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Published on BioPortfolio: 2018-05-21T18:19:10-0400
This study will test the ability of extended release nifedipine (Procardia XL), a blood pressure medication, to permit a decrease in the dose of glucocorticoid medication children take to ...
The purpose of this study is to develop a more physiological approach to the management of children and adolescents with salt wasting Congenital Adrenal Hyperplasia. We will administer th...
This is a multicenter Phase 2, multiple dose, dose escalation study to evaluate the safety, pharmacokinetics (PK), pharmacodynamics (PD), and efficacy of SPR001 in adult patients with clas...
This study was developed to determine if a combination of four drugs (flutamide, testolactone, reduced hydrocortisone dose, and fludrocortisone) can normalize growth in children with conge...
This is a Phase 2 multicenter, single-blind, multiple dose study to evaluate the safety and efficacy of orally administered ATR-101 in subjects with classic congenital adrenal hyperplasia ...
Congenital adrenal hyperplasia (CAH) patients are at risk for life-threatening adrenal crises. Management of illness episodes aims to prevent adrenal crises.
The objective of this study was to investigate the initial presenting features of children with classical congenital adrenal hyperplasia (CAH).
Non-classical congenital adrenal hyperplasia (NC-CAH) is a recessive autosomal disease caused by a deficiency of adrenal steroidogenesis enzymes. It must be distinguished from classical CAH, either si...
Management of congenital adrenal hyperplasia (CAH) involves suppression of the hypothalamic-pituitary-adrenal (HPA) axis using supraphysiological doses of exogenous glucocorticoids. This can pose a ch...
Salt wasting syndrome (hyponatremia, hyperkalemia, dehydration, metabolic acidosis) in early infancy could be caused by either mineralocorticoid deficiency as in congenital adrenal hyperplasia (CAH) a...
An adrenal microsomal cytochrome P450 enzyme that catalyzes the 21-hydroxylation of steroids in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP21 gene, converts progesterones to precursors of adrenal steroid hormones (CORTICOSTERONE; HYDROCORTISONE). Defects in CYP21 cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL).
A mitochondrial cytochrome P450 enzyme that catalyzes the 11-beta-hydroxylation of steroids in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP11B1 gene, is important in the synthesis of CORTICOSTERONE and HYDROCORTISONE. Defects in CYP11B1 cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL).
A group of inherited disorders of the ADRENAL GLANDS, caused by enzyme defects in the synthesis of cortisol (HYDROCORTISONE) and/or ALDOSTERONE leading to accumulation of precursors for ANDROGENS. Depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. The most common defect is in STEROID 21-HYDROXYLASE. Other defects occur in STEROID 11-BETA-HYDROXYLASE; STEROID 17-ALPHA-HYDROXYLASE; or 3-beta-hydroxysteroid dehydrogenase (3-HYDROXYSTEROID DEHYDROGENASES).
Neoplasm derived from displaced cells (rest cells) of the primordial ADRENAL GLANDS, generally in patients with CONGENITAL ADRENAL HYPERPLASIA. Adrenal rest tumors have been identified in TESTES; LIVER; and other tissues. They are dependent on ADRENOCORTICOTROPIN for growth and adrenal steroid secretion.
A microsomal cytochrome P450 enzyme that catalyzes the 17-alpha-hydroxylation of progesterone or pregnenolone and subsequent cleavage of the residual two carbons at C17 in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP17 gene, generates precursors for glucocorticoid, androgen, and estrogen synthesis. Defects in CYP17 gene cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL) and abnormal sexual differentiation.