Thyroid hormones play a vital role in the maturation of the cerebral cortex, especially in the development, differentiation, and functional maturation of the fetal nervous system.Insufficient thyroid hormones during the fetal and neonatal periods can lead to mental retardation, deafness, and cretinism; in children, they cause growth retardation; in adults, they result in memory loss and slow response.Therefore, thyroid function during pregnancy is critical for fetal development.
T4 reflects true thyroid function better than T3
In 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 free T4 (FT4) and free T3 (FT3), and the activity of T3 is 3–4 times that of T4.
All T4 in 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 peripherally from T4.Strictly speaking, only serum T4 truly reflects thyroid function; T3 does not.
In clinical laboratory tests, the most commonly used thyroid hormone indicators are T3, T4, FT3, and FT4.The units of T4 and FT4 are larger than those of T3 and FT3.
Another key clinical indicator related to thyroid hormones is thyroid‑stimulating hormone (TSH).TSH and 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.
This maintains the regulation and homeostasis of thyroid hormones.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, with minimal clinical significance.Notably, the hypothalamic‑pituitary‑thyroid feedback axis is not fully mature in children, so TSH levels may be higher—about 2–4 times those in adults.
Thyroid autoantibodies
Immune factors can cause thyroid‑related diseases, so thyroid antibody testing is used clinically for auxiliary diagnosis.Thyroid autoantibodies include:
Thyroid peroxidase antibody (TPOAb)
Thyroglobulin antibody (TgAb, referred to as TGA in the text)
TSH 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’ hyperthyroidism (toxic diffuse goiter).TRAb is mainly used for the etiological diagnosis of hyperthyroidism.
Other common thyroid indicators
Other commonly used clinical thyroid indicators are thyroglobulin (Tg) and thyroxine‑binding globulin (TBG).
Thyroglobulin measurement is mainly used for follow‑up after surgery for papillary and follicular thyroid carcinoma.
Thyroxine‑binding globulin is mainly measured during pregnancy, because TBG increases during pregnancy, leading to a corresponding rise in total serum T3.
Together with FT3, it helps identify coexisting hyperthyroidism.
TBG is not routinely measured in general clinical practice.FT3 and FT4 are the main indicators for diagnosing gestational hyperthyroidism
During pregnancy, basal metabolic rate increases, thyroid blood flow is abundant, acini proliferate, and the thyroid undergoes compensatory hyperplasia.Meanwhile, increased blood volume, hemodilution, elevated renal clearance, and increased iodine excretion lead to “iodine hunger”.Adequate iodine intake during pregnancy is therefore essential.The WHO recommends an iodine intake of 250 μg per day for pregnant and lactating women.
Human chorionic gonadotropin (HCG) during pregnancy has a subunit similar to TSH and can stimulate the release of TT4 and TT3, increasing total serum T4 (TT4) and TT3 levels to 1.5–2 times the non‑pregnant state.Hepatic production of thyroxine‑binding globulin (TBG) rises to 2–3 times normal.As a result, serum FT4 and FT3 levels do not increase, and FT3 and FT4 are the main indicators 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, predisposing to subclinical hypothyroidism.
Maternal TSH cannot cross the placenta, but thyroxine can.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 trimestersEarly 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 find that clinical maternal hypothyroidism is often associated with adverse pregnancy outcomes.Thyroid function screening during pregnancy should receive sufficient attention.