Thyrotoxicosis treatment with lithium corbanate. Cases reported

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.

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

Clinical & Investigative Medicine ◽

10.25011/cim.v32i1.5091 ◽

2009 ◽

Vol 32 (1) ◽

pp. 78 ◽

Cited By ~ 6

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.

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Graves’ Disease

10.5772/intechopen.97578 ◽

2021 ◽

Author(s):

Paula Aragão Prazeres de Oliveira ◽

Beatriz Nayara Muniz de Oliveira ◽

Eduarda da Silva Souza Paulino ◽

Fernanda Carolinne Marinho de Araujo ◽

Paula Gabriele Tabosa Lyra

Keyword(s):

Thyroid Gland ◽

Thyroid Hormones ◽

Radioactive Iodine ◽

Clinical Manifestations ◽

Nodular Goiter ◽

Graves Disease ◽

Decompression Surgery ◽

Excessive Sweating ◽

Toxic Nodular Goiter ◽

Diffuse Goiter

DG presents with three main presentations: hyperthyroidism with diffuse goiter, infiltrative ophthalmopathy and pre-tibial myxedema. Patients with Graves’ disease can rarely develop severe hyperthyroidism. The hyperthyroidism of Graves’ disease is characterized immunologically by the lymphocytic infiltration of the thyroid gland and by the activation of the immune system with elevation of the circulating T lymphocytes. In GD, goiter is characteristically diffuse. May have asymmetric or lobular character, with variable volume. The clinical manifestations of hyperthyroidism are due to the stimulatory effect of thyroid hormones on metabolism and tissues. Nervousness, eye complaints, insomnia, weight loss, tachycardia, palpitations, heat intolerance, damp and hot skin with excessive sweating, tremors, hyperdefecation and muscle weakness are the main characteristics. In the laboratory diagnosis, biochemical and hormonal exams will be done to assess thyroid hormones and the antithyroid antibodies. Additionally, imaging tests may be performed, such as radioactive iodine capture in 24 hours, ultrasonography, thyroid scintigraphy and fine needle aspiration. It is necessary to make the differential diagnosis of Graves’ disease for thyrotoxicosis, subacute lymphocytic thyroiditis and toxic nodular goiter. The treatment of DG aims to stop the production of thyroid hormones and inhibit the effect of thyroid hormones on the body. Hyperthyroidism caused by DG can be treated in the following ways: it may be the use of synthetic antithyroid medicines, thionamides, MMI being a long-term medicine, it allows a single daily dose, and adherence to treatment occurs, a disadvantage is that it cannot be used in pregnant women; beta-blockers, preferably used in the initial phase of DG with thionamides; radioactive iodine therapy (RAI), being the best cost–benefit and preventing DG recurrence; finally the total thyroidectomy, causing the withdrawal of the thyroid gland. Therefore, it should be discussed with the patient what is the best treatment for your case, with a view to the post and against each approach. If the patient develops Graves ophthalmopathy, in lighter cases the artificial tears should be used, and in more severe cases can be used as treatment, corticosteroids, orbital decompression surgery, prisms and orbital radiotherapy. In addition, the patient should keep their body healthy, doing exercise and healthy eating, following the guidance of their doctor.

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Clinical assessment and systemic manifestations of thyrotoxicosis

Oxford Textbook of Endocrinology and Diabetes ◽

10.1093/med/9780199235292.003.3162 ◽

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).

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Graves’ disease treated with thyroid arterial embolization

Clinical & Investigative Medicine ◽

10.25011/cim.v32i2.6034 ◽

2009 ◽

Vol 32 (2) ◽

pp. 158 ◽

Cited By ~ 8

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.

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Graves’ Disease

10.5772/intechopen.96418 ◽

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.

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THYROID DYSFUNCTION IN PATIENTS WITH CHRONIC KIDNEY DISEASE: THE STATE OF THE PROBLEM AND THE WAYS OF SOLVING

Nephrology (Saint-Petersburg) ◽

10.24884/1561-6274-2018-22-4-40-49 ◽

2018 ◽

Vol 22 (4) ◽

pp. 40-49 ◽

Cited By ~ 1

Author(s):

A. R. Volkova ◽

O. D. Dygun ◽

B. G. Lukichev ◽

S. V. Dora ◽

O. V. Galkina

Keyword(s):

Chronic Kidney Disease ◽

Thyroid Gland ◽

Kidney Disease ◽

Thyroid Hormones ◽

Thyroid Function ◽

Thyroid Dysfunction ◽

The Body ◽

Type I ◽

Low T3 ◽

Iodine Excretion

Disturbance of the thyroid function is often detected in patients with different profiles. A special feature of patients with chronic kidney disease is the higher incidence of various thyroid function disturbances, especially hypothyroidism. It is known that in patients with chronic kidney disease (CKD) iodine excretion from the body is violated, since normally 90% of iodine is excreted in urine. Accumulation of high concentrations of inorganic iodine leads to the formation of the Wolf-Chaikoff effect: suppression of iodine organization in the thyroid gland and disruption of the thyroid hormones synthesis. Peripheral metabolism of thyroid hormones is also disturbed, namely, deiodinase type I activity is suppressed and peripheral conversion of T4 into T3 is inhibited (so-called low T3 syndrome). Therefore, patients with CKD are often diagnosed with hypothyroidism, and the origin of hypothyroidism is not always associated with the outcome of autoimmune thyroiditis. The article presents an overview of a large number of population studies of thyroid gland dysfunction in patients with CKD, as well as experimental data specifying the pathogenetic mechanisms of thyroid dysfunction in patients with CKD. Therapeutic tactics are still not regulated. However, in a number of studies, replacement therapy with thyroid hormones in patients with CKD had some advantages.

