Normal tsh levels during pregnancy

In the US, the American Thyroid Association suggested that all adults should have serum TSH concentration measured at 35 years of age and every 5 years thereafter.
In pregnancy, oestrogen levels increase and thyroid-binding globulin concentrations rise, which leads to an increase in T4 and T3. Universal screening compared with case finding for detection and treatment of thyroid hormonal dysfunction during pregnancy did not result in a decrease in adverse outcomes.
TFTs should be monitored closely in pregnant women with hypothyroidism because thyroxine replacement often needs to be increased by 30% to 50% during the first trimester.
A serum TSH assay is the test of choice to screen for thyroid function disorders in the absence of hypothalamic or a pituitary pathology.
Previously, before improved FT4 and FT3 assays, total T4 and total T3 assays were ordered to evaluate an abnormal TSH assay. Illness, starvation, and poor nutrition may also decrease total T4 and total T3 levels by decreasing albumin and transthyretin levels and possibly interfering with the binding capacity of the carrier proteins. TSH-receptor antibodies (TRAb) are not routine tests but may be of use in selected cases where diagnosis is equivocal.
In the second and third trimesters of pregnancy, FT4 and FT3 decrease, sometimes below the non-pregnant woman's reference level.
In non-thyroid illness (sick euthyroid syndrome), TSH can be normal or low followed by rebound elevation during recovery from acute illness.
The following drugs may cause these results: dopamine, dopaminergic agonists, glucocorticoids, cytokines, or octreotide, because they inhibit pituitary TSH secretion.
In the first trimester of pregnancy, serum TSH falls due to the effect of human chorionic gonadotrophin. African-American people may have slightly lower TSH reference ranges for normal FT4 and FT3 compared with white people. If assay results are correct, the major diagnoses are a TSH-secreting pituitary tumour (TSH-oma) or a syndrome of resistance to thyroid hormone.

Thyroid hormone resistance syndrome can be confirmed by positive family history, absence of adenoma on pituitary MRI, and normal levels of serum alpha subunit glycoprotein. Thyroxine replacement therapy (for possible hypothyroidism) taken within a few hours of TFT can raise FT4 levels. Subclinical (or mild) hypothyroidism occurs when TSH is above reference range with a normal FT4 and FT3. Dopamine and its agonists, as well as glucocorticoids, cytokines, or octreotide, decrease TSH secretion. Oestrogens, tamoxifen, heroin, methadone, or raloxifene increase thyroxine binding globulin (TBG), total T4, and total T3 levels. Androgens, anabolic steroids, or glucocorticoids decrease TBG, total T4, and total T3 levels.
In the first trimester, serum TSH also falls due to the effect of human chorionic gonadotrophin (hCG), which may be associated with a slight and transient increase in FT4. However, total T4 and total T3 levels can be affected by changes in the levels of circulating thyroid hormone-binding protein levels. It may also help differentiate TSH secretory tumour from resistance to thyroid hormone syndrome (RTH).
Patients with subacute thyroiditis have elevated thyroid hormone levels initially, secondary to excessive release of stored T4 and T3 from the thyroid gland.
The finding of an elevated serum sex hormone-binding globulin (SHBG) and circulating free alpha subunit may support the diagnosis of TSH-oma, as may the finding of hyper- or hyposecretion of other pituitary hormones. By contrast, with a TSH-oma where TSH production is autonomous, T4 or T3 administration eventually suppresses the high TSH in thyroid hormone resistance syndrome. These changes are small and in most of the pregnant women, FT4 concentrations remain within the normal range for non-pregnant women. Later, thyroid hormone levels decrease below normal, before returning to normal when inflammation subsides.

Once released, T4 and T3 exert a negative feedback mechanism on the production of TRH and TSH. Therefore, any changes in the quantity or quality of thyroid-binding proteins will produce changes in circulating thyroid hormone levels. After delivery, thyroxine should be reduced to pre-pregnancy dose and TSH rechecked at 6 weeks to further adjust thyroxine if needed. Free T3 should be measured in evaluating patients with thyrotoxicosis, and when the FT4 is not elevated in the presence of a subnormal TSH. Acute illnesses, as well as certain drugs, may inhibit the process of converting T4 to T3 and, therefore, affect their serum levels.
Therefore, it is recommended to check TSH levels 6 to 8 weeks after thyroxine adjustment or any antithyroid drug treatment.
For this condition, thyroid replacement therapy is monitored by checking the levels of FT4 and FT3.
Rarely, TSH alterations can be caused by assay interference with heterophilic antibodies (antibodies to mouse IgG or other human anti-mouse monoclonal antibodies [HAMAs]). This may result in falsely low or high TSH results, although usually it causes elevated serum TSH. Repeat TSH testing using different commercial assays can neutralise the effect of heterophilic antibodies.

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