Abstract
Due to structural similarities between HCG and thyroid-stimulating hormone, thyroid stimulation during pregnancy starts in the first trimester (TSH). The volume of thyroid hormone distribution increases along with placental metabolism, maternal thyroxine transport, and estrogen-mediated changes in thyroxine-binding globulin (TBG), all of which cause a 20–40% rise in early pregnancy thyroid hormone demand. Due to the human chorionic gonadotropin alpha subunit's cross-reactivity with the TSH receptor, the reference range of laboratory values for TSH is lower. High serum protein levels may alter estimates rather than direct measurements of free thyroxine (FT4), leading to reported results that are inaccurate. The clinical range of thyroid dysfunction during pregnancy can include both hyperthyroidism (Graves' disease and transitory gestational thyrotoxicosis) and hypothyroidism (overt hypothyroidism, subclinical hypothyroidism, and autoimmune thyroid disease). The risk of preterm and infant respiratory distress syndrome is increased by this malfunction.
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