Thyroid eye disease (TED) has long been one of ophthalmology’s most challenging conditions to treat. Observed in approximately 50% of patients with Graves disease, TED affects women 5 times more frequently than men, with patients typically presenting in their 40s and exhibiting worse prognosis when diagnosed after age 50. Smoking is the strongest modifiable risk factor, whereas family history of autoimmune disorders and radioactive iodine therapy (especially in smokers) also contribute to disease risk and exacerbation.1 Patients suffer from debilitating symptoms, such as proptosis, diplopia, orbital pain, and—in severe cases—vision loss from optic nerve compression. For decades, our treatment arsenal was limited to corticosteroids for inflammation, supportive care, and surgical intervention for chronic complications. These approaches often provided only transient relief while carrying significant risks and side effects.
The landscape of TED treatment has been fundamentally transformed by advances in our understanding of disease pathophysiology, particularly the discovery of the insulin-like growth factor 1 receptor (IGF-1R) pathway as a key driver of pathogenesis. This mechanistic insight has enabled the development of targeted biologic therapies that address the underlying disease process rather than merely suppressing inflammation. Among these approaches, IGF-1R antagonism has emerged as the most transformative, offering the first truly disease-modifying treatment for TED.
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