Abstract Disclosure: G.I. Uwaifo: None. Thyroid cancer is often treatable and often involves iodine ablation therapy. Iodine based imaging and/or therapy can be complicated in patients with abnormal iodide metabolism. We present two patients with thyroid cancer and disparate abnormal iodide metabolism. Case 1 is a 35 yr old Caucasian lady with papillary thyroid cancer (PTC) stage 1 with no metastases. After total thyroidectomy and prior to I-131 remnant ablation she had a contrast Chest CT for shortness of breath. A month after serum iodine was elevated (545 Ug/L; 40—92). 24 hr urine iodine levels was also elevated; (2,300Ug/day; 150-500). She denied dietary intake of iodine rich foods. Ablation was postponed and she commenced a strict “zero” iodine diet. Despite this and despite having no further contrast imaging serum and urinary iodine remain elevated for nearly 3 yrs. Further history indicated episodes of sensitivity to several medications and Cytochrome P450 genetic profiling revealed two polymorphisms of CYP P450 2C19 and 2D6 associated with slow drug metabolizer phenotype. 34 months after her Chest CT with serum iodine of 127Ug/L and 24 hr Urine iodine of 652 she had radio iodine-ablation (RIA) with 130Mci of I-131. She had post treatment dysgeusia and parotitis. She remains on a low iodine diet and is presumably cured. Case 2 is a 66 yr old Caucasian man referred for second opinion regarding therapeutic options for known metastatic PTC with metastases to thoracic spine and lungs. He was diagnosed with follicular variant PTC 7 yrs ago. He had total thyroidectomy and repeated RIAs with a total accumulated dose of ∼ 850Mci and last RIA 3 yrs ago. His latest two whole body I-131 scans were -ve despite elevated thyroglobulins and metastatic disease. He was unable to tolerate sorefanib. He is on thyroid hormone repletion and quarterly denosumab. Contrast PET-CT scan a week prior showed extensive metastatic disease and thyroglobulins in the 300—650 ng/ml range. Work up for repeat whole body I-131 scan revealed curiously that serum iodine was 46 Ug/L (40-92) despite his recent contrast study and this was confirmed on two repeats. 24 hr urine iodine was reduced; 87 ug/day (150-500) and he had a typical diet with no excess intake of goitrogens. Based on history of often needing significantly higher doses of medications like opioids, anesthetics and sedatives cytochrome P450 genetic profile obtained showed two polymorphisms (of CYP P450 2C-19 and CVPs 3A4 +3A5) associated with fast metabolizer phenotype. Given his unusually rapid iodine clearance the utility of any further iodine based imaging and/or therapy was deemed dubious. His current management continues without change. We present two patients with extremes of iodine metabolic processing that had clinical management significance. Careful evaluation of ambient iodine status of patients is an important part of the preparation of thyroid cancer patients for iodine based imaging and/or therapy. Presentation: 6/1/2024
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