Chia-Hung Lin Taiwan

• Preoperative Molecular Testing for Thyroid Nodules
  Guodong FuCanada Speaker Preoperative Molecular Testing for Thyroid NodulesTitle: Preoperative Quantitative Molecular Testing for a Definitive Cancer Diagnosis among Patients with Thyroid Nodules Objective: Molecular testing is increasingly used in the assessment of thyroid nodules. Tumors harboring the same genomic variant may not behave the same because a gene variant is not expressed equally in tumor cells among patients. This study is to delineate interpatient variabilities in genomic variants in thyroid tumors and assess their diagnostic significance in definitive thyroid cancer diagnosis. Methods: Interpatient differences in BRAF V600E, TERT promoter, and RAS variants (ie, NRAS, HRAS, and KRAS) were analyzed in residual thyroid fine-needle aspiration (FNA) biopsies and compared with surgical histopathologic diagnoses. Malignancy rates, sensitivity, specificity, positive predictive values (PPV), and negative predictive values (NPV) were calculated. Results: This retrospective study enrolled 620 patients (470 [75.8%] female; mean [SD] age, 50.7 [15.9] years), including 438 surgically resected thyroid tumors and 249 thyroid nodule FNA biopsies. Of 438 tumors, 178 (40.6%) and 58 (13.2%) carcinomas were detected with interpatient variabilities of BRAF V600E and TERT promoter variants (C228T and C250T), with variant allele fraction (VAF) levels ranging from 0.03% to 48.56% and 0.13% to 54.74%, respectively. Furthermore, 89 (20.3%) were identified with the presence of RAS variants, including 51 (11.6%) with NRAS, 29 (6.6%) with HRAS, and 9 (2.1%) with KRAS, with VAF levels ranging from 0.15% to 51.53%. VAF assays of 249 residual FNA specimens identified 50 specimens (20.1%) with BRAF V600E, 25 FNAs (10.0%) with TERT promoter variants, and 36 specimens (14.5%) with RAS variants with interpatient variabilities (including 23 FNAs [9.2%] with NRAS, 10 FNAs [4.0%] with HRAS, and 3 FNAs [1.2%] with KRAS). Interpatient differences in the 5 gene variants (NRAS, HRAS, KRAS, BRAF, and TERT) were detected in 54 of 126 indeterminate FNAs (42.9%) and 18 of 76 ND FNAs (23.7%). Compared with the 5 gene variants detected in the matched surgical specimens, VAF assays on residual FNA biopsies exhibited a high agreement (κ = 0.80; P < .001) and demonstrated a sensitivity of 87.1% (95% CI, 69.2%-95.8%), specificity of 92.5% (95% CI, 78.5%-98.0%), PPV of 90.0% (95% CI, 72.3%-97.4%), and NPV of 90.2% (95% CI, 75.9%-96.8%). Conclusions: This diagnostic study delineated that quantitative discrimination of interpatient variabilities in genomic variants could facilitate cytology examinations in preoperative precision malignancy diagnosis among patients with thyroid nodules.
• Harnessing Molecular Diagnostics in Cytologically-Indeterminate Thyroid Nodules
  Samantha Peiling YangSingapore Speaker Harnessing Molecular Diagnostics in Cytologically-Indeterminate Thyroid NodulesCytologically indeterminate thyroid nodules (Bethesda III–IV) remain a common diagnostic challenge, as cytology alone cannot reliably distinguish benign from malignant disease. Molecular diagnostic tests have emerged as important adjuncts to refine malignancy risk and guide clinical management. This presentation reviews the molecular landscape of thyroid cancer relevant to indeterminate nodules, including key somatic alterations such as BRAF, RAS, and gene fusions (e.g., RET, NTRK, ALK), and discusses the performance of contemporary molecular diagnostic tests. Data from North America and emerging real-world experience in Singapore will be highlighted. The clinical utility of molecular diagnostics in reducing unnecessary diagnostic surgery and informing the extent of surgical management will be discussed, together with current guidance from the ATA 2025 guidelines on integrating molecular results with clinical, radiologic, and cytopathologic findings. Re-Differentiation Therapy in RAI-Refractory Thyroid CancerRadioactive iodine (RAI) therapy remains a cornerstone in the management of differentiated thyroid cancer. However, a subset of patients develop RAI-refractory disease due to loss of iodine-handling gene expression, including the sodium–iodide symporter (NIS). This loss is frequently associated with activation of the MAPK signalling pathway driven by oncogenic alterations such as BRAF and RAS mutations. While systemic therapy with multi-targeted or mutation-specific tyrosine kinase inhibitors (TKIs) can control disease progression, these treatments are generally not curative and do not consistently restore RAI sensitivity. Re-differentiation therapy has emerged as a promising strategy to restore iodine uptake by targeting MAPK signalling and re-inducing thyroid-specific gene expression. This presentation will review the biological rationale for re-differentiation therapy and summarize key clinical studies evaluating BRAF and MEK inhibition in patients with RAI-refractory thyroid cancer. Emerging approaches, optimal treatment duration, and potential predictors of response will also be discussed, highlighting the potential of re-differentiation therapy to restore the therapeutic benefit of RAI in selected patients.
• Preoperative Diagnosis of Thyroid Cancer
  Kiyomi HoriuchiJapan Speaker Preoperative Diagnosis of Thyroid Cancer

• Novel Biomarkers and Treatment Strategies in Thyroid Eye Disease
  Chia-Hung LinTaiwan Speaker Novel Biomarkers and Treatment Strategies in Thyroid Eye DiseaseThyroid Eye Disease (TED), also known as Graves' orbitopathy, remains a complex autoimmune condition that significantly impacts patients' vision and quality of life. Traditionally, management has relied mainly on non-specific anti-inflammatory therapies. However, as our understanding of its molecular pathogenesis evolves, there is an increasing clinical demand for more precise diagnostic tools and targeted therapeutic interventions. This presentation provides a comprehensive overview of the current landscape and future directions in the management of TED. We will discuss the emergence of novel serum and molecular biomarkers that offer potential for earlier diagnosis and more accurate prediction of disease progression. These biomarkers may bridge the gap between clinical observation and underlying immunological activity. Furthermore, we will explore the shift in treatment paradigms, moving from conventional systemic corticosteroids toward innovative biological agents. By targeting specific signaling pathways involved in orbital inflammation and remodeling, these new strategies aim to provide more effective and durable clinical outcomes. The integration of novel biomarkers and advanced treatment modalities is reshaping the management of TED. Moving toward a more individualized approach will allow clinicians to optimize therapeutic timing and selection, ultimately improving the long-term prognosis for patients with this challenging condition.
• Management of Thyroid Eye Disease: Insights from Clinical Experience and MRI Findings in Japan
  Ichiro YamauchiJapan Speaker Management of Thyroid Eye Disease: Insights from Clinical Experience and MRI Findings in JapanIn Japan, disease activity of thyroid eye disease (TED) is commonly assessed using magnetic resonance imaging (MRI) in addition to clinical activity score (CAS). Recently, we proposed an MRI-guided categorization of active moderate-to-severe TED based on our retrospective data. We retrospectively analyzed TED cases treated at our department between 2015 and 2022 with a combination of daily steroid pulse therapy and orbital radiation. Among 44 cases with diplopia, we classified 17 cases as severe (diplopia in the primary position) and 27 as non-severe (diplopia only in non-primary positions). The severe group was older (median 67 years) and had lower TSAb titers (median 324%) compared to the non-severe group (median 56 years, median TSAb 2443%). CAS was similar between the groups. MRI revealed that proptosis was more pronounced in the non-severe group (median 21.4 mm) than in the severe group (median 17.5 mm), whereas the difference in proptosis between eyes was larger in the severe group (median 2.0 mm) than in the non-severe group (median 0.9 mm). High signal intensity of orbital fat on STIR sequence was more frequently observed in the non-severe group (68.2%) than in the severe group (20.0%). These findings suggest that TED patients with severe diplopia are characterized by older age, lower TSAb titers, and greater asymmetry in proptosis. In contrast, CAS and STIR signal intensity of orbital fat were not indicative of severity. In this context, severe diplopia often develops despite low CAS and mild proptosis. We also present our clinical experience with teprotumumab, an anti–IGF-1 receptor antibody. Since its launch in Japan in 2024, we have treated several patients with severe TED, the majority of whom showed remarkable improvement in clinical features. However, adverse effects such as hearing impairment and hyperglycemia were occasionally observed, highlighting the importance of appropriate management. In conclusion, MRI-guided evaluation provides valuable insights for individualized management of TED. Evidence regarding the efficacy of teprotumumab remains limited in the subtype characterized by severe diplopia, which often presents with low CAS and mild proptosis. The MRI-guided approach may help clinicians select optimal therapeutic strategies, including steroid pulse therapy, teprotumumab, and other emerging agents.
• Update on Thyroid Eye Disease Management - Asia Pacific Perspectives
  Kelvin ChongHong Kong, China Speaker Update on Thyroid Eye Disease Management - Asia Pacific PerspectivesExisting guidelines/recommendations/consensus on the management of thyroid eye disease (TED)/Graves' orbitopathy (GO) pose significant difficulties when applied in the Asia Pacific region. The presenter will share his experiences and challenges in setting up the first thyroid eye clinic in Hong Kong, developing an image-guided medical and surgical decompression, while looking into the future of intelligence-based management of TED/GO.

