Thyroid Stimulating Immunoglobulin (TSI)

Thyroid marker

Thyroid Stimulating Immunoglobulin

Thyroid Stimulating Immunoglobulin (TSI)

Category: Thyroid
Unit: IU/L

An antibody that binds the TSH receptor and switches it on, driving the thyroid to overproduce hormone independently of TSH. The specific cause of Graves' disease.

PED Notes

This is the test that names the cause when thyroid function is genuinely overactive. That matters here because the picture it produces can be mistaken for something self-inflicted: suppressed TSH with raised free T4 and free T3 looks superficially like exogenous thyroid hormone use, and someone running T3 or T4 who develops Graves' can have it written off as their own dosing. The distinction is straightforward on paper. Exogenous T3 suppresses TSH while thyroglobulin falls and antibodies are absent; Graves' suppresses TSH with positive TSI and usually a diffusely enlarged gland. Do not interpret this while running thyroid medication without telling the clinician, because the two states are easy to confuse and the treatments are opposite. Also note that raised TSI in pregnancy crosses the placenta and can affect the fetal thyroid, so it carries weight beyond the person tested.

When high

A positive result identifies Graves' disease as the cause of an overactive thyroid, and it is diagnostic rather than something to manage yourself. This needs an endocrinologist.

Read it with the rest of the thyroid panel:

  • TSH suppressed, with raised Free T4 and Free T3, plus positive TSI, is the classic Graves' pattern.
  • Positive TSI with normal thyroid function can precede clinical disease and warrants monitoring rather than treatment.

The distinction that matters most in this population: exogenous T3 or T4 also suppresses TSH and raises free hormones, and can look similar at a glance. Antibodies separate them. If you are running thyroid medication, say so, because stopping it is the first step in interpreting the panel and nobody can do that safely without knowing.

Why it is not simply left alone: untreated hyperthyroidism causes atrial fibrillation, bone loss and, rarely, thyroid storm. Cardiac risk compounds with stimulants, raised haematocrit and elevated blood pressure, so see Resting Heart Rate and Systolic BP.

In pregnancy: TSI crosses the placenta and can cause fetal or neonatal hyperthyroidism even in a woman previously treated. Levels are measured in the third trimester for exactly this reason.

References:

  • Ross, D. S., Burch, H. B., Cooper, D. S., et al. (2016). 2016 American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid, 26(10), 1343-1421. DOI: 10.1089/thy.2016.0229
  • Barbesino, G., & Tomer, Y. (2013). Clinical review: clinical utility of TSH receptor antibodies. Journal of Clinical Endocrinology and Metabolism, 98(6), 2247-2255. DOI: 10.1210/jc.2012-4309
  • Kahaly, G. J., Bartalena, L., Hegedus, L., et al. (2018). 2018 European Thyroid Association guideline for the management of Graves' hyperthyroidism. European Thyroid Journal, 7(4), 167-186. DOI: 10.1159/000490384

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