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Thyroid EndNote LibraryEnM EndNote Library
Review Articles
Thyroid
Update from the 2022 World Health Organization Classification of Thyroid Tumors: A Standardized Diagnostic Approach
Chan Kwon Jung, Andrey Bychkov, Kennichi Kakudo
Endocrinol Metab. 2022;37(5):703-718.   Published online October 4, 2022
DOI: https://doi.org/10.3803/EnM.2022.1553
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  • 114 Web of Science
  • 131 Crossref
AbstractAbstract PDFPubReader   ePub   
The fifth edition of the World Health Organization (WHO) histologic classification of thyroid neoplasms released in 2022 includes newly recognized tumor types, subtypes, and a grading system. Follicular cell-derived neoplasms are categorized into three families (classes): benign tumors, low-risk neoplasms, and malignant neoplasms. The terms “follicular nodular disease” and “differentiated high-grade thyroid carcinoma” are introduced to account for multifocal hyperplastic/neoplastic lesions and differentiated thyroid carcinomas with high-grade features, respectively. The term “Hürthle cells” is replaced with “oncocytic cells.” Invasive encapsulated follicular and cribriform morular variants of papillary thyroid carcinoma (PTC) are now redefined as distinct tumor types, given their different genetic alterations and clinicopathologic characteristics from other PTC subtypes. The term “variant” to describe a subclass of tumor has been replaced with the term “subtype.” Instead, the term “variant” is reserved to describe genetic alterations. A histologic grading system based on the mitotic count, necrosis, and/or the Ki67 index is used to identify high-grade follicular-cell derived carcinomas and medullary thyroid carcinomas. The 2022 WHO classification introduces the following new categories: “salivary gland-type carcinomas of the thyroid” and “thyroid tumors of uncertain histogenesis.” This review summarizes the major changes in the 2022 WHO classification and their clinical relevance.

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Close layer
Thyroid
Clinical Relevance of Environmental Factors in the Pathogenesis of Autoimmune Thyroid Disease
Wilmar M. Wiersinga
Endocrinol Metab. 2016;31(2):213-222.   Published online May 13, 2016
DOI: https://doi.org/10.3803/EnM.2016.31.2.213
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AbstractAbstract PDFPubReader   

Genetic factors contribute for about 70% to 80% and environmental factors for about 20% to 30% to the pathogenesis of autoimmune thyroid disease (AITD). Relatives of AITD patients carry a risk to contract AITD themselves. The 5-year risk can be quantified by the so-called Thyroid Events Amsterdam-score, based on serum thyroid-stimulating hormone, thyroid peroxidase (TPO)-antibodies and family history. Subjects at risk may ask what they can do to prevent development of AITD. This review summarizes what is known about modulation of exposure to environmental factors in terms of AITD prevention. To stop smoking decreases the risk on Graves disease but increases the risk on Hashimoto disease. Moderate alcohol intake provides some protection against both Graves and Hashimoto disease. Low selenium intake is associated with a higher prevalence of thyroid autoimmunity, but evidence that selenium supplementation may lower TPO antibodies and prevent subclinical hypothyroidism remains inconclusive. Low serum vitamin D levels are associated with a higher prevalence of TPO antibodies, but intervention studies with extra vitamin D have not been done yet. Stress may provoke Graves hyperthyroidism but not Hashimoto thyroiditis. Estrogen use have been linked to a lower prevalence of Graves disease. The postpartum period is associated with an increased risk of AITD. Taking together, preventive interventions to diminish the risk of AITD are few, not always feasible, and probably of limited efficacy.

