3-deficient even if maternal T3 is normal. This is because during early development serum-derived T3 essentially does not contribute to cerebral T3. Studies have shown that normal concentrations of T3 alone in the maternal or fetal circulation without normal T4 concentrations have no protective effect on the fetal brain because during fetal and postnatal development cerebral structures depend entirely on the local generation of T3 from T4 by type II 5'-iodothyronine deiodinase (D2), the activity of which is inversely related to the availability of T4 17 . This might explain why in most cases of congenital hypothyroidism in a newborn with a mother who has normal thyroid function there is no permanent severe central nervous system damage when T4 is administered in the first 3 months of neonatal life. In this case, the fetal brain has not been severely damaged before birth and normal...

Causes of hypothyroidism

Hashimoto's thyroiditis most common cause associated with other autoimmune diseases (e.g., pernicious anemia, vitiligo, lupus). Look for positive antimicrosomal antibodies. Histology shows lymphocyte infiltration of the gland. 2. Subacute thyroiditis acute viral inflammation with fever and enlarged, tender thyroid gland. History of upper respiratory infection or mumps is common. Give NSAIDs for symptom relief. Patients often recover without treatment. 5. Iodine deficiency rare in. U.S. May cause cretinism in children (stunted growth and mental retardation).

Epidemiology of Congenital Hypothyroidism

The incidence of congenital hypothyroidism (CH) as detected by common neonatal screening programs, is approximately 1 3,000-1 4,000 in live births 1 . Very recently, in the Netherlands a higher incidence of 1 1,800 was observed using a screening based on thyroxine (T4), thyrotropin (TSH) and thyroxine-binding globulin (TBG) measurement 2 . With this strategy, the incidence of various types of CH was estimated 1 2,200 for permanent CH with 1 2,500 of thyroidal origin, 1 21,000 of central origin, and 1 12,000 for transient hypothyroidism. For unknown reasons, the female male ratio in CH is consistently 2 1. Newborn infants with Down syndrome have an increased risk for CH of approximately 1 140.

Genetic and Other Causes of Congenital Hypothyroidism

Severe central hypothyroidism due to isolated TSH deficiency frequently results from TSH-P subunit (TSHB) mutations 4, 5 . Similarly, TSH deficiency may be found as a component of combined pituitary hormone deficiencies Fig. 1. Anatomic and functional levels at which CH may occur, including exogenous and maternal causes of transient CH. *Antithyroid medication, iodine deficiency blocking TSHR antibodies. Fig. 1. Anatomic and functional levels at which CH may occur, including exogenous and maternal causes of transient CH. *Antithyroid medication, iodine deficiency blocking TSHR antibodies. Table 1. Genetic causes of congenital hypothyroidism Central (pituitary) hypothyroidism

Clinical Outcomes of Congenital Hypothyroidism

In contrast to physical signs, the neurodevelopmental outcome of patients with CH largely depends on the early initiation and maintenance of adequate postnatal L-T4 therapy, especially in cases of severe hypothyroidism (T4 < 5 xg dl). Despite neonatal screening, 10 of early treated infants with severe hypothyroidism are likely to require special education 17 . Subtle differences in intelligence, school performance and neuropsychological tests in comparison to control individuals, classmates and siblings have been detected in adults with CH despite early L-T4 treatment 18, 19 . While in some studies the severity of CH was correlated with poor developmental outcome, recent observations indicate that delayed and inadequate hormone substitution is a main predictor of clinical outcome 18, 20 . Children with CH may have selective deficits on visual, language, motor, attention and memory abilities 21 . Auditory brainstem evoked potentials were abnormal in 25 of early-treated patients with...

Experimental Autoimmune Thyroiditis in the Mouse

Experimental autoimmune thyroiditis (EAT) in mice is an excellent model for Hashimoto's thyroiditis (HT). It is induced with thyroglobulin (Tg), a known thyroid autoantigen that is common to both mouse and human and for which several conserved, thyroiditogenic epitopes have been identified. Basic Protocol 1 describes induction and evaluation of EAT. A homologous antigen, mouse (MTg), is used because it has additional unique epitope(s) and induces more severe and long-lasting thyroid inflammation than heterologous mammalian Tg induces. Susceptibility of mouse strains is based on major histocompatibility complex (MHC) class II genes H-2 haplotypes k and s are susceptible, b, d, and f are resistant, and q is intermediate. EAT is evaluated using appropriate assay parameters thyroid histology and in vitro proliferative response (see Support Protocol 2). Thyroid histology distinguishes susceptible from resistant strains and shows the extent of mononuclear cell infiltration and destruction...

Induction And Evaluation Of Experimental Autoimmune Thyroiditis

Two adjuvants, bacterial lipopolysaccharide (LPS) and supplemented complete Freund's adjuvant (CFA see Alternate Protocol), are widely used to facilitate induction of experimental autoimmune thyroiditis (EAT) with mouse thyroglobulin (MTg). These adjuvants are particularly useful if spleen cells (LPS) and lymph node cells (CFA) are to be used for adoptive transfer (see Basic Protocol 2). LPS is preferred to CFA because there is no antigen loss associated with preparing an emulsion, and the use of LPS as an adjuvant results in more uniform disease induction (see Background Information). Moreover, two injections of MTg are generally required to induce EAT, and some institutional animal care and use committees (IACUC) do not permit two CFA doses per animal.

Adoptive Transfer Of Experimental Autoimmune Thyroiditis

Adoptive transfer of experimental autoimmune thyroiditis (EAT) has recently been used to characterize T cell epitopes of thyroglobulin (Tg). Clones of the Tg gene have provided complete (human and bovine) or partial (porcine, rat, and mouse) amino acid sequences for the entire or large portions of the 660-kDa molecule (Kong et al., 1995). Thus far, no immunodominant epitopes have been uncovered, and the role of Tg peptides in patho-genesis can only be ascertained if they expand T cells in vitro and transfer thyroiditis to normal syngeneic recipients. This protocol can be used to examine conserved epitopes, the role of iodination of Tg peptides in immunogenicity, T cell receptor (TCR) VP gene usage, and the role of adhesion molecules in infiltration. The interval between immunization (Basic Protocol 1) and removal of lymphoid organs is similar to that listed for T cell proliferation assay (Support Protocol 2). After immunization with MTg and lipopolysaccharide (LPS), spleen cells can...

Induction Of Tolerance To Experimental Autoimmune Thyroiditis

Susceptible mice are normally unresponsive when immunized with mouse thyroglobulin (MTg) without adjuvant. However, they become resistant to experimental autoimmune thyroiditis (EAT) induction after pretreatment with two doses of deaggregated MTg (dMTg) given 7 days apart. Within 3 days after the second dose, EAT induction is virtually suppressed, and resistance lasts for > 73 days. Suppression is mediated by CD4+ cells. Thus, this protocol permits the study of regulatory T cell mechanisms in an autoimmune disease it simulates the endogenous release of circulatory MTg following thyroid-stimulating hormone infusion which also leads to CD4+ T-cell-mediated suppression. Note that two groups of mice are used tolerized and nontolerized mice.

Thyroid Disease in Diabetes Mellitus

Autoimmunthyroiditis describes a group of thyroid diseases with destruction of thyroid tissue due to an autoimmune reaction. Classification of these diseases is not consistent in the literature. Most frequently, Hashimoto thyroidi-tis with antibodies against thyroid antigens is found. These antibodies are directed towards thyroid peroxidase (TPO-Ab), thyreoglobulin (TG-Ab) and or TSH-receptor antigen (TRAK). The majority of patients with positive thyroid antibodies have normal thyroid function. Elevated TSH levels as a marker for subclinical hypothyroidism are found in about 15 in the antibody positive patient group. Overt primary hypothyroidism due to autoimmune thyroiditis is seen in 3-5 of patients 3, 8, 19 . Clinical findings of hypothyroidism like goiter, weight gain, fatigue, cold intolerance and bradycardia are rare because of screening for TSH and autoantibodies in patients with type 1 diabetes (table 1). In the study of Kaspers et al. 16 , evidence for thyroid disease was...

Iodine Deficiency and Supplementation

Iodine deficiency produces a spectrum of disorders - endemic goiter, hypothyroidism, cretinism, and congenital anomalies - that are termed the iodine deficiency disorders. Despite substantial global progress against iodine deficiency, it is estimated that 750 million people worldwide, or approximately 15 of the population, remain iodine deficient and goitrous. In iodine-deficient areas, multiple nutritional and environmental influences contribute to the prevalence and severity of iodine deficiency disorders. Even nowadays, iodine nutrition in children and iodine supplementation of pregnant women remains a medical challenge and ought to be optimized. In Europe, nearly two-thirds of the populations live in countries that are iodine deficient. Damage to reproductive function and to the development of the fetus and newborn is the most important consequence of iodine deficiency. The fetal brain is particularly vulnerable to maternal hypothyroidism in iodine deficiency, and iodine...

