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Though the exact cause of myxedema is still unclear, a wealth of research has demonstrated the importance of iodine. [10] In an important study [11] the researchers showed that in the myxedematous type of cretinism treatment with iodine normalizes thyroid function provided that the treatment is begun early in the postnatal period. If not, the ...
[10] [3] IL-1β has been shown to decrease liver D1, [10] as well as thyroid hormone receptor (THR) levels. IL-6 and TNFa downregulate D1 and suppress TSH, are negatively correlated with fT3, and are positively correlated with rT3. [3] NF-κB also inhibits D1, and decreases the expression of Thyroid receptors α and β. [3]
American guidelines recommend that treatment should be considered in people with symptoms of hypothyroidism, detectable antibodies against thyroid peroxidase, a history of heart disease, or are at an increased risk for heart disease if the TSH is elevated but below 10 mIU/L. [8] American guidelines further recommend universal treatment ...
Myxedema coma is an extreme or decompensated form of hypothyroidism and while uncommon, is potentially lethal. [1] [2] [3] A person may have laboratory values identical to a "normal" hypothyroid state, but a stressful event (such as an infection, myocardial infarction, or stroke) precipitates the myxedema coma state, usually in the elderly.
Certain medications can have the unintended side effect of affecting thyroid function. While some medications can lead to significant hypothyroidism or hyperthyroidism and those at risk will need to be carefully monitored, some medications may affect thyroid hormone lab tests without causing any symptoms or clinical changes, and may not require treatment.
The syndrome can present with variable symptoms, even between members of the same family harboring the same mutation. [1] Typically most or all tissues are resistant to thyroid hormone, so despite raised measures of serum thyroid hormone the individual may appear euthyroid (have no symptoms of over- or underactivity of the thyroid gland).
The abnormality in the channel is thought to lead to shifts of potassium into cells, under conditions of high thyroxine (thyroid hormone) levels, usually with an additional precipitant. Treatment of the low levels of potassium in the blood, followed by correction of the hyperthyroidism, leads to complete resolution of the attacks.
Thyroid function testing often shows decreased thyroid stimulating hormone and increased serum levels of triiodothyronine and thyroxine during the acute phase. Thyroid scans show minimal uptake during the acute phase due to disrupted thyroid follicles, but increase during recovery due to the thyroid gland's enhanced iodine trapping capacity.