scholarly journals Graves’ Disease and Pregnancy

2021 ◽  
Author(s):  
Nikolay Petrov Botushanov ◽  
Aleksandar Nikolaev Botushanov ◽  
Albena Dimitrova Botushanova
Keyword(s):  
Thyroid Gland ◽  
Beta Blockers ◽  
First Trimester ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Storm ◽  
Graves Disease ◽  
Maternal Complications ◽  
Low Birth Weight Infants ◽  
Organ Specific ◽  
And Function

Graves’ disease is an autoimmune organ specific disease characterized by excessive production of hormones from the thyroid gland and by its diffuse enlargement. The growth and function of the thyroid gland are stimulated by autoantibodies directed against the thyroid-stimulating hormone receptor. Pregnancies complicated by Graves’ disease are characterized with higher incidence of abortion, preterm delivery, low-birth- weight infants and neonatal mortality, as well as maternal complications such as heart failure, eclampsia and rarely thyroid storm. When fully controlled hyperthyroidism have excellent outcomes. Different therapeutic approaches are used in women with Graves’ planning pregnancy and in those when the disease is diagnosed after they became pregnant. Thionamides are the first choice for treatment, with Propylthyouracil being preferred for the first trimester and Methimazole for the second and third trimester. Aplasia cutis and some other malformations were associated with methimazole use during pregnancy. Monitoring the effect of treatment should ensure keeping maternal FT4 in the high normal range. Block-and replace regimen is not recommended and rdioiodine therapy is absolutely contraindicated. Thyroidectomy may be considered before pregnancy or in rare cases in the second trimester. Iodine is avoided because of the risk of fetal hypothyroidism and goiter. The use of beta-blockers is controversial. Noenatal thyrotoxicosis may occur in association with maternal Graves’ disease due to maternal TSAbs cross through the placenta.

Thyroid Disease I: Hyperthyroidism in Pregnancy

2020 ◽  
Author(s):  
Robert B. Martin ◽  
Brian Casey
Keyword(s):  
Hyperemesis Gravidarum ◽  
Beta Blockers ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Storm ◽  
Care Level ◽  
Hypermetabolic State ◽  
Life Threatening ◽  
Overt Hyperthyroidism ◽  
In Pregnancy ◽  
Stimulating Hormone

Thyroid physiologic adaptations in pregnancy may be confused with pathologic changes. Human chorionic gonadotropin rises early in pregnancy, stimulating thyrotropin secretion and suppressing thyroid stimulating hormone. These chemical changes are often seen in hyperemesis gravidarum and gestational transient thyrotoxicosis. Therefore, mild thyrotoxicosis may be difficult to differentiate from early pregnancy thyroxine stimulation.  However, overt hyperthyroidism usually includes classic symptoms seen outside of pregnancy in addition to suppressed TSH and T4 levels. Treatment includes thionamides propylthiouracil and methimazole.  Thyroid ablation is contraindicated in pregnancy. Often, in affected women, the fetus is euthyroid, but neonates can develop hyper or hypothyroidism with or without a goiter. Lastly, thyroid storm, though rare, is life threatening. Often presenting as a hypermetabolic state with cardiomyopathy and pulmonary hypertension, it generally results from decompensation from preeclampsia, anemia, sepsis, or surgery.  Treatment requires intensive care level management, with initiation of thionamides, iodine, and beta blockers.   This review contains 2 figures, 4 tables and 38 references. Keywords: Thyroid-releasing hormong, thyroid-stimulating hormone, thyromegaly, thyroid-stimulating immunoglobulins, thryotoxicosis, thionamides, thyroid storm

scholarly journals Graves Disease in Infancy

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A929-A930
Author(s):  
Kara A Beliard ◽  
Srinidhi Shyamkumarb ◽  
Mabel Yau ◽  
Cassie Mintz ◽  
Robert Rapaport
Keyword(s):  
Thyroid Gland ◽  
English Literature ◽  
Receptor Gene ◽  
Clinical Signs ◽  
Signs And Symptoms ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Free T4 ◽  
Ocular Changes ◽  
Clinical Signs And Symptoms

