View clinical trials related to Adrenocortical Hyperfunction.
Filter by:Background: The adrenal glands are 2 small organs that sit on top of each kidney. They release hormones; these are chemicals that control how the body works. Tumors on or outside the adrenal glands are called functional if they release hormones; they are called nonfunctional if they do not. Doctors who treat adrenal tumors need to know which type a person has. Researchers want to find better ways to learn whether an adrenal tumor is functional. Objective: To see if a new radioactive tracer ([68Ga]Ga-PentixaFor) can make it easier to identify functional adrenal tumors with positron emission tomography (PET) scans. Eligibility: People aged 18 years and older with 1 or more adrenal tumors. They must have increased levels of the hormones aldosterone or cortisol. They must also be enrolled in at least 1 other related NIH study (protocols 19-DK-0066, 18-CH-0031, or 09-C-0242). Design: Participants will be screened. They may have imaging scans. Their ability to perform normal activities will be reviewed. Participants will have one PET scan with the study tracer. The tracer will be given through a tube attached to a needle inserted into a vein. Participants will receive the tracer 1 hour before the scan. They will lie still on a bed while a machine captures images of the inside of their body. The scan will take 45 to 90 minutes. Participants heart rate, blood pressure, and rate of breathing will be checked before, during, and after the scan. Participants will have a follow-up visit 3 days after their scan. This visit can be by phone, email, or in person.
This cross-sectional, single-center study will assess the microvascular function using a nailfold video-capillaroscopy in patients with endogenous Cushing syndrome.
The congenital adrenal hyperplasias (CAHs) comprise a family of autosomal recessive disorders that disrupt adrenal steroidogenesis. Three specific enzyme deficiencies are associated with virilization of affected women. The most common form is 21-hydroxylase deficiency (21-OHD) due to mutations in the 21-hydroxylase (CYP21A2) gene. Other virilizing forms include 3b-hydroxysteroid dehydrogenase type 2 (HSD3B2) and 11b-hydroxylase deficiencies associated with mutations in the HSD3B2 and 11b-hydroxylase (CYP11B1) genes, respectively.