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08:30
09:10
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Steven KahnUnited States
Speaker
Revisiting the β-cell: The Key to the Type 2 Diabetes PuzzleIncretin-Based Therapies: Lessons Learned Beyond Diabetes
101
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09:10
09:50
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Harn-Shen ChenTaiwan
Moderator
Acromegaly and Cardiovascular Disease: The Research in Taipei Veterans General HospitalAcromegaly, characterized by chronic excess growth hormone (GH) and elevated insulin-like growth factor-1 (IGF-1), is associated with increased morbidity and premature mortality, particularly from cardiovascular (CV) complications. Research from Taipei Veterans General Hospital (Taipei VGH) over the past decade has systematically examined how biochemical control, metabolic status, and cardiac function influence patient outcomes, forming a comprehensive institutional understanding of acromegaly-related CV risk.
Early studies established the prognostic importance of postoperative hormonal normalization following trans-sphenoidal adenomectomy (TSA). Patients achieving stringent biochemical remission demonstrated markedly reduced long-term mortality, whereas persistent GH/IGF-1 elevation remained a strong predictor of premature death. Even partial hormonal improvement provided measurable survival benefit, highlighting the need for aggressive management and close monitoring after surgery.
Subsequent work addressed the metabolic impact of medical therapy, particularly long-acting octreotide. While effective in reducing GH/IGF-1 levels, somatostatin analogs impaired insulin secretion and frequently worsened glucose tolerance. These findings underscore the need to balance biochemical control with careful metabolic surveillance, especially in patients with preexisting glucose abnormalities.
In 2020, a nationwide epidemiological study expanded the perspective by detailing incidence, comorbidities, re-operation rates, cancer risk, and mortality trends across Taiwan. Despite modern advances, patients with acromegaly continued to exhibit elevated mortality—predominantly from CV and malignant causes—reinforcing the significance of early diagnosis and rigorous long-term management.
Complementing epidemiologic insights, a focused clinical study demonstrated that successful surgical remission led to significant improvements in traditional CV risk factors, including reductions in HbA1c, LDL cholesterol, total cholesterol, and blood pressure one year after TSA. These benefits were most pronounced in patients with normalized IGF-1.
The most recent study linked degrees of biochemical control to cardiac structure and function. Patients with uncontrolled or partially controlled acromegaly exhibited increased left ventricular mass and impaired diastolic function, indicating early acromegalic cardiomyopathy even when systolic function remained preserved.
Collectively, the Taipei VGH research program highlights that full biochemical remission is essential not only for reducing mortality but also for reversing metabolic abnormalities and preventing progressive cardiac dysfunction.
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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.
101
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09:50
10:10
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10:10
11:00
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ESROC & DAROC General Assembly
101
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11:00
12:30
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Updates in Endocrinology: Emerging Insights into Adrenal Disorders, Muscle Health, and Endocrine Diseases
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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.
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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.
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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.
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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.
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103
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Perspectives on Obesity in Asia-Oceania
Kathryn TanHong Kong, China
Moderator
Lipoprotein(a): What Endocrinologists Need to KnowLipoprotein(a) [Lp(a)] is a cholesterol-rich LDL-like particle with apolipoprotein(a) covalently linked to apolipoprotein B100 via a disulfide bond. Lp(a) is synthesized within the liver and there is a general inverse correlation between Lp(a) isoform size and plasma Lp(a) concentrations. About 90% of plasma Lp(a) concentration is genetically determined and plasma levels can modestly rise after menopause in women, and in conditions like hypothyroidism, nephrotic syndrome. It has been shown that elevated Lp(a) is an independent risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis. Although Lp(a) concentration does vary with ethnicity, relationships between Lp(a) concentration and ASCVD risk remain similar across different ethnic groups. Elevated Lp(a) is considered a cardiovascular risk-enhancing or amplification factor, and recent guidelines and consensus have increasingly recommended universal screening for Lp(a). There are as yet, no approved therapies for elevated Lp(a). Current management focuses on intensifying control of concurrent risk factors, particularly LDL-C, to reduce ASCVD risk. Amongst existing lipid-lowering drugs, only proprotein convertase subtilisin/kexin type 9 inhibitors can lower Lp(a) levels modestly. Emerging RNA-based and small-molecule therapeutics are under development and are showing promising Lp(a)-lowering effects up to 80-90%. Ongoing phase 3 cardiovascular outcomes trials will determine whether effectively lowering Lp(a) can translate to cardiovascular benefit.
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Vivien LimSingapore
Speaker
The Danger of Obesity in South East Asia and Practical Tips in the Clinic Obesity is steadily increasing in South East Asia (SEA) and with it comes complications naturally follow from it - metabolic, physical and mental. The talk will touch on the following:
- the prevalence of this and the changes over time
- the rising burden of it
- practical tips that can aid in the clinic including busting myths and misconceptions that hamper its management
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101
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Diabetic Neuropathy: from Pathophysiology to Clinical Practice
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Chih-Cheng ChenTaiwan
Speaker
Pathophysiological Mechanisms Underlying Diabetic NeuropathyDiabetic neuropathy is a prevalent complication of both type I and type II diabetes mellitus. However, although peripheral nerve degeneration is highly associated with painful neuropathy, the underlying mechanism remains largely unknown. Here we report a role of advillin in painful diabetic neuropathy in a mouse model of type I diabetes induced by multiple low doses of streptozotocin (STZ). Advillin is an actin-binding protein involved in regulating the organization of actin filaments and the dynamics of axonal growth cones. In mice, advillin is exclusively expressed in somatosensory neurons, ubiquitously expressed in all neuron subtypes during neonatal ages and particularly enriched in isolectin B4 positive (IB4+) non peptidergic neurons in adulthood. We previously showed that advillin plays a key role in axon regeneration of somatosensory neurons during peripheral neuropathy. Mice lacking advillin lost the ability to recover form neuropathic pain induced by oxaliplatin, chronic compression of sciatic nerve, and experimental autoimmune encephalitis. In the diabetic model, STZ-induced cold allodynia was resolved in 8 weeks in wild type (Avil+/+) mice, but could last more than 30 weeks in advillin-knockout (Avil-/-) mice. Additionally, Avil-/- but not Avil+/+ mice showed STZ-induced mechanical hypersensitivity of muscle. Consistent with the prolonged and/or worsened STZ-induced neuropathic pain, second-line coping responses to pain stimuli were greater in Avil-/- than in Avil+/+ mice. On analyzing intraepidermal nerve density, STZ induced large axon degeneration in the hind paws but with distinct patterns between Avil+/+ and Avil-/- mice. We next probed whether advillin knockout could disturb capsaicin induced axon regeneration ex vivo because capsaicin is clinically used to treat painful diabetic neuropathy by promoting axon regeneration. In a primary culture of dorsal root ganglion cells, 10 min capsaicin treatment selectively promoted neurite outgrowth of IB4+ neurons in Avil+/+ but not Avil-/- groups, which suggests that capsaicin could reprogram the intrinsic axonal regeneration by modulating the advillin-mediated actin dynamics. Together, advllin-dependent IB4+ axon regeneration plays an important role in the development of painful diabetic neuropathy.