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Thyroid
The Revised 2016 Korean Thyroid Association Guidelines for Thyroid Nodules and Cancers: Differences from the 2015 American Thyroid Association Guidelines
Ka Hee Yi
Endocrinol Metab. 2016;31(3):373-378.   Published online September 26, 2016
DOI: https://doi.org/10.3803/EnM.2016.31.3.373
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AbstractAbstract PDFPubReader   

Increased detection of thyroid nodules using high-resolution ultrasonography has resulted in a world-wide increase in the incidence of differentiated thyroid cancer (DTC). Despite the steep increase in its incidence, the age-standardized mortality rate of thyroid cancer has remained stable, which leads toward a trend of more conservative treatment. The latest American Thyroid Association (ATA) guidelines for thyroid nodules and thyroid cancer revised in 2015 suggested that fine needle aspiration biopsy should be performed for thyroid nodules larger than 1 cm and lobectomy might be sufficient for 1 to 4 cm intrathyroidal DTC. In addition, active surveillance instead of immediate surgical treatment was also recommended as a treatment option for papillary thyroid microcarcinoma based on the results of a few observational studies from Japan. The Korean Thyroid Association (KTA) has organized a task force team to develop revised guidelines for thyroid nodules and DTC after an extensive review of articles and intense discussion on whether we should accept the changes in the 2015 ATA guidelines. This paper introduces and discusses the updated major issues and differences in the ATA and the KTA guidelines.

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Thyroid
Radioactive Iodine-Refractory Differentiated Thyroid Cancer and Redifferentiation Therapy
Jierui Liu, Yanqing Liu, Yansong Lin, Jun Liang
Endocrinol Metab. 2019;34(3):215-225.   Published online September 26, 2019
DOI: https://doi.org/10.3803/EnM.2019.34.3.215
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AbstractAbstract PDFPubReader   ePub   

The retained functionality of the sodium iodide symporter (NIS) expressed in differentiated thyroid cancer (DTC) cells allows the further utilization of post-surgical radioactive iodine (RAI) therapy, which is an effective treatment for reducing the risk of recurrence, and even the mortality, of DTC. Whereas, the dedifferentiation of DTC could influence the expression of functional NIS, thereby reducing the efficacy of RAI therapy in advanced DTC. Genetic alternations (such as BRAF and the rearranged during transfection [RET]/papillary thyroid cancer [PTC] rearrangement) have been widely reported to be prominently responsible for the onset, progression, and dedifferentiation of PTC, mainly through activating the mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K) signaling cascades. These genetic alternations have been suggested to associate with the reduced expression of iodide-handling genes in thyroid cancer, especially the NIS gene, disabling iodine uptake and causing resistance to RAI therapy. Recently, novel and promising approaches aiming at various targets have been attempted to restore the expression of these iodine-metabolizing genes and enhance iodine uptake through in vitro studies and studies of RAI-refractory (RAIR)-DTC patients. In this review, we discuss the regulation of NIS, known mechanisms of dedifferentiation including the MAPK and PI3K pathways, and the current status of redifferentiation therapy for RAIR-DTC patients.

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Close layer
Thyroid
Effects of Increased Iodine Intake on Thyroid Disorders
Xin Sun, Zhongyan Shan, Weiping Teng
Endocrinol Metab. 2014;29(3):240-247.   Published online September 25, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.3.240
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AbstractAbstract PDFPubReader   

Iodine is a micronutrient essential for the production of thyroid hormones. Iodine deficiency is the most common cause of preventable mental impairment worldwide. Universal salt iodization (USI) has been introduced in many countries as a cost-effective and sustainable way to eliminate iodine deficiency disorders for more than 25 years. Currently, the relationship between USI and iodine excess has attracted more attention. Iodine excess can lead to hypothyroidism and autoimmune thyroiditis, especially for susceptible populations with recurring thyroid disease, the elderly, fetuses, and neonates. Nationwide USI was introduced in China in 1996. This review focused on the effects of iodine excess worldwide and particularly in China.

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Close layer
Thyroid
Bisphenols and Thyroid Hormone
Min Joo Kim, Young Joo Park
Endocrinol Metab. 2019;34(4):340-348.   Published online December 23, 2019
DOI: https://doi.org/10.3803/EnM.2019.34.4.340
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AbstractAbstract PDFPubReader   ePub   

In recent decades, attention has been directed toward the effects of bisphenol A (BPA) on human health. BPA has estrogenic activity and is regarded as a representative endocrine disruptor. In addition, mounting evidence indicates that BPA can disrupt thyroid hormone and its action. This review examined human epidemiological studies to investigate the association between BPA exposure and thyroid hormone levels, and analyzed in vivo and in vitro experiments to identify the causal relationship and its mechanism of action. BPA is involved in thyroid hormone action not only as a thyroid hormone receptor antagonist, but also through several other mechanisms. Since the use of bisphenols other than BPA has recently increased, we also reviewed the effects of other bisphenols on thyroid hormone action.