• Clinical Pathways for Obesity Management
  I-Weng YenTaiwan Speaker Clinical Pathways for Obesity ManagementObesity is a chronic disease driven by excess adiposity and associated complications, and relying on BMI alone is often insufficient, especially in Asian populations. In this presentation, I will introduce a structured clinical pathway for obesity management, based on a four-step approach including screening, adiposity verification, etiologic assessment, and complication-based staging. This framework emphasizes a shift from weight-centered care to a complication-driven, patient-centered model, with stage-based treatment strategies and shared decision-making, aiming to improve clinical outcomes and support upstream prevention of metabolic diseases such as diabetes.
• Anti-Obesity Medications: Clinical Use
  Kang-Chih FanTaiwan Speaker AI-Driven Precision Drug Therapy: Tailoring Personalized Treatment for Type 2 Diabetes Type 2 diabetes (T2D) is a highly heterogeneous syndrome where "one-size-fits-all" algorithms often fail to address individual pathophysiological variations. While recent guidelines prioritize cardiorenal protection, the choice between second-line agents—particularly SGLT2 inhibitors versus GLP-1 receptor agonists—remains largely empirical. This "trial-and-error" paradigm frequently results in therapeutic inertia and suboptimal glycemic durability. Artificial Intelligence (AI) and machine learning (ML) offer a paradigm shift from population-based guidelines to precision diabetology. By integrating high-dimensional data from electronic health records (EHR), continuous glucose monitoring (CGM), and routinely available clinical features, AI models can now quantify heterogeneous treatment effects (HTE) at the individual level. In this presentation, I will discuss: 1. Phenotypic Stratification: Moving beyond classic classification to identify data-driven clusters (e.g., severe insulin-resistant vs. age-related clusters) that dictate distinct disease trajectories. 2. Predictive Pharmacotherapy: Reviewing recent evidence where ML algorithms predict individual glycemic response, cardiorenal outcomes, and weight loss outcomes for specific drug classes. We will highlight how AI-driven decision support can optimize the selection between SGLT2 inhibitors and GLP-1 receptor agonists, maximizing efficacy while minimizing adverse events. 3. Real-World Implementation: Discussing the potential of leveraging large-scale longitudinal datasets, such as Taiwan’s National Health Insurance Research Database (NHIRD), to build robust, population-specific prediction models and facilitate the clinical adoption of explainable AI (XAI). Bridging the gap between data science and clinical practice, this session aims to demonstrate how AI can empower clinicians to prescribe the right drug for the right patient at the right time, fundamentally transforming T2D management.Anti-Obesity Medications: Clinical Use Obesity is a chronic, relapsing neurobehavioral disease requiring long-term management. Recent guidelines have shifted the treatment goal from BMI-centric weight loss to a "health-centered" approach, focusing on the remission of weight-related complications. With the advent of nutrient-stimulated hormone-based therapies, we have entered an era where pharmacotherapy can achieve double-digit weight loss comparable to bariatric surgery, offering systemic organ protection. In this session, we will navigate the clinical use of anti-obesity medications (AOMs) through three key dimensions based on the latest evidence: 1. Efficacy and Organ Protection: We will review the landmark trials establishing GLP-1 and dual GIP/GLP-1 receptor agonists as the cornerstone of treatment. Highlights include Semaglutide (STEP, SELECT, ESSENCE) and Tirzepatide (SURMOUNT, SUMMIT, SURMOUNT-OSA), demonstrating not only 15–20% weight loss but also breakthrough benefits in cardiovascular outcomes (MACE), heart failure with preserved ejection fraction (HFpEF), metabolic dysfunction-associated steatohepatitis (MASH), and obstructive sleep apnea (OSA). 2. Comorbidity-Directed Strategy: A practical framework for drug selection will be proposed, distinguishing between "Fat Mass Disease" (e.g., OSA, osteoarthritis), which benefits primarily from mechanical weight reduction, and "Sick Fat Disease" (e.g., T2D, CVD, MASH), which requires correction of adipose dysfunction. We will discuss how to prioritize agents like Semaglutide and Tirzepatide for high-risk profiles, while utilizing Naltrexone/Bupropion for emotional eating or Orlistat for patients requiring non-systemic options. 3. Asian Perspectives & Practical Management: We will present data confirming that Asian populations, who are highly sensitive to metabolic risks, achieve weight loss efficacy comparable to Western populations with Semaglutide and Tirzepatide (STEP-7, SURMOUNT-CN/J). Finally, we will address practical strategies for dose titration to mitigate GI adverse events and emphasize the necessity of chronic treatment to prevent weight regain. This presentation aims to equip clinicians with a precision medicine approach, ensuring the right AOM is prescribed to maximize both weight reduction and holistic health outcomes.
• Obesity Care in Special Populations
  Chun-Heng KuoTaiwan Speaker Obesity Care in Special PopulationsThis presentation, delivered by Chun-Heng Kuo, MD, MMSc, PhD, provides a comprehensive framework for obesity management across two distinct clinical cohorts: women of reproductive age and elderly populations. For women of reproductive age, the presentation defines a "Reproductive Continuum of Care" spanning fertility, preconception, pregnancy, and postpartum. It details obesity-related risks, including a 4% decline in conception rates per BMI unit, gestational diabetes (GDM), and intergenerational metabolic transmission. A critical clinical focus is the "Glucagon-like peptide-1 (GLP-1) receptor agonist Paradox," which weighs the metabolic benefits of preconception use against the risk of rapid weight rebound following discontinuation. Additionally, it advocates for localized Taiwan 2024 gestational weight gain (GWG) guidelines, which set tighter weight gain constraints than the Institute of Medicine (IOM) standards. In elderly populations, the focus shifts to the dangers of sarcopenic obesity and the "Obesity Paradox". Management transitions from pure weight loss to a "muscle-centric" strategy prioritizing a protein intake of 1.2–1.5 g/kg and resistance training to overcome anabolic resistance. The deck evaluates the Incretin Revolution and introduces the future of care: Activin Receptor Blockers (e.g., Bimagrumab), which promote muscle hypertrophy while reducing adiposity. Ultimately, geriatric care is defined by the preservation of physical function and quality of life.

