scholarly journals Thyroid arterial embolization for the treatment of hyperthyroidism in a patient with thyrotoxic crisis

2009 ◽  
Vol 32 (1) ◽  
pp. 78 ◽  
Author(s):  
Wei Zhao ◽  
Bu-Lang Gao ◽  
Gen-Fa Yi ◽  
Hui-Ying Yang ◽  
Hong Li
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Young Woman ◽  
Effective Means ◽  
Arterial Embolization ◽  
Graves Disease ◽  
Thyrotoxic Crisis ◽  
History Of ◽  
Serum Thyroid Hormones

Purpose: We report a case of hyperthyroidism in a young woman caused by Graves’ disease that was successfully treated with thyroid arterial embolization. Clinical details: A 35 year-old woman with a history of thyrotoxic crises was admitted after the last thyroid crisis. Thyroid arterial embolization was used to treat the hyperthyroidism after it had been controlled. Immediately after embolization, the enlarged thyroid gland shrank and vascular murmurs disappeared. Serum thyroid hormones increased on day 3 following embolization but decreased gradually. Thyroid hormone returned to normal 2 months after embolization and remained normal at three years. Conclusion: Thyroid arterial embolization is an effective means to treat refractory hyperthyroidism.

Clinical assessment and systemic manifestations of thyrotoxicosis

2011 ◽  
pp. 441-452
Author(s):  
Claudio Marcocci ◽  
Filomena Cetani ◽  
Aldo Pinchera
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Clinical Manifestations ◽  
Clinical Syndrome ◽  
Graves Disease ◽  
Free Triiodothyronine ◽  
Excessive Secretion ◽  
Almost All ◽  
Symptoms And Signs

The term thyrotoxicosis refers to the clinical syndrome that results when the serum concentrations of free thyroxine, free triiodothyronine, or both, are high. The term hyperthyroidism is used to mean sustained increases in thyroid hormone biosynthesis and secretion by the thyroid gland; Graves’ disease is the most common example of this. Occasionally, thyrotoxicosis may be due to other causes such as destructive thyroiditis, excessive ingestion of thyroid hormones, or excessive secretion of thyroid hormones from ectopic sites; in these cases there is no overproduction of hormone by thyrocytes and, strictly speaking, no hyperthyroidism. The various causes of thyrotoxicosis are listed in Chapter 3.3.5. The clinical features depend on the severity and the duration of the disease, the age of the patient, the presence or absence of extrathyroidal manifestations, and the specific disorder producing the thyrotoxicosis. Older patients have fewer symptoms and signs of sympathetic activation, such as tremor, hyperactivity, and anxiety, and more symptoms and signs of cardiovascular dysfunction, such as atrial fibrillation and dyspnoea. Rarely a patient with ‘apathetic’ hyperthyroidism will lack almost all of the usual clinical manifestations of thyrotoxicosis (1). Almost all organ systems in the body are affected by thyroid hormone excess, and the high levels of circulating thyroid hormones are responsible for most of the systemic effects observed in these patients (Table 3.3.1.1). However, some of the signs and symptoms prominent in Graves’ disease reflect extrathyroidal immunological processes rather than the excessive levels of thyroid hormones produced by the thyroid gland (Table 3.3.1.2).

scholarly journals Graves’ disease treated with thyroid arterial embolization

2009 ◽  
Vol 32 (2) ◽  
pp. 158 ◽  
Author(s):  
Wei Zhao ◽  
Bu-Lang Gao ◽  
Min Tian ◽  
Gen-Fa Yi ◽  
Hui-Ying Yang ◽  
...  
Keyword(s):  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Chronic Inflammation ◽  
Color Doppler ◽  
Thyroid Tissue ◽  
Arterial Embolization ◽  
Acute Ischemia ◽  
Graves Disease ◽  
Pathological Changes ◽  
Time Points

