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M S Elston, V B Crawford, M Swarbrick, M S Dray, M Head, and J V Conaglen

* Died shortly after first dose. AdenoCa, prostate adenocarcinoma; CS, Cushing’s syndrome; dx, diagnosis; hx, history; MR, mineralocorticoid. Of the reported cases of CS associated with SCPC most are due to ectopic ACTH production ( 24

Open access

Boni Xiang, Ran Tao, Xinhua Liu, Xiaoming Zhu, Min He, Zengyi Ma, Yehong Yang, Zhaoyun Zhang, Yiming Li, Zhenwei Yao, Yongfei Wang, and Hongying Ye

Introduction Cushing’s syndrome (CS) comprises diverse manifestations resulting from chronic exposure to excess glucocorticoids. The incidence is 0.2–5.0 per million people per year. Approximately 80% of endogenous CS is adrenocorticotrophin

Open access

Soraya Puglisi, Paola Perotti, Mattia Barbot, Paolo Cosio, Carla Scaroni, Antonio Stigliano, Pina Lardo, Valentina Morelli, Elisa Polledri, Iacopo Chiodini, Giuseppe Reimondo, Anna Pia, and Massimo Terzolo

Introduction Cushing’s syndrome (CS) is a condition of endogenous hypercortisolism caused by different pathological entities that is classified in two variants: (i) ACTH-dependent CS, due to a corticotroph pituitary adenoma or an ectopic tumor

Open access

Jingya Zhou, Meng Zhang, Lin Lu, Xiaopeng Guo, Lu Gao, Weigang Yan, Haiyu Pang, Yi Wang, and Bing Xing

Introduction Endogenous Cushing’s syndrome (CS) comprises signs and symptoms caused by pathological hypercortisolism, which seriously affects the metabolic and endocrine systems. Endogenous CS is divided between adrenocorticotropic hormone

Open access

Carla Scaroni, Nora M Albiger, Serena Palmieri, Davide Iacuaniello, Chiara Graziadio, Luca Damiani, Marialuisa Zilio, Antonio Stigliano, Annamaria Colao, Rosario Pivonello, and the Altogether to Beat Cushing’s Syndrome (ABC) study group

( 2 ). Under such conditions, there may be some clinical signs of hypercortisolism, which may be temporary or more persistent, giving rise to what is called pseudo-Cushing’s syndrome (PCS). The differential diagnosis of PCS and Cushing’s syndrome (CS

Open access

Benedetta Zampetti, Erika Grossrubatscher, Paolo Dalino Ciaramella, Edoardo Boccardi, and Paola Loli

ACTH-dependent hypercortisolism is highly suggestive of pituitary disease, this is not true for smaller lesions that still might be incidentaloma ( 16 , 17 ). The Consensus Statement on Diagnosis and Complications of Cushing’s Syndrome suggests 6mm as

Open access

Majunath R Goroshi, Swati S Jadhav, Anurag R Lila, Rajeev Kasaliwal, Shruti Khare, Chaitanya G Yerawar, Priya Hira, Uday Phadke, Hina Shah, Vikram R Lele, Gaurav Malhotra, Tushar Bandgar, and Nalini S Shah

Introduction Ectopic adrenocorticotrophic hormone (ACTH) syndrome (EAS) is a rare disorder, accounting for 5–15% cases of endogenous Cushing’s syndrome (CS) ( 1 , 2 ). Although initially construed to be caused by malignant tumours (such as

Open access

Kush Dev Singh Jarial, Anil Bhansali, Vivek Gupta, Paramjeet Singh, Kanchan K Mukherjee, Akhilesh Sharma, Rakesh K Vashishtha, Suja P Sukumar, Naresh Sachdeva, and Rama Walia

Introduction The differential diagnosis of ACTH-dependent Cushing’s syndrome (CS) as pituitary or ectopic source of ACTH production is often challenging for the physicians as none of the biochemical tests or imaging modalities have 100

Open access

Grethe A. Ueland, Thea Grinde, Paal Methlie, Oskar Kelp, Kristian Løvås, and Eystein Husebye

Objective: Autonomous cortisol secretion (ACS) is a condition with ACTH-independent cortisol overproduction from adrenal incidentalomas (AI) or adrenal hyperplasia. The hypercortisolism is often mild, and most patients lack typical clinical features of overt Cushing’s syndrome (CS). ACS is not well defined and diagnostic tests lack validation.

Methods: Retrospective study of 165 patients with AI evaluated clinically and by assay of morning plasma ACTH, late-night saliva cortisol, serum dehydroepiandrosterone sulphate (DHEAS), 24-hour urine free cortisol, and cortisol after dexamethasone suppression.

Results: Patients with AI (n=165) were diagnosed as non-functioning incidentalomas (NFI) (n = 82) or ACS (n = 83) according to current European guidelines. Late-night saliva cortisol discriminated poorly between NFI and ACS showing a high rate of false positive (37 %) and false negative (54 %) results. The conventional low dose dexamethasone suppression test (LDDST) did not improve the diagnostic specificity, compared with the 1 mg overnight DST. Receiver operating characteristic curve analysis of DHEAS in the two cohorts demonstrated an area under the curve of 0.76 (p<0.01) with a sensitivity for ACS of 58% and a specificity of 80% using the recommended cutoff at 1.04 µmol/L (40 µg/dL).

Conclusion: We here demonstrate in a large retrospective cohort of incidentaloma patients, that neither DHEAS, late night saliva cortisol nor 24-hour urine free cortisol are useful to discriminate between non-functioning adrenal incidentalomas and ACS. The conventional LDDST do not add further information compared with the 1 mg overnight DST. Alternative biomarkers are needed to improve the diagnostic workup of ACS.

Open access

Filippo Ceccato, Diego Cecchin, Michele Gregianin, Giacomo Ricci, Cristina Campi, Filippo Crimì, Marta Bergamo, Annibale Versari, Carmelo Lacognata, Federico Rea, Mattia Barbot, and Carla Scaroni

Introduction Cushing’s syndrome (CS), characterized by excessive endogenous cortisol secretion, is in most cases ACTH-dependent. Corticotropin (ACTH) secretion arises from a pituitary adenoma (Cushing’s disease) or, less frequently, from a non