• Long-Term Changes of Urinary Exosomal Peptide Levels after Thyroidectomy in Patients with Thyroid Cancer: A Prospective Observational Study
  Chih-Yuan WangTaiwan Speaker Obesity 2026 updateObesity remains one of the most critical and rapidly evolving global health challenges entering 2026, characterized by persistently rising prevalence, expanding clinical consequences, and profound societal and economic impacts. Over the past three decades, the prevalence of overweight and obesity has more than doubled among adults and increased nearly threefold among children and adolescents worldwide, driven by complex interactions between genetic susceptibility, obesogenic environments, sedentary lifestyles, dietary transitions toward energy-dense ultra-processed foods, and broader socio-economic determinants. Projections indicate that, if current trends continue, more than half of the global adult population and a substantial proportion of children will be living with obesity within the next two decades, with particularly rapid increases occurring in low- and middle-income countries undergoing nutritional and urban transitions. This epidemiologic shift has translated into a marked escalation in obesity-related non-communicable diseases, including type 2 diabetes, cardiovascular disease, chronic kidney disease, non-alcoholic fatty liver disease, osteoarthritis, and several obesity-associated malignancies, positioning excess adiposity as a leading contributor to global morbidity, mortality, and disability-adjusted life years. Alongside the growing disease burden, the conceptual framework of obesity has undergone important refinement. While body mass index remains a pragmatic population-level screening tool, its limitations in capturing adiposity distribution and metabolic risk have prompted international efforts to redefine obesity as a chronic, relapsing disease characterized by excess or dysfunctional adipose tissue with heterogeneous clinical expression. Emerging diagnostic paradigms increasingly emphasize waist-based measures, ectopic fat accumulation, and the presence of obesity-related complications, distinguishing pre-clinical obesity from clinically manifest disease and enabling more precise risk stratification and individualized management. Therapeutically, the obesity landscape has been transformed by advances in incretin-based pharmacotherapy, particularly glucagon-like peptide-1 receptor agonists and dual or multi-agonist agents, which have demonstrated unprecedented and sustained weight reduction alongside meaningful improvements in cardiometabolic outcomes. The recent development of effective oral formulations further expands treatment accessibility and has the potential to improve long-term adherence, although challenges related to cost, equity, and health-system implementation remain substantial. Importantly, pharmacotherapy alone is insufficient to address the obesity epidemic, and contemporary management strategies emphasize multimodal, life-course approaches integrating nutritional therapy, physical activity promotion, behavioral and psychological interventions, digital health technologies, and, when appropriate, metabolic and bariatric surgery, tailored to individual risk profiles and comorbidity burdens. At the population level, global policy initiatives increasingly recognize that obesity is not solely an individual responsibility but a systems-driven condition requiring coordinated action across healthcare, education, food systems, urban planning, and regulatory environments to create supportive contexts for healthy living. Concurrently, ongoing research continues to elucidate the complex pathophysiology of obesity, including the roles of genetics, epigenetics, gut microbiota, neuroendocrine regulation, and adipose tissue inflammation, while implementation science seeks to bridge gaps between evidence and real-world practice. Collectively, the 2026 obesity update portrays a paradoxical landscape of escalating global burden alongside unprecedented scientific and therapeutic progress, underscoring that meaningful and sustainable impact will depend on integrating biomedical innovation with structural policy reform, equitable access to care, and sustained public health commitment to reverse current trajectories and improve outcomes across the lifespan.Long-Term Changes of Urinary Exosomal Peptide Levels after Thyroidectomy in Patients with Thyroid Cancer: A Prospective Observational StudyIn this prospective observational study, we investigated whether longitudinal changes in urinary exosomal peptide profiles after thyroidectomy could predict recurrence risk in patients with papillary thyroid cancer, a disease with reported recurrence rates of up to 30%. Adults older than 20 years with newly diagnosed papillary thyroid cancer who had undergone thyroidectomy were enrolled, and urine samples were collected at 12 months after study entry and again one year later for exosomal peptide identification and comparison. Seventy patients were included and stratified according to the interval between surgery and enrollment (<5 years, 5–10 years, and >10 years). During the two-year follow-up after enrollment, no recurrences were observed. Across groups and time intervals, there were no significant differences in serum protein levels or urinary exosomal peptide concentrations, and established high-risk clinical factors showed only weak correlations with these biomarkers. Collectively, these findings delineate the long-term basal fluctuation ranges of serum proteins and urinary exosomal peptides in post-thyroidectomy thyroid cancer survivors, suggesting that biomarker levels remaining within these ranges may be indicative of a lower long-term risk of recurrence in high-risk patients following thyroidectomy.
• Salvage Radiofrequency Ablation Followed by External Beam Radiotherapy for Inoperable Recurrent Differentiated Thyroid Cancer
  Chen-Kai ChouTaiwan Speaker Salvage Radiofrequency Ablation Followed by External Beam Radiotherapy for Inoperable Recurrent Differentiated Thyroid Cancer
• Re-Differentiation Therapy in RAI-Refractory Thyroid Cancer
  Samantha Peiling YangSingapore Speaker Harnessing Molecular Diagnostics in Cytologically-Indeterminate Thyroid NodulesCytologically indeterminate thyroid nodules (Bethesda III–IV) remain a common diagnostic challenge, as cytology alone cannot reliably distinguish benign from malignant disease. Molecular diagnostic tests have emerged as important adjuncts to refine malignancy risk and guide clinical management. This presentation reviews the molecular landscape of thyroid cancer relevant to indeterminate nodules, including key somatic alterations such as BRAF, RAS, and gene fusions (e.g., RET, NTRK, ALK), and discusses the performance of contemporary molecular diagnostic tests. Data from North America and emerging real-world experience in Singapore will be highlighted. The clinical utility of molecular diagnostics in reducing unnecessary diagnostic surgery and informing the extent of surgical management will be discussed, together with current guidance from the ATA 2025 guidelines on integrating molecular results with clinical, radiologic, and cytopathologic findings. Re-Differentiation Therapy in RAI-Refractory Thyroid CancerRadioactive iodine (RAI) therapy remains a cornerstone in the management of differentiated thyroid cancer. However, a subset of patients develop RAI-refractory disease due to loss of iodine-handling gene expression, including the sodium–iodide symporter (NIS). This loss is frequently associated with activation of the MAPK signalling pathway driven by oncogenic alterations such as BRAF and RAS mutations. While systemic therapy with multi-targeted or mutation-specific tyrosine kinase inhibitors (TKIs) can control disease progression, these treatments are generally not curative and do not consistently restore RAI sensitivity. Re-differentiation therapy has emerged as a promising strategy to restore iodine uptake by targeting MAPK signalling and re-inducing thyroid-specific gene expression. This presentation will review the biological rationale for re-differentiation therapy and summarize key clinical studies evaluating BRAF and MEK inhibition in patients with RAI-refractory thyroid cancer. Emerging approaches, optimal treatment duration, and potential predictors of response will also be discussed, highlighting the potential of re-differentiation therapy to restore the therapeutic benefit of RAI in selected patients.

• Update in Osteoporosis
  Dolores ShobackUnited States Speaker Update in OsteoporosisMany issues in osteoporosis management are challenging in clinical practice. Factors in fracture risk assessment include those in the FRAX algorithm as well as imminent fracture risk in the next 1-5 years. Highest risk individuals benefit most from aggressive therapies targeted to increase bone mineral density (BMD) and reduce fracture rates as rapidly as possible to enhance bone strength. Sequential therapeutic strategies with repeated courses of both anabolic and antiresorptive treatments are becoming the norm for highest risk patients. Yet clinicians are often without trial data to predict clinical outcomes. Bisphosphonate treatment holidays are often employed to allow for a return of bone remodeling with the goal of microdamage repair and avoiding oversuppression of turnover. Yet the duration and monitoring of such treatment interruptions have not been rigorously established. The safety and efficacy of repeated courses of anabolic agents in the lifespan of a patient have not been well studied. The biologic basis for achieving effective BMD responses in sequential therapy is not known. Despite the long use of denosumab and bisphosphonates in clinical care, how to interrupt safely, and how to sequence these therapies most effectively are not known. Rebound increases in bone remodeling after stopping treatment with the RANK-ligand inhibitor denosumab and the challenges of treating patients with advanced chronic kidney disease with denosumab remain unsolved. The bifunctional monoclonal antibody to sclerostin romosozumab, while potent at increasing BMD due to its anabolic and antiresorptive actions, may have off-target cardiovascular adverse effects. Patients who are obese or with diabetes using GLP1 receptor agonists and SGLT2 inhibitors have risks to bone health with rapid weight loss and or direct effects on bone. Ultimately, clinicians must make decisions on patient management based on individual risk assessment and anticipated pathophysiology of the low BMD and risk in that patient.Challenging Parathyroid CasesThis session will review cases of primary, secondary and tertiary hyperparathyoidism and their management. The recommendations for screening patients with possible MEN1 and its manifestations will be reviewed. The role for parathyroid autotransplantation in the management of MEN1 hyperparathyroidism and in postsurgical hypoparathyroidism will be reviewed. A newly released form of parathyroid hormone (PTH) replacement will be discussed in the setting of chronic hypoparathyroidism in adults. Palopegteriparatide has been released for the treatment of chronic hypoparathyroidism and has shown strong efficacy on the control of the biochemical parameters (serum and urine calcium levels, serum phosphate, the Ca x phosphate product) as well as on the quality of life. Updated guidance on considering the use of PTH replacement is being developed and will be discussed. Additionally, the role combined functional and structural localization of parathyroid tissue(s) in the setting of recurrent primary hyperparathyroidism will be reviewed.

