Cushing Syndrome

Raff, Hershel

doi:10.1016/j.ecl.2014.10.005

Cited by 32 publications

(21 citation statements)

References 51 publications

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“…The presence of endogenous hypercortisolism and the possible source of Cushing syndrome-adrenal, pituitary, or ectopic-need to be established with a proper clinical history, detailed physical exam, and elaborate laboratory testing [1].…”

Section: Discussionmentioning

confidence: 99%

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PET imaging in ectopic Cushing syndrome: a systematic review

et al. 2015

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Cushing syndrome due to endogenous hypercortisolism may cause significant morbidity and mortality. The source of excess cortisol may be adrenal, pituitary, or ectopic. Ectopic Cushing syndrome is sometimes difficult to localize on conventional imaging like CT and MRI. After performing a multilevel thoracoabdominal imaging with CT, the evidence regarding the use of radiotracers for PET imaging is unclear due to significant molecular and etiological heterogeneity of potential causes of ectopic Cushing's syndrome. In our systematic review of literature, it appears that GalLium-based (Ga68) somatostatin receptor analogs have better sensitivity in diagnosis of bronchial carcinoids causing Cushing syndrome and FDG PET appears superior for small-cell lung cancers and other aggressive tumors. Further large-scale studies are needed to identify the best PET tracer for this condition.

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Section: Discussionmentioning

confidence: 99%

“…(b) If it is ACTH dependent, then is it from pituitary or ectopic (also called Ectopic ACTH Syndrome or EAS)? [1,2]. Ectopic CRH secretion is an extremely uncommon disorder with a very few cases reported, management and prognosis of which is similar to EAS [3].…”

Section: Introductionmentioning

confidence: 95%

PET imaging in ectopic Cushing syndrome: a systematic review

et al. 2015

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“…The salivary glands express corticosteroid 11β-dehydrogenase isozyme 2 (11β-HSD2), which converts cortisol into biologically inactive cortisone; in fact, salivary cortisone levels are 2- to 3-fold greater than salivary cortisol levels. Despite the greater analytical specificity of LC–MS/MS, we do not believe that it has clinical superiority [29, 30] and immunoassays may actually have better diagnostic sensitivity for the diagnosis of Cushing’s syndrome [31, 32]. Similar to UFC, salivary cortisol concentrations can be influenced by a variety of extrinsic factors such as food, exercise, smoking and various emotional/physical disturbances [33–35].…”

Section: Discussionmentioning

confidence: 99%

Late-night salivary cortisol may be valuable for assessing treatment response in patients with Cushing’s disease: 12-month, Phase III pasireotide study

et al. 2016

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Measuring salivary cortisol is a simple, convenient and accurate technique with potential value in monitoring patients with hypercortisolism. This analysis reports changes in late-night salivary cortisol (LNSC) during a 12-month, multicentre, Phase III study of patients with Cushing’s disease who were randomized to pasireotide 600 or 900 μg sc bid. LNSC assessment was an exploratory objective based on a single, optional measurement at midnight ± 1 h on the same day as one of the 24-h urinary free cortisol (UFC) measurements. Of 162 enrolled patients, baseline LNSC was measured in 93. Sixty-seven patients had levels above the upper limit of normal (ULN); median baseline levels were 19.7 and 20.7 nmol/L in the groups subsequently randomized to 600 μg (n = 40) and 900 μg (n = 27), respectively. Median LNSC levels decreased from baseline to month 12; median changes in patients who had baseline LNSC > ULN in the 600 and 900 μg groups were −13.4 nmol/L (–52.6 %; n = 19) and −11.8 nmol/L (–56.1 %; n = 14), respectively. LNSC normalized at months 6 and 12 in 25/67 (37.3 %) and 13/67 (19.4 %) patients, respectively; 10/25 and 8/13 patients also had normalized UFC, and 7/25 and 4/13 had partial UFC control (UFC > ULN and ≥50 % decrease from baseline). There was a moderate correlation (r = 0.55) on the log scale between individual patient LNSC and UFC values when all time points were pooled. Pasireotide decreased LNSC levels during 12 months of treatment. Salivary cortisol may be a simple, convenient biomarker for assessing treatment response in patients with Cushing’s disease.

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“…Algorithms used for the differentiation between EAS and CD are usually based on results of both imaging studies and biochemical tests (1,13). Classically, imaging studies are primarily directed at the pituitary gland in view of the prevalence of Cushing's disease (1, 52), while several biochemical tests, such as the CRH and high-dose dexamethasone test, are carried out to show differences in molecular equipment of EATs compared to pituitary corticotroph adenomas (134,135,136). However, pituitary MRI is associated with numerous false negative and positive results, and well-differentiated NETs may share molecular similarities with corticotropic pituitary adenomas, explaining overlapping responses to biochemical tests (see subsequent section).…”

Section: (B) Etiological Diagnosis (1) General Considerationsmentioning

confidence: 99%

MANAGEMENT OF ENDOCRINE DISEASE: Cushing’s syndrome due to ectopic ACTH secretion: an expert operational opinion

Young

Haissaguerre

Viera-Pinto

et al. 2020

European Journal of Endocrinology

153

186

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Ectopic ACTH syndrome (EAS) is rare but is frequently a severe condition because of the intensity of the hypercortisolism that may be dissociated from the tumoral condition. EAS should often be considered as an endocrine emergency requiring an emergency response both in terms of diagnostic procedures and therapeutic interventions. Patient management is complex and necessitates dual skills, in the diagnosis and treatment of CS and in the specific management of neuroendocrine tumors (NET). Therefore, initial management should be performed ideally by experienced endocrinology teams in collaboration with specialized hormonal laboratory, modern imaging platforms and intensive care units. Diagnostic procedures vary according to the endocrine and tumoral contexts but should be reduced to a minimum in intense hypercortisolism. Preventive and curative treatments of cortisol-induced comorbidities, non-specific management of hypercortisolism and etiological treatments should be considered simultaneously. Therapeutic strategies vary according to (1.) the intensity of hypercortisolism, the general condition of the patient and associated comorbidities and (2.) the tumoral status, ranging from resectable ACTH secreting tumors to non-resectable metastatic endocrine tumors or occult tumors. The ideal treatment is complete excision of the ACTH-secreting tumor that can be performed rapidly or after preoperative preparation using cortisol-lowering drugs. When this is not possible, the therapeutic strategy should be discussed by a multidisciplinary experienced team in a personalized perspective and include variable combinations of pharmacological agents, bilateral adrenalectomy and non-specific tumoral interventions. Here we discuss the diagnosis and therapeutic strategies including the modern, currently available tools and emphasize on the operational effectiveness of care.

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Cushing Syndrome

Cited by 32 publications

References 51 publications

PET imaging in ectopic Cushing syndrome: a systematic review

PET imaging in ectopic Cushing syndrome: a systematic review

Late-night salivary cortisol may be valuable for assessing treatment response in patients with Cushing’s disease: 12-month, Phase III pasireotide study

MANAGEMENT OF ENDOCRINE DISEASE: Cushing’s syndrome due to ectopic ACTH secretion: an expert operational opinion

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