The management of endogenous Cushing’s syndrome (CS) typically involves two key steps: (i) confirmation of autonomous hypercortisolism and (ii) localization of the cause to guide treatment. Adrenocorticotropic hormone (ACTH)-dependent CS is most commonly due to a pituitary corticotrope tumor which may be so small as to evade detection on conventional magnetic resonance imaging (MRI). Although biochemical testing (e.g., corticotropin stimulation; dexamethasone suppression) can provide an indication of the likely origin of ACTH excess, bilateral inferior petrosal sinus catheterization offers greater accuracy to distinguish pituitary-driven CS [Cushing’s Disease (CD)] from the ectopic ACTH syndrome [EAS, e.g., due to a bronchial or pancreatic neuroendocrine tumor (NET)]. In patients with CD, 40–50% may not have a pituitary adenoma (PA) readily visualized on standard clinical MRI. In these subjects, alternative MR sequences (e.g., dynamic, volumetric, fluid attenuation inversion recovery) and higher magnetic field strength (7T>3T>1.5T) may aid tumor localization but carry a risk of identifying coincidental (non-causative) pituitary lesions. Molecular imaging is therefore increasingly being deployed to detect small ACTH-secreting PA, with hybrid imaging [e.g., positron emission tomography (PET) combined with MRI] allowing precise anatomical localization of sites of radiotracer (e.g., ¹¹C-methionine) uptake. Similarly, small ACTH-secreting NETs, missed on initial cross-sectional imaging, may be detected using PET tracers targeting abnormal glucose metabolism (e.g., ¹⁸F-fluorodeoxyglucose), somatostatin receptor (SSTR) expression (e.g., ⁶⁸Ga-DOTATATE), amine precursor (e.g., ¹⁸F-DOPA) or amino acid (e.g., ¹¹C-methionine) uptake. Therefore, modern management of ACTH-dependent CS should ideally be undertaken in specialist centers which have an array of cross-sectional and functional imaging techniques at their disposal.

内源性库欣综合症（CS）的治疗通常涉及两个关键步骤：（i）确认自主性高皮质功能亢进和（ii）确定病因以指导治疗。促肾上腺皮质激素（ACTH）依赖的CS最常见是由于垂体皮质激素瘤引起的，其可能很小，以至于无法通过常规磁共振成像（MRI）进行检测。尽管生化检查（例如促肾上腺皮质激素刺激，地塞米松抑制）可提供可能的ACTH过量的迹象，但双侧下颌窦窦导管插入术可更好地区分垂体驱动的CS [Cushing's Disease（CD）]与异位ACTH综合征[例如，由于支气管或胰腺神经内分泌肿瘤（NET）引起的EAS]。在患有CD的患者中，40–50％的垂体腺瘤（PA）可能无法在标准的MRI上轻易观察到。在这些受试者中，替代性MR序列（例如，动态，体积，液体衰减倒置恢复）和更高的磁场强度（7T> 3T> 1.5T）可能有助于肿瘤定位，但存在识别偶然性（非致因性）垂体病变的风险。因此，越来越多的分子成像技术被用于检测分泌出少量ACTH的PA，而混合成像技术（例如，与MRI相结合的正电子发射断层扫描（PET））可实现放射性示踪剂部位的精确解剖定位（例如，5T）可能有助于肿瘤定位，但冒着鉴别巧合性（非致病性）垂体病变的风险。因此，越来越多的分子成像技术被用于检测分泌出少量ACTH的PA，而混合成像技术（例如，与MRI相结合的正电子发射断层扫描（PET））可实现放射性示踪剂部位的精确解剖定位（例如，5T）可能有助于肿瘤定位，但冒着鉴别巧合性（非致病性）垂体病变的风险。因此，越来越多的分子成像技术被用于检测分泌出少量ACTH的PA，而混合成像技术（例如，与MRI相结合的正电子发射断层扫描（PET））可实现放射性示踪剂部位的精确解剖定位（例如，¹¹ C-蛋氨酸）摄取。类似地，可以使用针对异常葡萄糖代谢（例如¹⁸ F-氟脱氧葡萄糖），生长抑素受体（SSTR）表达（例如⁶⁸ Ga-DOTATATE）的PET示踪剂检测在初始横截面成像中遗漏的小的ACTH分泌网。胺前体（例如¹⁸ F-DOPA）或氨基酸（例如¹¹ C-蛋氨酸）摄取。因此，理想情况下，应该在具有各种横截面和功能成像技术的专科中心对依赖ACTH的CS进行现代管理。