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Anti-TPO antibodies are the most common anti-thyroid autoantibody, present in approximately 90% of Hashimoto's thyroiditis, 75% of Graves' disease and 10–20% of nodular goiter or thyroid carcinoma. Also, 10–15% of normal individuals can have high level anti-TPO antibody titres.
The diagnosis of hyperthyroidism is confirmed by blood tests that show a decreased thyroid-stimulating hormone (TSH) level and elevated T 4 and T 3 levels. TSH is a hormone made by the pituitary gland in the brain that tells the thyroid gland how much hormone to make. When there is too much thyroid hormone, the TSH will be low.
A randomized control trial testing single dose treatment for Graves' found methimazole achieved euthyroidism (normal thyroid function that occurs within normal serum levels of TSH and T4 [23]) more effectively after 12 weeks than did propylthiouracil (77.1% on methimazole 15 mg vs 19.4% in the propylthiouracil 150 mg groups). [24]
The therapeutic target range TSH level for patients on treatment ranges between 0.3 and 3.0 μIU/mL. [18] For hypothyroid patients on thyroxine, measurement of TSH alone is generally considered sufficient. An increase in TSH above the normal range indicates under-replacement or poor compliance with therapy.
TSH may be useful to detect poor thyroid output and may reflect the state of thyroid hormones in the hypothalamic-pituitary-thyroid axis, but not the presence of hormones in other body tissues. [ 22 ] [ 79 ] [ 87 ] As a result, LT 4 monotherapy may not result in a "truly biochemically euthyroid state."
The body's need for thyroid hormone can also change over time, such as in the first months after radioactive iodine treatment (RAI). Thyroid autoimmune diseases can also be volatile [citation needed], as hyperthyroidism can interchange with hypothyroidism and euthyroidism. [2]