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Chi-Chao ChaoTaiwan
Speaker
Clinical Presentation and Diagnostic Evaluation of Diabetic NeuropathyDiabetic neuropathy (DN) is the most common microvascular complication of diabetes and a leading cause of peripheral neuropathy worldwide. With the global rise in diabetes prevalence, DN represents a growing clinical and public health challenge. Distal symmetric sensorimotor polyneuropathy (DSPN) is the predominant subtype, typically presenting with length-dependent sensory symptoms beginning in distal feet and progressing proximally. Patients commonly report various sensory symptoms like numbness, neuropathic pain, and imbalance. Although sensory manifestations predominate, motor weakness and autonomic dysfunction may occur and contribute to substantial morbidity, including foot ulceration, gait problem, cardiovascular and gastrointestinal complications.
The diagnosis of diabetic neuropathy requires compatible clinical symptoms and signs together with objective evidence of peripheral nerve dysfunction. Large-fiber involvement is assessed primarily by nerve conduction studies (NCS), which demonstrate reduced conduction velocity and action potential amplitudes in a length-dependent pattern. However, small-fiber neuropathy often occurs early and may precede detectable NCS abnormalities. Therefore, multimodal assessment is essential. Quantitative sensory testing (QST) allows functional evaluation of thermal (small-fiber) and vibratory (large-fiber) thresholds. Skin biopsy with intraepidermal nerve fiber density quantification provides morphologic confirmation of small-fiber degeneration. Corneal confocal microscopy offers a noninvasive surrogate marker of small-fiber integrity, while heat pain evoked potentials and autonomic function tests—including QSART and sudoscan—further characterize small-fiber and autonomic involvement. A comprehensive diagnostic approach integrating clinical evaluation with complementary large- and small-fiber testing improves diagnostic accuracy, enables earlier identification of high-risk individuals, and supports timely intervention to prevent disability.
This lecture reviews the clinical phenotypes, diagnostic criteria, and contemporary multimodal evaluation strategies for diabetic neuropathy, emphasizing the importance of early detection and precision phenotyping in clinical practice.
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Yen-Feng Wang Taiwan
Speaker
Evidence-Based Management of Diabetic Neuropathy: Pharmacologic and Non-Pharmacologic Approaches
102
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Novel Treatment and Diagnostic Approaches for Thyroid Cancer in Post-NGS Era
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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.
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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.
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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.
201BC
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Cushing’s Disease and Cushing’s Syndrome
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Cheng-Chia LeeTaiwan
Speaker
Stereotactic Radiosurgery for Cushing DiseaseCushing disease, caused by adrenocorticotropic hormone (ACTH)–secreting pituitary adenomas, remains a therapeutic challenge due to tumor invasiveness, difficulty in achieving complete resection, and the risk of recurrence following surgery. While transsphenoidal surgery is considered first-line treatment, a substantial proportion of patients experience persistent or recurrent hypercortisolism, necessitating adjuvant therapies. Stereotactic radiosurgery (SRS) has emerged as an effective and minimally invasive treatment modality for residual or recurrent Cushing disease, offering precise, high-dose radiation delivery to the target lesion while sparing surrounding critical structures. Clinical evidence demonstrates that SRS achieves long-term biochemical remission in a significant proportion of patients, with reported cortisol normalization rates increasing over time after treatment. Tumor control rates are consistently high, exceeding 90% in most series. Although the therapeutic effect of SRS is delayed compared to surgery, it provides durable disease control with an acceptable safety profile. Hypopituitarism remains the most common adverse effect, whereas cranial neuropathy and optic pathway injury are rare when strict dose constraints are observed. Advances in imaging, target delineation, and dose planning have further enhanced the efficacy and safety of SRS. Overall, stereotactic radiosurgery represents a critical component of multimodal management for Cushing disease, particularly in patients with surgically refractory disease, recurrent tumors, or contraindications to repeat surgery. Long-term endocrine follow-up remains essential to monitor treatment response and late radiation-related effects.
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Masaaki YamamotoUnited States
Speaker
Beyond Cushing’s Syndrome: The Future of Research in Cortisol DysregulationThe hypothalamic–pituitary–adrenal (HPA) axis is one of the most essential systems for maintaining physiological homeostasis and plays a central role in the stress response. Autonomous or excessive cortisol secretion leads to Cushing’s syndrome, whereas insufficient cortisol secretion results in adrenal insufficiency. Despite their clinical importance, globally unified diagnostic criteria for disorders of cortisol excess or deficiency are still lacking, and definitive diagnosis often requires invasive procedures and a high level of clinical expertise.
From a therapeutic standpoint, precisely replicating physiological cortisol secretion remains a major challenge. Chronotherapy—an approach that incorporates diurnal cortisol rhythmicity into treatment—has gained increasing attention in recent years. However, physiological cortisol secretion fluctuates dynamically under the influence of numerous factors, making it inherently difficult to delineate the boundary between “normal” and “pathological” states. Moreover, commonly used cortisol assays have several pitfalls, underscoring the need for biomarkers that more accurately reflect glucocorticoid action in vivo.
Recent advances also include the development of non-invasive wearable devices capable of real-time monitoring of cortisol secretion. In this lecture, I will present emerging concepts, diagnostic approaches, and therapeutic innovations related to disorders of cortisol dysregulation, and discuss future directions in this evolving field.