Abstract Background: Graves disease (GD) is the most common cause of hyperthyroidism worldwide. The usual age of presentation is between 20-30 years, and it is more common in females. Transient hyperthyroidism does occur in infants born to mothers with GD, however, the novo GD in infants is extremely rare. We are aware of only four cases of GD in children under the age of 2 years old previously reported in the literature, with the youngest being of 18 months. Although rare, the complications can be devastating, so identifying and treating GD in infants is vital. We describe an infant who presented at 12 months of life with poor weight gain. Patient Findings: A 12-month old female patient presented with weight loss, tachycardia, diaphoresis and hypertension. She had a palpable thyroid gland without ocular changes. She was found to have an undetectable Thyroid Stimulating Hormone (TSH) with an elevated free T4 of 2.1 ng/dL (normal 0.80 - 1.50 ng/dL). She was stabilized in the intensive care unit with beta-blocker and methimazole. The diagnosis of GD was subsequently confirmed with an extremely elevated elevated Thyroid Stimulating Immunoglobulins (TSI) titer of 263 Iu/L (normal 0.00-0.55 IU/L), her TSH receptor gene was normal. At 34 months of age, her TSI titer is still elevated at 34 IU/L and she still requires methimazole to maintain a euthyroid state. She is growing and developing appropriately. Conclusion: To our knowledge, this report describes the youngest child to be diagnosed with GD in the English literature. Only four patients between the ages of 18 - 24 months have been described. Autoimmune diseases are rare in infants, the reason for which GD developed at such a young age remains unclear. Clinical signs and symptoms of hyperthyroidism in infants can be subtle and easily missed: increased growth velocity, failure to gain weight, autonomic changes, and irritability. Most patients have an enlarged thyroid gland, and some have ocular changes. The major long-term complications of undiagnosed hyperthyroidism include craniosynostosis and permanent neurocognitive damage. A high index of suspicion is needed for the recognition and prompt treatment of GD in infants, leading to better clinical outcome.

scholarly journals Neurological manifestations of Graves’ disease: A case report and review of the literature

2016 ◽  
Vol 7 (01) ◽  
pp. 153-156 ◽  
Author(s):  
Swayamsidha Mangaraj ◽  
Arun Kumar Choudhury ◽  
Binoy Kumar Mohanty ◽  
Anoj Kumar Baliarsinha
Keyword(s):  
Similar Case ◽  
Clinical Manifestations ◽  
Autoimmune Disorder ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Diagnostic Dilemma ◽  
Ocular Manifestations ◽  
Thyroid Associated Ophthalmopathy ◽  
Organ Specific ◽  
High Degree

ABSTRACTGraves’ disease (GD) is characterized by a hyperfunctioning thyroid gland due to stimulation of the thyroid-stimulating hormone receptor by autoantibodies directed against it. Apart from thyrotoxicosis, other clinical manifestations include ophthalmopathy, dermopathy, and rarely acropachy. GD is an organ-specific autoimmune disorder, and hence is associated with various other autoimmune disorders. Myasthenia gravis (MG) is one such disease, which is seen with patients of GD and vice versa. Though the association of GD and myasthenia is known, subtle manifestations of latter can be frequently missed in routine clinical practice. The coexistence of GD and ocular MG poses a significant diagnostic dilemma to treating physicians. The ocular manifestations of myasthenia can be easily missed in case of GD and falsely attributed to thyroid associated ophthalmopathy due to closely mimicking presentations of both. Hence, a high degree of the clinical vigil is necessary in such cases to appreciate their presence. We present a similar case which exemplifies the above said that the clinical challenge in diagnosing coexistent GD and ocular myasthenia.

scholarly journals Sanguineous Pericardial Effusion and Cardiac Tamponade in the Setting of Graves’ Disease: Report of a Case and Review of Previously Reported Cases

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Peter V. Bui ◽  
Sonia N. Zaveri ◽  
J. Rush Pierce Jr.
Keyword(s):  
Atrial Fibrillation ◽  
Pericardial Effusion ◽  
Cardiac Tamponade ◽  
Low Voltage ◽  
Thyroid Stimulating Hormone ◽  
Ventricular Rate ◽  
Thyroid Storm ◽  
Graves Disease ◽  
Pericardial Effusions ◽  
Large Pericardial Effusion

