Lab result explainedThyroidLast updated November 11, 2026

TSI test and TRAb: normal range, what a high result means and how Graves' disease antibodies are read

TSI and TRAb (thyroid-stimulating antibodies) (TSI / TRAb) · Thyroid antibodies (ordered with TSH, free T4 and free T3 when hyperthyroidism is found; in pregnancy with a history of Graves' disease) · reported in IU/L for TRAb and automated TSI; percent of reference (% SRR) for the TSI bioassay; older reports used a 'TSI index' (normal 1.3 or lower)

TSI (thyroid-stimulating immunoglobulin) and TRAb (TSH receptor antibody) are two names for tests that detect the antibodies responsible for Graves' disease. In Graves', the immune system makes antibodies that lock onto the TSH receptor on thyroid cells and switch it on, driving the gland to make too much thyroid hormone regardless of what the pituitary wants. A positive result in someone with an overactive thyroid confirms Graves' disease as the cause, which matters because Graves' is treated differently from a toxic nodule or thyroiditis.

The two tests overlap but are not identical. TRAb assays detect any antibody that binds the TSH receptor, whether it stimulates, blocks or does neither, and are reported in IU/L with a cut-off of about 1.5 to 1.75 IU/L. TSI assays are designed to pick up only the stimulating antibodies, either with a cell-based bioassay reported as a percentage of a reference (positive above 140 percent) or with a newer automated immunoassay reported in IU/L (positive above 0.55 IU/L). Both are positive in roughly 95 to 97 percent of people with untreated Graves' disease, and either can be used to diagnose it.

Beyond diagnosis, the level is used to predict how Graves' will behave. A high level at diagnosis, or one that stays high after 12 to 18 months of antithyroid medication, means remission is unlikely and longer treatment or definitive therapy (radioactive iodine or surgery) is discussed. In pregnancy, a level more than three times the upper limit in the second or third trimester means the antibodies can cross the placenta and overstimulate the baby's thyroid, so the fetus is monitored. And the level tends to track with thyroid eye disease activity. The result is always read alongside TSH, free T4 and free T3.

TSI / TRAb at a glance

What it is: a blood test for antibodies against the TSH receptor, the cause of Graves' disease. TRAb detects all binding antibodies; TSI detects the stimulating ones.
Normal: TSI below 0.55 IU/L (automated immunoassay) or below 140 percent of reference (bioassay); TRAb below 1.75 IU/L on the most widely used assay (some labs use 1.5 or 1.22). Labs differ; use the printed cut-off.
Positive with a low TSH and high free T4: Graves' disease, with about 97–99 percent specificity. Negative in hyperthyroidism points to a toxic nodule, thyroiditis or excess thyroid hormone intake instead.
Higher levels predict more active disease and lower remission rates; a TRAb that is still above about 10 IU/L after 12–18 months of medication rarely remits.
In pregnancy with current or past Graves' disease: tested at 18–22 weeks; a level above 3 times the upper limit (TRAb above about 5 IU/L) prompts fetal monitoring and a repeat at 30–34 weeks.
Next step: TSH, free T4 and free T3 now; a thyroid uptake scan or ultrasound only if antibodies are negative; repeat TRAb before stopping antithyroid medication.

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What TSI / TRAb measures

The TSH receptor sits on the surface of thyroid follicular cells and normally responds only to TSH from the pituitary. In Graves' disease, B cells produce IgG antibodies that bind this receptor. Most of them mimic TSH and stimulate the cell (thyroid-stimulating antibodies, TSAb, measured as TSI), a minority block it (blocking antibodies, which can cause hypothyroidism and occasionally appear in Hashimoto's), and some bind without any effect. Because these antibodies are not under feedback control, they keep the gland running at full output, suppressing TSH to near zero while T4 and T3 rise. The same antibodies, acting on TSH receptors in the fat and fibroblasts behind the eye, drive Graves' eye disease.