201DE
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Paraganglioma
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Akiyo TanabeJapan
Speaker
Update in Management of Pheochromocytoma and ParagangliomaPheochromocytoma and paraganglioma (PPGL) are rare endocrine neoplasms. Because it is difficult to predict the future development of metastasis based on biochemical testing or pathological findings, all PPGLs were reclassified as malignant tumors with metastatic potential in the revised 2017 WHO Classification of Endocrine Tumors. In Japan, the clinical practice guidelines for PPGL were revised in 2025. The diagnosis of PPGL requires the presence of tumors with characteristic findings. A definitive diagnosis is made based on elevated serum and urinary metanephrine fractions, positive tumor 123I-MIBG scintigraphy, and pathological findings in surgical cases. Measurement of plasma or urinary catecholamine fractions is no longer recommended because of its limited diagnostic accuracy; instead, measurement of plasma or urinary metanephrine fractions, which are metabolites of catecholamines, is currently recommended. Imaging modalities include computed tomography (CT), magnetic resonance imaging (MRI), and 123I-MIBG scintigraphy; however, 68Ga-DOTATATE positron emission tomography, which offers higher specificity and superior spatial resolution, is increasingly being used as an alternative to 123I-MIBG scintigraphy. The first-line treatment is tumor resection, regardless of whether metastasis is present or not. In patients at high surgical risk, catecholamine synthesis inhibitors (metyrosine) may be administered preoperatively in combination with α-adrenergic blockers. Because there is no clearly established effective therapy for metastatic disease, multidisciplinary management is required, combining debulking surgery to control catecholamine excess, systemic therapies such as CVD chemotherapy, 131I-MIBG therapy, and somatostatin receptor radionuclide therapy, as well as local treatments including external beam radiotherapy and transarterial embolization. Although tyrosine kinase inhibitors and immune checkpoint inhibitors have been investigated, their therapeutic efficacy remains limited. Even in patients with metastatic disease, active surveillance without immediate treatment —so-called watch and wait— may be a reasonable option for those with slow tumor growth, well-controlled catecholamine-related symptoms, and a low risk of local organ damage, with active treatment initiated upon evidence of disease progression. Pathogenic variants in PPGL-associated genes are identified in approximately 20–40% of patients, and variant-specific diagnostic and therapeutic algorithms are increasingly being proposed.
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Roderick Clifton-BlighAustralia
Speaker
What's New in the Adrenal Medulla?Phaeochromocytomas (PCs) are adrenal chromaffin cell tumours; paragangliomas (PGLs) are derived either from parasympathetic paraganglia of the skull base and neck (HNPGLs: glomus caroticum, jugulare, tympanicum and vagale) and anterior/middle mediastinum, or from sympathetic-associated chromaffin paraganglia in the abdomen, pelvis and (rarely) the posterior mediastinum. PCs and PGLs (collectively, PPGLs) present in myriad ways, often dependent upon their specific genetic alteration (either germline or somatic).
This talk will highlight many recent advances in diagnosis and treatment of PPGLs, including an update on biochemical assessment, structural and functional imaging, histology, genetics and treatment. Since there is no known prevention, early detection of tumors and surgical resection remains the only chance of cure. It follows that appropriate surveillance of patients with genetic PPGL predisposition is the most effective means to reduce morbidity and mortality in these syndromes, albeit with many potential challenges including cost, parental concern about testing children, burden of a lifetime surveillance program, and concerns about accessing insurance.
Treatment of metastatic PPGL remains challenging, albeit with recent trials showing modest efficacy of multikinase inhibitors (e.g. sunitinib and cabozantinib) or HIF2-targeted therapy (belzutifan). Radionuclide therapy with either MIBG or Lutate may be appropriate for patients with slowly progressive disease. Machine-learning algorithms can now identify patients with high risk of developing metastatic disease, opening the potential for clinical trials to test efficacy of adjuvant therapies.
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Wan-Chen WuTaiwan
Speaker
Genetics of Paragangliomas (Pheochromocytomas)Background: Pheochromocytomas and paragangliomas (PPGLs) represent the most heritable human neoplasms, with nearly 80% of cases now attributable to either germline or somatic driver mutations. As we move into 2026, the paradigm of PPGL management has shifted from symptomatic treatment to genotype-driven precision care. This presentation integrates global molecular advancements with a specific focus on the unique genetic signatures identified within the Asia-Oceania region, particularly highlighting recent discoveries from the Taiwan research team.
Molecular Classification and Pathway Signatures: Advanced multi-omics profiling has refined the classification of PPGLs into at least eight distinct molecular subtypes, primarily converging on three key signaling clusters: Pseudohypoxia (e.g., SDHx, VHL, FH), Kinase Signaling (e.g., RET, NF1, HRAS), and Wnt-Altered pathways (e.g., MAML3 fusions, CSDE1). Each cluster is characterized by a unique "molecular-clinical-biochemical-imaging" quadruple phenotype, which dictates tumor location, secretory profile, metastatic potential, and responsiveness to specific functional imaging modalities.
The Asia-Oceania Perspective and the Taiwan Experience: Emerging data suggest significant ethnic variations in the genetic architecture of PPGLs. While Sino-Caucasian comparative studies have identified a higher prevalence of HRAS and FGFR1 mutations in Chinese cohorts, pioneering research from the National Taiwan University Hospital (NTUH) team has unveiled critical local nuances. A defining feature of the Taiwanese genetic landscape is the identification of a notable founder effect in the SDHD gene, which distinguishes local patients from other East Asian populations. These findings, alongside multicenter data from Korea, underscore the necessity of population-specific diagnostic algorithms in the Asia-Pacific region.
Clinical Translation and Precision Management: The high prevalence of pathogenic variants -even in "apparently sporadic" or "incidental" presentations - mandates universal genetic testing for all PPGL patients. For those with initial negative results, longitudinal multigene panel retesting is essential as the list of susceptibility genes expands. Genotype-informed care now guides every facet of clinical practice, from personalized surveillance and the selection of functioning scan (such as 68Ga-DOTATATE PET/CT) to the application of targeted therapies (such as HIF-2α inhibitors).
Conclusion: By bridging global molecular frameworks with localized research, such as the SDHD founder effect observed in Taiwan, we can achieve a higher standard of precision medicine. As we convene for AOCE 2026 in Taipei, these insights emphasize the importance of regional collaboration and the implementation of specific screening strategies to optimize the long-term outcomes for PPGL patients across Asia and beyond.
201AF
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Diabetes Mellitus and Emerging Complications
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Kuo-Meng LiaoTaiwan
Speaker
Diabetes and Heart Failure: A Dual EpidemicDiabetes mellitus (DM) and heart failure (HF) are tightly interconnected disease states that interact through complex and bidirectional cardio-metabolic mechanisms. Among HF phenotypes, heart failure with preserved ejection fraction (HFpEF) shows the strongest association with DM, reflecting shared pathophysiological pathways beyond traditional ischemic heart disease.