• Exploring the World of Autoimmune Disease: from Genetic Manipulation to Disease Reversal
  Huey-Kang SytwuTaiwan Speaker Exploring the World of Autoimmune Disease: from Genetic Manipulation to Disease ReversalAbstract for Asia Oceania Congress of Endocrinology 2026 Huey-Kang Sytwu1 2 1 National Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Taiwan 2 Department of Microbiology and Immunology, National Defense Medical University, Taiwan TITLE: Exploring the world of autoimmune disease: From genetic manipulation to disease reversal Abstract: Insulin-dependent diabetes mellitus (IDDM) is a T cell-mediated autoimmune disease. To delineate the protective roles of some immune modulatory molecules, such as soluble decoy receptor 3 (DcR3), cytotoxic T lymphocyte antigen 4 (CTLA4), program death ligand 1 and 2 (PD-L1 and 2), heme oxygenase 1 (HO-1), and chemokine receptor D6 in the autoimmune process and to search for potential preventive and/or therapeutic targets in this disease, we have generated (a) insulin promoter (pIns)-sDcR3 transgenic non-obese diabetic (NOD) mice, (b) pIns-single chain anti-CTLA4 transgenic NOD mice, (c) pIns-single chain anti-4-1BB transgenic NOD mice, (d) pIns-PD-L1 transgenic NOD mice, (e) pIns-HO-1 transgenic NOD mice, and (f) pIns-D6 transgenic NOD mice and demonstrated their immunomodulatory potential and underlying mechanisms. Meanwhile, to explore the modulatory potential of interleukin-12, 23 and 27 on autoimmune diabetes, we have generated following transgenic, knockout and knockdown NOD mice: (1) Th1 and Th2 doubly transgenic (2) IL-12 knockout (3) IL-23 knockdown (4) IL-27 knockdown NOD mice. Our results revealed that 20% IL-12-deficient NOD mice still developed autoimmune diabetes, the diabetic incidence of IL-23 knockdown NOD mice is lower than that of control littermates, and the number and percentage of Th1 cells are dramatically decreased and Th17 cells are increased in IL-27 knockdown mice, indicating a differential role of IL-12 cytokine family in modulating Th1 and Th17 cell development during autoimmune diabetogenic process. Previously, we demonstrated that overexpression of B lymphocyte-induced maturation protein-1 (Blimp-1) in T cells decreases IL-21 expression and suppresses autoimmune diabetes, whereas, lacking Blimp-1 in T cells upregulates IL-21 and results in severe colitis and autoimmune encephalomyelitis in NOD mice. Here, we further illustrated that Blimp-1 represses IL-21 by reducing chromatin accessibility and evicting an IL-21 activator, c-Maf on its promoter. Moreover, an IL-21-accelerating autoimmune diabetogenesis in SUMO-defective c-Maf transgenic mice can be overridden by Blimp-1 overexpression-mediated reduction of permissive chromatin structures at Il21 locus. We also explored the fundamental mechanisms by which a high-salt diet (HSD) affects susceptibility to or modifies autoimmune diseases. we generated T-cell–specific STE20/SPS1-related proline/alanine–rich kinase (SPAK) knockout NOD mice and demonstrated that SPAK deficiency in T cells significantly attenuated diabetes development in NOD mice by downregulating IL-21 expression in CD4+ T cells. Furthermore, HSD-triggered diabetes acceleration was abolished in HSD-fed SPAK knockout mice when compared with HSD-fed NOD mice, suggesting an essential role of SPAK in salt-exacerbated T-cell pathogenicity. Finally, by using gain- and loss-of-function approaches, we demonstrated that T cell-specific Mgat5 overexpression-induced higher tetra-antennary N-glycans exacerbate autoimmune diabetes, whereas mutant Mgat5L188R-associated tetra-antenna deficiency completely prevents disease in a CD8+ T cell-dependent manner. Making full use of these unique mouse strains, we are quantitatively and qualitatively investigating the immunopathogenic mechanisms of autoimmune diabetes and providing valuable information for the development of novel immunotherapies.

• Key Highlights of the American Thyroid Association Thyroid and Pregnancy Guidelines
  Angela M. LeungUnited States Speaker Key Highlights of the American Thyroid Association Thyroid and Pregnancy GuidelinesThis session will present the key highlights of the American Thyroid Association 2026 guidelines for thyroid disease in preconception, pregnancy, and postpartum that have been published by a multidisciplinary group of experts with global perspective. The discussion will provide an overview of the methodology used to prepare these updated guidelines in partnership with and endorsed by several other collaborating societies. The presentation will cover the most notable changes and new recommendations surrounding thyroid function testing, iodine nutrition, infertility and assisted reproductive techniques, hypothyroidism, hyperthyroidism (including Graves’ disease), thyroid nodules, and thyroid cancers for women planning pregnancy, are pregnant, or seen for postpartum care.Thyroid Risks of Iodine ExcessIodine is a micronutrient that is required for the production of thyroid hormone. Iodine is commonly obtained from consuming an iodine-rich diet or iodine-fortified foods, amiodarone use, iodine-containing supplements, and iodinated contrast media. This session will review the potential forms of thyroid dysfunction arising from an acute iodine load, due to the failure to escape from the Wolff-Chaikoff effect and to the Jod-Basedow phenomenon. The risks of iodine excess in vulnerable populations, and current guidelines regarding the screening and monitoring of iodinated contrast-induced thyroid dysfunction, will be summarized.
• Precision Medicine in Gestational Thyroid Disease: Taking Care of Mother and Baby
  Marjorie A. RamosPhilippines Speaker Precision Medicine in Gestational Thyroid Disease: Taking Care of Mother and BabyPrecision medicine is revolutionizing the management of thyroid disorders in pregnancy by emphasizing individualized diagnosis, trimester-specific reference ranges, and tailored treatment strategies. Thyroid dysfunction is the second most common endocrine abnormality during gestation which poses significant risks to both maternal and fetal health, including miscarriage, preterm delivery, and impaired neurodevelopment. Guidelines now emphasize routine screening in high-risk populations, with tailored management protocols based on trimester-specific TSH and free T4 targets. For hypothyroidism, levothyroxine therapy is initiated early and titrated to maintain TSH in the lower half of the trimester-specific reference range, while hyperthyroidism is managed with antithyroid drugs at the lowest effective dose to minimize fetal risks. Recent updates to clinical guidelines highlight recommendations, including the importance of shared decision-making for women with Graves’ disease, and a shift from antibody-based to timing-based criteria for the treatment of subclinical hypothyroidism. These updates reflect evolving evidence from large randomized trials and systematic reviews, underscoring the need for flexibility and individualization in clinical practice. Future directions in precision medicine include the integration of genetic and molecular profiling to predict disease risk, response to therapy, and long-term outcomes. Machine learning and artificial intelligence are also being explored to enhance diagnostic accuracy and personalize prevention strategies for high-risk subgroups. By combining cutting-edge diagnostics with tailored therapeutic interventions, precision medicine aims to maximize maternal and fetal well-being, reduce adverse outcomes, and improve the overall quality of care for pregnant women with thyroid disorders. This presentation will review the latest evidence, guideline updates, and future innovations in precision medicine for gestational thyroid disease, providing clinicians with practical tools and insights for optimizing patient management in clinical practice and research settings
• Iodine Status in Pregnant Women in Taiwan
  Fan-Fen WangTaiwan Speaker Iodine Status in Pregnant Women in TaiwanIn the 1940’s, endemic goiter was the fifth most common disease in Taiwan. Then, in 1967, an island-wide salt-iodization campaign using 33 ppm potassium iodate was started. Four years after implementation of the campaign, goiter rates among schoolchildren had decreased from 21.6% to 4.3%, suggesting successful elimination of iodine deficiency. However, the mandatory salt iodization policy was discontinued in 2002. In recent surveys, the iodine nutrition status of the overall Taiwanese population has been found to be sufficient, but is at borderline level in pregnant women. Socioeconomic, environmental factors contribute to the incident iodine deficiency in subgroups. While about 92% of pregnant women in Taiwan take nutritional supplements, only about 49% take iodine-containing multi-vitamins. The iodine content of daily meals in Taiwan is currently under investigation, to support targeted dietary education and food fortification programs, which are indicated to improve the iodine status of pregnant women in Taiwan.

