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Diagnosis starts with a history and physical examination. Screening for thyroid disease in patients without symptoms is a debated topic although commonly practiced in the United States. [8] If dysfunction of the thyroid is suspected, laboratory tests can help support or rule out thyroid disease.
Some patients in the early stage of the disease may experience symptoms of hyperthyroidism due to the release of thyroid hormones from intermittent thyroid destruction. [21] [25] While most symptoms are attributed to hypothyroidism, several studies have observed symptoms in hashimotos patients with normal thyroid hormone levels.
[7] [8] In 1926 the Japanese physician Tetsushiro Shinosaki, from Fukuoka, observed the high rate of thyroid disease in Japanese people with periodic paralysis. [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 ...
In 1971, the thyroid stimulating hormone (TSH) radioimmunoassay was developed, which was the most specific marker for assessing thyroid status in patients. [82] Many people who were being treated based on basal metabolic rate, minimizing hypothyroid symptoms, or based on serum protein-bound iodine, were found to have excessive thyroid hormone. [82]
Hashimoto's encephalopathy, also known as steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), is a neurological condition characterized by encephalopathy, thyroid autoimmunity, and good clinical response to corticosteroids.
Following this, a similar phenotype was noted in patients with critical illness, tumors, and uremia. [2] The alternative phenotype of type-2 thyroid allostasis was first predicted in 1968, when John W. Mason expected the concentrations of thyroid hormones to rise in situations of psychosocial stress. [25]
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