Hypothyroidism Introduction

Hypothyroidism is the result of inadequate thyroid hormone production to maintain body processes. It may be the result of congenital thyroid abnormality and therefore present in infancy or it may become notable during the first two years of life. It appears later when production is inadequate to maintain body processes as rapid growth increases the need for hormones. Acquired causes of the condition may be thyrotoxicosis, thyroidectomy, irradiation, infections, and dietary deficiency of iodine. Secretions of the thyroid gland include thyroid hormone (thyroxine, T4 and triiodothyronine, T3) which are bound to proteins in the blood (thyroxine-binding globulin, TBG) and thyrocalcitonin (maintains calcium levels in blood). The hormones are controlled by the thyroid-stimulating hormone (TSH) that is secreted by the anterior pituitary gland. Treatment of hypothyroidism is by thyroid hormone replacement, which involves prompt intervention in the infant and gradually increasing amounts of...

Hypothyroidism in Infancy Childhood and Adolescence

Hypothyroidism during childhood and adolescence can result from a variety of congenital or acquired defects (table 2). Table 3. Symptoms of childhood hypothyroidism Some children present with an asymptomatic goiter, whereas others may present with mild tenderness or a sensation of fullness in the anterior neck 41 . The course of hypothyroidism is often so insidious that neither the child nor the parents are aware of the physical changes that have occurred. These children often have marked growth retardation before the disease is recognized, and the expected effect on linear growth emphasizes the importance of serial growth measurements in all children. Children who develop hypothyroidism before age 2 years may suffer some irreversible central nervous system damage and developmental delay, the onset of hypothyroidism developed after infancy does not cause mental retardation 42 (table 3). Deceleration of linear growth is an important sign that is helpful in the early recognition of this...

Induction Of Experimental Autoimmune Thyroiditis Using Cfa As Adjuvant

Experimental autoimmune thyroiditis (EAT) can be induced by injecting mice with mouse thyroglobulin (MTg) emulsified in complete Freund's adjuvant (CFA) supplemented with Mycobacterium tuberculosis H37Ra and injected subcutaneously in the inner thigh. This method is used to obtain primed lymph node cells for in vitro T cell proliferation assays (see Support Protocol 2).

Diagnostic WorkUp of Congenital Hypothyroidism

Confirmatory serum measurements of TSH and T4 are required, along with thyroid hormone binding proteins and serum free T4. In cases of maternal autoimmune thyroid disorder, assessment of TSHR blocking antibodies may indicate a transient form of CH. Thyroglobulin levels tend to be high in dyshormonogenesis and low in thyroid agenesis. Thyroid ultrasonography and or thyroid scan are considered optional for management of CH 1 but are necessary to clarify the underlying source of CH, to distinguish between thyroid aplasia, ectopy or inborn errors of T4 synthesis. Testing thyroid function in first degree relatives may be informative because of the variable penetrance of inherited CH. Measurement of iodine or iodotyrosines in urine are helpful if iodine exposure, iodine deficiency or recycling defects are considered. It is clinically important to distinguish permanent or transient forms of CH. If imaging studies reveal ectopic or absent thyroid tissue, hypothyroidism is probably permanent....

Thyroid Disease in Turner Syndrome

An association between Turner syndrome (TS) and thyroid disease was first suggested by Atria et al. 1 in 1948 when they reported post mortem findings of a small thyroid gland with lymphocytic infiltration in a young woman with Turner syndrome. Many authors reported on a higher prevalence of hypothyroidism and an association with positive thyroid antibodies in TS patients (table 2) 2, 6, 7, 24, 29, 32, 37 . Hypothyroidism is found in up to 35 of TS patients. Thyroid autoimmunity seems to be even more common in females with Turner syndrome with a prevalence of up to 52 15 . A positive family history was reported by Wilson et al. 37 . This group found an increased incidence of thyroid antibodies in patients with TS and their first degree relatives. The incidence of thyroid antibodies was 30 in patients compared to 1.7 in an age matched control group and 22 in the mothers of the TS patients (vs. 6.6 in the controls). Larissa et al. 21 found a preferential parental segregation of...

Iodine Deficiency

Iodine is essential for thyroid hormone synthesis and is present in soil, water and air. Iodine deficiency disorders (IDD), which was referred to as endemic goiter up to thirty years ago refers to iodine deficiency that can be prevented by ensuring an adequate intake of iodine in population 64 . Goiter is the most frequent and visible manifestation of IDD and is an important health problem. It effects intellectual growth in neonates and children and almost 20 million people living in developing countries have some degree of brain damage due to the effects of iodine deficiency (ID). ID in the mother results in deficiency of the neonate. The most striking feature of ID is endemic cretinism. In severe iodine deficiency, endemic goiter and cretinism increased perinatal death, decreased fertility rate and increased infant mortality occur. Combined iodine and selenium deficiency causes a severe form of cretinism in some areas. Two types of endemic cretinism have been defined 65-67 . In...

The Hypothalamic PituitaryThyroid Axis

Thyroid hormones play an important role in normal growth and development of the maturing human. In the adult, thyroid hormones maintain metabolic homeostasis by regulating oxygen consumption, body weight and intermediate metabolism. Thyroid function is under hypothalamic-pituitary control. Thus, thyroid hormones are produced by the thyroid gland in response to stimulation by thyroid-stimulating hormone (TSH) produced by the anterior pituitary. TSH, in turn is regulated by the hypothalamic peptide, thyrotropin-releasing hormone (TRH). The function of the entire complex is modified by the availability of the thyroid hormones in a typical negative feedback manner leading to the concept of a functional unit, the hypothalamic-pituitary-thyroid (HPT) axis. After its secretion, TRH binds to a specific G-protein coupled receptor in the plasma membrane of the thyrotrophs to induce the synthesis and release of TSH, and in this way the production of thyroid hormones. TRH may also induce the...

Properties of arginine vasopressin antidiuretic hormone ADH

Plasma volume contraction cardiovascular volume receptors Fall in arterial blood pressure cardiovascular baroreceptors Hormonal beta-adrenergic stimulation angiotensin II hypothyroidism hypoadrenalism Drugs nicotine barbiturates vincristine Miscellaneous nausea and vomiting hypoglycaemia stress heat

Diseases Associated with Hirschsprungs Disease

Congenital anomalies associated with HD have been reported from various series and have an overall incidence of about 14.7 in 2856 patients.31 Down syndrome is the most common chromosomal abnormality associated with HD, and the genetic modifiers have been located on chromosome 21q 22.32 The diagnosis of HD in Down syndrome is often delayed because other associated anomalies take precedence and because constipation is often present in these patients due to hypotonia and hypothyroidism.

Fetal Maternal Relationships

Pregnancy affects thyroid homeostasis. An increased excretion of iodine in the urine accounts for the increase in thyroid volume even in areas of moderate dietary iodine intake 4 . Some studies, however, do not show an increase in urinary iodine during pregnancy. In either case the increase in thyroid volume is the result of imbalance between the intake and increased requirements of iodine during pregnancy 5 . Iodine deficiency during pregnancy is associated with maternal goitre and reduced maternal thyroxine (T4) level. While thyroid size increases in areas of iodine deficiency it does not do so in those regions that are iodine sufficient even in moderate iodine-deficient regions urinary iodine excretion is higher in all trimesters than in non-pregnant women and may be causative in maternal goitre formation as assessed by ultrasound. The increase in thyroid volume already referred to is substantially greater in iodine-deficient areas. This gestational goitrogenesis is preventable by...

Physiological Factors Metabolic

Endocrine disorders are associated with gastrointestinal complications, for example, constipation. Among the endocrinopathies discussed here are diabetes mellitus, hypothyroidism and hyperparathyroidism, multiple endocrine neo-plasia type lib (MEN lib), and pregnancy. The prevalence of bowel dysfunction in hypothyroidism was assessed by a colon transit study among patients who manifested with clinical hypothyroidism. The authors found a significant delay in the whole-gut transit in this population. The authors concluded that hypothyroidism may clinically manifest as a decrease in bowel movements, and is improved by replacement with thyroid hormones.25 Constipation is a common symptom of hypercal-cemia, secondary to hyperparathyroidism.26

Monitoring of the Fetus in a Mother with Graves Disease

(c) Subacute thyroiditis The diagnosis is suggested by the presentation of a painful thyroid in the presence of hyperthyroidism. As radionuclide evaluation (which would demonstrate a low iodine uptake) is contraindicated diagnosis may be made with a fine needle aspiration biopsy of the thyroid associated with an elevation in systemic markers of inflammation. Treatment is firstly with analgesics for pain and oral prednisolone therapy if inflammation is severe. Frequent monitoring of thyroid function is required as a small number of patients will develop hypothyroidism. Patients with Graves' disease may develop Graves' hyperthyroidism as a post partum phenomenon due to the immune rebound of TSH receptor antibodies. In Graves' disease patients, TSHR Abs have been shown to decrease during late gestation with a significant rebound in the late postpartum 44 . In this situation the hyperthyroidism of Graves' disease may be followed immediately by transient hypothyroidism due to co-existing...