Epidemiologically, DM confers a two- to four-fold increased risk of incident HF, with a disproportionate burden of HFpEF. Patients with HFpEF exhibit a high prevalence of DM and insulin resistance, accompanied by worse exercise intolerance, higher hospitalization rates, and increased mortality. These observations support the concept that DM is not merely a comorbidity but a central contributor to HFpEF pathogenesis.
Mechanistically, chronic hyperglycemia and insulin resistance initiate a cascade of systemic and myocardial abnormalities. Endothelial dysfunction, coronary microvascular inflammation, and impaired nitric oxide–cyclic GMP–protein kinase G signaling promote cardiomyocyte stiffness and diastolic dysfunction. Metabolic inflexibility, characterized by excessive fatty acid utilization and impaired glucose oxidation, reduces myocardial energetic efficiency. In parallel, advanced glycation end products, oxidative stress, mitochondrial dysfunction, and lipotoxicity drive myocardial fibrosis and adverse extracellular matrix remodeling. These myocardial changes are further amplified by extracardiac factors common in DM—obesity, chronic kidney disease, systemic inflammation, and autonomic imbalance—creating the multi-organ HFpEF syndrome.
Conversely, HF exacerbates insulin resistance through neurohormonal activation, inflammation, and skeletal muscle hypoperfusion, reinforcing a vicious cycle between metabolic and cardiac dysfunction. Recognition of this cross-talk has important therapeutic implications, as exemplified by sodium–glucose cotransporter 2 inhibitors, which improve HF outcomes through mechanisms extending beyond glucose lowering.
In summary, DM and HFpEF are linked through shared mechanistic pathways involving metabolism, microvascular dysfunction, and inflammation. A mechanistic understanding of this interaction is essential for developing integrated, phenotype-specific cardio-metabolic strategies.
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Jong-Ling FuhTaiwan
Speaker
Metabolic Dysfunction and Brain Health: Diabetes as a Risk Factor for DementiaType 2 Diabetes Mellitus (T2DM) is no longer confined to glucose dysregulation—it is a systemic accelerator of brain aging and a major modifiable risk factor for dementia. Epidemiologic and mechanistic studies reveal that poor glycemic control, including both hyper- and hypoglycemia, significantly increases dementia risk. Data from Taiwan’s National Health Insurance Database show that pronounced glycemic fluctuations more than double this risk, while meta-analyses identify prolonged diabetes duration, elevated HbA1c, hypertension, and insulin resistance as key predictors of cognitive decline.
Pathophysiological evidence links chronic hyperglycemia and insulin resistance to neuroinflammation, oxidative stress, and tau pathology. Neuroimaging studies show hippocampal atrophy and white matter degradation in patients with poorly controlled diabetes. Cardiovascular comorbidities amplify this burden: diabetes combined with coronary artery disease doubles the risk of vascular dementia.
Encouragingly, therapeutic innovation offers hope. Glucose-lowering agents such as GLP-1 Receptor Agonists (GLP-1RAs) and SGLT2 Inhibitors (SGLT2is) may extend their cardiometabolic benefits to the brain. GLP-1RAs have shown a 45% reduction in dementia risk in real-world and trial-based analyses, reinforcing the interconnectedness of metabolic, vascular, and neurodegenerative pathways.
In East Asia, where diabetes and dementia are surging, the clinical imperative is clear: brain health must be a core outcome of metabolic care. Early glycemic optimization, vascular protection, and neuroprotective therapies may define the next frontier in dementia prevention.
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Li-Pang ChuangTaiwan
Speaker
Sleep Apnea in Diabetes: A Silent AggravatorObstructive sleep apnea (OSA) is a highly prevalent clinical disease affecting more than 10% of the adult population. It is characterized by repetitive episodes of partial or total upper airway obstruction during sleep, resulting in subsequent sleep fragmentation and intermittent hypoxia. Accumulating studies reveal that OSA is an independent risk factor for consequent cardiovascular morbidities, such as myocardial infarction, heart failure, nocturnal dysrhythmias and pulmonary hypertension. Currently, OSA can be treated by means of positive airway pressure therapy, pharmacological therapy and surgical intervention.
OSA is a silent aggravator of diabetes because it worsens glucose metabolism and insulin resistance through mechanisms like intermittent hypoxia, sleep fragmentation, and sympathetic nervous system activation. This creates a bidirectional relationship where OSA increases the risk and severity of diabetes, and diabetes can worsen OSA. Treating OSA may improve glycemic control, and screening for it is crucial, especially in individuals with type 2 diabetes, particularly those who are obese.
3F Banquet Hall
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12:40
13:30
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Lunch Symposium 【Boehringer Ingelheim】
101
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Lunch Symposium 【Medtronic】
102
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Lunch Symposium 【Roche】
103
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Lunch Symposium 【Amgen】
201BC
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Lunch Symposium 【Daiichi Sankyo】
201DE
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Lunch Symposium 【Abbott】
201AF
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Lunch Symposium
3F Banquet Hall
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13:30
14:00
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Lee-Ling LimMalaysia
Speaker
Mechanistic Insights into the Gut–Liver–Brain Axis in MASLD: Metabolic Crosstalk and NeuroinflammationThe gut–liver–brain axis plays an important role in the pathogenesis and progression of metabolic dysfunction-associated steatotic liver disease (MASLD). Disruptions in gut microbiota, increased intestinal permeability, and microbial metabolites drive hepatic lipotoxicity and systemic inflammation. These hepatic signals, together with other metabolic dysfunctions, worsen neuroinflammatory responses and metabolic dysregulation. This lecture will discuss mechanistic links across the axis, and understanding these interconnected mechanisms offers opportunities to refine risk stratification and develop targeted interventions that address MASLD as a multisystem disease.Early-Onset Diabetes: Expanding the Spectrum of ComplicationsEarly-onset diabetes is increasing globally and is characterized by an accelerated trajectory of metabolic dysfunction. People diagnosed at a younger age experience a longer lifetime exposure to hyperglycaemia, adiposopathy, and inflammation, leading to an expanded spectrum of complications. Emerging evidence highlights earlier onset of kidney disease, heart failure, fatty liver disease, cognitive decline, and mental health disorders in this high-risk population. This lecture will synthesize current epidemiology, mechanistic insights, and evolving phenotypes, underscoring the urgent need for precision prevention, aggressive risk-factor modification, and integrated care models to reduce premature morbidity and mortality.