• Obesity 2026 Update
  Chih-Yuan WangTaiwan Speaker Obesity 2026 updateObesity remains one of the most critical and rapidly evolving global health challenges entering 2026, characterized by persistently rising prevalence, expanding clinical consequences, and profound societal and economic impacts. Over the past three decades, the prevalence of overweight and obesity has more than doubled among adults and increased nearly threefold among children and adolescents worldwide, driven by complex interactions between genetic susceptibility, obesogenic environments, sedentary lifestyles, dietary transitions toward energy-dense ultra-processed foods, and broader socio-economic determinants. Projections indicate that, if current trends continue, more than half of the global adult population and a substantial proportion of children will be living with obesity within the next two decades, with particularly rapid increases occurring in low- and middle-income countries undergoing nutritional and urban transitions. This epidemiologic shift has translated into a marked escalation in obesity-related non-communicable diseases, including type 2 diabetes, cardiovascular disease, chronic kidney disease, non-alcoholic fatty liver disease, osteoarthritis, and several obesity-associated malignancies, positioning excess adiposity as a leading contributor to global morbidity, mortality, and disability-adjusted life years. Alongside the growing disease burden, the conceptual framework of obesity has undergone important refinement. While body mass index remains a pragmatic population-level screening tool, its limitations in capturing adiposity distribution and metabolic risk have prompted international efforts to redefine obesity as a chronic, relapsing disease characterized by excess or dysfunctional adipose tissue with heterogeneous clinical expression. Emerging diagnostic paradigms increasingly emphasize waist-based measures, ectopic fat accumulation, and the presence of obesity-related complications, distinguishing pre-clinical obesity from clinically manifest disease and enabling more precise risk stratification and individualized management. Therapeutically, the obesity landscape has been transformed by advances in incretin-based pharmacotherapy, particularly glucagon-like peptide-1 receptor agonists and dual or multi-agonist agents, which have demonstrated unprecedented and sustained weight reduction alongside meaningful improvements in cardiometabolic outcomes. The recent development of effective oral formulations further expands treatment accessibility and has the potential to improve long-term adherence, although challenges related to cost, equity, and health-system implementation remain substantial. Importantly, pharmacotherapy alone is insufficient to address the obesity epidemic, and contemporary management strategies emphasize multimodal, life-course approaches integrating nutritional therapy, physical activity promotion, behavioral and psychological interventions, digital health technologies, and, when appropriate, metabolic and bariatric surgery, tailored to individual risk profiles and comorbidity burdens. At the population level, global policy initiatives increasingly recognize that obesity is not solely an individual responsibility but a systems-driven condition requiring coordinated action across healthcare, education, food systems, urban planning, and regulatory environments to create supportive contexts for healthy living. Concurrently, ongoing research continues to elucidate the complex pathophysiology of obesity, including the roles of genetics, epigenetics, gut microbiota, neuroendocrine regulation, and adipose tissue inflammation, while implementation science seeks to bridge gaps between evidence and real-world practice. Collectively, the 2026 obesity update portrays a paradoxical landscape of escalating global burden alongside unprecedented scientific and therapeutic progress, underscoring that meaningful and sustainable impact will depend on integrating biomedical innovation with structural policy reform, equitable access to care, and sustained public health commitment to reverse current trajectories and improve outcomes across the lifespan.Long-Term Changes of Urinary Exosomal Peptide Levels after Thyroidectomy in Patients with Thyroid Cancer: A Prospective Observational StudyIn this prospective observational study, we investigated whether longitudinal changes in urinary exosomal peptide profiles after thyroidectomy could predict recurrence risk in patients with papillary thyroid cancer, a disease with reported recurrence rates of up to 30%. Adults older than 20 years with newly diagnosed papillary thyroid cancer who had undergone thyroidectomy were enrolled, and urine samples were collected at 12 months after study entry and again one year later for exosomal peptide identification and comparison. Seventy patients were included and stratified according to the interval between surgery and enrollment (<5 years, 5–10 years, and >10 years). During the two-year follow-up after enrollment, no recurrences were observed. Across groups and time intervals, there were no significant differences in serum protein levels or urinary exosomal peptide concentrations, and established high-risk clinical factors showed only weak correlations with these biomarkers. Collectively, these findings delineate the long-term basal fluctuation ranges of serum proteins and urinary exosomal peptides in post-thyroidectomy thyroid cancer survivors, suggesting that biomarker levels remaining within these ranges may be indicative of a lower long-term risk of recurrence in high-risk patients following thyroidectomy.

• Incretin-Based Therapeutics: Bridging Theory and Practice, and Exploring New Horizons
  Daisuke YabeJapan Speaker Advancing toward a Cure for Diabetes: Insights from iPSC-Derived Islet Cell Transplantation TrialType 1 diabetes is characterized by absolute insulin deficiency and marked glycemic variability, creating a constant challenge for individuals who must maintain strict glycemic control to prevent complications and severe hypoglycemia. To address these persistent unmet medical needs, transplantation of pancreatic islet–like cells derived from embryonic stem (ES) or induced pluripotent stem (iPSC) cells has emerged as a promising therapeutic strategy. Encouraging advances have recently been reported from the United States and China. Notably, a world-first autologous transplantation of patient-specific iPSC-derived islet-like cells in China achieved insulin independence with near-normal glycemic control. Despite its promise, concerns remain regarding long-term safety, durability, and broad applicability, underscoring the need for further rigorous clinical evaluation. This lecture will provide an overview of current progress and ongoing challenges in β-cell replacement therapy aimed at curing type 1 diabetes. In addition, I will introduce the study design of our clinical trial at Kyoto University Hospital evaluating allogeneic transplantation of iPSC-derived islet cell sheets (OZTx-410). Through these insights, we aim to highlight both the steady steps already taken and the horizon of possibilities ahead in the pursuit of a functional cure for diabetes.Incretin-Based Therapeutics: Bridging Theory and Practice, and Exploring New HorizonsThe landscape of type 2 diabetes management has been transformed by the advent of incretin-based therapies, including dipeptidyl peptidase-4 (DPP-4) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists. In Japan—where more than 70% of individuals with diabetes are aged 65 years or older and commonly present with a non-obese phenotype and reduced insulin secretory capacity—DPP-4 inhibitors continue to serve as a fundamental treatment option, offering effective glycemic control with minimal risk of hypoglycemia. In contrast, among younger adults with obesity, GLP-1 receptor agonists have emerged as essential agents that not only improve glycemic control but also promote weight reduction and confer cardiovascular and renal benefits. A major advance in 2023 was the approval of tirzepatide, a dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 receptor agonist that engages both receptors. Tirzepatide has demonstrated robust glucose-lowering and weight-reducing effects in both clinical trials and real-world practice in Japan, further expanding therapeutic opportunities across the region. However, incretin-based therapies are not without challenges: gastrointestinal adverse events remain common, and potential associations with pancreatic and biliary diseases continue to require caution. In older adults, concerns regarding their impact on frailty and sarcopenia demand careful clinical judgment. Furthermore, inappropriate discontinuation of insulin therapy after initiating incretin treatment has occasionally resulted in severe clinical consequences, highlighting the critical need for decision-making that extends beyond the evidence from controlled trials. In response to these issues, the Japan Diabetes Society (JDS) Committee for the Safe Use of Medications released the Recommendations for the Safe Use of Incretin-Related Agents, Second Edition in 2024. Disseminating these recommendations across East Asia and the broader Asia–Oceania region will be essential to ensure the safe and effective application of incretin-based therapies in diverse clinical settings. In this plenary lecture, I will explore strategies to optimize type 2 diabetes management in Asia by harnessing the therapeutic potential of incretin-based agents while proactively mitigating associated risks. Together, we aim to build a future in which innovation, safety, and patient-centered care advance hand in hand.

