The 2025 award winners are named below and will be honored during the ATA’s 2025 Annual Meeting to be held September 10 – 14, 2025 in Scottsdale, AZ.

“We are thrilled to recognize the exceptional achievements and leadership of these outstanding ATA members, whose accomplishments, innovation, and dedication reflect those of our incredible and diverse ATA community,” said Ari Wassner, MD, Chair of the Awards Committee.

The 2025 honorees are:

Susan J. Mandel, MD, MPH – Lewis E. Braverman Distinguished Lectureship Award

The Lewis E. Braverman Distinguished Lectureship Award recognizes an individual who has demonstrated excellence and passion for mentoring fellows, students and junior faculty, has a long history of productive thyroid research, and is devoted to the ATA. Dr. Mandel is Sylvan H Eisman Professor of Medicine and Chief of the Division of Endocrinology, Diabetes and Metabolism at the Perelman School of Medicine, University of Pennsylvania. Her clinical practice focuses on thyroid neoplasia. Her research interests include sonography in the evaluation of patients with thyroid nodules and cancer. Dr. Mandel was on the writing groups for the 3 previous versions of the ATA Management Guidelines for Patients with Thyroid Nodules and Differentiated Thyroid Cancer and is co-chairing the 2025 ATA Guidelines for Patients with Thyroid nodules. She also was on the writing group for the ATA and Endocrine Society guidelines on the Management of Thyroid Disorders during Pregnancy. Dr. Mandel initiated and directed the Ultrasound workshops for the ATA and Endocrine Society. Dr. Mandel has received the Endocrine Society’s Distinguished Educator Award, the 2019 ATA WIT Woman of the Year award, and the AACE H. Jack Baskin Endocrine Teaching Award. She also received the Louis Duhring Outstanding Clinical Specialist Award from Penn Medicine. Dr. Mandel is past President of the Endocrine Society (2018-19) and of the Association of Program Directors in Endocrinology, Diabetes, and Metabolism (2009-2011). She currently serves as Secretary of the International Society of Endocrinology. During her 21-year tenure as Program Director of the Fellowship program at Penn, she trained over 70 fellows, eight of whom now serve as Endocrine Fellowship Program Directors. She has over 100 peer reviewed publications in journals including the New England Journal of Medicine, JAMA and the Annals of Internal Medicine. She has also authored chapters on thyroid disorders in Harrison’s Textbook of Medicine and thyroid nodules in Werner and Ingbar’s The Thyroid.

Kristien Boelaert, MD, PhD – Valerie Anne Galton Distinguished Lectureship Award

The Valerie Anne Galton Distinguished Lectureship Award recognizes an individual who has been instrumental in collaborative research that has significantly contributed to the advancement of our clinical knowledge of thyroid conditions. Dr. Boelaert is a Professor of Endocrinology at the University of Birmingham in the UK. She is an active researcher with an extensive portfolio spanning molecular, clinical and translational research into thyroid dysfunction, nodules and cancer. During her career she has attracted more than $12 million in research funding and published more than 200 research papers. In addition, Kristien is a prominent clinician who is actively involved in the setting of UK, European and ATA guidelines on the management of thyroid diseases. Recognizing her contributions to patient care, she was the recipient of the inaugural Outstanding Clinical Practitioner Award from the Society for Endocrinology in 2019. She is a strong believer in collaborative working and for many years has engaged closely with patient support organizations, policy makers and researchers in various disciplines across the world. Kristien has been an active member of the ATA since 2003, volunteering on several committees and currently serving as the co-chair of the ATA 2025 Annual Meeting. She has leadership roles in many international endocrine societies including President of the British Thyroid Association, Member of the European Thyroid Association Executive Committee and President Elect of the Society for Endocrinology.

Victor Joseph Bernet, MD, FACE, FACP – Distinguished Service Award

The Distinguished Service Award honors a member who has made important and continuing contributions to the American Thyroid Association (ATA). Dr. Bernet is the Director of the Mayo Clinic Endocrinology, Diabetes and Metabolism Fellowship in Jacksonville, Florida. He is a Professor of Medicine, Mayo Clinic College of Medicine and served as Chair of the Division of Endocrinology, Mayo Clinic Florida from 2012 to 2022. He is also an Adjunct Professor of Medicine, Uniformed Services University School of Medicine. Dr. Bernet served 21+ years in the U.S. Army Medical Corps retiring at the rank of Colonel. He was the Endocrinology Consultant to the Army Surgeon General and Director of the National Capitol Consortium Endocrinology, Diabetes and Metabolism Fellowship Program. Dr. Bernet is both a Distinguished Graduate and Distinguished Military Graduate of the Virginia Military Institute (1985). He graduated from the University of Virginia School of Medicine in 1989. He completed his internal medicine residency at Tripler Army Medical Center (1989-1992) and endocrinology fellowship at Walter Reed Army Medical Center (1992-1994). Dr. Bernet’s main academic interests are focused in the field of thyroid disorders with particular interest in thyroid nodules, thyroid cancer, challenging thyroid function tests as well as hormones found in OTC supplements. He has been the author/co-author of 70+ peer-reviewed articles and 19 book chapters. Dr Bernet served as President of the American Thyroid Association 2020-2021 and also as the ATA Secretary/ Chief Operating Officer from October 2015 to November 2019. Dr. Bernet serves as the Mayo Clinic representative on the National Comprehensive Cancer Network thyroid cancer guidelines and is a member of the ATA Thyroid Nodules Guidelines Task Force.

Paul M. Yen, MD – John B. Stanbury Thyroid Pathophysiology Medal

The John B. Stanbury Thyroid Pathophysiology Medal recognizes outstanding research contributions, either conceptual or technical, to the understanding of thyroid physiology or the pathophysiology of thyroid disease, as evidenced by having a major impact on research or clinical practice related to thyroid diseases. Dr. Yen is Professor at Duke-NUS Graduate Medical School in Singapore and Head of the Laboratory of Hormonal Regulation in the Cardiovascular and Metabolic Disorders Program. He also is Professor of Medicine at Duke University School of Medicine, Durham, NC and a member of the Duke Molecular Physiology Institute. He was formerly Assistant Professor at Harvard Medical School, Chief of the Neuro-endocrinology and Molecular Regulation Section of the Clinical Endocrinology Branch at NIDDK (at the National Institutes of Health, Bethesda, MD), and Associate Professor of Medicine and Pharmacology at Johns Hopkins University School of Medicine. He has served on the editorial boards of Endocrinology, Molecular Endocrinology, and Thyroid. He also is a U.S. board-certified physician in internal medicine and endocrinology. He is listed as a top 2% scientist worldwide by Stanford University and a leading World Expert on thyroid hormone by Expertscape. He has served as an Asia-Oceanic Thyroid Association (AOTA) Council Member and the AOTA delegate to the World Thyroid Foundation and Singapore Representative to the International Iodine Global Network. He was awarded the 2020 Nagataki-Fujifilm Prize for his contributions to basic and clinical thyroid hormone research in Asia by AOTA. At Duke-NUS, he has served as Master of Sheares Medical College since 2010. He also has served as the clinical faculty advisor for the Duke Overseas Volunteer Expedition (DOVE) program in which medical students deliver primary care in neighbouring underdeveloped countries since its inception in 2010. His laboratory uses molecular biological and genomic approaches to study hormonal regulation of transcription, autophagy, and metabolism as well as searching for ways to improve the diagnosis and treatment of non-alcoholic fatty liver disease (NAFLD).