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Close layer
Thyroid
Deiodinases and the Three Types of Thyroid Hormone Deiodination Reactions
Laura Sabatino, Cristina Vassalle, Cristina Del Seppia, Giorgio Iervasi
Endocrinol Metab. 2021;36(5):952-964.   Published online October 21, 2021
DOI: https://doi.org/10.3803/EnM.2021.1198
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AbstractAbstract PDFPubReader   ePub   
Thyroid hormone (TH) signaling is strictly regulated by iodothyronine deiodinase activity, which both preserves the circulating levels of the biologically active triiodothyronine (T3) and regulates TH homeostasis at the local level, in a cell- and time-dependent manner. Three deiodinases have been identified—namely iodothyronine deiodinase 1 (DIO1), DIO2, and DIO3—that differ in their catalytic properties and tissue distribution. The deiodinases represent a dynamic system that changes in the different stages of life according to their functions and roles in various cell types and tissues. Deiodinase activity at the tissue level permits cell-targeted fine regulation of TH homeostasis, mediating the activation (DIO1 and DIO2) and inactivation (DIO3) of THs. Deiodinase homeostasis is the driving force that leads T3-target cells towards customized TH signaling, which takes into account both the hormonal circulating levels and the tissue-specific response. This review analyzes the complex role of deiodinases in physiological and pathological contexts, exploring new challenges and opportunities deriving from a deeper knowledge of the dynamics underlying their roles and functions.

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Close layer
Thyroid
Prevalence and Risk Factors of Subclinical Thyroid Disease
Ye An Kim, Young Joo Park
Endocrinol Metab. 2014;29(1):20-29.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.20
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AbstractAbstract PDFPubReader   

Subclinical thyroid disease is defined biochemically by an abnormal thyrotropin (TSH) level and normal serum-free thyroxine level. The prevalence of this condition varies according to the reference range for TSH and geographic or demographic factors. Recently, several studies, including our community-based cohort studies, have reported on the incidence of subclinical thyroid disease in Korea. Using these studies, we reviewed the prevalence and risk factors of subclinical thyroid disease, focusing on subclinical hypothyroidism.

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Close layer
Thyroid
Long-Term Outcomes Following Thermal Ablation of Benign Thyroid Nodules as an Alternative to Surgery: The Importance of Controlling Regrowth
Jung Suk Sim, Jung Hwan Baek
Endocrinol Metab. 2019;34(2):117-123.   Published online June 24, 2019
DOI: https://doi.org/10.3803/EnM.2019.34.2.117
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AbstractAbstract PDFPubReader   ePub   

Thermal ablation (TA) procedures, such as radiofrequency ablation and laser ablation, are used for the treatment of benign thyroid nodules. Short-term studies (<2 years) have demonstrated that TA is an effective and safe procedure to improve cosmetic or symptomatic problems. However, studies including a longer follow-up period show that treated thyroid nodules can increase in size after 2 to 3 years. Several studies suggest that this results from regrowth at the undertreated nodule margins. Here, we review current data on regrowth after TA and describe factors related to it and possible approaches to prevent it.

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Original Article
Thyroid
Associations between Hashimoto Thyroiditis and Clinical Outcomes of Papillary Thyroid Cancer: A Meta-Analysis of Observational Studies
Shinje Moon, Hye Soo Chung, Jae Myung Yu, Hyung Joon Yoo, Jung Hwan Park, Dong Sun Kim, Young Joo Park
Endocrinol Metab. 2018;33(4):473-484.   Published online November 30, 2018
DOI: https://doi.org/10.3803/EnM.2018.33.4.473
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AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background

Epidemiological studies have suggested an association between Hashimoto thyroiditis (HT) and papillary thyroid cancer (PTC) development. Other studies, however, have reported a protective role of HT against PTC progression. Through this updated meta-analysis, we aimed to clarify the effects of HT on the progression of PTC.

