| Time |
Session |
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08:30
09:10
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09:10
09:50
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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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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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103
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Perspectives on Obesity in Asia-Oceania
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 Neuropathy
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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 Taiwan
201BC
|
Cushing’s Disease and Cushing’s Syndrome
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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
|
|
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 13
3F Banquet Hall
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13:30
14:00
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|
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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
|
Adrenal
-
Hirotaka ShibataJapan
Speaker
2026 Update in Primary AldosteronismDiagnosis and Management of Adrenal Insufficiency
201AF
|
|
14:00
15:30
|
Digital Endocrinology, Wearables, and Future Therapeutics in Asia
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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-based Insulin Titration & Digital Diabetes Care: Malaysia and Southeast Asia Experience
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Albert LinTaiwan
Speaker
Next-Generation Biomarkers for Thyroid Cancer and Endocrine Tumors
-
Siew Hui FooMalaysia
Speaker
Future Endocrine Therapeutics in Southeast Asia: From Super Mono, Dual to Triple Incretin Agonists and Beyond
-
103
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From AOCE to ISE: Mutual Collaboration
101
|
Insulin Therapy Across the Spectrum of Diabetes
-
-
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 Lin
Speaker
The New Era of Insulin Therapy: Ultra-Long Acting, Smart Delivery, and Beyond
102
|
Hormone Therapy in Transgenders
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Wayne Wing Ki TangHong Kong, China
Speaker
Management of Transgender Individuals: Psychiatrist PerspectivesThe psychiatrist plays a fundamental role in the care pathway for transgender and gender-diverse individuals, often providing supportive assessment and mental health care alongside the initiation of hormone therapy. This presentation outlines the key psychiatric considerations in managing this population, providing a complementary perspective to the endocrinologist's work within real-world, 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 gender incongruence and any dysphoria-related distress, supporting informed consent and shared decision-making, and identifying psychiatric comorbidities or psychosocial stressors that may benefit from parallel 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 physical congruence improves with hormonal treatment, psychological well-being is often more closely linked to psychosocial factors.
The session concludes by exploring how psychiatrists and endocrinologists can collaborate to support patients who face ongoing psychosocial stressors, ensuring a safe and sustainable transition process.
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-
201BC
|
Acromegaly
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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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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.
201DE
|
-
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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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201AF
|
-
-
I-Wen WuTaiwan
Speaker
AI-Assisted Discovery of Omic Signature in Diabetic Kidney Disease
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Dee Pei
Speaker
Applications of Machine Learning in Medical Research
3F Banquet Hall
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|
15:30
16:00
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|
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18:00
20:00
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Faculty Dinner (By Invitation Only)
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