3F Banquet Hall
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Steven KahnUnited States
Speaker
Revisiting the β-cell: The Key to the Type 2 Diabetes PuzzleIncretin-Based Therapies: Lessons Learned Beyond Diabetes
102
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Case Challenges
Chih-Yuan WangTaiwan
Moderator
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.
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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.
201BC
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Pituitary
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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.
201DE
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Adrenal
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Hirotaka ShibataJapan
Speaker
2026 Update in Primary AldosteronismPrimary aldosteronism (PA) is one of the most prevalent causes for secondary hypertension. Early diagnosis and treatment are mandatory, because patients with PA present markedly higher morbidity of cardiovascular diseases than those with essential hypertension whose blood pressure levels are equally managed. A recently published Endocrine Society Clinical Practice Guideline of PA emphasizes several points. First, screening for PA with serum/plasma aldosterone concentration and plasma renin (concentration or activity) is recommended in all individuals with hypertension. Second, in individuals who screen positive for PA, aldosterone suppression testing is suggested when screening results suggest an intermediate probability for lateralizing PA, but not all cases. Third, in individuals with PA, medical therapy or surgical therapy with the choice of therapy based on lateralization of aldosterone hypersecretion and candidacy for surgery. Fourth, in individuals with PA considering surgery, adrenal lateralization with CT scanning and adrenal venous sampling prior to deciding the treatment approach is suggested. Fifth, in individuals with PA receiving PA-specific medical therapy, mineralocorticoid receptor antagonists (MRAs) are suggested as the dose is titrated by monitoring potassium, renal function, renin (concentration or activity) and blood pressure response during follow-up. We should be aware that diversity exists with respect to aldosterone assays, cut-off values for screening and aldosterone suppression tests, AVS standardization issues, and choice of MRAs depending on countries.
Diagnosis and Management of Adrenal InsufficiencyThe diagnosis and management of adrenal insufficiency presents major clinical challenges. It is often unrecognized, which can lead to adrenal crisis and, if not identified and treated, death. There is a lack of understanding on who is at risk of adrenal insufficiency, how to test for it, and how to manage a life threatening adrenal crisis promptly. While primary and secondary adrenal insufficiency can be regarded as rare conditions, glucocorticoid-induced adrenal insufficiency might be quite common. One should consider glucocorticoid withdrawal syndrome that may occur during glucocorticoid taper. Patient education in raising awareness of glucocorticoid withdrawal syndrome, such as fatigue and reduced appetite, is important when tapering glucocorticoid doses. The symptoms of glucocorticoid withdrawal syndrome may resemble adrenal insufficiency, but HPA axis is normally functional. The degree and persistence of adrenal suppression after cessation of glucocorticoid therapy are dependent on overall exposure and recovery of adrenal function varies greatly among individuals. Upcoming ICE2026/JES2026: Enlightened Endocrinology in Unprecedented TimesWe are pleased to announce that the 22nd International Congress of Endocrinology (ICE2026) and the 99th Annual Congress of the Japan Endocrine Society (JES2026) will be held together at the Kyoto International Conference Center (ICC Kyoto) over five days from June 2 (Tue) to 6 (Sat), 2026 (ICE2026/JES2026).
The International Congress of Endocrinology (ICE) is held every two years, and after 1988 and 2010, this will be the third time that the Congress will be held in Japan. The Japan Endocrine Society (JES) has been actively involved in the International Society of Endocrinology (ISE) since its establishment, and as the JES will celebrate its 100th anniversary in fiscal year 2026, hosting the congress in Japan will be an especially valuable opportunity for JES members.
The theme of ICE2026/JES2026 is: Enlightened Endocrinology in Unprecedented Times. Globally, we are entering an unprecedented era, including digitalization, which has been rapidly accelerated by the experience of the COVID-19 pandemic; a super-aging society, which is mainly faced by developed countries; and extreme weather events, as exemplified by global warming. In the midst of these unprecedented times, we will gather in Kyoto - the birthplace of the Japan Endocrine Society - to discuss the new century of clinical and basic research in various fields of endocrinology.
Participants from all over the world are encouraged to present cutting-edge science from their respective countries, and through active discussions, we hope that you will experience the “Enlightened Endocrinology” of endocrinology in this unprecedented era.
In June, flowers bloom profusely at shrines and temples in Kyoto with the blessings of water, and shrine gardens and hydrangea gardens are open to the public.
We look forward to welcoming participants from all over the world to Kyoto - the ancient capital of Japan - and discussing the future of endocrinology!
201AF
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14:00
15:30
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Digital Endocrinology, Wearables, and Future Therapeutics in Asia
Yi-Sun YangTaiwan
Moderator
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.
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Jun-Sing WangTaiwan
Speaker
Continuous Glucose Monitoring (CGM) in Asia: Behavior Change, Physician Workflow, and New Care Models
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Chee Keong SeeMalaysia
Speaker
AI and Digital Diabetes Care: Awareness, Utilisation and Perspectives from Malaysia
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Yen Bo LinTaiwan
Speaker
Next-Generation Biomarkers for Thyroid Cancer and Endocrine Tumors
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Siew Hui FooMalaysia
Speaker
Future Endocrine Therapeutics in Southeast Asia: From Super Mono, Dual to Triple Incretin Agonists and BeyondThe role of incretin-based therapy is taking the front seat globally due to the high prevalence of obesity, diabetes and related complications worldwide. Similar scene is expected to take place in South East Asia that is facing the escalating burden of obesity driving up the already high burden of type 2 diabetes especially in the younger population despite consisting of relatively small countries in areas and population. This poses adverse socio-economic impact to the region due to increased risk of premature complications and death among the young in a region that is largely still developing.
The arrival of incretin-based therapy into South East Asia since the first daily glucagon-like peptide-1 receptor agonist (GLP-1 RA) injection in 2010 has picked up its pace in the last 5 years with the entry of weekly GLP-1 RA injection, oral GLP-1 RA and GLP-1 RA / GIP (glucose-dependent insulinotropic polypeptide) injection. This lecture will address the evidence behind its efficacy, tolerability as well as cardiovascular effects of these agents in the Asian populations. The future shift to the more potent high-dose GLP-1 receptor mono-agonist, dual, triple incretin receptor multi-agonist and beyond as these agents are approved for treatment for the twin epidemics of type 2 diabetes, obesity and related complications will be discussed along with the challenges especially on unequitable access, healthcare disparities, unregulated dispensing and the importance of a strengthened health system with multi-sectoral cooperation at the regional level to mitigate these issues.