TRAb tests are competitive binding assays: your serum is mixed with the TSH receptor and a labeled ligand (originally radiolabeled TSH, now a labeled monoclonal antibody called M22 in third-generation assays), and the degree to which your antibodies displace the label gives a concentration in IU/L calibrated against the WHO international standard. These assays cannot tell stimulating from blocking antibodies, but in a hyperthyroid patient that distinction is academic. Third-generation TRAb assays have a sensitivity of about 97 percent and specificity of 98 to 99 percent for Graves' disease.

TSI tests measure function rather than binding. The classic bioassay (for example Thyretain) exposes engineered cells carrying the TSH receptor to your serum and measures the cyclic AMP signal they produce, reported as a percentage of a reference serum; above 140 percent is positive. Since 2016, an automated TSI immunoassay (Immulite) uses a receptor configured to bind preferentially to stimulating antibodies and reports IU/L with a 0.55 IU/L cut-off; most US commercial labs now use this when 'TSI' is ordered. In practice TSI and TRAb results agree in over 90 percent of patients, and either is acceptable for diagnosis. High-dose biotin can interfere with the Immulite TSI assay and some TRAb platforms.

Normal range for TSI / TRAb

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (IU/L for TRAb and automated TSI; percent of reference (% SRR) for the TSI bioassay; older reports used a 'TSI index' (normal 1.3 or lower))	Notes
TSI, automated immunoassay (Immulite), negative	Below 0.55 IU/L	Most US commercial labs report TSI this way. Some quote below 0.10 IU/L as undetectable; 0.10–0.54 is still negative.
TSI bioassay (Thyretain), negative	Below 140 percent of reference serum (SRR)	Reported as a percentage. Values of 140–500 percent are typical of active Graves'; very active disease exceeds 500 percent.
TRAb, third-generation assay, negative	Below 1.75 IU/L (Roche) or below 1.5 IU/L (other platforms); some report below 1.22 IU/L	Cut-offs are manufacturer-specific. A 'borderline' or 'gray zone' result just above the cut-off is repeated in 4 to 8 weeks.
TRAb, positive, untreated Graves' disease	Typically 2–40 IU/L	About 95–97 percent of untreated Graves' patients are positive. The level correlates loosely with how overactive the gland is and with eye disease.
TRAb, predicting remission after antithyroid drugs	Below the cut-off at 12–18 months: about 50 percent remit; above 10 IU/L: under 10–20 percent remit	Used to decide whether to stop methimazole or move to radioiodine or surgery. Smoking, a large goiter and very high free T4 at diagnosis also lower remission odds.
Pregnancy, threshold for fetal risk	Above 3 times the assay's upper limit (roughly above 5 IU/L TRAb, or TSI above about 500 percent / 1.65 IU/L)	Measured at 18–22 weeks in women with current Graves' or a past history treated with radioiodine or surgery. Prompts fetal heart rate and thyroid ultrasound monitoring and a repeat at 30–34 weeks.
After radioactive iodine treatment	Often rises 2–3 fold for 6–12 months, then falls	An expected surge; it can worsen eye disease, which is why steroids are given with radioiodine in people with active eye disease.
Hashimoto's thyroiditis	Negative in 85–90 percent; low positives possible	Low-level TRAb in a hypothyroid person usually reflects blocking antibodies and does not mean Graves' disease.

High or positive TSI / TRAb

In someone with a suppressed TSH and a raised free T4 or free T3, a positive TSI or TRAb confirms Graves' disease with a specificity of about 98 to 99 percent. That settles the diagnosis without a nuclear uptake scan, which is why guidelines now recommend antibody testing as the first step in working up hyperthyroidism. The alternatives it rules out matter: a toxic multinodular goiter or toxic adenoma is antibody negative and does not remit on its own, thyroiditis is antibody negative and resolves without antithyroid drugs, and someone taking too much thyroid hormone is antibody negative with a low thyroglobulin. Occasionally Graves' presents with normal thyroid hormones but a suppressed TSH (subclinical hyperthyroidism) or with eye disease alone, and a positive antibody test is the finding that ties it together.

