Management of thyroid dysfunction in Graves’ Orbitopathy

Abstract

AbstractGraves’Orbitopathy (GO), generally associated with hyperthyroidism, may develop also before or after the onset of hyperthyroidism, or even in hypothyroid Hashimoto’s patients. The course and treatment modalities/outcomes of the thyroid disease may alter GO expression and severity. Restoration of euthyroidism with antithyroid drug (ATD) usually improves ocular conditions. However, recurrence of hyperthyroidism after ATD withdrawal, may favour GO progression. Therefore, radical treatment with radioiodine (RAI) or thyroidectomy, should be considered in relapsing patients with GO. RAI leads to a progression of GO in 15‐37% of patients. Several factors are predictive: a) pre‐existing ‘active’ GO, b) severity of hyperthyroidism, c) high serum TSH‐R Ab levels, d) cigarette smoking and e) occurrence of uncorrected post‐radioiodine hypothyroidism with elevated serum TSH. Progression of GO can be prevented by glucocorticoid (GC) therapy, 0.5 mg/Kg BW initially gradually withdrawn over 10‐12 weeks. In patients with inactive GO nor other risk factors, GC coverage is not necessary. In patients with ‘moderate‐severe and active GO’, if radical treatment with RAI is indicated, GO should be treated concomitantly with iv GC and/or orbital radiotherapy. Thyroidectomy is ‘neutral’ for GO. Total thyroid ablation (total thyroidectomy + RAI) might even be beneficial for GO. Iatrogenic hypothyroidism, whatever the treatment, is a significant risk factor of occurrence or progression of GO which warrants close control, and prompt correction, of thyroid function during ATD or after radical treatment. In conclusion, learned treatment strategy and close management of thyroid function are mandatory in Graves’ disease patients. In patients with GO, the combined endocrinological‐ophthalmological approach is the prerequisite for efficient global management.