Methods

We searched citation databases, including PubMed and Embase, for relevant studies from inception to September 2017. From these studies, we calculated the pooled odds ratios (ORs) of clinicopathologic features and the relative risk (RR) of PTC recurrence with 95% confidence intervals (CIs) using the Mantel-Haenszel method. Additionally, the Higgins I2 statistic was used to test for heterogeneity.

Results

The meta-analysis included 71 published studies with 44,034 participants, among whom 11,132 had HT. We observed negative associations between PTC with comorbid HT and extrathyroidal extension (OR, 0.74; 95% CI, 0.68 to 0.81), lymph node metastasis (OR, 0.82; 95% CI, 0.72 to 0.94), distant metastasis (OR, 0.49; 95% CI, 0.32 to 0.76), and recurrence (RR, 0.50; 95% CI, 0.41 to 0.61).

Conclusion

In this meta-analysis, PTC patients with HT appeared to exhibit more favorable clinicopathologic characteristics and a better prognosis than those without HT.

Citations

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Review Articles
Thyroid
Genome-Wide Association Studies of Autoimmune Thyroid Diseases, Thyroid Function, and Thyroid Cancer
Yul Hwangbo, Young Joo Park
Endocrinol Metab. 2018;33(2):175-184.   Published online June 21, 2018
DOI: https://doi.org/10.3803/EnM.2018.33.2.175
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AbstractAbstract PDFPubReader   ePub   

Thyroid diseases, including autoimmune thyroid diseases and thyroid cancer, are known to have high heritability. Family and twin studies have indicated that genetics plays a major role in the development of thyroid diseases. Thyroid function, represented by thyroid stimulating hormone (TSH) and free thyroxine (T4), is also known to be partly genetically determined. Before the era of genome-wide association studies (GWAS), the ability to identify genes responsible for susceptibility to thyroid disease was limited. Over the past decade, GWAS have been used to identify genes involved in many complex diseases, including various phenotypes of the thyroid gland. In GWAS of autoimmune thyroid diseases, many susceptibility loci associated with autoimmunity (human leukocyte antigen [HLA], protein tyrosine phosphatase, non-receptor type 22 [PTPN22], cytotoxic T-lymphocyte associated protein 4 [CTLA4], and interleukin 2 receptor subunit alpha [IL2RA]) or thyroid-specific genes (thyroid stimulating hormone receptor [TSHR] and forkhead box E1 [FOXE1]) have been identified. Regarding thyroid function, many susceptibility loci for levels of TSH and free T4 have been identified through genome-wide analyses. In GWAS of differentiated thyroid cancer, associations at FOXE1, MAP3K12 binding inhibitory protein 1 (MBIP)-NK2 homeobox 1 (NKX2-1), disrupted in renal carcinoma 3 (DIRC3), neuregulin 1 (NRG1), and pecanex-like 2 (PCNXL2) have been commonly identified in people of European and Korean ancestry, and many other susceptibility loci have been found in specific populations. Through GWAS of various thyroid-related phenotypes, many susceptibility loci have been found, providing insights into the pathogenesis of thyroid diseases and disease co-clustering within families and individuals.