Thomas S. Scanlan, PhD – Sidney H. Ingbar Distinguished Lectureship Award

Sidney H. Ingbar Distinguished Lectureship Award recognizes outstanding academic achievements in thyroidology, in keeping with the innovation and vision that epitomized Dr. Ingbar’s brilliant investigative career. The Ingbar award is conferred upon an established investigator who has made major contributions to thyroid-related research over many years. Dr. Scanlan is Professor of Physiology & Pharmacology in the Department of Chemical Physiology & Biochemistry at Oregon Health & Science University (OHSU) in Portland, Oregon.  Before that he was Professor of Pharmaceutical Chemistry and Cellular & Molecular Pharmacology at the University of California, San Francisco (UCSF).  Dr. Scanlan’s formal training is in organic chemistry, and in 1991 he began his independent career using chemical approaches to study thyroid hormone action.  Dr. Scanlan’s research accomplishments include the discovery and development of selective thyromimetics, most notably Sobetirome (GC-1) which has been studied clinically for different metabolic disease indications. Dr. Scanlan also discovered and characterized a novel class of biogenic amine thyroid hormone metabolites called thyronamines that have biological activities distinct from those of thyroxine and T₃.  Most recently Dr. Scanlan’s research has focused on the development of central nervous system penetrating thyromimetics, one of which is currently in clinical development for depression.  Dr. Scanlan has over 14,000 career citations and an h-index of 63. His honors include the National Science Foundation Career Award, the Alfred P. Sloan Research Fellow Award, the Arthur C. Cope Scholar Award from the American Chemical Society, the Resko Faculty Research and Mentoring Award, and the Technology Transfer Achievement Award (OHSU).

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Angela M. Leung, MD – Women in Thyroidology Woman of the Year

The Women in Thyroidology Woman of the Year Award recognizes an ATA member who is dedicated to the field and the advancement of women in thyroidology. Dr. Leung is a Health Sciences Associate Clinical Professor of Medicine in the Division of Endocrinology, Diabetes, and Hypertension, Department of Medicine at the University of California Los Angeles David Geffen School of Medicine and the VA Greater Los Angeles Healthcare System. Dr. Leung received her undergraduate degree from Occidental College, her MD from the Boston University School of Medicine, and MSc in Epidemiology from the Boston University School of Public Health. She completed her internal medicine internship and residency and endocrinology fellowship at Boston University School of Medicine/Boston Medical Center. Her clinical and research interests are focused on thyroid disease and include iodine nutrition, environmental thyroid disruptors, and maternal-child thyroid health. She has served on the ATA writing committees of the thyroid eye disease consensus statement, the updated differentiated thyroid cancer guidelines, and is co-chair of the updated thyroid and pregnancy guidelines. Dr. Leung has served on the ATA Board of Directors, Editor-in-Chief of Clinical Thyroidology^® and as Chair of the Women in Thyroidology.

About the American Thyroid Association^®

The American Thyroid Association (ATA) is dedicated to transforming thyroid care through clinical excellence, education, scientific discovery and advocacy in a collaborative and diverse community. ATA^® is an international professional medical society with over 1,700 members from 70 countries around the world. The ATA^® promotes thyroid awareness and information through Clinical Thyroidology^® for the Public, a resource that summarizes research for patients and families, and extensive, authoritative resources on thyroid disease and thyroid cancer in both English and Spanish. The ATA^® website www.thyroid.org serves as a bonafide clinical resource for patients and the public who look for reliable thyroid-related information.

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Sarimar Agosto Salgado, MD
Moffitt Cancer Center
Tampa, Florida
September 23, 2022

The mainstays of therapy for differentiated thyroid cancer cases include surgery, selective use of radioactive iodine (RAI) based on risk of tumor recurrence, and TSH suppression therapy with levothyroxine[1]. Although most patients have a favorable prognosis, a subset develop distant metastases (<10%), of which approximately two-thirds result in radioactive iodine refractory differentiated thyroid cancer (RAIR-DTC) [2]. Depending on the extent of metastatic disease, active surveillance under TSH suppression and localized therapies, including surgery, radiation, ablative therapies, and bone modulating agents for bone metastases, may assist in controlling the disease. Nevertheless, patients may require long-term systemic treatment for progressive RAIR-DTC. Evaluation for systemic therapy includes radiographic staging (including brain imaging), tumor testing for targetable mutations, comprehensive laboratories, cardiac function assessment, and close monitoring of comorbidities such as hypertension, diabetes, etc.

Initial systemic therapies approved for RAIR-DTC included multikinase inhibitors (MKIs) Lenvatinib and Sorafenib, which target multiple tumorigenic kinase pathways, including vascular endothelial growth factor receptors. Lenvatinib demonstrated impressive response rates of 65% and survival improvement in patients 65 years and older, leading to FDA approval in 2015 [3-5]. However, since tumors almost inevitably develop resistance mechanisms, additional therapies are being studied to expand the management options for RAIR-DTC; for example, Cabozantinib has recently been approved as a second line MKI [6].

Improved understanding of the molecular pathogenesis of thyroid cancer, coupled with increasingly comprehensive molecular testing platforms, has led to new insights. In fact, molecular testing has developed over time into an informative tool for prognostic and therapeutic implications. For example, BRAF V600E is the most common alteration in papillary thyroid cancer (PTC), present in at least 60% of cases [7]. BRAF inhibitors alone (e.g., Dabrafenib) or in combination with a MEK inhibitor (e.g., Trametinib) have shown overall responses between 42-54% in RAIR-DTC [8, 9]. A recent FDA approval in the summer of 2022, supported dabrafenib and trametinib combination for unresectable or metastatic BRAF V600E solid tumors with progression despite prior treatments. In addition, recently approved selective inhibitor options include Selpercatinib and Pralsetinib for RET fusion-driven thyroid cancer, and Larotrectinib and Entrectinib for tumors harboring NTRK fusions. Together, both MKI’s and selective inhibitors have brought a ray of hope for patients with RAIR-DTC[10]. However, practice variability still exists in terms of a) timing of initiation of systemic therapy, b) the definition criteria for RAI-refractory thyroid cancer, and c) decision regarding the first line of therapy when a targetable mutation is present.

Selective targeted therapies balance efficacy and tolerability, leading to new potential approaches to manage advanced thyroid cancer. A promising new strategy leverages the discovery that BRAF V600E mutations can lead to alteration-dysfunction in the sodium-iodine symporter and contribute to the development of RAIR-DTC. A short course of BRAF-inhibitor therapy may result in redifferentiation in BRAF-altered tumors; this is a promising approach to resensitize tumors to RAI, allowing for discontinuation of systemic therapy post-RAI and thereby limiting the toxicities of long-term chemotherapy [11, 12]. Similar capacity for redifferentiation has been reported in RAS altered, NTRK, or RET fusion-driven thyroid cancers after the treatment with a MEK inhibitor, Larotrectinib, and Selpercatinib, respectively [13-16]. Further studies are needed to determine the optimal candidates by molecular signature, standardization of protocols, and appropriate timing to implement a redifferentiation approach.

