Endocrine Abstracts

Immunopathogenesis: Orbital fibroblasts are recognized as the prime target cells of the autoimmune attack. There is good circumstantial evidence that autoimmunity against the TSH receptor is primarily involved, but a suitable animal model of GO is lacking. Autoimmunity against the IGF-1 receptor is nonspecific for Graves’ disease, but might contribute to the immune response in the orbit.

Diagnosis: Diagnosis of GO is based on: i) assessment of eye changes according to severity (lid aperture in mm, soft tissue changes, proptosis in mm, eye muscle motility, diplopia, corneal lesions, sight loss) and activity (clinical activity score); ii) Thyroid function tests (about 10% of GO patients is euthyroid, but most of them have detectable serum TSH receptor antibodies); iii) Exclusion of an alternative diagnosis (by orbital CT or MRI in unilateral or euthyroid cases).

Management: Management of GO is based on: i) To stop smoking. Smoking is associated with less favourable outcome of immunosuppression. ii) To restore and maintain euthyroidism. 131I therapy is associated with a risk on developing or worsening of GO, which can be largely prevented by a course of steroids (optimal dosage and duration are not well defined). Preventive steroids should be considered in high-risk patients (smokers, severe hyperthyroidism, active GO, or high TBII). Total thyroidectomy can be considered, as well as long-term treatment with antithyroid drugs (preferably as block-and-replace regimen). iii) To restore appearance and visual functions. In dysthyroid optic neuropathy urgent treatment is required (steroids, decompression). In moderately severe and active GO iv pulses of methylprednisolone are more efficacious and better tolerated than oral prednisone. Oral prednisone+cyclosporine or retrobulbar irradiation are useful in recurrences, and rituximab in resistant cases. In mild GO treatment with selenium has proven to be beneficial. In inactive cases rehabilitative surgery can be done.