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Very rare case of Graves’ disease with resistance to methimazole: a case report and literature review

Journal of International Medical Research ◽

10.1177/0300060521996192 ◽

2021 ◽

Vol 49 (3) ◽

pp. 030006052199619

Author(s):

Yusaku Mori ◽

Munenori Hiromura ◽

Michishige Terasaki ◽

Hideki Kushima ◽

Makoto Ohara ◽

...

Keyword(s):

Thyroid Hormone ◽

Rare Case ◽

Therapeutic Option ◽

Lithium Carbonate ◽

Graves Disease ◽

High Dose ◽

Hormone Concentration ◽

Thyroid Hormone Concentration ◽

Serum Thyroid Hormone ◽

Inorganic Iodine

Background Methimazole (MMI) is used to treat hyperthyroidism in Graves’ disease. It is rare to encounter patients in whom hyperthyroidism cannot be controlled using high doses of MMI. Case presentation: A 21-year-old woman was referred to our hospital because of MMI-resistant Graves’ disease. Although her MMI dose had been increased to 120 mg/day, her serum thyroid hormone concentration was too high to be measured. Additional therapy with lithium carbonate, and then with dexamethasone and inorganic iodine, was initiated. After 14 days, the patient’s serum thyroid hormone concentration normalized, while she was taking 150 mg/day MMI, 800 mg/day lithium carbonate, 6 mg/day dexamethasone and 306 mg/day inorganic iodine, and total thyroidectomy was then performed. The patient was discharged 8 days after the thyroidectomy and experienced no major complications. Conclusions We have presented a rare case of Graves’ disease that was resistant to high-dose MMI. Combination therapy of MMI with lithium carbonate, dexamethasone and inorganic iodine may represent a therapeutic option for the preoperative preparation of patients with MMI-resistant Graves’ disease.

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LACK OF EFFECT OF SOMATOSTATIN ON THYROID GLAND FUNCTION IN GRAVES' DISEASE

Clinical Endocrinology ◽

10.1111/j.1365-2265.1980.tb01038.x ◽

1980 ◽

Vol 13 (2) ◽

pp. 167-171 ◽

Cited By ~ 1

Author(s):

S. SKARE ◽

H. M. M. FREY

Keyword(s):

Thyroid Gland ◽

Graves Disease ◽

Thyroid Gland Function ◽

Gland Function

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Rescue pre-operative treatment with Lugol’s solution in uncontrolled Graves’ disease

Endocrine Connections ◽

10.1530/ec-17-0025 ◽

2017 ◽

Vol 6 (4) ◽

pp. 200-205 ◽

Cited By ~ 6

Author(s):

Jan Calissendorff ◽

Henrik Falhammar

Keyword(s):

Heart Rate ◽

Thyroid Hormone ◽

Side Effects ◽

Definitive Treatment ◽

Graves Disease ◽

Free T4 ◽

Hormone Levels ◽

Free T3 ◽

Adherence To Medication ◽

Thyroid Hormone Levels

Background Graves’ disease is a common cause of hyperthyroidism. Three therapies have been used for decades: pharmacologic therapy, surgery and radioiodine. In case of adverse events, especially agranulocytosis or hepatotoxicity, pre-treatment with Lugol’s solution containing iodine/potassium iodide to induce euthyroidism before surgery could be advocated, but this has rarely been reported. Methods All patients hospitalised due to uncontrolled hyperthyroidism at the Karolinska University Hospital 2005–2015 and treated with Lugol’s solution were included. All electronic files were carefully reviewed manually, with focus on the cause of treatment and admission, demographic data, and effects of iodine on thyroid hormone levels and pulse frequency. Results Twenty-seven patients were included. Lugol’s solution had been chosen due to agranulocytosis in 9 (33%), hepatotoxicity in 2 (7%), other side effects in 11 (41%) and poor adherence to medication in 5 (19%). Levels of free T4, free T3 and heart rate decreased significantly after 5–9 days of iodine therapy (free T4 53–20 pmol/L, P = 0.0002; free T3 20–6.5 pmol/L, P = 0.04; heart rate 87–76 beats/min P = 0.0007), whereas TSH remained unchanged. Side effects were noted in 4 (15%) (rash n = 2, rash and vomiting n = 1, swelling of fingers n = 1). Thyroidectomy was performed in 26 patients (96%) and one was treated with radioiodine; all treatments were without serious complications. Conclusion Treatment of uncontrolled hyperthyroidism with Lugol’s solution before definitive treatment is safe and it decreases thyroid hormone levels and heart rate. Side effects were limited. Lugol’s solution could be recommended pre-operatively in Graves’ disease with failed medical treatment, especially if side effects to anti-thyroid drugs have occurred.

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