Differential Diagnosis

Constipation is a disorder and not a disease. It may be secondary to several diseases, including colonic disease (stricture, cancer, anal fissure, proctitis), metabolic and endocrine disturbances (hypercalcemia, hypothyroidism, diabetes mellitus), neurologic disorders (Parkinson's disease, spinal cord lesions), or pharmaco-logic (antidepressive) (Table 5.2). Therefore, exclusion of both intestinal and systemic organic etiologies is an imperative step prior to referring the patient with functional symptoms to the physiology laboratory. Barium enema or colonoscopy is usually indicated and the primary pathology treated. Additional tests, dictated by the history and physical examination, may be necessary to exclude the above-named diseases. Hypothyroidism

Maternal Fetal Unit and the Function of the Fetal Thyroid Gland

(FT4) is much higher than in adult sera and the concentrations of T4 that are available to developing tissues reach values that are comparable to those know to be biologically active in their mothers 28, 29 (fig. 2). The T4-binding proteins and the concentrations of maternal T4 or FT4 that are allowed to pass the placental barrier determine the concentrations of FT4 in the fetal fluids and this is determined ontogenically. Therefore, it has become clear why an efficient barrier to complete maternal thyroid hormone transfer is necessary as the same concentrations that are available in the maternal sera might possibly be toxic to the developing fetal tissues 22, 30 . However, if the fetus is hypothyroid the placenta allows T4 from the mother to pass to the fetus in larger quantities 31 . In contrast to what happens with thyroid hormones the placenta allows the free passage of TRH and iodine from the mother to the fetus. As mentioned previously, if there is iodine insufficiency in the...

Function of the Thyroid Gland in the Neonate and Infant

After the large increase in the serum concentrations of the thyroid hormones and TSH which occur during the first days of neonatal life there is a gradual decrease in the levels of T4, T3 and TSH during the life of the neonate and infant. The most important difference between this period and adult life is that there is a larger production and utilization of T4 in the neonates and infants. The neonates produce 5-6 xg kg day of T4 with a gradual decrease during the first years of life to reach levels of 2-3 xg kg day of T4 at 3-9 years of age. This is in contrast to adults who produce 1.5 xg kg day of T4 42 . The weight of the neonatal thyroid gland is a good indicator of maternal iodine intake during pregnancy. On an adequate maternal iodine intake, the weight of the neonatal thyroid is less than 1.5 g 48 . Due to the increased turnover of iodine and consequently of thyroglobulin in the early neonatal period, decreased iodine intake will bring about an increased consumption of reserve...

Optimal Iodine Intake

These recommendations derive from consensus statements by several groups, including the International Council for Control of Iodine Deficiency Disorders, the World Health Organization, UNICEF, and the Food and Nutrition Board of the US National Academy of Sciences. The amounts are based on the following the calculated daily thyroid hormone turnover in euthyroidism, the iodine intake producing the lowest values for serum thyrotropin (TSH) and for serum thyroglobulin (TG), the amount of thyroid hormone replacement necessary to restore euthyroidism to athyreotic subjects, the iodine intake associated with the smallest thyroid volumes in populations, and the lowest incidence of transient hypothyroidism in neonatal screening with blood spot TSH. About 90 of iodine is eventually excreted in the urine. The median urinary iodine concentration in casual ('spot') samples, expressed as micrograms per liter ( g l), is currently the most practical biochemical laboratory marker of community iodine...

Step 2 Assess the history

Hyperthyroidism Hypothyroidism Diabetes mellitus Exogenous androgen use D. Step 4 Basic laboratory testing. In addition to measurement of serum hCG to rule out pregnancy, minimal laboratory testing should include measurements of serum prolactin, thyrotropin, and FSH to rule out hyperprolactinemia, thyroid disease, and ovarian failure (high serum FSH). If there is hirsutism, acne or irregular menses, serum dehydroepiandrosterone sulfate (DHEA-S) and testosterone should be measured.

Step 5 Followup laboratory evaluation

Prolactin secretion can be transiently increased by stress or eating. Therefore, serum prolactin should be measured at least twice before cranial imaging is obtained, particularly in those women with small elevations (< 50 ng mL). These women should be screened for thyroid disease with a TSH and free T4 because hypothyroidism can cause hyperprolactinemia.

More Than Adequate Iodine Intake

Although not excessive, studies in more than adequate iodine intake (see table 4) following iodine prophylaxis, also pointed out the possible development of thyroid autoantibodies. Zois et al. 85 investigated the iodine status and the impact of iodine prophylaxis on the prevalence of autoimmune thyroiditis among schoolchildren in a formerly iodine-deficient community in northwestern Greece. The findings were compared to those obtained from a similar survey carried out 7 years previously in the same area. A total of 302 schoolchildren (12-18 years of age) from a mountainous area of northwestern Greece were examined for the presence of goiter, and blood and urine samples were collected for assessment of thyroid function, antithyroid antibodies and urinary iodine excretion. Median urinary iodine concentration in the children was 200 xg l. Thyroid function was normal in all but 7 children, who had subclinical hypothyroidism (2.5 ). Antithyroid antibodies (antithyroid peroxidase and or...

Thyroid Hormone Transport

More than 99 of the circulating thyroid hormone is bound to plasma proteins but can be liberated with great rapidity for entry into cells. The thyroid hormone-binding proteins are comprised of thyroxine-binding globulin (TBG), transthyretin (TTR or thyroxine-binding prealbumin), human serum albumin (HSA) and lipoproteins. Their functions are most probably to ensure a constant supply of TH to the cells and tissues by preventing urinary loss 3 , protect the organism against abrupt changes in thyroid hormone production and degradation, protect against iodine deficiency 2 and target the amount of TH delivery by ensuring a site-specific, enzymatic alteration of TBG 4 . TBG has by far the highest affinity for T4, the result of which being that TBG binds 75 of serum T4, whereas TTR binds 20 and HSA 5 2 . Some of the properties of the binding proteins are displayed in table 1. Abnormalities of the TH-binding proteins do not cause alterations in the metabolic state of the individual nor do...

Deiodination of lodothyronines

D1 has both outer and inner ring deiodination activities, but appears particularly important for the generation of plasma T3 and clearance of reverse T3 by outer ring deiodination. D1 is positively regulated at the pretranscriptional level by T3, and is very potently inhibited by the antithyroid drug propylth-iouracil. In humans, therefore, it might be expected that hyperthyroidism would induce D1 with subsequent relative increase in T3 production. Hyperthyroidism is indeed commonly associated with a higher increase in plasma T3 compared to T4, and D1 activity has also been demonstrated to be approximately 3-fold elevated in thyroid glands from Graves' disease compared to euthyroid control glands 51 . D2, on the other hand, has only outer ring deiodination activity, preferring T4 over reverse T3 as substrate, and it is increased in hypo- and decreased in hyperthyroidism. This regulation by the thyroid state can occur both by pre- and posttranslational mechanisms. D2 is particularly...

Receptor Specific Nuclear Actions Genomic Actions

Response elements the transcriptional activity is altered by an interaction directly or indirectly with a complex array of transcriptional cofactors including corepressors, coactivators, integrators. Even unliganded TRs interact with core-pressors and repress expression rather than being an inactive passive receptor. This also explains that TR knockout mice are not suffering from as pronounced a hypothyroidism as might be expected 97 . Mutations have been demonstrated in the TR-p gene with resultant familial resistance to thyroid hormones. These patients are identified by their persistent elevation of circulating free T3 and T4 without a suppressed TSH concentration. The thyroid hormone resistance syndrome will be dealt with in more detail in a subsequent chapter.

Summary and Conclusions

Several transporters that mediate the cellular entry of TH have been identified, but most of them are not specific for thyroid hormones. Up to now only two truly TH-specific transporters have been found OATP1C1 with high preference for T4 and MCT8 with preference for T3 as the ligand 21 . Since delivery of TH to the cells is a crucial mechanism for subsequent TH action, abnormalities in these transporters probably result in disease, e.g. a described mutation in the MCT8 caused tissue-specific hypothyroidism in the brain with milder affection of other organs 39 .

Discharge And Home Healthcare Guidelines

GGoiter is the enlargement of the thyroid gland. It is usually a response to a thyroid hormone deficiency (primary hypothyroidism) that results in the hypersecretion of thyroid-stimulating hormone (TSH) from the anterior pituitary gland. Oversecretion leads to subsequent thyroid hypertrophy and hypervascularity. The body's response may compensate for thyroid hormone deficiency, leaving the patient asymptomatic. Goiter may also occur in conjunction with hyperthyroidism, known as Graves' disease. Finally, goiter may occur with the growth of thyroid tumors. Secondary hypothy-roidism occurs with TSH deficiency in the pituitary gland and is not associated with goiter. Most goiters are classified as simple (or nontoxic). They result from any enlargement of the thyroid gland that is not caused by an inflammation or a neoplasm. Simple goiters can be classified as sporadic or endemic and are not associated initially with either hyperthyroidism or hypothyroidism. Sporadic goiters occur after a...

Debate on Newborn Screening Programs

To detect CH, primary TSH screening is used in most European countries, Japan and Australia. However, using this approach, some forms of CH including delayed TSH elevation in infants with TBG deficiency or low birth weight, central hypothyroidism and hypothyroxinemia are missed. In North America, a T4-based program with additional measurement of TSH in samples with lowest T4 concentration is commonly used 1 . Primary T4 screening with backup TSH measurements has the potential to detect primary hypothyroidism, TBG deficiency and central hypothyroidism. The recall rate for primary hypothyroidism in both approaches is 0.05 , and the rate of false positive results is higher using the primary T4 strategy.

