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Endocrine Abstracts (2024) 101 PS1-05-01 | DOI: 10.1530/endoabs.101.PS1-05-01

1Helenic Endocrine Network, Endocrinology, Diabetes and Metabolism, Patras, Greece; 2Hellenic Endocrine Network, Patras, Greece; 3Hellenic Endocrine Network, Athens, Greece; 4Hellenic Endocrine Network, Kavala, Greece; 5Private Practice, Pvt, Chania, Greece; 6Private Practice for Endocrinology, Alexandroupolis, Greece; 7401 General Military Hospital of Athens, Endocrine Department - Thyroid Cancer Outpatient Clinic, Athens, Greece; 8University of Manchester, Manchester, United Kingdom; 9Hellenic Endocrine Network, Larisa, Greece; 10Loyola University Medical Center / Edward Hines Jr Va Hospital, Endocrinology, Diabetes and Metabolism, Hines, Il, United States; 11Euroclinic Hospital, Endocrine Surgery Center of Excellence, Athens, Greece


Introduction: Insulin resistance and diabetes have been lined to increased tumorigenesis and tumor aggressiveness in a multitude of cancers, but that link seems controversial when it comes to thyroid cancer. The present work aims to characterize the effects of various forms of diabetes [autoimmune = type 1 + LADA = DM1 vs. type 2 diabetes = DM2] on the incidence and features of tumor aggressiveness of thyroid cancers in comparison to the general population (non-diabetes = non-DM).

Methods: We performed a retrospective data collection from patients undergoing thyroid surgery in ten Endocrine Surgery and Endocrinology Clinics in Greece, between 2021-2023. We reviewed the data on pre-existing DM, the DM type, duration and treatment used, preoperative TSH, the surgical pathology report, the use of I-131 therapy and any potential structural recurrence. We compared the aggressiveness of thyroid cancers based on histology among subjects with and without DM and its subtypes.

Results: We studied 808 consecutive patients with thyroid cancer; n = 237 males (29.3%), with a mean age 47.3 ± 14.3 years, a mean BMI 27.0 ± 5.0 Kg/m2 and TSH 1.99 ± 2.21 mIU/l. Out of them, n = 692 had no DM, n = 10 had DM1 and n = 107 had DM2. Surgical pathology consisted of n = 5 poorly differentiated/ anaplastic, n = 13 medullary, n = 12 Hürthle cell, n = 17 follicular and n = 773 papillary thyroid cancers (PTC); n = 20 (2.5%) with aggressive histological subtypes of PTC, n = 5 (0.6%) with distant metastases (MET), n = 199 (24.6%) with extrathyroidal extension (ETE), n = 419 (51.9%) with capsular invasion (CI), n = 225 (27.8%) with lymph nodes involvement (LNi) while n = 23 had a structural tumor recurrence (CR) (2.8%). The incidence of aggressive histological types, CR, MET or number of I-131 treatments were not different between groups (P> 0.05). ETE, CI and LNi were found at a significantly higher rate in non-DM compared DM1 and DM2, while gross ETE was more common in DM2 over DM1 and non-DM (P < 0.001).

Conclusions: Autoimmune diabetes seems to confer a protective effect on several features of cancer aggressiveness in affected individuals as compared to DM2 and unaffected patients. Similarly, DM2 seems to significantly promote gross ETE. No statistically significant effects were observed pertaining to the risk for more aggressive tumors or histological subtypes of PTC. Although aggressiveness of thyroid cancer seems minimal in DM1 and potentially lower in DM2, a complex interplay between autoimmunity, hyperglycemia and tumoral biology is present, and requires significantly larger sample size to understand the interconnection between these parameters.

Volume 101

46th Annual Meeting of the European Thyroid Association (ETA) 2024

European Thyroid Association 

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