This review will examine the overall pathogenic mechanism linked to the immune cells of TED and then discuss the latest research findings on the immunomodulatory role of ICs in the development and pathogenesis of TED. This will offer fresh perspectives on the study of pathogenesis and the identification of potential therapeutic targets.
Recent studies have reported that the IGF-1 receptor (IGF-1R) plays an important role in the pathogenesis of TAO, and the IGF-1R inhibitor teprotumumab involves significantly improved disease endpoints in patients with active TAO. Thyroid-stimulating hormone (TSH) receptor (TSHR) and IGF-1R co-immunoprecipitate in orbital and thyroid tissues to form a functional complex; thus, combined therapy targeting TSHR and IGF-1R may be more effective than single therapy.
Treatment options include high doses of antithyroid medications or radioactive iodine and thyroidectomy in selected cases [2].Clinical case A 72-year-old female with a medical history of right-sided breast cancer treated with lumpectomy and radiation therapy in 2012 on anastrozole was referred for multinodular goiter (MNG) evaluation in 2018...The patient was also seen by ophthalmology and plans to start teprotumumab treatment...In this case, she was initially asymptomatic with an enlarged multinodular goiter; three years later, she developed subclinical hyperthyroidism due to Graves' disease and toxic multinodular goiter. Her symptom and thyroid function are well-controlled with low-dose methimazole.
She received teprotumumab for her eye disease, with resolution of symptoms. We believe our patient's elevated TSI was induced by benralizumab with subsequent progression of her thyroid cancer and new onset of thyroid eye disease. We should be aware of this potential adverse event of benralizumab and use it with caution in patients with Graves' disease.