• Genomic Alterations in Thyroid Cancer: Biological and Clinical Insights
  Maria E. CabanillasUnited States Speaker Genomic Alterations in Thyroid Cancer: Biological and Clinical InsightsGenomic alterations play a central role in the initiation, progression, and clinical behavior of thyroid cancers, offering critical insights into their underlying biology and therapeutic vulnerabilities. Follicular cell derived thyroid tumors commonly harbor driver mutations that constitutively activate the MAPK signaling pathway, most notably BRAFV600E and RAS mutations. These early events define major molecular subtypes and strongly influence differentiation status, tumor phenotype, and response to therapy. Progression toward aggressive or dedifferentiated forms, such as poorly differentiated and anaplastic thyroid carcinomas, is driven by additional alterations in key genes regulating chromatin remodeling, cell cycle control, and genomic stability, including TERT promoter mutations, TP53, PIK3CA, and EIF1AX. Actionable genomic alterations are increasingly leveraged to personalize treatment strategies in thyroid cancer and underscore the importance of genomic characterization in improving outcomes in thyroid cancer. Anaplastic Thyroid CancerAnaplastic thyroid cancer (ATC) is one of the most aggressive human malignancies, characterized by rapid local invasion, early metastasis, and near‑universal disease‑specific mortality and is considered a medical emergency. Current treatment strategies prioritize rapid assessment of resectability, with surgery pursued only when complete or near‑complete tumor removal is feasible, as partial debulking offers limited benefit. For unresectable disease, localized disease, combined modality therapy—typically external‑beam radiation with concurrent systemic therapy—remains the cornerstone of local control. Recent advances in molecular profiling have transformed systemic management, enabling targeted therapies for tumors harboring BRAFV600E mutations. These agents have demonstrated meaningful responses and, in select cases, have converted unresectable tumors to operable ones, expanding the role of surgery in modern care. However, due to the high risk of relapses, immunotherapy has been added to the treatment strategy. Patients with distant metastatic disease without a BRAFV600E mutation have a more complicated treatment regimen which is still under investigation but require systemic therapy combination strategies involving immunotherapy. These evolving strategies reflect a shift toward precision‑based, time‑critical management aimed at improving outcomes in this highly lethal cancer.

• Revisiting the β-cell: The Key to the Type 2 Diabetes Puzzle
  Steven KahnUnited States Speaker Revisiting the β-cell: The Key to the Type 2 Diabetes PuzzleIncretin-Based Therapies: Lessons Learned Beyond Diabetes

• Paraneoplastic Autoimmune Hypophysitis: A Novel Form Paraneoplastic Endocrine Syndrome
  Yutaka TakahashiJapan Speaker Paraneoplastic Autoimmune Hypophysitis: A Novel Form Paraneoplastic Endocrine SyndromeThe story begins with a fascinating case we encountered in 2003. It was an outlier of hypopituitarism that presented with acquired deficiencies in GH, PRL, and TSH. We subsequently accumulated similar cases and reported them as a novel disease entity named "anti-PIT-1 hypophysitis." We clarified that this condition represents a paraneoplastic syndrome associated with thymoma or malignancies. The mechanism of onset involves ectopic expression of PIT-1 in the tumor, leading to a breakdown of immune tolerance. As a result, anti-PIT-1 antibodies are produced in the blood, and PIT-1–expressing cells (those producing GH, PRL, and TSH) in the pituitary are damaged by cytotoxic T lymphocytes (CTLs). Recently, we have succeeded in establishing a disease model using co-culture of CTLs and patient-derived iPS cell–generated pituitary cells, demonstrating that CTLs are indeed the causatively involved. Interestingly, we found that a similar mechanism underlies some cases of isolated ACTH deficiency and immune checkpoint inhibitor–related hypophysitis (PD-1/PDL-1-related hypophysitis). Based on this, we proposed a broader new disease concept: “paraneoplastic autoimmune hypophysitis.” Very recently, we discovered a case of “immune checkpoint inhibitor–related anti–PIT-1 hypophysitis,” which clearly supports this concept. To elucidate the pathophysiology of such novel diseases, we emphasize the importance of a cross-disciplinary academic framework—beyond organ-specific medical practice and beyond endocrinology alone—which we refer to as "onco-immuno-endocrinology." In this lecture, I will introduce our research journey and share key insights and lessons for young physician-scientists aiming to reshape the textbooks of the future.Hypophysitis: Difficult CasesHypophysitis is defined as inflammation of the hypothalamo-pituitary region and is classified into primary and secondary forms. Primary hypophysitis refers to autoimmune hypophysitis (lymphocytic hypophysitis) and is essentially a diagnosis by exclusion of other diseases. Secondary hypophysitis can be classified into those associated with local lesions, systemic diseases, or drug-induced causes. Therefore, differential diagnosis from other conditions presenting with similar findings is crucial. Among the secondary forms, immune checkpoint inhibitor–related hypophysitis has emerged. In addition, the newly proposed entity paraneoplastic autoimmune hypophysitis have recently drawn considerable attention. That includes anti-PIT-1 hypophysitis, a component of isolated ACTH deficiency and PD-1/PDL-1-related hypophysitis, in which common mechanism underlies. Ectopic expression of pituitary antigens such as POMC and PIT-1 causes breakdown of immune tolerance and specific cytotoxic T cells injure anterior pituitary cells, results in a specific defect in ACTH or GH, PRL, and TSH, respectively. For systemic diseases, diagnosis proceeds by examining specific disease markers and searching for involvement of other organs. On the other hand, it is often difficult to differentiate lesions confined to the hypothalamo-pituitary region. In atypical cases, pituitary biopsy should be considered. When performing a biopsy, appropriate selection of the biopsy site is essential. If possible, the decision should be made before administering pharmacologic doses of glucocorticoids. In this Meet the Professor session, I would like to provide up-to-date information and foster discussion with audience on key points in the differential diagnosis of hypophysitis, with a focus on immune checkpoint inhibitor–related hypophysitis and paraneoplastic autoimmune hypophysitis, which represent emerging disease concepts.