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103
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Hiroshi ArimaJapan
Speaker
Network of AOCE could contribute to the development of ISEThe mission of the International Society of Endocrinology (ISE) is to promote endocrine and metabolic science, education, practice and advocacy worldwide. Around 50 national endocrine societies and 27, 000 representatives belong to the ISE, around 50% of whom are from Asia and Oceania countries. The number of board members in the ISE is proportional to that of membership in each region. Thus, Asian and Oceanian Endocrine societies play an important role in the ISE.
I had served as the president of the Japan Endocrine Society (JES) from 2021 to 2025. During the period, the Korean Endocrine Society (KES) and JES signed the memorandum of understanding, and we just published the Guideline for Cushing disease this year, which were published in Endocrine and Metabolism and Endocrine Journal, the official journals of the KES and JES, respectively. I believe we should extend the collaboration between the KES and JES to other societies in Asian and Oceania Endocrine Society, which will lead to the development of the ISE.
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Hirotaka ShibataJapan
Speaker
2026 Update in Primary AldosteronismPrimary aldosteronism (PA) is one of the most prevalent causes for secondary hypertension. Early diagnosis and treatment are mandatory, because patients with PA present markedly higher morbidity of cardiovascular diseases than those with essential hypertension whose blood pressure levels are equally managed. A recently published Endocrine Society Clinical Practice Guideline of PA emphasizes several points. First, screening for PA with serum/plasma aldosterone concentration and plasma renin (concentration or activity) is recommended in all individuals with hypertension. Second, in individuals who screen positive for PA, aldosterone suppression testing is suggested when screening results suggest an intermediate probability for lateralizing PA, but not all cases. Third, in individuals with PA, medical therapy or surgical therapy with the choice of therapy based on lateralization of aldosterone hypersecretion and candidacy for surgery. Fourth, in individuals with PA considering surgery, adrenal lateralization with CT scanning and adrenal venous sampling prior to deciding the treatment approach is suggested. Fifth, in individuals with PA receiving PA-specific medical therapy, mineralocorticoid receptor antagonists (MRAs) are suggested as the dose is titrated by monitoring potassium, renal function, renin (concentration or activity) and blood pressure response during follow-up. We should be aware that diversity exists with respect to aldosterone assays, cut-off values for screening and aldosterone suppression tests, AVS standardization issues, and choice of MRAs depending on countries.
Diagnosis and Management of Adrenal InsufficiencyThe diagnosis and management of adrenal insufficiency presents major clinical challenges. It is often unrecognized, which can lead to adrenal crisis and, if not identified and treated, death. There is a lack of understanding on who is at risk of adrenal insufficiency, how to test for it, and how to manage a life threatening adrenal crisis promptly. While primary and secondary adrenal insufficiency can be regarded as rare conditions, glucocorticoid-induced adrenal insufficiency might be quite common. One should consider glucocorticoid withdrawal syndrome that may occur during glucocorticoid taper. Patient education in raising awareness of glucocorticoid withdrawal syndrome, such as fatigue and reduced appetite, is important when tapering glucocorticoid doses. The symptoms of glucocorticoid withdrawal syndrome may resemble adrenal insufficiency, but HPA axis is normally functional. The degree and persistence of adrenal suppression after cessation of glucocorticoid therapy are dependent on overall exposure and recovery of adrenal function varies greatly among individuals. Upcoming ICE2026/JES2026: Enlightened Endocrinology in Unprecedented TimesWe are pleased to announce that the 22nd International Congress of Endocrinology (ICE2026) and the 99th Annual Congress of the Japan Endocrine Society (JES2026) will be held together at the Kyoto International Conference Center (ICC Kyoto) over five days from June 2 (Tue) to 6 (Sat), 2026 (ICE2026/JES2026).
The International Congress of Endocrinology (ICE) is held every two years, and after 1988 and 2010, this will be the third time that the Congress will be held in Japan. The Japan Endocrine Society (JES) has been actively involved in the International Society of Endocrinology (ISE) since its establishment, and as the JES will celebrate its 100th anniversary in fiscal year 2026, hosting the congress in Japan will be an especially valuable opportunity for JES members.
The theme of ICE2026/JES2026 is: Enlightened Endocrinology in Unprecedented Times. Globally, we are entering an unprecedented era, including digitalization, which has been rapidly accelerated by the experience of the COVID-19 pandemic; a super-aging society, which is mainly faced by developed countries; and extreme weather events, as exemplified by global warming. In the midst of these unprecedented times, we will gather in Kyoto - the birthplace of the Japan Endocrine Society - to discuss the new century of clinical and basic research in various fields of endocrinology.
Participants from all over the world are encouraged to present cutting-edge science from their respective countries, and through active discussions, we hope that you will experience the “Enlightened Endocrinology” of endocrinology in this unprecedented era.
In June, flowers bloom profusely at shrines and temples in Kyoto with the blessings of water, and shrine gardens and hydrangea gardens are open to the public.
We look forward to welcoming participants from all over the world to Kyoto - the ancient capital of Japan - and discussing the future of endocrinology!
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101
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Insulin Therapy Across the Spectrum of Diabetes
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Ju-Ying JiangTaiwan
Speaker
When, What, and How: Practical Approaches to Insulin Use in Type 2 DiabetesPractical insulin use in type 2 diabetes (T2D) requires clear decisions on when to start therapy, what regimen to choose, and how to titrate effectively. Insulin is indicated when lifestyle measures and non-insulin medications fail to achieve glycemic goals, especially when Hba1c is ≥10%, fasting glucose is >250–300 mg/dL, or when patients show symptomatic hyperglycemia or catabolic features. Insulin is also required during acute illness, surgery, pregnancy, or corticosteroid use.
Basal insulin remains the preferred first step due to its simplicity and lower hypoglycemia risk. Long-acting insulin analogues such as Glargine or Degludec are commonly initiated at 10 units or 0.1–0.2 U/kg/day with stepwise titration. When additional blood sugar control is needed, options include adding a GLP-1 receptor agonist, moving to basal-plus or basal-bolus regimens, or using premixed insulin for patients with fixed routines.
