PURPOSE OF REVIEW: Thyroid eye disease is a complex autoimmune disorder which 
causes substantial morbidity. It can result in orbital disfigurement, double 
vision, and visual loss. Consequently, it has a substantial negative effect on 
quality of life, mental health, and socioeconomic status. Most signs and 
symptoms of thyroid eye disease (TED) can be explained by the expansion of the 
orbital contents. Steroids are the mainstay of treatment in TED. However, 
recurrence may occur once steroids are withdrawn. Furthermore, in most cases, 
normal orbital anatomy is not restored, and skilled rehabilitative surgery is 
required to reduce disfigurement, double vision, and to preserve vision. 
Therefore, novel, causal, and more efficacious treatment strategies are 
warranted.
RECENT FINDINGS: In the last decade, the pathophysiology of TED has also been 
revised with the identification of new potential therapeutic targets. Recent 
clinical trials have shown that considerable benefit may be derived from the 
addition of antiproliferative agents (e.g., mycophenolate sodium) in preventing 
deterioration after steroid cessation. In addition, targeted biologic therapies 
have shown promise, including teprotumumab (anti-IGFR) which appears to 
substantially reduce proptosis, rituximab (anti-CD20) which reduces inflammation 
and tocilizumab (anti-IL-6) which potentially benefits both of these parameters.
SUMMARY: This short review summarizes the recent research developments in this 
area.