What is clinical hypothyroidism of pregnancy and hypothyroxinemia of pregnancy like?

  Definition of Clinical (or Subclinical) Hypothyroidism in Pregnancy and Hypothyroxinemia in Pregnancy Because of the widespread clinical use of ultrasensitive thyroid stimulating hormone (TSH) tests and the TSH-like effect of human chorionic gonadotropin (hCG) secreted by the placenta during pregnancy, the ATA has redefined the normal values of TSH in pregnancy: the upper limit of normal TSH in early pregnancy is 3.0 mIU/L in mid- and late pregnancy.  If a pregnant woman’s TSH exceeds the upper limit of the normal value for the corresponding gestational period, she should be considered as hypothyroid. Clinical hypothyroidism should be considered when the TSH of a pregnant woman is ≥, regardless of whether the free thyroxine (FT4) is normal or not.  Subclinical hypothyroidism in pregnancy means that TSH is within the range and FT4 is normal.  Hypothyroidism in pregnancy is defined as a pregnant woman with a normal TSH but an FT4 below the 5th (very hypothyroidism) or 10th percentile value (hypothyroidism) of the reference range.  Dangers of hypothyroidism in pregnancy Clinical hypothyroidism can increase the risk of pregnancy complications and may increase the risk of neurocognitive defects during fetal development.  Regarding the effect of subclinical hypothyroidism in pregnant women on fetal neurocognitive development, the ATA considers it biologically plausible but the clinical evidence is not sufficient.  There is also controversy regarding the negative impact of gestational hypothyroxinemia on the fetus.  Treatment of hypothyroidism in pregnancy Oral levothyroxine (LT4) therapy is recommended, targeting TSH ranges of 0.2 to 3.0 mIU/L and 0.3 to 3.0 mIU/L in early, mid and late pregnancy, respectively. Monitoring of hypothyroid pregnant women The body’s requirement for LT4 varies during pregnancy. 50% to 80% of hypothyroid pregnant women must increase their LT4 dosage by 20% to 50% during pregnancy to meet The body’s needs are increased by 20% to 50% during pregnancy. From the 4th to 6th week of gestation, the demand for exogenous LT4 starts to increase until the 16th to 20th week of gestation; after the 20th week of gestation, there is no significant change in the demand for LT4 until delivery; after delivery, the demand for LT4 returns to the prenatal level. Therefore, pregnant women using LT4 should have their TSH and FT4 checked every 4 weeks until 16-20 weeks of gestation, and TSH should be measured once every 6 weeks after delivery.  What level of TSH should be maintained in LT4-treated patients if they are preparing for pregnancy?  TSH is significantly lower in pregnant women because hCG secreted by the placenta after pregnancy stimulates the thyroid gland to produce more thyroid hormone. To avoid elevated TSH in early pregnancy, LT4-treated hypothyroid women should maintain TSH < until they are ready to become pregnant.  If a woman with normal thyroid function but positive thyroid antibodies is preparing for pregnancy, is it possible to use such patients with low conception rate, high rate of miscarriage after pregnancy, low success rate of assisted reproduction and a tendency to elevated TSH after pregnancy.  There is a lack of studies on the effect of LT4 on pregnant women with purely positive thyroid antibodies. It is recommended that their thyroid function be tested every 4-6 weeks after pregnancy and that they be treated with LT4 if their TSH exceeds the upper limit of normal values in pregnancy.