Condition: ACTH · Cushing's Syndrome · Sponsor: National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Between 10% and 15% of patients with endogenous hypercortisolism (Cushing syndrome) have ectopic (non-pituitary) production of adrenocorticotropin hormone (ACTH) that causes cortisol excess. In approximately 50% of these patients, the tumoral source of ACTH cannot be found initially despite very detailed and extensive imaging, including studies such as computed tomography, magnetic resonance imaging, and octreotide scan (Octreoscan) using the standard dose of indium- 111 pentetreotide (\[111In-DTPA-D-Phe\]-pentetreotide). The sensitivity and specificity of structurally based imaging studies depends on anatomic alterations and the size of the tumor. In contrast, positron emission tomography (PET) and somatostatin ligand imaging detect pathologic tissue based on physiologic and biochemical processes within the abnormal tissue. This protocol tests the ability of \[18F\]-L-3,4-dihydroxyphenylalanine (18F-DOPA) PET, and the somatostatin imaging analogue, 68Ga-DOTATATE-PET, to localize the source of ectopic ACTH production.
This description comes directly from the study's public registry record.
Raven N McGlotten, R.N. · (301) 827-0190 · mcglottenr@mail.nih.gov
Lynnette K Nieman, M.D. · (301) 496-8935 · niemanl@mail.nih.gov
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| National Institutes of Health Clinical Center | Bethesda, Maryland, United States | Recruiting |
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Source record: clinicaltrials.gov/study/NCT02019706