Do You Understand Thyroid Hormone Markers?

Thyroid hormones play a critical role in the maturation of the cerebral cortex, especially in the development, differentiation, and functional maturation of the fetal nervous system.Insufficient thyroid hormone during the fetal and neonatal periods can lead to intellectual disability, deafness, and cretinism; in children, it causes growth retardation; in adults, it results in memory loss and slow response.Therefore, thyroid function during pregnancy is vital for fetal development.
T4 better reflects true thyroid function than T3In a broad sense, thyroid hormones include thyroxine (T4), triiodothyronine (T3), reverse triiodothyronine (rT3), diiodothyronine (T2), and monoiodothyronine (T1).Most thyroid hormones in peripheral blood bind to thyroid-binding proteins; the biologically active forms are mainly free T4 (FT4) and free T3 (FT3). The activity of T3 is 3–4 times that of T4.
All T4 in the serum is secreted directly by the thyroid gland, whereas only a small portion (10%–20%) of serum T3 comes directly from the thyroid; the vast majority (80%–90%) is converted from T4 in peripheral tissues.Strictly speaking, only serum T4 truly reflects thyroid function; T3 does not.
In clinical laboratory testing, the most commonly used thyroid hormone markers are T3, T4, FT3, and FT4. The units for T4 and FT4 are larger than those for T3 and FT3.
Another key clinical marker related to thyroid hormones is thyroid‑stimulating hormone (TSH).TSH and circulating thyroid hormones form a negative feedback regulatory system:

When thyroid hormone secretion is insufficient, the pituitary gland is stimulated to secrete more TSH, which in turn stimulates the thyroid to produce more hormones.
When thyroid hormone secretion is excessive, TSH secretion from the pituitary is inhibited, reducing thyroid hormone output and restoring homeostasis.

Thyroid hormone levels show no racial differences and little variation across most age groups, except that T3 is slightly lower in the elderly and slightly higher in children—differences with limited clinical significance.Notably, the hypothalamic‑pituitary‑thyroid feedback axis is immature in children, so TSH levels may be higher, reaching 2–4 times those of adults.
Immune factors contribute to thyroid diseases, so thyroid antibodies are measured for 辅助 diagnosis.Thyroid autoantibodies include:

Thyroid peroxidase antibody (TPOAb)
Thyroglobulin antibody (TGAb)
Thyrotropin receptor antibody (TRAb)
Thyroid hormone antibody (TAb)

TPOAb and TGAb are mainly used in the diagnosis of chronic lymphocytic thyroiditis (Hashimoto’s thyroiditis) and Graves’ disease (toxic diffuse goiter).TRAb is used primarily for the etiological diagnosis of hyperthyroidism.
Other commonly used thyroid markers are thyroglobulin (Tg) and thyroxine‑binding globulin (TBG).

Thyroglobulin is mainly measured for follow‑up after surgery for papillary and follicular thyroid carcinoma.
Thyroxine‑binding globulin is often measured during pregnancy, because TBG increases in gestation, leading to a rise in total serum T3. Together with FT3, it helps identify coexisting hyperthyroidism. It is not routinely measured in general practice.

FT3 and FT4 are the main markers for diagnosing gestational hyperthyroidismDuring pregnancy, basal metabolic rate increases, thyroid blood flow and acinar hyperplasia occur, and the thyroid undergoes compensatory enlargement.Increased blood volume, renal clearance, and iodine excretion lead to “iodine deficiency.” Thus, adequate iodine intake is essential in pregnancy.The WHO recommends 250 μg of iodine per day for pregnant and lactating women.
Human chorionic gonadotropin (HCG) during pregnancy shares a similar subunit with TSH and can stimulate the release of TT4 and TT3, increasing total serum T4 (TT4) and TT3 to 1.5–2 times non‑pregnant levels.Hepatic production of TBG also increases to 2–3 times non‑pregnant levels.However, serum FT4 and FT3 do not increase, making FT3 and FT4 the primary markers for diagnosing gestational hyperthyroidism.
Physiological changes in pregnancy increase maternal demand for thyroxine.Iodine deficiency and chronic thyroiditis may cause relative FT4 insufficiency and elevated TSH, increasing the risk of subclinical hypothyroidism.
Maternal TSH does not cross the placenta, but thyroxine does.The early fetus cannot synthesize T4 on its own, so maternal thyroxine is critical for early embryonic brain development.Recommended upper limits of normal serum TSH:

2.5 mU/L in the first trimester
3.0 mU/L in the second and third trimesters

Early embryonic brain development depends on maternal thyroid hormones.Animal studies show that hypothyroidism in early pregnancy causes irreversible brain underdevelopment in offspring.Observational studies in humans also link clinical maternal hypothyroidism to adverse pregnancy outcomes.Thyroid function screening during pregnancy deserves strong emphasis.