Introduction. Pericardial effusion in the setting of hyperthyroidism is rare. We present a patient with Graves’ disease who developed a sanguineous pericardial effusion and cardiac tamponade.Case Description. A 76-year-old man presenting with fatigue was diagnosed with Graves’ disease and treated with methimazole. Two months later, he was hospitalized for uncontrolled atrial fibrillation. Electrocardiography showed diffuse low voltage and atrial fibrillation with rapid ventricular rate. Chest radiograph revealed an enlarged cardiac silhouette and left-sided pleural effusion. Thyroid stimulating hormone was undetectable, and free thyroxine was elevated. Diltiazem and heparin were started, and methimazole was increased. Transthoracic echocardiography revealed a large pericardial effusion with cardiac tamponade physiology. Pericardiocentesis obtained 1,050 mL of sanguineous fluid. The patient progressed to thyroid storm, treated with propylthiouracil, potassium iodine, hydrocortisone, and cholestyramine. Cultures and cytology of the pericardial fluid were negative. Thyroid hormone markers progressively normalized, and he improved clinically and was discharged.Discussion. We found 10 previously reported cases of pericardial effusions in the setting of hyperthyroidism. Heparin use may have contributed to the sanguineous nature of our patient’s pericardial effusion, but other reported cases occurred without anticoagulation. Sanguineous and nonsanguineous pericardial effusions and cardiac tamponade may be due to hyperthyroidism.

scholarly journals Graves’ Disease

2021 ◽  
Author(s):  
Vasudha Bakshi ◽  
Gollapalli Rajeev Kumar
Keyword(s):  
Thyroid Gland ◽  
Hormone Receptor ◽  
Treatment Options ◽  
Positive Family History ◽  
Current Treatment ◽  
Thyroid Stimulating Hormone ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Autoimmune Thyroid ◽  
Stimulating Hormone

Graves’ disease (GD) is an autoimmune thyroid disorder where autoantibodies are produced against TSH (Thyroid Stimulating Hormone) receptor causing thyrotoxicosis. It is characterized by goiter, ophthalmopathy, and occasionally pretibial myxedema. The autoimmune mechanism causing disease is not well understood and it is complex. It involves multifactorial etiology involving environmental and genetic factors. Smoking and positive family history contributing to the development of GD. GD can be diagnosed based on the clinical manifestation and demonstrating low concentration of TSHs, high TRab (Thyroid Stimulating Hormone receptor autoantibodies), and high FT4 (Free thyroxine) concentration. Current treatment options aimed at stable restoration of euthyroidism by following different modalities of suppressing thyroid gland using antithyroid drugs, removing/ablating thyroid gland by surgery, and radioactive iodine treatment with iodine- 131.

scholarly journals Cytomorphological alterations of thyroid gland consequent upon fluorosis

2019 ◽  
Vol 7 (2) ◽  
pp. 544
Author(s):  
Jwalaram Kumar Chaluvadi ◽  
Srinivasulu Kande ◽  
Viswa Kumar Ramalinga ◽  
Vijay Kumar Kutala ◽  
Vijay Kumar J.
Keyword(s):  
Thyroid Gland ◽  
Thyroid Function ◽  
Biochemical Parameters ◽  
Follicular Adenoma ◽  
Thyroid Function Test ◽  
Thyroid Stimulating Hormone ◽  
Structure And Function ◽  
Free Triiodothyronine ◽  
And Function ◽  
The Impact

Background: Study aimed at assessing the impact of elevated fluoride from drinking water on thyroid gland structure and function in fluorosis prone areas. Iodine is incorporated in the thyroid synthesis by thyroid gland but in the presence of low Iodine levels fluoride is likely to interfere with the concentrating capacity of thyroid of iodine in thyroid production, consequently reflecting changes in thyroid parameters and also cytomorphological features manifesting hypothyroidism in association with different pathological entities.Methods: Prakasam district in Andhra Pradesh is fluorosis prone zone and subjects are picked up from highly vulnerable zone in this district and their specimens are collected to study cytomorphological changes of the thyroid gland and biochemical parameters of blood samples for thyroid function test were considered. Cytological study by way of Fine Needle Aspiration Cytology (FNAC) of thyroid gland, biochemical parameters pertaining to function of thyroid gland namely Free triiodothyronine (FT3), Free Thyroxine (FT4) and Thyroid stimulating hormone (TSH) were assessed in the subjects from fluorosis prone zone.Results: The results were statistically significant with concurrent association of different cytological alterations of thyroid gland in these subjects like Hashimoto’s thyroiditis of hypothyroidism, adenomatous goitre, colloid goitre and few of follicular adenoma/neoplasm. FNAC makes cytological changes evident showing different morphological features that comprise different pathological entities largely with an evidence of hypothyroidism in most of the cases in the given study.Conclusions: The results of the study strongly suggest assessing the magnitude of the problem of fluorosis and also magnitude of its influence on thyroid structure and function that warrants assessment of the thyroid function by biochemical and cytological studies.

