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Subclinical hypothyroidism is a biochemical diagnosis characterized by an elevated serum TSH level, but with a normal serum free thyroxine level. [47] [48] [49] The incidence of subclinical hypothyroidism is estimated to be 3-15% and a higher incidence is seen in elderly people, females and those with lower iodine levels. [47]
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 ...
Thyroiditis is a group of disorders that all cause thyroidal inflammation. Forms of the disease are Hashimoto's thyroiditis, the most common cause of hypothyroidism in the US, postpartum thyroiditis, subacute thyroiditis, silent thyroiditis, drug-induced thyroiditis, radiation-induced thyroiditis, acute thyroiditis, Riedel's thyroiditis. [8]
Hypothyroidism is common in pregnancy with an estimated prevalence of 2-3% and 0.3-0.5% for subclinical and overt hypothyroidism respectively. [8] Endemic iodine deficiency accounts for most hypothyroidism in pregnant women worldwide while chronic autoimmune thyroiditis is the most common cause of hypothyroidism in iodine sufficient parts of the world.
It is the most common cause of hypothyroidism in developed countries. [10] It typically begins between the ages of 30 and 50. [3] [4] Rates of the disease have increased. [9] It was first described by the Japanese physician Hakaru Hashimoto in 1912. [11] Studies in 1956 discovered that it was an autoimmune disorder. [12]
The first case of HE was described by Brain et al. in 1966. [10] The patient was a 48-year-old man with hypothyroidism, multiple episodes of encephalopathy, stroke-like symptoms, and Hashimoto's thyroiditis confirmed by elevated antithyroid antibodies.
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[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]