As an oncologic endocrinologist, given the evolving landscape of therapeutic options for RAIR-DTC, it is essential to highlight the importance of timely evaluating patients with advanced thyroid cancer. High-risk thyroid cancer patients should be referred to expert multidisciplinary patient-centered teams; this ensures patients receive a comprehensive assessment to delineate treatment plans and incorporate the use of precision oncology.

References:
1. Haugen, B.R., et al., 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer: The American Thyroid Association Guidelines Task Force on Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid, 2016. 26(1): p. 1-133.
2. Fullmer, T., M.E. Cabanillas, and M. Zafereo, Novel Therapeutics in Radioactive Iodine-Resistant Thyroid Cancer. Front Endocrinol (Lausanne), 2021. 12: p. 720723.
3. Schlumberger, M., et al., Lenvatinib versus placebo in radioiodine-refractory thyroid cancer. N Engl J Med, 2015. 372(7): p. 621-30.
4. Brose, M.S., et al., Effect of Age on the Efficacy and Safety of Lenvatinib in Radioiodine-Refractory Differentiated Thyroid Cancer in the Phase III SELECT Trial. J Clin Oncol, 2017. 35(23): p. 2692-2699.
5. Brose, M.S., et al., Sorafenib in radioactive iodine-refractory, locally advanced or metastatic differentiated thyroid cancer: a randomised, double-blind, phase 3 trial. Lancet, 2014. 384(9940): p. 319-28.
6. Brose, M.S., et al., Cabozantinib for radioiodine-refractory differentiated thyroid cancer (COSMIC-311): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet Oncol, 2021. 22(8): p. 1126-1138.
7. Landa, I., et al., Genomic and transcriptomic hallmarks of poorly differentiated and anaplastic thyroid cancers. J Clin Invest, 2016. 126(3): p. 1052-66.
8. Shah, M.H., et al., Results of randomized phase II trial of dabrafenib versus dabrafenib plus trametinib in BRAF-mutated papillary thyroid carcinoma. Journal of Clinical Oncology, 2017. 35(15_suppl): p. 6022-6022.
9. Busaidy, N.L., et al., Dabrafenib Versus Dabrafenib + Trametinib in BRAF-Mutated Radioactive Iodine Refractory Differentiated Thyroid Cancer: Results of a Randomized, Phase 2, Open-Label Multicenter Trial. Thyroid, 2022.
10. Cabanillas, M.E., M. Ryder, and C. Jimenez, Targeted Therapy for Advanced Thyroid Cancer: Kinase Inhibitors and Beyond. Endocr Rev, 2019. 40(6): p. 1573-1604.
11. Dunn, L.A., et al., Vemurafenib Redifferentiation of BRAF Mutant, RAI-Refractory Thyroid Cancers. J Clin Endocrinol Metab, 2019. 104(5): p. 1417-1428.
12. Rothenberg, S.M., et al., Redifferentiation of iodine-refractory BRAF V600E-mutant metastatic papillary thyroid cancer with dabrafenib. Clin Cancer Res, 2015. 21(5): p. 1028-35.
13. Groussin, L., J. Clerc, and O. Huillard, Larotrectinib-Enhanced Radioactive Iodine Uptake in Advanced Thyroid Cancer. N Engl J Med, 2020. 383(17): p. 1686-1687.
14. Lee, Y.A., et al., NTRK and RET fusion-directed therapy in pediatric thyroid cancer yields a tumor response and radioiodine uptake. J Clin Invest, 2021. 131(18).
15. Ho, A.L., et al., Selumetinib-enhanced radioiodine uptake in advanced thyroid cancer. N Engl J Med, 2013. 368(7): p. 623-32.
16. Jaber, T., et al., Targeted Therapy in Advanced Thyroid Cancer to Resensitize Tumors to Radioactive Iodine. J Clin Endocrinol Metab, 2018. 103(10): p. 3698-3705.

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

For more information on Thyroid Topics please visit: https://www.thyroid.org/thyroid-information/

We invite you to submit any questions or comments regarding this blog post below, for potential response in a future blog or social media post.

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Iñigo Landa, PhD
Brigham and Women’s Hospital & Harvard Medical School
Boston, MA
May 20, 2022

Thyroid cancers are driven by a handful of genetic alterations. Papillary thyroid cancer (PTC), the most frequent thyroid tumor with excellent survival rates, primarily harbors mutations involving BRAF, RAS or RET genes, which in turn constitutively activate the MAPK pathway, a key process for cell proliferation (1). A subset of PTCs can evolve to more aggressive forms, namely poorly differentiated (PDTC) and anaplastic thyroid cancers (ATC), which account for most of the disease-associated morbidity and mortality (2, 3). TERT (telomerase reverse transcriptase) is one of the genes that is most often mutated as thyroid cancer progresses. Mutations in TERT occur in its promoter region, which is the non-coding portion of a gene acting as an on/off switch. The acquisition of a TERT promoter mutation (TPM) reactivates the expression of telomerase, a bona fide oncogene that is otherwise silenced in human adult cells.

TPMs were discovered in advanced melanomas in 2013 (4, 5), then found at high rates in certain tumor types, such as glioblastomas, bladder and hepatocellular carcinomas (6), and shortly after reported in thyroid carcinomas (7-10). Remarkably, TPMs display a stepwise increase across thyroid specimens, tracking with tumor virulence. Less than 10% of the mostly indolent PTCs harbor TPMs; this prevalence increases in high grade PTCs and PDTCs, rising to more than 70% in the highly aggressive ATCs (11-13). Within each tumor type, TPMs systematically associate with poor prognosis. They correlate with an increased frequency of metastasis, persistent disease and lower survival in PTC patients, particularly when they co- occur with BRAFV600E or RAS oncogenic mutations (14-16). In advanced disease, patients with TERT-mutant PDTCs develop more metastasis, whereas survival of ATC patients whose tumors carry TPMs is further diminished (12). Overall, TERT promoter mutations have become a promising biomarker of poor prognosis which is progressively being incorporated in the guidelines for the management of thyroid cancer patients (17, 18).

Telomerase reactivation, which in thyroid tumors mainly occur via the acquisition of TPMs, likely enhances several molecular functions of TERT, which are relevant for the biology of cancer cells. The best-known role of telomerase is its ability to prevent the critical shortening of chromosomal ends (called “telomeres”), thus circumventing the molecular clock for cells to stop dividing (19). There are, however, multiple non-telomeric TERT functions that likely favor cancer fitness (20, 21). The elucidation of which of these cellular processes are unleashed in aggressive thyroid tumors is a topic of great interest for research, and has the potential to unveil novel nodes for genotype-driven and mechanism-oriented therapeutic intervention for thyroid cancer patients harboring TPMs.