The height of the level carries prognostic weight. At diagnosis, very high values (TRAb above 10 to 12 IU/L or TSI several times the cut-off) go with a larger goiter, more severe thyrotoxicosis, a higher chance of thyroid eye disease and a lower chance that 12 to 18 months of methimazole will produce a lasting remission. Levels fall in most people on treatment as the immune activity settles, and the value measured before stopping medication is one of the best predictors of what happens next: with a negative TRAb, roughly half stay in remission, while with a persistently high level, relapse within a year is the rule, and radioactive iodine or surgery is usually recommended rather than another course of tablets.

In pregnancy the stakes are different because TSH receptor antibodies are IgG and cross the placenta from mid-gestation. A level above three times the upper limit of normal at 18 to 22 weeks means the fetal thyroid may be overstimulated, producing fetal tachycardia, goiter, growth restriction and, after birth, neonatal Graves' disease in about 1 to 5 percent of babies of affected mothers. This applies even to women whose hyperthyroidism was treated years earlier by radioiodine or surgery, because the antibodies can persist after the gland is gone. A low or negative level at 18 to 22 weeks means no further antibody monitoring is needed in that pregnancy. In thyroid eye disease, higher and rising levels track with activity, and a falling level is one sign the eye disease is settling.

Common causes

Graves' disease (untreated or active)
By far the most common cause. Stimulating antibodies drive both the hyperthyroidism and, when present, the eye and skin manifestations. About 95–97 percent of untreated patients are positive on third-generation assays; a small minority have antibodies below the detection limit.
Graves' disease in remission or after treatment
Antibodies fall on antithyroid drugs and often disappear, but can persist at low levels for years after radioiodine or surgery, which is why women with a history of treated Graves' are still tested in pregnancy.
Recent radioactive iodine therapy
Radioiodine releases thyroid antigens and typically raises TRAb two- to threefold over the following 6–12 months before it declines. This surge can trigger or worsen thyroid eye disease.
Thyroid eye disease (Graves' ophthalmopathy)
TSH receptor antibodies act on orbital fibroblasts; levels correlate with eye disease activity and severity, and the test is positive in most people with eye disease even when thyroid function is normal ('euthyroid Graves').
Neonatal Graves' disease
Maternal antibodies crossing the placenta stimulate the baby's thyroid; the newborn is positive at birth and the antibodies clear over 1–3 months as the hyperthyroidism resolves. Cord blood or day 3–5 testing is used when the mother's level was high.
Hashimoto's thyroiditis with blocking antibodies
TRAb assays cannot distinguish stimulating from blocking antibodies, so 10–15 percent of people with autoimmune hypothyroidism have a low positive TRAb (TSI bioassays are negative). Rarely, blocking antibodies cause hypothyroidism outright, or a patient switches between blocking and stimulating over time.
Hashitoxicosis and the overlap syndromes
Some people have both TPO antibodies and TSH receptor antibodies, with a phase of Graves'-type hyperthyroidism followed by hypothyroidism as the gland is destroyed.
Immune reconstitution and immunotherapy
Alemtuzumab for multiple sclerosis causes Graves' disease in 20–40 percent of patients 1–3 years after treatment; checkpoint inhibitors, interferon-alpha and antiretroviral therapy restoring CD4 counts in HIV can also trigger TRAb-positive Graves'.
Assay interference and borderline results
High-dose biotin can produce false results on streptavidin-based platforms; heterophile antibodies rarely cause false positives. A result just above the cut-off with normal thyroid function is repeated rather than acted on.

