title: The tale of radioiodine and Graves' orbitopathy.
abstract: BACKGROUND
  Autoimmunity against the thyrotropin receptor (TSH-R) is a key pathogenic element in Graves' disease (GD) and the autoimmune aberration may be modified by antithyroid treatment. An association between radioactive iodine (RAI) therapy for GD and the development or worsening of Graves' orbitopathy (GO) is widely quoted. RAI-associated leakage of thyroid antigen(s) leads to an increased production of TSH-R antibodies that may initiate the eye injury.
  
  
  CONCLUSIONS
  RAI therapy leads to prolonged worsening of autoimmunity against the TSH-R, and the number of patients entering remission of TSH-R autoimmunity is considerably lower than with other antithyroid therapies. Scientific evidence has indicated that RAI treatment for GD is associated with increased risk of occurrence or progression of GO compared with antithyroid drugs (ATD) and thyroid surgery. The risks of developing new GO or worsening of preexisting GO is around 20% after RAI and around 5% after ATD. The risk of developing severe GO after RAI is around 7%. Smoking, high levels of pretreatment serum triiodothyronine, and post-RAI hypothyroidism are associated with increased risk of GO, whereas a high TSH-R autoantibody titer is an independent risk factor for the progression of GO. In patients with mild preexisting GO, steroid prophylaxis is effective in preventing deterioration of GO. Also, routine use of prophylactic oral steroids with RAI therapy should be considered in GD patients without overt GO, but even more so in those at higher risks of eye complications such as smokers, old men, and those with severe hyperthyroidism or high TSH-R antibody titers.
  
  
  CONCLUSIONS
  In contrast to ATD, remission of TSH-R autoimmunity after RAI therapy is less common, and RAI for GD is associated with definite increased risk of GO. Oral steroids are beneficial for patients with preexisting GO, particularly smokers.
authors.affiliation: Department of Ophthalmology, Gutenberg University Medical Center, Mainz, Germany.
authors.forename: Katharina A
authors.initials: KA
authors.lastname: Ponto
authors.forename: Stephanie
authors.initials: S
authors.lastname: Zang
authors.forename: George J
authors.initials: GJ
authors.lastname: Kahaly
mesh_terms: D013956:Antithyroid Agents / Q000009:adverse effects* / Q000627:therapeutic use; D015551:Autoimmunity / Q000528:radiation effects; D018450:Disease Progression; D004198:Disease Susceptibility; D006111:Graves Disease / Q000150:complications / Q000276:immunology / Q000532:radiotherapy*; D049970:Graves Ophthalmopathy / Q000188:drug therapy / Q000209:etiology* / Q000517:prevention & control; D006801:Humans; D007457:Iodine Radioisotopes / Q000009:adverse effects* / Q000627:therapeutic use; D011837:Radiation-Protective Agents / Q000009:adverse effects / Q000627:therapeutic use; D011989:Receptors, Thyrotropin / Q000276:immunology; D012307:Risk Factors
chemical_list: D013956:Antithyroid Agents; D007457:Iodine Radioisotopes; D011837:Radiation-Protective Agents; D011989:Receptors, Thyrotropin