DOCSLIB.ORG

Fetal Goitre in Maternal Graves' Disease A.M

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Fetal Goitre in Maternal Graves' Disease A.M 1300 EDITORIAL doi: 10.4183/aeb.2018.85 FETAL GOITRE IN MATERNAL GRAVES’ DISEASE A.M. Panaitescu1,*, K. Nicolaides2 1Filantropia Hospital, Bucharest, Romania, 2Fetal Medicine Research Institute, King’s College Hospital, London, UK Abstract to the fetus and increasing requirements for maternal Fetal goitre is found in about 1 in 5,000 births, hormone production; the gland itself may increase in usually in association with maternal Graves’ disease, due to size up to 40% in some women thus decreasing serum transplacental passage of high levels of thyroid stimulating thyroglobulin. Also, iodine clearance is increased antibodies or of anti-thyroid drugs. A goitre can cause during pregnancy making hormone production in complications attributable to its size and to the associated iodine deficient areas potentially insufficient (1). thyroid dysfunction. Fetal ultrasound examination allows easy recognition of the goitre but is not reliable in Changes in the thyroid hormones during distinguishing between fetal hypo- and hyperthyroidism. pregnancy relate to the necessity of delivering thyroxine Assessment of the maternal condition and, in some cases, to the fetus, especially to the fetal brain. Maternal T4 is cordocentesis provide adequate diagnosis of the fetal thyroid effectively metabolised into inactive reverse T3 by the function. First-line treatment consists of adjusting the dose placenta, however a small but physiologically relevant of maternal anti-thyroid drugs. Delivery is aimed at term. In amount of T4 is still transferred to the fetus and this is cases with large goitres, caesarean-section is indicated. essential for normal fetal development (2). Normal fetal brain development depends on maternal derived T4 at Key words: Graves’ disease, fetal goitre, fetal least until 16 weeks’ gestation when the fetal thyroid thyroid, pregnancy. starts to produce the thyroid hormones.(3) In the fetal brain deiodinase type 2 is found in high levels and is responsible for converting T4 to active T3, thus making INTRODUCTION it readily available (3). In healthy women thyroid physiological changes happen seamlessly, however in The thyroid gland undergoes extensive changes cases with uncorrected thyroid dysfunction there may during pregnancy, delivery and lactation. These be deleterious effects on the fetus during pregnancy changes are supported by the interaction between the such as development of fetal hypo- or hyperthyroidism fetal-placental unit and the maternal endocrine system or fetal goitre and long term neurodevelopmental (Fig. 1) and are reflected in the thyroid function tests, sequalae (4). which differ from outside pregnancy as early as first Along with gestational and preexisting diabetes, trimester. During pregnancy, there is an increase in thyroid disorders are the most common endocrine thyroid binding globulin which leads to increased disorders in pregnant women (5). Hypothyroidism, levels of serum thyroid hormones (T4 - thyroxine and either clinical or subclinical, is encountered in about T3 - tri-iodothyronine); the placenta produces hCG 2-3% of pregnant women (6). Thyrotoxicosis is also (human chorionic gonadotrophin), a glycoprotein common and is usually due to Graves’ disease, but hormone with molecular similarity of its α-subunit during the first part of pregnancy may also be the with TSH (thyroid stimulating hormone) which acts consequence of elevated hCG levels (7) (gestational as an agonist of TSH raising transiently free T4 levels transient thyrotoxicosis) and is often associated with and decreasing serum TSH levels; plasma volume hyperemesis gravidarum. expands thus increasing total T4 and T3 pool size; This review will only discuss maternal Graves’ in the placenta, type 3 iodothyronine deiodinase is disease and its fetal consequences and will focus on the highly expressed converting T4 into inactive reverse management of prenatally detected fetal goitre in the T3 and thus controlling the availability of T3 and T4 case of maternal Graves’ disease. *Correspondence to: Anca Maria Panaitescu MD, Filantropia Hospital, 11 Ion Mihalache Blvd., Bucharest, 011161, Romania, E-mail: [email protected] Acta Endocrinologica (Buc), vol. XIV, no. 1, p. 85-89, 2018 85 A.M. Panaitescu and K. Nicolaides Graves’ disease during pregnancy treatment, radioiodine therapy or surgical removal Graves’ disease is an autoimmune disorder of the gland in those affected by Graves’ disease. characterised by the presence of immunoglobulins Therefore, indications for testing for thyroid stimulating that bind the TSH receptors in the thyroid gland and immunoglobulins in pregnant women with known stimulate the production