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Thyroid
Current Status and Future Perspectives in Differentiated Thyroid Cancer
Tae Yong Kim, Won Gu Kim, Won Bae Kim, Young Kee Shong
Endocrinol Metab. 2014;29(3):217-225.   Published online September 25, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.3.217
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AbstractAbstract PDFPubReader   

Thyroid cancer is increasing all over the world. The exact cause of this increase is still debated and there are conflicting reports. Sophisticated molecular studies suggest that environmental chemicals may have effects of thyroid carcinogenesis. The development of powerful molecular biology techniques has enabled targeted next-generation sequencing for detection of mutations in thyroid cancer, and this technique can make a specific diagnosis of thyroid cancer in cytologically indeterminate cases. The initial treatment of well-differentiated thyroid cancer (DTC) is surgery followed by radioiodine remnant ablation. However, further studies are needed to determine the optimal dosage of radioactive iodine for DTC patients with lateral neck metastasis. DTC is an indolent tumor and may cause death even decades later. Thus, long-term follow-up is mandatory. Recently, dynamic risk stratification (DRS) has begun to use stimulated thyroglobulin level at 1 year after the initial treatment and restratified the risk in accordance with the response to the initial treatment. This DRS strategy accurately predicts disease free survival and can be widely used in daily clinical settings. For the iodine refractory metastatic disease, redifferentiation therapy and targeted therapy are two promising alternative treatments. Sorafenib is the first approved agent for the treatment of progressive iodine refractory advanced thyroid cancer in Korea and may be very helpful for radioactive-refractory locally advanced or metastatic DTC. Selumetinib may be an effective redifferentiating agent and could be used within several years.

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Thyroid
The Diagnosis and Management of Hyperthyroidism in Korea: Consensus Report of the Korean Thyroid Association
Jae Hoon Moon, Ka Hee Yi
Endocrinol Metab. 2013;28(4):275-279.   Published online December 12, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.4.275
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AbstractAbstract PDFPubReader   

Hyperthyroidism is one of the causes of thyrotoxicosis and the most common cause of hyperthyroidism in Korea is Graves disease. The diagnosis and treatment of Graves disease are different according to geographical area. Recently, the American Thyroid Association and the American Association of Clinical Endocrinologists suggested new management guidelines for hyperthyroidism. However, these guidelines are different from clinical practice in Korea and are difficult to apply. Therefore, the Korean Thyroid Association (KTA) conducted a survey of KTA members regarding the diagnosis and treatment of hyperthyroidism, and reported the consensus on the management of hyperthyroidism. In this review, we summarized the KTA report on the contemporary practice patterns in the diagnosis and management of hyperthyroidism, and compared this report with guidelines from other countries.

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Close layer
Thyroid
Graves' Disease: Can It Be Cured?
Wilmar M. Wiersinga
Endocrinol Metab. 2019;34(1):29-38.   Published online March 21, 2019
DOI: https://doi.org/10.3803/EnM.2019.34.1.29
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AbstractAbstract PDFPubReader   ePub   

Whether or not Graves' hyperthyroidism can be really cured, depends on the definition of “cure.” If eradication of thyroid hormone excess suffices for the label “cure,” then all patients can be cured because total thyroidectomy or high doses of 131I will abolish hyperthyroidism albeit at the expense of creating another disease (hypothyroidism) requiring lifelong medication with levothyroxine. I would not call this a “cure,” which I would like to define as a state with stable thyroid stimulating hormone (TSH), free thyroxine, and triiodothyronine serum concentrations in the normal range in the absence of any thyroid medication. Surgery and radioiodine are unlikely to result in so-defined cures, as their preferable aim as stated in guidelines is to cause permanent hypothyroidism. Discontinuation of antithyroid drugs is followed by 50% recurrences within 4 years; before starting therapy the risk of recurrences can be estimated with the Graves' Recurrent Events After Therapy (GREAT) score. At 20-year follow-up about 62% had developed recurrent hyperthyroidism, 8% had subclinical hypothyroidism, and 3% overt hypothyroidism related to TSH receptor blocking antibodies and thyroid peroxidase antibodies. Only 27% was in remission, and might be considered cured. If the definition of “cure” would also include the disappearance of thyroid antibodies in serum, the proportion of cured patients would become even lower.