References:
1. Fagin JA, and Wells SA, Jr. Biologic and Clinical Perspectives on Thyroid Cancer. N Engl J Med. 2016;375(23):2307.
2. Nikiforov YE, and Nikiforova MN. Molecular genetics and diagnosis of thyroid cancer. Nat Rev Endocrinol. 2011;7(10):569-80.
3. Smallridge RC, and Copland JA. Anaplastic thyroid carcinoma: pathogenesis and emerging therapies. Clin Oncol (R Coll Radiol). 2010;22(6):486-97.
4. Huang FW, Hodis E, Xu MJ, Kryukov GV, Chin L, and Garraway LA. Highly recurrent TERT promoter mutations in human melanoma. Science. 2013;339(6122):957-9.
5. Horn S, Figl A, Rachakonda PS, Fischer C, Sucker A, Gast A, et al. TERT promoter mutations in familial and sporadic melanoma. Science. 2013;339(6122):959-61.
6. Killela PJ, Reitman ZJ, Jiao Y, Bettegowda C, Agrawal N, Diaz LA, Jr., et al. TERT promoter mutations occur frequently in gliomas and a subset of tumors derived from cells with low rates of self-renewal. Proc Natl Acad Sci U S A. 2013;110(15):6021-6.
7. Landa I, Ganly I, Chan TA, Mitsutake N, Matsuse M, Ibrahimpasic T, et al. Frequent somatic TERT promoter mutations in thyroid cancer: higher prevalence in advanced forms of the disease. J Clin Endocrinol Metab. 2013;98(9):E1562-6.
8. Liu T, Wang N, Cao J, Sofiadis A, Dinets A, Zedenius J, et al. The age- and shorter telomere-dependent TERT promoter mutation in follicular thyroid cell-derived carcinomas. Oncogene. 2013.
9. Liu X, Bishop J, Shan Y, Pai S, Liu D, Murugan AK, et al. Highly prevalent TERT promoter mutations in aggressive thyroid cancers. Endocr Relat Cancer. 2013;20(4):603-10.
10. Vinagre J, Almeida A, Populo H, Batista R, Lyra J, Pinto V, et al. Frequency of TERT promoter mutations in human cancers. Nature communications. 2013;4:2185.
11. Cancer Genome Atlas Research N. Integrated genomic characterization of papillary thyroid carcinoma. Cell. 2014;159(3):676-90.
12. Landa I, Ibrahimpasic T, Boucai L, Sinha R, Knauf JA, Shah RH, et al. Genomic and transcriptomic hallmarks of poorly differentiated and anaplastic thyroid cancers. J Clin Invest. 2016;126(3):1052-66.
13. Pozdeyev N, Gay L, Sokol ES, Hartmaier RJ, Deaver KE, Davis SN, et al. Genetic analysis of 779 advanced differentiated and anaplastic thyroid cancers. Clin Cancer Res. 2018.
14. Melo M, Rocha AG, Vinagre J, Batista R, Peixoto J, Tavares C, et al. TERT promoter mutations are a major indicator of poor outcome in differentiated thyroid carcinomas. J Clin Endocrinol Metab. 2014:jc20133734.
15. Xing M, Liu R, Liu X, Murugan AK, Zhu G, Zeiger MA, et al. BRAF V600E and TERT promoter mutations cooperatively identify the most aggressive papillary thyroid cancer with highest recurrence. J Clin Oncol. 2014;32(25):2718-26.
16. Song YS, Lim JA, Choi H, Won JK, Moon JH, Cho SW, et al. Prognostic effects of TERT promoter mutations are enhanced by coexistence with BRAF or RAS mutations and strengthen the risk prediction by the ATA or TNM staging system in differentiated thyroid cancer patients. Cancer. 2016;122(9):1370-9.
17. Bible KC, Kebebew E, Brierley J, Brito JP, Cabanillas ME, Clark TJ, Jr., et al. 2021 American Thyroid Association Guidelines for Management of Patients with Anaplastic Thyroid Cancer. Thyroid. 2021;31(3):337-86.

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

For more information on Thyroid Topics please visit: https://www.thyroid.org/thyroid-information/

We invite you to submit any questions or comments regarding this blog post below, for potential response in a future blog or social media post.

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Carolyn Dacey Seib, MD, MAS
Stanford University School of Medicine
Stanford, CA
April 19, 2022

The parathyroids are small, oval-shaped glands that tightly regulate serum calcium levels through the production of parathyroid hormone (PTH), which stimulates the release of calcium from bone, increased GI absorption of calcium, and decreased renal excretion of calcium. Most commonly, each person has four parathyroid glands that are located in the neck, with two on each side, behind and just below each lobe of the thyroid gland.

Given their proximity to the thyroid and critical role in maintaining calcium homeostasis, it is important for surgeons to identify and protect the parathyroid glands during thyroid surgery. They can be as small as a grain of rice and encased in fat, making them difficult to identify. In addition, each parathyroid gland has a delicate blood supply and may be adherent to the capsule of the thyroid. Therefore, fine dissection is needed to preserve them in situ and with intact blood flow. If all parathyroid glands are injured, devascularized, or inadvertently removed during total or completion thyroidectomy, patients may experience temporary or permanent hypoparathyroidism, which is decreased production of PTH that results in hypocalcemia. Symptoms of hypocalcemia due to hypoparathyroidism include numbness and tingling in the fingers and around the mouth, muscle cramps or, when more severe, laryngospasm, seizures and dysrhythmias due to QT prolongation. The mainstay of treatment for hypoparathyroidism is supplementation with calcium and active vitamin D, which can be cumbersome for patients if large or frequent doses are required to prevent symptoms.

Permanent hypoparathyroidism is associated with impaired quality of life and long-term renal complications.(1,2) Although historically thought to be rare, recent studies suggest this complication may occur in up to 5% to 15% of patients following thyroidectomy.(3,4) As a result, there has been a renewed focus on techniques to identify and preserve parathyroid glands during operations in the neck. The most promising methods include near-infrared autofluorescence (NIRAF), which comes in probe-based and image-based systems, and parathyroid angiography using the fluorescent dye indocyanine green (ICG). NIRAF relies on the fact that parathyroids exhibit fluorescence, meaning when illuminated with light of a specific wavelength they reflect light back with a different wavelength. This allows the parathyroid glands to be differentiated from surrounding thyroid, fat, or lymph nodes and more easily identified.(5) In randomized clinical trials, NIRAF has been shown to improve the identification of parathyroid glands during thyroid surgery and decrease the rates of parathyroid autotransplantation, inadvertent parathyroid removal, and postoperative hypocalcemia.(6,7) However, autofluorescence is an intrinsic property of parathyroid tissue, detectable when the gland is in or out of the body, and does not predict viability. Parathyroid angiography with ICG can assess parathyroid gland perfusion at the conclusion of thyroidectomy to make decisions about parathyroid autotransplantation and guide postoperative calcium supplementation.(8,9) Given the documented short-term benefits of these tools are promising, additional studies are underway to determine long-term outcomes with their use. In addition to meticulous surgical technique, fluorescence imaging systems hold promise as adjunct tools to identify and preserve functional parathyroid glands during thyroid operations and reduce the risk of postoperative hypoparathyroidism.