of thyroid hormones leading to Graves’ disease include (a) mothers with untreated hyperthyroidism (the occurrence of inhibiting antibodies or drug-treated hyperthyroidism in pregnancy, (b) a being exceptional). Affected individuals are treated by previous history of Graves’ disease with past treatment radioiodine therapy or surgical removal of the gland with radioiodine or total thyroidectomy, (c) a previous followed by the administration of the synthetic thyroid history of delivering an infant with hyperthyroidism, or hormone levothyroxine. Some patients are treated by (d) a known history of thyroidectomy for the treatment anti-thyroid drugs, such as propylthiouracil, carbimazole of hyperthyroidism in pregnancy. A level of antibodies and methimazole; these drugs inhibit the enzyme of 3 times the upper limit of normal is an indication thyroperoxidase which facilitates the addition of iodine for establishing close follow-up of the fetus (10). Anti- to tyrosine in the production of thyroglobulin (Fig. 1), an thyroid drugs used during pregnancy can also cross the essential step in the formation of thyroid hormones. placenta and may be teratogenic and act on the fetal Graves’ disease is found in 1 in 500 pregnant thyroid gland, leading to hypothyroidism and fetal women (8). During pregnancy, thyroid stimulating goitre. If possible, it is recommended that anti-thyroid immunoglobulins can cross the placenta by using medication is avoided in the first trimester of pregnancy the physiological maternal-fetal antibody transfer and this can be achieved in some stable cases of pathways (9) and can act on the fetal thyroid gland Graves’ disease as the general autoimmunity decreases resulting in the development of fetal hyperthyroidism during pregnancy (11). However, when treatment and sometimes to fetal goitre. Thyroid stimulating is necessary, propylthiouracil is generally favoured immunoglobulins may persist for years after medical due to its safer fetal profile compared to carbimazole and methimazole which have been associated with development of aplasia cutis, choanal and oesophageal atresia, abdominal wall defects and ventricular septal defects. After the first trimester, consideration can be given to switching to carbimazole or methimazole to decrease the risk of liver failure in the mother (10). Fetal goitre The exact incidence of fetal goitre is not P<0.05 is considered as significant known but it may be up to 1 in 5,000 births, usually, but not exclusively, in association with maternal Graves’ disease (12). Thus, the incidence of Graves’ disease during pregnancy is about 1 in 500 (8) and incidence of fetal goitre in mothers with treated or untreated Graves’ disease is about 10% (13-17). Thyroid stimulating immunoglobulins in maternal Graves’ disease can cross the placenta and act Figure 1. Production of thyroid hormones and its control. The hypothalamus produces thyroid releasing hormone (TRH) which on the fetal thyroid gland resulting in the development stimulates the pituitary gland to release thyroid stimulating of fetal hyperthyroidism and in some cases of fetal hormone (TSH) which acts on TSH receptors on the thyroid gland goitre. However, most cases of fetal thyroid goitre are and stimulates the production of thyroid hormones. They in turn the consequence of fetal hypothyroidism due to trans- control their production through negative feedback on both the hypothalamus and pituitary gland. During pregnancy, the placenta placentally derived anti-thyroid drugs used for the produces human chorionic gonadotrophin (hCG) which stimulates treatment of maternal hyperthyroidism. (13-15). the TSH receptor. Placenta controls the availability of maternal Less common causes of fetal goitre are thyroid hormones to the fetus through the enzyme iodothyronine inadequate or excessive iodine availability (18) or deiodinase type 3 (D3) which inactivates T4 and T3. A small, but physiologically relevant amount of T4 is transferred from the congenital thyroid dyshormonogenesis due to defects mother to the fetus. This is essential for normal early neurological in genes involved in the pathway of thyroid hormone fetal development. Within the fetal brain, deiodinase type 2 is production (19). specifically expressed and converts T4 into active T3. 86 Fetal goitre in maternal Graves Ultrasound diagnosis fetal hypothyroidism or hyperthyroidism. In uncertain Fetal goitre can be diagnosed prenatally by cases, cordocentesis and measurement of fetal blood ultrasound with the demonstration of an anterior thyroid hormones and TSH can help distinguish cervical echogenic mass of variable size (Fig. 2). Large between hypothyroidism, with low thyroid hormones fetal goitres may lead to obstruction of fetal swallowing and high TSH, due to anti-thyroid drugs or congenital with consequent polyhydramnios; the neck may be dyshormonogenesis, and hyperthyroidism, with