Purpose: To study pathological changes in the thyroid gland of patients with Graves’ disease (GD) treated with thyroid arterial embolization. Methods: Thirty-seven patients with GD were treated through transcatheter thyroid arterial embolization. Of these patients, twenty-two had biopsy of the thyroid gland at different time points before and after the embolization for the study of pathology. Serum thyroid hormones, TSH and TRAb were also studied at these time points. Thyroid size was evaluated in all patients using color Doppler ultrasound or CT scan. Results: Thyroid size decreased immediately or several days following embolization. Pathological study demonstrated mainly acute infarction and necrosis at 7 days post embolization. At 6 months, chronic inflammation and fibrous hyperplasia were the primary findings in the gland, and at 3 years following embolization, mesenchyma hyperplasia and follicle atrophy were primarily present in the embolized thyroid tissue. The thyroid hormones and TSH gradually resumed to normal range after embolization while TRAb decreased significantly. Conclusion: Thyroid arterial embolization can cause GD thyroid gland a series of pathological changes of acute ischemia and necrosis and later, chronic inflammation, fibroplasia and atrophy to decrease secretion of thyroid. The pathological changes within the thyroid gland after embolization form the basis of thyroid arterial embolization in treating GD hyperthyroidism.

scholarly journals Graves’ Disease

2021 ◽  
Author(s):  
Thenmozhi Paluchamy
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
The Body ◽  
Graves Disease ◽  
Doctor Who ◽  
Exophthalmic Goiter ◽  
Circulating Autoantibodies ◽  
Thyroid Profile ◽  
Radioactive Iodine Uptake

Graves’ disease is an autoimmune disease characterized by hyperthyroidism due to circulating autoantibodies. Graves’ disease was originally known as “exophthalmic goiter” but is now named after Sir Robert Graves, an Irish doctor who first described the condition in 1835. A number of conditions can cause hyperthyroidism, but Graves’ disease is the most common, affecting around 1 in 200 people. It most often affects women under the age of 40, but it is also found in men. It affects an estimated 2–3 percent of the world’s population. Thyroid-stimulating immunoglobulin (TSIs) binds to and activates thyrotropin receptors, causing the thyroid gland to grow and the thyroid follicles to increase synthesis of thyroid hormone. The overproduction of thyroid hormones can have a variety of effects on the body causes exophthalmic goiter, graves ophthalmopathy, graves dermopathy etc.,. Thyroid profile including antithyroid antibodies, radioactive iodine uptake study, and thyroid scan are the main diagnostic investigations to rule out Graves’ disease. The major aim of the treatment is to inhibit the overproduction of thyroid hormones by targeting the thyroid gland, to reduce the symptoms, and prevention of complication is also major challenges.

EFFECT OF THE COMBINATION OF DEXAMETHASONE AND SODIUM IPODATE ON SERUM THYROID HORMONES IN GRAVES' DISEASE

1983 ◽  
Vol 19 (5) ◽  
pp. 619-627 ◽  
Author(s):  
E. ARTEAGA ◽  
J. M. LÓPEZ ◽  
J. A. RODRÍGUEZ ◽  
P. MICHAUD ◽  
G. LÓPEZ
Keyword(s):  
Thyroid Hormones ◽  
Graves Disease ◽  
Sodium Ipodate ◽  
Serum Thyroid Hormones

scholarly journals Thyrotoxicosis treatment with lithium corbanate. Cases reported

2021 ◽  
Vol 17 (3) ◽  
pp. 22-26
Author(s):  
I. A. Matsueva ◽  
A. B. Dalmatova ◽  
T. V. Andreychenko ◽  
E. N. Grineva
Keyword(s):  
Side Effects ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Toxic Hepatitis ◽  
Lithium Carbonate ◽  
Graves Disease ◽  
Allergic Reactions ◽  
Low Doses ◽  
Short Course ◽  
Toxic Goiter