References:
1. Büttner M, Musholt TJ, Singer S. Quality of life in patients with hypoparathyroidism receiving standard treatment: a systematic review. Endocrine. 2017;58(1):14-20.
2. Mitchell DM, Regan S, Cooley MR, et al. Long-Term Follow-Up of Patients with Hypoparathyroidism. The Journal of Clinical Endocrinology & Metabolism. 2012;97(12):4507-4514.
3. Maurer E, Maschuw K, Reuss A, et al. Total versus near-total thyroidectomy in Graves disease: results of the randomized controlled multicenter TONIG-trial. Annals of surgery. 2019;270(5):755-761.
4. Lončar I, Noltes ME, Dickhoff C, et al. Persistent Postthyroidectomy Hypoparathyroidism in the Netherlands. JAMA Otolaryngology–Head & Neck Surgery. 2021.
5. Solórzano CC, Thomas G, Berber E, et al. Current state of intraoperative use of near infrared fluorescence for parathyroid identification and preservation. Surgery. 2021;169(4):868-878.
6. Benmiloud F, Godiris-Petit G, Gras R, et al. Association of Autofluorescence-Based Detection of the Parathyroid Glands During Total Thyroidectomy With Postoperative Hypocalcemia Risk: Results of the PARAFLUO Multicenter Randomized Clinical Trial. JAMA Surgery. 2020;155(2):106-112.
7. Dip F, Falco J, Verna S, et al. Randomized Controlled Trial Comparing White Light with Near-Infrared Autofluorescence for Parathyroid Gland Identification During Total Thyroidectomy. Journal of the American College of Surgeons. 2019;228(5):744-751.
8. Vidal Fortuny J, Belfontali V, Sadowski S, Karenovics W, Guigard S, Triponez F. Parathyroid gland angiography with indocyanine green fluorescence to predict parathyroid function after thyroid surgery. Journal of British Surgery. 2016;103(5):537-543.
9. Vidal Fortuny J, Sadowski S, Belfontali V, et al. Randomized clinical trial of intraoperative parathyroid gland angiography with indocyanine green fluorescence predicting parathyroid function after thyroid surgery. Journal of British Surgery. 2018;105(4):350-357.

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

For more information on Thyroid Topics please visit: https://www.thyroid.org/thyroid-information/

We invite you to submit any questions or comments regarding this blog post below, for potential response in a future blog or social media post.

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Danica M. Vodopivec, MD
The University of Texas MD Anderson Cancer Center
Houston, TX
March 24, 2022

Medullary thyroid cancer (MTC) is a rare thyroid malignancy and considered a neuroendocrine type of tumor. It originates from the parafollicular or C-cells of the thyroid, which are neural crest derivatives and produce a variety of biogenic amines, including calcitonin and carcinoembryonic antigen (CEA) ─ used as tumor markers. MTC represents up to 4% of thyroid cancer cases, and accounts for about 14% of all thyroid cancer related deaths(1,2).

MTC can be sporadic (or acquired via somatic mutation) in 75% of the cases and hereditary (or familial via germline mutation) in the remaining 25%, with the latter comprising the polyglandular cancer syndrome known as multiple endocrine neoplasia 2 (MEN2) types A and B. The RET oncogene is the most common genetic alteration in MTC, being present in 100% of MEN2 syndromes and in about 45% of sporadic MTC. Mutually exclusive point mutations of RAS has been reported in sporadic MTC but with less frequency (approximately 15%), and the remainder cases of sporadic MTC do not have identifiable mutations(3).

Many patients are diagnosed incidentally in the absence of symptoms, although some may experience compressive symptoms, diarrhea, and/or flushing. MTC is initially diagnosed by US-guided fine-needle aspiration (FNA) biopsy of a thyroid nodule. There are no distinctive ultrasound features between MTC and a follicular-derived thyroid cancer; hence, cytology findings suggestive of MTC should be further assessed with immunohistochemistry. MTC stains positive for calcitonin, chromogranin, and CEA, and negative for thyroglobulin. The advent of molecular genetic testing for thyroid nodules has significantly improved diagnosis among indeterminate FNA samples(4–7). After a cytological diagnosis of MTC (prior to surgery), the serum calcitonin and CEA levels should be measured followed by a genetic testing for a RET germline mutation. All patients with MTC should undergo genetic testing because up to 7% of apparent sporadic MTC are indeed de-novo hereditary mutations, meaning not inherited from either parent. In addition, up to 75% of patients with MEN2B have a de-novo germline RET mutation. It is important that pediatricians, primary providers, and dentists be able to recognize the characteristic MEN2B body features ─ including a marfanoid body habitus, eye abnormalities (thickened and everted eyelids and inability to produce tears), mucosal neuromas in the eyelids and aerodigestive tract (visible in the lips, tongue, nostrils), and diffuse ganglioneuromas of the gastrointestinal tract leading to chronic constipation, abdominal pain, and possible intestinal obstruction(1).

Total thyroidectomy with cervical lymph node dissection is the standard treatment. Unfortunately, there is only a 10% cure rate when cervical lymph nodes are involved at the time of initial surgery(1). Post-operative levothyroxine should be administered to maintain euthyroidism, and radioactive iodine treatment is not indicated. For persistent locoregional and/or distant metastases, repeat surgery, external beam radiation, or other focal therapies can be implemented. When these therapies are no longer options due to progressive or symptomatic disease, systemic therapy should be considered. There are 4 FDA approved kinase inhibitors for MTC. The non-selective multi-kinase inhibitors, vandetanib and cabozantinib(8,9), were the first drugs approved for MTC. The selective RET-inhibitors, selpercatinib and pralsetinib, were approved in 2020 and may be used as first or subsequent lines of therapy for RET mutated MTC(10,11). New treatments with immunotherapy, tumor vaccines, peptide receptor radionuclide therapy (PRRT) are being studied in clinical trials for MTC.

References:
1. Wells SA, Asa SL, Dralle H, et al. Revised American Thyroid Association guidelines for the management of medullary thyroid carcinoma. Thyroid 2015; 25: 567–610.
2. Roman S, Lin R, Sosa JA. Prognosis of medullary thyroid carcinoma: demographic, clinical, and pathologic predictors of survival in 1252 cases. Cancer 2006; 107: 2134–2142.
3. COSMIC https://cancer.sanger.ac.uk/cosmic.
4. Wirth LJ, Waguespack SG, Busaidy NL, et al. Genomic landscape of FNAs positive for medullary thyroid cancer (MTC) and potential impact on systemic therapy. JCO 2019; 37: 6087–6087.
5. Hu MI, Waguespack SG, Dosiou C, et al. Afirma Genomic Sequencing Classifier and Xpression Atlas Molecular Findings in Consecutive Bethesda III-VI Thyroid Nodules. J Clin Endocrinol Metab 2021; 106: 2198–2207.
6. Ciarletto AM, Narick C, Malchoff CD, et al. Analytical and clinical validation of pairwise microRNA expression analysis to identify medullary thyroid cancer in thyroid fine-needle aspiration samples. Cancer Cytopathol 2021; 129: 239–249.
7. Nikiforov YE, Baloch ZW. Clinical validation of the ThyroSeq v3 genomic classifier in thyroid nodules with indeterminate FNA cytology. Cancer Cytopathology 2019; 127: 225–230.
8. Wells SA, Robinson BG, Gagel RF, et al. Vandetanib in Patients With Locally Advanced or Metastatic Medullary Thyroid Cancer: A Randomized, Double-Blind Phase III Trial. JCO 2012; 30: 134–141.
9. Elisei R, Schlumberger MJ, Müller SP, et al. Cabozantinib in Progressive Medullary Thyroid Cancer. JCO 2013; 31: 3639–3646.
10. Wirth LJ, Sherman E, Robinson B, et al. Efficacy of Selpercatinib in RET -Altered Thyroid Cancers. N Engl J Med 2020; 383: 825–835.
11. Subbiah V, Hu MI, Wirth LJ, et al. Pralsetinib for patients with advanced or metastatic RET-altered thyroid cancer (ARROW): a multi-cohort, open-label, registrational, phase 1/2 study. The Lancet Diabetes & Endocrinology; 0. Epub ahead of print 9 June 2021. DOI: 10.1016/S2213-8587(21)00120-0.

