Article

Hyperthyroidism: Diagnosis and treatment

University of Louisville School of Medicine, Louisville, Kentucky, USA.
American family physician (Impact Factor: 1.82). 09/2005; 72(4):623-30.
Source: PubMed

ABSTRACT The proper treatment of hyperthyroidism depends on recognition of the signs and symptoms of the disease and determination of the etiology. The most common cause of hyperthyroidism is Graves' disease. Other common causes include thyroiditis, toxic multinodular goiter, toxic adenomas, and side effects of certain medications. The diagnostic workup begins with a thyroid-stimulating hormone level test. When test results are uncertain, measuring radionuclide uptake helps distinguish among possible causes. When thyroiditis is the cause, symptomatic treatment usually is sufficient because the associated hyperthyroidism is transient. Graves' disease, toxic multinodular goiter, and toxic adenoma can be treated with radioactive iodine, antithyroid drugs, or surgery, but in the United States, radioactive iodine is the treatment of choice in patients without contraindications. Thyroidectomy is an option when other treatments fail or are contraindicated, or when a goiter is causing compressive symptoms. Some new therapies are under investigation. Special treatment consideration must be given to patients who are pregnant or breastfeeding, as well as those with Graves' ophthalmopathy or amiodarone-induced hyperthyroidism. Patients' desires must be considered when deciding on appropriate therapy, and dose monitoring is essential.

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    • "Conventional principal management of thyrotoxicosis includes antithyroid drugs, radioactive iodine, and surgery. Adjunctive treatment in the form of beta-blockers, corticosteroids , inorganic iodide, and iopanoic acid may also be used for more prompt control of symptoms [3] [4] [5] [6]. However, a few cases may require additional treatment despite these conventional modalities to achieve euthyroid state. "
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    ABSTRACT: Background. Conventional management of thyrotoxicosis includes antithyroid drugs, radioactive iodine, and surgery while adjunctive treatment includes beta-blockers, corticosteroids, inorganic iodide and iopanoic acid. Very rarely, patients may be resistant to these modalities and require additional management. Case Presentation. A 50-year-old lady presented with weight loss and palpitations diagnosed as atrial fibrillation. Her past history was significant for right thyroid lobectomy for thyrotoxicosis. Thyroid functions tests at this presentation showed free T4 of 6.63 ng/dl (normal range: 0.93-1.7) and TSH of <0.005 μIU/mL (normal range: 0.4-4.0). She was given aspirin, propranolol, heparin and carbimazole; however free T4 failed to normalize. Switching to propylthiouracil (PTU) did not prove successful. She was then given high doses of prednisolone (1 mg/kg/day) and lithium (400 mg twice daily) which prepared the patient for radioactive iodine treatment by reducing free T4 levels (2.82 ng/dl). Two doses of radioactive iodine were then administered 6 months apart. Subsequently she became hypothyroid and was started on thyroid replacement therapy. Conclusion. This case highlights management options in patients with resistant thyrotoxicosis. Radioactive iodine and surgery are definitive modes of treatment in such complex cases while steroids and lithium play an important role in preparing patients for more definitive treatment.
    08/2011; 2011:649084. DOI:10.4061/2011/649084
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    • "Therefore, even in the euthyroid state, GD leads to an increase in oxidative stress. Increased oxidative stress may play a role in the pathogenesis of GD [19] [20] Consequently, markers indicating increased oxidative stress may be observed in GD patients, even in the euthyroid state. "
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    ABSTRACT: The aim of our study was to evaluate the oxidant/antioxidant status of thyroid tissue in Graves' disease (GD) patients and to compare the results of GD thyroid tissue with plasma of patients and healthy controls. We studied 25 consecutive patients with GD hyperthyroidism who underwent surgical treatment. The patients were divided into groups according to the duration of antithyroid drug treatment, the type of antithyroid drugs used, the presence of ophthalmopathy, and recurrence after a complete course of antithyroid drugs. Thiobarbituric acid-reacting substances (TBARS), glutathione peroxidase (GPx) activity, superoxide dismutase (SOD) activity, and total thiol (t-SH) content of tissue and plasma samples were determined. TBARS concentrations were found to be significantly increased in GD patients' plasma compared with controls' plasma (0.1+/-0.02 nmol/mg protein vs. 0.062+/-0.01 nmol/mg protein). Significantly decreased t-SH concentrations were measured in GD patients' plasma compared with controls (8.26+/-1.9 nmol/mg protein vs. 13.03+/-3.3 nmol/mg protein). Tissue TBARS, t-SH, GPx, and SOD measurements in GD patients indicated significantly increased concentrations compared with the plasma levels of patients. Patients with shorter treatment duration before the operation had significantly increased plasma and tissue TBARS and decreased plasma and tissue t-SH concentrations. Patients on propylthiouracil treatment had significantly lower plasma and tissue concentrations of TBARS than patients on methimazole. Patients with recurrence had significantly higher plasma and tissue TBARS and lower plasma and tissue t-SH concentrations than patients treated for the first time. In euthyroid GD patients on antithyroid drugs, increased oxidative stress and a compensatory increase in the antioxidant defense system are more prominent in thyroid tissue than in plasma. Patients who relapsed had markers indicating increased oxidative stress. Thus, ongoing autoimmunity may contribute to increased oxidative stress in GD patients, even in the euthyroid state.
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