Thyroid gland disorders

2020 ◽  
pp. 289-312
Author(s):  
Gary Butler ◽  
Jeremy Kirk
Keyword(s):  
Thyroid Gland ◽  
Lymphocytic Infiltration ◽  
Thyroid Stimulating Hormone ◽  
Hormone Deficiency ◽  
Graves Disease ◽  
Childhood And Adolescence ◽  
Inborn Errors ◽  
Autoimmune Hypothyroidism ◽  
Thyroid Hormone Metabolism ◽  
Drug Of Choice

• The thyroid gland produces all of the T4 and 20% of T3. • Congenital hypothyroidism is caused by: ◦ anatomical defects: agenesis/dysgenesis, ectopic, sublingual ◦ inborn errors of thyroid hormone metabolism ◦ secondary (pituitary thyroid-stimulating hormone (TSH)) or tertiary (hypothalamic thyrotropin-releasing hormone) deficiency ◦ iodine deficiency (commonest cause worldwide of hypothyroidism, patients are usually euthyroid). • Genetic causes are rare. • In most countries worldwide, newborn TSH screening is performed at 0–5 days of age. Treatment with l-thyroxine is (usually) lifelong. • Neonatal thyrotoxicosis due to transplacental passage of thyroid-stimulating immunoglobulins (TSIs) from mothers with thyrotoxicosis/Graves’ disease and may require antithyroid drugs (ATDs). • Acquired autoimmune hypothyroidism in children and adolescents: ◦ is caused by lymphocytic infiltration of the thyroid gland (Hashimoto’s disease/thyroiditis) • raised thyroid peroxidase antibodies are diagnostic • treatment is with l-thyroxine. • Hyperthyroidism (Graves’ disease, Hashimoto’s stimulatory phase (Hashitoxicosis)): ◦ is caused by autoantibodies to the TSH receptor (TSI, or TRAbthyrotropin receptor antibody) ◦ the first-line drug of choice is the ATD carbimazole ◦ thyroidectomy or radioiodine treatment can be considered for drug-resistant cases or after relapse. • Thyroid cancer is rare in childhood and adolescence, usually presenting with a nodule, but can be part of the multiple endocrine neoplasia syndromes.

Thyroid disease

2018 ◽  
Author(s):  
John Newell-Price ◽  
Alia Munir ◽  
Miguel Debono
Keyword(s):  
Thyroid Gland ◽  
Thyroid Disease ◽  
Thyroid Nodules ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Storm ◽  
Amiodarone Therapy ◽  
Multinodular Goitre ◽  
Normal Range ◽  
Threatening Condition ◽  
Life Threatening

This chapter addresses six topics in thyroid disease: hypothyroidism; thyrotoxicosis/hyperthyroidism; thyroiditis; amiodarone-induced thyroid disease; thyroid storm; and multinodular goitre and solitary adenomas. Hypothyroidism occurs when there is insufficient secretion of thyroid hormones, commonly caused by autoimmune disease. Subclinical hypothyroidism is when the plasma level of thyroid-stimulating hormone is elevated, but free thyroxine is in the normal range. Myxoedema is severe hypothyroidism with accumulation of mucopolysaccharides in the dermis and other tissues. Thyrotoxicosis results from exposure to excessive thyroid hormone. The term ‘hyperthyroidism’ denotes those conditions in which thyroid hyperfunction results in thyrotoxicosis. Thyroiditis is inflammation of the thyroid gland, and often leads to transient thyrotoxicosis followed by hypothyroidism. Abnormalities of the thyroid occur in up to half of those on amiodarone therapy, with both thyrotoxicosis and hypothyroidism. Thyroid storm occurs as a result of exacerbation of thyrotoxicosis, and is a rare but life-threatening condition. Thyroid nodules are common, and may be multiple or single, functioning or non-functioning, and benign or malignant.

