Background: Graves disease (GD) as a consequence of radioactive iodine (RAI) therapy is rare, usually presenting as post-therapeutic-RAI immunogenic hyperthyroidism. The present study describes a patient with a thyroid remnant after surgery and no metastases of papillary thyroid cancer who was treated with low activity RAI. Her RAI-induced GD manifested clinically as Graves orbitopathy (GO), and she had high levels of antibodies to thyroid stimulating hormone receptor (TRAb). Case presentation: A 49-year-old woman with a history of non-toxic nodular goiter was referred for postoperative evaluation after total thyroidectomy for papillary thyroid microcarcinoma. Physical examination revealed no ocular symptoms, and ultrasound of the neck revealed no focal lesions in the thyroid bed. Immunoassays showed normal levels of TRAb and anti-thyroglobulin antibodies, and elevated levels of thyroid peroxidase antibodies (TPOAb). A diagnostic whole body scan (WBS) showed negligible uptake of iodine on the left side of the thyroid bed. Three months later, the patient developed clinically significant orbitopathy and her TRAb level was elevated. She was started on methylprednisolone therapy while tapering doses. Four months later, her TRAb had decreased and she showed clinical improvements in ocular symptoms and signs. Conclusions: To our knowledge, this is the first case report describing GD/GO induced by a low activity RAI and the presence of a thyroid remnant after total thyroidectomy. RAI-induced GD/GO should be considered in the differential diagnosis of TPO-positive patients, even if their thyroids had been removed. Background: Graves disease (GD) as a consequence of radioactive iodine (RAI) therapy is rare, usually presenting as post-therapeutic-RAI immunogenic hyperthyroidism. The present study describes a patient with a thyroid remnant after surgery and no metastases of papillary thyroid cancer who was treated with low activity RAI. Her RAI-induced GD manifested clinically as Graves orbitopathy (GO), and she had high levels of antibodies to thyroid stimulating hormone receptor (TRAb). Case presentation: A 49-year-old woman with a history of non-toxic nodular goiter was referred for postoperative evaluation after total thyroidectomy for papillary thyroid microcarcinoma. Physical examination revealed no ocular symptoms, and ultrasound of the neck revealed no focal lesions in the thyroid bed. Immunoassays showed normal levels of TRAb and anti-thyroglobulin antibodies, and elevated levels of thyroid peroxidase antibodies (TPOAb). A diagnostic whole body scan (WBS) showed negligible uptake of iodine on the left side of the thyroid bed. Three months later, the patient developed clinically significant orbitopathy and her TRAb level was elevated. She was started on methylprednisolone therapy while tapering doses. Four months later, her TRAb had decreased and she showed clinical improvements in ocular symptoms and signs. Conclusions: To our knowledge, this is the first case report describing GD/GO induced by a low activity RAI and the presence of a thyroid remnant after total thyroidectomy. RAI-induced GD/GO should be considered in the differential diagnosis of TPO-positive patients, even if their thyroids had been removed.

Background: Multiple endocrine neoplasia type 2A (MEN2A) is a rare, hereditary syndrome resulting from a germline mutation in the RET proto-oncogene and characterized primarily by medullary thyroid cancer (MTC), pheochromocytoma (PHEO), and hyperparathyroidism. Types of RET mutation have been associated with age at onset, clinical outcomes of MTC, and the penetrance of other components. Patients classified as ‘high-risk’ by the American Thyroid Association (ATA), based on the aggressiveness of MTC and the penetrance of other components, are recommended to undergo early prophylactic thyroidectomy at age ≤ 5 years and to be screened for PHEO at age ≥ 11 years. Patients with RET codon C634R mutations have been classified as high-risk. Case presentation: The present study describes a 71-year-old woman newly diagnosed with hereditary MTC related to a RET C634R germline mutation. Her basal serum calcitonin level was high, but there was no evidence of distant metastases. Surgery revealed bilateral MTC with two metastatic lymph nodes. Because microscopic resection was incomplete and extranodal extension was observed, the patient underwent adjuvant external beam radiotherapy. Response to therapy was excellent. Follow-up after 1.5 years showed no evidence of disease or other manifestations of MEN2A. Conclusion: Despite RET C634R carriers being classified as high-risk by the ATA, this patient did not present with either distant MTC or PHEO until her seventies. To our knowledge, only one other patient has shown a similar late identification of a RET C634R mutation, but MTC could not be diagnosed because the patient was lost to follow-up. Further research is required to develop optimal protocols that could allow patients requiring prophylactic thyroidectomy to be differentiated from those who can be monitored closely without early surgery.