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Close layer
Thyroid
Current Guidelines for Management of Medullary Thyroid Carcinoma
Mijin Kim, Bo Hyun Kim
Endocrinol Metab. 2021;36(3):514-524.   Published online June 22, 2021
DOI: https://doi.org/10.3803/EnM.2021.1082
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AbstractAbstract PDFPubReader   ePub   
Medullary thyroid carcinoma (MTC) is a rare neuroendocrine tumor originating from the parafollicular cells. The diagnostic and therapeutic strategies for the condition are different from those used for well-differentiated thyroid cancer. Since the 2015 American Thyroid Association guidelines for the diagnosis and treatment of MTC, the latest, including the National Comprehensive Cancer Network and European Association for Medical Oncology guidelines have been updated to reflect several recent advances in the management of MTC. Advances in molecular diagnosis and postoperative risk stratification systems have led to individualized treatment and follow-up strategies. Multi-kinase inhibitors, such as vandetanib and cabozantinib, can prolong disease progression-free survival with favorable adverse effects. In addition, potent selective rearranged during transfection (RET) inhibitors (selpercatinib and pralsetinib) have shown a promising efficacy in recent clinical trials. This review summarizes the management of MTC in recent guidelines focused on sporadic MTC.

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  • Diagnostic capabilities of PET/CT with 18F-DOPA in biochemical recurrence of medullary thyroid carcinoma: a retrospective study
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    Diagnostic radiology and radiotherapy.2024; 15(1): 87.     CrossRef
  • LINC00887 Acts as an Enhancer RNA to Promote Medullary Thyroid Carcinoma Progression by Binding with FOXQ1
    Daxiang Liu, Wenjing Wang, Yanzhao Wu, Yongle Qiu, Lan Zhang
    Current Cancer Drug Targets.2024; 24(5): 519.     CrossRef
  • Spontaneous and Treatment-Related Changes of Serum Calcitonin in Medullary Thyroid Cancer: Long-Term Experience in a Patient With Multiple Endocrine Neoplasia Type 2B
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  • False-Negative 68Ga-FAPI PET/CT in Pediatric Thyroid Medullary Carcinoma Seen With 68Ga-DOTATOC PET/CT and 18F-FDG PET/CT
    Mohamad B. Haidar, Farah A. Abou Zeid, Zarouhie Z. Meguerian, Akram N. Al-Ibraheem, Peter E. Noun
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    Dušan Ilić, Sanja Ognjanović, Bojana Popović, Valentina Elezović-Kovačević, Milica Opalić-Palibrk, Lena Radić, Katarina Krstić, Đuro Macut
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    Endocrine.2024; 86(3): 1081.     CrossRef
  • Pancreas as an Unusual Metastatic Site of Medullary Thyroid Carcinoma: A Case of Very Long-term Follow-up Under Prolonged Treatment with Somatostatin Analogues
    Salvatore Raia, Sabrina Chiloiro, Antonella Giampietro, Maria Grazia Maratta, Fabia Attili, Maria Gabriella Brizi, Vittoria Rufini, Laura De Marinis, Alfredo Pontecorvi, Guido Rindi, Giovanni Schinzari, Antonio Bianchi
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    Thifhelimbilu Emmanuel Luvhengo, Maeyane Stephens Moeng, Nosisa Thabile Sishuba, Malose Makgoka, Lusanda Jonas, Tshilidzi Godfrey Mamathuntsha, Thandanani Mbambo, Shingirai Brenda Kagodora, Zodwa Dlamini
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  • DLK1 Is Associated with Stemness Phenotype in Medullary Thyroid Carcinoma Cell Lines
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  • Update on Management of Medullary Thyroid Carcinoma: Focus on Nuclear Medicine
    Giorgio Treglia, Vittoria Rufini, Arnoldo Piccardo, Alessio Imperiale
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  • Physical activity and reduced risk of fracture in thyroid cancer patients after thyroidectomy — a nationwide cohort study
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  • The Evolving Treatment Landscape of Medullary Thyroid Cancer
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  • Psychosocial Characteristics and Experiences in Patients with Multiple Endocrine Neoplasia Type 2 (MEN2) and Medullary Thyroid Carcinoma (MTC)
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  • Aggressive clinical course of medullary thyroid microcarcinoma
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  • Update on the Diagnosis and Management of Medullary Thyroid Cancer: What Has Changed in Recent Years?
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