Symptoms that can go with it

Palpitations, a fast or irregular heartbeat and breathlessness on exertion
Weight loss despite a good appetite, heat intolerance and sweating
Tremor of the hands, anxiety, irritability and poor sleep
Eye symptoms: gritty or watery eyes, swelling around the eyes, a staring or bulging appearance, double vision
A diffusely enlarged, sometimes tender thyroid (goiter), occasionally with an audible bruit
Frequent bowel movements, muscle weakness (especially climbing stairs) and, in women, lighter or missed periods
Thickened, reddish skin over the shins (pretibial myxedema) in a small minority
None, when the antibody is found in treated Graves', in pregnancy screening or with blocking antibodies in Hashimoto's

Negative or low TSI / TRAb

A negative TSI or TRAb in someone with hyperthyroidism makes Graves' disease unlikely (it misses roughly 3 to 5 percent of cases) and shifts attention to the other causes: a toxic adenoma or toxic multinodular goiter, which show up as hot areas on a radioiodine uptake scan; painless or subacute thyroiditis, which shows near-zero uptake and resolves over weeks to months; and excess thyroid hormone from tablets or supplements, which also shows low uptake but with a suppressed thyroglobulin. A negative result in someone with eye symptoms makes thyroid eye disease less likely but does not exclude it, and an orbital specialist may still be involved.

In someone known to have Graves' disease, a level that has fallen below the cut-off after 12 to 18 months of antithyroid medication is good news: it is the strongest single predictor that medication can be stopped with a reasonable chance (about 50 percent, higher if the goiter is small and the person does not smoke) of lasting remission. In pregnancy, a negative level at 18 to 22 weeks in a woman with a history of Graves' means the fetus is not at risk from maternal antibodies and no further antibody testing is needed. A low positive result in a hypothyroid person usually reflects blocking antibodies and is interpreted as part of Hashimoto's thyroiditis, not as Graves' disease.

Common causes

Hyperthyroidism from a cause other than Graves'
Toxic multinodular goiter and toxic adenoma account for most antibody-negative hyperthyroidism, particularly in people over 50 and in iodine-deficient regions; thyroiditis (subacute, silent, postpartum, amiodarone- or checkpoint-inhibitor-induced) is the other main group.
Graves' disease in remission
Falling antibodies on treatment reflect quieting autoimmunity. Levels are rechecked before stopping methimazole and, if negative, the drug is tapered off with follow-up thyroid tests at 2–3 months and then yearly.
Excess thyroid hormone intake
Levothyroxine over-replacement, liothyronine, desiccated thyroid, or weight-loss and 'thyroid support' products containing thyroid hormone suppress TSH without any antibody; thyroglobulin is low and uptake scan shows little uptake.
Early or mild Graves' below the assay threshold
A small minority of people with Graves' have antibodies below the detection limit, particularly in mild disease; if the clinical picture still fits, a TSI bioassay or a repeat in 2–3 months may turn positive, or an uptake scan settles it.
Timing and treatment effects
Antibodies can be transiently undetectable during heavy immunosuppression and are lower in people on high-dose glucocorticoids; a sample drawn years after thyroidectomy for Graves' is often negative.

Symptoms that can go with it

None; a negative result is the expected finding in people without Graves' disease
If you have hyperthyroid symptoms with a negative antibody test, the symptoms still need a cause, and an uptake scan or ultrasound is the usual next step
A sore, tender neck with hyperthyroid symptoms and negative antibodies suggests subacute thyroiditis

Read it alongside

TSH — suppressed (often below 0.01 mU/L) in active Graves'; the first test that prompts antibody testing and the one used to monitor treatment, although it can lag behind thyroid hormones by months.
Free T4 and free T3 — confirm and grade the hyperthyroidism; Graves' often raises T3 proportionally more than T4 (a T3:T4 ratio above 20 ng/dL per µg/dL favors Graves' over thyroiditis).
TPO antibodies — positive in about 70–80 percent of Graves' patients as well as in Hashimoto's; they confirm thyroid autoimmunity but do not distinguish the two.
Thyroglobulin antibodies — a second marker of thyroid autoimmunity; useful mainly in the overlap with Hashimoto's.
Thyroglobulin — high in Graves' and thyroiditis, low or undetectable in hyperthyroidism from taking thyroid hormone; helps when antibodies are negative.
Radioactive iodine uptake and scan — the alternative to antibody testing: diffusely high uptake in Graves', focal hot spots in toxic nodules, near-absent uptake in thyroiditis or exogenous hormone. Not used in pregnancy or breastfeeding.
Thyroid ultrasound with Doppler — shows a diffusely enlarged, highly vascular gland in Graves' and is the imaging of choice in pregnancy.
Complete blood count, liver enzymes and alkaline phosphatase — a baseline before antithyroid drugs (which can lower white cells and affect the liver) and because untreated hyperthyroidism itself raises alkaline phosphatase and can lower neutrophils.

