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1 emia due to pituitary corticotroph adenomas (Cushing disease).
2 tary adenomas in 80% of patients with proven Cushing disease.
3 rbances mimicking hypercortisolism caused by Cushing disease.
4 nomously, resulting in hypercortisolemia and Cushing disease.
5 ctive pituitary targeted pharmacotherapy for Cushing disease.
6 gnaling may be a novel strategy for treating Cushing disease.
7 EGFR might provide a therapeutic target for Cushing disease.
8 but the long-term survival of patients with Cushing disease after transsphenoidal surgery has not be
12 etrospective analysis included patients with Cushing disease (CD) but prior negative or inconclusive
14 ne (ACTH) secretion from a pituitary tumour (Cushing disease (CD)) or non-pituitary tumour (ectopic A
15 s (PitNETs) of the corticotroph type lead to Cushing disease (CD), a condition associated with signif
16 pling of the petrosal sinuses to distinguish Cushing disease from the ectopic adrenocorticotropic hor
17 for paediatric patients with prolactinomas, Cushing disease, growth hormone excess causing gigantism
18 ntral to peripheral ACTH were diagnostic for Cushing disease (> 2 before administration of CRH and >
21 , we discuss challenges in the management of Cushing disease in adults and provide information to gui
22 ell as a handful of other cases of infantile Cushing disease in the literature, suggests that feature
26 ors in 43 patients (20 pheochromocytomas, 13 Cushing disease or syndrome, and 10 others), nonfunction
27 rgery, and clinical outcome in patients with Cushing disease, particularly those with repeated negati
28 Other management approaches are required if Cushing disease persists or recurs following surgery, in
29 rom 16 of 20 patients with surgically proven Cushing disease (sensitivity, 80% [95% CI, 56% to 96%]).
30 rom 19 of 20 patients with surgically proven Cushing disease (sensitivity, 95% [CI, 75% to 99%]).