Treatment of thyrotoxicosis caused by Graves’ disease or multinodular toxic goiter, is not difficult, in most cases, since the prescription of thionamides allows to normalize the level of thyroid hormones quickly and safety. But in a number of cases this therapy might be associated with serious side effects (agranulocytosis, toxic hepatitis, cholestasis), severe allergic reactions and also individual intolerance on thionamides. In such cases lithium carbonate is used, especially in severe thyrotoxic syndrome. It is known, that lithium can accumulate in the thyroid gland at a concentration 3–4 times higher than in the plasma. Perhaps, lithium uses Na+/I- ions. It can inhibit the synthesis and secretion thyroid hormones of thyroid gland. The article presents the cases reported the use of lithium carbonate in thyrotoxicosis treatment before thyroidectomy. Administering low doses of carbonate lithium (900 mg/ per day) renders significant decrease or normalization of thyroid hormones concentration within 7–14 days, thus it let perform thyroidectomy on the patients. No side effects have been identified with such a short course of lithium carbonate treatment.

LINGUAL AND SUBLINGUAL THYROID GLANDS IN EUTHYROID CHILDREN

PEDIATRICS ◽  
1966 ◽  
Vol 38 (4) ◽  
pp. 647-651
Author(s):  
Wellington Hung ◽  
Judson G. Randolph ◽  
Domenic Sabatini ◽  
Theodore Winship
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Physical Examination ◽  
Thyroid Hormones ◽  
Hormone Therapy ◽  
Surgical Intervention ◽  
Ectopic Thyroid ◽  
Lingual Thyroid ◽  
Thyroid Glands ◽  
Careful Physical Examination

Five clinically euthyroid children with lingual or sublingual thyroid glands were seen during a 12-month period. Certain recommendations have been formulated based upon our experience with these patients. A careful physical examination should be performed to demonstrate the presence of a normally located thyroid gland in all children presenting with midline masses in the lingual or sublingual areas. When the thyroid gland cannot be palpated with certainty in these children, a scintiscan with I-131 should be carried out to determine if the mass is an ectopic thyroid gland and if a normally located thyroid gland is present. All children with lingual on sublingual thyroid glands should have a trial of full replacement thyroid hormone therapy before excision is contemplated. Thyroid therapy will prevent further hypertrophy and hyperplasia. Surgical intervention should be reserved for those children in whom there is dysphagia, dysphonia, ulceration, or hemorrhage due to a lingual thyroid gland or if the ectopic thyroid gland fails to decrease in size following a course of treatment with thyroid hormones.

Iodide Metabolism and Effects

2020 ◽  
pp. 25-33
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Dietary Supplement ◽  
Thyroid Function ◽  
Thyroid Stimulating Hormone ◽  
Hormone Synthesis ◽  
Serum Tsh ◽  
Tsh Stimulation ◽  
Sensitive Marker

Iodine (I2) is essential in the synthesis of thyroid hormones T4 and T3 and functioning of the thyroid gland. Both T3 and T4 are metabolically active, but T3 is four times more potent than T4. Our body contains 20-30 mg of I2, which is mainly stored in the thyroid gland. Iodine is naturally present in some foods, added to others, and available as a dietary supplement. Serum thyroid stimulating hormone (TSH) level is a sensitive marker of thyroid function. Serum TSH is increased in hypothyroidism as in Hashimoto's thyroiditis. In addition to regulation of thyroid function, TSH promotes thyroid growth. If thyroid hormone synthesis is chronically impaired, TSH stimulation eventually may lead to the development of a goiter. This chapter explores the iodide metabolism and effects of Hashimoto's disease.

Autoantibodies to thyroxin and triiodothyronine in the immunoglobulin G fraction of serum.