What usually happens next

A positive result with a low TSH and high free T4 or free T3 establishes Graves' disease; the next conversation is about the three treatment options (antithyroid drugs, radioactive iodine, surgery), each with its own trade-offs, and about a beta-blocker for symptoms in the meantime.
Ask whether your level is high or low relative to the cut-off; a very high level at diagnosis, a large goiter, smoking and severe hyperthyroidism all lower the chance of remission on tablets and may shift the discussion toward definitive treatment or a longer course.
If you are on methimazole, expect the antibody to be repeated after 12 to 18 months before any attempt to stop; a negative result supports a trial off medication with thyroid tests 6 to 8 weeks later and then every few months for the first year, since most relapses occur within 12 months.
If you are pregnant or planning pregnancy and have current or past Graves' disease, ask for a TRAb or TSI in the first trimester and at 18 to 22 weeks; a level above three times the upper limit means fetal monitoring and a repeat at 30 to 34 weeks, and the baby is checked after birth.
If the result is negative but you are hyperthyroid, a radioiodine uptake scan (or ultrasound with Doppler if pregnant or breastfeeding) distinguishes toxic nodules from thyroiditis, which are managed very differently.
Mention eye symptoms (grittiness, swelling, double vision, bulging) at every visit; active eye disease changes the choice of treatment, since radioiodine can worsen it, and selenium and steroid cover may be discussed.

Diet, lifestyle and natural levers with evidence

What can move TSI / TRAb once the cause is known. Nothing here replaces finding the cause.

Stop smoking

Strong evidence

Smoking is the strongest modifiable factor in Graves' disease. Smokers have about a twofold higher risk of developing Graves', a sevenfold to eightfold higher risk of thyroid eye disease, worse eye disease outcomes, a poorer response to eye treatments, and roughly half the chance of remission after antithyroid drugs compared with non-smokers; in cohort studies, TRAb levels fall more slowly and relapse is more common in smokers. The risk of eye disease declines toward non-smoker levels within a few years of quitting.

Selenium (for mild thyroid eye disease)

Moderate evidence

In the European Group on Graves' Orbitopathy trial of 159 people with mild, recent-onset thyroid eye disease, 100 µg of sodium selenite twice daily for 6 months improved quality of life and eye findings and slowed progression to more severe disease (7 percent progressed versus 26 percent on placebo). Trials of selenium added to methimazole for the hyperthyroidism itself show faster normalization of thyroid hormones in some studies but no consistent effect on TRAb levels or remission rates, so its established role is in mild eye disease.

Doses above 400 µg a day are toxic; long-term supplementation in selenium-replete people has been linked to a higher risk of type 2 diabetes. Discuss with your clinician rather than self-prescribing for years.

Correct vitamin D deficiency

Preliminary evidence

People with Graves' disease have lower vitamin D levels than controls in most observational studies, and a Danish randomized trial of 278 people found that 70 µg (2,800 IU) a day of vitamin D3 did not reduce relapse after antithyroid drugs. One small trial in people with Graves' eye disease suggested a modest benefit on recurrence. The reasonable position is to test and correct a deficiency (25-hydroxyvitamin D below 20 ng/mL) for bone health, which hyperthyroidism already threatens, without expecting it to change the antibodies.

