[Symposium] Pituitary (2)
22 Mar 2026
11:00
12:30
201DE
Cushing’s Disease and Cushing’s Syndrome
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11:00
11:30
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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.
201DE
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11:30
12:00
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Seung Shin ParkSouth Korea
Speaker
Treatment of Recurrence/Persistence of Cushing Disease: Role of Medical TherapyCushing’s disease (CD) remains a challenging disorder despite advances in pituitary surgery, as a substantial proportion of patients experience persistent or recurrent hypercortisolism following initial treatment. In these clinical settings, medical therapy has emerged as a central component of disease management. Recent international collaborative efforts, including a joint consensus statement developed by the Korean Endocrine Society and the Japan Endocrine Society, emphasize the expanding role of pharmacologic treatment across multiple stages of CD care.
This lecture provides a practical overview of contemporary medical therapies for persistent or recurrent CD based on a mechanism-oriented framework. Tumor-directed therapies aimed at suppressing adrenocorticotropic hormone secretion, including cabergoline and pasireotide, will be discussed in the context of patient selection and regional practice differences. Adrenal-directed steroidogenesis inhibitors—particularly osilodrostat, ketoconazole, and metyrapone—will be reviewed with emphasis on clinical positioning, efficacy, and safety considerations. In addition, the unique therapeutic role of glucocorticoid receptor antagonism with mifepristone will be highlighted, focusing on indications and monitoring challenges distinct from cortisol-lowering therapies.
Special attention will be given to real-world treatment strategies, including drug selection, combination therapy, and region-specific clinical considerations in Asian populations. Key concepts from the upcoming treatment consensus will be integrated to provide a clinically applicable framework for individualized management.
This session aims to offer a practical, consensus-informed approach to optimizing medical therapy in patients with persistent or recurrent Cushing’s disease.
201DE
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|
12:00
12:30
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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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