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

For more information on Thyroid Topics please visit: https://www.thyroid.org/thyroid-information/

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Catherine F. Sinclair, BSc (Biomed), MBBS (Hons), FRACS, FACS
Monash University, Malvern, Australia
Icahn School of Medicine at Mount Sinai, New York, NY
January 20, 2022

The rise of thyroid thermal ablative (TA) techniques in North America over the past 3 years has been rapid. These techniques have emerged as compelling alternatives to surgery for benign nodular disease. Multiple international studies have shown excellent long-term nodule volume reductions, minimal complications, rapid recovery, and efficacy in avoidance of thyroid hormone supplementation. Long-term follow-up data for North American populations is not yet available, however early results mirror those of international series. Future randomized trials comparing long-term outcomes of TA to surgery will better define the value of TA for thyroid nodule management.

Disease indications for TA are gradually evolving from benign nodules to include malignancy, regional metastatic disease, and hyperparathyroidism. The most promising of these new indications is papillary thyroid microcarcinoma (PTMC) where recent case series with 2-5 years follow-up have demonstrated low to non-existent rates of disease progression and metastases. If this data is validated in larger trials with longer follow-up durations, TA may well become the preferred treatment modality for select, localized PTMC although patient selection guidelines and indications for treatment will need to be carefully considered and characterized.

Apart from disease indications, some fundamental aspects of TA are still being refined.

• Is there an optimal patient age range for TA?
• Should TA be utilized prophylactically on smaller nodules that are not yet symptomatic in anticipation of future symptoms?
• What is the optimal energy to be delivered to ensure sustained nodule volume reduction?
• How much does nodule composition determine treatment response?
• What is the optimal follow-up protocol for ablated nodules and optimal timing for repeat ablation procedures?
• Should there be regulation of pre-requisite skills / training for physicians wishing to commence TA programs?

These are just some of the questions that will need to be addressed to ensure our patients are selected appropriately, are adequately counselled about risks and benefits, are assured of optimal procedural safety, and experience consistent treatment outcomes. Answering these questions will require multidisciplinary collaboration and forward planning and will ultimately define TA’s role in treatment algorithms for neck endocrine disease.

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

For more information on Thyroid Topics please visit: https://www.thyroid.org/thyroid-information/

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Sara Ahmadi, MD, ECNU
Brigham and Women’s Hospital
Boston, MA
November 19, 2021

Thyroid nodules and thyroid cancer are common clinical problems in adults. The yearly incidence of thyroid cancer in the United States has almost tripled from 4.9 per 100,000 in 1975 to 14.3 per 100,000 in 2009. It has been predicted that thyroid cancer will replace colorectal cancer as the fourth leading cancer diagnosis by 2030(1,2).

Surgery is the primary treatment for thyroid cancer. Most patients with differentiated thyroid cancer have an excellent outcome with a 98% long-term disease-specific survival.

Traditional therapy with total thyroidectomy and radioactive iodine(RAI) has not shown added benefit in patients with low-risk differentiated thyroid cancer and might result in more harm. Thyroid lobectomy, selective use of radioactive iodine, and active surveillance have gained attention in recent years. They have been recommended as potential management options for low-risk thyroid cancer and micropapillary thyroid cancer in the current American Thyroid Association guidelines(2). This has led to significant changes in clinical practice. A study of 35,291 patients using National Surgery Quality Improvement Program Data showed that there has been a 10-fold increase in the rate of thyroid lobectomy rather than total thyroidectomy after the publication of 2015 ATA guidelines(3).

However, many patients with differentiated thyroid cancer may overestimate the mortality implications, which may drive their willingness to undergo more aggressive treatment(4).

The Discrete Choice Survey Study of a cohort of 150 patients with newly diagnosed differentiated thyroid cancer or thyroid nodule requiring surgery showed that risk of thyroid cancer recurrence impacted patient’s preference around surgical treatment options the most, followed by risk of requiring completion thyroidectomy and recurrent laryngeal nerve injury. The risk of hypocalcemia and hypothyroidism had the least impact on patients’ preferences around treatment options. This study also showed that the average patient would prefer total thyroidectomy unless the risk of requiring completion thyroidectomy can be reduced to 30% or less(5).

Patients’ concern and worry can also limit their acceptability of less aggressive treatment options. A survey of 243 patients with papillary thyroid cancer enrolled in an active surveillance program showed cancer worry is common among these patients. However, the patient’s level of concern improves over time(6).

Patient-physician communication also plays an essential role in providing the patient with a good understanding of the risks and benefits of different treatment options and an informed decision-making process. Computerized patient decision aids in addition to usual care can be associated with a significant increase in patients’ medical knowledge around treatment options and a reduction in decisional conflict at the time of decision making(7). In a recent study, 1319 patients with thyroid cancer in whom selective use of radioactive iodine was recommended were surveyed to assess patient perspectives regarding RAI decision making. More than half of the patients perceived they did not have a choice regarding RAI. These patients were also more likely to receive RAI and to have lower decision satisfaction(8).

There has been a significant change in clinical practice since the publication of the 2015 ATA guidelines. It is of vital importance that we improve our understanding of patients’ preferences, ensure excellent patient-physician communication, and use educational decision aids in conjunction with physician counseling to facilitate shared-decision making.

References:
1. Rahib L, Smith BD, Aizenberg R, Rosenzweig AB, Fleshman JM, Matrisian LM. Projecting cancer incidence and deaths to 2030: the unexpected burden of thyroid, liver, and pancreas cancers in the United States. Cancer research. 2014;74(11):2913-2921.
2. Haugen BR, Alexander EK, Bible KC, et al. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer: The American Thyroid Association Guidelines Task Force on Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid : official journal of the American Thyroid Association. 2016;26(1):1-133.
3. Ullmann TM, Gray KD, Stefanova D, et al. The 2015 American Thyroid Association guidelines are associated with an increasing rate of hemithyroidectomy for thyroid cancer. Surgery. 2019.
4. Dixon PR, Tomlinson G, Pasternak JD, et al. The Role of Disease Label in Patient Perceptions and Treatment Decisions in the Setting of Low-Risk Malignant Neoplasms. JAMA Oncol. 2019.
5. Ahmadi S, Gonzalez JM, Talbott M, et al. Patient Preferences Around Extent of Surgery in Low-Risk Thyroid Cancer: A Discrete Choice Experiment. Thyroid : official journal of the American Thyroid Association. 2020;30(7):1044-1052.
6. Davies L, Roman BR, Fukushima M, Ito Y, Miyauchi A. Patient Experience of Thyroid Cancer Active Surveillance in Japan. JAMA Otolaryngol Head Neck Surg. 2019;145(4):363-370.
7. Sawka AM, Straus S, Rodin G, et al. Thyroid cancer patient perceptions of radioactive iodine treatment choice: Follow-up from a decision-aid randomized trial. Cancer. 2015;121(20):3717-3726.
8. Wallner LP, Reyes-Gastelum D, Hamilton AS, Ward KC, Hawley ST, Haymart MR. Patient-Perceived Lack of Choice in Receipt of Radioactive Iodine for Treatment of Differentiated Thyroid Cancer. J Clin Oncol. 2019;37(24):2152-2161.