L-carnitine for symptoms of thyroid hormone excess

Preliminary evidence

L-carnitine blocks thyroid hormone entry into cell nuclei. In a randomized trial of 50 women deliberately made hyperthyroid with levothyroxine, 2 to 4 g a day prevented or reversed symptoms such as palpitations, tremor and weakness, and small studies in Graves' report symptom relief alongside standard treatment. It does not lower antibody levels or thyroid hormones and is not a substitute for antithyroid medication.

May cause a fishy body odor and digestive upset; discuss with your clinician if you take warfarin or have a seizure disorder.

Avoid excess iodine and check supplements

Moderate evidence

Iodine loads (kelp and seaweed supplements, iodine drops, some multivitamins with several hundred micrograms, amiodarone, iodinated contrast) can precipitate or worsen hyperthyroidism in people with Graves' and reduce the effectiveness of antithyroid drugs and radioiodine; population studies after iodine fortification show a transient rise in Graves' incidence. Normal dietary iodine (around 150 µg a day) is appropriate; what to avoid is the supplement-sized dose. Separately, high-dose biotin (5 mg or more, common in hair and nail products) can distort TSI, TSH and free T4 results on common platforms, so stop it 2 to 3 days before testing.

Do not stop prescribed iodine-containing medication (such as amiodarone) without medical advice.

When to see a clinician promptly

Fever, agitation or confusion, a heart rate above 130–140, vomiting or diarrhea with known or suspected hyperthyroidism: possible thyroid storm, a medical emergency; call emergency services.
A new irregular heartbeat, chest pain, fainting or sudden breathlessness; untreated Graves' is a common cause of atrial fibrillation, particularly over age 60.
Sore throat, mouth ulcers or fever while taking methimazole or propylthiouracil: possible agranulocytosis (dangerously low white cells), which needs a same-day blood count. Also report yellowing of the skin or eyes, dark urine or severe abdominal pain, which can signal liver injury.
Eye pain, worsening double vision, reduced or dimmed color vision or difficulty closing the eyes: sight-threatening thyroid eye disease needs urgent specialist review.
A positive antibody test in pregnancy, or hyperthyroid symptoms in pregnancy, needs an endocrinologist and obstetric team promptly; propylthiouracil is preferred in the first trimester and fetal monitoring may be needed.
Hyperthyroid symptoms returning after stopping medication (weight loss, tremor, palpitations, heat intolerance): relapse is most common in the first year and is confirmed with TSH and free T4.

Frequently asked questions

What is a normal TSI level?

On the automated immunoassay most US labs now use, TSI is normal below 0.55 IU/L; some labs report anything under 0.10 IU/L as undetectable. On the older cell-based bioassay, normal is below 140 percent of the reference serum, and a few labs still report a 'TSI index' where 1.3 or lower is normal. Check which unit your report uses before comparing numbers; the cut-off is printed next to the result.

What is the difference between TSI and TRAb?

TRAb measures every antibody that binds the TSH receptor, whether it stimulates, blocks or does nothing, and is reported in IU/L (normal usually below 1.75). TSI measures only the stimulating antibodies that actually cause Graves' disease. In a hyperthyroid person the two agree more than 90 percent of the time and either confirms Graves'. TRAb is the test used worldwide and in pregnancy guidelines; TSI is more specific when the question is whether a low positive TRAb in a hypothyroid person is a blocking antibody.

What does a high TSI mean?

In someone with a low TSH and high thyroid hormones, a high TSI confirms Graves' disease: antibodies are switching on the thyroid. The higher the level, the more active the disease tends to be, the more likely eye involvement, and the lower the odds that 12 to 18 months of medication will produce a lasting remission. A high level in someone with normal thyroid function can mean early Graves', euthyroid Graves' eye disease, or treated Graves' with persisting antibodies.

Can you have Graves' disease with negative antibodies?