Load more

Recommended publications
  • Basedow's Bonanza-Graves' Disease
    Journal of Liver Research, Disorders & Therapy Short Communication Open Access The prosperous goitre: basedow’s bonanza-graves’ disease Keywords: graves’ disease, auto-antibodies, thyroid gland, goiter, HLA CD40, CTLA-4, thyroglobulin, TSH receptor, PTPN 22, T cell Volume 4 Issue 3 - 2018 cytokines, toxic goitre, autoimmune hyperthyroidism, oncocytes Anubha Bajaj Abbreviations: TS Ab, thyroid stimulating antibody; TBII, Laboratory AB Diagnostics, India TSH binding inhibitor immunoglobulin; TSB Ab: thyroid stimulation blocking antibody; Anti TPO Ab, anti thyroid peroxidase antibody; Correspondence: Anubha Bajaj, Laboratory A.B. Diagnostics, Anti TG Ab, anti thyroglobulin antibody; TG, thyroglobulin; TSH R, A-1, Ring Road, Rajouri Garden, New Delhi 110027, India, Email [email protected] thyrotropin receptor; HLA, human leucocyte antigen; TRAb, TSH receptor autoantibodies Received: April 6, 2018 | Published: May 11, 2018 Introduction iodide symporter (a protein located in the baso-lateral membrane of An autoimmune disease constituting of hyperthyroidism due the thyrocytes) with an enhanced iodine uptake and a deficiency of to circulating auto-antibodies against thyrotropin (TSH receptor) TSH receptor which mobilizes protein C kinase pathway to control is delineated as Graves Disease.1 An upsurge in thyroid hormone cell proliferation. Pituitary secretion of TSH is restricted with synthesis, secretions and glandular enlargement is elucidated. Aberrant the antagonistic feedback mechanism of the accumulated thyroid glandular stimulation
    [Show full text]
  • Non Myxedematous Hypothyroidism
    University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1935 Non myxedematous hypothyroidism Norton L. Francis University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Francis, Norton L., "Non myxedematous hypothyroidism" (1935). MD Theses. 383. https://digitalcommons.unmc.edu/mdtheses/383 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. -Senior Thesis- Non-Myxedematous HYpothyroidism Norton L. Francis April 24, 1935. University of Nebraska College of Medicine -Table of Contents- Introduction Definition History Incidence Etiology Symptomatology Physical Findings Diagnosis Differential Diagnosis Treatment Summary 480690 -Introduction- The condition hypothyroidism of a non-myxedematous nature is not mentioned as such in the modern textbooks of medicine. Rather, hypothyroidism is mentioned as a condition which occurs either early in life, as creti­ nism, or in adult life as myxede~. These two subdivisions represent the inadequate discussion of hypothyroidism, as it is usually presented. In this treatise, an attempt will be made to present that condition reported in the literature as non-myxe­ dematous hypothyroidism or mild hypothyroidism. It is that condition reported in the varying degrees of severity between the conventional normal and clinical entity of true myxedema or absolute thyroid failure.
    [Show full text]
  • Goitre and Hypothyroidism in the Newborn After Cutaneous Absorption of Iodine
    Arch Dis Child: first published as 10.1136/adc.53.6.495 on 1 June 1978. Downloaded from Archives of Disease in Childhood, 1978, 53, 495-498 Goitre and hypothyroidism in the newborn after cutaneous absorption of iodine J. P. CHABROLLE AND A. ROSSIER From the Department ofPaediatrics B, H6pital Saint Vincent de Paul, Faculte de Medecine Cochin Port-Royal, University ofParis suMMARY Iodine goitre and hypothyroidism in 5 newborn infants in an intensive care unit were induced by cutaneous absorption of iodine, after numerous skin applications of iodine alcohol. The infant's skin permeability allows severe iodine overloading of the thyroid, resulting in goitre and hypothyroidism. loduria should always be sought in a newborn infant showing hypothyroidism. Iodine should not be used as a skin disinfectant in young infants. Goitre in the newborn infant resulting from maternal thyroxine index (FTI), triiodothyronine (T3), total ingestion of iodine-containing drugs is a well-known blood iodine (TBI), and urine analysis for 24 hour condition (Job et al., 1974). Parenteral sources of ioduria (UL). T3 and TBI could not always be iodine have also led to thyroid insufficiency both in measured, due to the amount of blood required. the infant (Mornex et al., 1970) and in the fetus TSH was measured by radioimmunoassay (normal (Denavit et al., 1977). We now describe thyroid range .1 ng/ml), as were T4 I, T3, and T3 test disorder in 5 newborn infants who had been treated (resin T3 uptake in vitro). TBI and Ul were measured in an intensive care unit where iodine solutions were by Technicon Autoanalyser.
