Thyroxine-Binding Globulin (TBG) Unit Converter
Thyroxine-Binding Globulin (TBG) Unit Converter
Convert TBG between mg/L, µg/mL, mg/dL and µg/dL — mg/L and µg/mL are the same number — and see why the one thing this rarely ordered measurement is for is explaining a total T4 that does not match the patient.
Thyroxine-Binding Globulin (TBG) converter
mg/L = µg/mLTBG 20 mg/L in a woman taking the combined oral contraceptive, whose total T4 is 13.5 µg/dL and TSH normal
The unit ladder, and why there is no molar unit
mg/dL = mg/L ÷ 10 µg/dL = mg/L × 100
TBG is a ~54 kDa variably glycosylated glycoprotein, so it is reported as a mass concentration and has no clinically used molar unit
- mg/L = µg/mL
- identical concentrations. Mayo report µg/mL, others mg/L, and the numbers are the same — a TBG of 20 mg/L is 20 µg/mL
- mg/dL
- the mg/L figure divided by ten, so 20 mg/L is 2.0 mg/dL. A TBG reported as "2.0" is in mg/dL, not mg/L
- no nmol/L
- thyroxine-binding globulin is a glycoprotein of about 54 kDa whose glycosylation varies with oestrogen exposure, and immunoassays report it against a manufacturer's standard. A molar value would imply a fixed mass it does not have
- the alternative to measuring it
- a T3 uptake or thyroid hormone binding ratio, and the free thyroxine index derived from it, address the same question indirectly — they estimate unoccupied binding capacity rather than the protein itself
- capacity, not just concentration
- TBG carries about 70% of circulating T4 but is normally only a few per cent saturated, which is why a change in its concentration moves total hormone so much and free hormone so little
Worked example
TBG 20 mg/L in a woman taking the combined oral contraceptive, whose total T4 is 13.5 µg/dL and TSH normal
20 mg/L = 20.0 µg/mL = 2.00 mg/dL = 2,000 µg/dL — one concentration, four units
20 mg/L sits inside Mayo's female interval of 11–27 µg/mL, so the binding protein is not the explanation here and the raised total T4 needs another one — a free T4 is the next test
Change the number and the reasoning changes with it. A TBG of 40 mg/L in the same woman would account for the whole of the raised total T4, and nothing further would need doing
Or the mirror image: a man with a total T4 of 3.2 µg/dL, a normal TSH and a TBG of 4 mg/L has inherited TBG deficiency, not hypothyroidism — the total T4 will be low for the rest of his life and levothyroxine would be a mistake
In late pregnancy the same logic runs against Mayo's 47–59 µg/mL, because oestrogen raises TBG two- to three-fold by mid-gestation
What changes a TBG concentration
| Raises TBG | Lowers TBG |
|---|---|
| Pregnancy — two- to three-fold by mid-gestation | Androgens and anabolic steroids |
| Oestrogen replacement, the combined oral contraceptive, tamoxifen | High-dose glucocorticoids |
| Acute hepatitis and other liver injury with regeneration | Nephrotic syndrome and protein-losing enteropathy — urinary and enteric loss |
| Acute intermittent porphyria | Cirrhosis, malnutrition, severe systemic illness |
| Methadone, heroin, mitotane, 5-fluorouracil | Major surgery and critical illness |
| Inherited TBG excess — X-linked, lifelong, no disease | Inherited TBG deficiency — X-linked; complete deficiency affects roughly one in 15,000 male births, again with no disease |
A discordant total T4 — what TBG can and cannot explain
| Pattern | Explanation | How it is confirmed |
|---|---|---|
| High total T4, normal free T4, normal TSH | Raised TBG — pregnancy, oestrogen, inherited excess | A raised TBG, or a normal free thyroxine index |
| Low total T4, normal free T4, normal TSH | Reduced TBG — androgens, protein loss, illness, inherited deficiency | A low TBG, often strikingly low in inherited complete deficiency |
| High total T4, high free T4 on some assays, normal TSH | Familial dysalbuminaemic hyperthyroxinaemia, or a transthyretin variant — a different carrier, not TBG | A normal TBG; equilibrium dialysis free T4, family studies, or genetic testing |
| High total and free T4 with a normal or raised TSH | Assay interference, biotin, thyroid hormone resistance, a TSH-secreting adenoma | Not a binding problem — investigate as discordant thyroid function tests |
| Low total T4 with a raised TSH | Genuine primary hypothyroidism | TBG adds nothing here and should not be measured |
The carrier protein, and the only question it is measured to answer
Thyroxine-binding globulin is reported as a mass concentration, and the units are simpler than they look: milligrams per litre and micrograms per millilitre are the same number, milligrams per decilitre are that number divided by ten, and micrograms per decilitre are it multiplied by a hundred. So a TBG of 20 mg/L is 20 µg/mL, 2.0 mg/dL and 2,000 µg/dL. There is no molar unit, because TBG is a glycoprotein of about 54 kilodaltons whose glycosylation itself varies with oestrogen exposure, and immunoassays report it against a manufacturer’s standard rather than as an amount of substance.
