Background: The prevalence and clinical significance of de novo detection of anti-thyroglobulin antibodies (TgAbs) during the follow-up of patients with differentiated thyroid cancer (DTC) is unknown. Methods: We utilized the National Thyroid Cancer Treatment Cooperative Study registry . Patients registered after 1996 (n = 3318) were analyzed. We identified 1545 subjects who had available TgAb status (TgAb cohort) between years 1996 and 2012, of whom 1325 were TgAb negative at first postoperative follow-up testing. From this initial TgAb-negative group, we excluded 513 patients: 423 patients who had less than 3 years of follow-up and/or fewer than three follow-up visits, 86 patients with persistent disease after initial treatment, and 4 patients with data entry errors. The remaining 812 patients were included for analysis, comprising the TgAb persistently negative group (defined as TgAb negative for at least 3 consecutive follow-up visits and at least 3 years of follow-up) (n = 772) and the de novo TgAb-positive group in whom TgAbs became detectable (n = 40). We then assessed whether de novo appearance of TgAb was associated with DTC structural recurrence by using the Kaplan-Meier method. Results: The de novo detection of TgAb occurred in 5% of DTC patients. Recurrence of DTC in the TgAb persistently negative group compared with the de novo TgAb-positive group did not differ significantly (9.6% vs. 15.0%, p = 0.23). Baseline characteristics, histology, history of radiation exposure, staging, and median duration of follow-up were similar between the two groups. Interestingly, in all six patients who suffered a recurrence in the de novo TgAb-positive group, the TgAbs were negative at the time of recurrence detection and became positive at a median of 2.1 (0.7-8.7) years after the structural recurrence. Conclusions: Utilizing a large North American DTC registry, we found the prevalence of de novo TgAb detection to be 5% among initially TgAb-negative patients. We did not find a statistically significant association between de novo TgAb development and DTC structural recurrence. Larger prospective studies are required to confirm these findings and further assess the significance of de novo TgAb detection in the follow-up of DTC.

Introduction Automated immunoassays used to evaluate thyroid function tests (TFTs) are susceptible to various forms of interference that can lead to inaccurate results and misdiagnosis. Case Description A 55-year-old male was diagnosed with abnormal TFTs since 2017 [TSH 7.32 mIU/L (range 0.4-4.5), FT3 5.1 pg/mL (range 2.3-4.2), and FT4 1.2 ng/dL (range 0.9-2.2)]. Thyroid peroxidase antibody and thyroglobulin antibody were positive. He was on levothyroxine 50 mcg daily since 2017, and he did not feel significantly different despite treatment. He was referred to endocrine clinic in 2021. He had no symptoms of hypothyroidism or hyperthyroidism except occasional palpitations and headache. He reported blurred vision due to cataracts. He denied thyroid diseases in first degree relatives. He denied taking biotin or desiccated thyroid extract. Physical examination was unremarkable. Differentials included TSH-producing adenoma, assay interference, exogenous T3 use, T3 thyrotoxicosis with interference of TSH assay, and thyroid hormone resistance. Levothyroxine was discontinued in May 2021. Other pituitary hormones including alpha-subunit and MRI pituitary were unremarkable, which ruled out TSH-producing adenoma. Human anti mouse antibody (HAMA) was normal. In June 2021, prior to seeing genetics, FT4, FT3 and Total T3 were checked with equilibrium dialysis method and values were 1.2 ng/dL (range 0.9-2.2), 238 pg/dL (range 210-440) and 105 ng/dL (range 76-181), respectively and TSH 9.13 mIU/L (range 0.40-4.50), thyroglobulin 0.6 ng/ml (range 2.8-40.9), reverse T3 LC/MS/MS 12 ng/dL (range 8-25). Labs were therefore consistent with subclinical hypothyroidism, and he was started back on levothyroxine 75 mcg every morning. Discussion TFTs are usually measured by automated immunoassays, and this will have accurate results in most cases. However, immunoassays are vulnerable to interferences that can affect clinical decisions. It is important to consider assay interference such as this and to confirm with equilibrium dialysis method before pursuing further aggressive workup. Conclusion Potential interferences in TFTs should always be suspected whenever discrepancies arise. Awareness of these conditions is critical to the institution of appropriate therapy and preventing misdiagnosis. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

Introduction Thyroid storm is a rare, life-threatening condition with a high mortality rate approaching 10-30%. The mainstay of treatment includes initiation of therapy directed against the thyroid, supportive intensive care, and treatment of any precipitating factors. We report three cases of patients with thyroid storm and successful therapeutic use of plasmapheresis when traditional therapy was contraindicated. Clinical Cases Case 1 A 22-year-old male with no known past medical history, presented with fever, shortness of breath, and syncope. Labs showed TSH 0. 014 mIU/L (range 0.4-4.5), FT4 4.30 ng/dL (range 0.9-2.2), TSI 546% (range <140), and TPO 20 U/mL (range <60). He was diagnosed with thyroid storm due to Graves’ disease (Burch-Wartofsky score of 60). He was initially treated with propylthiouracil (PTU), hydrocortisone, propranolol, and Lugol's iodine solution. He developed transaminitis and shock liver so was not able to continue PTU or trial methimazole. He underwent 4 rounds of plasmapheresis with improvement in thyroid hormone levels and eventually had thyroidectomy. Case 2 A 37-year-old female with known Graves’ disease (non-adherent to antithyroid drug), presented with shortness of breath and palpitations. Labs showed TSH <0. 01 mIU/L (range 0.4-4.5), FT4 4.83 ng/dL (range 0.9-2.2), and FT3 6. 0 pg/mL (range 2.3-4.2). Burch-Wartofsky score was 40 and supported the diagnosis of thyroid storm. She was initially treated with methimazole, hydrocortisone, propranolol, and Lugol's iodine solution. She developed transaminitis and there was also concern for methimazole-induced insulin autoimmune syndrome, so methimazole was discontinued. She underwent 3 rounds of plasmapheresis with improvement in thyroid hormone levels and eventually had thyroidectomy. Case 3 A 31-year-old female with no known past medical history, presented with shortness of breath and altered mental status requiring intubation. Labs showed TSH <0. 01 mIU/L (range 0.4-4.5), FT4 4.65 ng/dL (range 0.9-2.2), FT3 25.2 pg/mL (range 2.3-4.2), TSI 467% (range <140), TPO 375 U/mL (range <60). She was diagnosed with thyroid storm due to Graves’ disease (Burch-Wartofsky score of 90). She was initially treated with methimazole, hydrocortisone, propranolol, and Lugol's iodine solution. She developed pulmonary alveolar hemorrhage and it was unclear if this was due to methimazole, thus methimazole was discontinued. She underwent 5 rounds of plasmapheresis with improvement in thyroid hormone levels and eventually had thyroidectomy. Conclusion Plasmapheresis can be an effective and safe treatment option in thyroid storm when there are contraindications for antithyroid drugs or when rapid normalization of thyroid hormone levels is needed. It should be considered as a stabilizing measure as it leads to marked improvement of thyrotoxicosis within 3-5 days, allowing thyroidectomy for definitive therapy. Presentation: No date and time listed

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