Controversies in Ophthalmology

Thyroid orbitopathy (thyroid associated orbitopathy or Graves’ ophthalmopathy) is a common cause of proptosis, eyelid retraction, orbital congestion, and motility disturbances in adults. Each patient experiences a unique combination of symptoms and signs for an unpredictable duration and with varying severity. Although orbital manifestations typically improve within 2–5 years, these years feel like a century to the extremely uncomfortable and discontented patients. In addition, visual loss due to optic nerve compression does occur. Radiotherapy has a key role in the management of moderate to severe inflammatory symptoms and is effective treatment for optic nerve compromise. Our understanding of the link between systemic thyroid disease and orbitopathy has expanded greatly over the past 20 years, although the precise pathogenesis remains uncertain. An unknown mechanism allows thyroid antigen to stimulate the immune system and produce antibodies to the thyroid stimulating hormone (TSH) receptor and other antigens that alter the release of thyroid hormones. Shared orbit thyroid antigens result in the production of activated T lymphocytes that invade the orbital connective tissue. 2 Orbital fibroblasts proliferate, resulting in increased synthesis and release of glycosaminoglycans. Locally produced cytokines amplify the inflammatory response. This combined cell mediated and humoral response results in inflammatory cell migration and production of oedema in the orbit. The result is thickening of extraocular muscle and an increase in orbital fat volume. External beam radiation can intervene in this process by arresting the fibroblast proliferation and diminishing the orbital inflammation permanently.