Hyperthyroidism: Diagnosis and treatment

University of Louisville School of Medicine, Louisville, Kentucky, USA.
American family physician (Impact Factor: 2.18). 09/2005; 72(4):623-30.
Source: PubMed


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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    • "Disruptions of thyroid function by endogenous or exogenous factors may produce various subclinical effects22 or direct clinical manifestations.23 A clear example is the clinical hyperthyroidism also known as thyrotoxicosis, which can be activated by different disorder with a resultant upshot of excess thyroid hormones.24 "
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    ABSTRACT: Background: Cyanide is one of the major environmental pollutants termed thyroid disruptor. Regardless of its origin, it is a primary toxic agent. This study was designed to understand the impact of prolonged low dose cyanide exposure on the structure and function of the thyroid gland. Materials and Methods: Twelve F1 male Wistar rats were used for this study. They were divided into two groups of six animals each. The first group served as the control group and received 0.25M sucrose while the second group being the treated group received 2 mg/kg body weight (BW) potassium hexacyanoferrate III solution. The treatment duration was 56 days following which the animals were sacrificed by cervical dislocation. Blood samples were drawn to determine serum FT3, FT4 and thyroid stimulating hormone (TSH) levels. The thyroid gland was also excised and processed for light microscopic studies. Result: An increase in serum FT3 and FT4 with decrease serum TSH was obtained in the treated group. Application of one-way analysis of variance (ANOVA) statistical analysis showed that there were highly significant differences (P < 0.05) in the activities of FT3, FT4 and TSH when compared with those of the control group. Light microscopic examination of thyroid gland from the treated group revealed marked epithelial hyperplasia with cellular degeneration and scanty cytoplasm while the control group revealed normal thyroid architecture. Conclusion: Results obtained revealed that hyperthyroidism was induced by cyanide.
    Journal of the Nigeria Medical Association 05/2014; 55(3):246-9. DOI:10.4103/0300-1652.132060
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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.
    Journal of Thyroid Research 08/2011; 2011:649084. DOI:10.4061/2011/649084
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    • "Euthyroid GD patients remain at risk for developing TED [62, 63]. Furthermore, TED does not usually occur in patients with non-Graves’ hyperthyroidism [64]. It has been suggested that the orbit is a secondary target of autoimmune attack, involving the same autoantigen (TSH-R), but resulting in consequences distinct from those in the thyroid [50, 58, 65]. "
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    ABSTRACT: Thyroid eye disease (TED) is an autoimmune condition in which intense inflammation leads to orbital tissue remodeling, including the accumulation of extracellular macromolecules and fat. Disease progression depends upon interactions between lymphocytes and orbital fibroblasts. These cells engage in a cycle of reciprocal activation which produces the tissue characteristics of TED. Peroxisome proliferator-activated receptor-gamma (PPARgamma) may play divergent roles in this process, both attenuating and promoting disease progression. PPARgamma has anti-inflammatory activity, suggesting that it could interrupt intercellular communication. However, PPARgamma activation is also critical to adipogenesis, making it a potential culprit in the pathological fat accumulation associated with TED. This review explores the role of PPARgamma in TED, as it pertains to crosstalk between lymphocytes and fibroblasts and the development of therapeutics targeting cell-cell interactions mediated through this signaling pathway.
    PPAR Research 02/2008; 2008:895901. DOI:10.1155/2008/895901 · 1.64 Impact Factor
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