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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 ...
In the US, hypothyroidism and hyperthyroidism were respectively found in 4.6 and 1.3% of the >12y old population (2002). [3] In some types, such as subacute thyroiditis or postpartum thyroiditis, symptoms may go away after a few months and laboratory tests may return to normal. [4] However most types of thyroid disease do not resolve on their own.
Some do so only a few months after treatment while others may not be affected for 20–30 years. Hypothyroidism patients must begin a lifelong regimen of thyroid replacement hormones. While the onset of hypothyroidism is most common with radio-iodine treatment, the condition has been observed in patients treated with medication series and surgery.
Sub-clinical hyperthyroidism has been reported in 63% of euthyroid Graves' disease, [56] but only in 4% of cases where Graves' disease was in remission. [57] Subclinical hyperthyroidism has an 8% risk of converting to overt hyperthyroidism at 1 year, and a 26% risk at 5 years. [50]
The most common type of hyperthyroidism, Graves' disease, may additionally cause eye problems (Graves' ophthalmopathy) and skin changes of the legs (pretibial myxedema). [6] Thyroid disease may also cause muscle weakness in the form of thyrotoxic myopathy, but this is constant rather than episodic. [5]
Normal thyroid levels are also seen, and occasionally also hypothyroidism, which may assist in causing goiter (though it is not the cause of the Graves' disease). Hyperthyroidism in Graves' disease is confirmed, as with any other cause of hyperthyroidism, by measuring elevated blood levels of free (unbound) T3 and T4. [citation needed]
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Toxic multinodular goiter (TMNG), also known as multinodular toxic goiter (MNTG), is an active multinodular goiter associated with hyperthyroidism.. It is a common cause of hyperthyroidism [2] [3] in which there is excess production of thyroid hormones from functionally autonomous thyroid nodules, which do not require stimulation from thyroid stimulating hormone (TSH).