Thyroid eye disease treatment depends on disease activity and severity and involves both pharmacologic and non-pharmacologic strategies. Intravenous methylprednisolone remains the standard first-line therapy for active moderate-to-severe disease, offering rapid inflammation control with well-established protocols. It is effective but carries some risks such as systemic adverse effects and relapses in some patients. Biologic therapies have significantly advanced care. Teprotumumab, targeting the IGF-1 receptor, has shown strong and durable improvements in proptosis and diplopia, though it requires careful monitoring for hyperglycemia and hearing changes. Additionally, Tocilizumab is effective in steroid-resistant disease, while rituximab remains a selective option due to mixed trial results. These therapies provide more targeted inflammation control, though cost, access, and safety monitoring must be considered. Non-pharmacologic measures are also essential. Smoking cessation, tight thyroid control, ocular surface protection, and selenium supplementation in deficient regions improve outcomes and may reduce disease activity. Orbital radiation can support refractory cases, and staged surgical interventions address residual proptosis or diplopia once the disease becomes inactive. Optimizing treatment involves matching therapy to disease stage, clinical features, and patient risk factors. Biologics may be prioritized for prominent proptosis or steroid intolerance, while conventional therapy remains effective and accessible for many.
Management of thyroid eye disease now reflects a more individualized and targeted approach. Intravenous glucocorticoids, especially methylprednisolone, remain a cornerstone for controlling active inflammation, reducing orbital congestion, and stabilizing vision in moderate-to-severe disease. These regimens are supported by strong clinical data, though their limitations include incomplete control of proptosis, potential relapse, and systemic side effects that can restrict use in patients with comorbidities. Biologic therapy has altered the therapeutic landscape. Teprotumumab, by blocking the IGF-1 receptor pathway, has demonstrated significant improvements in both proptosis and diplopia, achieving outcomes that steroids alone rarely provide. Tocilizumab and rituximab offer additional options for patients with inadequate steroid response or intolerance, expanding flexibility in tailoring therapy. Although these treatments carry their own risks, particularly metabolic and otologic effects in the case of teprotumumab, their targeted mechanisms provide more durable disease control for selected patients. Non-pharmacologic strategies remain integral to comprehensive care. Maintaining stable thyroid function, eliminating smoking exposure, and implementing ocular surface protection reduce disease activity and enhance response to medical therapy. Radiation therapy can offer additional benefit in specific active, resistant cases, while surgical intervention remains a critical component of long-term management, particularly for rehabilitating proptosis and diplopia in the inactive phase. Choosing the best treatment depends on disease activity, clinical features, and patient-specific factors such as comorbidity profile, disease severity, and treatment goals.