Teprotumumab - the new biological target in the management of thyroid orbitopathy

Abstract

Background. Thyroid orbitopathy (OT) represents a complex autoimmune condition with a varied ocular clinic such as diplopia, diminished vision and progressive alterations in facial appearance. Traditional treatments show limited efficacy regarding the structural components of the disease such as proptosis and diplopia. Objective(s). Highlighting innovative treatment methods in OT particularly focusing on targeted biological treatment represented by Teprotumumab - a monoclonal antibody directed against the IGF-1R receptor. Materials and methods. Review of current data analyzing PubMed, ScienceDirect and Elsevier scientific publications and articles, published between 2016-2022 regarding the pathogenetic mechanism of OT, underlining the results obtained regarding the efficacy of teprotumumab - the antibody directed against the insulin-like growth factor receptor 1. Results. By blocking the IGF-1R/TSHR pathway, teprotumumab reduces the release of proinflammatory cytokines. This causes the stimulation of orbital fibroblasts and the deposition of hyaluronan - thus contributing to the expansion of adipose tissue and extraocular muscle, the development of edema and inflammation. Therefore, this monoclonal antibody can reduce the signaling initiated at either receptor, blocking any pathological immune response in Thyroid Orbitopathy. Its efficacy in reducing proptosis, improving diplopia and decreasing disease activity has led to its approval as the first targeted biologic treatment for OT. Conclusion(s). Recent clinical studies with reference to the pathogenesis of thyroid orbitopathy indicate an advanced transition from nonspecific anti-inflammatory therapies to individualized biological approaches. Therefore, teprotumumab marks a significant advance in this direction.