title: Reduced final height outcome in congenital adrenal hyperplasia under prednisone treatment: deceleration of growth velocity during puberty.
abstract: BACKGROUND
  Normal to decreased final height (FH) has been reported in patients with congenital adrenal hyperplasia (CAH).
  
  
  OBJECTIVE
  The objective was to determine FH outcome and influences of steroid treatment.
  
  
  METHODS
  The effects of glucocorticoid treatment for classical CAH were retrospectively studied in 125 patients (77 females). Growth pattern, FH, and pubertal development were recorded.
  
  
  RESULTS
  Corrected FH was in the lower range of genetic potential [females with simple virilizing (SV)-CAH, -0.6 +/- 1.0 sd score (SDS) vs. females with salt-wasting (SW)-CAH, -0.6 +/- 0.9 SDS; males with SV-CAH, -1.1 +/- 0.9 SDS vs. males with SW-CAH, -0.9 +/- 0.9 SDS]. Total pubertal growth was significantly reduced in comparison with a reference population (females with SV-CAH, 11.9 +/- 6.5 cm, and females with SW-CAH, 13.8 +/- 7.6 cm vs. reference 20.3 +/- 6.8 cm, P < 0.01; and males with SV-CAH, 15.4 +/- 6.6 cm, and males with SW-CAH, 18.5 +/- 6.9 cm vs. reference 28.2 +/- 8.2 cm, P < 0.01). Thirty-three patients had been treated with prednisone, which resulted in reduced FH compared with patients (n = 92) treated with hydrocortisone (-1.0 +/- 0.9 SDS vs.-0.6 +/- 0.9 SDS; P < 0.05). FH correlated negatively with hydrocortisone dose given at the start of puberty (r = -0.3; P < 0.05). Pubertal development started early in boys [9.8 +/- 2.3 yr (SV) and 10.6 +/- 1.9 yr (SW)] and was timely in girls [9.8 +/- 1.9 yr (SV) and 10.3 +/- 1.5 yr (SW), menarche at 13.3 +/- 1.7 yr (SV) and 13.7 +/- 1.5 yr (SV)].
  
  
  CONCLUSIONS
  Patients with CAH are able to achieve adequate FH with conventional therapy. Total pubertal growth is significantly decreased, and treatment with prednisone results in decreased FH. In addition to biochemical analysis, treatment should be adjusted to normal growth velocity, especially during puberty.
authors.affiliation: University Children's Hospital, Department of Endocrinology, Ludwig Maximilians University, Lindwurmstrasse 4, D-80337 Munich, Germany. wbonfig@web.de
authors.forename: Walter
authors.initials: W
authors.lastname: Bonfig
authors.forename: Susanne
authors.initials: S
authors.lastname: Bechtold
authors.forename: Heinrich
authors.initials: H
authors.lastname: Schmidt
authors.forename: Dietrich
authors.initials: D
authors.lastname: Knorr
authors.forename: Hans Peter
authors.initials: HP
authors.lastname: Schwarz
mesh_terms: D000293:Adolescent; D000312:Adrenal Hyperplasia, Congenital / Q000188:drug therapy* / Q000473:pathology*; D001827:Body Height / Q000502:physiology*; D015992:Body Mass Index; D001940:Breast / Q000254:growth & development; D002648:Child; D005260:Female; D006128:Growth / Q000187:drug effects* / Q000502:physiology*; D006728:Hormones / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000627:therapeutic use; D008297:Male; D011241:Prednisone / Q000627:therapeutic use*; D011627:Puberty / Q000502:physiology*; D012189:Retrospective Studies; D013255:Steroid 21-Hydroxylase / Q000235:genetics; D013737:Testis / Q000254:growth & development; D016896:Treatment Outcome
chemical_list: D006728:Hormones; D013255:Steroid 21-Hydroxylase; D011241:Prednisone; D006854:Hydrocortisone