    [Show full text]
  • Evaluation of Thyroid Functions in Critically Ill
    EVALUATION OF THYROID Malnutrition and illness influence every FUNCTIONS IN CRITICALLY aspect of thyroid hormone economy, from the control of secretion to the delivery, me- ILL INFANTS tabolism and ultimate action. This has led to the terminology known as "Sick Euthyroid Syndrome" which is characterized by sig- N.K. Anand nificant decrease in serum tri-iodothyronine Vineeta Chandra (T3) slight decrease in serum thyroxin (T4) R.S.K. Sinha increase in reverse T3 level and no signifi- Harish Chellani cant change in thyroid stimulating hormone (TSH) level(l-5). During the past two de- ABSTRACT cades, considerable progress has been made The degree to which thyroid functions are in the understanding of the peripheral me- affected by non-thyroid illness and an assess- tabolism of thyroid hormones in diseases ment of its correlation with mortality was evalu- that do not primarily affect thyroid gland. ated. Thirty infants (20 M, 10 F) with a mean Interestingly, all the conditions in which age of 433±3.28 months (±1 SD), with severe sick euthyroid syndrome has been docu- acute systemic illness and 30 healthy controls, mented have nothing more in common than age and sex matched, were studied for total catabolic state. Hence, it has been suggested serum T3, T4 and TSH levels at admission and recovery or before death. Serum thyroid hor- that the decrease in thyroid hormone level mones were measured using standard techniques. may be a protective phenomenon to limit There was no significant change in thyroid protein catabolism and lower energy re- indices with age, sex, nutritional status, serum quirements in non-thyroidal illness protein and C-reactive protein.
    [Show full text]
  • Thyroid Hormone Resistance in Two Patients with Papillary
    case report Thyroid hormone resistance in two patients with papillary thyroid microcarcinoma and their BRAFV600E mutation status 1 Diskapi Yildirim Beyazit Training and Research Hospital, Melia Karakose1, Mustafa Caliskan1, Muyesser Sayki Arslan1, Department of Endocrinology 1 2 1,3 and Metabolism, Ankara, Turkey Erman Cakal , Ahmet Yesilyurt , Tuncay Delibasi 2 Diskapi Yildirim Beyazit Training and Research Hospital, Department of Stem Cell and Genetic Diagnostic Center, Ankara, Turkey SUMMARY 3 Hacettepe University, School of Medicine (Kastamonu), Department Resistance to thyroid hormone (RTH) is a rare autosomal dominant hereditary disorder. Here in, we of Internal Medicine, Ankara, Turkey report two patients with RTH in whom differentiated thyroid cancer was diagnosed. Two patients were admitted to our clinic and their laboratory results were elevated thyroid hormone levels with Correspondence to: Melia Karakose unsuppressed TSH. We considered this situation thyroid hormone resistance in the light of laboratory Diskapi Hospital, and clinical datas. Thyroid nodule was palpated on physical examination. Thyroid ultrasonography Irfan- Bastug Caddesi, showed multiple nodules in both lobes. Total thyroidectomy was performed. The pathological fin- Ankara, Turkey [email protected] dings were consistent with papillary thyroid microcarcinoma. BRAFV600E mutation analysis results were negative. RTH is very rare and might be overlooked. There is no consensus on how to overcome Received on May/16/2014 the persistently high TSH in patients with RTH and differentiated thyroid cancer (DTC). Further studies Accepted on Nov/24/2014 are needed to explain the relationship between RTH and DTC which might be helpful for the treat- DOI: 10.1590/2359-3997000000091 ment of these patients. Arch Endocrinol Metab.
