Therapeutic Landscape—Steroids, Biologics, Radiotherapy, and Surgery

The treatment landscape for thyroid eye disease has changed significantly with the advent of targeted biologic therapy. In this segment, Andrea Kossler, MD, contrasts traditional temporizing measures—such as systemic corticosteroids and orbital radiotherapy—with teprotumumab, a monoclonal antibody directed against the insulin-like growth factor 1 receptor (IGF‑1R). She explains that corticosteroids, whether administered intravenously or orally at high doses, can reduce inflammatory activity but often confer only transient benefit and carry meaningful risks for patients with comorbidities such as diabetes mellitus or uncontrolled hypertension.

Andrea Kossler, MD, describes high-dose intravenous glucocorticoids as “bridge” therapy, sometimes used to stabilize patients while more definitive options are pursued. Radiotherapy remains in use within some practices, although she notes that it does not address the underlying pathophysiology and may be associated with scarring. In contrast, she characterizes teprotumumab as the first agent to modify the course of TED, citing its targeted mechanism against IGF‑1R and the superior clinical outcomes observed with biologic immunomodulation compared with older off-label immunosuppressive regimens.

Despite these advances, surgery retains an important role. Dr Kossler highlights orbital decompression for patients with sight-threatening optic nerve compression or severe, disfiguring proptosis. She notes that experienced oculoplastic surgeons can achieve excellent results, but procedural timing and sequencing relative to medical therapy must be carefully considered. Collectively, her comments underscore an evolving paradigm in which biologics, bridge therapies, and surgery are deployed in a more strategic, individualized fashion.

Andrea Kossler, MD, delineates a clear distinction between legacy therapies for thyroid eye disease and newer biologic options. Systemic corticosteroids remain widely used for short-term control of active inflammation, often via high-dose intravenous regimens. However, she underscores that their benefits are frequently temporary; disease activity can recur once steroids are tapered, and prolonged exposure is problematic in patients with diabetes mellitus, hypertension, prior radiation exposure, or other contraindications. Consequently, steroids function primarily as a bridge rather than as definitive disease-modifying therapy.

Radiotherapy occupies a more limited role in her algorithm. Although still used by some practitioners, orbital radiotherapy may induce scarring and does not directly address the immunologic drivers of TED. In contrast, teprotumumab, an IGF‑1R–targeted monoclonal antibody, represents a paradigm shift as the first approved therapy to alter disease trajectory. Dr Kossler notes that manufacturer-sponsored programs can sometimes facilitate rapid access to initial doses, and that patients receiving biologic immunomodulation typically achieve more robust and sustained improvements than with older immunosuppressive strategies.

Surgical intervention, particularly orbital decompression, remains indispensable for select patients, especially those with compressive optic neuropathy or severe proptosis. Andrea Kossler, MD, emphasizes the skill of contemporary oculoplastic surgeons but cautions that appropriate sequencing relative to medical therapy is critical. Biologic treatment may reduce inflammatory burden and optimize surgical conditions, whereas surgery itself can theoretically trigger disease flares in some cases. Her approach reflects a multidisciplinary, staged strategy that leverages steroids, biologics, radiotherapy, and surgery according to disease severity, activity, and individual risk factors.