Treatment Recommendations

Because poor compliance has major consequences, initial and ongoing counseling of parents is of utmost importance. Education of parents by trained professionals should address the etiology of hypothyroidism, the benefit of early diagnosis in preventing mental retardation, the appropriate L-T4 application, and the importance to follow treatment regimens and regular visits. Thus, the pediatrician plays a central role to provide a medical home for every child with CH to coordinate care and lifelong disease management. 1 American Academy of Pediatrics Update of newborn screening and therapy for congenital hypothyroidism. Pediatrics 2006 117 2290-2303. 2 Kempers MJE, Lanting CI, van Heijst AFJ, et al Neonatal screening for congenital hypothyroidism based on thyroxine, thyrotropin, and thyroxine-binding globulin measurement potentials and pitfalls. J Clin Endocrinol Metab 2006 91 3370-3376. 3 Olivieri A, Stazi MA, Mastroiacovo P, et al A population-based study on the frequency of additional...

Primary Nursing Diagnosis

The primary treatment is dietary management, weight reduction, increased physical activity, and the restriction of saturated animal fat and cholesterol intake. Adding polyunsaturated vegetable oils to the diet helps reduce LDL-C concentration. Secondary treatment is aimed at reducing or eliminating aggravating factors, such as alcoholism, diabetes mellitus, or hypothyroidism. To reduce risk factors that contribute to atherosclerosis, the regimen includes treating hypertension, implementing an exercise program, controlling blood sugar, and stopping smoking. For type V hyperlipoproteinemia, female patients are taken off oral contraceptives. Medications may also be prescribed to lower the plasma concentration of lipoproteins, either by decreasing their production or by increasing their removal from plasma.

Gender Ethnicracial And Life Span Considerations

Hyperthyroidism is most frequently found in women as compared with men, and some experts suggest that the hormone cycles of women may in some way affect the incidence of thyroid disease. Although it can affect all ages, it is most typically diagnosed in 20- to 40-year-olds and is unusual in children, teenagers, and people over 65 years of age. When hyperthyroidism occurs in the elderly, their symptoms may be more subtle than those of younger persons, and the classic signs may even be absent. Occasionally, an elderly person with hyperthyroidism has apathy or withdrawal instead of the more typical hypermetabolic state. No specific gender and ethnic racial considerations exist in hyperthyroidism.

Resistance to Thyroid Hormone in Childhood

Occasionally, a patient is seen in the clinic with apparent hypo- and or hyperthyroid symptoms but with conflicting results of thyroid function tests they have a nonsuppressed or even slightly increased TSH inappropriate for the invariably increased free T4 in serum. This combination of hormone levels can have several causes but there are two major ones namely a TSH-producing pituitary adenoma and resistance to thyroid hormone (RTH). The latter will be the subject of this chapter. The basic problem in RTH is a decreased sensitivity of tissues to thyroid hormone. The decreased sensitivity is also present in the pituitary, where it leads to a blunting of the feedback of thyroid hormone on the pituitary. This in turn results in the above mentioned increased secretion of TSH and thereby of T4. As will be explained below, the insensitivity is caused by mutations in the thyroid hormone receptor beta isoform that reduce thyroid hormone binding affinity. This does not just lead to a...

Pharmacologic Highlights

Treatment consists of replacing the deficient hormone with synthetic thyroid hormone low doses are initially used, and the dose is increased every 1 to 2 months based on the clinical response and serial laboratory measurements that show normalization of thyroid-stimulating hormone (TSH) levels in primary hypothyroidism. The patient begins to experience clinical benefits in 3 to 5 days, which level off after approximately 4 to 6 weeks. After the dose is stabilized, patients can be monitored with laboratory measurement of TSH annually. The patient with myxedema is generally weak and therefore progressively immobile. Hypothyroidism exposes the patient to the risk of skin breakdown. One goal is to increase the patient's mobility while accommodating her or his extreme weakness with frequent rest periods. Provide meticulous skin care.

Mechanisms of Thyroid Autoimmunity

It is well established that a complex interplay of diverse environmental and genetic susceptibility factors interact in predisposing an individual to autoimmune thyroid disease (fig. 1). Moreover, the contribution that each factor makes varies from patient to patient, and as yet there are no clear genotype-phenotype correlations. We have shown that polymorphisms in the thyroid stimulating hormone receptor (TSH-R) are associated with Graves' disease but not autoimmune Clinical autoimmune thyroid disease Clinical autoimmune thyroid disease Fig. 1. Interaction of factors predisposing to autoimmune thyroid disease. hypothyroidism 2 . The other known genetic loci associated with thyroid autoimmunity, namely HLA, CTLA-4 and PTPN22, are shared between these 2 thyroid conditions, as well as many other autoimmune diseases reviewed in 3 . Several environmental factors have been delineated but some of these remain controversial and of unknown action, such as smoking and stress 4, 5 . Evidence...

Clinical manifestation

Onset in early childhood organs most involved the bone, the viscera, the connective tissue, and the brain lichenified, dry, thick skin with diminished elasticity increased pigmentation on the dorsum of the hands sclerodermalike changes hypertrichosis of the extremities pale colored hair neurologic symptoms hypertensive hydrocephalus syndrome, changes in the tonus of the musculature and the tendon reflex, and damage of the cranial nerves myxedema in patients with associated hypothyroidism dwarfism hepat-osplenomegaly cardiovascular involvement progressive deterioration of intellect after a period of apparently normal development speech disturbances ocular symptoms progressive clouding of the cornea, megalocornea, hereditary glaucoma, and congestion and atrophy of the optic disc death often occurs before age 10 years from progressive neurologic and cardiovascular deterioration

Effects of Hyperthyroidism on Mother and Child

Congestive heart failure and thyroid storm may also occur and the risk of pre-eclampsia is significantly higher in women with poorly controlled hyperthyroidism and low birth weight may be up to nine times as common. Neonatal hyperthyroidism, prematurity and intra-uterine growth retardation may be observed. A retrospective review documented a 5.6 incidence of fetal death or stillbirth in 249 pregnancies from hyperthyroid mothers and a further 5 fetal and neonatal abnormalities. Women with thyroid hormone resistance who, despite being euthyroid, had high levels of circulating T4 had a significantly increased miscarriage rate compared to euthyroid unaffected couples 30 . However, a recent study of women with subclinical hyperthyroidism, comprising 1.7 of women, showed no significant adverse pregnancy outcomes suggesting that treatment of this condition in pregnancy is not warranted 31 . Nevertheless, there is no doubt that overt clinical and biochemical hyperthy-roidism should...

Studies in Experimental Animal Models

The suppressive effect of GA in EAE is a specific one, since GA lacked any suppressive effect on the immune response in several systems - humoral and cellular immune responses to a variety of antigens and vaccination against various induced infections. GA treatment also did not suppress other experimental autoimmune diseases, including myasthenia gravis, thyroiditis, diabetes, and systemic lupus erythematosus.5,17 However, it has been reported to inhibit another autoimmune disorder, namely experimental uveoretinitis,18 a disease interrelated with MBP and EAE. Recently, GA was also shown to be effective in the case of experimental colitis.19 In addition, GA also had an effect on a murine model for graft-versus-host disease, as well as in three systems of graft rejection.20

Directions for the Future

The discovery of the genetic cause of Pendred syndrome opened up new opportunities in the study of thyroid, ear and kidney physiology. The next challenge is to translate these findings into clinically relevant interventions. Genetic testing can identify carriers in high-risk populations, and this information can then be used for genetic counseling and family planning. The thyroid disease per se does not cause overwhelming disability however, early, complete thyroid

Prevention and Optimization

Control of blood sugar levels and with awareness maintained of the correlation with vascular disease which may impact on flap survival and wound healing. Pulmonary status should be evaluated fully with pulmonary function tests and preoperative arterial blood-gas levels in patients for whom there is concern about persistent postoperative aspiration or chronic ventilator requirement. Subclinical hypothyroidism may be associated with poor wound healing however, we do not routinely obtain thyroid function tests preoperatively unless the patient has symptoms of hypothyroidism or a history of radiotherapy to the head and neck. Patients with chronic steroid use are started on preoper-ative vitamin A supplementation to aid in wound healing, as shown in studies by Hunt et al.13 Finally, some consideration should be given to the patient's age. Although elderly patients undergoing major resection have complication rates similar to those of younger patients, they suffer from more severe medical...

Evaluation of Patient

It is important that every effort be made to locate the primary tumor. If found, the primary can be adequately and appropriately treated and the patient's prognosis therefore better assessed. In addition, locating the primary lesion may avoid extensive mucosal radiation and therefore avoid the often severe adverse effects of wide-field mucosal irradiation. These adverse effects include severe xerostomia, dental caries, laryngeal edema, osteoradionecrosis of the mandible, laryngeal chondritis, persistent pain, dysphagia due to submucosal fibrosis of the pharynx, hypothyroidism, hypopituitarism, and aspiration.5-8

Roussel And Dunn 2004 Thyroid Function

8 Delange F Iodine deficiency in Europe and its consequences an update. Eur J Nucl Med 2002 29(suppl 2) S404-S416. 9 WHO, UNICEF and ICCIDD Indicators for Assessing Iodine Deficiency Disorders and Their Control Through Salt Iodization. Geneva, WHO, WHO NUT 94.6, 1994. 10 World Health Organization WHO global database on iodine deficiency. Internet http www3. who.int whosis micronutrient. Accessed 18 May, 2006. 11 Dumont JE, Ermans AM, Maenhaut G, Coppee F, Stanbury JB Large goiter as a maladaptation to iodine deficiency. Clin Endocrinol (Oxf) 1995 43 1-10. 12 WHO, UNICEF and ICCIDD Assessment of Iodine Deficiency Disorders and Monitoring Their Elimination. Geneva, WHO, WHO NHD 01.1, 2001. 13 Delange F Iodine deficiency as a cause of brain damage. Postgrad Med J 2001 77 217-220. 15 Pemberton HN, Franklyn JA, Kilby MD Thyroid hormones and fetal brain development. Minerva Ginecol 2005 57 367-378. 17 Vulsma T, Gons MH, de Vijlder J Maternal-fetal transfer of thyroxine in congenital...