    [Show full text]
  • Time to Reconsider Nonsurgical Therapy of Benign Non-Toxic Multinodular Goitre
    European Journal of Endocrinology (2009) 160 517–528 ISSN 0804-4643 REVIEW Time to reconsider nonsurgical therapy of benign non-toxic multinodular goitre: focus on recombinant human TSH augmented radioiodine therapy Søren Fast, Viveque Egsgaard Nielsen, Steen Joop Bonnema and Laszlo Hegedu¨s Department of Endocrinology and Metabolism, Odense University Hospital, DK-5000 Odense C, Denmark (Correspondence should be addressed to S Fast; Email: [email protected]) Abstract The treatment of benign multinodular goitre (MNG) is controversial, but surgery is recommended in large compressive goitres. While some patients decline surgery others may have contraindications due to comorbidity, since MNG is prevalent in the elderly. Therefore, non-surgical treatment alternatives are needed. Until recently, levothyroxine therapy was the preferred non-surgical alternative, but due to low efficacy and potential side-effects, it is not recommended for routine use in recent international guidelines. Conventional radioiodine (131I) therapy has been used for two decades as an effective and safe alternative to surgery in the treatment of symptomatic non-toxic MNG. Since much higher activities of 131I are employed when treating non-toxic rather than toxic MNG, there has been reluctance in many countries to use this treatment modality. Frequently, the 131I -uptake in a non-toxic MNG is low, which makes 131I therapy less feasible. Another challenge is the negative correlation between the initial goitre size and goitre volume reduction (GVR). With its ability to more than double the thyroid 131I-uptake, recombinant human TSH (rhTSH) increases the absorbed radiation dose and thus enhances the GVR by 35–56% at the expense of up to fivefold higher rate of permanent hypothyroidism.
    [Show full text]
  • THYROTOXICOSIS BV SIR CARRICI ROBERTSON, F.R.C.S., F.R.A.C.S., Hon
    57' Postgrad Med J: first published as 10.1136/pgmj.24.277.571 on 1 November 1948. Downloaded from THYROTOXICOSIS BV SIR CARRICI ROBERTSON, F.R.C.S., F.R.A.C.S., Hon. F.A.C.S. Auckland, New Zealand A goitre is an enlargement of the thyroid gland. lating hormone (T.S.H.) goes forth from the It may be either a diffuse smooth enlargement or pituitary which causes increased activity in the a lumpy one. The lumps are due to the presence thyroid and a rise in the production of the thy- of nodules, varying in size from a pea to a cricket roxin. The opposite effect takes place if there is ball; this type used to be called adenomatous not sufficient thyroxin in the blood stream. goitre, but the pathologists say these nodules are A few years ago, it was discovered that the pro- formed by alternating phases of hyperplasia and duction of thyroxin by the thyroid gland could be involution (Reinhoff & Lewis) and are not true suspended by administering thiourea, thiouracil adenomata, so it is better to reserve the name or other thio compounds by the mouth. These 'adenoma' for the single adenoma which may drugs act by their toxic effect on the thyroid gland occur in the thyroid as in any other glandular itself: they render it incapable of synthesizing organ. Both the diffuse and the nodular enlarge- the blood iodine into thyroxin. Continued admin- ments can be present without doing apparent harm istration of the drug eventually leads to a state of to the patient: but as time goes on, something myxoedema.