Effects of photoperiod on thyroid gland development and function in growing chicks: a biochemical and morphometric study

2021 ◽  
Vol 61 (16) ◽  
pp. 1652
Author(s):  
Seckin Ozkanlar ◽  
Hulya Kara ◽  
Cihan Gür ◽  
Semin Gedikli ◽  
Adem Kara ◽  
...  
Keyword(s):  
Thyroid Gland ◽  
Continuous Light ◽  
Thyroid Stimulating Hormone ◽  
Morphometric Study ◽  
Broiler Chicks ◽  
Free Triiodothyronine ◽  
Follicle Diameter ◽  
And Function ◽  
Gland Development ◽  
Thyroid Development

Context Light treatment has a regulatory role in some growth-related functions, including thyroid development in chicks. Aims This study aimed to investigate the effects of different photoperiod treatments on thyroid organ weight and serum thyroid hormone concentrations of broilers by use of biochemical and histological methods. Methods After the hatching, 120 broiler chicks (Ross) were divided into two main groups according to sex. Both groups were then split into two sub-groups based on photoperiod treatment: 16 h (i.e. 16 h light:8 h dark) and 24 h (24 h light:0 h dark). Thyroid gland and blood samples of six animals from each group were obtained after slaughtering at 7-day intervals from Day 14 after hatching to Day 42. Serum concentrations of free triiodothyronine (FT3), free thyroxin (FT4) and thyroid-stimulating hormone (TSH) were determined by the chemiluminescence method for all groups. Thyroid weight, bodyweight and thyroid follicle diameter were also measured. Key results Thyroid weight:bodyweight ratio generally started to increase from Day 14 to Day 42, with no significant (P > 0.05) difference among the groups at the same age. For both male and female broiler chicks, morphometric measures increased as birds grew. Serum FT3 and TSH concentrations slightly decreased and serum FT4 concentrations increased in growing chicks of both sexes. Conclusions Extending the photoperiod from 16 to 24 h had no effects on thyroid gland development or functions in terms of both biochemical and morphometric parameters in broiler chicks. Implications Continuous light has minimal effects on thyroid functions of growing broiler chicks to Day 42.

Graves Disease (Thyroid Storm) with Polyautoimmune Disorders (Autoimmune Hemolytic Anemia and Probable Autoimmune Hepatitis)

2021 ◽  
Vol 28 (1) ◽  
pp. 97
Author(s):  
Mabruratussania Maherdika ◽  
Banundari Rachmawati ◽  
Andreas Arie Setiawan
Keyword(s):  
Autoimmune Hepatitis ◽  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Cytotoxic T Lymphocyte ◽  
Thyroid Stimulating Hormone ◽  
The Body ◽  
Thyroid Storm ◽  
Graves Disease ◽  
Autoimmune Thyroid ◽  
Indirect Bilirubin

Graves' disease is caused by IgG antibodies that bind to the Thyroid Stimulating Hormone (TSH) receptor on the surfaceof the thyroid gland. These bonds drive the growth of stimulated thyroid follicular cells causing the glands to enlarge andincrease the production of thyroid hormones. Previous studies mention the association of HLA-B8 and HLA-DR3 withGraves' disease and the Cytotoxic T-lymphocyte-associated-4 (CTLA-4) gene on chromosome 2q33 as a result of reducingT-cell regulation, resulting in autoimmune disease. Autoimmune thyroid disease is often found together with otherautoimmune disorders (polyautoimmune). A 51-year-old male complained of dyspnea, yellowing of the body, and a lumpon the neck. One year ago, he was diagnosed with hyperthyroidism. Graves' disease was suspected due to a score of 22 forthe Wayne index, FT4 96.9 pmol/L, TSHs <0.01 μIU/mL, TRAb 10.8 IU/L, thyroid uptake test for toxic diffuse struma. Inaddition, the patient had atrial fibrillation and a thyroid storm with a Bruch Wartofsky index score of 65. Laboratoryexamination found normocytic normochromic anemia, thrombocytopenia, reticulocytosis, direct coomb test and autocontrol results positive one, SGOT 87 U/L, SGPT 59 U/L, alkali phosphatase 166 U/L, total bilirubin 38.13 mg/dL, directbilirubin 16.59 mg/dL, indirect bilirubin 21.54, LDH 318 U/L, establishing the diagnosis of Autoimmune Hemolytic Anemia(AIHA). Autoimmune hepatitis score: 15, so a diagnosis of probable autoimmune hepatitis was made.

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