Childhood Hyperthyroidism

Hyperthyroidism occurs much less commonly in children than hypothyroidism, yet is a far more virulent condition 7, 8 . In children the most common cause of childhood thyrotoxicosis is Graves' disease, which is characterized by diffuse goiter, hyperthyroidism and occasionally ophthalmopathy 6, 9-11 . Other causes of childhood hyperthyroidism include toxic nodules, toxic multinodular goiters, acute and subacute thyroiditis, and the ingestion of thyroid hormone 6, 9-11 .

Measurement Of T Cell Proliferative Response To Mouse Thyroglobulin

The T cell proliferation assay is used as an adjunct to histologic examination of the thyroid for assessment of experimental autoimmune thyroiditis (EAT). It correlates well with thyroid infiltration after mouse thyroglobulin (MTg) immunization in that only cells from susceptible strains respond to in vitro stimulation with MTg. In addition, this assay can be used to detect the presence of T cells that have been primed to respond to thyroglobulins (Tgs) from various species or to synthetic peptides.

Background Information

Induction of murine experimental autoimmune thyroiditis (EAT) and its genetic linkage to the major histocompatibility complex (MHC), which was first shown by Vladutiu and Rose (1971), form the basis for many subsequent studies on autoimmune diseases and their MHC association in humans and other species. Hashimoto's thyroiditis (HT) and mouse thyroglobulin (MTg)-induced EAT share the persistent characteristics of mononu-clear cell infiltration, follicular destruction, autoantibody production, and T cell prolifera-tive response to thyroglobulin (Tg). As reviewed recently (Kong, 1994 Kong and Gi-raldo, 1994), studies of EAT have provided insights into cellular infiltration kinetics (the role of T cell subsets and macrophages), short-and long-term effects of immunotherapy, involvement of cytotoxic T cells, and the role of regulatory T cells in preventing EAT induction. Moreover, the usefulness of EAT as a model for HT is fortified by two recent findings evidence for HLA-DRB1 association...

Antithyroid Drug Therapy

In contrast to oral iodine therapy (see below), thiouracil drugs do not prevent thyroid gland hyperplasia. Thus, thyroid enlargement may occur during therapy. The thyroid gland may become softer and the outlines of the gland more difficult to distinguish 99 . Because radioactive iodine is less effective in large than in small glands 59, 99, 107 , thyroid size should be continuously monitored for progressive thyroid enlargement that may make the patient an unsuitable candidate for radioactive iodine treatment. If the gland enlarges, this may also be due to hypothyroidism. Thus, patients should be monitored for TSH elevations. Although MMI and PTU promptly inhibit hormone formation, they do not inhibit hormone release. Thus, levels of circulating thyroid hormones may remain elevated for several weeks as stored hormone is released. Until circulating levels of thyroid hormones normalize, the signs and symptoms of hyperthyroidism may be controlled with beta-blockers such as atenolol (25 or...

Treatment Approaches for Children

When radioactive iodine is used, it is important that higher doses of 131I be used in children. The goal of radioactive iodine therapy in children should be to ablate thyroid gland and achieve hypothyroidism. If no thyroid tissue remains, the risk of thyroid cancer will be very small if present at all. To achieve this goal we now use doses of 131I of 250-300 xCi g thyroid tissue. Finally, irrespective of the treatment option selected, careful follow-up is needed for all patients treated for Graves' disease. Long-term follow-up should include regular examination of the thyroid gland and measurement of circulating levels of thyroid hormones once or twice a year. All newly appearing thyroid nodules should be biopsied or excised.

Hyperthyroidism and Pregnancy

Subacute thyroiditis causes such as hyperemesis gravidarum, toxic multinodular goitre, toxic adenoma and subacute thyroiditis may occur. It should be noted that most women with nausea and vomiting in pregnancy do not have hyperthyroidism. Rarer causes include struma ovarii, hydatidiform mole and one reported case of a TSH receptor mutation activated only during pregnancy 27 (table 3).

Pendrins Function in the Thyroid

Thyroid Pendrin

Iodination of thyroglobulin and formation of thyroid hormone. Thus, patients with severe mutations in either will have severe congenital hypothyroidism. In contrast, in the total absence of pendrin, organification is only partially inhibited and most patients remain clinically euthyroid. Thus, an alternative, as yet unidentified, pathway, or pathways, must exist by which iodide can exit the apical border of the cell. It is possible that mutations in the components of these other pathways may explain the disease in patients with clinical Pendred syndrome, but without PDS mutations.

Fetal Thyroid Development and Function

Important in the development of many organs including the brain. It is now well accepted that maternal circulating T4 crosses the placenta into the fetus at all stages of pregnancy, first shown by Vulsma et al. 20 . The precise mechanism of placental T4 transport is not clear but the important role of both the type 2 and type 3 deiodinase enzymes, both expressed in the placenta, has been recognised. Type 2 deiodinase is also located in the uterus and other parts of the genital tract and may have a role in fetal implantation 21 . In the fetus it is expressed in the brain and its action supplies that developing organ with T3. Type 3 deiodinase (D3), which degrades thyroid hormones, is also expressed in pregnant uterus, placenta, fetal and neonatal tissues. Analysis of a D3 knock out mouse has revealed a critical role for this enzyme in the maturation and function of the thyroid axis 22 . As thyroid hormone receptors have been localised in different brain areas well before fetal thyroid...

Thyroid hormone synthesis

* Secretion of thyroid hormones follows proteolysis of thyroglobulin within endocytotic vesicles by endosomal and lysosomal enzymes. Proteolysis is initiated by cathepsins D, B and L. Exopeptidases release free T3 and T4. The thyroid predominantly produces T4, which is converted in peripheral tissues to the metabolically active form T3. Increasing iodide intake may occasionally either reduce total organic iodine (Wolf-Chaikoff effect) or increase organic iodine, especially in iodine deficiency areas (Jod-Basedowphenomenon).

Hypothalamicpituitarythyroid axis

The hypothalamic-pituitary-thyroid axis is an integrated organ complex providing for the regulated production of thyroid hormones. It is affected by the following factors Hypothalamic TRH production Increased dopamine, noradrenaline Decreased T3, T4, glucocorticoids Pituitary TSH production Increased TRH e Serum thyroid hormones T4, free T4, T3, free T3, thyroglobulin. i Basal serum TSH a normal level virtually rules out thyrotoxicosis or hypothyroidism Primary hypothyroidism Secondary hypothyroidism (pituitary failure) Tertiary hypothyroidism (hypothalamic failure) Primary hyperthyroidism Secondary hyperthyroidism

Imaging of the Normal and Affected Thyroid in Childhood

Imaging has undergone major advances over the past three decades and has revolutionized the evaluation of patients with thyroid disease. However, the use of thyroid imaging is in general not evidence-based, and there have been few cost-benefit evaluations of medical imaging 1 .

Highurine osmolality urine osmolality serum osmolality

High-urine sodium (> 40 mEq L) and normal volume is most likely caused by water retention due to a drug effect, hypothyroidism, or the syndrome of inappropriate antidiuretic hormone secretion. In SIADH, the urine sodium level is usually high. SIADH is found in the presence of a malignant tumor or a disorder of the pulmonary or central nervous system.

Selenium Deficiency and Supplementation

The essential trace element selenium is involved in thyroid hormone synthesis, metabolism and action. In several regions of the world people are exposed to inadequate selenium supply because selenium contents of surface soils have been depleted by erosion and glacial washout similar to iodine. Therefore, plant and animal food chains contain inadequate amounts of both of these elements. Deficiencies of selenium and iron can act in concert with iodine deficiency to impair thyroid metabolism and modify the response to prophylactic iodine. The effects of selenium and iron status on iodine and thyroid metabolism share certain parallels. Selenium deficiency reduces the activity of the selenium-dependent deiodinase and peroxidase enzymes and thereby impairs thyroid metabolism in iodine-deficient populations 21-24 . Similarly, iron deficiency reduces heme-dependent thyroperoxidase activity, impairs thyroid metabolism, and influences the response to iodine in iodine deficiency disorders....

Iron Deficiency and Supplementation

Iodine deficiencies often coexist in regions of West and North Africa, 20-30 of school-age children suffer from both goiter and iron-deficiency anemia. Data from animal studies indicate that iron deficiency, with or without anemia, impairs thyroid metabolism. Iron deficiency also impairs thyroid metabolism in human trials. Overall, these studies suggest that iron deficiency blunts the thyrotropic response to exogenous TRH lowers serum T3 and T4 levels, and lowers utilization of thyroid hormones 25-30 . Clinical trials were done in primary schools in an area of endemic goiter in the mountains of Cote d'lvoire. At that time, the median urinary iodine concentration and the goiter rate by palpation in school-aged children in this region were 28 xg l and 45 , respectively, indicating moderate to severe iodine deficiency. Goitrous, school-aged children were divided into two groups nonan-emic or with iron deficiency anemia. All children received an oral dose of 0.4 ml iodized poppy seed oil...

