- Last Update On : 2014-02-09
All forms of autoimmune thyrotoxicosis (Graves disease, Hashitoxicosis, neonatal thyrotoxicosis) are caused by the production of TSHR-stimulating autoantibody (TSHR-antibody), which are also known as long-acting-thyroid-stimulator (LATS) or thyroid-stimulating immunoglobulins (TSI). These autoantibodies bind to the thyrotropin receptor and activate it, leading to stimulation of the thyroid gland independent of normal thyrotropin (TSH) stimulation. TSHR autoantibody may be detected before autoimmune thyrotoxicosis becomes clinically apparent.
TSHR-antibody is a binding assay that detects both TSI and TSHR-blocking autoantibodies. It can be used instead of this TSI assay for most applications. TSHR-antibody test has a shorter turnaround time than the TSI assay, is less expensive, and if interpreted within the clinical context, has excellent correlation with the TSI assay. A TSHR antibody cutoff point of 1.75 IU/L has a sensitivity of 97% and a specificity of 99% for detection of Graves disease.
Since none of the treatments for Graves disease are aimed at the underlying disease process, but rather at thyroid ablation or thyroid hormone synthesis, TSI may persist after clinical cure. This is particularly important for pregnant women with a history of Graves disease that were treated with thyroid-ablative therapy. Some of these women may continue to produce TSI. Since TSI are IgG antibodies, they can cross the placental barrier and cause neonatal thyrotoxicosis. Significant neonatal thyrotoxicosis is likely if a pregnant woman with a history of Graves disease has TSHR Ab concentrations of >3.25 IU/L during the last trimester.
Specimen requirement is a red top tube of blood.