TBG carries roughly 70% of the thyroxine in blood, with transthyretin and albumin taking the rest, and it is normally only a few per cent saturated. That combination of high affinity and large spare capacity is why its concentration matters so much to a total hormone measurement and so little to a free one: add carrier and more hormone is held in the bound pool, so the total rises while the free concentration the pituitary defends barely moves. Oestrogen raises TBG two- to three-fold in pregnancy, mainly by increasing sialylation and slowing clearance; androgens, glucocorticoids, protein loss through kidney or gut, cirrhosis, malnutrition and severe illness lower it.
The measurement is rarely ordered, and it has essentially one job: explaining a total T4 or total T3 that does not fit the patient. A high total T4 with a normal free T4 and a normal TSH in a pregnant woman or a woman on the combined pill is a TBG effect, and once that is understood nothing further needs doing. The most instructive version is inherited. Thyroxine-binding globulin abnormalities are X-linked: complete deficiency occurs in roughly one in 15,000 male births and TBG excess in around one in 25,000, and both produce a lifelong markedly abnormal total T4 alongside a normal free T4, a normal TSH and a completely well patient. That pattern — a total hormone concentration far outside the reference interval in someone with no symptoms and a normal TSH — is precisely what this measurement exists to identify, and identifying it prevents years of unnecessary levothyroxine or antithyroid treatment.
A normal TBG is informative too, because it moves the problem elsewhere: to familial dysalbuminaemic hyperthyroxinaemia or a transthyretin variant, where a different carrier binds thyroxine avidly and some free T4 immunoassays are also misled; to drugs that displace hormone from its carriers, such as phenytoin, carbamazepine, furosemide and high-dose salicylates; or to assay interference. Where a credible free T4 is available it usually answers the question before a TBG is needed, and the free thyroxine index — total T4 corrected for binding capacity — addresses the same question by a different route.
Frequently asked questions
Is a TBG of 20 mg/L the same as 20 µg/mL?
Yes, identical — a milligram per litre and a microgram per millilitre are the same concentration. The same value is 2.0 mg/dL and 2,000 µg/dL. There is no molar unit for TBG because it is a variably glycosylated glycoprotein of about 54 kDa reported against an immunoassay standard.
When is a TBG worth measuring?
When a total T4 or total T3 does not fit the TSH and the free hormone, and you need to know whether the carrier protein is the reason. Typical cases are a strikingly high or low total T4 in a patient with no symptoms and a normal TSH, and the investigation of a suspected inherited binding abnormality. It is not a thyroid function test, it adds nothing when the TSH is clearly abnormal, and where a credible free T4 is available that usually answers the question first.
What is inherited TBG deficiency?
An X-linked variation in the TBG gene that reduces or abolishes the protein. Complete deficiency affects roughly one in 15,000 male births; TBG excess is rarer, at around one in 25,000. Affected people have a markedly abnormal total T4 for life — very low in deficiency, high in excess — alongside a normal free T4, a normal TSH and no thyroid disease whatsoever. Recognising it matters because the alternative is years of unnecessary levothyroxine or antithyroid treatment.
Why does pregnancy raise TBG?
Oestrogen increases the sialylation of thyroxine-binding globulin, which slows its clearance from the circulation, so the concentration rises two- to three-fold by mid-gestation. More carrier holds more hormone, so total T4 and total T3 rise while free hormone stays appropriate. Mayo quote 47–59 µg/mL in late pregnancy against 11–27 µg/mL in non-pregnant women. The combined oral contraceptive and oestrogen replacement do the same thing more modestly.
If the TBG is normal but the total T4 is high, what else could it be?
A different carrier or a different problem. Familial dysalbuminaemic hyperthyroxinaemia involves a variant albumin that binds thyroxine avidly, and transthyretin variants do something similar; both raise total T4 with a normal TSH, and both can also mislead some free T4 immunoassays. Drugs that displace hormone from its binding proteins, assay interference including biotin, thyroid hormone resistance and a TSH-secreting adenoma are the other possibilities, and they are investigated as discordant thyroid function tests rather than as a binding-protein problem.
Related calculators
References
- Mayo Clinic Laboratories. Test ID: TBGI — Thyroxine-Binding Globulin (TBG), Serum. Solid-phase chemiluminescent assay. Reference values: males 12–26 mcg/mL; females 11–27 mcg/mL; late pregnancy 47–59 mcg/mL.
- Refetoff S. Inherited thyroxine-binding globulin abnormalities in man. Endocr Rev. 1989;10(3):275–293.
- Baloch Z, Carayon P, Conte-Devolx B, et al. Laboratory medicine practice guidelines. Laboratory support for the diagnosis and monitoring of thyroid disease. Thyroid. 2003;13(1):3–126.
- Alexander EK, Pearce EN, Brent GA, et al. 2017 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum. Thyroid. 2017;27(3):315–389.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.