    [Show full text]
  • Toxic Multinodular Goitre: a Surprising Finding Marlene Rodrigues,1 Helena Ferreira,2 Ana Antunes,1,3 Olinda Marques3,4
    Images in… BMJ Case Reports: first published as 10.1136/bcr-2017-221913 on 12 September 2017. Downloaded from Toxic multinodular goitre: a surprising finding Marlene Rodrigues,1 Helena Ferreira,2 Ana Antunes,1,3 Olinda Marques3,4 1Department of Pediatrics, DESCRIPTION Hospital de Braga, Braga, A 16-year-old healthy adolescent boy was referred Portugal 2 to the paediatric endocrinology clinic because of Department of Pediatrics, multiple thyroid nodules detected by cervical Hospital da Senhora da Oliveira ultrasound, in the context of cervical lymphade- Guimaraes EPE, Guimaraes, Portugal nopathies. There was no family history of thyroid Figure 1 Cervical ultrasound revelling multiples 3Pediatric Endocrinology Unit, disease. He denied recent infections, asthenia, nodules in the right thyroid lobe. (A) Predominantly Hospital de Braga, Braga, weight loss, sweating, palpitations, mood or sleep cystic nodule, (B) characteristic mixed nodule and (C) Portugal disturbances, dysphagia or dysphonia. At physical predominantly solid nodule. 4Department of Endocrinology, examination, an enlarged, irregular and fibro- Hospital de Braga, Braga, elastic thyroid, with a predominant right lobe, Portugal was identified. The remaining examination was Thyroid nodules are a frequent incidental normal. finding with an incidence between 9.4% and Correspondence to The analytical profile was thyroid stimulating 27.0%.1 In contrast to adults, TMNG is an Dr Marlene Rodrigues, rodrigues. f. marlene@ gmail. com hormone (TSH) <0.01 uUI/mL (normal 0.5–4.8 uncommon thyroid disease in paediatric age. The uUI/mL), free triiodothyronine (FT3) 7.27 pg/mL presence of hyperthyroidism determines the need Accepted 3 September 2017 (normal 2.3–4.2 pg/mL) and free thyroxine (FT4) for a definitive therapy in multinodular goitre, and 2.02 ng/dL (normal 0.8–2.3 ng/dL).
    [Show full text]
  • Some Aspects of Thyroid System Status in Persons Exposed to the Chernobyl Accident
    IAEA-CN-67/18 XA9745557 SOME ASPECTS OF THYROID SYSTEM STATUS IN PERSONS EXPOSED TO THE CHERNOBYL ACCIDENT Anatoly K.Cheban, Dmitry E.Afanasyev, Olga Y.Boyarskaya Paediatric Endocrinology Department, Endocrinology Departmant Radiation Medicine Scientific Centre of Ukrainian Medical Sciences Academy Melnikova str. No53, Kiev 254050, Ukraine ABSTRACT The thyroid system status estimation held in post-accidental period dynamics among 7868 children evacuated from the 30-km Chernobyl zone and resident now in Slavutich city (Cs-137 contaminated area), among contaminated regions permanent residents, among native kievites and evacuated from 30-km zone. The thyroid pathology incidence dependence on residence place during Chernobyl Accident and after that was revealed. The immune-inflammatory thyroid disorders are characteristic for 30-km zone migrants, goitre different forms - for the radionuclides contaminated territories residents. No thyroid function abnormalities frequency confidential increase was registered during the research activities run. The total serum cholesterol level application unavailability is revealed in Chernobyl accident survivors thyroid hormones metabolic effects estimation. Data concerning Chernobyl accident consequences cleaning up participants (CACCP) presented additionally. INTRODUCTION The thyroid gland and thyroid system in general posses the important place among nuclear facilities accidents. That is particular in case of Chernobyl nuclear power plant accident (CNPPA) [1]. Because of radioiodine high content in CNPPA fallout and iodine metabolism features the thyroid irradiation doses can exceed 10 - 20 Gy [2]. That unavoidably leads to thyroid pathology risk amplification [3]. Children are characteristic with higher thyroid irradiation doses compared to that in adults [4]. The radioecologic situation after the CNPPA in Ukraine is peculiar with extreme irregularity of present soil contamination level and radioiodine-produced thyroid irradiation doses in 1986.
    [Show full text]
  • Goitre – Causes, Investigation and Management
    Thyroid Goitre Causes, investigation and management Kiernan Hughes Creswell Eastman Background Goitre refers to an enlarged thyroid gland. Causes of goitre Goitre refers to an enlarged thyroid. Common causes of goitre include autoimmune disease, the formation of one or more include autoimmune disease, thyroid nodules and iodine thyroid nodules and iodine deficiency (Table 1). Goitre deficiency. occurs when there is reduced thyroid hormone synthesis Objective secondary to biosynthetic defects and/or iodine deficiency, This article outlines the causes, investigation and leading to increased thyroid stimulating hormone (TSH). management of goitre in the Australian general practice This stimulates thyroid growth as a compensatory setting. mechanism to overcome the decreased hormone synthesis. Elevated TSH is also thought to contribute to an enlarged Discussion Patients with goitre may be asymptomatic, or may present thyroid in the goitrous form of Hashimoto thyroiditis, in with compressive symptoms such as cough or dysphagia. combination with fibrosis secondary to the autoimmune Goitre may also present with symptoms due to associated process in this condition. In Graves disease, the goitre hypothyroidism or hyperthyroidism. Thyroid stimulating results mainly from stimulation by the TSH receptor hormone is the appropriate first test for all patients with goitre; antibody (Figure 1). if this hormone is low a radionuclide scan is helpful. Thyroid ultrasound has become an extension of physical examination When diffuse enlargement of the thyroid occurs in the absence of and should be performed in all patients with goitre. Ultrasound nodules and hyperthyroidism, it is referred to as a diffuse nontoxic can determine what nodules should be biopsied. Treatment goitre. This is sometimes called ‘simple goitre’ because of the options for goitre depend on the cause and the clinical absence of nodules, or ‘colloid goitre’ because of the presence of picture and may include observation, iodine supplementation, uniform follicles that are filled with colloid.
