Thyroid Eye Disease: Advancements in Orbital and Ocular Pathology Management

Abstract

Thyroid Eye Disease (TED) is a debilitating autoimmune condition often associated with thyroid dysfunction, leading to significant ocular and orbital morbidity. This review explores recent advancements in the management of TED, focusing on both medical and surgical innovations. The introduction of Teprotumumab, the first FDA-approved drug specifically for TED, marks a pivotal development in medical therapy. Teprotumumab targets the insulin-like growth factor-1 receptor (IGF-1R), effectively reducing inflammation and tissue remodeling. Clinical trials demonstrate its efficacy in reducing proptosis and improving quality of life, making it a cornerstone in the treatment of active, moderate-to-severe TED. Surgical management remains critical for patients with chronic TED or those unresponsive to medical therapy. Advancements in orbital decompression surgery, including image-guided and minimally invasive techniques, offer improved outcomes and reduced complications. Innovations in eyelid and strabismus surgery enhance functional and cosmetic results, further improving patient satisfaction. The management of TED necessitates a multidisciplinary approach involving endocrinologists, ophthalmologists, oculoplastic surgeons, radiologists, and other specialists. This collaborative strategy ensures comprehensive care, addressing the diverse aspects of TED from thyroid dysfunction to ocular health and psychological well-being. Future directions in TED treatment include emerging pharmacological therapies targeting different aspects of the disease's pathophysiology and advanced surgical techniques aimed at enhancing precision and safety. This review underscores the importance of a personalized, multidisciplinary approach in managing TED, highlighting current advancements, and exploring potential future innovations to improve patient outcomes and quality of life.

Keywords: autoimmune; dry eye; insulin growth factor; orbital pathologies; proptosis; teprotumumab; thyroid eye disease.

Figure 1

Pathogenesis of Thyroid Eye Disease (TED). ↑ (increased secretion); APC (Antigen Presenting Cell); IFN-γ (Interferon gamma); IGF-1 (Insulin-like Growth Factor 1); IL- (Interleukin); MHC-II (Major Histocompatibility Complex class II); RANTES (Regulated on Activation, Normal T Cell Expressed and Secreted); TGF-β (Transforming Growth Factor beta); TNF-α (Tumor Necrosis Factor alpha).

Figure 2

Thyroid Eye Disease clinical manifestations.

Figure 3

Teprotumumab mechanism of action. CD40 (Cluster of Differentiation 40); IGF-1 (Insulin-like Growth Factor 1); IGF-1R (Insulin-like Growth Factor 1 Receptor); MHC-II (Major Histocompatibility Complex class II).