Vitamin A Supply and Zinc Status

In a double-blind, randomized clinical trial, children with vitamin deficiency were given iodized salt and either vitamin A or placebo at 0 and 5 months. At baseline, increasing severity of vitamin A deficiency was a predictor of greater thyroid volume and higher concentrations of TSH and thyroglobulin. In children with vitamin A deficiency, the odds ratio for goiter was 6.51 (95 CI 2.94-14.41). Severity of vitamin A deficiency was also a strong predictor of higher concentrations of total T4 the odds ratio for hypothyroidism in vitamin A deficiency was 0.06 (95 CI 0.03-0.14). During the intervention, mean thyroglobulin, median TSH, and the goiter rate significantly decreased in the vitamin A-treated group compared with those in the placebo group. The findings indicate that vitamin A deficiency in severely iodine deficient children increases TSH stimulation and thyroid size and reduces the risk for hypothy-roidism. This effect could be due to decreased vitamin A-mediated suppression of...

Thyroid Hormone Therapy

Effect Thyroid Hormornes Cells

Thyroid hormones accelerate metabolism. Their release (A) is regulated by the hypophyseal glycoprotein TSH, whose release, in turn, is controlled by the hypothalamic tripeptide TRH. Secretion of TSH declines as the blood level of thyroid hormones rises by means of this negative feedback mechanism, hormone production is automatically adjusted to demand. Replacement therapy of hypothyroidism. Whether primary, i.e., caused by thyroid disease, or secondary, i.e., resulting from TSH deficiency, hypothy-roidism is treated by oral administration of T4. Since too rapid activation of metabolism entails the hazard of cardiac overload (angina pectoris, myocar-dial infarction), therapy is usually started with low doses and gradually increased. The final maintenance dose required to restore a euthyroid state depends on individual needs (approx. 150 jg d). able to a level at which hypothyroidism is averted. Therefore, the thyroid increases in size. In addition, intrathyroid depletion of iodine...

The Thyroid and Autoimmunity in Children and Adolescents

Thyroid autoimmunity is the commonest disease process to affect thyroid function. The prevalence of thyroid autoimmunity increases throughout life, with a possible decline in frequency in the very old as a 'healthy survivor' effect. The mere presence of thyroid autoimmunity, as demonstrated by the presence of thyroid autoantibodies or focal thyroiditis, for example, does not equal thyroid disease, since the majority of people with focal thyroiditis do not become hypothyroid 1 . On the other hand, as far as we know the formation of thyroid-stimulating antibodies (TSAb) leads to Graves' disease in the great majority of subjects, even if in rare cases their levels may oscillate and be associated with a fluctuating clinical course. After a brief review of the basic immunological mechanisms which underlie autoimmune thyroid diseases, this chapter will focus on the comparatively few studies which have looked specifically at the pathogenic mechanisms in these disorders in children and...

Post 131I Cancer Risks

It is important to note that iodine deficiency and exposure to nuclides other than 131I may have contributed to the increased risk of thyroid cancer in the young following the Chernobyl reactor explosion 70-72 . In comparison, rates of thyroid cancer were not increased in the more than 3,000 children exposed to 131I from the Hanford reactor site in an iodine replete region 75 . An increase in thyroid cancer has not been observed in about 6,000 children who received 131I for diagnostic procedures 72, 76 .

Patients with Concomitant Disease Neurologic Diseases

Constipation occurs commonly among patients with other diseases. In many instances, these conditions are the actual cause of an individual's constipation. For example, hypothyroidism is well known to cause constipation. In other cases the associations may be coincidence or may be the result of shared etiologic risk factors. To investigate this possibility, Johanson et al24 examined the Health Care Financing Administration (HCFA) database comprising 11 million Medicare beneficiaries to assess the association of constipation with other coexisting diseases. Not surprisingly, a number of recognized causes of constipation were found to be strongly associated with constipation including laxative abuse odds ratio (OR) 18.8 , Hirschsprung's disease (OR 6.5), intestinal obstruction (OR6.3), and hypothyroidism (OR 1.6). These findings served to corroborate the validity of the results.

Classification of Diabetes Mellitus and the Metabolic Syndrome

Immune-mediated diabetes, previously referred to as insulin-dependent diabetes, type I diabetes, and juvenile-onset diabetes, accounts for 5-10 of all cases of diabetes. Immune-mediated diabetes typically develops in childhood and adolescence, but has a variable age of onset ranging from infancy to the eighth and ninth decades of life. Abnormalities in glucose homeostasis result from severe insulin deficiency due to cell-mediated autoimmune inflammation (insulitis) and subsequent destruction of the b-cells of the pancreas. In T1DM, daily exogenous insulin administration is a life-sustaining intervention, and the absence of insulin can result in a state of acute metabolic decompensation known as diabetic ketoacidosis (DKA). Individuals with T1DM are at increased risk for other autoimmune disorders such as Graves' disease, Hashimoto's thyroiditis, Addison's disease, vitiligo, celiac sprue, autoimmune hepatitis, myasthenia gravis, and pernicious anemia.

Hormones Thyroid Agent

1 Weetman AP Autoimmune thyroid disease propagation and progression. Eur J Endocrinol 2003 148 1-9. 9 Penhale WI, Farmer A, McKenna RP, Irvine WJ Spontaneous thyroiditis in thymectomized and irradiated Wistar rats. Clin Exp Immunol 1973 15 225-236. 11 Chen F, Day SL, Metcalfe RA, Sethi G, Moses S, Kapembwa M, Brook G, Churchill D, de Ruiter A, Robinson S, Lacey CJ, Weetman AP Characteristics of autoimmune thyroid disease occurring as a late complication of immune reconstitution in patients with advanced human immunodeficiency virus (HIV) disease. Medicine (Baltimore) 2005 84 98-106. 13 McIntosh RS, Asghar MS, Weetman AP The antibody response in human autoimmune thyroid disease. Clin Sci 1997 92 529-541. 15 McLachlan SM, Braley-Mullen H, Chen C-R, Aliesky H, Pichurin PN, Rapoport B Dissociation between iodide-induced thyroiditis and antibody-mediated hyperthyroidism in NOD.H-2h4 Mice. Endocrinology 2005 146 294-300. 16 Weetman AP Cellular immune responses in autoimmune thyroid disease....

Side Effects

Despite concerns regarding resorcinol and sa-licylate toxicity, Jessner's solution has been extremely well tolerated with minimal side ef-3 fects. Allergic reactions to resorcinol are reported to be rare 9,10 .Although the potential to induce thyroid disease has been reported, a recent toxicological review on the risk of resorcinol in inducing thyroid abnormalities did not support an association 9 . However, resorcinol administered at high doses to rodents can disrupt thyroid hormone synthesis and can produce goitrogenic effects. Clinical case reports from patients undergoing resorcinol therapy for dermatological indications reveal thyroid side effects in instances where copious amounts of resorcinol-containing ointments are applied to integrity-compromised skin for months to years. However, a risk assessment comparing potential worst-case exposures to resorcinol through its use in dermatological preparations supports the conclusion that under real-life conditions, human exposures to...

Thyroid Drugs

Levothyroxine sodium Action Kinetics The thyroid manufactures two active hormones thy-roxine and triiodothyronine, both of which contain iodine. These thyroid hormones are released into the bloodstream, where they are bound to protein. Synthetic derivatives include liothyronine (T3), levothyro-nine (T4), and liotrix (a 4 1 mixture of T4 and T3). The thyroid hormones regulate growth by controlling protein synthesis and regulating energy metabolism by increasing the resting or basal metabolic rate. This results in increases in respiratory rate body temperature CO oxygen consumption HR blood volume enzyme system activity rate of fat, carbohydrate, and protein metabolism and growth and maturation. Excess thyroid hormone causes a decrease in TSH, and a lack of thyroid hormone causes an increase in the production and secretion of TSH. Normally, the ratio of T4 to T3 released from the thyroid gland is 20 1 with about 35 of T4 being converted in the periphery (e.g., kidney, liver) to T3. Uses...


Action Kinetics Predominantly beta-1 blocking activity. Has no membrane stabilizing activity or intrinsic sympathomimetic activity. Low lipid solubility. Peak blood levels 2-4 hr. tVi 6-9 hr. 50 eliminated unchanged in the feces. Uses Hypertension (either alone or with other antihypertensives such as thiazide diuretics). Angina pectoris due to hypertension, coronary atherosclerosis, and AMI. Non-FDA Approved Uses Prophylaxis of migraine, alcohol withdrawal syndrome, situational anxiety, ventricular arrhythmias, prophylacti-cally to reduce incidence of supraven-tricular arrhythmias in coronary artery bypass surgery. Contraindications Hypersensitiv-ity to atenolol, cardiogenic shock, 2nd or 3rd degree heart block, sinus bradycardia, congestive heart failure, cardiac failure. Special Concerns Aortic or mitral valve disease, asthma, COPD, diabetes mellitus, major surgery, renal disease, thyroid disease, well-compensated heart failure. Side Effects Oral Dry mouth. CV Bradycardia, CHF, cold...

