Pathophysiology and clinical aspects of graves' orbitopathy: An analysis of the current state of knowledge and therapeutic trends

Graves’ orbitopathy (GO), also referred to as thyroid eye disease (TED) or endocrine orbitopathy (EO), is the most common extrathyroidal manifestation of Graves’ disease, affecting approximately 25–40% of patients. The pathogenesis of GO is complex and multifactorial, primarily involving autoimmune processes driven by antibodies against the thyrotropin receptor. These antibodies interact with both the TSH receptor and the insulin-like growth factor 1 receptor, leading to the activation of orbital fibroblasts, which results in chronic inflammation, soft tissue swelling, and fibrosis. The clinical presentation varies from mild symptoms to severe complications, such as dysthyroid optic neuropathy. Smoking remains the most critical modifiable risk factor, significantly worsening prognosis and reducing treatment efficacy. Diagnosis relies on a comprehensive assessment, including the Clinical Activity Score, laboratory evaluation of TRAb levels, and orbital imaging to determine disease activity and severity. Treatment strategies depend on the clinical phase: intravenous glucocorticosteroids are the first-line therapy for active moderate-to-severe disease, while modern biological therapies are increasingly used for refractory cases. In the inactive phase, surgical and rehabilitative interventions are primarily indicated. Due to the potential for relapse and the impact on quality of life, a multidisciplinary approach involving endocrinologists and ophthalmologists is essential for long-term management and improved patient outcomes.