# The therapeutic revolution in thyroid eye disease: from orbital radiotherapy to teprotumumab and AI

## TL;DR

This paper reviews the evolving treatment of thyroid eye disease, focusing on new biological therapies and the role of artificial intelligence.

## Contribution

The paper highlights the recent therapeutic shift toward IGF-1R inhibition and emerging immunotherapy targets in thyroid eye disease.

## Key findings

- Thyroid eye disease involves TSHR and IGF-1R synergy causing fibroblast activation and tissue changes.
- Targeted biological agents like IGF-1R inhibitors are transforming TED treatment.
- Artificial intelligence is emerging as a tool for diagnosis and prognosis in TED.

## Abstract

Thyroid eye disease (TED) is a vision-threatening and quality-of-life-impairing manifestation of autoimmune thyroid disease, driven by orbital fibroblast activation, inflammation, and tissue remodeling. This review synthesizes current evidence on TED epidemiology and pathogenesis, with a particular focus on the pathogenic synergy between the thyrotropin receptor (TSHR) and the insulin-like growth factor-1 receptor (IGF-1R). We discuss how this receptor complex propagates intracellular signaling that leads to disease hallmarks: fibroblast proliferation, glycosaminoglycan secretion, and adipogenesis. While we outline the established paradigm of management—encompassing glucocorticoids, orbital radiotherapy, and surgery—a key emphasis is placed on the recent therapeutic revolution ushered in by targeted biological agents, most notably IGF-1R inhibition. As well as research on new targets for immunotherapy such as Tregs and other aspects such as IL-6 or TNF-α. Finally, we explore the nascent role of artificial intelligence in refining diagnosis and prognostic assessment. This overview aims to equip clinicians and researchers with a forward-looking perspective on the evolving landscape of TED management.