• Pheochromocytoma: Current Concepts and Emerging Evidence
  Min Jeong ParkSouth Korea Speaker Pheochromocytoma: Current Concepts and Emerging EvidencePheochromocytoma and paraganglioma: Current Concepts and Emerging Evidence Min Jeong Park1 1Department of Internal Medicine, College of Medicine, Korea University, Seoul, South Korea Pheochromocytoma and paragangliomas (PPGLs) are rare neuroendocrine tumors. Over the past decade, rapid progress in molecular genetics, diagnostic and follow-up strategies, and systemic therapy has reshaped the landscape of these tumors. In this lecture, I will summarize current concepts and emerging evidence with particular attention to evolving clinical phenotype and long-term management challenges. Recent evidence suggests that a subset of PPGL patients exhibit autonomous hypercortisolemia in addition to catecholamine excess. In such cases, our group discovered higher rates of metabolic comorbidities – including diabetes mellitus and hypertension – compared with PPGL without cortisol excess. It infers the need for evaluation of pre and postoperative adrenal cortical function and metabolic comorbidities in patients with PPGL. PPGL are now recognized as among the most heritable human tumors, with 30-40% harboring germline mutation across more than 20 susceptibility genes. Molecular profiling had led to classification into three major clusters: Pseudohypoxia, kinase signaling, and Wnt-pathway – which informs biochemical phenotype, imaging patterns, and metastatic behavior. Multi-omics analyses identify ATRX/TERT alterations, copy-number burden, and immune microenvironmental features as potential prognostic biomarkers. Surgery remains curative for localized disease with alpha-blockade based perioperative optimization. For metastatic or unresectable disease, tyrosine kinase inhibitors, radionuclide therapies, and immune checkpoint inhibitors form an evolving systemic therapy for PPGL. Prediction of recurrence is also a major unmet domain. Current guideline recommend more than 10 years of surveillance for all resected PPGL and lifelong follow-up for high-risk patients; however, criteria for discontinuing surveillance in low-risk patients after 10 years remain undefined. Our group investigated features of the very-low risk group, which may discontinue follow-up after free of recurrence for 10 years of follow-up. This lecture will integrate recent advances in PPGL biology and management with practical consideration for metabolic assessment and long-term surveillance, including new data that may guide personalized decision-making for folllow-up cessation in selected low-risk patients.
• Translational Research for Developing Blood-Based Biomarkers of Sarcopenia
  Beom-Jun KimSouth Korea Speaker Translational Research for Developing Blood-Based Biomarkers of SarcopeniaSarcopenia, characterized by the progressive loss of skeletal muscle mass and function, is a major determinant of frailty and adverse health outcomes in aging populations. Consequently, the identification of reliable blood-based biomarkers is critical for early diagnosis, risk stratification, and the development of therapeutic interventions. This lecture provides an overview of our translational research efforts aimed at discovering and validating novel biomarkers using multi-omics approaches in both preclinical and clinical models of sarcopenia. In animal models, we have integrated proteomics and metabolomics to identify candidate biomarkers reflecting key pathophysiological mechanisms of muscle degeneration. Concurrently, in human cohorts, we employed multi-omics profiling of circulating biomarkers to detect signatures associated with muscle mass, strength, and physical performance. A central focus of our research is the cross-validation of these biomarkers between animal and human models to ensure translational relevance. By leveraging comparative bioinformatics analyses, we aim to establish robust biomarkers with high sensitivity and specificity for detecting sarcopenia and monitoring disease progression. Furthermore, this lecture will discuss the potential clinical utility of these biomarkers in personalized risk assessment. By bridging preclinical discoveries with human validation studies, our work contributes to the advancement of precision medicine for sarcopenia. Ultimately, establishing reliable blood-based biomarkers will facilitate the early identification of high-risk individuals, improve patient stratification in clinical trials, and enable targeted therapeutic strategies.
• Anxiety in Patients with Thyroid Nodules: What Clinicians Need to Know
  Edy KorneliusTaiwan Speaker Anxiety in Patients with Thyroid Nodules: What Clinicians Need to KnowThyroid nodules are commonly encountered in endocrine practice, and while the majority are benign, the diagnostic and surveillance process often imposes a substantial psychological burden on patients. Anxiety related to fear of malignancy, uncertainty surrounding ultrasonographic findings, fine-needle aspiration results, and long-term follow-up is frequently underestimated and insufficiently addressed in routine clinical care. Emerging evidence suggests that anxiety in patients with thyroid nodules may persist even after reassurance of benign disease and can significantly affect quality of life, healthcare utilization, and decision-making preferences. Cancer-related worry is often disproportionate to the actual risk of malignancy and may be exacerbated by repeated imaging, indeterminate cytology, ambiguous terminology, and lack of clear follow-up strategies. Heightened anxiety has been associated with increased demand for diagnostic interventions and preference for aggressive management, potentially leading to overtreatment. This presentation reviews current evidence on the prevalence, determinants, and clinical consequences of anxiety among patients with thyroid nodules, integrating published literature with real-world clinical experience. Practical approaches for identifying psychological distress in outpatient settings and strategies for improving communication and expectation management will be discussed. Recognizing and addressing anxiety as an integral component of thyroid nodule care is essential for delivering holistic, patient-centred, and value-based endocrinology.
• Impaired Fasting Glucose and Musculoskeletal Disorders
  Yi-Sun YangTaiwan Speaker Impaired Fasting Glucose and Musculoskeletal DisordersThe Continuum of Glycemic Dysregulation and Musculoskeletal Health: From Impaired Fasting Glucose to Established Diabetes. As the global medical community transitions into the "Next ERA" of endocrinology, there is an urgent need to broaden our focus beyond traditional microvascular and macrovascular complications toward the pervasive, yet often neglected, musculoskeletal (MS) burden associated with dysglycemia. While the debilitating effects of established Type 2 Diabetes Mellitus (T2DM) on physical function are well-documented, emerging clinical evidence suggests that the musculoskeletal system is an early "silent" target of metabolic injury, with pathological changes manifesting as early as the Impaired Fasting Glucose (IFG) stage. This presentation explores the MS burden across the full glycemic spectrum, highlighting how the transition from normoglycemia to IFG, and ultimately to T2DM, correlates with a progressive increase in chronic pain, structural tissue damage, and functional disability.
• Discussion