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

For more information on Thyroid Topics please visit: https://www.thyroid.org/thyroid-information/

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Ulla Feldt-Rasmussen, MD, DMSc
University of Copenhagen
Copenhagen, Denmark

October 18, 2021

Endocrine disruptors are chemical pollutants in the environment that can affect the action of endocrine glands, including the thyroid gland. Some are suspected to influence thyroid function negatively, while a direct causative relationship may not have been scientifically verified. This is especially the case with triclosan, a polychloro phenoxy phenol with hormonal disrupting properties and widespread use in toothpaste and cosmetic and household products.

To appreciate that an influence from triclosan can be detrimental to human health, it is important to understand the significance of intact thyroid function, and how triclosan may impair it. The thyroid gland produces primarily thyroxine (T4), which is paramount for metabolism in every single cell and organ by conversion to the metabolically active triiodothyronine (T3). T4 is thus essential for maintenance of optimal organ function, including the brain, heart, bones, and muscles, and it is vital to fetal neurological and cognitive development.

Triclosan is structurally similar to T4, and it is therefore possible that it can interfere with the function of T4 at one or more sites of the thyroid function pathways. Triclosan may potentially result in hypothyroidism in the person who has been directly exposed to it, but it can also potentially indirectly compromise neurodevelopment through placental transfer to the fetus.

So, why is triclosan problematic for human health? Triclosan is a broad spectrum antimicrobial used as an antiseptic, disinfectant or preservative in clinical settings and various consumer products including cosmetics, household cleaning products, plastic materials, toys, paints, etc. It was detected in the urine of 97% of young Danish men in 2013, with a decreasing tendency over 8 years, consistent with Denmark’s restriction of the use of triclosan before the official recommendations. Results from The National Health and Nutrition Examination Survey (NHANES) of a nationally annual representative sample of about 5,000 persons from different places within the USA also demonstrated declined concentrations of triclosan, but the NHANESIII 2019 study measured concentrations three to ten times higher in young Americans compared to young Danes.

Both the FDA and the EU introduced regulations with triclosan limits up to 0.3% due to suspicion of skin reactions, cancer development and hormonal disruption in both humans and animals, but it is unknown if these regulations suffice as thyroid protection. It is also unknown if people living in relative iodine deficient areas and people, mainly women, with a low thyroid reserve such as thyroid autoimmunity are more prone to the negative influence on thyroid function.

It is largely unknown if the rest of the world complies with the levels in FDA and EU regulations, but in China and Vietnam for example, triclosan is measured at very high levels in household dust. This is possibly due to slow leakage from its incorporation onto surfaces of medical devices, plastic materials, textiles, kitchen utensils, etc., intended for a long period of biocidal effect in these household products.

The global threat from triclosan as a thyroid disrupter is therefore not solved. As a traveler or online shopper importing potentially affected products, it is therefore important to bear this in mind. It remains necessary to explore the effects of triclosan in human thyroid health in more detail by both clinical and basic research.

References:
1. https://www.thyroid.org/patient-thyroid-information/ct-for-patients/march-2020/vol-13-issue-3-p-11-12/
2. https://ec.europa.eu/health/scientific_committees/opinions_layman/triclosan/en/l-3/2-uses-cosmetics-disinfectant.htm

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

For more information on Thyroid Topics please visit: https://www.thyroid.org/thyroid-information/

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Larry A. Fox, MD
Nemours Children’s Health
Jacksonville, Florida

September 22, 2021

Background
Pediatricians and other practitioners are regularly faced with ordering thyroid function tests (TFTs) in children for a variety of clinical reasons. Sometimes it is a child displaying symptoms suggesting hypothyroidism, development of a goiter, or a decline in growth velocity. It is also common for physicians to order TFTs because the patient is obese, and quite often these thyroid labs are abnormal. With the epidemic of childhood obesity, our clinic is seeing an increasing number of referrals for abnormal TFTs in the setting of obesity. It is important for pediatricians to understand how TFTs are affected by obesity, when thyroid function tests should be ordered, and when a referral is necessary.

The relationship between thyroid function tests and obesity
The effect obesity has on thyroid function has been well documented in adults and children. In most studies, TSH is proportional to BMI. TSH results may be within the assay reference range, but are often slightly above. Thus, it is quite common for obese children (and adults) to have elevated TSH (with slightly increased free or total T3 and normal free T4), suggesting compensated hypothyroidism. In fact, TSH levels are above the reference range in up to 25% of obese children, and several population studies suggest TSH reference ranges need to be adjusted for obesity. Changes in TSH are thought to be mediated by increased leptin causing an increased pituitary release of thyrotropin releasing hormone and a rise in TSH. These changes increase resting energy expenditure and thus are adaptive to the obesity. They do not cause the obesity as evidenced by a decline in TSH with weight loss, either with bariatric surgery (in adults) or lifestyle changes in children and adults.

When should thyroid functions tests be done in an obese child?
Under many clinical circumstances checking TFTs (TSH, free T4) in the setting of obesity is reasonable, such as poor growth, goiter, and/or more specific symptoms suggesting hypothyroidism (such as cold intolerance, generalized dry skin, fatigue or constipation). Simply being overweight or obese (BMI >85th or >95th percentile, respectively) are not symptoms of hypothyroidism and ordering TFTs would not be indicated. Obtaining TFTs in overweight or obese patients without clear indications could lead to unnecessary additional testing, treatment, or referrals. Because the TFT changes are adaptive and do not cause the obesity, treatment is thought not to be necessary.

What should one do if the TSH is abnormal?
If the TSH is elevated above the reference range in an obese individual, the practitioner must decide whether further testing, treatment and/or referral is needed. Because autoimmune disorders are more common in obese individuals, it is reasonable to obtain markers of autoimmune (Hashimoto) thyroiditis (i.e., thyroid peroxidase and thyroglobulin antibody titers). If antibody titers are elevated, referral to a thyroid specialist is reasonable. If the child has a goiter or a nodule is palpable, a thyroid ultrasound would also be informative. If the ultrasound reveals a nodule or cyst, the patient should be referred to a thyroid specialist.
Otherwise, mild elevations in TSH without a goiter do not need treatment and a referral would not be necessary. Instead, rechecking TSH and free T4 in 3-6 months to document the trend in TFTs indicated.

Conclusion
TFTs are commonly abnormal in obese patients, with serum TSH concentrations often above the reference range. These laboratory abnormalities are due to changes in leptin and reflect an adaptation to obesity. Most often the abnormal TFTs do not require treatment. In some circumstances, however, a referral to a thyroid specialist is warranted.