Specific History

Diseases reported to provoke urticaria atopy, systemic lupus, dermatomyositis, lymphoma, dysproteinemias, hyper- and hypothyroidism. With the exception of hyperthyroidism, these are rare associations. Atopy and thyroid disease are associated with common hives while the others are usually associated with urticarial vasculitis, a disease distinct from common hives that will be covered in the differential diagnosis section.


Because D1 is a selenoprotein, one might expect to find decreased D1 enzyme activity in selenium deficiency, and in rats this was indeed demonstrated for hepatic and renal D1 70, 71 . There are, however, differences in the organ sensitivity to selenium deficiency, so studies may show difference in results depending on the organs studied. Furthermore, it is difficult to study in humans, because it is difficult to find pure, isolated selenium deficiency. Yet, mildly elevated serum T4 levels have been described in selenium-deficient humans 70-73 . Selenium supplementation in an area with both iodine and selenium deficiency has resulted in an unexpected reduction of serum T4, and in some an increase of serum TSH as indication of worsening of hypothy-roidism 74, 75 . This reaction might be explained by selenium deficiency causing reduced Dl-catalyzed inner ring deiodination of iodothyronines, thereby protecting against hypothyroidism. These results are in contrast to a study by Roti et al....

Causes of anemia

Vitamin B)2 deficiency (macrocytic) most commonly due to pernicious anemia (antiparietal cell antibodies). Remember the physiology ofBJ2 absorption and the association with vitiligo and hypothyroidism. Other causes include gastrectomy, terminal ileum resection, diet (strict vegan), chronic pancreatitis, and Diphyllobothiium latum (fish tapeworm) infection. Peripheral smear looks the same as in folate deficiency (macrocytes, hypersegmented neutrophils), but the patient has neurologic deficiencies (loss of sensation or position sense, paresthesias, ataxia, spasticity, hypcrreflexia, positive Babinskt sign, de mentia). Look for low serum B13 , achlorhydria (no stomach add secretion, elevated stomach pH), and antibodies to parietal cells. A Schilling test usually determines the etiology. Usual replacement route is intramuscular, because most patients cannot absorb Bl2.

Codeine sulfate

Contraindications Premature infants or during labor when delivery of a premature infant is expected. Special Concerns May increase the duration of labor. Use with caution and reduce the initial dose in clients with seizure disorders, acute abdominal conditions, renal or hepatic disease, fever, Addison's disease, hypothyroidism, prostatic hypertrophy, ulcerative colitis, urethral stricture, following recent GI or GU tract surgery, and in the young, geriatric, or debilitated clients. Additional Drug Interactions

Newborn Screening

Newborn screening (NS) for congenital hypothyroidism (CH) is one of the major achievements of preventive medicine 1, 2 . Although since 1972 the problem of CH has been resolved in developed countries by the implementation of NS for CH, the problem exists for developing countries that still have no NS programs for CH 2, 3 . Since diagnosis based on clinical findings is delayed in most instances because of few symptoms and signs, hypothyroidism in the newborn period is almost always overlooked and delayed diagnosis leads to the most severe outcome of CH, mental retardation. In a study from Denmark, it was emphasized that only 10 of the affected infants were diagnosed within the first month of life, 35 within 3 months. 70 were diagnosed within the first year, while in the remainder the diagnosis was delayed to the 3rd and 4th years of life 4 . In a retrospective analysis of 1,000 cases of CH from Turkey, the mean age at diagnosis was 49 months and only 3.1 of cases were diagnosed within...


Most patients have corrected themselves by increasing their serum thyroid hormones in the presence of normal TSH 12, 14 . No treatment is necessary in these cases. When the patient presents with hyperthyroid symptoms, especially tachycardia, beta-blockers can be used. The thyroid hormone analogue 3,5,3'-triiodothyroacetic acid (TRIAC) has also been used successfully to treat some symptoms of RTH in children such as increased TSH and goiter 15-18 . This is due to the fact that TRIAC has a higher affinity for the TRp then for the TRa, and is metabolized more rapidly then T3. Because of this it has a limited effect on organs like the heart with a predominance of TRa. Similar treatment successes with D-T4 19, 20 have no clear explanation. In cases where previous erroneous diagnosis has occurred resulting in postsurgical or postradiation hypothyroidism, treatment with thyroid hormone can be started. As an outcome for successful therapy serum TSH can be used required T4 doses can be as high...

Radioactive Iodine

If a patient is taking antithyroid medication, as is often the case, treatment should be stopped 3-5 days before the administration of radioactive iodine. If antithyroid medication is stopped too soon before radioactive iodine administration, there can be accumulation of thyroid hormones within the gland leading to thyroid storm following radioactive iodine treatment 35 . After 131I administration, circulating levels of thyroid hormones may then rise within 4-10 days as thyroid hormone is released from degenerating follicular cells 36 . Progressive decline in thyroid hormone levels will then occur. Until the patient becomes biochemically euthyroid or hypothyroid, which usually takes 6-12 weeks after treatment, symptoms of hyperthyroidism can be controlled using beta-blockers 36-38 . The use of SSKI or Lugol's solution started one week after the administration of radioactive iodine will also attenuate biochemical hyperthyroidism and not adversely affect the outcome of radioiodine...


Total thyroidectomy is the procedure of choice for Graves' disease 68, 91, 92 . New surgical techniques, such as minimally invasive thyroidectomy and minimally invasive video-assisted thyroidectomy have recently been described 93 . Whereas it can take several months for the hyperthyroid state to remit after 131I treatment, the hypothyroid state occurs much sooner after surgery, being dependent on the clearance of circulating thyroid hormone. Following subtotal thyroidectomy, relief of hyperthyroidism is achieved in about 80 of children and adults, and hypothyroidism develops in about 60 of individuals 94, 95 . Hyperthyroidism recurs in about 10-15 of patients after subtotal thyroidectomy 68, 94, 95 . In comparison, hyperthyroidism recurs in less than 3 of children and adults who undergo total thyroidectomy, and hypothyroidism is nearly universal 68, 94-96 .


Kong, Y.M., McCormick, D.J., Wan, Q., Motte, R.W., Fuller, B.E., Giraldo, A.A., and David, C.S. 1995. Primary hormonogenic sites as conserved autoepitopes on thyroglobulin in murine autoimmune thyroiditis Secondary role of io-dination. J. Immunol. 155 5847-5854. Kong, Y.M., Lomo, L.C., Motte, R.W., Giraldo, A.A., Baisch, J., Strauss, G., Hammerling, G.J., and David, C.S. 1996. HLA-DRB1 polymorphism determines susceptibility to autoimmune thyroiditis in transgenic mice Definitive association with HLA-DRB1*0301 (DR3) gene. J. Exp. Med. 184 1167-1172. Lewis, M., Fuller, B.E., Giraldo, A.A., and Kong, Y.M. 1992. Resistance to experimental autoimmune thyroiditis is correlated with the duration of raised thyroglobulin levels. Clin. Immunol. Immunopathol. 64 197-204. Nakashima, M., Kong, Y.M., and Davies, T.F. 1996. The role of T cells expressing TcR VP13 in autoimmune thyroiditis induced by transfer of mouse thyroglobulin-activated lymphocytes Identification of two common CDR3 motifs. Clin....

Clinical Syndrome

In contrast, the thyroid disease associated with Pendred syndrome rarely presents in infancy, usually appearing in late childhood or early adolescence as diffuse or multinodular goiter. Typically, the patients are clinically euthyroid, although mild, compensated hypothyroidism, characterized by elevated TSH with normal thyroxin and tri-iodothyronine levels, is often present. However, clinical presentation is variable and Massa et al. recently described a case of documented Pendred syndrome in whom the presenting thyroid pathology was a painless, benign solitary thyroid nodule that resolved after hormone replacement 8 . The size of the goiter is also variable, and may be small, detectable only on close physical examination, or may reach massive proportions, causing significant cosmetic problems or even tracheal compression (fig. 1) 9 . Although the goiter tends to recur after surgery, partial thyroidectomy may be required. The histological appearance of the thyroid tissue is...

Iodine Excess

Of iodine are given to subjects with normal thyroid function a transient decrease in the synthesis of the thyroid hormones occurs for 48 h. This acute inhibitory effect of iodine on thyroid hormone synthesis is called the acute Wolff-Chaikoff effect and is due to increased intrathyroid iodine concentrations. The escape from or adaptation to the acute Wolff-Chaikoff effect is a decrease in the thyroid iodide trap, thereby decreasing the intrathyroid iodide concentration 68 , due to a decrease in the sodium iodide symporter (NIS) mRNA and protein expression 69 . For this reason, most people can tolerate high doses of iodine without developing thyroid abnormalities. Excess iodine ingestion (up to 1.5-3.0 mg day) also decreases the release of T4 and T3 from the thyroid resulting in small decreases in serum T4 and T3 concentrations with compensatory increases in basal and TRH-stimulated TSH concentrations, all values remaining well within the normal range. These iodine-treated subjects...


Chen F, Day SL, Metcalfe RA, Sethi G, Kapembwa MS, Brook MG, Churchill D, De Ruiter A, Robinson S, Lacey CJ, and Weetman AP (2005). Characteristics of autoimmune thyroid disease occurring as a late complication of immune reconstitution in patients with advanced human immunodeficiency virus (HIV) disease. Medicine (Baltimore) 84(2) 98-106.

