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Subclinical hyperthyroidism is a milder form of hyperthyroidism characterized by low or undetectable serum TSH level, but with a normal serum free thyroxine level. [32] Although the evidence for doing so is not definitive, treatment of elderly persons having subclinical hyperthyroidism could reduce the number of cases of atrial fibrillation ...
Hyperthyroidism. Graves-Basedow disease; Toxic multinodular goitre; Thyrotoxic myopathy; ... List of MeSH codes (C19) List of ICD-9 codes 240-279: Endocrine ...
Even then, upon cessation of the drugs, the hyperthyroid state may recur. The risk of recurrence is about 40–50%, and lifelong treatment with antithyroid drugs carries some side effects such as agranulocytosis and liver disease. [27] Side effects of the antithyroid medications include a potentially fatal reduction in the level of white blood ...
Thyroid diseases are highly prevalent worldwide, [10] [11] [12] and treatment varies based on the disorder. Levothyroxine is the mainstay of treatment for people with hypothyroidism, [13] while people with hyperthyroidism caused by Graves' disease can be managed with iodine therapy, antithyroid medication, or surgical removal of the thyroid ...
Acute infectious thyroiditis (AIT) also known as suppurative thyroiditis, microbial inflammatory thyroiditis, pyrogenic thyroiditis and bacterial thyroiditis. [1] [2] [3]The thyroid is normally very resistant to infection.
The term is sometimes used to refer to hyperthyroidism, but hyperthyroidism is a more general term. [2] When the level of thyroxine (T4) in the blood exceeds normal range, it can lead to symptoms such as irritability and unexplained weight loss. [3] Types include: Familial dysalbuminemic hyperthyroxinemia; Familial euthyroid hyperthyroxinemia
The dose is typically 0.15–0.37 MBq (4–10 μCi) of 131 I iodide, or 3.7–7.4 MBq (100–200 μCi) of 123 I iodide. [2] The RAIU test is a reliable measurement when using a dedicated probe with a reproducibility of 1 percent and a 95%-least-significant-change of 3 percent.
[9] [10] The first English-language report, in 1931, originated from Dunlap and Kepler, physicians at the Mayo Clinic; they described the condition in a patient with features of Graves' disease. [ 2 ] [ 10 ] In 1937 periodic paralysis was linked with hypokalemia, as well as precipitation of attacks with glucose and insulin.