References:
1. Popovic V, Duntas LH. Leptin TRH and ghrelin: influence on energy homeostasis at rest and during exercise. Horm Metab Res. 2005;37:533-7.
2. Reinehr T. Obesity and thyroid function. Mol Cell Endocrinol. 2010;316:165-71.
3. Reinehr T. Thyroid function in the nutritionally obese child and adolescent. Curr Opin Pediatr. 2011;23:415-20.
4. Gertig AM, Niechcial E, Skowrońska B. Thyroid axis alterations in childhood obesity. Pediatr Endocrinol Diabetes Metab. 2012;18:116-9.
5. Valdés S, Maldonado-Araque C, Lago-Sampedro A, et al. Reference values for TSH may be inadequate to define hypothyroidism in persons with morbid obesity: Di@bet.es study. Obesity. 2017;25:788-793.
6. Song R-H, Wang B, Yao Q-M, et al. The impact of obesity on thyroid autoimmunity and dysfunction: a systematic review and meta-analysis. Front Immunol. 2019;10:2349.
7. Gyuricsko E. The “slightly” abnormal thyroid test: What is the pediatrician to do? Curr Probl Pediatr Adolesc Health Care. 2020;50:100770.
8. Oron T, Lazar L, Feldhamer I, et al. Pediatric reference values of TSH should be personalized according to BMI and ethnicity. Eur J Endocrinol. 2020;183:419-426.
9. Tsigalou C, Vallianou N, Dalamaga M. Autoantibody production in obesity: Is there evidence for a link between obesity and autoimmunity? Curr Obes Rep. 2020;9:245-254.
10. Gokosmanoglu F, Aksoy E, Onmez A, et al. Thyroid homeostasis after bariatric surgery in obese Cases. Obes Surg. 2020;30:274-278.
11. Mohareb OA, Saqaaby MA, Ekhzaimy A, et al. The relationship between thyroid function and body composition, leptin, adiponectin, and insulin sensitivity in morbidly obese euthyroid subjects compared to non-obese subjects. Clin Med Insights Endocrinol Diabetes. 2021;14:1179551420988523. eCollection 2021.
12. Aykota MR, Atabey M. Effect of sleeve gastrectomy on thyroid-stimulating hormone levels in morbidly obese patients with normal thyroid function. Eur Rev Med Pharmacol Sci. 2021;25:233-240.

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

For more information on Thyroid Topics please visit: https://www.thyroid.org/thyroid-information/

The post Thyroid Health Blog: Obesity and Thyroid Function Tests in Children appeared first on American Thyroid Association.

Kaniksha Desai, MD, FACE
Stanford University
Palo Alto, CA

August 24, 2021

Thyroid hormone replacement is a critical element in the overall management of patients with thyroid cancer. For a long period of time, aggressive TSH suppression with long-term high doses of thyroid hormone was advocated for all thyroid cancer patients to prevent cancer recurrence by reducing the stimulation of cancer cells. Recently, a growing body of evidence has suggested a limited benefit to aggressive TSH suppression in many patients. In addition, there appears to be significant risks of long-term TSH suppression to cardiovascular health, bone health, and mental health including the development of osteoporosis, atrial fibrillation, and mood disorders, which can significantly impact Quality of Life in thyroid cancer patients. Benefits of preventing cancer recurrence should be balanced with risks of excessive thyroid hormone replacement. Therefore, thyroid hormone replacement should be tailored to provide appropriate levels of TSH suppression based on a dynamic risk stratification in thyroid cancer patients.

Currently best practice for the management of thyroid cancer patients determines individualized thyroid hormone replacement therapy based on risk stratification of cancer recurrence following initial surgery and the patient’s response to subsequent treatment.

After initial surgery, patients are risk-stratified based upon their surgical pathology and extent of tumor metastasis. They are categorized into three groups for their risk of recurrence: low (<5%), intermediate (5-30%) and high (30-50+%). Thyroid hormone replacement is initiated with TSH goals based upon this risk stratification. Low risk patients that have had their cancer completely resected, including lobectomy patients, are given replacement doses to make them euthyroid with a TSH goal of 0.5 to 2.0 mu/L. Intermediate risk patients, often with lymph node involvement, have mild suppression of their TSH with thyroid hormone replacement dosed to a TSH goal of 0.1 to 0.5 mu/L. High risk patients including those who have extensive metastatic disease or incomplete resection are given higher doses of thyroid hormone with a TSH goal of <0.1 mu/L to prevent cancer recurrence.

At subsequent follow up visits, patients are evaluated for their response to overall cancer treatment and are categorized into four groups: 1) excellent response to treatment (no evidence of cancer recurrence), 2) biochemical incomplete response (elevations in thyroglobulin tumor marker levels), 3) structural incomplete response (local or metastatic disease present) or 4) indeterminate response (nonspecific imaging findings or slight elevations in tumor marker levels). Patients with high risk of recurrence, as well as those with structural incomplete response benefit the most from aggressive TSH suppression and are treated accordingly. In patients with excellent response to treatment with no evidence of disease, thyroid hormone treatment can be decreased, even in initially high-risk patients after 5 years. If a patient has a recurrence, then a higher dose of thyroid hormone treatment may be recommended in the future.

In summary, thyroid hormone replacement should be tailored to patients individually based on their initial risk for thyroid cancer recurrence as well as their response to treatment over time to avoid under treatment of high-risk patients and overtreatment of low risk patients. Risk of thyroid cancer growth and recurrence should be balanced with risk of long-term side effects of over-suppression.

References:
1. Haugen BR, Alexander EK, Bible KC, Doherty GM, Mandel SJ, Nikiforov YE, Pacini F, Randolph GW, Sawka AM, Schlumberger M, Schuff KG, Sherman SI, Sosa JA, Steward DL, Tuttle RM, Wartofsky L. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer: The American Thyroid Association Guidelines Task Force on Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid. 2016 Jan;26(1):1-133.
2. Tarasova VD, Tuttle RM. A Risk-adapted Approach to Follow-up in Differentiated Thyroid Cancer. Rambam Maimonides Med J. 2016 Jan 28;7(1):e0004. doi: 10.5041/RMMJ.10231. PMID: 26886955; PMCID: PMC4737510.
3. Tuttle RM, Alzahrani AS. Risk Stratification in Differentiated Thyroid Cancer: From Detection to Final Follow-up. J Clin Endocrinol Metab. 2019 Mar 15;104(9):4087–100.
4. Grani G, Ramundo V, Verrienti A, Sponziello M, Durante C. Thyroid hormone therapy in differentiated thyroid cancer. Endocrine. 2019 Oct;66(1):43-50.
5. Biondi B, Cooper DS. Thyroid Hormone Suppression Therapy. Endocrinol Metab Clin North Am. 2019 Mar;48(1):227-237.
6. Grani G, Zatelli MC, Alfò M, Montesano T, Torlontano M, Morelli S, Deandrea M, Antonelli A, Francese C, Ceresini G, Orlandi F, Maniglia CA, Bruno R, Monti S, Santaguida MG, Repaci A, Tallini G, Fugazzola L, Monzani F, Giubbini R, Rossetto R, Mian C, Crescenzi A, Tumino D, Pagano L, Pezzullo L, Lombardi CP, Arvat E, Petrone L, Castagna MG, Spiazzi G, Salvatore D, Meringolo D, Solaroli E, Monari F, Magri F, Triggiani V, Castello R, Piazza C, Rossi R, Ferraro Petrillo U, Filetti S, Durante C. Real-World Performance of the American Thyroid Association Risk Estimates in Predicting 1-Year Differentiated Thyroid Cancer Outcomes: A Prospective Multicenter Study of 2000 Patients. Thyroid. 2021 Feb;31(2):264-271.

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

For more information on Thyroid Topics please visit: https://www.thyroid.org/thyroid-information/

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