Importantly, once-weekly basal insulin formulations—such as insulin icodec—are emerging as a future option, offering flatter pharmacokinetics and the potential to improve adherence by reducing injection frequency. These agents may simplify initiation and long-term management for patients hesitant about daily injections.
Overall, individualized regimen selection, structured titration, and patient-centered education remain essential for safe and effective insulin therapy.
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Jia-Hong LinTaiwan
Speaker
The New Era of Insulin Therapy: Ultra-Long Acting, Smart Delivery, and BeyondInsulin therapy is entering a transformative era driven by innovations in pharmacology, delivery systems, and data integration, fundamentally reshaping diabetes management. The development of ultra-long-acting basal insulin analogues has markedly improved glycemic stability by providing flatter, more predictable pharmacokinetic and pharmacodynamic profiles with extended duration of action. These agents reduce glycemic variability, lower the risk of nocturnal and overall hypoglycemia, and allow greater dosing flexibility, thereby improving treatment adherence and quality of life for people with diabetes.
Beyond molecular advances, smart insulin delivery technologies are redefining how insulin is administered and titrated. Continuous subcutaneous insulin infusion (CSII) systems integrated with continuous glucose monitoring (CGM) have evolved into automated insulin delivery (AID) or hybrid closed-loop systems that dynamically adjust basal insulin and deliver correction boluses based on real-time glucose data. These systems consistently demonstrate superior time-in-range, reduced hypoglycemia, and decreased patient burden compared with conventional multiple daily injections or sensor-augmented pump therapy. Increasingly, algorithm refinement, interoperability, and personalization are enabling broader clinical applicability across age groups and diabetes phenotypes.
Collectively, these advances signal a paradigm shift from reactive glucose control toward proactive, personalized, and technology-enabled insulin therapy. The integration of ultra-long-acting insulins, smart delivery systems, and digital innovations promises to further improve glycemic outcomes, safety, and patient-centered care in the management of diabetes.
102
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Hormone Therapy in Transgenders
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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.
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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.
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201BC
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Acromegaly
Naoko InoshitaJapan
Moderator
Consensus in Pituitary Pathology: Impact after New Classification for JapanIn Japan, the brain tumor handling rules are essentially based on the WHO classification. However, the introduction of the term pituitary neuroendocrine tumour (PitNET) has occasionally led to misunderstanding in clinical practice, particularly regarding the implication of malignancy.
In this lecture, I will present a consensus-oriented approach in pituitary pathology, focusing on practical strategies developed through multidisciplinary collaboration for the benefit of clinicians and patients. First, I will show how the addition of touch smear cytology to frozen section diagnosis during surgery can improve the accuracy of margin assessment and increase the likelihood of achieving the intended surgical goal, including adequate removal of hormone-producing tumours. Second, I will emphasize that truly malignant PitNETs are extremely rare, and that the term “NET” should not be equated with malignancy. Third, I will discuss the well-known discrepancy between hormone immunohistochemistry and clinical functionality, highlighting the importance of careful pathological interpretation.
These perspectives reflect our pathology team’s commitment to accurate communication and clinically relevant pathological diagnosis.
Szu-Tah ChenTaiwan
Moderator
The Impact of the 2022 WHO PitNET Classification to the Clinical Practitioners. Does Silence Equal Acceptance?The 2022 World Health Organization (WHO) Classification of Endocrine and Neuroendocrine Tumors redefined pituitary adenomas as pituitary neuroendocrine tumors (PitNETs) within the International Classification of Diseases for Oncology, 3rd Edition (ICD-O/3). This change reflects updated insights into tumor biology, recognizing a spectrum of clinical behaviors beyond the traditionally benign designation.
A narrative review of the WHO 2022 classification updates was conducted, focusing on their clinical, diagnostic, and epidemiologic implications for practitioners in endocrinology, neurosurgery, and oncology.
The reclassification emphasizes the potential for variability in tumor aggressiveness, recurrence, and invasiveness. Clinically, this shift necessitates more careful risk stratification, closer follow-up in selected cases, and a reassessment of treatment algorithms. From a reporting perspective, ICD-O/3 alignment may affect cancer registry data and epidemiologic tracking, altering disease burden estimates. Importantly, the new terminology presents challenges in patient communication, as the label “neuroendocrine tumor” may cause undue anxiety despite the indolent nature of most PitNETs.
The WHO 2022 reclassification of pituitary adenomas as PitNETs represents a significant change for clinical practice. While it enhances awareness of potential aggressive behavior, it also requires balanced application in patient care to avoid overtreatment and misperceptions. Practitioners must adapt by refining diagnostic vigilance, tailoring follow-up strategies, and delivering clear patient-centered communication.
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Harn-Shen ChenTaiwan
Speaker
Acromegaly and Cardiovascular Disease: The Research in Taipei Veterans General HospitalAcromegaly, characterized by chronic excess growth hormone (GH) and elevated insulin-like growth factor-1 (IGF-1), is associated with increased morbidity and premature mortality, particularly from cardiovascular (CV) complications. Research from Taipei Veterans General Hospital (Taipei VGH) over the past decade has systematically examined how biochemical control, metabolic status, and cardiac function influence patient outcomes, forming a comprehensive institutional understanding of acromegaly-related CV risk.
Early studies established the prognostic importance of postoperative hormonal normalization following trans-sphenoidal adenomectomy (TSA). Patients achieving stringent biochemical remission demonstrated markedly reduced long-term mortality, whereas persistent GH/IGF-1 elevation remained a strong predictor of premature death. Even partial hormonal improvement provided measurable survival benefit, highlighting the need for aggressive management and close monitoring after surgery.
Subsequent work addressed the metabolic impact of medical therapy, particularly long-acting octreotide. While effective in reducing GH/IGF-1 levels, somatostatin analogs impaired insulin secretion and frequently worsened glucose tolerance. These findings underscore the need to balance biochemical control with careful metabolic surveillance, especially in patients with preexisting glucose abnormalities.
In 2020, a nationwide epidemiological study expanded the perspective by detailing incidence, comorbidities, re-operation rates, cancer risk, and mortality trends across Taiwan. Despite modern advances, patients with acromegaly continued to exhibit elevated mortality—predominantly from CV and malignant causes—reinforcing the significance of early diagnosis and rigorous long-term management.
Complementing epidemiologic insights, a focused clinical study demonstrated that successful surgical remission led to significant improvements in traditional CV risk factors, including reductions in HbA1c, LDL cholesterol, total cholesterol, and blood pressure one year after TSA. These benefits were most pronounced in patients with normalized IGF-1.