1988 ◽  
Vol 34 (12) ◽  
pp. 2561-2562 ◽  
Author(s):  
L Li Calzi ◽  
S Benvenga ◽  
S Battiato ◽  
F Santini ◽  
F Trimarchi
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Human Serum ◽  
Immunoglobulin G ◽  
Subacute Thyroiditis ◽  
Total Serum ◽  
Graves Disease ◽  
Carrier Proteins ◽  
Weak Binding ◽  
Idiopathic Myxedema

Abstract Thyroid hormone antibodies (THAbs)--i.e., antibodies to thyroxin (T4) and triiodothyronine (T3)--are detected rarely in human serum, where they are searched for, possibly because of a quantitatively minimal interaction between thyroid hormones (the haptens) and serum IgGs (the antibodies). The weak binding could result from these facts: (a) there are already six physiological carrier proteins for thyroid hormones; (b) THAbs usually account for a very small fraction of the total serum IgGs; (c) THAbs may have--as reported in the literature--a relatively low affinity. To ascertain whether THAbs could pass undetected in serum, we measured antibodies to T3 and T4 in both the serum and the corresponding IgG fraction of six normal persons and 45 patients with various thyroid diseases (Graves' disease, idiopathic myxedema, Hashimoto's thyroiditis, subacute thyroiditis, tumors), using radioimmunoprecipitation. The prevalence of antibodies to T4 was 0/51 in both the sera and the IgG fractions; the prevalence of antibodies to T3 was 1/51 in both materials. Because all of the sera that tested THAb negative were confirmed to be so in the THAb assay of the IgG fraction, we conclude that the prevalence of serum THAbs is not underestimated and that autoimmunization against thyroid hormones is really a rare phenomenon.

scholarly journals Dendritic cells produce interleukin-12 in hyperthyroid mice

1999 ◽  
pp. 625-629 ◽  
Author(s):  
M Tamura ◽  
B Matsuura ◽  
S Miyauchi ◽  
M Onji
Keyword(s):  
Dendritic Cells ◽  
Thyroid Hormone ◽  
Mouse Model ◽  
Thyroid Hormones ◽  
Normal Subjects ◽  
Interleukin 12 ◽  
Graves Disease ◽  
Hyperthyroid State ◽  
Thyroid Glands

We previously reported that serum interleukin-12 (IL-12) levels were significantly increased in patients with hyperthyroid Graves' disease and in normal subjects after administration of thyroid hormone. In the present study, we investigated which cells produce IL-12 and the interactions between IL-12 and thyroid hormones, using a hyperthyroid mouse model. Thyroid hormones induced IL-12 production, and IL-12 was mainly produced by dendritic cells outside the thyroid glands in a hyperthyroid state.

scholarly journals Relative contribution of cysteine and methionine to glutathione content and thyroid hormone levels in the rat

1987 ◽  
Vol 58 (1) ◽  
pp. 105-111 ◽  
Author(s):  
C. Suberville ◽  
P. Higueret ◽  
D. Taruoura ◽  
H. Garcin ◽  
D. Higueret
Keyword(s):  
Thyroid Hormone ◽  
Pisum Sativum ◽  
Thyroid Hormones ◽  
Reduced Glutathione ◽  
Pea Protein ◽  
Relative Contribution ◽  
Methionine Supplementation ◽  
Serum Thyroid Hormone ◽  
Thyroid Hormone Levels ◽  
Serum Thyroid Hormones

1. For a period of 24 d rats were given diets containing either casein or pea (Pisum sativum) protein at two different concentrations (180 and 120 g/kg) without or with cysteine or cysteine + methionine supplementation.2. The effects of these diets on levels of blood and liver reduced glutathione (GSH) and serum thyroid hormones were studied.3. When compared with the 180 g casein/kg diet, the 120 g casein/kg diet decreased liver GSH and serum thyroid hormone concentrations. These changes were related to dietary cysteine supply since supplementation induced an increase in these variables.4. When compared with 180 g pea protein/kg diet, the 120 g pea protein/kg diet decreased liver GSH and serum thyroid hormone concentrations. These changes could not be corrected by cysteine or cysteine + methionine supplementation.

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