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D1, D2, and D3 regulate the levels of T4, T3, and rT3. Three primary deiodinases are responsible for thyroid hormone conversion and breakdown. Type 1 (D1) deiodinates T4 to the biologically active T3, as well as the hormonally inactive and possibly inhibitory rT3. [3] [5] Type 2 (D2) converts T4 into T3, and breaks down rT3. D3 produces rT3 ...
Free T4 and total T3 can be measured when hyperthyroidism is of high suspicion as it will improve the accuracy of the diagnosis. Free T4, total T3 or both are elevated and serum TSH is below normal in hyperthyroidism. If the hyperthyroidism is mild, only serum T3 may be elevated and serum TSH can be low or may not be detected in the blood. [14]
Desiccated thyroid has roughly a 4:1 ratio of thyroxine (T4) to triiodothyronine (T3). In humans, the ratio is 11:1. [10] A combination of various ratios of T4 and T3 might not provide benefits over T4 alone. Some controlled trials have shown inconsistent benefits of various ratios of T4 and T3. [11] [12]
Normalization of TSH does not mean that other abnormalities associated with hypothyroidism improve entirely, such as elevated cholesterol levels. [63] In people with central/secondary hypothyroidism, TSH is not a reliable marker of hormone replacement and decisions are based mainly on the free T 4 level.
Low-T3 syndrome and high-T3 syndrome: Consequences of step-up hypodeiodination, e.g. in critical illness as an example for type 1 allostasis, [20] or hyperdeiodination, as in type 2 allostasis, including posttraumatic stress disorder. [12] Resistance to thyroid hormone: Feedback loop interrupted on the level of pituitary thyroid hormone receptors.
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Thyroid hormone binding ratio (THBR) is a thyroid function test that measures the "uptake" of T3 or T4 tracer by thyroid-binding globulin (TBG) in a given serum sample. This provides an indirect and reciprocal estimate of the available binding sites on TBG within the sample. The results are then reported as a ratio to normal serum.
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