The most recent study linked degrees of biochemical control to cardiac structure and function. Patients with uncontrolled or partially controlled acromegaly exhibited increased left ventricular mass and impaired diastolic function, indicating early acromegalic cardiomyopathy even when systolic function remained preserved.
Collectively, the Taipei VGH research program highlights that full biochemical remission is essential not only for reducing mortality but also for reversing metabolic abnormalities and preventing progressive cardiac dysfunction.
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Cheol Ryong KuSouth Korea
Speaker
Medication Management for AcromegalyPharmacological management of acromegaly plays a central role in patients with persistent disease following surgery; however, treatment strategies vary substantially across countries due to differences in healthcare systems and reimbursement policies. Understanding real-world approaches within specific national frameworks provides valuable insight into optimizing long-term disease control. This lecture aims to present the Korean reimbursement-based treatment algorithm for acromegaly and share institutional clinical outcomes using contemporary medical therapies, including pasireotide, pegvisomant, and lanreotide autogel with extended dosing interval (EDI) strategies. In addition, emerging therapeutic candidates under development at our institution will be briefly introduced.
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Michio OtsukiJapan
Speaker
Acromegaly: GH Response Pattern to Oral Glucose Load and Personalized MedicineAcromegaly is characterized by elevated levels of growth hormone (GH) and insulin-like growth factor-1 (IGF-1), with resultant signs and symptoms of hypersomatotropism. To examine autonomous secretion of GH, an oral glucose tolerance test (OGTT) is used. In most healthy individuals, GH levels decrease to a nadir below 0.4 mg/L after OGTT. In contrast, patients with acromegaly fail to suppress serum GH levels after OGTT. Interestingly, a paradoxical GH response to oral glucose (OG) load is found in one third of acromegalic patients. The mechanism of this paradoxical response in acromegaly is mediated by glucose-dependent insulinotropic polypeptide, which is released after OG administration
We found that the paradoxical GH response to OG load reflected the clinical characteristics. The patients the paradoxical GH response to OG load (OG responders) had substantially greater IGF-1 SD scores than nonresponders. Regarding glucose metabolism, 120-minute plasma glucose and immunoreactive insulin after OG administration and hemoglobin A1c were significantly greater in OG responders than in nonresponders. GH levels during octreotide or bromocriptine testing were decreased more significantly in OG responders than in nonresponder. The proportion of pituitary tumors with hypointensity on T2-weighted MRI was significantly greater in OG responders than in nonresponders.
OGTT is essential to evaluate autonomous secretion of GH. The paradoxical GH response to OG load is the useful for evaluation of the clinical characteristics of acromegaly and leads to the personalized medicine of acromegaly.
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Iris Isip-TanPhilippines
Speaker
AI applications and insulin managementArtificial intelligence is evolving from novel research concepts to practical clinical tools. This presentation will provide a broad overview of the current AI ecosystem, from automated insulin delivery (AID) systems to machine learning algorithms designed for glucose prediction and clinical decision support. The unique regional perspective will be addressed, exploring how diverse healthcare infrastructures and reimbursement models influence the adoption of AI innovations. The discussion will conclude by identifying key challenges in implementation, such as algorithmic equity and data security, to outline a framework for the future integration of AI into daily practice.
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I-Wen WuTaiwan
Speaker
AI-Assisted Discovery of Omic Signature in Diabetic Kidney DiseaseDiabetic kidney disease (DKD) is a leading cause of chronic kidney disease and end-stage renal disease, posing significant global health and economic burdens. Traditional management of DKD relies on standardized approaches, which often fail to account for the complexity of individual patient profiles.
Precision medicine leverages individualized patient data—spanning genetic, proteomic, metabolic, and clinical information—to optimize diagnosis, risk assessment, and therapeutic interventions. However, translating this paradigm into clinical practice presents significant challenges and opportunities.
This presentation focuses on the practical aspects of integrating precision medicine into DKD management. Key themes include the role of genetic and epigenetic biomarkers in risk stratification, the integration of multi-omics data with machine learning for predictive modeling and the design of personalized treatment regimens using tools such as pharmacogenomics.
By examining real-world implementation strategies and overcoming barriers, this presentation aims to guide healthcare providers, researchers, and policymakers toward a sustainable and patient-centered precision medicine framework for DKD.
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Dee PeiTaiwan
Speaker
The roles of Machine Learning in Medical ResearchArtificial intelligence (AI) is fundamentally transforming clinical research by democratizing access to advanced analytical tools and establishing new standards for scientific publication. This presentation outlines a comprehensive framework for integrating machine learning (ML) methodologies into clinical studies—from raw data preparation to manuscript submission—while addressing critical challenges in model development, validation, and interpretation. We emphasize that financial barriers to sophisticated analysis have largely dissolved with the advent of open-source AI platforms, enabling researchers to move beyond legacy statistical software toward reproducible, transparent ML pipelines.
The workflow begins with strategic data preparation, including appropriate imputation techniques (k-NN, MissForest, MICE) and feature standardization. For binary classification tasks—common in clinical prediction—It is advocate a rigorous protocol encompassing stratified cross-validation, hyperparameter tuning via nested CV, and explicit overfitting controls (regularization, feature limitation to ≥10 events per variable). Model selection should prioritize algorithms matching the clinical question: logistic regression for interpretability, random forests for robust baselines, and gradient boosting for maximal performance—while acknowledging trade-offs in complexity and calibration risk.
Evaluation must extend beyond conventional ROC-AUC to include precision-recall curves (especially for imbalanced data), calibration assessment (slope ~1, intercept ~0), Brier score, and decision curve analysis for clinical utility. SHAP values provide essential interpretability for "black-box" models, translating complex predictions into clinically actionable insights. Crucially, it is stressed that accuracy alone is misleading in medical contexts; minimizing false negatives often carries greater clinical consequence than overall accuracy.
Reproducibility demands fixed random seeds, complete pipeline documentation, and packaging preprocessing steps with final models for deployment. As journals increasingly expect ML-enhanced analyses, studies relying solely on traditional statistics face diminished publication prospects. It is concluded that AI integration is no longer optional but essential for contemporary clinical research seeking impact, rigor, and real-world applicability in an era where algorithmic insight complements—not replaces—clinical expertise.
3F Banquet Hall
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15:30
16:00
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18:00
20:00
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Faculty Dinner (By Invitation Only)
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