• Advances in the Treatment of Radioactive Iodine-Refractory Differentiated Thyroid Cancer: Multikinase Inhibitors and Beyond – An Asian Perspective
  Won Gu KimSouth Korea Speaker Advances in the Treatment of Radioactive Iodine-Refractory Differentiated Thyroid Cancer: Multikinase Inhibitors and Beyond – An Asian PerspectiveDifferentiated thyroid cancer (DTC) arising from follicular cells generally has a good prognosis; however, about 5-10% of patients experience recurrence or distant metastasis. High-dose radioactive iodine (RAI) therapy is the mainstay of treatment for metastatic DTC, but its efficacy depends on the iodine avidity of the tumor. Iodine uptake of metastatic lesions tends to decline over time, and ultimately, around 60-70% of metastatic cases become refractory to RAI therapy. Patients whose metastases remain RAI-avid have a median survival approaching 10 years, whereas those with RAI-refractory disease have a roughly 10% of 10 10-year survival. Because the clinical course of RAI-refractory DTC is variable, it is critical to determine which patients should receive systemic therapy with a tyrosine kinase inhibitor (TKI) and how to integrate local treatment before and during systemic therapy. TKIs such as sorafenib and lenvatinib, which primarily inhibit tumor angiogenesis, have been approved. The DECISION trial reported that sorafenib achieved a median progression-free survival (PFS) of 10.8 months compared with 5.8 months in the control group. The SELECT trial showed that lenvatinib achieved a median PFS of 18.3 months versus 3.6 months in controls. Based on these results, sorafenib and lenvatnib are now widely used as the first-line treatments for patients with RAI-refractory DTC who have progressive or symptomatic metastatic disease. A recent multi-center real-world study in Korea suggested that lenvatinib provides better efficacy and longer PFS (median 35.3 months) than sorafenib (median 13.3 months, p<0.001). However, lenvatinib is also associated with higher rates of adverse events such as hypertension (95%) and proteinuria (80%). These TKIs show activity irrespective of the underlying genetic alterations that drive thyroid cancer. Recently, selective NTRK and RET inhibitors have been developed for solid tumors harboring NTRK or RET gene fusions, and their efficacy has been confirmed in clinical trials. In addition, genetic testing to identify actionable mutations is increasingly being incorporated into practice, and personalized treatment approaches are reflected in current clinical guidelines. A recent Korean multicenter study found that approximately 31% of patients with RAI-refractory thyroid cancer who had wild-type BRAF carried targetable gene fusions. The choice and sequencing of TKI, the optimal timing of their use, strategies to prevent and manage adverse events, and individualized treatment plans based on patient characteristics will be crucial for improving clinical outcomes in patients with RAI-refractory thyroid cancer.
• Translating the Genetic Landscape of Thyroid Cancer to Precision Diagnosis and Therapy
  Young Joo ParkSouth Korea Speaker Translating the Genetic Landscape of Thyroid Cancer to Precision Diagnosis and TherapyThyroid cancer is characterized by a relatively low mutational burden compared with other solid tumors, with recurrent alterations mainly involving BRAF, RAS, and various fusion genes. Several novel driver candidates have also been identified through next-generation sequencing studies. The frequency and pattern of these genomic alterations differ across thyroid cancer subtypes and are often associated with distinct histopathological phenotypes, providing valuable clues for differential diagnosis. Moreover, molecular subtypes defined by driver mutations are closely linked to tumor biology and clinical behavior, allowing more accurate prediction of disease aggressiveness and prognosis. Most differentiated thyroid cancers (DTCs) harbor a single dominant driver alteration; however, acquisition of additional mutations such as TERT promoter, tumor suppressor genes, or PI3K–AKT pathway alterations may lead to dedifferentiation and progression to aggressive or metastatic disease. Advances in our understanding of these genetic alterations have refined the pathological classification of thyroid cancer and enabled improved prognostication, treatment selection, and follow-up strategies. Importantly, the identification of actionable genetic alterations—including RET and NTRK fusions, as well as BRAF mutations—has revolutionized therapeutic approaches. Targeted agents such as selpercatinib, pralsetinib, larotrectinib, and entrectinib demonstrate substantial clinical efficacy with fewer adverse events than multikinase inhibitors, while dabrafenib plus trametinib has shown marked benefit in anaplastic thyroid cancer. With multiple targetable mutations being uncovered, incorporating comprehensive genomic testing into the diagnostic workflow is essential to guide precision therapy for patients with thyroid cancer.
• Redifferentiation Strategies in Refractory Thyroid Cancer: First Insights from Taiwan
  He-Jiun JiangTaiwan Speaker Redifferentiation Strategies in Refractory Thyroid Cancer: First Insights from TaiwanBackground: Patients with BRAF p.V600E-mutated radioactive iodine-refractory differentiated thyroid cancer (RAIR-DTC) face a poor prognosis. While MAPK pathway inhibition can restore radioiodine (RAI) avidity, standard full-dose protocols (e.g., MERAIODE) are often associated with significant toxicity (Grade 3/4 adverse events >20%). This study investigates the efficacy and safety of a novel low-dose, pulsed redifferentiation strategy in a real-world Asian cohort. Methods: We conducted a retrospective cohort study of 24 patients with metastatic BRAF p.V600E RAIR-PTC. Patients received a 60-day induction regimen of Dabrafenib (75 mg BID) and Trametinib (2 mg QOD, every other day). A "Treat-All" strategy was employed, omitting diagnostic scanning to avoid stunning effects, followed by a fixed therapeutic dose of 131-I (150-200 mCi). Primary endpoints included RAI uptake restoration, objective response rate (ORR), disease control rate (DCR), and safety profile. Results: RAI avidity was restored in 83.3% of patients. The regimen demonstrated an exceptional safety profile without Grade 3/4 adverse events. While the ORR was 16.7%, the DCR reached 83.3% at 6 months. Age <55 years was identified as the most significant predictor for objective tumor regression (p=0.007). Furthermore, the study highlights the clinical value of "TKI-Free Survival," with 88.9% of prior TKI users achieving a sustained drug holiday. Conclusion: The low-dose, pulsed BRAF/MEK inhibition protocol offers a highly tolerable and effective redifferentiation strategy. While tumor shrinkage is less pronounced than with full-dose regimens, the high rate of disease control and excellent safety profile make it a viable option for stabilizing disease and improving quality of life, particularly for younger patients (<55) or those intolerant to standard TKI therapy.

• Incretin-Based Therapies: Lessons Learned Beyond Diabetes
  Steven KahnUnited States Speaker Revisiting the β-cell: The Key to the Type 2 Diabetes PuzzleIncretin-Based Therapies: Lessons Learned Beyond Diabetes

• Challenging Cases in Endocrinology
  Ronald MaHong Kong, China Speaker Precision Medicine in Diabetes: Perspectives from AsiaPrecision Medicine in Diabetes: Perspectives from Asia Abstract Diabetes is traditionally classified into type 1 diabetes, type 2 diabetes and gestational diabetes as the main forms of diabetes. However, there is increasing recognition that there is significant hidden heterogeneity within diabetes. Resolving this heterogeneity of diabetes can help facilitate personalized treatment and precision medicine in diabetes. For example, identification of specific monogenic forms of diabetes may facilitate tailored choices of diabetes medications. Precision diagnosis also includes the use of biomarkers to correctly identify adults presenting with autoimmune diabetes for appropriate treatment. Recent advances have included the use of clinical characteristics to empower subtyping of adult-onset diabetes through different clustering strategies. Regardless of the approach of subclassification, the essence of diabetes subtyping is to differentiate between individuals with diabetes due to different underlying pathophysiological defects, and hence have different prognosis towards complications or response to treatment. Recent advances in precision prognostics have also highlighted strategies that can identify high-risk individuals for more intensive treatment. An international consortium initiated by the American Diabetes Association and European Association for the Study of Diabetes (EASD) has reviewed the landscape for precision medicine in diabetes to map our current understanding, as well as outline future directions. The ability to resolve the heterogeneity in diabetes, and thereby provide treatment that is best tailored to the underlying pathophysiology, provides exciting opportunities to realize precision medicine in diabetes towards better patient outcomes. References 1. Leslie RD, Ma RCW, Franks PW, Nadeau KJ, Pearson ER, Redondo MJ. Understanding diabetes heterogeneity: key steps towards precision medicine in diabetes. Lancet Diabetes Endocrinol. 2023 Nov;11(11):848-860. 2. Tobias D, Merino J et al, Second International Consensus report on gaps and opportunities for the clinical translation of precision diabetes medicine. Nature Medicine 2023; 29: 2438-2457. Challenging Cases in EndocrinologyIn this meet the professor session, we will use 4-5 case scenarios to illustrate diagnostic challenges around clinical endocrinology and diabetes and discuss management strategies.

• Psychiatric Perspectives in Gender-Affirming Care
  Wayne Wing Ki TangHong Kong, China Speaker Psychiatric Perspectives in Gender-Affirming CareThe psychiatrist plays a fundamental role in the multidisciplinary care of transgender and gender-diverse individuals, moving beyond traditional gatekeeping to provide supportive assessment and mental health care alongside the initiation of hormonal therapy. This presentation outlines the key psychiatric considerations in providing holistic care for this population, offering a complementary perspective to the endocrinologist's work within culturally specific service settings. We will review the current diagnostic framework (ICD-11 Gender Incongruence) and the practical aspects of the pre-/peri-treatment psychiatric consultation. The focus will be on understanding the individual’s unique gender journey and identifying co-occurring mental health conditions or psychosocial stressors that may benefit from concurrent support during medical transition. Furthermore, we will discuss the longitudinal intersection between medical intervention and mental health. While Gender-Affirming Hormone Therapy (GAHT) is effective in alleviating gender incongruence and often reduces distress, clinical experience and local data suggest that medical transition alone may not universally resolve concurrent depressive or anxiety symptoms. We will briefly illustrate this using recent findings from a Hong Kong cohort, which highlight that while gender congruence improves with hormonal treatment, psychological well-being is often more closely linked to psychosocial stressors. The session concludes by exploring how psychiatrists and endocrinologists can collaborate to support patients who face these ongoing challenges, ensuring a safe and sustainable transition process.
• Gender-Affirming Hormone Therapy for Transgender and Gender Diverse Adults
  Brendan NolanAustralia Speaker Gender-Affirming Hormone Therapy for Transgender and Gender Diverse AdultsGender-affirming hormone therapy (GAHT) is used by many transgender and gender-diverse adults to align physical characteristics with their gender identity, reduce gender incongruence and improve psychological functioning. This presentation will provide an overview of the initiation and monitoring of GAHT in trans adults. Trans individuals treated with testosterone typically receive standard testosterone doses and formulations recommended for cisgender men, whereas those receiving estradiol-based GAHT are typically treated with estradiol in combination with an anti-androgen in those without orchidectomy. Proactive monitoring and mitigation of cardiovascular risk factors is pertinent in all trans adults and bone health is an important consideration in those using estradiol-based GAHT.
• Gender-Affirming Hormone Therapy in Taiwan
  Pei-Lung ChenTaiwan Speaker Gender-Affirming Hormone Therapy in Taiwan