The Philippines

Many studies have shown that micronutrient deficiencies are widespread their serious consequences for health, survival, and intellectual development are now well known. Deficiency of vitamin A, while decreasing in clinical form, affects some 30 percent of children subclinically, with relatively little decline in recent years. Iodine deficiency, as goiter, is seen in at least 10 percent of the population and may even be increasing, a serious concern since even mild deficiency can adversely affect cognitive development. Anemia, for which iron deficiency is a major cause, affects more than 30 percent of the population and may also be increasing


Subacute thyroiditis is rare in childhood 35 and most often presents with thyrotoxicosis and elevated erythrocyte sedimentation rate and is associated with neck pain and tenderness. Reduced or no thyroid uptake on a scintiscan supports the diagnosis (fig. 11). Fig. 11. 99mTc pertechnetate thyroid scintigraphy of a 14-year-old girl with transient thyrotoxicosis and painful swelling of the thyroid gland following an episode of flu-like symptoms. Low tracer uptake, compatible with subacute thyroiditis, is seen. Fig. 11. 99mTc pertechnetate thyroid scintigraphy of a 14-year-old girl with transient thyrotoxicosis and painful swelling of the thyroid gland following an episode of flu-like symptoms. Low tracer uptake, compatible with subacute thyroiditis, is seen.


In a recent retrospective review of PET CT images, obtained in 78 patients with non-head and neck cancers, the accumulation of FDG was described 46 . Intense tracer uptake is usually seen in the palatine tonsils, soft palate, and lingual tonsils. In the normal thyroid gland, the tongue, and inferior conchae the uptake is minimal. FDG accumulation is variable in the sublingual, submandibular and parotid glands 46 . Thus, the normal thyroid shows very low-grade FDG uptake, and is usually not visualized on the whole-body FDG-PET scan. Diffuse thyroid FDG uptake is usually an indicator of chronic autoimmune thyroiditis, as supported by the presence of thyroid autoantibodies and changes on sonography in one study 50 . Occasionally, focally or diffusely increased FDG uptake is seen as an incidental finding in the thyroid. The dilemma is to differentiate physiologic from pathologic FDG uptake 51 . Although a high FDG uptake in a thyroid tumor suggests malignancy even low levels of FDG uptake...


Because of the superficial location of the thyroid gland, high-resolution real-time gray-scale and color Doppler sonography can demonstrate the normal thyroid anatomy and pathologic conditions with remarkable clarity 58 . With increasing availability, this technique has come to play an ever more important role in the diagnostic evaluation of thyroid diseases. High-frequency transducers (7.5-15.0 MHz) provide both deep ultrasound penetration (up to 5 cm) and a high-definition image, with a resolution of 0.7-1.0 mm. It can distinguish solid nodules from cysts and allows accurate estimation of size, shows vascular flow (Doppler), and aids in the accurate placing of needles for diagnostic or therapeutic purposes 59 . It is also an excellent tool for use in the follow-up for estimation of changes in size of a lesion or the entire thyroid gland over time. Finally, it allows in utero investigation of the fetal thyroid 60 and can be helpful in fetal diagnosis of thyroid dysfunction 61 . The...

Treatment Strategies

Anemia Hypogonadism Adrenal insufficiency Hypothyroidism Infections Malnutrition Depression Inactivity Primary adrenal insufficiency can be treated with oral hydrocortisone or dexamethasone replacement therapy (Dufour et al., 2005). Hypothyroidism improves with levothyroxine administration, which has also been found to improve quality of life and energy levels in HIV patients with no evidence of hypothyroidism (Derry, 1995).

Computed Tomography

Supported by the availability of equal, or in some instances superior, imaging modalities. Furthermore, the need for sedation in newborn and smaller children makes CT less attractive compared to US, as an initial examination of neck masses in children. CT-guided biopsy is possible but more cumbersome than is US-guided biopsy. It can be valuable in poorly accessible or deep-seated lesions of the neck 135 . Neither CT nor MRI is routinely indicated in the pediatric population with thyroid disorders, and never in case of hyper- or hypothyroidism. Localization of thyroid tissue is valuable in the workup of hypothyroidism (including congenital hypothyroidism) during childhood or in rare cases of stridor 136 . For this purpose, US is recommended as an initial screening examination in addition to scintigraphy. However, in a small series of 19 patients with congenital hypothyroidism, enhanced CT (Omnipaque intravenously) identified ectopic (sublingual) thyroid tissue in 7 patients, which was...


Isotretinoin and etretinate have subsequently been replaced by acitretin and the third generation of retinoids, bexarotene, for the treatment of CTCL. An optimal dose of bexarotene of 300 mg m2 day is recommended. Although higher doses (500-600 mg m2 day) may be more effective, dose-limiting hypertriglyceridemia with pancreatitis is more common. The most significant side effects of bexarotene are hypertriglyceridemia, hypercholesterolemia, leukopenia, central hypothyroidism, and headache. Hypertriglyceridemia occurs in 82 of the patients and requires additional treatment with lipid-lowering agents such as fenofibrate, HMG-CoA reduc-tase inhibitors or statins. Gemfibrozil is not recommended since it increases bexarotene-induced hypertriglyceridemia (44).

Hair Loss

A high fever or severe infection can produce hair loss, as can an overactive or underactive thyroid gland. Other causes of hair loss include an inadequate amount of protein in your diet, iron deficiency, or cancer treatment. Certain prescription medications such as those for gout, arthritis, depression, heart disease, or high blood pressure can cause hair loss in some people. Large doses of vitamin A also can cause hair loss. If you notice that your hair is falling out in large amounts after you brush or comb your hair, see your doctor as soon as possible to determine the cause.


Despite significant progress, deficiencies of iodine and other trace elements, e.g. selenium and iron, remain major public health problems affecting more than 30 of the global population. These deficiencies often coexist in children. Recent studies have demonstrated that a high prevalence of iron deficiency among children in areas of endemic goiter may reduce the effectiveness of iodized salt programs. These findings argue strongly for improving iron status in areas of overlapping deficiency, not only to combat anemia but also to increase the efficacy of iodine prophylaxis. The dual fortification of salt with iodine and iron may prove to be an effective and sustainable method to accomplish these important goals. Iron deficiency impairs thyroid hormone synthesis by reducing activity of heme-dependent thyroid peroxidase. Iron-deficiency anemia blunts and iron supplementation improves the efficacy of iodine supplementation. Combined selenium and iodine deficiency leads to myxedematous...

Eruptive Xanthoma

Eruptive Xanthomas And Lipemia Retinalis

Diabetic xanthoma, xanthoma diabetacorum Serum hypertriglyceridemia and or elevated VLDL Diabetes mellitus, oral estrogens, acute ethanol ingestion, lipoprotein lipase deficiency, Type IV V hyperlipoproteinemia, pregnancy, nephrotic syndrome, hypothyroidism, intravenous miconazole, oral 13-a's-retinoic acid Eruptive xanthoma (EX) is a serious systemic dyslipid-emia with distinctive cutaneous features. Although the dermatologic manifestations are not in themselves serious, their presence may be the harbinger of serious visceral disease. EX is an uncommon disease with a near equal gender incidence, principally seen in two age groups with different predisposing factors. Among children and young adults genetic disturbances in lipid metabolism are largely responsible and include lipoprotein lipase deficiency and Type I and V hyperlipoproteinemia (1). In older adults, acute ethanol ingestion and endocrinologic disturbances including hypothyroidism and diabetes mellitus are often observed....

Potential causes

Tis, vasculitis, eosinophilic fasciitis, polymyalgia rheumatica, fibromyalgia. Alcohol, drugs, hypothyroidism. Metabolic myopathies. Muscle strain. Neuromyotonia. Stiff-man syndrome Muscle cramps Idiopathic, exercise-induced, pregnancy, uremia, hypothyroidism, electrolyte imbalance hypothyroidism, female carrier of trait (Duchenne Becker muscular dystrophy), incipient myopathy (muscular dystrophy, myositis, glycogen storage disease), hereditary 1 Hypokalemic or hyperkalemic form. 2 Table 66. 3 Hypothyroidism or hyperthyroidism, acromegaly, Cushing disease, hyperparathyroidism, Conn syndrome, Cushing syndrome. 4 Myopathia distalis tarda hereditaria. 5 Elevation of creatine kinase (CK) levels in serum without clinical evidence of myopathy risk of malignant hyperthermia (related to general anesthesia, see p. 346).

Child Development

Thyroid hormones are major factors for the normal development of the brain. The mechanisms of actions of thyroid hormones in the developing brain are mainly mediated through two ligand-activated thyroid hormone receptor isoforms 50 . It is known that thyroid hormone deficiency may cause severe neurological disorders resulting from the deficit of neuronal cell differentiation and migration, axonal and dendritic outgrowth, myelin formation and synapto-genesis 23 . This is the situation well documented in iodine-deficient areas where the maternal circulating thyroxine concentrations are too low to provide adequate fetal levels particularly in the first trimester. Recent work has raised concern that in an iodine-sufficient area maternal thyroid dysfunction (hypothyroidism, subclinical hypothyroidism or hypothyroxinaemia) during pregnancy results in neuro-intellectual impairment of the child. Two studies, have shown that a low thyroid hormone concentration in early gestation can be...

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