1, Free triiodothyronine (FT3), in pg/ml 2, Free tetraiodothyronine (FT4), in pg/ml 3, Triiodothyronine (T3), in ng/ml 4, Thyroxine (T4), in ng/ml 5, Thyrotropin (TSH), in uIU/ml 6, Human serum TM antibody <20%, sometimes IU/ml 7, Human Human serum TG antibody <30%, sometimes IU/ml 8. Human thyroglobulin, IU/ml In peripheral blood, 99.97% of T4 is in a bound state (e.g., bound to T4-binding proteins, albumin, etc.), and only 0.03% is free, able to enter the cell and be converted to the active form of T3. reflect the functional state of thyroxine. Total T4 (TT4) cannot do this. But why test it at all? It is to get enough information. Doctors should be awake and not be misled by this information. For example, during pregnancy, the serum T4-binding protein is much higher than usual in response to estrogen, resulting in a much higher TT4 than usual, but a completely normal FT4. Conversely, in starvation, and in certain liver and kidney diseases, the level of binding proteins is very low, resulting in a decreased level of TT4, but FT4 is also normal at this time. For these reasons, testing TT4 alone is not sufficient to correctly reflect thyroid function; it must also be combined with FT4.(items 1 and 2 above) In the hyperthyroid state, T3 is able to reflect thyroxine levels. This is because under immune attack, T3 is released directly from the destroyed thyroid cells (rather than being converted from peripheral T4). Of course FT3 is more accurate, but TT3 in its usual state is sufficient information because the T3 released from the destroyed thyroid is much larger than the peripherally converted T3. however, if it is in a hypothyroid state, TT3 is not as accurate as FT3. (These are items 3 and 4.) Sometimes it is not enough to diagnose hyperthyroidism or hypothyroidism on the basis of FT4 levels alone, and this is because FT4 is a range, an average of a population, although this population can be very large. For example, in a laboratory, the FT4 range is 0.8-2.1, but for a specific person, whose optimal level is 1.2, and who takes medication to raise it to 2.0, it may appear to be in the normal range (0.8-2.1), but in reality, he may already be showing signs of hyperthyroidism. Based on this, the thyroid function needs to be evaluated in conjunction with other items, which is the TSH. in the case just described, the TSH may have been well below normal. (This is item 5) There are three main types of anti-thyroid antibodies: anti-peroxidase (TPOAb: thyroid peroxidase antibody) antibodies, also known as anti-microsomal antibodies (TMAb: thyroid microsomal antibody). It attacks the follicular cells of the thyroid gland, such as in Hashimoto's thyroiditis, and is present in more than 95% of patients. It can be used to confirm the diagnosis. The second antibody associated with Hashimoto is the antithyroglobulin antibody (TGAb: thyroglobulin antibody), which attacks thyroglobulin (TG).TG monitors for recurrence of thyroid cancer, so the presence of TGAb may interfere with the doctor's judgment. The third antibody is thyroid stimulating immunoglobulin (TSI, also known as thyroid stimulating antibody or TSA). It can irreversibly take over the receptors for TSH and keep stimulating thyroxine production, eventually leading to hyperthyroidism. It also attacks the eye muscles, causing symptoms of proptosis. In hyperthyroidism, TPOAb and TGAb are constantly destroying the thyroid gland, and TSI is constantly stimulating thyroxine secretion, so all three antibodies are measured; in Hashimoto, only the first two are detected (these are items 6 and 7) TG is the only protein synthesized in the thyroid gland, and when TSH stimulates the thyroid to do its job it prompts the follicular cells to synthesize TG. a portion of this is stored as a colloid in the follicular lumen for backup, and another portion binds to iodine and synthesizes TG. One part is stored in the follicular lumen as gel and the other part is combined with iodine to synthesize T3T4, which is released into the bloodstream along with some of the TG. Measuring TG in the blood therefore gives an indication of the state of the thyroid gland. Generally, TG levels reflect the amount of thyroid tissue in the body (or its working condition). When TSH levels are high (the patient may be hypothyroid), TG levels are also high (TSH promotes thyroid work), and when TSH levels are low (the patient may be taking thyroxine), TG levels are also low (TSH suppresses thyroid work). However, in the case of hyperthyroidism, when the thyroid is not regulated by TSH, it is stimulated by TSI to secrete desperately, and TG levels will be high. In Hashimoto, the cells are destroyed and TG is also released into the bloodstream, resulting in elevated test levels. The most important application of TG is the follow-up of patients with thyroid cancer. After the thyroid is removed, the source of TG is cut off, and if elevated TG is detected, it often means that the cancer has recurred. It is important to note that in Hashimoto, the presence of TGAb may interfere with the detection of TG. The cancer has recurred, but it is not detected in the blood, and is actually masked by TGAb. (This is item 8).