    [Show full text]
  • Graves Disease Can Occur at Any Age in Women and Men but More Commonly Affetcs Women Aged 20 Or Older
    Vermaak en Vennote CPD March 2015 Compiled by: M Fourie Grave’s Disease Graves' disease is an autoimmune disease in which the patient's own immune system attacks the thyroid gland, causing it to produce too much thyroxine (FT4). Graves' disease is a form of hyperthyroidism. When FT4 levels are high the patient's metabolic rate increases; this can have an effect on their physical appearance as well as moods. Healthy people’s immune systems attack pathogens, organisms and substances that are bad for us eg: bacteria. In an autoimmune disease a person’s immune system starts to attack normal healthy tissue. The thyroid gland is a butterfly gland situated in the neck below the adams apple. The thyroid gland is part of the endocrine system and produces hormones that regulate metabolism. The thyroid gland produces 2 hormones thyroxine (FT4) and triiodothyronine (FT3). FT4 affects many body systems and has a key role in regulating our body's metabolic rate - the rate at which chemical reactions occur in our body; the rate at which our bodies break things down to produce energy, and build new tissue (metabolism). Graves disease can occur at any age in women and men but more commonly affetcs women aged 20 or older. This disease can cause the thyroid gland to enlarge to twice its normal size known as a goitre. Graves disease can also affect the eyes, causing bulging eyes (exophthalmos). Symptoms of Graves disease: Anxiety Moodiness and irritability Insomnia Tiredness Arrhythmia (irregular heart beat) Tachycardia (accelerated heart beat) Tremor in the hands and fingers Sensitivity to heat Weight loss, even though the patient eats properly Brittle hair Goitre (thyroid gland is enlarged) Menstrual cycle changes Bowel movements are more frequent Cause Thyroid stimulating antibodies binds to the TSH receptor found on the thyroid gland and chronically stimulates it and results in high production of thyroid hormones.
    [Show full text]
  • Introduction Case
    Case Report General Surgery Medical Journal of Islamic World Academy of Sciences Recently Unusual Surgical Educational Case: A Real Giant Nodular Goiter Murat B. YILDIRIM1, Doğukan DURAK1, Ersin G. DUMLU2, Mehmet KILIÇ1, Abdüssamed YALÇIN1 ¹Departmant of General Surgery, Yıldırım Beyazıt University, Ankara, Turkey 2Departmant of General Surgery, Atatürk Education and Research Hospital, Ankara, Turkey ABSTRACT Goitre is a common endocrine abnormality. It is an enlargement of the thyroid gland. If goitre left untreated. they became giant goitre. Giant goitres are becoming increasingly infrequent because of imaging techniques. Although goitre are asymptomatic,they can compress the trachea or oesophagus and cause clinical symptoms such as dyspnea or dysphagia. We present a case of a giant goitre. A 77-year-old woman consulted our clinic. She had the swelling of her neck, had rapidly progressive increase in shortness of breath and had difficulty in swallowing. The huge mass was surgically removed without complications. The pathological result of the patient reported follicular carcinoma of the thyroid/Hurthle cell carcinoma. As such cases have the risk of malignancy, operations must be performed after getting a diagnosis to prevent complicated situations. Keywords: Giant goitre, Multi-nodular, Thyroid INTRODUCTION Normal thyroid tissue has a homogeneous structure, but sometimes thyroid tissue may show nodule formation. These nodules may occur with follicles junction that is full of colloid or they may occur with less adenoma or cysts. A 5% nodular goiter incidence is seen at nonendemic regions and 15% at endemic regions (1). Nodules, which are larger than 1 cm, can only be realized with palpation at physical examination.
    [Show full text]