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J Pediatr Endocrinol Metab ; 23(1-2): 179-87, 2010.
Article in English | MEDLINE | ID: mdl-20432821

ABSTRACT

BACKGROUND: CAH, most often due to a molecular defect in the 21-OH enzyme, results in inadequate cortisol production and subsequent life-long GC replacement. AIMS: To heighten awareness for risk of GIO in children with CAH including (1) ongoing assessment of GC dosing, (2) screening for bone health, and (3) prophylactic measures/early intervention once GIO is identified. PATIENT: 23 year-old male with 21OHD CAH referred for osteopenia. METHODS: Chart review; radiological, serological and urine assessment. RESULTS: Patient has old vertebral compression fractures and diminished BMD, the onset of which likely corresponds to excessive GC dosing during adolescence. CONCLUSION: As with other GC-dependent conditions, children with CAH may represent a previously unrecognized population at risk for GIO. Physicians need to be cognizant of the consequences of excessive GC dosing on bone health, especially during infancy and adolescence, critical periods for both linear growth as well as bone accretion.


Subject(s)
Adrenal Hyperplasia, Congenital , Bone Density , Bone Diseases, Metabolic , Osteoporosis/prevention & control , Spinal Fractures , Adrenal Hyperplasia, Congenital/diagnosis , Adrenal Hyperplasia, Congenital/epidemiology , Adrenal Hyperplasia, Congenital/metabolism , Bone Diseases, Metabolic/diagnostic imaging , Bone Diseases, Metabolic/epidemiology , Bone Diseases, Metabolic/metabolism , Fractures, Compression/diagnostic imaging , Fractures, Compression/epidemiology , Fractures, Compression/metabolism , Glucocorticoids/adverse effects , Humans , Male , Osteoporosis/chemically induced , Radiography , Risk Factors , Spinal Fractures/diagnostic imaging , Spinal Fractures/epidemiology , Spinal Fractures/metabolism , Steroid 21-Hydroxylase/metabolism , Young Adult
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