Rarely. Third-generation TRAb and TSI assays pick up about 95 to 97 percent of untreated Graves' disease, so roughly 1 in 30 people with Graves' will test negative, usually in mild disease. If the picture still fits (diffuse goiter, eye signs, no nodules), a radioiodine uptake scan showing high diffuse uptake makes the diagnosis, or the antibody test can be repeated in 2 to 3 months or run on a different assay.

Does a falling TSI or TRAb mean Graves' is going into remission?

It is the best available sign. Antibody levels fall in most people on methimazole as the immune activity settles, and a level that has dropped below the cut-off after 12 to 18 months is associated with about a 50 percent chance of remission after stopping, higher in non-smokers with a small goiter. A level that stays high, especially above 10 IU/L, predicts relapse in most people, which is why many clinicians recommend radioiodine or surgery rather than another course of tablets in that situation.

Why do I need a TRAb test in pregnancy if my Graves' was treated years ago?

The antibodies can outlast the thyroid. After radioiodine or surgery you no longer have a gland for them to overstimulate, but they still cross the placenta from about 20 weeks and can stimulate the baby's thyroid. Guidelines recommend testing at 18 to 22 weeks in any woman with current Graves' or a history of it treated with radioiodine or surgery; a level above three times the upper limit means the baby's heart rate, growth and thyroid are monitored and the test is repeated at 30 to 34 weeks. A negative result means no further monitoring is needed.

Can TSI be positive in Hashimoto's or hypothyroidism?

A TRAb test can be low positive in 10 to 15 percent of people with Hashimoto's because it also detects blocking antibodies, which lower thyroid function rather than raise it; a true TSI bioassay is usually negative in these people. Some people have both stimulating and blocking antibodies and swing between hyperthyroidism and hypothyroidism over the years. A low positive TRAb in someone with a high TSH is read as part of autoimmune hypothyroidism, not as Graves' disease.

Do I need to fast or stop medication for a TSI test?

No fasting is needed and you should continue methimazole, propylthiouracil, levothyroxine and beta-blockers as prescribed; the test is measuring antibodies, which these drugs do not change over hours. The one supplement to pause is high-dose biotin (5 mg a day or more), for 2 to 3 days beforehand, because it can interfere with the immunoassay. Tell the lab if you had radioactive iodine in the past year, since levels are expected to be higher then.

References

Thyroid antibodies. MedlinePlus, US National Library of Medicine (2023)View source
Ross DS, Burch HB, Cooper DS, et al.. 2016 American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid (2016)View source
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)View source
Kahaly GJ, Bartalena L, Hegedüs L, Leenhardt L, Poppe K, Pearce SH. 2018 European Thyroid Association guideline for the management of Graves' hyperthyroidism. European Thyroid Journal (2018)
Tozzoli R, Bagnasco M, Giavarina D, Bizzaro N. Diagnostic accuracy of TSH receptor antibody assays in Graves' disease: a systematic review and meta-analysis. Autoimmunity Reviews (2012)
Barbesino G, Tomer Y. Clinical utility of TSH receptor antibodies. Journal of Clinical Endocrinology and Metabolism (2013)
Marcocci C, Kahaly GJ, Krassas GE, et al.. Selenium and the course of mild Graves' orbitopathy. New England Journal of Medicine (2011)View source
Grove-Laugesen D, Ebbehoj E, Watt T, et al.. Effect of vitamin D supplementation on relapse of Graves' disease: the DAGMAR trial. Thyroid (2023)
Benvenga S, Ruggeri RM, Russo A, Lapa D, Campenni A, Trimarchi F. Usefulness of L-carnitine, a naturally occurring peripheral antagonist of thyroid hormone action, in iatrogenic hyperthyroidism: a randomized, double-blind, placebo-controlled clinical trial. Journal of Clinical Endocrinology and Metabolism (2001)
Wiersinga WM. Smoking and thyroid. Clinical Endocrinology (2013)
Hyperthyroidism. Merck Manual Professional Version (2024)
Graves' disease. American Thyroid Association (2023)View source

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